close

Enter

Log in using OpenID

FOR WHOLESALE BANKING CUSTOMERS USE ONLY Indication

embedDownload
Intern Handbook
1998 – 2000
References Available from Medical Education
What follows is a compilation of various
references, which may be useful,
educational or amusing.
*****************************************
INTERN'S CREDO
There's no admission like
no admission.
Anonymous
*****************************************
2
THE HOUSE OFFICER'S 15 LAWS OF HOSPITAL PRACTICE...........................................................................11
THE HOUSE OFFICER'S 10 LAWS OF OUTPATIENT PRACTICE ......................................................................11
THE HOUSE OFFICER'S FIVE RULES FOR LAB TESTS ....................................................................................11
SIX MEDICAL TRUISMS .........................................................................................................................................11
10 MEDICAL CLICHES ...........................................................................................................................................11
OCCUPATIONAL HAZARDS FOR PHYSICIANS PRACTICING IN THE UNITED STATES................................12
THE LECTURER (POEM)........................................................................................................................................12
WHAT IS THE SINGLE MOST IMPORTANT SKILL TO LEARN EARLY IN YOUR RESIDENCY? .....................12
CARDIAC ARREST -- VF & PULSELESS VT* .......................................................................................................13
CARDIAC ARREST -- PULSELESS ELECTRICAL ACTIVITY..............................................................................13
CARDIAC ARREST -- ASYSTOLE .........................................................................................................................14
CARDIAC DYSRHYTHMIAS ...................................................................................................................................18
SINUS BRADYCARDIA...........................................................................................................................................18
SINUS TACHYCARDIA ...........................................................................................................................................18
SUPRAVENTRICULAR EXTRASYSTOLE .............................................................................................................18
ATRIAL FLUTTER, ATRIAL FIBRILLATION .........................................................................................................18
CODE DRUGS ACLS ..............................................................................................................................................19
ANTI-ARRHYTHMICS .............................................................................................................................................20
VASODILATOR DRUGS .........................................................................................................................................21
DOPAMINE INFUSION ............................................................................................................................................21
ATRIOVENTRICULAR (AV) HEART BLOCK DURING ANESTHESIA .................................................................22
SUPRAVENTRICULAR (SV) TACHYCARDIA .......................................................................................................22
SV-TACHYCARDIA WITH PREEXCITATION-SYNDROME (WPW, LGL) ............................................................22
BRADYCARDIA DYSRHYTHMIA AND AV-BLOCK ..............................................................................................22
BRADYCARDIA AND HYPOTENSION IN THE PRESENCE OF BETA-BLOCKADE ..........................................22
VENTRICULAR DYSRHYTHMIA ............................................................................................................................22
PROLONGED QT-INTERVAL .................................................................................................................................22
3
VENTRICULAR EXTRASYSTOLES CAUSED BY DIGITALIS INTOXICATION ...................................................22
VENTRICULAR FIBRILLATION..............................................................................................................................23
DIGITALIZATION.....................................................................................................................................................23
DIGITALIS INTOXICATION .....................................................................................................................................23
LOWN CLASSIFICATION .......................................................................................................................................23
SWAN GANZ CATHETER.......................................................................................................................................23
'7-3' - RULE FOR FLUID MONITORING.................................................................................................................24
MEDICAL HISTORY-TAKING IN THE MODERN ERA ..........................................................................................24
HISTORY, PHYSICAL, & NOTES ...........................................................................................................................25
MEDICAL HISTORY (ALTERNATIVE) ...................................................................................................................27
PHYSICALEXAMINATION ......................................................................................................................................28
CARDIAC PHYSICAL EXAM SIGNS ......................................................................................................................31
MINI-MENTAL STATUS EXAM ...............................................................................................................................32
PROGRESS/SOAP NOTE (NON-ICU) ....................................................................................................................33
PROGRESS NOTE (ICU).........................................................................................................................................33
OPERATIVE NOTE..................................................................................................................................................34
PROCEDURE NOTE................................................................................................................................................34
DISCHARGE SUMMARY ........................................................................................................................................34
LABOR AND DELIVERY H&P ................................................................................................................................34
DELIVERY NOTE (EXAMPLE)................................................................................................................................35
INCOMPLETE ABORTION ADMIT ORDERS.........................................................................................................35
PREGNANCY AND DRUGS TO BE AVOIDED-.....................................................................................................35
APGAR SCORE.......................................................................................................................................................35
NEONATAL/BIRTH H&P .........................................................................................................................................36
PRIMITIVE REFLEXES OF INFANCY ....................................................................................................................36
PEDIATRIC H&P......................................................................................................................................................36
ESTIMATING BODY SURFACE AREA IN CHILDREN..........................................................................................37
4
ABBREVIATED PSYCH HISTORY .........................................................................................................................37
MENTAL STATUS EXAM:.......................................................................................................................................37
ABBREVIATED NEUROLOGICAL EXAM..............................................................................................................38
GLASGOW COMA SCALE .....................................................................................................................................38
DERMATOMES, ANTERIOR VIEW ........................................................................................................................39
DERMATOMES, POSTERIOR VIEW ......................................................................................................................40
EKG LEADS.............................................................................................................................................................42
MEDICAL ORDERS.................................................................................................................................................42
SIGN-OUT NOTE .....................................................................................................................................................43
DISCHARGE ORDERS............................................................................................................................................43
PRESENTING PATIENTS .......................................................................................................................................43
ACUTE PAIN MANAGEMENT ................................................................................................................................44
EVIDENCE BASED..................................................................................................................................................47
CENTRAL LINES: PLACEMENT AND PROBLEMS..............................................................................................49
DRAIN MANAGEMENT ...........................................................................................................................................50
NASOGASTRIC TUBE MANAGEMENT.................................................................................................................52
NEEDLE STICKS AND OTHER EXPOSURES TO BLOOD AND BODY FLUIDS ................................................52
WOUND COMPLICATIONS ....................................................................................................................................52
PROCEDURES ........................................................................................................................................................53
GRAM STAIN ...........................................................................................................................................................54
FLUIDS & ELECTROLYTES ...................................................................................................................................55
NORMAL PHYSIOLOGIC VALUES ........................................................................................................................55
ACID-BASE DISORDERS .......................................................................................................................................57
NORMAL LAB VALUES..........................................................................................................................................58
ACID-BASE..............................................................................................................................................................62
APPROACH TO INTERPRETING ACID-BASE STATUS ......................................................................................62
ARTERIAL BLOOD GAS LECTURE SLIDES ABGS.............................................................................................63
5
ACUTE RESPIRATORY FAILURE LECTURE SLIDES ARF.................................................................................82
HYPERCALCEMIA ..................................................................................................................................................96
HYPERKALEMIA.....................................................................................................................................................98
HYPERNATREMIA ..................................................................................................................................................99
HYPOKALEMIA .................................................................................................................................................... 100
HYPOMAGNESEMIA............................................................................................................................................ 101
HYPONATREMIA ................................................................................................................................................. 102
HYPOPHOSPHATEMIA ....................................................................................................................................... 103
MAGNESIUM TOXICITY....................................................................................................................................... 103
CONVERSIONS EQUATIONS ............................................................................................................................. 104
RENAL FUNCTION............................................................................................................................................... 104
ACUTE RENAL FAILURE .................................................................................................................................... 104
OLIGURIA (SUDDEN)- ......................................................................................................................................... 107
ACUTE TUBULAR NECROSIS (ATN) ................................................................................................................. 108
CHRONIC RENAL FAILURE................................................................................................................................ 109
MYOCARDIAL ISCHEMIA.................................................................................................................................... 111
MYOCARDIAL INFARCTION (MI) ....................................................................................................................... 115
THE USE OF BETA-BLOCKERS FOR ACUTE MYOCARDIAL INFARCTION ................................................. 117
RECOMMENDED IV DOSAGE OF BETA-BLOCKERS FOR PATIENTS WITH ACUTE MYOCARDIAL
INFARCTION ON ADMISSION ............................................................................................................................ 117
THROMBOLYTIC AGENTS IN ACUTE MYOCARDIAL INFARCTION .............................................................. 117
CONTRAINDICATIONS TO THROMBOLYSIS ................................................................................................... 118
CONGESTIVE HEART FAILURE (CHF) .............................................................................................................. 118
DIASTOLIC HEART FAILURE (DHF) .................................................................................................................. 122
TORSADES DES POINTES (POLYMORPHIC VT) ............................................................................................. 123
PULMONARY ARTERY CATHETERIZATION .................................................................................................... 123
HEMODYNAMIC EXAMPLES .............................................................................................................................. 126
SWAN GANZ CATHETER WAVE FORMS.......................................................................................................... 127
6
GOLDMAN MULTIFACTORIAL CARDIAC RISK INDEX (MCRI)....................................................................... 128
HYPERTENSIVE CRISIS-..................................................................................................................................... 128
HYPERTENSIVE CRISIS AND SPECIFIC DRUG THERAPY- ............................................................................ 129
AORTIC DISSECTION:......................................................................................................................................... 130
SUBARACHNOID HEMORRHAGE: .................................................................................................................... 130
ISCHEMIC STROKE:............................................................................................................................................ 130
ISCHEMIC HEART DISEASE OR MYOCARDIAL INFARCTION: ..................................................................... 130
LEFT VENTRICULAR FAILURE:....................................................................................................................... 130
HYPERADRENERGIC STATES........................................................................................................................... 130
ECLAMPSIA: ........................................................................................................................................................ 130
POST-OPERATIVE HYPERTENSION: ............................................................................................................... 130
ACUTE RENAL INSUFFICIENCY:....................................................................................................................... 130
PERICARDITIS- .................................................................................................................................................... 133
CARDIAC TAMPONADE- .................................................................................................................................... 134
CAUSES OF ORTHOSTATIC HYPOTENSION:................................................................................................. 137
CHRONIC OBSTRUCTIVE PULMONARY DISEASE.......................................................................................... 140
DIFFERENTIAL DIAGNOSES OF PULMONARY ABNORMALITIES ................................................................ 146
PULMONARY FUNCTION TESTING PFT ........................................................................................................... 148
PULMONARY EMBOLISM LECTURE SLIDES(DR. GOFF) .............................................................................. 152
TB MYCOBACTERIUM TUBERCULOSIS........................................................................................................... 164
TEN RULES FOR READING CHEST X-RAYS.................................................................................................... 165
CHEST RADIOGRAPHY LECTURE BY DR. GOFF............................................................................................ 166
RULES ON OXYGEN THERAPY -- WHAT EVERY HOUSE OFFICER.............................................................. 182
SIGNS OF OBVIOUS BREATHING (WOB) ......................................................................................................... 183
THE FOUR MOST IMPORTANT EQUATIONS IN CLINICAL PRACTICE.......................................................... 183
NORMAL RANGES FOR VENTILATORY VALUES ........................................................................................... 189
PLEURAL EFFUSIONS ........................................................................................................................................ 190
7
ABDOMINAL PAIN ............................................................................................................................................... 196
CHARACTERISTIC PHYSICAL FINDINGS IN THE ACUTE ABDOMEN........................................................... 196
GASTROINTESTINAL BLEEDING (ACUTE UPPER)-........................................................................................ 197
ALCOHOLISM ...................................................................................................................................................... 199
ALCOHOLIC WITHDRAWAL-.............................................................................................................................. 201
ALCOHOL-............................................................................................................................................................ 201
VIOLENT PATIENTS- ........................................................................................................................................... 202
RANSON'S CRITERIA: FOR DETERMINING PROGNOSIS OF ACUTE PANCREATITIS ............................... 203
MODIFIED CHILD'S INDEX FOR GRADING SEVERITY OF LIVER DZ ........................................................... 203
ACUTE BLINDNESS ............................................................................................................................................ 203
ACUTE DYSTONIC REACTION........................................................................................................................... 204
SEIZURES............................................................................................................................................................. 205
STATUS EPILEPTICUS........................................................................................................................................ 208
LUMBAR PUNCTURE TESTS ............................................................................................................................. 208
CSF ANALYSIS .................................................................................................................................................... 209
STROKE RISK FACTORS AND PREVENTION THERAPY................................................................................ 209
COMA (COMMON CAUSES)- .............................................................................................................................. 210
ANTIBIOTICS & INFECTIOUS DISEASE ............................................................................................................ 210
HIV & AIDS STATS, ETC ..................................................................................................................................... 211
DIARRHEA............................................................................................................................................................ 214
ANTIRETROVIRAL (AIDS) AGENTS, DAILY DOSAGE AND MAJOR TOXICITIES -....................................... 214
PROPHYLAXIS OF OPPORTUNISTIC INFECTIONS AIDS ............................................................................... 215
CDC RECOMMENDATIONS FOR REDUCING PERINATAL HIV TRANSMISSION ......................................... 216
FEVER CLUES- DIAGNOSTIC SIGNIFICANCE BY MAGNITUDE OF THE TEMPERATURE: ..................... 217
FEVER OF UNKNOWN ORIGIN- FUO................................................................................................................ 218
HEAT STROKE..................................................................................................................................................... 219
NEUROLEPTIC MALIGNANT SYNDROME- ....................................................................................................... 220
8
MENINGITIS- COMMON CAUSES OF MENINGITIS BY AGE: ...................................................................... 221
DIABETIC KETOACIDOSIS DKA ........................................................................................................................ 225
DIFFERENTIAL DIAGNOSIS DKA HNKC ........................................................................................................... 225
HEMOGLOBIN A1C [GLYCOHEMOGLOBIN] AND BLOOD GLUCOSE ......................................................... 228
THYROID DISEASE INTRODUCTION................................................................................................................. 229
THYROTOXIC CRISIS-......................................................................................................................................... 231
THYROID STORM ................................................................................................................................................ 231
ADRENAL INSUFFICIENCY- ............................................................................................................................... 231
ANTICOAGULATION TREATMENT .................................................................................................................... 232
ANTICOAGULANT INR RECOMMENDATIONS FOR VARIOUS SITUATIONS-............................................... 233
BLEEDING DISORDERS- .................................................................................................................................... 234
BLOOD TRANSFUSION COMPLICATIONS-...................................................................................................... 234
MEDICAL EVALUATION OF SURGICAL RISK .................................................................................................. 236
THROMBOEMBOLISM PROPHYLAXIS IN SURGICAL PROCEDURES .......................................................... 239
ANTIBIOTICS FOR ENDOCARDITIS PROPHYLAXIS ....................................................................................... 240
POISONING .......................................................................................................................................................... 241
ACETAMINOPHEN TOXICITY- ............................................................................................................................ 241
CARBON MONOXIDE POISONING- ................................................................................................................... 242
CIGUATERA FISH POISONING- ......................................................................................................................... 244
ANAPHYLAXIS..................................................................................................................................................... 244
SCABIES-.............................................................................................................................................................. 245
ACUTE ARTHRITIS .............................................................................................................................................. 246
PRESSURE ULCERS IN ADULTS: ..................................................................................................................... 247
PULMONARY BEDSIDE REFERENCE ............................................................................................................... 251
ENDOTRACHEAL TUBE PLACEMENT .............................................................................................................. 253
MASSIVE HEMOPTYSIS (ANY OF THE BELOW) .............................................................................................. 253
GUIDELINES FOR FLUID CHALLENGES BY CVP OR PCWP ......................................................................... 255
9
EVIDENCE BASED MEDICINE LECTURES ....................................................................................................... 256
WORKSHEET FOR USING AN ARTICLE ABOUT THERAPY OR PREVENTION........................................... 274
WORKSHEET FOR USING AN ARTICLE ABOUT ASSESSING DIAGNOSTIC TESTS................................... 291
WORKSHEET FOR USING AN ARTICLE ABOUT PROGNOSIS ...................................................................... 293
WORKSHEET FOR USING AN ARTICLE ABOUT CAUSATION OF HARM..................................................... 294
WORKSHEET FOR USING AN ARTICLE ABOUT AN ECONOMIC ANALYSIS............................................... 298
WORKSHEET FOR USING AN ARTICLE REPORTING VARIATIONS IN THE OUTCOMES OF HEALTH
SERVICES............................................................................................................................................................. 300
INDEX.................................................................................................................................................................... 302
10
THE HOUSE OFFICER'S 15 LAWS OF HOSPITAL PRACTICE
(http://www.mtsinai.org/pulmonary/books/house/rules-a.html)
1. (Wherever you are . . .) if it happens here it happens everywhere.
2. Money not spent on the terminally ill will not go to feed hungry children. (This law is a corollary of: money not spent on
military hardware . . .)
3. There is always family. When a patient is admitted with "no family" you just haven't found them yet.
4. When a consensus is needed for DNR status, there's always a key family member who is out of town.
5. If you order a CAT scan and a weight measurement on the same patient at the same time, the former will be done and
charted before a scale is found.
6. Hospitalized patients can invariably be divided into two distinct groups. One group wants to go home as soon as
possible and the other group never wants to leave.
7. The medical literature deals with patients who have only one disease. Most of your patients have more than one
disease.
8. The number of layers of clothing through which the chest is auscultated directly correlates with the house officer's level
of training.
9. After a patient is in the hospital for three days no one will know the patient's complete list of medications.
10. Any chart note worth writing is worth being legible; if a peer can’t quickly and easily read it, it might as well not have
been written.
11. If God wanted us to have plastic tubes we'd be born with them: use it or remove it.
12. Dyspnea in a hospitalized patient is never due to anxiety. If a physician attributes dyspnea to anxiety the physician is
either a fool or has completed an exhaustive workup for causes of dyspnea. Most of the time the physician is a fool.
13. The top three causes of fever in a hospitalized patient are: infection, infection, and infection.
14. When you assume another cause of fever remember the previous law.
15. In 1920 about 90% percent of all diagnoses were made with just a thorough medical history; in the 1990s the
percentage is the same. Ditto for the next century.
THE HOUSE OFFICER'S 10 LAWS OF OUTPATIENT PRACTICE
1. A drug proven effective after multi-center trials costing millions of dollars doesn't work very well if patients don't take it.
2. No study has ever shown that an outpatient can reliably ingest more than three drugs for more than three weeks.
3. No study has even shown the efficacy of more than three drugs taken simultaneously.
4. The drugs you think your patient is taking are never exactly the same as what your patient is taking.
5. Drugs for which blood monitoring is necessary should be avoided unless unequivocally needed - they all have a narrow
therapeutic window. Examples: theophylline, digoxin, coumadin, procainamide.
6. The more complicated your patient, the more likely your patient is seeing other physicians for the same or related
problems.
7. Outpatients can invariably be divided into two groups: those with no questions, and those who always have one more
question.
8. An appointment every three months for a patient with two or more diseases taking two or more medications is about as
helpful as no appointment at all.
9. Often the best treatment for a patient with chronic disease is the doctor's phone number.
10. You will be retired before your hospital's outpatient department implements a really useful record keeping system.
THE HOUSE OFFICER'S FIVE RULES FOR LAB TESTS
(NOTE: chest x-rays have their own set of rules)
1. Don't order a test if the outcome will have no effect on the management of your patient.
2. If the ordering of a lab test is equivocal, pretend you are the one paying for it. Then make your decision.
3. If a test result surprises you because it is abnormal, consider repeating it or obtaining a complementary test (e.g., CRP
for
ESR). If the test is abnormal a second time believe it.
4. Only people can lie. Lab tests are not people. Lab tests don't lie.
5. A hundred things can screw up a lab test result, from improper labeling to improper data transcription. The better you
know your patient the better you will recognize a screw up.
SIX MEDICAL TRUISMS
1. Not all asthmatics wheeze. However, finding a dyspneic asthmatic "without wheezing" usually means the patient was
not auscultated during forced expiration (I question this. / Dr.Goff.).
2. Daily weights are seldom accurate because no one pays for them. A "weight service" that could charge per patient
would maintain the scales and provide accurate daily weights.
3. Chronic complainers, hypochondriacs and Munchausen patients can contract the same diseases as everyone else.
4. The most underrated piece of medical equipment is the fax machine.
5. American hospitals have 19th century record keeping systems because they spend 19th century dollars on the problem.
6. An on-time patient deserves an on-time doctor.
10 MEDICAL CLICHES
(Some of which are true some of the time)
11
10. Not charted not done.
9. Doctors make the worst patients.
8. Doctors' relatives have the most complications.
7. Doctors are lousy investors.
6. Only nice people get cancer.
5. Nasty people don't get bad diseases.
4. See one, do one, teach one.
3. Doctors bury their mistakes.
2. The patient is the one with the disease.
1. If something can go wrong, it will.
Occupational Hazards for Physicians Practicing in the United States
(Other countries may present different infectious disease risks; hazards are listed alphabetically)
AIDS - Rare, but AIDS transmission from a patient's blood has been documented
Assault- including murder - particularly at risk are ED physicians and psychiatrists who see patients with psychosis or a
character disorder
Asthma - mainly from formaldehyde, among pathologists
Infectious hepatitis - particularly among surgeons
Non-infectious hepatitis - mainly from halothane, among anesthesiologists
Sclerotherapist's conjunctivitis - endoscopists occasionally squirt their eyes with sclerotherapy chemical
Stress and burnout - all physicians at risk, and of course the problem is not unique to the medical profession
Substance abuse - risk increased because of easy access to drugs
Suicide - rate is definitely higher in some medical specialties (e.g., psychiatry) than in the general population
Tuberculosis - particularly among physicians who work with multi-drug resistant TB
THE LECTURER (poem)
Tell us what we need to know.
Please don't bore us with your show.
Your slides, dear sir, put one to sleep.
The words you use are way too deep.
The problem, alas, is clear to see,
You address a special fraternity.
Who know the line, arcane reference;
But none of them in this audience.
Solution? None, I fear.
You're too insensitive to hear
What all of us show so well.
You've simply lost us, truth to tell.
Polite we'll be and clap the end.
And hide the message we wish to send.
Applause is for one reason, true
Thank God, dear sir, you are through!
1. Determine the question
2. Establish urgency (emergent, urgent, elective)
3. Look for yourself (not everything is in the chart)
4. Be brief (short notes, <= 5 recommendations)
5. Be specific (spec drugs, mode of admin, duration,)
6. Provide contingency plans
7. Honor thy turf (discuss with surgeon before
patient)
8. Teach...with tact
9. Talk is cheap...and effective (call requesting MD
and discuss the findings)
10. Follow-up (if needed)
What is the Single Most Important Skill to Learn Early in Your Residency?
"How to take a history,"
"How to talk to patients,"
"How to write orders,"
"How to obtain DNR," or "
How to Interpret a Chest x-ray/EKG/blood smear, etc."
12
My answer is:
How to perform Advanced Cardiac Life Support or "ACLS."
If you don't know ACLS, basically what to do in a life-threatening cardiac emergency, and how to do it, the patient can die
within minutes. All other skills mentioned are obviously important, and in the career of most physicians will no doubt be
much more useful than knowing ACLS.
ACLS, taught in an intensive one or two day course, is now a requirement of virtually all hospital residents (it is also
required of all ICU and CCU nurses). ACLS certification is good for two years, at which time the course is taken again.
While the various cardiac treatment algorithms change somewhat over time, the basics do not. You need to know how to
quickly insert a peripheral intravenous line and ventilate an apneic patient with a bag-valve mask device (AMBU bag). You
need to know how to intubate, should that become necessary. (In many hospitals an always-available, in-house
anesthesiologist intubates chest team patients. If your hospital is set up this way, fine.) You need to know where the
defibrillator is kept, how to use it, what drugs to use for which arrhythmias and, not least important, when to stop. You
need to feel comfortable when a chest team is called. You need to know enough so that if the patient doesn't survive, it is
not because you didn't know something, but because there was nothing else to do.
Cardiac Arrest -- VF & Pulseless VT*
ABCs
Initiate basic CPR
Attach defibrillator
Defibrillate at 200 Joules
Defibrillate at 300 Joules
Defibrillate at 360 Joules
Continue CPR
Intubate
IV Access
Epinephrine 1 mg IV push
may repeat 3-5 min; may use higher doses
Defibrillate 360 J after every dose
Lidocaine 1.5 mg/kg IV push
may repeat 3-5 min, up to 3 mg/kg
Defibrillate 360 J after every dose
Bretylium 5 mg/kg IV push
may repeat 5 min at 10 mg/kg
Defibrillate 360 J after every dose
Continue: Drug-Shock-Drug-Shock, etc.
________
Cardiac Arrest -- Pulseless Electrical Activity
ABCs
Initiate Basic CPR
Intubate
IV Access
Consider Possible Causes while checking for blood
flow with Doppler Ultrasound
HYPOVOLEMIA
HYPOXIA
CARDIAC TAMPONADE
TENSION PNEUMOTHORAX
HYPOTHERMIA
PULMONARY EMBOLISM
DRUG OVERDOSE
HYPERKALEMIA
ACIDOSIS
MYOCARDIAL INFARCTION
Epinephrine 1 mg IV push
Atropine 1 mg IV push
13
Cardiac Arrest -- Asystole
ABCs
Initiate CPR
Intubate
IV access
Confirm asystole in more than one monitor lead
Consider possible causes:
HYPOXIA
HYPERKALEMIA
HYPOKALEMIA
ACIDOSIS
DRUG OVERDOSE
HYPOTHERMIA
Consider transcutaneous pacing (available on some defibrillator models)
Epinephrine 1 mg IV push
Atropine 1 mg IV push
Anti-Arrhythmic Drugs:
Beta-Blockers:
Calcium Antagonists:
14
15
16
17
Cardiac Dysrhythmias
_______________________
Sinus Bradycardia
Atropine
Isoprenaline
Pacemaker
Sinus Tachycardia
Rectify cause
Beta Blocker (in the presence of Coronary
Heart Disease (CHD))
Digitalis (Heart failure)
Supraventricular Extrasystole
Digitalis (in the presence of CHD with hemodynamic disturbances)
Beta-Blocker (Attention: Heart Failure)
Quinidine
Atrial Flutter, Atrial Fibrillation
Verapamil (Isoptin) 2.5mg iv as a Bolus, max. 7.5mg for awake patients (see below)
Beta-Blocker (Attention: Do not combine with Verapamil)
Propafenone
Cardioversion / Defibrillation in the presence of hemodynamic disturbances
Chronic: Digoxin, Quinidine
18
Code Drugs ACLS
19
Anti-Arrhythmics
20
Vasodilator Drugs
Dopamine Infusion
21
Atrioventricular (AV) Heart Block during Anesthesia
Reduce frequency: Adrenaline 5mcg IV repeat Bolus
Increase frequency: Phenylephrine 50-100mcg IV if hypotensive
Esmolol 100 - 200 mg iv if normotensive
Supraventricular (SV) Tachycardia
Propranolol: 1 - 10 mg i.v., in 0.5 - 1 mg increments
Verapamil: 2.5 mg iv as a Bolus, max. 7.5 mg for awake patients.
Attention: Volatile agents can cause Myocardial depression
Propafenone
Cardioversion / Defibrillation
SV-Tachycardia with Preexcitation-Syndrome (WPW, LGL)
Valsalva Maneuver, Aortic pressure / Carotid pressure
Procainamide: 1.5mg/kg IV (in the presence of VHF and WPW: Cardioversion)
Propafenone: 1mg/kg iv
Verapamil (see above)
Propranolol: 1-10mg i.v., in 0.5 - 1mg increments
Attention: No Digitalis,
Do note combine Beta-Blockers and Verapamil!
Bradycardia Dysrhythmia and AV-Block
Atropine: 0.5-1mg i.v.
Isoprenaline: Start with 0.5 - 5mcg/min i.v.
Pacemaker
Bradycardia and Hypotension in the presence of Beta-Blockade
Atropine: 0.5-1mg IV
Isoprenaline: Start with 0.5 - 5mcg/min IV
Pacemaker
Calcium (as Inotrope)
Aminophylline: 4 - 6mg/kg i.v.
Glucagon: (5 - 10mg)
Ventricular Dysrhythmia
Hypoxemia ?, Hypercapnia ?, Myocardial
Ischaemia ?, Central Catheter ?, Hypokalemia ?,
Digitalis Intoxication ?
Lidocaine Bolus: (1 mg/kg) i.v., Infusion 1 – 4 mg/min, Procaine
Propafenone: 35 mg i.v. or
Propranolol: 0.5 mg i.v. repeated
Potassium (Aim: > 4mmol/l)
Magnesium
Prolonged QT-Interval
Attention: No Succinylcholine - it lengthens QT!
Possibly aforementioned Beta block, possibly
aforementioned left Stellate (ganglion) block
Thiopental for induction
Avoid: Lidocaine, Procainamide, Quinidine
Ventricular Extrasystoles caused by Digitalis Intoxication
22
Lidocaine 1mg/kg iv
Beta-blocker
Magnesium
Alternative : Phenytoin (Epanutin) 3.5 - 5mg/kg IV (max. 50mg/min)
Ventricular Fibrillation
See: Resuscitation (REA) Figure
DIGITALIZATION
Quick saturation: 0.25 - 0.5 (-1.0) mg slowly iv, then in 4 - 6 hourly intervals 0.25 - 0.5 mg iv
Medium saturation: 1.0 to 1.5 mg po, then every 6 hours 0.25 mg po until compensation
Slow saturation: 0.5 - 1.5 mg po daily, divided into a number of single doses
Maintenance: 0.125 - 0.75 mg po/ day
Therapeutic plasma concentration: 0.5 - 2.0 ng/ml
Reduce dosage in the presence of :
Kidney insufficiency, liver insufficiency, pulmonary heart disease, CHD, Hypothyroidism, Medicines (Erythromycin,
Tetracycline, Quinidine, Verapamil, Spironolactone, Amiodarone), Acidosis, Hypoxia.
Rule: Reduce digoxin dose by same % as reduction in clearance!
Contra-indications: AV-Block 2. В° Or 3. В°, Sinus Bradycardia, Sinus-Arrest, Hypokalemia, WPW-Syndrome
DIGITALIS INTOXICATION
Indications: AV - Blocks, Ventricular Extrasystoles
(VES), Sinus Tachycardia (ST) decreasing
Plasma level: toxic > 3 ng/ml
Laboratory: Potassium, Magnesium, Calcium,
Creatinine-Clearance, ABGA
Therapy:
Remedy Hypokalemia / Hypoxia
Lidocaine
Atropine
Phenytoin (Epanutin) 3.5 - 5 mg/kg iv (max. 50 mg / min)
Digitalis anti-bodies (FAB-Fragments)
Digitalis antidote BM (Attention: Extremely expensive); use your knowledge of approximate glycoside levels in the
body to decide dose: 80 mg Digitalis (Digibind) antibodies bind 1 mg Digoxin. If glycoside levels unknown,
administer ca. 6 injection bottles (Demand 24-hour duty from clinical pharmacology !)
Beta-blocker
LOWN Classification
I
II
III
IVa
IVb
V
< 30 PVC/h
> 30
Multifocal PVCs
PVCs in runs
Ventricular tachycardia
R-on-T phenomenon
SWAN GANZ Catheter
Possible Indications:
Unstable angina pectoris
23
Left trunk stenosis (> 90%) or equivalent (prox. RIVA + prox. Circumflex.)
Acute myocardial infarction
Complications from a MI (VSD, Mitral insuff.)
Poor LV Function (EF < 30%)
Two-valve surgery
Replacement of the mitral valve
Apparent cardiac insufficiency
Severe pulmonary arterial hypertension (at rest)
Repeat heart operation
Major vascular surgery
'7-3' - Rule for fluid monitoring
Initial PCWP Fluid
< 10 mmHg 200 ml in 10 minutes
10-15 mmHg 100 ml in 10 minutes
> 15 mmHg 50 ml in 10 minutes
Reaction Therapy
PCWP increases > 7 mmHg Stop
PCWP increases 3 - 7 mmHg Wait 10 minutes
Always > 3 mmHg Stop
PCWP increases < 3 mmHg more fluid
MEDICAL HISTORY-TAKING IN THE MODERN ERA
The "art" of history taking means getting the story in as complete a fashion as possible, so that you learn what is worth
knowing. What is worth knowing includes: 1) the sequence of events that culminated in placing the patient before you; 2)
an understanding of the patient's complaint, and 3) an appreciation of the patient as a human being. It does no good to
learn every detail of the HPI if you are clueless about the patient's anxieties, fears, and perceptions. Similarly, you may be
the most empathic, perceptive doctor around, but if you don't know who treated the patient last week and for what, or don't
know the medications your patient is taking and why, you won't be very effective.
SUMMARY: The history should be logical, complete, and answer all questions the reasonable reviewer might ask. To
learn what is bothering the patient, you must care about, and listen to, the patient.
Unfortunately, the house officer's response in many situations is all too often, "The patient is a poor historian," a response
that suggests it is the patient's obligation to render a well-organized, coherent history! In fact, labeling the patient a poor
historian often signifies one thing only: the physician is not trained to assemble a comprehensive history.
Instead of blaming the patient for an inadequate history, emphasis should be on the vitally important "verifiable past
medical history." Verifiable PMH covers events one can document, usually meaning specific past medical contacts
(doctor, emergency room, pharmacy, laboratory, radiology department, etc.). Pity the poor house officer who, after
spending an hour with a patient eliciting every nuance of her vague symptoms, has failed to learn of a recent complete
evaluation at another hospital for the same complaints! (Oh? Then why didn't the patient say so? Simple: because the
house officer didn't ask.)
It is amazingly common that patients we see in the hospital, the ER, or the outpatient clinic, have verifiable, recent medical
history pertinent to their current problem(s): lab tests; x-rays; office visits to other physicians; pharmacy prescriptions;
hospital discharge summaries; workers' compensation records; operative reports. It is also amazingly common how often
this verifiable history goes undetected by the treating house officer.
You will be amazed how often your patients have been treated and evaluated for the same problems you are treating
them for; or how often they are taking medications pertinent to their current problem which they "forgot" to tell you about.
When you learn that important verifiable information exists, take advantage of those modern medical tools the phone and
fax machine and work to get the information.
Questions Regarding Verifiable Medical History
What physicians have you seen in the past year? Where? What for?
When was the last time you saw a doctor for any reason? And the time before that?
Have you had any operation in the past 5 years? Have you spent the night in a hospital in the last 5 years?
Have you visited an emergency room or urgent care center in the last 5 years?
24
Have you seen a podiatrist, chiropractor, or psychologist recently?
When was the last time you had a prescription filled? Do you remember what it was for? What drugs do you take? What
else do you take? What else do you take when these drugs don't work?
Where do you get your medicine? Where else do you get your medicine?
The task may not be easy. Say you've learned that verifiable information does exist, and you've requested it be sent via
fax. How long should you wait for it to arrive? Not long. You can minimize delays by remembering three rules.
Rule 1: Always record the name and phone number of the person you speak with, the one who agrees to send you the
information.
Rule 2: Records mailed will never arrive in time to help an already-hospitalized patient. They must be faxed or,
alternatively, important information relayed verbally over the phone.
Rule 3: Since record-keeping departments are often under-staffed and chaotic, the best intentions may not result in the
records being sent to you. The record personnel may forget the request, or their fax machine may be inoperable, or the
old records may not be found. After a reasonable wait (a few hours at most) call back: "Hello, this is Dr. Jones. I spoke
with you earlier about records on my patient, Mr. Smith. We still haven't received those records. Have they been sent?
Oh? Well, we need to make some important decisions; could you please fax them now?"
Summary: Don't blame the patient for an inadequate medical history. Always assume verifiable past medical history exists
and work hard to find out what and where it is. If you need prior records, find out where they are and set out determinedly
to obtain them. Be polite but aggressive.
Summary: No one pays doctors for time-consuming, high-quality history taking. Nonetheless, it stands to reason that the
more thorough your history, the better will be your care of the patient.
HISTORY, PHYSICAL, & NOTES
Introductory Sentence
This sentence should include the number of hospital admissions or clinic visits followed by the patient's age, race, parity,
sex, occupation, and the patient's chief complaint or complaints (C.C.) in his own words.
Source
Source of history and assessment of reliability.
Present Illness
The present illness should be told in chronological sequence with reference to calendar date or time prior to admission,
outlining the course of the illness from its beginning. Expound on each symptom thoroughly and its course. Previous
treatment and hospitalizations should be noted; identify all significant medications received. Items of past medical history,
family history, occupational history or social history that might have a bearing on the present illness should be included.
Any symptoms suggested by the clinical picture, which are not present, should be noted and denied, i.e. "pertinent
negatives".
Past Medical History PMH
General Health: Patient's general health throughout life.
Childhood Health: General health and development. Note important deviations. Also, specifically mention acute febrile
illnesses
of childhood.
Medical Illnesses: List and/or describe all illnesses requiring hospitalizations or a physician's care.
Give dates.
Operations and Injuries: Describe briefly and date each operation. Identify the hospital and surgeon, if known. Give dates
of
severe lacerations, head trauma, sprains, broken bones, or gunshot wounds.
Describe sequelae.
Medications: List all prescription and OTC medications including dosages.
Allergies and Immunizations: Record all known allergies, specifically allergies to drugs.
Remark on the state of immunization of the patient.
Family History
25
Ask about diseases in parents, siblings, and children including present age, age at death, and the cause of death where
applicable.
Specific diseases to be asked about are: cancer, diabetes, gout, Tb, bleeding disorders, arthritis, anemia, hypertension,
migraine headaches, allergies, mental or nervous disorders, or diseases of the cardiovascular system.
Personal and Social History
Inquire about: alcohol use (quantity and type), smoking (how much, how long), unusual drug habits, occupation, economic
status, leisure activities, home, family and marital history.
Review of Systems
Skin: moisture, temperature, color, texture, changes in hair or nails, itching, rashes, lesions
Head: headache, head injury
Eyes: vision, glasses, pain, photophobia, proptosis, diplopia, scotomata, lacrimation, inflammation, infection, discharge
Ears: hearing acuity, pain, tinnitus, vertigo, infection, discharge
Nose: head colds, discharge, epistaxis, obstruction, sinus pain, anosmia
Mouth & Throat: lesions in mouth, tongue or lips, pain in mouth or tongue, condition of teeth and gums, sore throats,
postnasal discharge, speech difficulty, hoarseness
Neck: stiffness, pain, limitations of motion, goiter, swelling
Breasts (both sexes): pain, swelling, discharge, masses
Respiratory: cough sputum (character, amount), hemoptysis, chills, fever, night sweats, dyspnea, wheezing, asthma, pain,
pleurisy, bronchitis, and pneumonia
CVS: cyanosis, exertional dyspnea, paroxysmal nocturnal dyspnea, edema, palpitations, irregular rhythm, precordial pain
(character, radiation, duration, location; relation to exercise, posture, eating, effect of medication), known hypertension,
heart disease, or lipid disorder, claudication, varicose veins, phlebitis
GI: appetite, food intolerance, dysphagia, belching, water-brash, heart-burn, sour stomach, nausea, vomiting,
hematemesis, rectal pain, hemorrhoids, jaundice, hernia, "gas" (flatus, belching, borborygmus), change in bowel habits
(regularity, frequency, laxative use), stools (color, consistency, size, shape, odor, bloody or tarry), epigastric distress (rel.
to meals, relief by antacids, belching or food), abdominal pain (loc. & radiation; sharp, knife-like, colicky, dull, aching,
gnawing; constant or intermittent; severity; relationship to eating, defecation, urination or menstruation; relieved by
belching, vomiting, doubling up, defecation, urination, enema or drugs)
GU: dysuria, urgency, frequency, nocturia, polyuria, incontinence, hesitancy, dribbling, size of stream, retention, oliguria,
anuria, smoky urine, hematuria, pyuria, back or CVA pain, history of UTI, stones or gravel, gonorrhea and syphilis by
name or symptoms
OB-GYN: age of menarche, menses (freq., regularity, duration, amount, dysmenorrhea, recent changes in cycle, passage
of clots, intermenstrual bleeding), menopause (spontaneous or surgical, date, complications, subsequent vaginal
bleeding), vaginal discharge, genital lesions, infertility, past use of birth control pills, pregnancies (number, abortions,
complications)
Bones, Joints, and Muscles: pain, tenderness, swelling, stiffness limitations of movement, previous injuries and
deformities
Endocrine: general (weight change, easy fatigability, behavioral changes), diabetes (polyuria, polydipsia, infections),
change in size of features, hands, feet, impotence, decrease in libido, change in body hair or distribution, thyroid disease
(goiter, heat or cold intolerance, sweating, exophthalmos, tremor, skin and hair changes)
Neurological: syncope, convulsions, unconsciousness, dizziness, vertigo, ataxia, tremor, weakness, paralysis,
incoordination, pain, numbness, paresthesias, difficulty with speech or swallowing, difficulty with bladder or bowel control,
localized or generalized symptoms Psychiatric: rapid changes in mood, memory loss, phobias, hallucinations, antisocial
behavior, sleep disturbances, previous emotional illness and treatment
Physical Examination
General Appearance: A brief sentence to characterize the overall appearance of the patient including body habitus,
muscular development, nutrition, and whether the patient appears to be of stated age, acutely ill, in acute distress, pain,
dyspneic, coughing, etc.
Vital Signs: ht, wt, (percentiles and FOC in pediatrics), temp, blood pressure (which arm and whether supine, sitting, or
standing), pulse, and respiration.
Skin: hands, nails, hair; color, pigmentation, texture, moisture, temperature, and lesions.
Lymph Nodes: posterior auricular, submaxillary, cervical, epitrochlear, axillary, and inguinal.
Head: symmetry, deformities, skull size, scars, tenderness, tumors, or lesions.
Eyes: visual acuity and fields, exophthalmos, EOM, nystagmus, strabismus, inflammation, discharge, conjunctivae, sclera,
corneal scars, opacity, ulcerations, arcus. Iris (iridectomy or lesions). Pupil size, regularity, equality, and reaction to light
and accommodation (PERRLA). Lens (cataract, or dislocation).
Fundi: disc (color, margins, cupping, and papilledema); vessels (size, tortuosity, AV nicking); hemorrhages, exudates, or
lesions.
Ears: hearing acuity, symmetry, tenderness, discharge, perforation, tophi; Weber, and Rinne test results.
Nose: deformity, septal deviation or perforation, obstruction, mucosa (discharge, bleeding, polyps).
Mouth and Throat: lips and mucous membranes (colors, lesions), tongue (size, color, papillae, lesions). Teeth and gums.
Soft Palate. Uvula. Tonsils and pharynx (inflammation, exudate, and tonsillar size).
Neck: symmetry, scars, ROM, stiffness, tenderness; thyroid (size, symmetry, nodules, and tenderness); trachea midline;
JVD, carotid pulses; masses.
26
Spine: curvature, symmetry, mobility, tenderness.
Chest: shape, symmetry, respiratory excursions, masses, tenderness, fremitus, percussion, rales, rhonchi, breath sounds,
egophony, wheezes, friction rubs.
Heart: heart sounds, rhythm, precordial heave or thrill, PMI location and character, pulsations, enlargement, murmurs
(intensity, timing, location, and radiation), rubs and gallops.
Breast: shape, retractions, discharge, masses, tenderness, scars.
Abdomen: contour, scars, striae, venous pattern, abnormal movements; auscultation for bowel sounds (frequency and
character) and bruits; percussion for liver and splenic dullness, ascites (shifting dullness); palpation for liver, spleen,
kidneys, bladder, colon, masses, aortic pulsations; CVA tenderness, abdominal tenderness (direct and rebound), hernias.
Genitalia: Male--size and development of penis and testes, hydrocele, varicocele, masses, discharge, lesions. Female-External genitalia, Bartholin's glands, urethral orifice, clitoris, cystocele, rectocele, prolapse, vaginal or cervical discharge,
lesions, bleeding, cervix, uterus, adnexa, or masses (note size, location, mobility, and tenderness), Pap smear.
Rectal: hemorrhoids, fissures, ulcerations, bleeding, sphincter tone, masses, tenderness, prostate, and stool for occult
blood test. Extremities: atrophy, tremor, clubbing, edema, redness, tenderness, limitation of joint motion, deformities.
Neurological: mental status, behavior, alertness, orientation, mood, memory (recent and remote), speech; gait, Romberg,
cranial nerve function, muscle (coordination, strength, tremor, abnormal movements), sensation (light touch, pin prick,
temperature, position, vibration, two point discrimination), reflexes (abdominalis, cremasteric, biceps, triceps, radials,
Hoffman, patellar, Achilles, plantar), clonus. Stick figures are helpful for reflexes.
Summary
One or two sentences that contain only those points of the history and physical which contribute directly to the
establishment of a diagnosis.
Problem List Numbered in order of importance, include date of entry.
Impression List of tentative diagnosis based on the history and physical exam to explain the problems noted under the
problem list. This section should express your impressions diagnostically as to possible explanations for the problems
found and most importantly why you feel these diagnoses should be considered. Likewise, reasons you feel certain
disease processes are operative should also be discussed.
Plan Record all planned diagnostic and therapeutic procedures and plan for education of the patient based on the
problem list generated.
MEDICAL HISTORY (alternative)
A. Identification and Vital Statistics
1. Name, (residence), age; birth date, place of birth where relevant
2. Nationality, race, marital status, occupation where relevant
3. Informant- relationship to patient, name
B. Chief Complaint(s) - problem/condition that motivated patient to seek care-duration
C. Present Illness
1. Symptoms and pertinent negatives
2. Onset and duration; associations with specific events
3. Character and quality of condition
4. Current level of activity and degree of disability
D. Past Medical History
1. General Health- lifetime summary, list of relevant risk factors
2. Infectious Diseases- dates, complications, therapies
3. Operations, Injuries- names, dates, operative diagnoses
4. Previous hospitalizations- dates and names of hospitals
5. Transfusion History
E. Medications - names, doses, allergies
F. Review of Systems
1. Integument
a. Skin: color, pigmentation, temperature, moisture, lesions, pruritus, scaling, bleeding
b. Hair: hair color, texture & distribution
c. Nail: color, changes, brittleness, ridging, pitting, clubbing
2. Lymph Nodes - enlargement, pain, suppuration, draining sinuses, location
3. Connective Tissue
a. Bones: fractures, dislocations, sprains,
b. Joints: arthritis, pain, swelling, stiffness, migratory distribution, degree of disability
c. Muscles: weakness, wasting, atrophy, pain, night cramps
4. Hematopoietic System
a. Anemia (type, therapy, response)
b. Bleeding (spontaneous, traumatic, familial, transfusions
c. Lymphadenopathy, Infections
5. Endocrine
27
a. General : history of growth, body configuration and weight, head, and feet
b. hair distribution, skin pigmentation, dryness of skin and hair
c. Thyroid: goiter, exophthalmos, heat or cold intolerance, tremor
d. Diabetes: polyphagia, polydipsia, polyuria, glycosuria
e. Secondary sex characteristics, impotence, sterility, treatment
6. Allergic/Immunologic System
a. Vaccinations and immunizations
b. Vasomotor rhinitis, asthma, hay fever,
c. Dermatitis, urticaria, angioneurotic edema, conjunctivitis, eczema
d. Seasonal incidence of the foregoing, known sensitivity to pollen, food, drugs,
e. Previous skin tests & results, desensitization, serum injections
f. TB test results
7. Head- headaches, migraines, trauma, vertigo, syncope, convulsive seizures
8. Ears- deafness, tinnitus, vertigo, discharge, pain, mastoiditis, operations
9. Eyes- visual loss, color blindness, diplopia, hemianopsia, trauma, inflammation, glasses
10. Nose- coryza, rhinitis, sinusitis, discharge, obstruction, epistaxis, frequency of colds
11. Mouth- soreness, symptoms referable to teeth
12. Throat- hoarseness, sore throats, tonsillitis, voice changes
13. Neck- swelling, lymph node character, goiter, stiffness, range of motion
14. Breasts
a. Development, lactation, gynecomastia
b. Trauma, lumps, pain, nipple discharge and/or changes
15. Respiratory System
a. Dyspnea: nocturnal, rest, exertional, orthopnea, pain, and cyanosis
b. Wheezing, cough, sputum, night sweats, pleurisy, bronchitis, smoking
c. Pneumonia, hemoptysis, other respiratory infections, tuberculosis (exposure)
16. Cardiovascular System
a. Chest pain, shortness of breath, exertional, rest, smoking, hypertension
b. Palpitation, tachycardia, irregular rhythms, cyanosis
c. Exercise tolerance, edema, ascites, and claudication
d. Cardiac Drugs, rheumatic fever, syphilis, diphtheria
e. Cold extremities, phlebitis, postural or permanent skin color changes
f. Cocaine abuse, other recreational drug abuse
17. Gastrointestinal System
a. Appetite, changes in weight, dysphagia, flatulence, abdominal pain or colic
b. Nausea, vomiting, diarrhea, constipation, frequency, consistency
c. Hematemesis, jaundice (pain, fever, duration, color of urine)
d. Stools - color, frequency, consistency, odor, gas, cathartics), hemorrhoids
e. Change in bowel habits.
18. Genitourinary System
a. Urine: color, polyuria, oliguria, nocturia, dysuria, hematuria, pyuria, urinary retention, frequency,
incontinence, pain, passage of stones or gravel.
b. Menstrual history - age at onset, frequency, regularity, duration, amount of flow, leukorrhea,
dysmenorrhea, date of last period, date & character of menopause, postmenopausal bleeding.
c. Pregnancy history -number, abortions, miscarriages, stillbirths, chronologic sequence,
complications.
d. Venereal history - chancre, buboes, papillomas, penile discharge, treatment
19. Nervous System
a. Cranial Nerves - disturbance of smell or vision, orofacial paresthesias and chewing difficulty,
facial
weakness, disturbed hearing and/or equilibrium, difficulty with speech, swallowing and/or taste,
limited neck motion.
b. Motor system - paralyses, atrophy, involuntary movements / seizures, gait, coordination
c. Sensory system - pain, lightning pain, girdle pain, paresthesia, hypesthesia, anesthesia
d. Autonomic system - control of urination and defecation, sweating, erythema, cyanosis, pallor,
reaction
to heat and cold.
20. Psychiatric History
a. Reactions to and influences of parents, siblings, spouse, children, friends and associates
b. Sexual adjustments, successes and failures, illnesses, lability of mood, hallucinations
c. Grandiose ideas, nervous breakdowns, sleep disturbances
PHYSICALEXAMINATION
A. General
28
1. Overall appearance, nutritional status, weight, height
2. Communication skills, behavior, awareness, orientation, cooperation with examination
B. Vitals
1. Blood pressure, pulse, respiratory rate, temperature
2. Oxygen saturation where indicated
C. Skin
1. Color, integrity, texture, temperature, hydration, diaphoresis, edema
2. Lesions
3. Hair, nails
D. Head
1. Size, contour, scalp appearance, symmetry and spacing of facial features
2. Edema, puffiness, erythema, other lesions
E. Eyes
1. Appearance of orbits, conjunctivae, sclerae, eyelids, eyebrows
2. Extraocular movements,
3. Corneal light reflex
4. Pupil shape, consensual response to light (and accommodation)
5. Visual fields (acuity optional)
6. Ophthalmoscopic findings
a. Retina, optic disc, macula
b. Retinal vessel size, caliber, arteriovenous crossings (optional cornea, lens findings)
F. Ear
1. Configuration, position, and alignment of auricles
2. Otoscopic findings: canals and tympanic membrane
3. Hearing Assessment
a. Weber Test: base of vibrating tuning fork on vertex midline of head
• normally hear sounds best in both ears
• if better in one ear, then sound is lateralized
• occlude this ear with finger and repeat the test
• sound lateralized to deaf ear in conductive loss, to better ear in sensorineural loss
b. Rinne Test: base of vibrating tuning fork on mastoid
• time the interval until sound no longer heard
• then move fork to place vibrating tines with 1-2cm of auditory canal
• normally, hearing is ~2X longer with air than bone
• conductive loss: bone heard longer than air; sensorineural air is less than 2X bone
G. Nose
1. External appearance, nasal patency, discharge, crusting, flaring
2. Internal Exam: appearance of turbinates, polyps, septal alignment
3. Presence of sinus swelling or tenderness, odor discrimination
H. Throat/Mouth
1. Appearance of lips, tongue, buccal and oral mucosa
2. Condition of teeth, presence of dental appliances
3. Floor of mouth, pharynx, tonsils, hard and soft palates, uvula
4. Gag reflex, voice quality
I. Neck
1. Mobility, suppleness (range of motion), strength, trachea position
2. Thyroid size, shape, tenderness, anomalies (eg. masses)
3. Lymphadenopathy, swollen salivary glands
J. Chest
1. External Appearance
a. Anteroposterior diameter
b. Symmetry of movement with respiration, respiratory rate, use of accessory muscles
2. Auscultation
a. Air movement
b. Abnormal sounds - rales (crackles), rhonchi, wheezes, stridor, rubs
K. Breasts
1. External Appearance: Symmetry, masses, scars, discharge, dimpling, erythema
2. Palpation: Tenderness, thickening, masses
3. Lymph node examination: esp axillary
L. Cardiac
1. Surface location of apical impulse, rate, rhythm, amplitude
2. Contour and symmetry of apical impulse and pulse in extremities
3. Comparison between extremities
4. Findings on auscultation
a. Characteristics of S1 and splitting of S2
b. Presence of murmurs: first listen for systolic murmurs, then diastolic (usually quieter)
c. Gallops: suspect S4 in young persons, or hypertension, or hypertrophic cardiomyopathy
d. Suspect S3 in systolic congestive heart failure, low ejection fraction
29
e. Clicks (synthetic valve), snaps (mitral valve prolapse)
5. Signs of Heart Failure
a. Jugular venous distention
b. Hepatojugular reflux
c. Peripheral edema
d. Presence of S3 gallop
6. Signs of Vascular Disease
a. Presence of carotid, abdominal, renal, or femoral bruits
b. Strength of distal pulses, temperature of extremities
M. Abdomen
1. Shape, contour, visible aorta pulsations
2. Auscultation findings (Bowel Sounds)
a. Normal
b. Normal pitch, hyperactive: gaseous distension, partial obstruction
c. High pitch: partial or complete mechanical obstruction
d. Decreased or absent: ileus (functional obstruction), peritonitis, perforation
3. Palpation findings
a. Each of four quadrants
b. Pelvic area
c. Costovertebral angle
d. Spleen - not a sensitive test in low risk patients
4. Percussion findings
a. Liver - total span
b. Spleen
N. Rectum / Anus
1. External Structures
a. Hemorrhoids, fissures, skin tags
b. Sphincter control: "Anal Wink" test
2. Rectal Digital Examination
a. Rectal wall contour, tenderness, prostate size, contour and consistency
b. Color and consistency of stool, occult blood
O. Genitalia
1. Female
a. Appearance, pubic hair, external genitalia
b. Palpation findings
c. Vaginal speculum exam: appearance, lesions, discharge (Pap smear)
d. Bimanual findings: size, tenderness of uterus, adnexa and ovaries
2. Male
a. Appearance, circumcision status, location and size of urethral opening
b. Discharge, lesions, pubic hair, palpation findings
c. Scrotum: hernia, scrotal swelling, pain
P. Extremities
1. Temperature, color, hair distribution, skin texture and nails of lower extremities, edema,
2. Swelling, venous distention,
3. Evaluation of Thrombosis: tenderness, erythema, cord, Homans' sign
4. Pulses:
a. Radial pulse, (brachial pulse)
b. Femoral, Dorsalis pedis and posterior tibial pulses, (Popliteal Pulse)
Q. Neurologic
1. Cranial Nerves (findings for each or specify those tested)
2. Cerebellar and motor function (gait, balance, coordination)
3. Sensory function and symmetry
4. Deep tendon reflexes (symmetry and grade)
5. Mental status (thought processes, cognitive function, speech and language)
R. Musculoskeletal
1. Alignment of extremities and spine, symmetry of body parts
2. Muscle strength
3. Joints
a. Joint appearance, deformities
b. Range of motion passive and active, presence of pain, tenderness, crepitus
S. Lymphatic
1. Size, shape, tenderness, discreetness, mobility
2. Presence in neck, epitrochlear, axillary, or inguinal areas
30
CARDIAC PHYSICAL EXAM SIGNS
PULSES:
Paradoxes: fall in BP >10 w/inspiration
-seen in Tamponade & Obstructive Lung Dz.
Pulsus Parvus: weak upstroke due to decreased stroke volume(hypovolemia, LV-failure, AS, MS
Pulsus Tardus: delayed upstroke (AS)
APICAL IMPULSES:
-Lat & Downward: LV dilatation
-Prominent Presystolic Impulse: HTN, AS, Hypertrophic Cardiomyopathy
-Double Systolic Apical Impulse: Hypertrophic cardiomyopathy
HEART SOUNDS:
S1: shutting of mitral valve
Very Loud: MS
Very Soft: CHF, MR, COPD
S2: Closing of the Aortic Valve
Wide Split: MR, Pulm Stenosis
Fixed Split: ASD
Narrow Split: Pulm HTN
Paradoxical Split: narrow sw/inp: AS
Loud A2: systemic HTN
Soft A2: AS
Loud P2: Pulm Art Htn
Soft P2: Pulm Stenosis
S3: Rapid Ventricular Filling heard best w/bell @ apex nml in kids. In Adults indicated Volm
Overload
S4: Atrial Contraction w/reduced vent contraction heard best w/bell @ apex reflects noncompliant
Ventricle heard in AS, HTN, ischemic & HTN cardiomyopathy
Opening Snap: Mitral Valve Opening follows S2 heard @ LLSB (in MS) (apex in MS):
MURMERS
SEM: related to blood flow across semiLunar valves: "midsystolic" + Spaces between S1 & S2
PANSYSTOLIC: no space between S2: Occurring w/regurgitant flow across AV valves.
EARLY DIASTOLIC: typically w/regurgitant flow Across incompetent semilunar valves
AS: Loud Crescendo / Decrescendo (SEM)
- heard best @ base & rad to neck
- increase w/ squatting
- decrease w/ Valsalva, standing
- Late slow rising carotid upstroke w/ decreased intensity
- strong apical impulse
- narrow pulse pressure(in severe AS)
MR: Holosystolic w/radiation to axilla
- increase w/ squatting
- decrease w/ Valsalva, standing
- no correlation between intensity of murmur & severity of MR
** LOUD S1
AI: Low Pitched Early Diastolic murmur Immediately after S2
- early SEM
- high pitched
- widened pulse pressure(sig > SBP)
- Bounding pulses
- Water Hammer pulse @ wrist w/ rapid rise & sudden collapse
- Capillary pulsation @ nail bed base
** absent or diminished S1
PI: same as AI
MS: Mid-to-Late Diastolic: low pitched
-increase w/ L lat position or cough
-diastolic rumble & opening snap
- accentuated S1
31
MINI-MENTAL STATUS EXAM
EYE SIGNS IN NEURO EXAMINATION
Frontal Eye Fields: in each lobe
normally: Rt side moves eyes to Lt
Lt side moves eyes to Rt
Lesion: eyes deviate toward area of
32
lesion.
Dolls Eyes: Oculocephalic Reflex
(valid only if pt unconscious)
Nmlly: eyes move opp of head mvt
Lesion: front eye fields: can't move
eyes away on head mvt on
side of lesion
brainstem: can't move bilat
PUPILS:
Asymmetrical: idiopathic or Trauma
Pinpoint: Pontine lesion
Oval (other one=pinpoint): midbrain
--occulomotor N. damage
Argyle-Robinson: No light Reflex w/ intact accommodation
Optokinetic Reflex: move stripped tape to Lt - nml eyes w/nystagmus to right
Calorics:
Cold water: nystagmus away
Warm water: nystagmus same side
Cold in both ears: nystagmus up
Warm in both ears: nystagmus down
In COMA: cold H2O: slow deviation to side of stim- may fixate
ICP: papiledema
no venous pulsations
check for increased blind spot
MLF: (from ?MS vs DM)
opposite eye stops @ midline on lateral gaze / converges normally
Progress/SOAP Note (non-ICU)
Hospital day #__ Postop day #__ Antibiotic day #__
Subjective: how the patient feels, new complaints, continuing
complaints,
dizziness, pain, bowel movement, flatus, nausea, vomiting, etc.
Objective:
Vital signs
PE by system including any surgical wounds
Labs
Studies (CXR, MRI, EEG, etc.)
Assessment: List each problem and its current status, eg
#1 IDDM--still poorly control, patient doesn't understand
disease
#2 HTN--well controlled on current meds
Plan: What are you going to do? eg:
#1--increase insulin to 30 units NPH q am, will contact
diabetic teaching for education
#2--continue current meds and doses
Progress Note (ICU)
System oriented. Objective, assessment
and plan done for each system in turn.
Vitals (can include weight, growth esp. if pedi)
Meds: list all medications pt is on
Systems: Remember you have 11 systems in alphabetical order and you'll do great:
A/B: airway, breathing, vent settings, apneic episodes, ABG's, pO2 by pulse ox, etc.
CVS: heart, pulses
CNS ("Da brain"):
F/E/N: fluids, electrolytes, nutrition (include I/O’s, TPN and residuals, Chem. 7 (lytes))
GI: abdominal exam, pertinent studies, BM's, flatus, guaiac
Heme: jaundice, CBC with differential, PT/PTT, etc.
ID: infectious disease (include antibiotics, peak and trough levels, fever status, etc.)
33
Joints/Bones/Muscles:
Kidney:
Lines: List each and number of days it has been in place, whether local erythema, etc.
Skin: rashes, decubitus ulcers
Grade I = superficial
Grade II = subcutaneous
Grade III = muscle exposed
Grade IV = bone exposed
Operative Note
Date of procedure:
Procedure performed:
Pre-op diagnosis:
Post-op diagnosis:
Surgeon:
Assistant(s):
Type of anesthesia:
Anesthesiologist:
Pump Time(if applicable):
Clamp Time(if applicable):
Findings:
Specimen(s):
Tubes/drains: (NG, ETT, Foley, wound drains)
EBL: estimated blood loss, ask anesthesiologist
Fluids in: type and amount
Fluids out: eg. urine output, NG drainage
Complications: (if not "none", a resident/attending should be writing this note)
Pt's condition/disposition (eg. pt transferred to RR awake, extubated and stable)
Procedure Note
Procedure: type, date, time, indications, who performed
Consent form: explained, signed, and on chart
Description: Pt draped and prepped in a sterile manner. Local anesthesia achieved with ...
Findings: Describe fluid withdrawn, specimens sent to lab or pathology, how pt tolerated.
Complications: (if there are complications, best to have resident or attending write the procedure note)
Discharge Summary
Dictated by ____, medical student, for ____, MD/DO on ____(date)
Patient name, medical record number
Admit date, admit diagnosis
Discharge date, discharge diagnosis
Date and type of surgery, procedure(s) this admission
Brief summary of pt's history & physical
Summary of hospital course
Pathology reports (if any)
Disposition: discharge medications, follow-up instructions, discharged to home/nursing home/etc., discharge diet
and activity
Copies to:
Repeat dictated by ____ for ____ on ____(date)
Pt name and medical record number
Labor and Delivery H&P
CC: age, race, female, gravida, parity
Dates: LMP, CGA and EDD by dates, with ultrasound on
date, and CGA by scan
Current labor: presents with contractions (regularity, interval, duration, radiation to back, associated fever, vaginal
bleeding, mucus show, SROM, meconium
Prenatal history:
34
prenatal care: where, since date, # of visits, EGA at first visit
prenatal screening labs (on POPRAS) should include following and dates:
PAP smear; CBC; UA; ABO; Rh; antibody screen; GTT glucose screen, PRP; rubella titer; HSsAg titer; urine cx;
chlamydia cx.
Medications: prenatal vitamins (PNV), Fe, other prescription meds
Complications: substance abuse (alcohol, tobacco, IVDA); UTI's HTN; DM; gestational DM; PIH; large babies; h/o
twins; h/o congenital anomalies
Past OB history: for each pregnancy (not each child) note date of birth, location, sAb/tAb/c-section/NSVD/forceps;
at gestational age; anesthesia used; fetal sex; weight; complications
Past GYN history: age at menarche, interval, duration, flow, regularity use of contraceptives; h/o STD's treatment
Past Med hx: highlight DM, HTN, asthma, renal disease, hepatitis
Past Surg hx: procedure, age, location, surgeon, complications; any trauma
Social hx: tobacco, alcohol; IVDA, animal exposure (Toxo)
Family hx: medical hx; birth complications
PE: vital signs, head to toe, and including Extremities: reflexes, edema are important
Fundal height, Fetal heart tones (type of monitor, BTBV,
rate, reactivity, decels), Pelvic exam: dilation/efface/present/station/membranes eg.
dilation = FT to 10 cm
efface = 0 to 100%
present = vertex, breech (footling or frank), LOA, ROA, etc.
station = +3 to -3
membranes = intact, SROM/AROM, time of rupture, +meconium A/P:
1) Term IUP in active labor
2) Routine labor room care and admitting lab work
3) Expectant management
Glucose Screening in OB--glucose screening between 24 and 28 weeks gest.
Fasting 100 mg/dl
1 hour after 50-gm glucose load 135
2 hour after 100-gm glucose load 140 if a fasting, or 1 hour,
or 2 hour screening Serum Glucose level is above, order a 2 hour or
3 hour Glucose Tolerance Test
Delivery Note (example)
Diagnosis: Term IUP s/p NSVD over a 2o MLE with extension to 3o
Anesthesia: epidural/local with 3-5 cc anesthetic agent
Physician: MS/Resident
Episiotomy/Lacerations: 2o midline episiotomy was cut with extension to 3o.
Repaired with ___(suture types/sizes) in ___ layers. EBL: Estimated blood loss
Findings: Term male/female infant, APGAR's 81/95, weight 7lb 5oz born at 08:12 with nuchal cord x 1, easily
moved. Placenta delivered at 08:21, Schultze (or Duncan) and intact with 3 vessel cord noted. Cord blood and
placental
cultures sent to lab.
Complications: none
Disposition: Mother to recovery room in good condition; baby to
TCN (or NICU) in ___ condition.
INCOMPLETE ABORTION ADMIT ORDERS
1.Admit to...
2.NPO
3.Bedrest
4.IV D5RL @ 8hour rate with 2 amps Pitocin
5.Vitals Q2hours or routine
6.Watch for excessive bleeding
7.CBC, Astra 8, T & S 2u PRBC
8.Tetnus toxoid .5cc IM
9.OCOR: Bicitra 30cc PO
10.Rhogam if indicated
PREGNANCY AND DRUGS TO BE AVOIDEDCoumarin compounds, colchicine, doxycycline, ergotamine, erythromycin estolate, ethacrynic acid, griseofulvin,
lindane, lisinopril, mebendazole, metolazone, metronidazole, misoprostol, norfloxacin, phenylbutazone,
piroxicam, tetracycline, tolazamide, tolbutamide, valproic acid.
APGAR Score
APGARS
35
_____________________________________________________________
0
1
2
Hear rate
none
<100
>100
Respiration
none
slow, irreg
good cry
Tone
none
floppy
active
Color
blue
acrocyanotic all pink
Reflex irritability none
grimace
cry
_____________________________________________________________
Neonatal/Birth H&P
DOB___ DOL#___
Gestational age (WBD=wks by dates/WBE=wks by exam), birth wt,
SGA/AGA/LGA male/female:
BTA (born to a): mom's age, parity (GPA), labs (ABO/ HepB /RPR/Rub),> complications of pregnancy (maternal
DM, PIH, PTL,chorio, smoking, ETOH/drug abuse, HIV, etc), maternal temp at delivery /fever during labor
Delivered via: SVVD/C-sect with nuchal cord x 1, ROM (spontaneous or artificial) at 05:20 with meconium
Perinatal course: Infant to NICU warmer, suctioned with ETT x 1 with NBTC (no meconium below the cords),
suctioned by NGT x 1 with ___ cc of meconium-stained fluid removed, dried & stimulated, APGARS 81/95.
Infant transferred to TCN for transitioning
PE: Vitals, weight, length, FOC (%tiles)
HEENT: fontanelles, red reflex
Heart/Lungs/Abd/GU
Extremities: hip click
Neuro: reflexes of infancy
Labs: Infant's ABO
Primitive Reflexes of Infancy
Reflex
Age of Appearance
Moro
Grasp
Rooting
Placing
Crossed extension
Tonic neck
Trunk incurvation
Landau
birth
birth
birth
birth
birth
birth
birth
6-8 months
Age of Disappearance
4-6 months
4-6 months
4-6 months
4-6 months
4-6 months
4-6 months
9-6 months
15 mo-2 yrs
Pediatric H&P
Chief complaint
Informant (parent, guardian, etc.)
HPI
PMH: Hosp/surgeries
Allergies
Medications
Complete birth history for child and siblings
Dietary history
Immunizations
Developmental milestones
Travel
Pets
Fam Hx: Include Tb exposure
Psych / SocHx: who cares for, day care
ROS:
PE: Vitals
Growth: weight, height, FOC (and %tiles)
HEENT: fontanelles, red reflex
Neck: stiffness, adenopathy
Lungs/Heart/Abd
GU: Tanner staging
Mental Status
Neuro and developmental
36
Estimating Body Surface Area in Children
Weight (lb)
Body Surface Area (m2)
3
6
12
18
24
30
36
42
48
60
>60
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
1.0
add 0.1 for each additional 10 lb
Abbreviated Psych History
Organizational components: identifying data, referral source, chief complaint, history of present problem, medical
history, drug and alcohol history, mental status exam, formulation, diagnostic impression, treatment plan. HPI:
Onset of problems (time, setting)
Duration and course (chronic vs. episodic)
Psychological symptoms
Symptoms of psychoses
Cognitive Problems
Mood Changes (irritability, depression, elation)
Somatic symptoms
Medical conditions
Vegetative signs (anorexia, weight loss, insomnia, anergy, agitation or retardation, decreased sexual energy and
interest, diurnal mood variation)
Neurological symptoms
Somatic complaints without organic basis
Severity of problems-degree of impairment in functioning
Possible precipitants.
Past History:
Family relations (father, mother, siblings, others at home, important family relationships, major losses and
separations) Infancy (birth order, birth history, developmental milestones)
Childhood (health-hospitalizations, preschool years, friendships)
Adolescence (onset of puberty, early sexual experiences, peer relationships, experimentation with drugs, smoking,
ETOH)
Adulthood (education, military experience, employment, social life & friendships, romantic relationships, sexual
history, marriage, children)
Mental Status Exam:
Appearance and behavior (dress and grooming, posture and gait, physical characteristics, facial expressions, eye
contact, motor activity, specific mannerisms) Speech (rate, pitch, volume, clarity, abnormalities)
Emotions (mood, affect-variability, intensity, lability, appropriateness)
Thought Process (flow of ideas, quality of associations)
Content
(Distortions -delusions, ideas of reference, depersonalization)
(Preoccupation’s - obsession, phobias, somatic concerns)
(Suicidal or homicidal ideation)
Perception (Illusions or hallucinations)
Sensorium and Intellect
Consciousness
Orientation
Time- "What is today's date?"
Place- "What is the name of this place?"
Person- "What is your full name?"
Concentration: Serial 7's (or 3's)- ask patient to subtract 7's (or 3's) in succession, starting from 100.
Memory Immediate- Digit span (Ask patient to repeat a series of random numbers, first forward, then backward)
Recent- Ask patient to remember 3 unrelated objects then recall them after 15 minutes.
Remote- Ask about names and dates in patients earlier life; ask patient to name the U.S. Presidents
beginning with the current one and going backwards.
Fund of Knowledge ("Who is the Vice-president of the U.S.?", "What are the colors of the American flag?", "How
far is it from New York to Los Angeles?", What is a thermometer?")
Abstraction Proverbs- Ask patient to interpret a Proverb (a stitch in time saves nine, the grass is always greener
on the
other side of the fence, a rolling stone gathers no moss, etc.)
37
Similarities-ask the patient what two things have in common (a table and chair, an orange and a baseball)
Judgment - Ask what the patient would do in a social situation that requires judgment (smelling smoke in a
crowded
theater; finding a stamped, addressed, sealed letter on the street)
Insight- Ask patient if he knows why he is in hospital or if he thinks that he currently has any problems.
Attitude toward interviewer
ABBREVIATED NEUROLOGICAL EXAM
Mini Mental Status Exam
Orientation
What is the year, season, month, day, date? {1 point each}
Where are we (state, county, city, hospital, floor)? {1 point each}
Registration
Name 3 objects taking one second to say each. Ask pt. To repeat all 3 immediately after you say them. Repeat
until he/she learns all three. {1 point each}
Attention & Calculation
Serial 7's (stop after 5 correct), or spell "world" backwards. {1 point each up to 5}
Recall
Ask pt. to name the three objects named above. {1 point each}
Language
Name 2 objects that you show (i.e. pencil, pen, cup). {1 point each}
Repeat "no ifs, ands, or buts". {1 point}
Follow a three step command (i.e. take the piece of paper, fold it in half, and toss it on the floor). {1point each
step}
Write a sentence. {1 point}
Copy a complex polygon. {1 point}
Total 30 points <27 considered abnormal Serial exams will reveal progress, no change, or deterioration.
Glasgow Coma Scale
Eye opening: Spontaneous
To voice
To pain
None
4
3
2
1
Verbal response: Oriented
Confused
Inappropriate words
Incomprehensible sounds
None
5
4
3
Motor response:
Obeys commands
Purposeful movement
Withdrawn
Flexion
Extension
None
2
1
6
5
4
3
2
1
Cranial Nerves, Motor, Cerebellar, Sensory, Gait
Cranial Nerves
I test sense of smell II visual acuity III, IV, VI extraocular movements (LR6,SO4,all others3) V facial pinprick/touch
(optional
corneal reflex) VII upper/lower facial muscles (optional taste test for Bell's Palsy) VIII hearing (check for nystagmus) IX, X
midline palate elevation XI turn head in both directions XII tongue protrudes in midline Motor Tone: degree of stiffness
Strength: selected distal and proximal muscle groups
C5 = elbow flexors
C6 = wrist extensors
C7 = elbow extensors
38
C8 = finger flexors
T1 = small finger abductors
L2 = hip flexors
L3 = knee extensors
L4 = anterior foot dorsiflexors
L5 = long toe extensor
Reflexes
biceps = C5
brachioradialis = C6
triceps = C7-8
knee = L2-4
ankle = S1
Pathological Reflexes: i.e. Babinski, clonus
Cerebellar
Finger-to-nose
Heel-to-shin
Rapid alternating movement
Sensory
compare side vs. side, upper vs. lower in ability to discern pinprick,
light touch, vibration, and proprioception.
Gait heel walking, toe walking
Dermatomes, anterior view
39
Dermatomes, posterior view
40
41
EKG Leads
Medical Orders
Admission Orders (Remember "ABC VANDALISM")
Admit to: (floor, service, MD)
Diagnosis: (Because)
Condition: (good, fair, poor, critical, guarded)
Vital Signs: (q shift, q 4o, per routine, etc.)
Allergies:
Nursing: (I/O’s, daily weights, turn patient q 4o, etc.)
Diet: (regular, clear or full liquid, 4 g Na, low or hi protein,
ADA calories, etc.)
Activity: (ad lib, bedrest with/without bathroom privileges,
OOB tid, etc.)
Labs: (also x-rays, EKG's, etc.)
IV Fluids: (type, added KCl, rate)
Studies: (CXR, MRI, CT, EKG, EEG, etc.)
Meds:
Call house officer if T> 101, BP>170/110 or <90/50,
HR>120 or <50
Pre-op Orders
Diagnosis:
Procedure planned:
Labs: (lytes, CBC, PT/PTT, UA, amylase if applicable)
CXR
EKG (if > 35 yo or h/o heart disease)
Type and crossmatch
Prep and shave surgical field
NPO after midnight
Void on call to OR
Foley catheter (if indicated)
Consent form signed and on chart
History and Physical on chart
42
SIGN-OUT Note
An effective sign-out system saves everyone time. Use a printed, pocket-sized sign-out card. Interns complete a
card on each patient, updating the information as needed. The cards are delivered to the covering house officer
and retrieved the following morning. The card is printed with the following information, and the intern caring fills in
the blanks for the patient. If the covering intern interacts with the patient, it also is noted on the card.
Team_________________ Intern_____________________
Res._____________________
Pt____________________ ID#_______________________
Ward____________________
Age__________________
Allergies__________________________________________
Code: DNR FC IV: Yes No CX: Yes No
Problems:
Main Meds:
Potential Problems (if this, then ______________):
To Do List:
Discharge Orders
Discharge: when and to where
Diagnosis:
Discharge Medications: (also need to fill out prescriptions)
Diet:
Condition:
Activity: (eg. ad lib with 4 weeks pelvic rest for postpartum
patients)
Follow up: (eg. return to clinic in 1 week)
Presenting Patients
Now that you've got the history, what do you do with it? One of your more important tasks is to transmit the information
you've gathered to other health care professionals. This is frequently accomplished through a combination of written
documentation (the medical record) and verbal presentation (face to face or over the telephone). Developing these skills is
essential for your medical career. The following outline summarizes the elements of a good case presentation.
Documenting vs. Communicating
Keep in mind that a case presentation is not simply reading your write-up. The medical record and your presentation are
complimentary. The former serves as the primary documentation of the patient's clinical situation. The latter is a
formalized way of communicating the patient's story to your colleagues. A good case presentation includes all the
"important" details in a very terse, easy to assimilate package. Knowing which details are important and which can be left
out is an acquired skill that comes with practice. Finally, the length of the presentation (and thus the level of detail) will
vary depending on the purpose. In a busy clinic this might be only 1 or 2 minutes. A formal case presentation to a large
group might last as long as ten minutes or more.
Opening Statement
Begin with an arresting sentence; close with a strong summary; in between speak simply, clearly, and always to the point;
and above all be brief. - William J. Mayo
The opening statement sets the stage for the presentation, so it is worth looking at in detail. You should include a bit of
demographic information ("Jean Smith is a 40 year old woman who...") and a description of the patient's problem or chief
complaint ("...came to clinic because of increasing dyspnea.") Note that, unlike the subjective section of the written record,
it is okay to use medical terms and state exactly what you think. The entire presentation is your interpretation of what is
going on.
43
Personal Information
The opening statement may also contain additional information about who the person is as an individual (what they do for
a living, their general level of health, where they live). Including this information helps the listener paint a more complete
mental picture of the patient and prevents the discussion from becoming totally focused on the disease. Source and
Validity
Finally, you may want to comment about the source(s) and validity of the information you are reporting. If you don't
otherwise state it, your listener will assume that you got the history from the patient and that you consider the information
valid. If the patient is mentally incapacitated or otherwise unable to communicate well (e.g. speaks a language you don't
understand), say so!
Time Course
Remember that you are telling a story. As with any story, the events of the patient's illness unfold in a specific sequence.
This sequence is referred to as the clinical time course or chronology. Think of it as the scaffold on which all the other
details of the history of present illness (HPI) will hang. Elements of the time course should include:
When did the problem start? (Onset) How has it progressed? What is its current status? Influential Factors
Once you've established the time course, you should fill in the details that are "pertinent" to the case. These include other
elements of the HPI such as:
Precipitating and exacerbating factors Relieving or moderating factors Prior treatment and response to it
Note that what is not present is often more important as what is. These are called pertinent negatives and should always
be included. For example, in a patient with shortness of breath, the absence of chest pain is significant because it makes
certain diagnoses less likely.
Analysis At this point your listeners will expect you to "put it together" for them. What pathologic processes might explain
the symptoms you've presented? As part of your analysis you will be expected to develop and prioritize a list possible
causes (differential diagnosis). You should bring in elements of the HPI; family, social, and past medical history; review of
systems; and physical exam that support or oppose each diagnosis. At the end of this process you should have narrowed
the field to one or two possibilities. These are your working diagnoses - what you think is actually going on. The remainder
of your presentation should explain what you intend to treat or better characterize these diagnoses.
Keep in mind that medicine has a bias towards simpler explanations. A single cause is always preferred over a
combination of causes. This doesn't mean that a patient can't have more than one thing going on. If you believe there are
two distinct symptom complexes present, say so at the beginning of your presentation and develop a differential diagnosis
for each.
Acute Pain Management
Special considerations for Elderly Persons
44
Elderly people often suffer multiple chronic, painful illnesses and take multiple medications. They are at greater
risk for drug-drug and drug-disease interactions. Pain assessment presents unique problems in the elderly, as
these patients may exhibit physiologic, psychologic, and cultural changes associated with aging. Misunderstanding
of the relationship between aging and pain is common in the management of elderly patients. Many health care
providers and patients alike mistakenly consider pain to be a normal part of aging. Elderly patients sometimes
believe that pain cannot be relieved and are stoic in reporting their pain. The frail and oldest-old (>85 years) are at
particular risk for under treatment of pain. Aging need not alter pain thresholds or tolerance. The similarities of pain
experience between elderly and younger patients are far more common than are the differences. Cognitive
impairment, delirium, and dementia are serious barriers to assessing pain in the elderly. Sensory problems such
as visual and hearing changes may also interfere with the use of some pain assessment scales. However, as with
other patients, the clinician should be able to obtain an accurate self-report of pain from most patients. When
verbal report is not possible, clinicians should observe for behavioral cues to pain such as restlessness or
agitation. The absence of pain behaviors does not negate the presence of pain. NSAIDS can be used safely in
elderly persons, but their use requires vigilance for side effects, especially gastric and renal toxicity. Opioids are
safe and effective when used appropriately in elderly patients. Elderly people are more sensitive to analgesic
effects of opiate drugs. They experience higher peak effect and longer duration of pain relief.
45
46
Evidence Based
47
48
CENTRAL LINES: PLACEMENT AND PROBLEMS
Immediate Questions When Line's Not Working
A. Does it change with respiration? A CVP should have a slowly undulating waveform that varies with the patient's
respirations, if properly positioned in the chest.
B. Does it flush and can it be aspirated?
C. When was the last chest x-ray? The tip should be in the superior vena cava.
Differential Diagnosis
A. Catheter in incorrect position.
B. Kinked catheter.
C. Other mechanical problems.
D. Infected catheter. Any question of sepsis originating in a central venous line requires expeditious evaluation. The best
technique involves drawing cultures through the catheter, removing the line, and culturing the tip. Remove & replace @
an alternate site
Plan:
A. Unless the line is infected, it can be changed over a guide wire. All line manipulations should be performed using sterile
technique with the patient in Trendelenburg (head-down) position to prevent air embolus.
B. A line thought to be clotted can often be declotted safely with a syringe. The catheter can be gently aspirated or flushed
with a 1 cc tuberculin syringe.
Internal Jugular Insertion:
49
A. Materials for central line placement are available in a kit, which you can obtain on the hospital unit.
B. IJ lines have less risk of pneumothorax and are preferred if hyperinflation or mechanical ventilation are present.
Because direct pressure can be applied, the IJ line also is preferred if coagulopathy is present. For IJ lines use a 25
gauge needle and 1% lidocaine to raise a small skin wheal. Change to a 22-gauge needle to anesthetize the deeper
layers, and then use gentle aspiration, with the same needle, to initially locate the internal jugular vein. Direct the needle
through the skin wheal, directed toward the ipsilateral nipple and at a 30-degree angle to the frontal plane. If the vein is
not entered, withdraw the needle slightly and redirect it 5 to 10 degrees more laterally.
Subclavian Insertion:
A. Materials for central line placement are available in a kit, which you can obtain on the hospital unit.
B. Subclavian lines usually are more comfortable for the patient and easier to fix to the skin. However, it results in a
pneumothorax in 1 to 2% of insertions.
C. Most commonly for subclavian lines, the patient is placed in Trendelenburg position, with a roll between the scapulae.
This presumably makes the clavicles flatten and vein more prominent and simplifies puncture. The artery is above and
behind the vein, so slow entry will allow going into the vein before the artery. The needle is passed below the clavicle and
aimed toward the sternal notch, with the bevel upward. Turn the bevel to 3:00 when the vein is entered.
Other lines:
Femoral lines are acceptable when there is no upper body alternative and when rapid access is needed during
cardiopulmonary resuscitation.
Complications:
Pneumothorax, hemothorax, hydrothorax, arterial puncture with hematoma and catheter tip embolus.
A. Obtain help from an experienced house officer to assist with line placement.
B. Always obtain and review a CXR following line placement.
C. Air can enter an open system when intrathoracic pressure decreases, (as during an inspiration). An air embolus
obstructs the pulmonary artery and can produce acute right heart failure. If you suspect that air embolization has occurred,
place the patient head down and turned left side down to keep air in the right atrium. Obtain a stat CXR to look for air in
the atrium.
D. If you suspect a pneumothorax, order a stat portable CXR in the upright position in expiration. Hypotension, tachypnea
and pleuritic chest pain after central line insertion are suggestive of a pneumothorax. Order O2 by mask at 10 L/min.
E. Tension pneumothorax is a medical emergency requiring urgent treatment.
F. Massive unilateral pleural effusion can occur if the IV line is emptying into the pleural space. Stop the IV fluid, and
thoracentesis will be required if the patient is markedly SOB. Hemothorax can occur when a vessel is perforated.
DRAIN MANAGEMENT
Immediate Questions:
A. What operative procedure did the patient have and what surgical sites are being drained?
B. What type of drain was placed intraoperatively? Surgical drains are of two basic types: passive or active. Passive
drainage is accomplished by gravity or capillary action. Drainage is further facilitated by transient increases in intraabdominal pressure, as with coughing. Passive surgical drains include Penrose, Foley, Malecot, and Word catheters.
Active drainage is accomplished by suction from a simple bulb device or a suction pump. These systems may be closed,
like the Hemovac and Jackson-Pratt drains.
C. What is the nature of the drainage fluid? Examine the fluid for color, odor and volume. Also examine the tube for clots
or other obstructing material.
Differential Diagnosis:
50
A. Increased drainage Increased bloody drainage can be due to vessel leakage and may be caused by catheter erosion
into a vessel. Document rate of bleeding every 30-60 minutes. Increased serous drainage may be from increased lymph
drainage, particularly with increased activity. Drainage of urine may represent fistulas anywhere along the urinary tract.
B. Purulent drainage This indicates infection.
C. Sudden cessation of drainage Tissue debris, especially in smaller catheters, is a principal source of catheter occlusion.
Drains can be walled off from the general peritoneal cavity within about 6 hours. Intra-abdominal fluid can be collecting
without drainage from the catheters. Therefore, regular examinations of the abdomen are necessary for early identification
of intra-abdominal fluid collections.
D. Drain exit wound infection Erythema, induration and pain at the drain exit site are indicators of infection in the
subcutaneous tract.
Misc. Drain Management
Usually drain management does not require emergent or urgent action with the exception of mediastinal tubes on the
cardiac surgery service.
1. Increased output. Almost always due to blood. Document rate of bleeding by accurately noting output every 30-60
minutes and following serial hematocrits. Measure coagulation parameters and correct as needed.
2. Decreased output. A sudden decrease in output may be due to a clot in the tube and lead to an episode of cardiac
tamponade.
FOLEY CATHETER PROBLEMS
Immediate Questions:
A. What has the urine output been? If the urine output has slowly tapered off, then the problem may be oliguria rather than
a nonfunctioning Foley.
B. Is the urine grossly bloody and are there clots in the tubing or bag?
C. Is the patient complaining of any pain? Bladder distention often causes severe lower abdominal pain.
Differential Diagnosis:
A. Low urine output. If the catheter irrigates freely, evaluate for decreased urine output (see section on Oliguria below).
B. Obstructed or improperly positioned Foley catheter
1. Kinking of catheter or tubing
2. Clots and tissue fragments (especially if after a TURP)
3. Sediment/stones
Management:
A. Verify function. A rule of thumb is that a catheter that will not irrigate is in the urethra and not in the bladder. Start by
irrigating the catheter with aseptic technique using a catheter-tipped 60 mL syringe and sterile normal saline. Catheter
irrigation or replacement in any patient who has undergone bladder surgery must be done with extreme care.
B. Spasms. A patient with bladder spasms may complain of severe suprapubic pain, pain radiating to the perineum, or
urine loss from around the catheter. Spasms are common after bladder surgery. Bladder spasms can be treated with
oxybutynin (Ditropan), propantheline (Pro-Banthine) or belladonna and opium (B&O) suppositories.
C. Faulty balloon. There are several techniques to deflate a balloon that will not empty.
1. Injecting 5-10 mL of mineral oil into the inflation port will cause the balloon of a latex catheter to rupture in 5-10 minutes.
2. Threading a 16 French central venous catheter into the inflation channel (after the valve is removed) may bypass the
obstruction.
3. As a last resort, ultrasound-directed transvesical needle puncture of the balloon may be needed.
51
NASOGASTRIC TUBE MANAGEMENT
Immediate Questions:
A. How long has the NG tube been in place? A tube that has just been placed may have bloody drainage from the trauma
of insertion or as a result of recent gastric surgery.
B. What is the volume and description of the output? How much bloody drainage has there been? Is the patient having
abdominal distress?
Database: An abdominal radiograph is useful to identify the tube's location. Look for a large stomach bubble indicating
poor gastric emptying. Check the position of the tube tip and verify that it is in the stomach.
Plan:
A. Decreased output:
1. Verify position. This is based on x-ray confirmation. Flushing the tube with 40-60 cc of air and listening over the
stomach results in a typical crackle or pop; however, this may also be heard with the tube in the distal esophagus or
duodenum. Based on x-ray findings, you may want to advance or retract the tube, as needed.
2. Verify function. Sump tubes should whistle continuously on low suction. Most tubes need to be flushed with saline (30
mL) every 3-4 hours to maintain patency.
3. If the tube's position and function are not problems, then decreased output can indicate return of bowel function.
B. Increased output:
1. Poor gastric emptying (no obstruction).
2. Distal obstruction
3. Ileus
C. Blood in the NG output (See GI Bleeding Below):
1. Determine whether the cause of bleeding is serious enough to require specific aggressive therapy. Is there hypotension
or hemodynamic instability? For either and signs of significant bleeding, place a large-bore IV and begin fluid and blood
replacement. Bleeding may be due to trauma, all the causes of upper GI bleeding, and a coagulopathy. Place in ICU!
NG irrigation; H2 blockers or antacids.
NEEDLE STICKS and OTHER EXPOSURES TO BLOOD and BODY FLUIDS
All exposures (needle sticks, splashes, scrapes, etc.) should be reported as soon as possible. During working hours,
report to Employee or Student Health, and after hours, report to the Emergency Department. A team of experts available
will do evaluation and management for both the exposed and the exposure source.
In several epidemiologic studies, 7% - 35% of house officers, depending on prevalence of HIV in the patient population,
had a reported needle or mucous membrane exposure to HIV. However, closer study of these groups indicated that only
one-third of house staffs' exposures were reported due to concern regarding confidentiality and lack of knowledge about
reporting procedures.
Blood and body fluid exposures are evaluated for infectious disease transmission and wound care. HIV, hepatitis B and
hepatitis C checked by lab studies. Prophylactic treatments and boosters are offered appropriately. Risks of tetanus are
evaluated and boosters given when needed. The exposure source will be evaluated for other blood borne pathogens as
well. Detailed algorithms for evaluation and management of blood or body fluid exposure are available.
Remember:
* Always use universal precautions. Always be careful. * Immediately wash affected area with soap and water. * Always
report blood or body fluid exposures as soon as possible.
WOUND COMPLICATIONS
Immediate Questions:
52
A. Is there a wound dehiscence, and if so, to what extent? Did any fluid leak from the wound? Always evaluate the wound
yourself as soon as possible; see how much of the wound has opened and if there is an evisceration. An "open wound" is
not a dehiscence unless the fascia opens.
B. Are there findings of an infection?
Plan:
A. Initial management. Determine by wound examination if there is an evisceration, fascial disruption without evisceration,
or a superficial wound separation. In all cases, it is safe to make the patient NPO and start antibiotics to cover skin
organisms, until a final plan is formulated.
B. Evisceration/fascial dehiscence. Cover the wound with saline soaked sterile gauze, then cover with a large sterile
dressing. Notify the senior staff since evisceration requires operative repair.
C. Fascial dehiscence with evisceration. If the overlying skin and subcutaneous tissues are intact but there is clearly a
fascial defect, it may be treated by operative repair or observation. Without treatment, a ventral hernia will develop.
D. Superficial wound separation. Healing by secondary intention is mandatory when there is an associated superficial
wound infection, and is the safest management in any case.
E. Wound infection. Culture and antibiotics selected based on type of surgery. See the Stanford/Parkland guide for
antibiotic choice, which varies with surgery type for:
1. surgery not involving GI or female GU tract
2. surgery involving GI tract (including oropharynx) and female GU tract
3. extremity, +/- sn sepsis
PROCEDURES
Blood Tube Type
CBC: purple top
PT/PTT: blue top
Chem. 7: small red top
Chem. 20: large red top
ABGs: heparinized syringe with air bled out and on ice
TFT's: red top
Ammonia: green top on ice
Others: call lab but usually red top
Body Fluid Routine Labs
Lumbar Puncture
Tube 1: Gram stain & cultures
Tube 2: protein, glucose
Tube 3: cell count with differential
Tube 4: special studies
Thoracentesis
specific gravity, protein, LDH, pH, cell count with differential, glucose, Gram
stain, cultures, AFB smear & cultures, fungal smear & culture
Paracentesis
cell count with differential, Gram stain & cultures, lactic acid, pH, protein,
glucose, LDH, specific gravity, amylase, cytology
Arthrocentesis
Un-heparinized tube: viscosity, mucin clots
53
heparinized tube: glucose, Gram stain, culture, cytology, cell count & differential
glass slide for polarized light examination
Pleural/Peritoneal Effusions
Exudate (IU/dl) Transudate (IU/dl) Fluid LDH >200 <200 Fluid protein >3 g <3
g Fluid/serum LDH ratio >0.6 <0.6 Fluid/serum protein ratio >0.5 <0.5 Specific
gravity >1.016 <1.016
Gram Stain
1.Air dry specimen after smearing thinly on slide.
2.Heat fix by quickly passing the slide through a flame 2-3 times.
3.Cover the entire slide with Crystal Violet for 30 seconds.
4.Rinse with water.*
5.Cover slide with Iodine for 1 minute.
6.Rinse with water.
7.Hold slide at 45&degree; and decolorize with acetone/ethanol for 5 10 seconds or until no more blue runs off.
8.Rinse with water.
9.Cover slide with Safranine for 30 seconds.
10.Rinse with water and blot dry with bibulous paper.
*NOTE: use distilled water for rinsing when available
Urinalysis
1.Dipstick urine and record values. Pour sample of urine off into test tube for dipstick. Do not contaminate sterile
specimen cup with dipstick.
2.Spin urine in centrifuge for 3-5 minutes.
3.Pour most of the supernatant off, leaving a few drops in the bottom of the test tube.
4.Put a few drops of the remaining mixture on each of 2 slides, put a cover slip on one (wet prep) and examine
under the microscope while the other dries.
5.If there are more than 5 WBC's per high-powered field in spun urine, then it is considered infected. If you see
WBC's then you will probably want to gram stain the slide you left to dry to see if you can see any bacteria. If the
wet prep is clear, there is no reason to gram stain the other slide.
6.Other things to look for include: RBC's, yeast, Trich, sperm, epithelial cells, etc. If the specimen contains many
epithelial cells it is considered a dirty catch and you had best start with another specimen from that patient.
54
Fluids & Electrolytes
NORMAL PHYSIOLOGIC VALUES
Hemodynamic Values
Heart Rate..........................……….60-100 beats/min.
Pressures
Systemic Arterial
Peak Systolic/End-Diastolic.........100 - 140/60 - 90mmHg
Mean (MAP)..........................
70 - 105 mmHg
(2 * diastolic + systolic)/3
Left Ventricle
Peak Systolic/End-Diastolic.........100 -140/3 - 12 mmHg
Left Atrium (PCWP)
Mean................................2 - 12 mmHg
a wave..............................3 - 10 mmHg
55
v wave..............................3 - 15 mmHg
Pulmonary Artery
Peak Systolic/End-Diastolic.........15 - 30/4 - 14 mmHg
Mean................................9 - 17 mmHg
Right Ventricle
Peak Systolic/End-Diastolic.........15 - 30/2 - 7 mmHg
Right Atrium
Central Venous Pressure (CVP).......less than 5 mmHg
Mean................................2 - 6 mmHg
a wave..............................2 - 8 mmHg
v wave..............................2 - 7 mmHg
Resistances
Systemic Vascular Resistance (SVR)...700 - 1600
dyne-sec/cm-5
SVR = [(MAP-CVP)/CO] * 80
Pulmonary Vascular Resistance (PVR)..100 - 300
dyne-sec-cm-5
PVR = [(PAP-PCWP)/CO] * 80
Flow
Cardiac Output (CO)...................3.5-5.5 liters/min
CO = HR * SV
Cardiac Index (CI)...................2.4 - 3.8 L/min/m2
CI = CO/BSA
Ejection Fraction = (SV/End-Diastolic Volume) * 100
Arterial Blood Gases
pH.....................................7.4
pCO2...................................40 mmHg
pO2....................................90 mmHg
SaO2...................................90+ %
Mixed Venous Blood Gases
pH.....................................7.36
pCO2...................................45 mmHg
pO2....................................40 mmHg
SvO2...................................0.75
Oxygen Content-Arterial Blood .....19 ml/100cc
CaO2 = (1.34 * Hgb * (SaO2/100)) + (0.003 * PaO2)
Oxygen Content-Venous Blood........14 ml/100cc
CvO2 = (1.34 * *Hgb * (SvO2/100)) + (0.003 * PvO2)
Oxygen Content-Capillary Blood.....22 ml/100cc (FiO2=1)
CcO2 = (1.34 * *Hgb) + (0.003 * (713-PaCO2)FiO2)
Alveolar Gas Equation
PAO2 = PiO2 - PaCO2/R = (PB-PH2O)(FiO2) - (PaCO2/R)
= (760-47)(0.21) - (40 * 1.25) = 100 at sea
level, room air
Simplified Alveolar Gas Equation
PAO2 = (700 * FiO2) - (PaCO2 * 1.25)
Alveolar-Arterial Gradient
A - a = PAO2 - PaO2
56
Acid-Base Disorders
See below for much more
57
Normal Lab Values
58
59
60
61
Acid-Base
Metabolic Acidosis
Acute Respiratory Acidosis
Metabolic Alkalosis
Respiratory Alkalosis
Approach to interpreting Acid-Base Status
Metabolic Acidosis
A. Anion Gap Acidosis (Normal Anion Gap = Na - [Cl + HCO3] = 8 - 14)
Paraldehyde
Ketones (DKA, AKA, rarely starvation)
Uremia (BUN usually >=40, gap 15-25)
Salicylates (associated with respiratory alkalosis)
Methanol (retinal edema, papillitis)
Ethylene glycol (calcium oxalate crystals)
Lactic acid
B. Normal Gap Acidosis
1. Normokalemic
Obstructive uropathy
Hypoaldosteronism
2. Hypokalemic
GI loss
Acetazolamide
Ileal loop
RTAs (lithium, amphotericin, hyperparathyroidism., autoimmune, etc.)
Acute Respiratory Acidosis
Pulmonary
CNS depression
Chest wall weakness (Guillain-BarrГ©, drugs [e.g., succinylcholine])
Metabolic Alkalosis
A. Chloride responsive (saline responsive) urine Cl <10 mEq/L
Vomiting, NG suction
Diuretics
"Contraction" alkalosis
B. Chloride unresponsive
Bartter’s
Severe potassium depletion
Mineralocorticoid excess
Respiratory Alkalosis
CNS (tumor, inflammation, infection, anxiety, cirrhosis)
Hypoxia
Airway irritation (tumor, fibrosis, pulmonary emboli)
Drugs (ASA, progesterone, xanthines)
Pregnancy
Approach to Interpreting Acid-Base Status
A. Measure electrolytes and ABGs
B. Compare calculated and measured HCO3 to r/o lab error; H+ = 24 (PaCO2 / HCO3)
C. Compute anion gap
D. Compare PaCO2 and pH to see whether pH change is directly related PaCO2 change or other processes are
ongoing
62
H+
70
60
50
40
32
25
pH
7.16
7.22
7.3
7.4
7.5
7.6
Useful Mnemonic
MUDPILES (for causes of increased anion gap)
ELM PARK
AMPLE SUDS
Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde, Phenformin, Metformin, Propylene glycol
Iron, INH
Lactic acidosis
Ethanol, Ethylene glycol
Salicylate, Starvation
BEDROCK LAB TESTS
Arterial blood gases (pH, PaO2, PaCO2, SaO2)
Chest x-ray (PA and lateral)
Complete blood count (hematocrit, WBC, differential, platelet count)
Electrocardiogram (12-lead)
Serum electrolytes, BUN and blood glucose
Spirometry
Sputum analysis (Wright's stain, Gram's stain)
Urinalysis
Arterial Blood Gas Lecture Slides ABGs
Pulse Oximetry
63
Accuracy of Pulse Oximetry
64
ABG’s in Pulmonary Embolism
65
Normal ABG Ranges
66
Oxyhemoglobin Desaturation Curve
67
Oxygen Transport System
68
Oxygen Dosing
69
Scoring for Acute Lung Injury and Acute Respiratory Distress Syndrome
70
Acute Lung Injury ALI
Acute Respiratory Distress Syndrome ARDS
71
72
73
Anion Gap
74
Bicarbonate Gap
Anion Gap Gap
Delta Gap
75
Acid Base Algorithm
76
Anion Gap
77
Bicarbonate Gap
Anion Gap Gap
Delta Gap
78
79
80
Arterial Blood Gas Diagnostic Worksheet
Normal Ranges
Equations
Aa O2 Diff <= 1.1 x (2.5 + .21 x Age)
[H+] = 24 x (PaCO2/HCO3)
OH Dissociation [email protected]%; [email protected]%; [email protected]%; [email protected]%
AG <= (.5 xHCO3) +16 Not Organic Acidosis
AG gap = AG – 12 [24 – AG gap = HCO3]
SOsm - [ (2xNa) + (BUN/2.8) + (BS/18) ] <= +/- 10 mOsml
Aa Diff = [ (760 – 47) FiO2 – (pCO2/0.8)] – pO2
Bicarb Gap = Na – Cl – 39 (AG + vCO2 on lytes) = +/- 6
pH = 7.38-7.42
PaCO2 = 38-42
PaO2 on 21% O2
>= .9 x (104.2 - .27 x Age) Normoxia
>=.8 x
“
Mild Hypoxia
>= 55
“ Moderate Hypoxia
< 55 mm Hg
Severe Hypoxia
Compensation for Simple Acid-Base Disorders (Narins, RG, Medicine, 1980; 59, 161-187)
Primary Disorder
Metabolic Acidosis
Initial Change
HCO3 Decrease
Compensatory
PaCO2 Decrease
Metabolic Alkalosis
HCO3 Increase
PaCO2 Increase
Respiratory Acidosis
PaCO2 Increase
HCO3 Increase
Respiratory Alkalosis
PaCO2 Decrease
HCO3 Decrease
Age:
Temp:
Ht:
BP:
Ventilatory Mode:
FiO2 =
%
Wt:
AR:
Primary Process?
COHb=
/
Barometric Pressure:
RR:
Settings:
- emia ?
pH =
PCO2 =
PaO2 =
SaO2 =
SpO2 =
H&H=
Anion Gap =
LFT’s
=
Glucose =
Expected Range
*PCO2= [1.5( HCO3)+8] +/-2
*PCO2 = Last 2 digits of pH
deltaPCO2=1 to1.3x(deltaHCO3)
PCO2 Variable Increase
PCO2 = (.9 x HCO3) + 9
PCO2 .6 Incr per 1 Incr HCO3
Acute:
delta[H+] = .8 x delta PCO2
pH = 7.40 – [ .008 * ( pCO2-40) ]
HCO3 Inc 1 for 10 Inc PCO2
Chronic:
delta[H+] = .3 x delta PCO2
pH = 7.40 – [ .003 * ( pCO2-40) ]
HCO3 Inc 3.5 for 10 Inc PCO2
Acute:
delta[H+] = .8 x delta PCO2
pH = 7.40 + [ .008 * ( 40 - pCO2)]
HCO3 dec 2 for 10 dec PCO2
Chronic:
delta[H+] = .17 x delta PCO2
pH = 7.40 – [ .0017 * ( 40 - pCO2)]
HCO3 dec 5 for 10 dec PCO2
Compensation Appropriate?
MetHb=
Na =
CL=
BUN=
Toxic=
K=
CO2=
Creat=
Urine =
Diagnoses:
81
Lactate=
Ketones=
ETOH =
Acute or Chronic
Calculations:
HCO3 =
AaDif =
OHD =
PaO2/FiO2=
Hb=
PCO2 Compensation =
HCO3 Compensation =
pH Compensation
=
Serum Osm calc
=
Acute Respiratory Failure Lecture Slides ARF
82
Systemic Inflammatory Response Syndrome SIRS
83
Multiorgan Dysfunction Syndrome MODS
84
85
ARDS
86
Hypoxia-Hypoxemia
87
Respiratory Muscles and Innervations
88
89
90
91
92
93
94
Mechanical Ventilation in Acute Respiratory Failure ARF
95
HYPERCALCEMIA
Immediate Questions:
A. Vital signs? Mental status?
B. Underlying condition(s)?
Differential Diagnosis:
A. Among outpatients, malignancy and primary hyperparathyroidism are leading diagnoses. Malignancy predominates as
an etiology for hypercalcemia among hospitalized individuals.
B. Potential etiologies:
1. Malignancy: bone mets, ectopic PTH, osteoclast activating factor
2. Primary hyperparathyroidism
3. Myeloma
4. Vitamin D excess
5. Sarcoid / granulomatous disease
6. Milk alkali
96
7. Other: hyperthyroidism, thiazide diuretics, lithium, immobilization (especially children)
Therapy: Patients usually are profoundly volume depleted and can require several liters of NS volume replacement.
Volume replacement is the initial step in management. Lasix can be added to help increase a saline diuresis (>2500 ml
urine/day) and calcium excretion but should only be used following volume replacement.
Agent Dose Comments
Saline + furosemide 40-80 mg IV each 2 hours monitor hourly urine output,
(Diuretic only if adequately hydrated) output plus NS equal to urine monitor electrolytes frequently
Mithramycin 25 mcg/kg IV every response takes 24 hours; can 2-3 days cause bone marrow suppression
Pamidronate 60-80 mg IV over 6 to response in 3 to 4 days, which (mainstay of therapy) 24 hours lasts up to 7 to 14 days
Prednisone 40-60 mg per day antagonizes actions vitamin D; decreases calcium absorption and increases calcium
excretion; in most cases, effect lasts only for a few days
HYPERCALCEMIA- (HC). HC is most commonly caused by cancer and primary hypoparathyroidism. In cancer patients
the parathyroid hormone is low, and in primary hyperparathyroidism the parathyroid is high. Hypercalcemia in cancer
patients and primary hyperparathyroidism is due to parathyroid-like hormone and parathyroid hormone, respectively,
which stimulates osteoclast reabsorption of bone. Also, these two hormones stimulate renal tubular reabsorption of
calcium, which further elevates the calcium. The hypercalcemia itself interferes with reabsorption of sodium and water
and this leads to polyuria and dehydration. Moreover, many cancer patients are immobilized which further increases the
calcium.
SYMPTOMS OF HYPERCALCEMIA: HC can be divided traditionally into Gastrointestinal (anorexia, nausea, vomiting,
constipation and pancreatitis), Renal (polyuria, polydipsia and nephrocalcinosis), CNS (drowsiness, coma, apathy) and
Cardiovascular (short QT interval on EKG, digitalis sensitivity, and hypertension depending on degree of hydration).
OTHER CAUSES OF HYPERCALCEMIA: Sarcoidosis, histoplasmosis, coccidioidomycosis, tuberculosis, leprosy, lithium,
thiazide diuretics, estrogens and antiestrogens, multiple myeloma, Vitamin A and D toxicity, familial hypocalciuric
hypercalcemia, milk alkali syndrome, immobilization, acute and chronic renal insufficiency, parenteral nutrition,
pheochromocytoma, thyrotoxicosis, vasoactive intestinal polypeptide hormone- producing tumor and thyrotoxicosis.
If the serum calcium after being corrected for albumin is 14 mg/dl, then immediate therapy is indicated. If the albumin is
elevated then the calcium should be adjusted downward. If the albumin is low, then the calcium should be adjusted
upward.
TREATMENT OF HYPERCALCEMIA: The decision to treat is usually clear-cut if the calcium is 14 or greater.
However, calcium levels between 10.5 and 14 depend on several factors such as age, concomitant conditions, stage of
cancer, and symptoms. There are four classes of treatment and include: hydration, enhance the renal excretion of
calcium, inhibit bone resorption and treating the underlying condition. These will subsequently be discussed.
Hydration with isotonic saline is usually the first step. Various amounts and time schedules have been used, but in
general give 2.5 to 4 liters of saline daily with attention to the cardiovascular and renal status. When there has been
restoration of intravascular volume then one could reasonably expect a diminution of 1.6 to 2.4 mg reduction of the
calcium level. This occurs because of increased renal calcium clearance, decreased calcium absorption in the proximal
renal tubule, and obligatory kaluresis with increased presentation of sodium and water to the distal renal tubule.
Furosemide is usually given along with isotonic saline in order to inhibit reabsorption of calcium in the thick ascending
loop of Henle, and to protect the patient from saline overload. Thiazide diuretics should never be given as they increased
the absorption in the distal tubule. Always precede loop diuretic agents as furosemide with saline hydration, because
furosemide depends on the delivery of calcium to the loop. Depending on the degree of hypercalcemia and symptoms,
the furosemide needs to be adjusted possibly from 20 mg every 6 hours to 80 mg every two hours. Careful attention
must be given to electrolyte depletion.
Etidronate works by inhibiting osteoclasts. The reduction in calcium begins at about 2 days and has a peak reduction at 7
days. The patient should be well hydrated as the etidronate works better under this situation. The dose is 7.5 mg/kg IV
over a four-hour period daily for 3-7 days. The length of treatment depends on the response. Etidronate is safe with
transient increases in creatinine and phosphate.
Pamidronate is more potent than etidronate. Giving a single 24-hour IV infusion of up to 90 mg will normalize the serum
calcium in 70-100% of patients. Other schedules include giving a slow IV infusion of 15-45 mg daily for up to six days
depending on the response. Pamidronate can also be given orally as 1200 mg daily for up to 5 days, but many
hypercalcemic patients are unable to tolerate orally because of nausea and vomiting. Onset of action and peak action is
about the same as Etidronate. Side effects are mild with transient increase of temperature, which is usually less than 2
degrees C, transient hypophosphatemia and leukopenia.
97
Plicamycin is given at 25 micrograms/kg over a 4-6 hour period and can be repeated at 1-2 day intervals depending on
limiting side effects of the drug which include: hepatic and renal toxicity, thrombocytopenia, and cellulitis with
extravasation of the drug. The onset of lowering the calcium starts at 12 hours and peaks at 48-72 hours.
Calcitonin is usually given as salmon calcitonin at 4 units/kg every 12 hours and is the drug of choice if a rapid reduction
of calcium is needed. The calcium starts to drop after a few hours and the peak drop is at 12-24 hours. The drawback is
that calcitonin is fairly weak and doesn't lower the calcium to degrees that the bisphosphonates and plicamycin do. In
spite of this, severe hypercalcemia can be treated with a combination of calcitonin, which can be given for 1 to 2 doses
and either plicamycin, bisphosphonates or gallium nitrate. Calcitonin also possesses pain relief properties that can relieve
metastatic bone pain. Calcitonin is safe and causes mild nausea, flushing, abdominal cramps and allergic reactions to
salmon. Skin testing with 1 unit of salmon calcitonin prior to therapy is recommended.
Gallium nitrate is given as a continuous IV infusion at 200-mg/square meter of body surface in 1 liter of fluid daily for 5
days. Gallium appears to be more effective in lowering the calcium to normal and prolonging this effect than calcitonin.
However, normal calcium levels are not obtained until the 5 days of therapy is completed and the lowest levels are at 3
days post infusion. Also, it appears that gallium is more effective than etidronate in normalizing the calcium by about 50%.
The main side effect is nephrotoxicity and should not be given if renal insufficiency is present. Patients should not be
given other renal toxic drugs, as aminoglycosides and hydration should be maintained. Decreased hemoglobin and
phosphates can also occur.
Steroids useful if the patient has multiple myeloma, lymphoma, vitamin D intoxication, or granulomatous disease and is
given as 200-300 mg of hydrocortisone IV daily for 3-5 days.
Hyperkalemia
Immediate Questions:
A. What are the vital signs?
B. Is the lab result correct? Consider pseudohyperkalemia, especially if the ECG shows no changes of hyperkalemia.
There are a number of causes of factitious hyperkalemia, the most common being the tourniquet method of drawing
blood. A tight tourniquet around an extremity can elevate the potassium. Hemolysis of a blood sample prior to the
chemical determination is another source of error. Extreme leukocytosis (>70,000) or thrombocytosis (>1,000,000) can
elevate the serum potassium. If there is a question, obtain a plasma potassium.
C. What is the patient's urine output?
D. What does the ECG show? The ECG is the most important test, (besides the potassium level). It provides more of a
"bioassay" than the serum potassium. Changes seen with potassium increase include peaked T waves, flat P waves,
prolonged PR interval and a widened QRS complex, progressing to a sine wave and arrest. E. Is the patient taking any
medication that could raise the potassium level? Is the patient receiving potassium in an intravenous solution? If the
patient is receiving spironolactone, triamterene, indomethacin and other NSAIDS; ACE-inhibitors, trimethoprim /
sulfamethoxazole, pentamidine, succinylcholine; stop these medications immediately.
Differential Diagnosis:
A. Redistribution 1. Acidosis drives potassium out of the cells and can cause hyperkalemia 2. Cellular breakdown a.
Rhabdomyolysis b. Hemolysis c. Tumor lysis syndrome
B. Increased total body potassium 1. Inadequate excretion a. Renal caused (acute or chronic renal failure) b.
Mineralocorticoid deficiency or Addison's disease c. Drug-induced (potassium sparing diuretics [e.g., spironolactone] and
ACE-inhibitors) 2. Excessive intake
C. Pseudohyperkalemia 1. Hemolysis of the specimen
2. Prolonged period of tourniquets occlusion prior to blood draw
3. Thrombocytosis/leukocytosis
Plan:
The severity of hyperkalemia (as judged by the serum level and the ECG) dictates treatment.
A. Repeat any abnormal value, taking care to avoid hemolysis, while assessing for increased WBC or platelets.
B. Prevention of further hyperkalemia; discontinue any potassium administration and any contributing drugs.
C. Calcium administration. Calcium counteracts membrane effects and protects the heart. Calcium antagonizes the
membrane effects of hyperkalemia and restores normal excitability within minutes. Administer one to two ampules of
calcium gluconate, (10-20 mL of a 10% solution IV over 3-5 minutes), with the patient on a cardiac monitor.
98
D. Potassium can be quickly shifted into cells by the administration of alkali or glucose plus insulin (one ampule D50 and
10 units regular insulin).Sodium bicarbonate (1 ampoule [44 mmol] of bicarbonate) may be administered intravenously
over several minutes.
E. Remove potassium from body. Kayexalate may be administered orally or as an enema. Remember that this will trade
potassium for sodium and result in a sodium load. Normal saline diuresis can assist removal of potassium.
ACUTE THERAPY OF HYPERKALEMIA
Condition: ECG changes of hyperkalemia
Therapy: Calcium gluconate (10%) 10 ml IV over 3 minutes. Repeat in 5 minutes if needed. Follow with 10 units regular
insulin IV; the insulin may be by IV push, but must be followed with 1 ampule D50 IV push; alternatively, 10 units regular
insulin in 500cc D20 may be infused over 30 to 60 minutes.
Comment: Lasts only 30 to 60 minutes. No bicarbonate after calcium.
Condition: After acute phase or if no ECG changes
Therapy: Kayexalate: Oral dose of 30 to 60 grams in 50 ml sorbitol (20%). Rectal dose of 50 grams in 200 ml sorbitol
(20%) as retention (30 to 45 minutes) enema.
Comment: Oral dose preferred (enemas are only if patient cannot take po).
Condition: If renal failure
Therapy: Hemodialysis as soon as possible. Kayexalate also will be effective, but not immediately.
HYPERKALEMIACalcium gluconate 10%: 10-30 ml IV. Lasts 30-60 min.
Glucose and insulin: 50 grams glucose hourly and 5 units regular insulin q 15 min. Duration 2 hrs.
Sodium bicarbonate: 50-100 mEq IV. Duration 3-6 hrs.
Albuterol: 10-20 mg by inhaler. Duration 2 hrs.
Sodium polystyrene sulfonate (Kayexalate) 15-60 gms with sorbitol PO or 50-100 gms with retention enema
(retain for 30-60 min).
Furosemide: 40-240 mg IV over 30 min.
Ethacrynic acid: 50-100 mg IV over 30 min.
Bumetanide: 1-8 mg over 30 min.
Hemodialysis which is much more effective than peritoneal dialysis.
HYPERNATREMIA
Immediate Questions:
A. What is the patient's mental status?
B. What have been intake, output and serial weights?
Clinical Findings:
A. Na+ serum is usually 150 mEq/L before symptoms manifest; a rapid rate of increase is more likely to result in problems
B. Na+ 160 mEq/L: irritability, anorexia, ataxia, cramping
C. Na+ 180 mEq/L: confusion, stupor, and seizure
Diagnostic Considerations:
Extracellular Fluid Volume State
Management:
A.
B.
99
Assess the extracellular fluid volume.
"Hypernatremia with increased volume": Therapy is diuresis (e.g., furosemide), and replacement of the urine output
with water (D5W).
C.
"Hypernatremia with " normal volume": Hypovolemia usually is not evident because of the large intracellular water
reserve. Acute
therapy is water (D5W) replacement, and evaluation for possible DI.
D.
"Hypernatremia with decreased volume", (i.e., water loss Na+ loss): Estimate the degree of volume depletion by
using:
Water depletion approximately (0.6 X body weight) X [measured serum sodium / 140] -1) *Correct volume with normal
saline, and follow with half-normal saline. * If initial serum Na+ >175, prevent cerebral edema by monitoring serum Na+
hourly until it reaches 155 mEq/L, allowing a decline of at most 2 mEq/L/hr.
Replace one-half this volume over the first 24 hours, the remainder over the next 1-2 days.
HYPOKALEMIA
Immediate Questions:
100
A. Is the patient symptomatic? Symptoms of hypokalemia include weakness, nausea, vomiting and abdominal tenderness.
Severe hypokalemia can depress reflexes and cause weakness.
B. What medications is the patient taking? Loop diuretics and amphotericin causes potassium wasting by direct renal
effects.
C. Is there a history of vomiting, nasogastric suction, diarrhea or renal problems (such as renal tubular acidosis)?
Database:
Because potassium is the principle intracellular cation, measured serum hypokalemia usually represents a significant loss
of body potassium. Thus, serum levels of 3.0 meg/L (mmol/L) often reflect total deficits of 100-200 mEq or more. Look for
coexisting hypocalcemia and hypomagnesemia. Check ABG's, as acid-base disorders may coexist and obtain an ECG.
Severe hypokalemia can cause blunting of reflexes, paresthesia and paralysis.
Plan:
A. Aggressive potassium replacement should be performed only after adequate renal function has been documented.
B. Parenteral replacement should be considered for digoxin toxicity, significant arrhythmia, and severe hypokalemia (<3.0
mmol/L). Maximum concentrations of KCl used in peripheral veins generally should not exceed 10-meq/100 cc, due to the
damaging effects of high concentrations on the veins.
C. For lesser degrees of hypokalemia that require parenteral replacement, 10 to 15 mEq/h may be infused peripherally.
The maximum infusion rate is 10 mEq/hour. Check serum levels frequently (every 2-4 hours depending on clinical
response) to avoid hyperkalemia. ICU monitoring is required if arrhythmias are present or for rapid infusions of KCl.
D. Oral replacement includes liquids and tablets. Slow-release pills typically contain 8, 10 or 20-mEq tablet. Thus, it will
take several days to replete the potassium depletion. Replacement doses should be 40-120 mEq qd in divided doses,
depending on the patient's weight and level of hypokalemia. More than 20 mEq in one dose can cause GI upset.
HYPOMAGNESEMIA
Immediate Questions:
A. What are the patient's vital signs? Cardiac arrhythmias including atrial fibrillation, ventricular tachycardia and ventricular
fibrillation can occur.
B. Is the patient tremulous? Tremor, tetany, muscle fasciculations, and seizures are all associated with magnesium
deficiency. Determining the presence of these neurologic problems will help guide the urgency of treatment.
Differential Diagnosis:
Hypomagnesemia can be caused by medications; especially diuretics, antibiotics (ticarcillin, amphotericin B),
aminoglycosides, cisplatin, and cyclosporin, often cause hypomagnesemia. Alcoholism and reduced intake/ malabsorption
also can cause hypomagnesemia.
Laboratory Data:
Electrocardiograph findings may include prolongation of the PR, QT, and QRS intervals, as well as ST depression and T
wave changes. Rhythm disturbances include supraventricular arrhythmias, as well as ventricular tachycardia and
ventricular fibrillation.
Plan:
A. Asymptomatic individuals can be treated with oral magnesium. Oral magnesium oxide (20 meq of magnesium per 400
mg tablet) can be administered as 1 or 2 tablets per day; oral administration is most appropriate for chronic maintenance
therapy.
B. Magnesium sulfate 1 g (2 mL of a 50% solution of MgSO4) equals 98 mg of elemental magnesium. For moderate
depletion, infuse 6 GMs (12 ml of 50% MgSO4 = 6 GMs) in 500 ml saline can be given IV over 3 hours, followed by 5 gm
in 500 ml saline over the next 6 hours. The 50% solution must be diluted for IV use. For slightly less urgent situations, 1
g/h may be given q3-4h with close monitoring of deep tendon reflexes. As long as signs and symptoms of
hypomagnesemia are improving, the infusion can then be slowed so that the patient receives approximately 10 g of
magnesium sulfate in the first 24 hours.
Intramuscular magnesium sulfate. Give 1-2 g IM q4h for 5 doses during the first 24 hours.
101
HYPONATREMIA
Important Questions:
A. Is the lab value real? Repeat any abnormal lab. Was it drawn above IV site? What's the glucose? What are lipids?
B. What's the volume state, based both on the patient's history and current exam? What fluids have been administered?
C. CNS sx? Are there any recent prior sodium levels to document the chronicity of the hyponatremia? The urgency of
correction depends on the patient's symptoms and the acuteness of the hyponatremias onset.
Differential Diagnosis:
The initial differentiation is between true hyponatremia and laboratory artifact. True hyponatremia may be classified
according to the volume status of the patient: hypovolemic, euvolemic or hypervolemic. Hypovolemic hyponatremia may
be further classified by serum and urine chemistries.
DIFFERENTIAL DIAGNOSIS of SIADH
102
1. Malignant neoplasia
a. Carcinoma (bronchogenic, duodenal, pancreatic,
Ureteral, prostatic, bladder)
b. Lymphoma and leukemia
c. Thymoma, mesothelioma, and Ewing's sarcoma
2. CNS disorders
a. Trauma, subarachnoid hemorrhage, subdural hematoma
b. Infection (encephalitis, meningitis, brain abscess)
c. Tumors
d. Porphyria
e. Stroke
3. Pulmonary disorders
a. Tuberculosis
b. Pneumonia
c. Mechanical ventilators with positive pressure
d. Lung abscess
4. Drugs (including vasopressin, chlorpropamide, thiazide
diuretics, oxytocin, vincristine, haloperidol, nicotine,
phenothiazine, tricyclic antidepressants)
5. Others
a. "Idiopathic" SIADH
b. Hypothyroidism
HYPONATREMIA CLASSIFIED BASED ON SERUM
OSMOLALITY, VOLUME STATE and URINE SODIUM
Calculated Na Deficit = 0.6 (Wt. in kg) (140 - Na) + (140)
(Volume deficit in L) (mEq)
Corrected Na for LIPID, PROTEIN and GLUCOSE
% serum H2O = 99 - 1.03 (lipids in gm/L) - 0.73 (protein in
gm/dl)
corrected Na = measured Na X 93/% serum H2O
change in Na = 0.016 (measured glucose - 100)
corrected Na = 0.016 (measured glucose - 100) + measured Na
HYPOPHOSPHATEMIA
Immediate Questions:
A. Is the patient an alcoholic, recovering from DKA or refeeding orally or parenterally?
B. Symptoms or signs of weakness? (Clinical findings may not be prominent, despite PO4 of less than 1.0 mg/dl).
Treatment:
A. IV replacement is used for levels less than 1.0 mg/dl (even without symptoms).
B. Monitor K, Mg, Ca, as abnormalities of other cations often coexists.
MAGNESIUM TOXICITY
(Consideration when treating preeclampsia)
Immediate Questions:
A. What dose of magnesium sulfate was the patient receiving? Most patients receive 1-2 MgSO4 IV every hour. This dose
is regulated by following serum levels and changes in physical examination such as decreased patellar reflexes, which are
suggestive of high serum magnesium levels. Magnesium sulfate used in patients with premature labor may require doses
of up to 3g/h.
103
B. What was her last serum magnesium level? Clinically significant hypermagnesemia can begin to be seen at levels as
low as 4 mEq/L. Most patients who are being maintained on magnesium sulfate for the prevention of eclampsia will be
held at 4-6 mEq/L.
Management:
1. Magnesium. Toxicity may be seen at levels as low as 4 mEq/l. Most patients are maintained at 4-6 mEq/l to prevent
eclampsia. Respiratory depression can appear at magnesium levels of 8-10 mEq/l, and cardiotoxicity, while not usually
seen until levels exceed 10 mEq/l, can occur at any serum magnesium level.
2. Electrocardiogram. Obtain a baseline study. Hypermagnesemia may manifest itself as a shortened Q-T interval up
through complete heart block.
3. Calcium gluconate. Administer 1 g IV over approximately one minute, while waiting for serum magnesium and
electrolyte values. If calcium administration improves the patient's status, then magnesium toxicity is most likely the
correct diagnosis: magnesium is a calcium antagonist, and calcium should reverse its toxicity.
4. Urine output. The kidneys secrete magnesium. Urine output should be maintained at a minimum of 30 mL/h.
CONVERSIONS Equations
TEMP: 40C=104F/39=102.2/38=100.4/37=98.6
C=(F-32) x 5/9
F=(C x 1.8) + 32
1inch=2.54cm 1cm=0.3973
1lb=0.454kg 1kg=0.45kg
1L=1.06qt=33.81oz
RENAL FUNCTION
CREATININE CLEARANCE:
(cockroft-gault eq)
(140-Age) (wgt in Kg)
--------------------- (X 0.85 if Female)
(72) (Serum Cr)
Endogenous Creatinine: primarily excreted
by glomerular filtration
Affected by: age, sex, dietary protein
exercise, drugs & Dz
DRUGS requiring dose change w/renal fxn
- H2 BLOCKERS: accumulates w/renal dz
& may interfere w/Cr excretion
thus increasing serum levels
- AMINOGLCOSIDES:
- Some Beta LACTAM Antibiotics:
- Some Beta BLOCKERS:
Renal FXN & the Elderly: Cr Clearance
may decrease w/age from nml renal
aging & GFR may decline @ 10cc/min
for each decade over 40
REF: Friedman: Corr of Est Renal Fxn
JAMA 37:145-149,1989
ACUTE RENAL FAILURE
A. Symptoms
1. Polyuria, Oliguria or Anuria
2. Hematuria
3. Dysuria
4. Uremia
a. Definition: symptomatic azotemia
b. Acidosis (В± tachypnea)
104
c. Mental Status changes
d. Hypervolemia / Hypertension
e. Hyperkalemia
f. Pericarditis
5. Duration <3 months
B. Etiologies
1. Location of Lesion
a. Prerenal - ~70% of cases
b. Intrinsic - ~25% of cases
c. Post-renal (obstructive) - <5% of cases
2. Pre-renal azotemia
a. Renal Artery Stenosis (atherosclerosis, fibromuscular dysplasia)
b. CHF - reduced ejection fraction, hypoperfusion
c. Hepatorenal syndrome (cirrhosis with ascites may show similar picture)
d. Shock - renal hypoperfusion (usually hypovolemia and/or hypotension)
3. Parenchymal Damage
a. Nephritis (inflammation): glomerular vs. interstitial
b. Tubular Injury: most common cause of ARF
c. Nephrotic Syndrome (total protein losses)
4. Obstruction of Outflow (~5%)
a. Urinary Tract Infection (UTI) with Pyelonephritis
b. Urinary Calculus disease (renal stones)
c. Crystal Deposition
d. Bladder tumors with extensive invasion
e. Prostatic Enlargement: BPH vs. Carcinoma
f. Unilateral obstruction with only one functioning kidney
5. Vascular
a. Hypertension
b. Atherosclerotic (atheroembolism) - cholesterol emboli, 5-10% of hospitalized ARF [8]
c. Trauma
d. Vasculitides
e. Post-operative - aortic aneurysm repair, aortic cross-clamping
6. Pathophysiology
a. Ischemia is the underlying problem in many patients with ARF
b. This leads to depletion of cellular ATP and release of calcium
c. Reactive oxygen species are produced leading to further cell death
d. Calcium release leads to phospholipase activation
e. Neutrophils may mediate reperfusion injury (ICAM-1 is involved)
f. Many nephrotoxins are renal vasoconstrictors (eg. cyclosporine, radiocontrast)
C. Initial Evaluation
1. Consider possible etiologies and direct evaluation towards these
2. Medications should always be suspected in contributing to or causing ARF
a. Non-steroidal anti-inflammatory drugs (NSAIDS)
b. ACE Inhibitors
c. Aminoglycoside
d. Radiocontrast Agents
e. Amphotericin
f. Cyclosporine
g. Cisplatin
h. Interstitial Nephritis - sulfonamides, NSAIDS, other antibiotics
3. Standard Blood Testing
a. Electrolyte and renal panel, Ca2+, Phosphate, Mg2+, Albumin
b. Complete Blood Count (В± reticulocyte count and ESR)
4. Foley catheter must be placed to rule out bladder obstruction
5. Urine for electrolytes, dipstick and microscopic analysis
a. Osmolality, creatinine, Na+, K+, Clb. Urine spot protein to creatinine ratio (normal is <0.2)
c. Pigment: Hemoglobin (myoglobin)
d. Cells, Casts, Crystals, Organisms
e. Consider Urine culture
6. Renal and Pelvic Ultrasound - stones, hydronephrosis, mass compression
7. Consider Abdominal radiograph if ultrasound is not done to rule out stones
8. Consider sedimentation rate, ASO titer, ANA, Complement Levels, Anti-GBM Abs
9. Renal Biopsy should be considered in rapidly progressing disease
a. ANCA and Anti-GBM diseases – consider cyclophosphamide + glucocorticoids
b. Idiopathic rapidly progressive glomerulonephritis is often ANCA positive
c. However, other inflammatory diseases such as bacterial endocarditis can given ANCA+
D. Pathology Summary
1. Glomerular Involvement
a. Diffuse: all glomeruli in a tissue section are diseased
105
b. Focal: some glomeruli in a section are diseased
c. Segmental: some parts of an individual glomerulus are affected
2. Focal Glomerulonephritis:
a. Some of the glomeruli are dead b. Death can include necrosis, collapse, or sclerosis
c. Acute or chronic inflammation is often seen
3. Crescent Glomerulonephritis
a. Crescent (moon shaped) formation in glomerulus
b. Affected glomeruli are non-functional
c. Very poor prognosis
4. Focal and Segmental Glomerulosclerosis: portions of many glomeruli are destroyed
5. Minimal Change Glomerulonephritis
a. Glomeruli appear okay, but function is poor
b. Electron microscopic evidence of basement membrane disease
c. Response to glucocorticoids is usually very good
6. IgA Deposition
a. IgA nephropathy
b. Deposition of IgA immune complexes
c. Differential includes Systemic Lupus and Henoch-Schönlein Purpura
7. Proliferative Glomerulonephritis
a. Increase in mesangial cell number
b. Usually follows insults (eg. Post-Streptococcal)
c. May be seen in collagen vascular disease, especially Systemic Lupus
8. Collapsing Glomerulonephritis
a. Major form seen in HIV nephropathy
b. Usually late stage
c. Rapid progression to renal failure (weeks to months)
d. No effective therapy to date
9. Tubular Necrosis
a. Tubular cells die and slough off basement membrane
b. The dead tubular cells form casts, which can occlude lumen
c. Glomerular basement membrane may also be damaged
E. Management
1. Renal Diet
a. Low phosphate, potassium, sodium, and protein
b. High calcium and vitamin D
c. Various multivitamin formulas available for renal patients, eg. Nephro-ViteВ®
d. Low protein diet may slow progression slightly in chronic renal disease [3]
2. Phosphate and Calcium
a. Dangerous if product of Calcium and Phosphate > ~70 (mg/dl) (will lead to precipitation)
b. If product is close to 70, then phosphate should be lowered with aluminum compounds
c. These compounds should be given with meals to bind the phosphate directly
d. If product is <60, then calcium should be given 500-1000mg po tid with meals
e. If calcium is low but phosphate normal, then calcium should be given before meals
f. Consider using 1,25 dihydroxyvitamin D supplements
3. Acidosis
a. Renal tubular acidosis (RTA) is common in early renal failure
b. Oral Bicitra (citrate replaces bicarbonate) may be used
c. Bicitra is contraindicated in edematous states due to high sodium content
4. Hyperuricemia
a. Check uric acid levels
b. Uric acid deposition in renal tubules may worsen progression of renal failure
c. Allopurinol may be given (100-200mg po qd) to attempt normalization of uric acid
5. Adjust medication dosages for the renal failure
a. 24 hour urine collection for accurate GFR determination
b. Discontinue NSAIDS and other nephrotoxic medications
6. Hypertension
a. ACE inhibitors generally contraindicated in moderate to severe renal failure
b. Calcium blockers such as nifedipine are effective
c. Labetalol is also very effective but patient should have LV EF>50% and no bronchospasm
d. Consider Hydralazine for afterload reduction
e. Pure alpha-adrenergic blocking agents may be effective, but tachyphylaxis may occur
f. Diuretic agents may improve hypertension and volume overload
7. Volume overload
a. Attempt to maximize cardiac output and improve intravascular volume
b. Diuretics often worsen renal failure but may be necessary to prevent pulmonary edema
c. In general, potassium sparing diuretics should be avoided (high risk hyperkalemia)
d. Dopamine or mannitol can be tried, but are usually not effective
e. Albumin infusions are probably not helpful, but may help diuresis in low albumin states
f. Dialysis may be required particularly in severe volume overload situations
106
8. Protein Load
a. Thought to reduce incidence of azotemia
b. Appears to slow progression of chronic renal failure [4]
c. Patients with moderate renal disease – some decrease in progression on low protein diet
d. Patients with severe renal disease show no benefit on low protein diet [3]
9. Hospital inpatients with acute renal failure have ~50% mortality rate
10. Newer Agents
a. Atrial natriuretic factor (ANF) are dilators with diuretic activities
b. ANF (AuriculinВ®) may have some efficacy in oliguric renal failure [6]
c. ANF may increase renal dysfunction in diabetics receiving radiocontrast [7]
d. Other vasodilators (eg. calcium channel blockers) are not effective
e. Renal growth and regeneration factors are under investigation
F. Dialysis Indications
1. Serum abnormalities unresponsive to medical therapy
a. Severe Acidosis
b. Severe Hyperkalemia
2. Uremia
a. Mental status changes (usually delirium)
b. Nausea and vomiting
c. Pericarditis (pericardial friction rub)
3. Volume Overload
4. Renal function and initiation of dialysis
a. Native kidneys may continue with minimal function for 6-12 months
b. After that, native kidneys usually shut down permanently
G. Kidney Transplantation
1. Excellent (and improving) results with cadaveric grafts
2. New kidney usually placed in extraperitoneally in the pelvis
3. Cyclosporin usually required for life
4. Prednisone В± azathioprine may be required for life
5. Other immune suppression, eg. OKT3, mycophenolic acid, FK506 may also be used
OLIGURIA (Sudden)PRERENAL AZOTEMIA: BUN: creatinine > 20:1; urine osmolality > 500; urine spot urine sodium < 20; FEna < 1%; urine
sediment may show hyaline casts; Signs of intravascular volume depletion include low cardiac output states as CHF,
tamponade, arrhythmias, cardiogenic shock, massive pulmonary embolism, OR intravascular volume depletions
secondary to hemorrhage, renal losses with diuretics, osmotic diuresis, sequestration of fluid in a third space such as
diarrhea, pancreatitis, peritonitis, skin looses from burns, excessive sweating OR increased renal/systemic vascular
resistance such as vasodilation from antihypertensive drugs, anaphylaxis, anesthesia, sepsis, drug overdose, OR renal
vasoconstriction from alpha adrenergic agonists or high dose dopamine, surgery, anesthesia, hepatorenal
syndrome, OR impaired renal autoregulation from prostaglandin synthesis inhibitors such as NSAIDS in the presence of
CHF, nephrotic syndrome, cirrhosis, hypovolemia or preexisting liver disease, ACE inhibition in the presence of
bilateral renal artery stenosis or CHF.
POSTRENAL AZOTEMIA: (Obstructive uropathy) BUN: creatinine > 20:1; urine osmolality variable; urine spot sodium is
variable, may be < 20; FEna variable; may be < 1%; urine sediment is normal or may contain RBCs, WBCs, or crystals;
urine volumes fluctuate day to day; bilateral hydronephrosis or hydroureter on sonography; enlarged bladder or
prostate. Ureteral obstruction may be caused by papillary necrosis, blood clots, sulfonamide or uric acid crystals,
fungus balls, stones, retroperitoneal hemorrhage and fibrosis, ureteral ligation during pelvic surgery, and tumors of the
prostate, cervix and uterus. Bladder outlet obstruction can be caused by bladder carcinoma, stones, clots, functional
impairment from neuropathy or ganglionic blocking agent, prostatic hypertrophy or malignancy. Urethral obstruction is
caused by congenital valves, strictures, and phimosis.
INTRINSIC RENAL DISEASE: acute tubular necrosis will produce a BUN: creatinine < 20:1; urine osmolality < 350; urine
spot sodium > 20; FEna > 1%; urine sediment shows granular casts, renal tubular epithelial cells, and cellular debris,
pigment, and crystals. There may be a history of significant hypotension and renal hypoperfusion, and exposure
to nephrotoxins. Nephrotoxins include aminoglycoside, amphotericin B, radiographic contrast media,
immunosuppressive drugs as cyclosporin, heavy metals as lead, arsenic, chemotherapeutic agents as cisplatin,
methotrexate, organic solvents as ethylene glycol, myoglobin, hemoglobin, calcium, uric acid and oxalates. Acute
glomerulonephritis and vasculitis will produce a BUN: creatinine > 20:1; urine osmolality > 500; urine spot sodium < 20;
FEna <1%. The urine sediment shows RBCs and RBC casts. There may be systemic evidence of vasculitis as SLE or
other collagen vascular disease. There may be a history of sore throat and strep infections. The causes include
glomerulonephritis, toxemia of pregnancy, hemolytic uremic syndrome, DIC, malignant hypertension, and radiation
injury. Acute interstitial nephritis shows a BUN: creatinine less than 20:1; urine osmolality is variable; urine spot sodium
is variable; FEna variable; urine sediment shows WBC and WBC casts and eosinophils. There may be a history of
allergic reaction, drugs, infections, peripheral eosinophilia and thrombocytopenia. Causes include fungal infections,
bacterial infections, viral infections, drugs as beta lactam antibiotics, sulfonamides, rifampin, NSAIDS, cimetidine, and
phenindione. Renovascular occlusion (Arterial) shows a BUN: creatinine < 20:1; urine osmolality is variable; urine spot
107
sodium is variable; FEna is variable; urine sediment is variable; renal vein thrombosis is associated with nephrotic
syndrome or with compression or invasion of the renal vein by tumor. The causes include renal artery embolism,
thrombosis, dissection (postangioplasty or traumatic), aortic aneurysm, and thrombotic microangiopathy.
Renovascular occlusion (Venous) shows a BUN/creatinine < 20:1; urine osmolality variable; urine spot sodium variable;
FEna variable; urine sediment variable. Renal vein thrombosis is associated with nephrotic syndrome or with
compression or invasion of renal vein by tumor. Causes include renal vein thrombosis and compression, Individuals
with sudden occlusion of one or both of their main renal arteries may have acute flank pain, fever, livedo reticularis,
marked elevation of LDH (found in large quantities in renal cells), increased ESR, decreased serum complement
levels, thrombocytopenia, eosinophilia and/or evidence of thrombotic thrombocytopenic purpura. There may be
abdominal bruits, aneurysms, reduced or absent femoral pulses, or peripheral or cerebral vascular diseases.
There may be atrial fibrillation, recent MI or endocarditis that embolizes. A history of aortic catheterization may point
to cholesterol embolization. The FEna (fractional excretion of sodium) = Una x Pcr / Pna x Ucr x 100 where the Una=urine
sodium (mEq/L), Pna=plasma sodium (mEq/L), Pcr=plasma creatinine (mg/dL), and the Ucr=spot urine creatinine
(mg/dL).
ACUTE TUBULAR NECROSIS (ATN)
A. Pathophysiology [1]
1. Renal medulla receives blood supply after oxygen has been extracted in the cortex
2. In addition, low blood flow in medulla is required to maintain osmotic gradients
3. Therefore, medulla is especially susceptible to hypoxia, usually from hypoperfusion
4. ATN is the most common cause of acute renal failure in hospital
5. Renal Vasodilators help prevent ischemic injury
a. Nitric oxide
b. Prostaglandin - especially PGI2 (prostacyclin)
c. Adenosine
d. Dopamine
e. Urodilatin
6. Renal Vasoconstrictors
a. Endothelin
b. Angiotensin II
c. Vasopressin
7. Electrolyte transport inhibitors can also limit damage (by reducing energy needs)
a. Prostaglandin E2
b. Adenosine
c. Dopamine
d. Platelet activating factor
B. Etiology
1. Drugs
a. Aminoglycoside
b. Cis-platinum, methotrexate, mitomycin
c. Cyclosporin
d. Radiocontrast Agents (Intravenous)
e. Amphotericin
2. Myoglobinuria (Rhabdomyolysis) and possibly Hemoglobinuria (hemolysis)
3. Ischemia / Hypotension
a. Hemorrhage / Shock / Anesthesia (intubation)
b. Sepsis
c. Pre-renal azotemia prolonged (eg. dehydration, hypotension)
d. Obstetric Complications
4. Factors Contributing to Likelihood of Renal Damage
a. Underlying renal disease – especially diabetes mellitus, hypertension, myeloma
b. Non-steroidal anti-inflammatory drugs (NSAIDS)
c. Baseline hypoxemia - COPD mainly
C. Signs and Symptoms
1. Oliguria or anuria
2. Epithelial ("muddy brown") Casts in Urine
3. Previous Toxin Exposure
4. Rapidly progressive azotemia – creatinine elevation 0.5-1mg/dl per day
5. Urine sodium usually high due to inability to reclaim electrolytes
6. Uremia
D. Treatment
1. Hydration - usually the most effective method, least toxicity
2. Mild diuresis to hasten toxin removal
a. Mannitol: increases lumen fluids, may prevent obstruction by casts and dead cells
b. Furosemide: increases toxin removal, theoretical sparing of tubules by blocking ATPase
c. Mannitol and furosemide are not effective in preventing contrast nephropathy
3. Dopamine (low dose, 2-4Вµg/kg/min) may improve urinary flow
108
a. Especially in patients with poor renal perfusion such as heart failure
b. However, no clear benefit in patients after major vascular surgery [3]
c. Use reasonable in patients who require diuresis with poor cardiac function and perfusion
d. This agent is probably worth trying in many patients, especially with above medicines
4. Discontinue any renal toxins and implicated medications
5. Dialysis
6. Atrial Natriuretic Protein (ANP, ANF; AuriculinВ®)
a. Produced in cardiac atria in response to elevated atrial pressures
b. Induces natriuretic diuresis
c. May improve outcome in oliguric renal failure
CHRONIC RENAL FAILURE
(CRF)
A. Etiology
1. Azotemia means abnormally high BUN (>28) and creatinine (>1.5) levels due to reduced GFR
2. Prerenal azotemia
a. Renal hypoperfusion
b. Usually with heart failure or liver failure
c. Renal artery stenosis
3. Intrinsic Renal Azotemia
a. Intrinsic disease, usually glomerular
b. Hypertension (~28%) and Diabetes (~33%) are the most common causes
c. Glomerulonephritis accounts for ~12% of current cases
d. Renal (glomerular) deposition diseases
4. Postrenal azotemia - obstruction of some type
5. Long-term progression of (cumulative) insults to kidney
6. CRF requires duration >3 Months
7. Common Underlying Causes of CRF
a. Hypertension - systolic BP >210 or diastolic >120 mm has 22X increased risk of CRF [3]
b. Diabetes - over 30% of persons with CRF have diabetes mellitus
c. Renal Deposition Diseases – amyloidosis and others
d. Renal Vascular Disease - renal artery stenosis, atherosclerotic vs. fibromuscular
e. Medications - especially causing tubulointerstitial diseases
B. Electrolyte Abnormalities
1. Excretion of Na+ is initially increased, probably due to natriuretic factors
2. As glomerular filtration rate (GFR) falls, fractional sodium excretion rises
a. Maintain volume until GFR <10-20ml/min, then edema will occur
b. In renal failure with nephrotic syndrome, edema occurs early
c. Can not conserve Na+ when GFR <25ml/min, and Fe Na rises with falling GFR
3. Tubular K+ secretion is decreased
a. Aldosterone mediated. Also increased fecal loss of K+ (up to 50% of K ingested)
b. Can not handle bolus K+, so must avoid drugs high in K+
c. Do not use K+ sparing diuretics
4. Control of acids
a. Normally, produce ~1mEq/kg/day H+
b. When GFR <40ml/min then decrease NH4+ excretion adds to metabolic acidosis
c. When GFR <30ml/min then urinary phosphate buffers decline and acidosis worsens
d. Bone CaCO3 begins to act as the buffer and bone lesions result (renal osteodystrophy)
e. Usually will not have wide anion gap even with acidosis if can make urine
f. Acidosis caused by combination hyperchloremia and hyper sulfatemia (SID reduction)
g. Defect in renal generation of HCO3-, as well as retention of nonvolatile acids
5. Loss of urine diluting and concentrating abilities
a. Osmotic diuresis due to high solute concentration for each functioning nephron
b. Reduce urinary output only by reducing solute excretion
c. Major solutes are salt and protein, so these should be decreased
6. Bone metabolism
a. GFR reduction leads to elevated blood phosphate, low calcium and acidosis
b. In addition, reduced tubular resorption of calcium augments hypocalcemia
c. Other defects include acidosis and decreased dihydroxy-vitamin D production
d. Bone acts as a buffer for acidosis, leading to chronic bone loss in renal failure
e. Low vitamin D causes poor calcium absorption and hyperparathyroidism (high PTH)
f. Increased PTH maintains normal serum Ca2+ and PO42- until GFR <30ml/min
g. Chronic hyperparathyroidism and bone buffering of acids leads to severe osteoporosis
7. Other abnormalities
a. Slight hypermagnesemia with inability to excrete high magnesium loads
b. Uric acid retention occurs with GFR <40ml/min
109
c. Vitamin D conversion to dihydroxy-Vitamin D is severely decreased
d. Erythropoietin (EPO) levels fall and anemia develops
8. Accumulation of normally excreted substances, "uremic toxins", MW 300-5000 daltons
C. Uremic Syndrome
1. Symptomatic azotemia
2. Fever, Malaise
3. Anorexia, Nausea
4. Mild neural dysfunction
D. Associated Problems and Treatment
1. Immunosuppression
a. Patients with CRF, even pre-dialysis, are at increased risk for infection
b. Cell mediated immunity is particularly impaired
c. Hemodialysis seems to increase immunocompromise
d. Complement system is activated during hemodialysis
e. Patients with CRF should be vaccinated aggressively
2. Anemia
a. Due to reduced erythropoietin production by kidney
b. Occurs when creatinine rises to >2.5-3mg/dL
c. Rarely clinically significant until 6-12 months prior to dialysis
3. Hyperuricemia
4. Hyperphosphatemia
a. Decreased excretion by kidney
b. Increased phosphate load from bone metabolism (by high PTH levels)
5. Hypertension
a. ACE inhibitors shown be most effective at preserving renal function [ 1, 6]
b. Blood pressure control is very important to slowing progression of renal failure
c. Patients with grade IV (severe) HTN have 22X-increased risk vs. normal for CRF [3]
d. Targeted mean pressure 92-98mm Hg in patients with renal failure and proteinuria [2]
e. ACE inhibitors are avoided in patients with serum creatinine >2.5-3mg/dL
6. Poor coagulation
a. Platelet dysfunction - usually with prolonged bleeding times
b. May be partially reversed with DDAVP administration
7. Proteinuria >0.25gm per day is an independent risk factor for renal decline [2]
E. Evaluation
1. Search for underlying causes (see above)
2. Laboratory
a. Full Electrolyte Panel
b. Calcium, phosphate, uric acid, magnesium and albumin levels
c. Urinalysis, microscopic exam, quantitation of protein in urine (protein: creatinine ratio)
d. Calculation of creatinine clearance and protein losses
e. Complete blood count - anemia can occur, low erythropoietin levels
f. Consider complement levels, protein electrophoresis, and antinuclear antibodies, ANCA
g. Renal biopsy - particularly in mixed or idiopathic disease
3. Radiographic Evaluation
a. Renal Ultrasound - evaluate for obstruction, stones, tumor, kidney size, chronic change
b. Duplex ultrasound or angiography or spiral CT scans to evaluate renal artery stenosis
c. Magnetic resonance angiography preferred over contrast agents
4. Bone Evaluation
a. Severe secondary hyperparathyroidism can lead to osteoporosis
b. Some patients will require parathyroidectomy to help prevent this
c. Unclear when bone densitometry should be done on patients with CRF
F. Pre-Dialysis Treatment
1. Maintain normal electrolytes
a. Potassium, calcium, phosphate are major electrolytes affected in CRF
b. Discontinue ACE inhibitors in most patients with creatinine >3.0mg/dL
c. Reduce or discontinue other renal toxins (including NSAIDS)
d. Diuretics (eg. furosemide) may help maintain potassium in normal range
e. Renal diet including high calcium and low phosphate
2. Reduce protein intake to <0.6gm/kg body weight [5]
a. Appears to slow progression of diabetic and non-diabetic kidney disease
b. In type 1 diabetes mellitus, protein restriction reduced levels of albuminuria
3. Underlying Disease
a. Diabetic nephropathy should be treated with ACE inhibitors until creatinine >2.5-3mg/dL
b. Hypertension should be aggressively treated (ACE inhibitors may be preferred) [1]
c. Caution with use of ACE inhibitors in renal artery stenosis
G. Hemodialysis
1. Indications
a. Uremia - azotemia with symptoms and/or signs
b. Severe Hyperkalemia
110
c. Volume Overload - usually with congestive heart failure (pulmonary edema)
d. Toxin Removal - ethylene glycol poisoning, theophylline overdose, etc.
2. Procedure for Chronic Hemodialysis
a. An arteriovenous fistula in the arm is created surgically
b. Catheters are inserted into the fistula for blood flow to dialysis machine
c. Blood is run through a semi-permeable filter membrane bathed in dialysate
d. Composition of the dialysate is altered to adjust electrolyte parameters
e. Electrolytes and some toxins pass through filter
f. By controlling flow rates (pressures), patient's intravascular volume can be reduced
g. Most chronic hemodialysis patients receive 3 hours dialysis 3 days per week
3. Efficacy
a. Some acids, BUN and creatinine are reduced
b. Phosphate is dialyzed, but quickly released from bone
c. Very effective at reducing intravascular volume and potassium levels
d. Once dialysis is initiated, kidney function is often reduced further
e. Not all uremic toxins are removed and patients generally do not feel "normal"
f. Response of anemia to erythropoietin is often suboptimal with hemodialysis [4]
4. Chronic Hemodialysis Medications
a. Anti-hypertensives - often labetalol, calcium blockers, ACE inhibitors
b. Erythropoietin (EpogenВ®) - given for anemia, in ~80% of dialysis patients
c. Vitamin D Analogs - calcitriol given intravenously
d. DDAVP may be effective for patients with symptomatic platelet problems
MYOCARDIAL ISCHEMIA
A. Symptoms
1. Classical
a. Chest Pain, squeezing
b. Radiation to left, both, or right arms (shoulders)
c. Nausea and vomiting
d. Diaphoresis
e. Shortness of Breath
f. Responds to rest or to nitroglycerin
2. Non-Classical
a. Burning chest pain - may be increased in women
b. Tingling in arms
c. Abdominal or Epigastric Pain
d. No symptoms (silent ischemia)
3. Silent Ischemia
a. Most common in diabetics and women [27]
b. Patients with heart transplants have no somatic pain inputs from new heart
c. Both peripheral and central nervous systems are involved in lack of pain sensation
d. Frontal cortical activation is present in patients with pain, absent without pain [28]
4. Initial Evaluation
a. History, especially cardiac risk factors, previous cardiac events
b. Targeted physical exam – jugular venous distension, lungs, heart, extremities (edema)
c. Comorbid conditions: stroke, peripheral vascular disease, and renovascular disease
d. Vital signs including pulse-oximetry or arterial blood gas
e. ECG; old ECG is very helpful for interpretation of ECG abnormalities
f. Consider Chest Radiograph
g. Women should be evaluated similar to men, particularly post-menopausal patients
5. Assess Coronary Artery Disease (CAD)
B. ECG Changes
1. Reversible ST segment Depression
a. Down-sloping depression most specific
b. Horizontal depression is less specific
c. Up-sloping (with J point) is most likely a normal variant
d. Patients may have abnormal (CAD) or normal (Syndrome X) Coronary Arteriograms
2. Variant Angina (Prinzmetal's)
a. ST segment elevation
b. Vasospasm induced, relieved when spasm stops
c. May be due to underlying plaque / thrombus which is variably lodged / dislodged
d. Overall good prognosis; related to tobacco use
e. Other vasospastic diseases are commonly found (eg. migraine, Raynaud's Disease)
C. Stable Angina
1. Definition
111
a. Angina on exertion, relieved by resting В± nitrates
b. Cardiac etiology confirmed by ECG or ETT
c. Most patients have demonstrable epicardial coronary artery disease (CAD)
2. Etiology
a. Epicardial coronary artery disease (CAD) present in most patients
b. Stable atherosclerotic plaques present in majority
c. TRUE cardiac angina in patients with normal epicardial vessels is called "Syndrome X" or
microvascular angina
d. Syndrome X patients may have vasospasm, abnormal vessel dilation (see below)
3. Evaluation
a. Medical history suggestive of cardiac angina
b. Concomitant risk factors
c. Exercise Treadmill Test
d. Dobutamine echocardiography
e. Catheterization for high-risk patients who are candidates for PTCA or cardiac surgery
f. The most important part of evaluation is patients history and cardiac risk factors
g. This provides a pre-test probability of coronary disease
h. Tests are done to rule out coronary disease and avoid unnecessary cardiac angiography
4. Exercise Treadmill Testing (ETT)
a. Walking (or arm) ergometry to increase myocardial workload
b. Workload includes increased heart rate, blood pressure, and myocardial vessel dilation
c. In general, attempt to achieve >90% of maximal heart rate: max HR ~ 220 - Age
d. Monitor symptoms and ECG for specific changes (ST depressions most specific)
e. Test is gauged by Rate Pressure product (RPP) = SBP x Maximum HR
f. A "good" (interpretable) test usually has RPP > 20,000
g. Combination with thallium or technetium (MIBI) improves specificity and sensitivity
h. Patients with the following abnormal results have high risk for coronary disease:
• Decrease in or no change in blood pressure during test
• Global ischemia
• Lung uptake (thallium)
• Reversed cavity dilatation
i. ETT may be less useful in women and in persons with poor exercise tolerance [27]
j. Women have increased number of false positives with ETT vs. men
k. However, nuclear tests often show large number of false positives in low risk patients
l. In women and patients with baseline ECG anomalies, especially LBBB, nuclear studies or
dobutamine
(stress) echocardiography must be used
m. However, in patients with normal ECG, nuclear scans add cost but no information [1]
n. Due to low pre-test probability of CAD for normal ECG
5. Stress-Echocardiography [2]
a. Assessment of wall motion abnormalities (implies ischemia) at high cardiac work
b. Similar sensitivity and specificity as other pharmacologic stress tests
c. Dobutamine (10-40Вµg/kg/min) is usually used to increase cardiac work (as above)
d. Atropine (0.25-1mg iv) may be added to increase heart rate to >90% predicted
e. Ultrasound (echocardiogram) is used to detect work-induced wall motion abnormalities
f. Wall motion abnormalities usually occur prior to development of symptoms
g. Test is useful for evaluation of chest pain to rule out myocardial source
h. Extremely useful in preoperative assessment in patients who cannot exercise
i. Negative predictive value for late cardiac events ~87% in patients with suspected coronary disease
j. Positive predictive value ~25%; therefore, best used to rule out cardiac ischemia
6. Classification
a. Class I: Angina with prolonged exertion
b. Class II: Angina with walking >2 blocks
c. Class III: Angina with walking <2 blocks
d. Class IV: Angina with minimal or no exertion
D. Therapy of Exertional Angina [3]
1. Control of Cardiac Risk Factors
a. Hypertension itself can cause angina
b. Cholesterol reduction is critical
c. Diabetes control
d. Tobacco abuse
2. Pharmacologic Agents
a. Goal is control of rate-pressure product (ie. control pulse and blood pressure)
b. Гџ-Blockers are preferred over calcium channel blocking agents
• ß-blockers have been proven to reduce mortality in angina as well as MI
• Use Calcium blockers only when ß-Blockers are contraindicated
• Calcium blockers reduce anginal symptoms but do not reduce mortality
112
c. All patients should be on ASA if tolerated (consider sulfinpyrazone as substitute)
d. Vitamin E (alpha-tocopherol) supplementation, but not Гџ-carotene, provided a minor decrease in
incidence of angina in persons with no known coronary artery disease [25]
3. Specific Therapy
a. Atenolol/Metoprolol (Гџ-blockers) are excellent agents for the treatment of stable angina
b. Adding nifedipine or IsordilВ® (or both) to atenolol does not improve overall symptoms
c. Long acting nitrates reduce anginal symptoms but do not reduce mortality
d. Some calcium blockers cause vasodilatation, increased ischemia, and coronary "steal"
4. In patients not controlled on monotherapy, further evaluation of angina may be indicated
a. Patients with high-risk ETT results should undergo coronary angiography
b. Other causes of angina should be considered
E. Unstable Angina
1. Definitions
a. Originally defined as angina at rest
b. Now includes new onset angina and accelerating angina also
c. Crescendo (accelerating or increasing) non-rest angina
2. Mechanisms
a. Likely similar to that for MI; may be precursor lesion
b. Vasospasm and transient clot formation are likely contributors
c. Non-occlusive thrombi often form on top of severely obstructed coronary lesions
d. Vasoconstrictors (Serotonin, thromboxanes, ADP, PAF, etc.) are likely involved
e. Many of the patients with unstable angina have multi-vessel disease
3. Evaluation
a. Medical history is the key element here
b. Exercise treadmill test is contraindicated in unstable angina
c. Patients with recurrence, on medications, should undergo coronary angiography
d. Dobutamine echocardiography may be reasonable pre-angiography screening test
4. Decision to Treat [4]
a. Risk stratification important: high or moderate risk patients are admitted to hospital
b. Patients with known CAD, age >60-70, ECG changes, hemodynamic changes are high risk
c. Diabetes - very important risk factor, especially since patients may not have pain
d. 2-10% of hospitalized patients with unstable angina will progress to MI
5. Treatment of High Risk Patients (hospitalized)
a. Aspirin: All patients without contraindications should be given one EC-ASA (325mg) qd
b. Aspirin must be given prior to stopping heparin to prevent recurrent ischemia
c. Ticlopidine (TiclidВ®) should be considered in patients intolerant to aspirin
d. IIb/IIIa in route to cath lab
e. Heparin (standard): therapeutic levels important
f. Low Molecular Weight Heparin - Nadroparin more effective than standard heparin]
g. Hirudin or Hirulog, direct platelet inhibitors, are about as effective as heparin
h. Morphine for resistant pain (and consider further evaluation)
i. Reduce Heart Rate - ischemia is exacerbated by high HR; Гџ-blockers preferred
j. Angioplasty in appropriate candidates
k. Angioplasty probably safer than atherectomy
l. Patients with pre-infarction angina who do progress to MI are likely to have very rapid reperfusion
(mean
~40 minutes) with thrombolytic therapy
m. Thrombolytics of no benefit overall in patients with unstable angina (without MI)
n. Nitrates: sublingual given initially, iv nitroglycerin if pain continues, otherwise paste
6. Outpatient Management
a. Begin Гџ-blocker (preferred) or calcium blocker to HR 50-60
b. Control blood pressure with systolic 130-150 and diastolic <80 if possible
c. Begin ASA (81-325mg qd) or ticlopidine (250mg po bid; monitor blood counts)
d. Consider nitrates (eg. patch or oral formulation)
7. Additional Therapy [6]
a. Consider coumadin or low molecular weight heparin in outpatients [24]
b. Consider ticlopidine for patients allergic to aspirin
c. Aspirin / coumadin combinations
d. In hospitalized patients to receive anti-coagulation, Hirulog has less bleeding than heparin [21]
e. Abciximab (ReoProВ®), an anti-platelet antibody, is safe and effective in unstable angina
F. Microvascular Angina [16]
1. Definition
a. Chest Pain
b. Abnormal ECG, ETT with ST depressions
c. No significant coronary artery stenosis on angiography
d. ~5% of patients with myocardial infarction will have normal coronaries
e. Previously called "Syndrome X" (distinct from insulin resistance syndromes)
2. Etiology [ 8, 9]
a. Vasospasm vs. microvascular disease
b. Abnormal arterial dilatory responses (inadequate vasodilator reserve)
113
c. Role of hyperinsulinemia, insulin resistance, and dyslipidemia
3. Treatment [10]
a. Agents above, but also agents to reduce vasospasm (eg. diltiazem, nicardipine)
b. Aspirin should probably be used as described below
c. Ca agents probably more effective than Гџ-blockers in this syndrome (no real data)
d. Tricyclic antidepressants may have efficacy (eg. Imipramine 25-50mg po qhs)
e. Prognosis is excellent; disease is benign (communicate this to the patient)
G. Summary of Pharmacologic Agents
1. Nitrates
a. Vasodilation: Nitroglycerin (iv or paste): short acting primarily venodilator
b. Isosorbide Dinitrate (IsordilВ®): direct, long acting vasodilator, mainly venous action
c. Isosorbide Mononitrate (ISMOВ®): 20mg bid (7 hours apart) or qd, reduced tolerance and rebound
compared with dinitrates
d. The Mononitrate is the major active metabolite of dinitrate with ~100% bioavailability
2. Aspirin
a. 325mg po qod or 81mg qd (strongly consider H-2 blocker to prevent GI ulcers)
b. Sulfinpyrazone is not effective
c. Ticlopidine 250mg bid may be as effective as ASA; consider in ASA-allergic patients
3. Гџ-Blockers
a. Excellent anti-ischemic agents (anti-inotropic, anti-chronotropic)
b. Also control premature ventricular contractions (PVC) and other arrhythmias
c. Demonstrated benefit on survival
d. Contraindications: bronchospasm, diabetes, low-EF states, impotence
e. Suggest Metoprolol 50-100mg bid-tid or Atenolol 50-100mg qd (both oral)
4. ACE inhibition
a. Excellent afterload reduction / anti-hypertensives
b. Strongly recommended in diabetics with hypertension
c. Effective and safe in patients with COPD, arrhythmias, peripheral vascular disease
d. Examples: captopril, enalapril, lisinopril, etc.
5. Heparin [14] and other anti-coagulants
a. IV bolus then drip for 2-3 days in all patients with unstable angina or rule out MI
b. Consider warfarin in patients with PTCA, diabetes, high risk of MI or ASA intolerant
c. ASA must be given before heparin is stopped or recurrent unstable angina likely to occur
d. Hirudin, a direct thrombin inhibitor from leeches, has reduced early events after PTCA compared
with
heparin, but no improvement in late events [20]
e. Hirulog, a synthetic direct thrombin inhibitor, has reduced bleeding compared with heparin, more
easily
dosed, but no overall improvement in mortality outcomes
6. Calcium Antagonists
a. Verapamil most effective for hypertrophic cardiomyopathy and to slow heart rate
b. Diltiazem excellent for slowing heart rate with less anti-inotropic activity
c. Nifedipine: peripheral vasodilation, good for BP reduction, but causes reflex tachycardia
d. Felodipine, amlodipine, isradipine, nicardipine have less anti-inotropic effects
e. Calcium blockers can induce coronary steal syndromes
• Non-diseased vessel dilatation is greater than that of diseased vessel
• Therefore, blood is shuttled into dilated healthy vessels, away from ischemic areas
f. In general, calcium antagonists are not recommended post-MI
g. They should be considered if patients are intolerant of Гџ-blockers
7. Cholesterol Reduction
a. Clear data that secondary prevention (post-MI) is beneficial
b. Cholesterol reduction, especially in patients with coronary artery disease, as a primary measure is
still
debated but very reasonable.
c. Cholesterol reduction leads to plaque stabilization and sometimes regression [17]
d. Increased dietary fiber intake reduced risk of CAD independent of cholesterol [26]
8. Antioxidant Vitamins
a. Oxidized form of LDL is major contributor to atherosclerosis
b. Antioxidants can prevent LDL oxidation
c. Vitamin E >100U per day po supplement reduced coronary artery disease progression
d. Main effect occurred only in patients on colestipol-niacin for high cholesterol [18]
e. Vitamin E slightly reduced incidence of angina in primary prevention cohort [25]
f. Randomized studies are complete and pending publication
9. Other Agents
a. Ticlopidine may be used in aspirin intolerant / allergic patients
b. Lamifiban - platelet aggregation inhibitor with efficacy in unstable angina
c. Newer anti-platelet agents (RGD inhibitors of platelet integrin function)
114
Myocardial Infarction (MI)
RISK FACTORS
A. Risk Factors for MI
1. Smoking
a. Responsible for ~21% of all mortality from heart disease
b. Quitting within 5 years decreased risk 50-70%; quit >5 years has near non-smoker risk
c. Smoking
d. Smoking + Oral Contraceptives ~39X increased risk
2. Lipid Profile
a. 2-3% decrease in risk for each 1% decrease in serum cholesterol
b. Low HDL (<35mg/dl) is independent risk factor
c. Hypertriglyceridemia is a risk factor only in setting of high LDL:HDL ratio
d. High lipoprotein a {Lp(a)} levels is a risk factor in hypertriglyceridemic white men
e. High Lp(a) levels is best correlate of CAD in patients with high LDL-C [37]
f. Lowering cholesterol improves coronary artery endothelial dilatory responses
g. Reduction of cholesterol in persons with high cholesterol reduces MI risk ~37%
3. Hypertension
a. 2-3% decrease in risk for each 1mm diastolic BP decreased to DBP ~85 mm
b. Interaction with diabetes, cholesterol
c. HTN also major risk for stroke
4. Left Ventricular Hypertrophy (LVH)
a. LVH appears to be an independent risk factor for MI and premature death
b. LVH as a risk is also independent of coronary artery disease
c. LVH is a more important single risk factor than HTN, smoking, high cholesterol
5. Genetic
a. Family History
b. Male Sex; Post-menopausal women
c. Other genetic disease (hyperlipidemias, homocystinuria, thrombotic disorders, etc)
6. Hyperhomocystinemia
a. Autosomal recessive genetic trait affecting 1:20,000 persons
b. Many patients with atherosclerosis have high homocysteine serum levels
c. ~20% of patients with hereditary homozygous disease (cystathionine Гџ-synthase deficiency) will
have a
thromboembolic event by age 20
d. Patients with CAD should probably take B vitamin complex to lower serum homocysteine
e. Folic acid 1mg po qd will usually reduce homocysteine levels; may add vit B6/B12 also
f. Studies ongoing to determine role of high serum homocysteine levels in CAD [35]
g. Appears that each 5ВµM increase in homocysteine increases cardiac risk as much as a 20mg/dL
increase in total cholesterol
h. Low serum folate is a risk factor for heart disease, may correlate with homocysteine [3]
7. Cocaine
a. Potent vasoconstrictor, also increase cardiac oxygen demand
b. Synergistic with smoking to cause ischemia and myocardial infarctions
8. High levels of fibrinogen, von Willebrand factor antigen, tissue plasminogen activator are mild risk factors for
CAD
(~2 fold increase each compared to low levels) [25]
9. Summary of Risk Factors For MI
a. Left Ventricular Hypertrophy (LVH)
b. Male age >45 or Female age >55 yrs.
c. Hypercholesterolemia
d. Low HDL (<35mg/dl)
e. Smoking
f. Hypertension
g. Diabetes
h. Family History
i. Sedentary Lifestyle
j. Obesity
k. Fibrinogen Elevation [15]
l. Cocaine abuse
m. Serum Homocysteine Elevations
B. Cardiovascular Risk Reduction
1. Exercise [ 5, 6]
a. Fairly good data show risk reduction ~50% for active life style
b. Aerobic activity may be of maximal benefit
c. Sudden exertion in sedentary persons is definite risk for infarction
2. Aspirin, Low Dose
a. PHS (Physicians' Health Study)
115
b. Randomization to ASA or not (325mg qod) for 22,071 male physicians
c. Total MI ~50%; 75% in fatal MI in ASA group (p<.006 in all groups)
d. Stroke incidence increased ~15% though p>0.1 in all (fatal, nonfatal, total) groups
e. Data on low (160mg and 80mg po qd) dose not yet available
f. Risk of bleeding and possibly stroke are increased
3. Estrogen Replacement Therapy (ERT)
a. Cardioprotective effects of estrogen
b. Estrogen may be inotropic agent as well as anti-atherosclerotic (alters lipid profile)
c. ~45% decreased risk in women who take estrogen vs. those who do not
d. Progesterone may partially decrease estrogen's protective effect
4. Elevated HDL Levels
a. HDL subtypes 2 and 3 are major cardioprotectant
b. They are anti-atherosclerotic
c. Levels of total HDL > 60mg/dL are considered protective
5. Alcohol: Mild-Moderate consumption may decrease risk of MI 25-45%
a. Appears to correlate with decrease HDL2 and HDL3 sub fractions [7]
b. No significant changes in total cholesterol or triglycerides
c. Moderate alcohol also increase endogenous tissue plasminogen activator levels [8]
6. Anti-Oxidants [36]
a. No clear benefit of anti-oxidant vitamin C, trend benefit only for Гџ-carotene, in CAD
b. Vitamin E taken for 2 years reduces risk of CAD in men and women 30-60%
c. Probucol + lovastatin may improve dilation of atherosclerotic coronary arteries
7. Other Factors
a. High Fish Oil (marine n-3 fatty acids) does not decrease risk of coronary disease
b. Moderate n-3 fatty acid (seafood) intake does reduce risk of cardiac arrest [32]
c. Highest quartile dietary fiber intake was independently associated with 40% risk reduction for MI
compared with lowest quartile intake [38]
d. High doses of folate and/or vitamin B6 (pyridoxine) may reduce serum homocysteine
C. Symptoms of Coronary Artery Disease
1. Crushing or squeezing substernal chest pain
2. Usually radiates to left shoulder
3. High suspicion with shortness of breath, vomiting, and/or diaphoresis
4. Must distinguish from gastrointestinal pain (usually esophageal pain)
5. In women, diabetics, elderly, symptoms may be atypical, very mild or even absent
6. Good correlation between suspicion of CAD from history and physical and results of testing
7. Physician suspicion and exercise stress (thallium) tests correlate well
D. Blood Test Results
1. Creatine Kinase (CK) elevation (normal 25-125)
a. MB isozyme specifically (MM=striated muscle; BB=brain)
b. Note that skeletal muscle <5% MB form
c. Peaks 20-24 hours post MI
d. Specific CK MB isozyme analysis may detect MI within 6-12 hr [17]
2. Cardiac Troponin T testing is available for diagnosis of MI
3. Lactate Dehydrogenase
a. LDHI/LDHII > 1 implies MI
b. Peaks 2-3 days post event
c. Note LDH not useful in hemolytic or megaloblastic anemia or renal insufficiency
4. AST peaks 24-48hrs post-MI
5. Leukocytosis - due to stress response: epinephrine and cortisol production
E. Pathophysiology of MI [ 18, 19, 20]
1. Prevalence of coronary occlusion during early hours of transmural MI
a. ~90% of patients seen within 4 hours of onset of symptoms have total occlusion
b. ~65% of patients seen 12-24 hours of onset had total occlusion
2. Etiology of Occlusion [40]
a. Total arterial thrombotic occlusion is found in most cases of infarction
b. The thrombus has formed on a newly ruptured atherosclerotic plaque
c. Coronary artery vasospasm is responsible for occlusion in minority of cases
d. Unstable angina is usually caused by a non-total thrombotic occlusion (mural thrombus)
e. The underlying problem is initial formation of atherosclerotic plaque, which ruptures
f. Platelets adhere to exposed surface of ruptured plaque and activate thrombus formation
3. Involvement of Vasoconstrictors
a. Thromboxane A2
b. Serotonin - vasoconstrictive effects on diseased (but not healthy) arteries
c. Platelet activating factor (PAF)
d. Thrombin
e. ADP
4. Lack of Vasodilator Substances
a. Insufficient nitric oxide (EDRF)
b. Adenosine
c. Prostacyclin
116
5. Occlusion often resolves over next 24-48 hours without treatment
6. Reperfusion Injury
a. Tissue ischemia and necrosis stimulates complement and other systems
b. Increase in neutrophil migration into dead / dying tissue
c. Release of toxic oxygen species may contribute to injury
F. Prognosis
1. Ejection Fraction (EF) is most accurate predictor of prognosis
a. Echocardiography usually used to determine EF
b. Radio ventriculography more accurate but gives no valve function data
c. Cardiac catheterization can provide a good estimate of EF
d. Note that cardiac output, not just EF, is important for determining heart function
2. Complications post-MI indicate poor prognosis (eg. arrhythmias, bundle branch block, CHF)
3. Even asymptomatic ventricular arrhythmias have 2 fold increased incidence of death.
4. Stress thallium test may be done 3-6 weeks post-MI
a. Exercise test preferred to evaluate functional status
b. Thallium should be used to assess dead vs. ischemic myocardium
c. Determine if coronary angiography is indicated
d. That is, is there additional myocardium at risk?
The Use of Beta-Blockers for Acute Myocardial Infarction
Contraindications
Bradycardia of < 50 beats/min
Significant first-degree atrioventricular block
(pulse rate > 240 ms)
Systolic blood pressure of less than 90 mm Hg
High-degree atrioventricular block
Acute congestive heart failure
Severe asthma
Recommended IV Dosage of Beta-Blockers for Patients with Acute Myocardial Infarction on Admission
Propranolol 0.1 mg/kg (IV) divided into three equal doses given at 5-minute intervals Metoprolol (Lopressor) three
5 mg (IV)doses given at 2-minute intervals. If 15mg tolerated, start 50mg PO dose 15 minutes after IV dose
finished. Esmolol (Brevibloc) Loading dose: 0.5 mg/kg/min for 1 minute followed by a maintenance infusion of 50
ug/kg/min. If an inadequate therapeutic effect is observed, the loading dose should be repeated over 1 minute
followed by an increased maintenance dose and orally administered beta-blockers without intrinsic
sympathomimetic activity (e.g., atenolol, metoprolol, propranolol, or timolol) are then used 30 to 60 minutes after
the intravenous dose. (See PDR for additional titration information.)
Thrombolytic Agents in Acute Myocardial Infarction
Administration of Thrombolytic
Agents
1. Start two 18-g peripheral intravenous lines.
2. No ABGs or central lines may be used or started before treatment.
Streptokinase (Kabikinase, Streptase)
1.Dilute two 750,000-unit vials of streptokinase with 5 ml of 5% dextrose in water.
2.Gently swirl to dissolve.
3.Add this dose of 1.5 million units to 150 mL of 5% dextrose in water.
4.This should be infused over 60 minutes.
5.Monitor for the first few hours for signs of anaphylaxis or allergic reaction. Infusion should be slowed if the blood
pressure drops 25 mm Hg or terminated if asthmatic symptoms appear.
6.Begin a 5,000- to 10,000-unit bolus dose of heparin followed by 1,000 units per hour approximately 3 to 4 hours
after completion of streptokinase infusion or when partial thromboplastin time is < 100 seconds.
7.Monitor prothrombin time, partial thromboplastin time, and fibrinogen levels during therapy.
Alteplase, recombinant (tPA Activase)
1.Dilute two 50-mg vials with sterile water for injection provided in the package.
117
2.Gently swirl to dissolve.
3.The total dose is 100 mg over 1.5 hours. (For patients who weigh < 65 kg, use 1.25 mg/kg.)
4.Add this dose to a 100-mL bag of 0.9% sodium chloride for a total volume of 200 mL.
5.Infuse 15 mg (30 ml) over 1 to 2 minutes.
6.Infuse 50 mg (100 ml) over the remainder of the first 30 minutes.
7.Begin a 5,000- to 10,000-unit bolus dose of heparin followed by continuous infusion of 1,000 units per hour.
8.Infuse 35 mg over the next hour.
9.Check partial thromboplastin time 3 to 4 hours after the end of the infusion.
Contraindications to Thrombolysis
Absolute
Active bleeding
Possible Aortic dissection
Prolonged CPR
Head injury
Central nervous system neoplasm
Hemorrhagic retinopathy
Pregnancy
Streptokinase or anistreplase allergy
Blood pressure > 200/120 mm Hg after sublingual
nifedipine
Prior cerebral bleeding
Trauma or surgery within 2 weeks
Relative
Trauma/surgery longer than 2 weeks
Chronic severe hypertension
Active peptic ulcer disease
History of cerebrovascular accident
Bleeding diathesis
Anticoagulant medication
Liver dysfunction
Previous Streptokinase / Alteplase
CONGESTIVE HEART FAILURE (CHF)
A.
Introduction to Cardiac Pump Function
1. Cardiac output depends on filling of heart (preload) and resistance to emptying (afterload)
2. Starling Curve is a graphic relationship between cardiac output and Preload/Afterload
a. Relationship between venous return to the LV (Preload, or Left Atrial Filling Pressure)
b. And Afterload (vascular resistance) as they determine the cardiac output (LV)
3. The curve shows that as left ventricular end diastolic volume (LVEDV) increases, LV stroke volume also
increases
a. This probably occurs up to a maximal LV output
b. After this, further filling of the heart may lead to decreased cardiac output
4. The curve also shows that as afterload (resistance to emptying) increases, Cardiac Output decreases
5. For a given clinical situation, preload and/or afterload may be suboptimal
6. It should be noted that preload here refers to LV preload, or return from the lungs
7. The central venous (R sided) pressure may not be a reliable indicator of LV preload
8. Invasive monitoring with a may be indicated
a. A catheter is inserted through the RA, to the RV, into the pulmonary artery
b. The catheter balloon is inflated ("wedged") to estimate LA pressures
c. This LA pressure, pulmonary capillary wedge pressure (PCWP)are usually related
d. LVEDV ~ LV end diastolic pressure ~ pulmonary capillary wedge pressure
e. SEE BELOW…
B. Considerations in Evaluation of CHF
1. Underlying Etiology
a. By anatomy
b. By function (systolic or diastolic)
c. Hypertension is/was present in >90% of CHF patients [32]
2. Anatomy of the failing heart
118
3. Severity and Disability
4. Polypharmacy
C. Anatomic Types [1]
1. Hypertrophic
a. Hypertensive
b. Aortic Stenosis
c. Hereditary
2. Dilative
a. Viral
b. Alcoholic
c. Post-MI (ie. infarction due to coronary disease)
d. Mitral Regurgitation
e. Familial
f. Small Vessel: microvascular angina
g. Hemochromatosis
h. Cobalt toxicity
i. Tachycardia induced dilation - may be reversible
3. Restrictive
a. Pericardial process (usually post-inflammatory)
b. Amyloidosis
c. Hemochromatosis
d. Scleroderma
e. Sarcoidosis
D.
Major Symptoms and Signs
1. Left Sided Failure
a. Rales (pulmonary congestion)
b. S3 Gallop - rapid filling of dilated ventricle
c. Displaced point of maximal impact / Left heart border
d. Tachycardia / arrhythmia - tachycardia can also induce LV dysfunction
e. Narrow pulse pressure due to peripheral vasoconstriction
f. Acute pulmonary edema with hypoxia, dyspnea, may progress to hypercarbia
g. Cardiac Cachexia (weight loss, muscle loss) partly due to high heart rate [6] and TNF [7]
2. Right Sided Failure
a. Usually seen with L sided failure, but may be unilateral (eg. patients with lung disease)
b. Jugular venous distension
c. Pedal Edema (pitting)
d. Hepatojugular reflex / Hepatomegaly
e. Hypotension
3. Elevated BUN and Creatinine (due to renal hypoperfusion)
E. Newer Classification of CHF [ 2, 3]
1. Systolic Dysfunction
a. LV Ejection Fraction (EF) < 40%
b. Loss of heart muscle with inability to pump; remodelling then occurs (including fibrosis)
c. Good filling (preload) of ventricle, poor unloading
d. Compensation by increased preload, tachycardia, hyperadrenergic ("cold, clammy") state
e. Occurs in ~60-70% of CHF cases [28]
2. Diastolic Dysfunction (see Below)
a. Diastole, with LV muscle relaxation, requires ATP
b. Poor ventricular filling (impedence to filling)
c. Typically hypertensive cardiomyopathy, aortic stenosis, diabetics with LVH
d. Patients tend to be older and have less coronary disease than patients with systolic CHF
e. Growth factors, including angiotensin II, may be responsible for LVH
f. Occurs in ~30-40% of CHF cases [28]
g. Diastolic dysfunction also occurs in constrictive and restrictive pericarditis
3. Clinical signs are unreliable indicators of type of CHF
4. Echocardiography is indicated for evaluation of CHF and proper management [30]
F. Mortality from Heart Failure
1. Arrhythmias
a. Bradycardia, VT, VF
b. May be asymptomatic until sudden cardiac death occurs
c. Amiodarone may prolong survival in CHF with asymptomatic ventricular arrhythmias [26]
2. Cardiogenic shock
3. Fulminant Respiratory Failure due to Pulmonary edema
4. Mortality Rates
119
a. Class II or III: 50% mortality at 5 years
b. Class IV: 50% morality < 1 year
5. Over 750,000 new cases per year; >250,000 deaths per year
G. Therapy of Systolic Failure
1. General Considerations [20]
a. Fluid Restriction 1.5-3L per day depending on symptoms
b. Low Salt Diet - 3gm/d initially; lower to 2gm/d if continued fluid retention
c. Diuretics as needed for symptomatic relief
d. TEDs stockings - very effective and underutilized
e. Oxygen as needed
f. ETOH restricted to 30ml/day
g. Activities as tolerated
2. Types of Agents
a. Afterload reduction
b. Vasodilators, nonspecific
c. Diuretics (preload reduction)
d. Inotropic Agents
e. Anti-ischemics
f. Low dose Гџ-adrenergic blockers
3. Afterload Reduction
a. ACE inhibitor: most efficacious agents for symptomatic and asymptomatic CHF [25]
b. Enalapril appears to lower mortality more than the hydralazine - nitrate combination
c. Hydralazine (see below)
d. Amlodipine (NorvascВ®) may show some benefit in improving symptoms in early studies
4. ACE Inhibitors in heart failure
a. A large number of studies have been done using ACE Inhibitors in heart failure
b. Overall reduction in mortality (usually from progressive CHF) was ~30%
c. Additional reduction in hospitalizations for progressive CHF
d. Patients with lowest ejection fraction (EF) have the greatest benefit
e. These agents are highly preferred as first line therapy in CHF
f. Long term (2-4 year) followup of ACE inhibitor (trandolapril) use 3-7 days post-MI with reduced EF confirmed
the
mortality and morbidity benefits of shorter term studies [29]
5. Vasodilator Combinations [ 9, 10]
a. Combination of isosorbide dinitrate and hydralazine decreases morbidity for CHF
b. Prazosin in high dose (20mg qd) is no better than control
c. Recent comparison of captopril + IsordilВ® vs. hydralazine + IsordilВ® shows ACE better
6. Inotropic Agents [11]
a. Digitalis decreases mortality from CHF only combined with diuretics
b. Should be avoided in diastolic dysfunction
c. Should be avoided in elderly, patients on quinidine, etc. [12]
d. Digitalis + ACE Inhibitors more effective (improved symptoms, EF, delayed progression) than ACE inhibitor
therapy alone in EF 35% Class II or III CHF [13]
e. Milrinone is a new positive inotropic agent developed for treatment of heart failure
- Increases cellular cAMP
- Dosing 10mg po qid
- Therapy with milrinone increases morbidity and mortality in severe CHF [14]
f. Vesnarinone, 60mg po qd, shown to have impressive effect in improving quality of life and preventing mortality
in
late stage heart failure. Higher doses worsen condition [15]
7. Гџ-Blocking agents [ 16, 27]
a. Low doses of metoprolol may prolong survival in patients with LV EF<40%
b. Appear to prevent high output failure and improve responses to other agents
c. Overall mean EF was actually increased and hospital admissions were decreased
d. Begin at 6.25mg bid and increase to 50mg po bid (then consider qd agent)
e. Bisopropyl had significant improvement in CHF symptoms, trend improved survival [24]
f. Carvedilol therapy showed moderate improvement in symptoms, EF, exercise [27]
g. Carvedilol reduced hospitalization and mortality in patients with EF<35% [31]
h. Bucindolol is another new Гџ-blocker for CHF in Phase III trials ("BEST" Trial)
8. Anti-Coagulation
a. Many experts recommend anti-coagulation for EF <15-20%
b. This is independent of rhythm or presence of intracardiac clots
c. No compelling data to support empiric anticoagulation in CHF in normal sinus rhythm [21]
d. Patients with known clots or in atrial fibrillation should be anti-coagulated
9. Diuretics
a. Useful for symptomatic relief and acute therapy
b. Generally use furosemide (LasixВ®) or other loop diuretic
c. Thiazide type diuretic (distal tubule function) can be added
120
d. Diuretics long term may deplete thiamine, leading to poorer LV function
e. Supplementation with thiamine in such patients may improve LV dysfunction (~4%) and diuresis (~500cc/day)
10. Arrhythmia Therapy
a. High risk of sudden cardiac / arrhythmia associated death with dilated cardiomyopathy
b. Patients with CHF and frequent ventricular arrhythmias have mortality ~15% per year
c. Amiodarone may provide some benefit in patients with non-ischemic dilated cardiomyopathy and
asymptomatic
ventricular arrhythmias [26]
d. However, AICD devices are usually recommended for symptomatic arrhythmias
e. Гџ-blockers may provide some benefit (low doses) in CHF with arrhythmias
11. Endstage Failure
a. Heart Transplant
b. Cardiomyoplasty
c. Role of bypass surgery is unclear but may improve function in ischemic disease [22]
d. Risk of surgery greatly increases as EF declines; EF~10% carries ~30% mortality risk
e. Angioplasty can be considered in patients with moderate-severe LV dysfunction and CAD
12. Severe CHF (ICU Setting)
a. Inotropic support with Dobutamine initially (В± dopamine)
b. If chronotropic activity not tolerated, substitute amrinone iv for dobutamine
c. Afterload reduction with nitroprusside may be required if tolerated
d. Further inotropic support with vasopressor activity may require epinephrine
e. Aortic balloon pump support may be required as bridge to surgery or transplantation
f. Magnesium levels should be maintained high (may reduce arrhythmias) [17]
H. Current Recommendations: Step Therapy for Systolic CHF
1. ACE Inhibition: afterload reduction and remodeling
a. Captopril to 50mg po tid
b. Enalapril to 10mg po bid
c. Lisinopril to 20mg po qd or bid
d. Newer Agents (early studies only; eg. ramipril, fosinopril)
e. Note: these agents were only effective at (near) maximal doses (lower doses not studied)
2. Hydralazine for afterload reduction (if failed ACE inhibitor)
a. Cardiac remodeling has not been studied with these agents
b. Doses 10-75mg po qid (100mg po tid) as tolerated by blood pressure
c. Concern for development of lupus-like syndrome
3. Digitalis: adds inotropism in low (eg. <35%) EF states.
a. Titrate to therapeutic levels
b. Should be avoided in hypertrophic cardiomyopathy and diastolic dysfunction
4. Diuretics
a. Primarily symptomatic relief (peripheral and pulmonary edema)
b. Titrate to desired patient weight
c. Loop diuretics (furosemide, bumetanide, torsemide) usually first line
d. Caution when initiating diuretics with ACE inhibitors
5. Гџ-Blockers
a. Systolic Dysfunction: Low to moderate dose only in systolic dysfunction
b. Consider higher doses in diastolic dysfunction
c. Reduce hyperadrenergic states; decrease high cardiac output failure conditions
d. Mortality benefit likely; clear benefit on morbidity
6. Nitrates
a. Major effect is to lower preload
b. Provide rapid symptomatic relief, may decrease ischemia induced cardiac dysfunction
c. May worsen CHF caused by diastolic dysfunction or aortic stenosis (preload reduction)
7. Consider vesnarinone for additional inotropic support
I. Therapy of Diastolic Failure
1. Treat underlying hypertension aggressively
a. ACE inhibitors, especially in diabetics or with accompanying systolic dysfunction
b. ACE inhibitors may be preferred agents because they may inhibit hypertrophy
c. Calcium blockers, especially verapamil or nifedipine (if severe)
2. Slow Heart Rate
a. Гџ-Blockers are highly preferred by most cardiologists (high dose if tolerated)
b. Verapamil (or diltiazem, if co-existent systolic dysfunction)
c. Anti-inotropic agents are recommended to improve diastolic relaxation
d. Nodal blocking agents are very useful atrial fibrillation associated with diastolic CHF
3. Other
a. Low dose diuretics for symptomatic improvement
b. Low dose nitrates for ischemia (which may worsen diastolic dysfunction)
c. The use of preload reducing agents (venodilators, diuretics) should be limited
d. This is because diastole in LVH is highly dependent on adequate preload for filling
121
e. Digoxin and other inotropes are contraindicated in diastolic CHF patients
4. Efficacy
a. Many patients with severe diastolic CHF will improve
b. No change in exercise capacity with verapamil or nadolol in mild-moderate hypertrophy
J. Treatment of Acute Pulmonary Edema Due to CHF
1. Nitrates: sublingual or paste
a. Dilation of coronary vessels
b. Preload reduction
c. Some afterload reduction
d. Should be used iv in severe situations
e. IV preferred in diastolic dysfunction, since preload reduction may worsen condition
2. Loop Diuretics, Given Intravenously
a. Furosemide (LasixВ®) or Bumetanide (BumexВ®)
b. Reduced preload volume by increasing urine output
c. Direct vasodilators (when given iv)
d. May be combined with thiazides or mixed diuretics in patients with renal insufficiency
3. Morphine
a. Coronary vasodilator
b. Decreases respiratory drive (decreases tachypnea) and anxiety
4. Reduces Blood Pressure (Afterload)
a. ACE inhibition
b. Hydralazine
c. Severe hypertension should be treated aggressively with IV nitroprusside
d. Nifedipine (may use sublingual or 10mg po tid-qid)
5. Dilative cardiomyopathy
a. Consider digitalis loading: Digoxin: 0.25mg iv q8 hours.
b. Decrease preload and afterload
6. Mnemonic: "LMNOP"
a. LasixВ® (Furosemide) or Ethacrynic acid in patients with allergy to furosemide
b. Morphine
c. Nitrates
d. Oxygen
e. Posture (upright)
7. Intensive Care Setting
a. IV Nitroprusside or Nitroglycerin
b. IV furosemide or bumetanide
c. ACE Inhibition
d. Intubation may be required; usually it is not prolonged (eg. 1-3 days)
e. Morphine
f. If ischemic cause, consider aspirin and heparin
g. Consider invasive monitoring, especially with intubation and/or sepsis
DIASTOLIC HEART FAILURE (DHF)
40% all CHF w /nml systolic Fxn - w/
diastolic dysfxn w/better prog than
w/systolic dysfunction
(Systolic dysfxn is often complicated
by sig diastolic component)
INCREASED DIASTOLIC FILLING PRESSURE
FROM NON-COMPLIANT VENTRICLE:
1. enlarged heart reaches limits of
pericardial expansion
2. hypertrophic myocardium stretches
less than nml myocardium
3. Interstitial or regional fibrosis
causes restricted diastolic filling
Seen in Pts w/
-mild-moderate HTN or ischemic Heart Dz
Dx of Diastolic Dysfunction: NO GOLD STD
(Dx of Exclusion)
1. Maintain high index of suspicion
2. Consider complete CHF Dif-Dx
3. r/o systolic dysfxn: nml EF & size
4. ECHO: LVEF & heart size
122
5. Assessment of rate of diastolic
filling & Г»rate of filling in both
rapid phase & atrial contraction
phase: w/worsening diastolic fxn,
amt of filling from atrial contrac
increases & ratio of filling from
atrial contraction/rapid phase
is > 1.
(complicated by changes in preload,
afterload, age, MR
CAUSES OF CHF:
1. Restrictive diastolic filling:
pericarditis & mitral stenosis
2. Myocardial Overload: MR & AS
3. Myocardial Dysfxn: MI, myocarditis
or idiopathic cardiomyopathy
TX:
- No Dig:
- No Afterload Reduction: assumes
poorly fxning heart & won't
improve CO
*Cautious Diuresis: overdiuresis may
lead to low output state from
increased filling pressures
for nml CO.
-Ca+ blockers & ГЎ-blockers may improve
fxn (particularly in IHSS)
-Ca+ blockers may improve active
relaxation & passive filling
-ГЎ-blockers slow rate for increased
filling time
Systolic Dz:
-Dig: Inotropy
-Nitrates & diuretics: reduce Preload
-ACEI's: reduce afterload
Torsades Des Pointes (Polymorphic VT)
stop 1a antiarrhythmics
may use overdrive pacer
or iv magnesium
due to low mg, quinidine
follow corrected q-t int:
corrected for rate: q-t/square root of r-r
IF UNSTABLE
cardiovert + lidocaine + ISOPROTERONOL
PULMONARY ARTERY CATHETERIZATION
A. Description
1. Catheter is a flow directed, balloon tipped devise inserted through a large vein
2. Fed through Right Atrium into ventricle then "wedged" into the Pulmonary Artery (PA)
3. Wedging is accomplished by inflating a balloon at the end of the catheter.
4. Pressures are recorded with balloon inflated while catheter is inserted forward
5. Allows determination of R sided pressures, PA pressures, and "Wedge" pressure
6. The "wedge" pressure is approximately the pulmonary capillary pressure (hence "PCWP")
7. Generally, PCWP = LAEDP (end diastolic pressure) = LV filling pressure (LVEDP, see below)
8. Other Uses of PA Catheter
a. Permits determination of oxygen consumption and cardiac output
b. Pacing from atrial and ventricular sites
c. Measurement of core body temperature
d. Measurement of intracavitary potentials
e. Infusion of medications and fluids
B. Theoretical Pressure Tracing
1. Catheter is fed through a dilator-sheath device ("cordice")
123
2. This devise is usually inserted into the R-Internal Jugular, L-Subclavian, or femoral veins
3. Balloon is inflated when RA is reached
a. Central venous pressure can be determined
b. Catheter is further inserted with balloon up into the RV
c. Arrhythmias are often seen (usually briefly) as tricuspid valve is passed
4. Once in the RV (note pressure tracing change), further advance into the pulmonary artery
a. In the wedged, balloon-up position in PA, PCWP is determined
b. The PCWP is used to estimate LV filling (see above)
5. Order of pressures is IVC/SVC (0-6cm) leads RA (0-8cm) leads to RV (20-25/6-12cm) leads to PA (20-25/10cm)
leads to Wedge (6-12 cm)
C. Indications
1. General Considerations
a. Majority of patients are hypotensive and/or with low (or no) urine output
b. Catheter is used to determine whether problem is with volume or heart pump function
c. This will help guide volume manipulations and choice of vasopressor agents
d. Especially useful in patients with >2 components of hypotension
e. Thus, volume status and pump function are determined from catheter data
2. Complicated MI See Card "MI-Complications"
a. Cardiogenic Shock
b. Severe Left Ventricular Failure
c. Right Ventricular (RV) Failure
d. Acute Mitral Regurgitation
e. Ventricular Septal Rupture
f. Cardiac Tamponade
g. Recurrent severe post-infarction ischemia
3. Respiratory Distress
a. Severe respiratory dysfunction of any cause
b. Adult Respiratory Distress Syndrome (ARDS)
c. Cardiogenic or non-cardiogenic pulmonary edema
d. Massive pulmonary embolism (PE)
e. Toxic inhalations
f. Mechanically ventilated patients, especially with high PEEP
4. Evaluation of specific causes of CHF
a. Dilative Cardiomyopathy
b. Constrictive vs. Restrictive Disease
c. Pre-capillary pulmonary hypertension
5. High Risk Obstetric Patients
a. Pre-existing Cardiac Disease
b. Pre-eclampsia and Eclampsia
c. Abruptio placentae
6. Multiorgan-System Failure Syndromes (MODS)
a. Severe Sepsis
b. Extensive Burns
c. Pancreatitis
d. Extensive Trauma
e. Persistent low output syndrome
7. Shock
a. Septic Shock
b. Hypovolemic Shock
c. Cardiogenic Shock
d. RV Failure due to Pulmonary Embolism
e. Cardiac Tamponade
8. Other Indications
a. Acute Renal Failure for volume management
b. Cirrhosis with ascites - volume management
c. Post- and intra-operative open heart and other surgeries
D. Limitations of PCWP and LVEDP Equivalency
1. PA inflated balloon pressure increase PCWP
a. Increased PVR
b. Heart Rate > ~120 beats per minute
c. Veno-occlusive disease (VOD)
2. PCWP increase Pulmonary Venous Pressure
a. Catheter tip location
b. Severe hypovolemia
c. PEEP
3. Pulmonary Venous Pressure increase LA Pressure
a. Veno-occlusive disease
b. Tumor venous occlusion
4. LA Pressure increase LVEDP
a. Mitral Valve disease
124
b. Increased intrapleural pressure
c. Aortic Valve disease
d. Decreased LV compliance (with increased atrial systole)
E. Complications of Swan-Ganz Catheter Placement
1. Arrhythmia
2. Complete heart block or R bundle branch block
3. Thrombosis
4. Infection
5. Pulmonary Infarction
6. Balloon rupture
7. Pulmonary artery rupture / hemorrhage
8. Cardiac Tissue injury
9. Catheter knotting
F. Normal Values and Calculations
1. Cardiac Output (CO)
a. Various methods for calculation
b. Fick Method uses assumed oxygen consumption and is good for cardiac disease
VO2i (=OCI)
CI = -----------------------------------CaO2-CvO2
c. Thermodilution measures flow and is good in septic patients
d. Normal value 3.0-7.0L/min, cardiac index (CI) 2.5-4.5 L/min/m2 (CI=CO/BSA)
2. Systemic Vascular Resistance (SVR) = (Mean SBP-CVP) Г· CO (nl 1000-1500 dyne/sec/cm2)
3. Pulmonary Vascular Resistance (PVR) = (Mean PAP-PCWP) Г· CO (nl 120-250 dyne/sec/cm2)
4. Mixed venous saturation can be obtained from blood sample during insertion / proximal port
a. Normal MVO2 ~ 75%
b. MVO2 is decreased in cardiogenic shock
c. MVO2 is increased in septic shock (due to AV shunting and poor perfusion)
5. Stroke index = cardiac index/heart rate (nl 50-75ml/contraction)
125
Hemodynamic Examples
H. Additional Notes and Waveforms
1. Acute Tricuspid Regurgitation
a. Increased CVP, right atrial, and RV end diastolic pressures
b. Blunted "X" descent, steep "Y" descent
c. RA and RV pressures equalized
2. Constrictive Pericarditis
a. Increased RA and PCW pressures
b. Dip and plateau in RV pressure
c. "M" or "W" shaped jugular venous pressures
d. Preserved "X" and steep "Y" descents
3. Restrictive Cardiomyopathy
a. PCWP may be higher than RA pressure
b. Similar findings to constrictive pericarditis
4. Acute Ventricular Septal Rupture
a. Reduced CO, increased SVR, tachycardia, hypotension
b. Oxygen step-up from RA to RV and PA (due to Left to Right shunt
126
Swan Ganz Catheter Wave Forms
127
Goldman Multifactorial Cardiac Risk Index (MCRI)
Variable
S3 gallop or JVD
MI in past 6 mos
Rhythm other than sinus or PACs on last preop EKG
Age >70 years
5
Emergency operation
Intraperitoneal, intrathoracic, or aortic operation
Suspected critical aortic stenosis
Poor general medical condition
K<3.0, HCO3<20, pO2<60 or pCO2>50, BUN>50 or
Creat>3.0, abnormal LFTs, bedridden
Points
11
10
7
4
3
3
3
Stage Points Risk of life threat complications/death
I 0-5 0.7% / 0.2%
II 6-12 5% / 2%
III 13-25 11% / 2%
IV >=26 22% / 56
HYPERTENSIVE CRISISNITROPRUSSIDE: Give 0.5-1.5 ug/kg/min to start with, then maintenance up to10 ug/kg/min. Add 50 mg of reconstituted
sodium nitroprusside to 250 ml of either 5% dextrose in water or normal saline. The solution should be covered with an
aluminum foil or paper bag to protect it from light. Nitroprusside has its onset of action within 3-5 min. It acts directly on
vascular smooth muscle producing mostly arterial, and to a lesser extent, venous dilation. The heart rate (HR), cardiac
output (CO) and extracellular fluid (ECF) all may increase or have no change. There is a decrease of systemic
resistance (SVR). The pulmonary capillary wedge pressure (PCWP) will decrease or have no change. There will be an
increase of the plasma renin activity (PRA), and angiotensin II (ANG II). SIDE EFFECTS: Side effects are cyanide
and thiocyanate toxicity. Clinical signs of thiocyanate toxicity include headache, nausea and vomiting,
tremulousness, confusion, drowsiness, psychosis and coma. Deaths due to cyanide poisoning are extremely rare. If
the patient is given an infusion of nitroprusside for more than 24 hours, serum thiocyanate levels should be done daily.
Concentration > 10 mg/dL are associated with toxicity; > 20 mg/dL could be fatal. Always monitor the renal status as
thiocyanate is excreted via the kidney. Oral antihypertensives should be started as soon as possible; usually
when the diastolic reaches 100 mm Hg. If needed hemodialysis is used for treating thiocyanate toxicity. Nitroprusside
is indicated for hypertension associated with CNS events, CHF, and aortic dissection and hypertensive encephalopathy.
LABETALOL: Use 20 mg IV over 2 minutes to start with by bolus. If a response is not seen, then double the dose q 10
min to a total of 300 mg. Onset of action is in minutes and lasts for 4-6 hours. A labetalol infusion may be prepared by
adding 200 mg of labetalol (40 mL) to 160 mL of either 5% dextrose in water or normal saline. The infusion rate is
0.5 mg/min. This is then titrated to obtain the desired blood pressure. In most cases, hypertension is under control
when labetalol is given at a dose of 2 mg/min. Infusion rates up to 4 mg/min may be used. There is a decrease or no
change in the HR and CO. There is a decrease of the SVR. The PCWP and ECF may either increase or have no
change. There is a decrease in both the PRA and ANG II. Labetalol is a sympatholytic agent and is unique in that
there is both post synaptic non-cardioselective Beta blockade and Alpha1 blockade. Since there is an oral form, the
patient can be switched to oral labetalol after BP is controlled. SIDE EFFECTS: There is a relative contraindication in
patients with CHF, bradydysrhythmia, and bronchospastic lung disease. Watch for paradoxical hypertension that
occasionally happens. Also, there may be orthostatic dizziness. Labetalol is useful in hypertensive encephalopathy,
angina, renal failure, pheochromocytoma, antihypertensive withdrawal, and interactions between monamine oxidase
inhibitors and drugs or food.
PHENTOLAMINE: Give a test dose of 1 mg IV over 2 minutes. If there is no marked hypotension then give 5-10 mg
(.1-.2 mg/kg IV) over the next 4 minutes. It can be given every 5-15 minutes. Phentolamine is useful in
hyperadrenergic states such as pheochromocytoma, but has a very short half life and the BP will start to rise again in 10
minutes, at which time the phentolamine can be given in intermittent boluses or a drip of 100 mg/hr. Because of a
reflex tachycardia, a beta blocker should be used.
ENALAPRILAT (Vasotec): Start with 1.25 mg (1 ml of a 2 ml vial) given over a 5 minute period. Increase to 5-10 mg as
needed, then give q 6 hours. The peak effect usually is seen in 30 minutes, but may not be until 4 hours. Hypotension is
very infrequent but can be treated with fluids. Diuretics will enhance the effect. Enalaprilat has no effect on the HR but
does cause a decrease in the SVR, PCWP, and ECF. The CO is increased. The PRA is increased and the ANG II is
decreased. Enalaprilat is excreted primarily by the kidneys. Enalaprilat is useful in CHF.
HYDRALAZINE: The initial dose is 10-20 mg IV ever 20 minutes as needed or 10-50 mg IM (onset of action in 30
minutes) every 6 hours IM. The peak effect occurs at about 60 minutes. If hydralazine is used as a continuous
infusion, 200 mg of drug is added to 1 liter of 5% dextrose in water or normal saline, and infused at 0.2 mg/min initially,
and subsequently titrated. The onset of action by continuous infusion occurs within 10 to 20 minutes. Peak effect
is seen at 20-40 minutes with continuous infusion. Hydralazine should not be used in myocardial ischemia. It is
most useful in pre-eclampsia and eclampsia. Hydralazine is a direct acting arterial vasodilator. It exerts little effect on
the venous system. Reflex tachycardia, increased myocardial oxygen consumption and increased cardiac output are
128
the major effects. There is a decreased SVR and increase in PCWP and ECF. The PRA and ANG II are both
increased. Hydralazine is metabolized primarily by the liver by acetylation. Some patients, genetically, are rapid
acetylator and metabolize hydralazine rapidly, and therefore a more frequent dosing schedule may be needed. SIDE
EFFECTS: Side effects include headache, palpitations, orthostatic dizziness and edema. There may be exacerbation
of angina. Drug induced lupus erythematosus occurs rarely with parenteral administration and much more commonly
with oral hydralazine. In this syndrome there may be rash, fever, arthralgias, arthritis, serositis, elevated
sedimentation rate and antinuclear antibodies.
NITROGLYCERIN: Nitroglycerine is given as an infusion of 5-100 ug/min by adding 50 mg/250 ml of 5% dextrose and
water and then titrating to desired BP. Can give up to 300ug/min. Nitroglycerin is useful in myocardial infarction,
pulmonary edema, and unstable angina.
NIFEDEDPINE [FELT Contraindicated in HTN Crisis d/t risk of stroke!]: Can be given as 10 mg, and then biting
and swallowing or sublingually. The peak effect is seen in 30-45 minutes. Nifedipine should be avoided in unstable
angina or evolving MI as it may lower perfusion pressure. Nifedipine maintains or increases the cerebral blood
flow. Nifedipine causes an increase or no effect in the cardiac output, and conduction in the sinoatrial node and
atrioventricular node. There is an increase in the HR and coronary blood flow. There is a decrease or no change of
myocardial contractility. There is a fairly marked decreased in PVR and an increase in sodium retention. There is a lack
of a predictable response to nifedipine. The duration of response is 2-6 hours.
CLONIDINE: Clonidine is given initially as .1-.2 mg orally followed by .1 mg/hr to a total dose of 0.6 - 0.7 mg over 6-7
hours. The onset of action is at 30-60 min and peaks at 2-4 hours. It does not cause reflex tachycardia and can be
used in CHF and myocardial ischemia. It can be useful in hyperadrenergic states as cocaine toxicity, clonidine
withdrawal, MAO inhibitors with tyramine ingestion and phenylpropanolamine. The major disadvantage is sedation.
Therefore, it shouldn't be used in hypertensive encephalopathy, stroke, or subarachnoid hemorrhage. It can cause
significant bradycardia and rebound hypertension if stopped abruptly.
CAPTOPRIL: Give as a 25 mg tablet and onset will occur in 15 minutes and peak in 2-3 hours. There may be a
precipitous drop if used in patients with CHF, scleroderma crisis, renovascular disease and those on diuretics and
vasodilators. Lisinopril and enalapril have slower onsets and shouldn't be used when a rapid reduction is needed. It
doesn't cause reflex tachycardia or salt retention. It will maintain cerebral blood flow. It is useful in malignant
hypertension, CHF, renovascular and cerebrovascular disease. There is an increase in the CO and PRA and a decrease
in SVR, PCWP, ECF and ANG II. Side effects are rash, agranulocytosis, and angioedema.
MINOXIDIL: The initial dose is 5 mg with a repeat dose in 6 hours if needed. It should be used with a beta blocker and
diuretic. It doesn't cause a rapid decrease in blood pressure and should not be used with CHF, myocardial ischemia or
pheochromocytoma because of the reflex tachycardia.
DIAZOXIDE: Diazoxide can be given at 50-150 mg (1-2 mg/kg) IV over a 5-10 second period, and can be repeated
every 10-15 minutes as needed, or can be given as a 7.5-30 mg/min IV infusion. Diazoxide acts directly on vascular
smooth muscle. There is an increase of HR, CO, PCWP, ECF, PRA and ANG II. There is a decrease in SVR. There is
onset of action within 5 minutes and a peak effect within 3-5 minutes if given as an IV bolus. The duration of effect
ranges from 4-12 hours. SIDE EFFECTS: The most serious effect is prolonged hypotension. This occurs less
frequently when mini boluses are given rather than the full 300 mg given as a bolus. There may be palpitations and
tachyarrhythmias and peripheral edema. It may produce hyperglycemia by inhibiting Beta islet cell function. If
extravasation occurs there may be superficial thrombophlebitis, cellulitis and necrosis as diazoxide is very alkaline.
TRIMETHAPHAN CAMSYLATE: Trimethaphan can be started as a .3 -.5 mg/min IV infusion by adding 500 mg in 500 ml
of 5% dextrose in water and then titrating to the desired level. In most patients the hypertension is controlled by
giving 1-4 mg/min. Trimethaphan is a ganglionic blocking agent and will decrease the HR, CO, SVR, PCWP and
increase the ECF. SIDE EFFECTS: Trimethaphan can cause postural hypotension and patients should be kept at
bed rest and may be placed in a 15 degree reverse Trendelenburg position to optimize the hypotensive effect.
Other side effects include adynamic ileus, urinary retention and mydriasis. In very high doses of greater than 5
HYPERTENSIVE CRISIS AND SPECIFIC DRUG THERAPYMost hypertensive crisis can be controlled with the following drugs: Nitroprusside, labetalol, diazoxide, nimodipine,
nitroglycerin, calcium antagonists, nicardipine and hydralazine. However, it is important that the appropriate drug be
matched up with the condition producing the hypertensive crisis, and that certain drugs not be given as they may
exacerbate the hypertension or underlying disease.
In most cases hypertensive crisis can be defined as an elevation of the diastolic pressure greater than 120. However,
this rule needs to be modified in some cases depending on whether the patient has had pre-existing hypertension or
normal blood pressure. If a patient has had normal blood pressure in the past, and then suddenly develops a diastolic BP
of 100-110 this rapid change could be disastrous. On the other hand, if a patient has chronic elevation of the BP and
suddenly develops elevation of the diastolic pressure the results may not be as severe with diastolic pressures greater
than 120 mm Hg. Hypertensive crisis usually affects patients that have pre-existing elevation of the BP. Blacks,
smokers and men tend to be affected. Hypertensive crisis, to place it in perspective, will only occur in about 1-2% of
those that have hypertension.
129
AORTIC DISSECTION:
In this disease the blood pressure should rapidly be reduced to around 120/80 in order to reduce the shearing force and
reduce the chance of further dissection. Aortic dissection is suspected if the patient has chest, back or abdominal pain
associated with abnormal abdominal pulsation, aortic regurgitation, peripheral pulse deficits, and widening of the
mediastinum on chest x-ray. Aortic dissection of the ascending aorta is a surgical emergency whereas dissection
beyond the left subclavian artery is treated medically. MRI, transesophageal echocardiography, CT and angiography
all have been used for diagnosis. Recently MRI and transesophageal echocardiography have emerged as the
procedures of choice.
DRUGS USED IN AORTIC DISSECTION: Beta blockers plus nitroprusside or trimethaphan, OR labetalol used
alone. Avoid hydralazine and diazoxide.
SUBARACHNOID HEMORRHAGE:
Subarachnoid hemorrhage may be due to rupture of a berry aneurysm or an arteriovenous malformation. Reduction of
BP in the face of subarachnoid hemorrhage is somewhat controversial because of possible induction of cerebral
spasm. However, if the BP is severely elevated, a cautious, slow reduction over several hours may be attempted to
reduce the pressure to around 170/100 or 20% of the patient's BP. Nimodipine is now standard therapy in
subarachnoid therapy as it has been shown to reduce death, disability and the vegetative state by about 40%.
Nimodipine will help reduce the cerebral spasm, but in the recommended oral dose, the BP is not significantly lowered.
DRUGS USED IN SUBARACHNOID HEMORRHAGE:
Nimodipine: 60 mg po QID for 21 days. Start within 96 hours of the subarachnoid hemorrhage. Nitroprusside and
labetalol may be used. Avoid beta blockers, diazoxide, clonidine, and methyldopa.
ISCHEMIC STROKE:
The same precautions for reduction of hypertension in ischemic stroke should be followed as for subarachnoid
hemorrhage because decreases can precipitate decreased cerebral perfusion. Reduce slowly and by about 20%.
DRUGS USED IN ISCHEMIC STROKE: Nitroprusside and labetalol. Avoid diazoxide, methyldopa, clonidine and beta
blockers.
INTRACEREBRAL HEMORRHAGE:
Treatment should only be given if the BP is exceedingly high such as greater than 200/130. The outcome prognosis is
usually poor with intracerebral bleeds and treatment doesn't usually change the course.
TREATMENT FOR INTRACEREBRAL HEMORRHAGE: Treat with Labetalol or nitroprusside only if BP is greater than
200/130. Otherwise, no treatment is required.
ISCHEMIC HEART DISEASE OR MYOCARDIAL INFARCTION:
An effort should be made to decrease peripheral vascular resistance, sympathetic activity and increase coronary
perfusion which will in turn decrease oxygen demands and wall tension.
TREATMENT OF ISCHEMIC HEART DISEASE AND MYOCARDIAL INFARCTION: Nitroglycerine is the drug of
choice and should be given IV, titrated to reduce the ischemic pain and/or reduction of diastolic BP to 100 mm Hg.
Labetalol given IV as well as calcium channel blockers may also be used as they will favorably influence the BP.
Nitroprusside should be reserved for those that are refractory to the above measures. Avoid hydralazine and
diazoxide.
LEFT VENTRICULAR FAILURE:
Treatment of left ventricular failure associated with a hypertensive crisis should be treated with drugs that will reduce
preload and or afterload.
TREATMENT USED IN LEFT VENTRICULAR FAILURE: Nitroprusside and nitroglycerin are the drugs of choice. Avoid
beta blocker and labetalol.
HYPERADRENERGIC STATES
: Hyperadrenergic states can be caused by cocaine overdose, pheochromocytomas, clonidine withdrawal and
amphetamines. All of these conditions can cause arrhythmias and myocardial ischemia.
TREATMENT USED IN HYPERADRENERGIC STATES: Phentolamine, labetalol, and nitroprusside are the drugs
of choice. Reinstitution of clonidine is used for clonidine withdrawal.
ECLAMPSIA:
TREATMENT FOR ECLAMPSIA: Hydralazine, magnesium sulfate, labetalol and calcium antagonists. Avoid
diuretics, ACE inhibitors, and trimethaphan.
POST-OPERATIVE HYPERTENSION:
TREATMENT FOR POST-OPERATIVE HYPERTENSION: Labetalol, nitroglycerin, nitroprusside,
nicardipine. Avoid trimethaphan.
and
ACUTE RENAL INSUFFICIENCY:
TREATMENT FOR ACUTE RENAL INSUFFICIENCY Labetalol, nitroprusside, and nicardipine. Avoid beta blockers
and trimethaphan. SPECIFIC DRUGS: Propranolol (Inderal): Give a loading dose of 1-10 mg, then 3 mg/hour IV
followed by 80-640 mg/day orally in divided doses. Nitroprusside (Nipride): 0.25-10 ug/kg/min IV with titration to
desired BP. (Add 50 mg to 250 ml of D5W). Trimethaphan camsylate (Arfonad): Give 2-4 mg/min IV infusion.
(Add 500 mg to 500 ml D5W). Labetalol (Trandate): Give 20 mg IV bolus (0.25 mg/kg), then 20-80 mg boluses IV
130
every 10 minutes and titrate to desired BP. (maximum of 300 mg). For infusion give 0.5-2 mg/min. (max 300 mg/day).
Follow orally with 100-400 mg po BID. Magnesium sulfate: Give 1-2 grams (2-4 ml) 50% solution (8-16 mEq) IV bolus
over 5-15 minutes. For infusion drip, add 2 grams of Magnesium sulfate to 250 ml of D5W and drip at 3-20 mg/min.
Start at 10 mg/min or 75 ml/hour. Hydralazine (Apresoline): 10 mg IV every 20 minutes prn to keep diastolic below 100.
Nicardipine: 20 mg tid initially po. Maximum of 120 mg daily. Nicardipine SR (Cardene): 30-60 mg bid. Nitroglycerin: 5100 ug/min IV, titrated to desired BP up to 300 ug/min. Add 50 mg of nitroglycerin to 250 ml of D5W. Nimodipine: 60
mg QID for 21 days. Diazoxide: 50-150 mg IV over 5-10 seconds, repeat every 10 minutes as needed or give infusion
at 7.5-30 mg/min IV. Phentolamine (Regitine): Give 5-10 mg IV and repeat as needed up to 20 mg. Clonidine
(Catapres): Give .2 mg po initially,
Hypertensive Emergencies Lancet
2000; 356: 411 – 417
A hypertensive emergency is a situation in which uncontrolled hypertension is associated with acute end-organ damage.
Most patients presenting with hypertensive emergency have chronic hypertension, although the disorder can present in
previously normotensive individuals, particularly when associated with pre-eclampsia or acute glomerulonephritis. The
pathophysiological mechanisms causing acute hypertensive endothelial failure are complex and incompletely understood
but probably involve disturbances of the renin-angiotensin-aldosterone system, loss of endogenous vasodilator
mechanisms, upregulation of proinflammatory mediators including vascular cell adhesion molecules, and release of local
vasoconstrictors such as endothelin 1. Magnetic resonance imaging has demonstrated a characteristic hypertensive
posterior leucoencephalopathy syndrome predominantly causing oedema of the white matter of the parietal and occipital
lobes; this syndrome is potentially reversible with appropriate prompt treatment. Generally, the therapeutic approach is
dictated by the particular presentation and end-organ complications. Parenteral therapy is generally preferred, and
strategies include use of sodium nitroprusside, Гџ-blockers, labetelol, or calcium-channel antagonists, magnesium for preeclampsia and eclampsia; and short-term parenteral anticonvulsants for seizures associated with encephalopathy. Novel
therapies include the peripheral dopamine-receptor agonist, fenoldapam, and may include endothelin-1 antagonists.
Causes of hypertensive emergencies
Essential hypertension
Renal parenchymal disease
Acute glomerulonephritis
Vasculitis
Haemolytic uraemic syndrome
Thrombotic thrombocytopenic purpura
Renovascular disease
Renal-artery stenosis (atheromatous or fibromuscular
dysplasia)
Pregnancy
Eclampsia
Endocrine
Phaeochromocytoma
Cushing's syndrome
Renin-secreting tumours
Mineralocorticoid hypertension (rarely causes hypertensive
emergencies)
Drugs
Cocaine, sympathomimetics, erythropoietin, cyclosporin,
antihypertensive withdrawal
Interactions with monoamine-oxidase inhibitors (tyramine),
amphetamines, lead intoxication
Autonomic hyper-reactivity
131
Guillain-BarrГ© syndrome, acute intermittent porphyria
Central-nervous-system disorders
Head injury, cerebral infarction/haemorrhage, brain
tumours
End
organ
Aorta
132
Complications
Therapeutic considerations
Aortic dissection
Гџ-blockade, labetalol (decrease dp/dt), sodium
nitroprusside with Гџ-blockade, avoid isolated
use of pure vasodilators
Brain
Hypertensive
Avoid centrally acting antihypertensive drugs
encephalopathy
such as clonidine
Cerebral infarction
Avoid centrally acting agents; avoid rapid
or haemorrhage
decreases in blood pressure
Heart
Myocardial ischaemia Intravenous glyceryl trinitrate, Гџ-blockade
Myocardial infarction
Diuretics and ACE inhibitors useful, ГџHeart failure
blockers
with caution
Kidney
Renal insufficiency Diuretics with caution, calcium antagonists
useful
Placenta Eclampsia
Hydralazine, labetalol, calcium antagonists
useful; avoid sodium nitroprusside
dp/dt=change in pressure/change in time.
Table 1: End-organ complications of hypertensive emergencies
Drug
Sodium
Dose
0В·25-10 Вµg kg1
min1
Onset
Duration Adverse effects
Hypotension,
Immediate 1-2 min
nausea,
nitroprusside
*
Labetalol
Hydralazine
vomiting, cyanate
20-80 mg bolus
(every 10 min)
2 mg/min infusion
10-20 mg bolus
5-10 min 2-6 h
2-6 h
10-15
Fenoldopam 0В·1-0В·6 Вµg kg1 min1 5-10 min
min
Glyceryl
trinitrate
Enalaprilat
5-100 Вµg/min
Nicardipine
2-10 mg/h
10 min
1-3 min
1В·25-5В·00 mg bolus 15 min
toxicity
Nausea, vomiting,
heart block,
bronchospasm
Reflex tachycardia
Hypotension,
headache
5-15 min Headache, vomiting
4-6 h
5-10 min 2-4 h
Hypotension, renal
failure
Reflex tachycardia,
flushing
Reflex tachycardia
Phentolamine 5-10 mg/min
1-2 min 3-5 min
*Risk of toxic effects in patients with renal impairment.
Table 2: Commonly used parenteral antihypertensive drugs
PERICARDITISCOMMON CAUSES OF PERICARDITIS:
133
Most causes are idiopathic or due to a viral infection. Most cases can readily be diagnosed in the clinical setting. For
instance, if a patient has a malignancy and develops pericarditis, there is a possibility of metastatic disease to the
pericardium. In a young healthy person, viral or idiopathic would be suspected. Pericarditis that develops a few weeks
after cardiac surgery could be due to post-pericardiotomy syndrome. Pericarditis in a uremic patient could be due to
advanced kidney disease. VIRAL: Viral pericarditis can be caused by echovirus, Coxsackie, adenovirus, mumps,
varicella, mononucleosis, hepatitis and AIDS. Males under the age of 50 are the most susceptible to viral etiologies.
Confirmation may be obtained by rising viral titers in paired sera. Cardiac enzymes may be slightly elevated.
Pericarditis usually starts after an upper respiratory infection. Indomethacin 100-150 mg/day in divided doses or ASA
650 mg QID is usually effective, but if not, prednisone may be added. Most cases will resolve after a few days to
weeks. However, there may be recurrences and rarely this may cause constrictive pericarditis. Tamponade occurs in <
5%.
TUBERCULOUS: Tuberculous pericarditis is rare in the USA. Associated clinical involvement of the lungs may be
absent, but pleural effusions are common. The patients may have fever, fatigue, night sweats with a subacute
presentation for days to months. Spread is usually by lymphatics or hematogenous. The effusions are usually
small or moderate. Pericardial biopsy has a higher yield than pericardiocentesis fluid and diagnosis may be made at
another site of involvement. Patients usually respond to standard anti-tuberculous pharmacologic therapy, but
constrictive pericarditis may be a sequela.
MALIGNANT: Common causes of neoplastic pericarditis include carcinoma of the breast and lungs, renal
carcinoma, leukemia, lymphomas, Hodgkin's disease and melanoma. Neoplastic pericarditis is a common cause of
pericardial tamponade and frequently is painless, but presenting with hemodynamic consequences. Diagnosis is by
cytologic exam of the pericardial effusion and/or pericardial biopsy, which may be difficult if the patient has had
mediastinal radiation within the last year. CT and MRI may be of some benefit in visualizing proximal tumor. Once
the patient has malignant invasion of the pericardium, the prognosis is very poor with only a few surviving for a
year. Palliation can be achieved by drainage, followed by instillation of chemotherapeutic agents or tetracycline in an
effort to reduce recurrence of fluid accumulation. Partial pericardiectomy may be of some benefit while pericardial
windows are rarely helpful. Be careful not to assume that the cause is neoplastic in a patient that has cancer, as
radiation, infection and autoimmune disorders may be instrumental. Rarely, mesotheliomas are causative.
RADIATION: Radiation for neoplastic disease may present months or years after radiation. The patients may present as
acute, or subacute pericarditis or constrictive pericarditis due to fibrinous and scar formation of the pericardium as
well as the myocardium, conducting system and coronary arteries. Radiation pericarditis usually develops if there is
more than 4000 cGy delivered to ports including more than 30% of the heart.
POST MI AND DRESSLER'S SYNDROME: Dressler's syndrome is probably an autoimmune disease. It occurs weeks
to months after open heart surgery or MI, and can be recurrent. The sedimentation rate is elevated, there is
leukocytosis, pain, malaise, and fever, and pleural effusions. The pericardial effusions tend to be large and
tamponade is rare after MI, but not so in postcardiotomy pericarditis. Treatment is with NSAIDS and corticosteroids.
Pericarditis accompanying MI usually occurs 2-5 days post MI. Large effusions are rare. Differential from
progressive ischemic changes may be difficult as evolutionary repolarization changes of the pericarditis may
simulate ischemic changes. There is usually a rub. Spontaneous resolution usually occurs after a few days. NSAIDS
or ASA will help the pain.
ACUTE BACTERIAL INFECTION: Staphylococcus, pneumococci, streptococci, Legionella, Neisseria gonorrhoeae,
Neisseria meningitidis.
INFLAMMATORY DISEASE: SLE, rheumatoid arthritis, scleroderma, polyarteritis nodosa,
amyloidosis, sarcoidosis, acute rheumatic fever, and inflammatory bowel disease. DRUGS:
Procainamide, hydralazine, isoniazid, phenytoin, dantrolene, phenylbutazone, methysergide and
cyclophosphamide.
CARDIAC TAMPONADECardiac tamponade occurs when ventricular and atrial filling are compromised by increased
intrapericardial volume and pressure, with subsequent decreased cardiac output and hypotension.
Pericardial effusions may be due to fungal infections, TB, malignancy, trauma, thyroid disease,
autoimmune diseases, acute and chronic renal failure, aortic dissections, endocarditis and in postcardiac surgery. Echocardiography can ascertain if there is pericardial effusion and/or tamponade.
Tamponade criteria include right ventricular diastolic or right atrial systolic collapse, swinging
heart, respiratory variation in the left and right ventricular chamber sizes and right atrial indentation.
Confirmation of these findings may be necessary by inserting a balloon flow directed pulmonary
artery catheter and determining equalization of right atrial, left atrial and ventricular end-diastolic
pressures. Ancillary bedside findings of a pulsus paradoxus (augmented respiratory variation in
the pulse pressure of greater than 10 mm Hg), along with distended neck veins, dyspnea,
orthopnea, tachycardia, tachypnea, decreased heart sounds and hypotension are usually present.
Electrical alternans on ECG, and water bottle cardiomegaly may also be present.
134
TREATMENT: The first line of treatment is fluid loading and dopamine in order to stabilize the
patient until pericardiocentesis can be accomplished which is essential for treatment and
diagnosis. Under echocardiographic, fluoroscopic or electrocardiographic guidance, an
intrapericardial catheter should be introduced using the Seldinger method. Having a tube in place
for at least 24 hours will allow drainage of large effusions, and provide access for instillation of
chemotherapeutic, sclerosing or anti-infective agents. In patients that have malignant effusions
from lung cancer, breast cancer, melanoma, leukemia, lymphoma or Hodgkin's disease,
sclerotherapy with bleomycin, tetracycline or fluorouracil may decrease the recurrence of
tamponade. If the patient has a life expectancy of > 6 months or the effusion cannot be
controlled with sclerosis, pericardiectomy may be indicated. Open surgical drainage has the
advantage of a generous biopsy sample, lysis of adhesions for loculated fluid and less danger of
laceration of a coronary artery or muscle. Hemodialysis patients are treated by increasing the
frequency of dialysis or pericardiocentesis and triamcinolone instillation.
AORTIC DISSECTIONAortic dissection occurs when there is a tear in the aortic intima. The etiology of this tear may be
degenerative changes in the smooth muscle and elastic tissue of the media. Sometimes there is
associated cystic medial necrosis. Hypertension is the most common cause of medial degeneration,
and about 66% of patients will have hypertension. The peak age for hypertension depends on the
etiology, but in general is in the 6th and 7th decade. Patients that have proximal dissections
tend to be somewhat younger. Approximately 60% of patients have intimal tears in the proximal
ascending aorta. Males predominate in a ratio of 3:1.
Marfan's syndrome as a cause of aortic dissection commonly presents in the 3rd and 4th decade.
Other causes of aortic dissection include Marfan's and Ehlers-Danlos syndromes, Turner's
syndrome, relapsing polychondritis, coarctation of the aorta, bicuspid aortic valves, patent ductus
arteriosus, arteriosclerosis, trauma, and injury from arterial catheterization and other vascular
procedures such as cross clamping injuries.
As the tear progresses the media is separated from the adventitia with production of a false channel
which extends distally, and to a lesser extent proximally. The proximal dissection will produce
incompetency of the aortic valve. Distal dissections may occlude vital tributaries of the aorta with
symptoms contingent upon the vessels that are compromised. The most common site of
origination of the tear is within about 5 cm of the aortic valve, and in the descending aorta
near the ligamentum arteriosum and just distal to the origin of the left subclavian artery.
Rupture may occur into the pericardial cavity or left pleural space and produce mortality. Without
treatment 90% will be dead in 3 months. If the patient is fortunate enough to be treated 60% of
those that are released from the hospital after treatment will be alive 5 years later, and 40%
10 years later.
CLASSIFICATIONS OF DISSECTIONS: Aortic dissections are considered acute if they are less than
2 weeks or chronic if > 2 weeks. There are two main systems used for classification. The
DeBakey system has been in place for many years and reflects the site of the intimal tear while
the Stanford University system does not address the site of the tear, but only involvement of the
ascending aorta. In the Stanford type A tear, all ascending aorta tears are addressed, and type B
dissections address all tears that do not involve the ascending aorta. In the DeBakey classification
there are 3 types of dissection. Type I starts in the proximal aorta and extends beyond the
brachiocephalic tributaries. Type II originates at the same place but is confined to the ascending
aorta. Type III originates in the descending thoracic aorta just beyond the origin of the left
subclavian artery.
CLINICAL: Patients present with sudden pain that has been described as ripping or tearing and
is excruciating. There is no crescendo tempo to the pain. The pain is maximal at the start. If the
dissection is proximal, the pain tends to be in the anterior chest, while pain in the back in the
interscapular area suggests a distal dissection. As the dissection extends, the initial pain will
migrate to another area. This can be an important diagnostic feature.
Other symptoms depend on the tributaries that are occluded. Some may develop myocardial
infarction, stroke, or paraparesis. There may be pain in an arm due to ischemia or there may be
abdominal pain secondary to mesenteric insufficiency or infarction. Syncope may be caused by
rupture into the pericardium producing tamponade. Congestive heart failure may develop
secondary to severe aortic regurgitation. If blood flow is interrupted to the kidneys there is renal
dysfunction and further elevation of the blood pressure due to excessive renin release from the
ischemic kidney.
Physical exam may reveal the BP to be elevated with a difference in BP between the arms.
There may be jugular vein distention, pericardial friction rub and pulsus paradoxus suggesting
rupture into the pericardium. Other patients may present with hypotension, become clammy and
complain of chest pain simulating a myocardial infarction. Hypotension suggests rupture into the
135
peritoneal cavity, cardiac tamponade or pleural space. Check the femoral and brachial pulses
as a decrease in these will reflect a distal aortic dissection. About 16% of patients with distal
dissections will have diminished or absent pulses. About 50% with proximal dissections will have
diminished pulses. Check the brachiocephalic branches for dissection of the proximal ascending
aorta.
Aortic regurgitation associated with proximal dissection occurs in about 2/3 of cases. This will
produce a diastolic murmur. If the aortic regurgitation is severe, as well as acute, the murmur may
be difficult to hear, and the patient may develop congestive heart failure.
LABORATORY: The patient may have an elevated LDH, bilirubin and anemia secondary to
hemolysis of the RBCs in the false lumen of the aorta. The BUN and creatinine may be elevated if
there is compromise of the renal blood flow to the kidneys. If the dissection extends into the
coronary arteries there may be EKG, and enzyme changes secondary to myocardial infarction.
The AST and CK are usually normal unless there is a concomitant myocardial infarction. A precise
diagnosis must be made before thrombolytic therapy is given for a myocardial infarction. The chest
x-ray will demonstrate widening of the aorta in about 90% of cases. There may also be displacement
of an aortic plaque of 5-10 mm or more. If there is rupture into the pericardium, the heart may be
enlarged. There may be a left pleural effusion.
IMAGING PROCEDURES:
TRANSESOPHAGEAL ECHOCARDIOGRAPHY (TEE) has a specificity of 90% or greater and a
sensitivity of almost 100%. It can be done fairly rapidly, is portable, can show the status of the
coronary arteries and can demonstrate aortic regurgitation. A typical exam can be done in about
15 minutes. At the present time with the new multiplane probe, images can be imaged in the
transverse and longitudinal planes and various in-between planes. TEE can show the true and
false lumens and the intimal flap as well as the branch vessels and thrombi in the false lumen.
Pericardial effusions may also be detected. With the advent of the multiplane probe, false
positive intimal flaps have been eliminated to a large degree. Transthoracic echocardiography has
a sensitivity at the best of about 85% and a 63-96% specificity. It is best for detection of ascending
aorta dissection.
MAGNETIC RESONANCE IMAGING has a sensitivity and specificity of 99%. However, it can
not be used in an emergent situation because it is too time consuming. It also is not available
at all institutions and is very expensive. Intravenous contrast is not needed which is an asset if there
is renal compromise or allergies. The true and false lumens are visualized. The intimal flap is best
seen when the blood flow is rapid. Secondary signs of aortic dissection may be seen as widening of
the aorta and thickening of the aortic wall. If cine-MRI is used, aortic regurgitation can be
diagnosed with correlation paralleling Doppler studies. However, utilizing cine-MRI will extend the
imaging time by another 15-30 minutes so that the total time of imaging can be over an hour. This
is unacceptable in acute unstable aortic dissections. Disadvantages include the inability to visualize
branch vessels and coronary arteries. MRI cannot be used in patients with mechanical prosthetic
valves, metal implants, surgical clips or pacemakers.
COMPUTED TOMOGRAPHY has a sensitivity of about 90% and specificity of 95%. Most
institutions now have CT machines. It can demonstrate both the true and false lumens and flap.
False positives can occur due to motion and streak artifacts, and false negatives may occur due to
insufficient contrast in the false lumen. It is non-invasive but does require intravenous contrast
agents. Branch vessels and coronaries are not visualized.
AORTOGRAPHY is mandatory if surgical therapy is planned. It will define the origin and extent of
the dissection, the magnitude of aortic regurgitation, and involvement of the branches of the aorta
and any coronary occlusion. It has a sensitivity of 90% and specificity of 95%. It is invasive,
requires contrast and is somewhat time consuming.
TREATMENT: For dissections of the proximal aorta, surgery is usually required while distal aortic
dissections are treated medically. Patients should have intra-arterial catheters inserted for
blood pressure monitoring. Pulmonary artery catheters also are helpful, monitoring for pulmonary
edema and volume changes due to dissection and rupture. The goal in medical treatment is to
reduce the systemic blood pressure and the rate of pressure change in the aorta (dP/dT). The
systolic blood pressure should be reduced to around 120 mm Hg. The combination of sodium
nitroprusside and propranolol is a useful combination. Nitroprusside should not be used alone
because it can increase the dP/dT initially. Nitroprusside is prepared by adding 50 mg in 250 ml of
5% D5W with a starting drip rate of 25ug/min and then titrating to the desired BP level.
Propranolol may be given at .5-1 mg every 3-5 minutes to a total of .15 mg/kg or until the pulse slows
to around 60 beats/min. IV labetalol can also be used with nitroprusside. The dose is 10-20
mg initially and then 20-40 mg every 15 minutes until the BP is controlled. The total dose should not
be greater than 300 mg. Additional doses of labetalol in the same range may be given prn every 4-8
hours. Constant infusions of labetalol can also be used by giving the drug at 1-2 mg/min. Other
136
beta blocker alternatives that can be used are esmolol, metoprolol and atenolol. If patients are not
candidates for beta blockers because of congestive heart failure, bradycardia, heart block, asthma
or left ventricular systolic dysfunction, calcium channel blockers, and nifedipine may be used.
Verapamil may be given at .05-.1 mg/kg IV and nifedipine 10-20 mg sublingually every 2-4 hours.
Trimethaphan camsylate may be used alone at a dose of 1-5 mg/min IV. It is initially effective, but
tachyphylaxis may rapidly develop. Furthermore, blurred vision, urinary retention and ileus are side
effects.
SURGERY is usually indicated in acute dissections of the ascending aorta. Complications as
stroke and myocardial are not absolute contraindications for surgery. Unless there is dissection
into branch vessels or impending rupture, dissections of the aortic arch and distal aorta are
treated medically. The mortality associated with aortic dissection is about 15%. The dissected
portion of the aorta is excised with reconstitution of the aorta with a synthetic graft. If there is
significant aortic regurgitation, valve replacement should be done. All patients, whether they are
initially treated with surgery or by medical means, should be chronically treated with a combination of
beta blockers or calcium antagonists plus an ACE inhibitor. Hydralazine, minoxidil or beta
blockers that possess intrinsic sympathomimetic properties, as acebutolol or pindolol, should
not be used. All patients should be followed for any recurrence of dissection, aneurysmal
development or progressive aortic valve insufficiency.
SYNCOPECARDIOVASCULAR
CAUSES
OF
SYNCOPE:
COMMON:
1....Aortic stenosis
2....Arrhythmia - slow or fast
3....Carotid sinus hypersensitivity
4....Drugs
5....Low cardiac output with cardiomyopathy
6....Neurally mediated
7....Orthostatic hypotension
8....Vasovagal
UNCOMMON:
1....Atrial myxoma
2....Cardiac tamponade
3....Congenital lesions as tetralogy of Fallot, Eisenmenger’s complex.
4....Obstructive hypertrophic cardiomyopathy
5....Primary pulmonary hypertension
6....Pulmonary stenosis
CAUSES OF ORTHOSTATIC HYPOTENSION:
COMMON:
1....Decreased circulating volume as bleeding, dehydration, fever, widespread burns,
pregnancy, diabetes insipidus, hemodialysis
2....Deconditioning
3....Drugs
UNCOMMON:
1....Autonomic nervous system dysfunction as:
2....Bradbury Eggleston syndrome (sympathetic dysfunction in older men) 3....Shy-Drager syndrome
4....Riley Day syndrome
5....Alcoholic or diabetic neuropathies
6....Subacute combined sclerosis
7....Tabes dorsalis
8....Spinal cord disease or trauma
9....Adrenal insufficiency
10...Pheochromocytoma
11...Amyloidosis
DRUGS THAT COMMONLY CAUSE SYNCOPE:
1....Antidepressants
2....Antihypertensives
3....Beta blockers
4....Calcium channel blockers
5....Cardiac glycosides
6....Nitrates
7....Phenothiazine derivatives
137
8....Diuretics
9....Antiarrhythmics - causes proarrhythmia
10...Antidepressants - causes arrhythmias
11...Cardiac glycosides - causes arrhythmias
12...Phenothiazine--causes arrhythmias
TREATMENT OF REFRACTORY ORTHOSTATIC HYPOTENSION:
1....Atrial pacing
2....Caffeine
3....Clonidine
4....Diet high in sodium
5....Fludrocortisone acetate(Florinef)
6....Indomethacin
7....Elastic stockings
8....Monoamine oxidase inhibitors
9....Inderal
CARDIAC WORKUP FOR SYNCOPE:
1....CAROTID SINUS MASSAGE - Put in an IV line in place and continuous EKG monitoring and
appropriate medication such as atropine sulfate should be available. Response may be slowing
of the heart (cardioinhibitory) or fall in BP (vasodepressor response) or a combination of the
two. One half seconds of pressure per side should be done. Only unilateral pressure should be
applied. An abnormal response is 5 seconds or more of ventricular asystole or a fall in systolic
BP of more than 30 mm Hg.
2....EKG - look for arrhythmias, left ventricular hypertrophy as in hypertension or aortic stenosis,
previous MI that may predispose to arrhythmias, prolonged QT interval and WPW.
3....HOLTER - The diagnostic yield is low.
4....ECHO - Look for valvular lesions, poor contraction, and pericardial effusion.
5....EXERCISE STRESS - Look for a positive test for ischemia.
6....SIGNAL AVERAGED EKG - This test is most useful for assessing the possibility of ventricular
tachycardia in a patient with coronary artery disease. A high percentage of patients with sustained
VT or subsequent sudden cardiac death show late potentials on the surface EKG. It has a high
sensitivity but low specificity. It is most useful when used in patients with known organic heart
disease in whom the absence of late potentials makes significant ventricular arrhythmias
unlikely as a cause of syncope.
7....ELECTROPHYSIOLOGIC STUDY - is expensive and is invasive and uncomfortable and
may result in complications. It should be used only when a complete noninvasive workup is
unrevealing.
8....TILT TABLE TESTING - Beta blocker, Norpace, Transderm or dual chamber cardiac pacing
have been used with varying degrees of success. a....Head up tilt testing should be done in young
patients who have no history of cardiac disease initially. In older patients LV function should be
assessed by echo or radionuclide isotope imaging. Echo can also identify LV outflow obstructive
syndromes. Head up tilt testing will identify patients that have neurocardiogenic dysfunction.
b....Head up tilt test - Patients lie on a tilt table that has a footboard for support. The head of the
table is elevated to 70 degrees from horizontal. They remain in this position for 15 minutes
during which arterial pressure and EKG leads are monitored continuously. If syncope occurs the
test is discontinued. If after 15 minutes there is no syncope the table is placed in the horizontal
position and infusion of Isoproterenol is started to raise the heart rate by 20% over the baseline. The
table is then placed in 70 degrees for another 15 minutes.
c....If the head up tilt test is negative then an electrophysiologic study should be done to evaluate
sinus node dysfunction, AV conduction abnormalities, supraventricular tachycardia and rarely
ventricular tachycardia. Supraventricular tachycardia remains an important cause of syncope in
young patients with or without evidence of overt ventricular preexcitation.
d....If the patient has had an old myocardial infarction, or has Q waves on EKG from previous
MI or has LV ejection fraction less than 40 % then ventricular tachycardia must be ruled out if the
patient has syncope. A signal averaged electrocardiogram may be useful. If this reveals
abnormalities then electrophysiologic studies to induce ventricular tachycardia is higher. Twenty four
hour ambulatory Holter monitoring has a low yield for detection of arrhythmic syncope.
e....Get potassium and magnesium levels as these can precipitate ventricular tachycardia, as
can transient myocardial ischemia, orthostatic hypotension, LV outflow obstruction,
antihypertensives, vasodilator therapy or autonomic dysfunction.
TREATMENT OF CARDIAC SYNCOPE:
1....Patients with sinus node dysfunction or AV block do well with permanent pacing. In selected
cases, radiofrequency modification and ablation may help supraventricular tachycardia arising
in the AV junction. Flecainide and Encainide are the most effective drugs. However, class I agents
are useful.
2....For ventricular tachycardia, class I and III, catheter or surgical ablation and implantation of an
automatic cardioverter defibrillator may be used.
138
3....For Neurocardiogenic dysfunction, drugs that decrease the force of myocardial contraction as
beta blockers and disopyramide (Norpace) are helpful. Beta blockers are the best. To predict the
efficacy of oral beta blocking agents head up tilt testing sessions after treatment with IV Esmolol
(Brevibloc) are useful. Oral theophylline and Transderm-Scop may also be helpful.
SYNCOPE CAUSESCardiovascular: carotid sinus syncope, vasodepressor syncope, aortic, mitral and pulmonary
stenosis, pulmonary hypertension, myxoma, hypertrophic cardiomyopathy, tetralogy of Fallot,
neurocardiogenic, arrhythmic, structural abnormalities, cardiovascular drugs, postural
hypotension, brain stem ischemia, cardiac tamponade, pulmonary embolism, aortic dissection, brady
and tachyarrhythmias, pump failure due to myocardial infarction and cardiomyopathy.
Neurologic diseases: cerebrovascular disease, seizures, trigeminal and glossopharyngeal
neuralgia, autonomic neuropathies.
Psychiatric disorders: panic disorder, hysteria, orthostatic hypotension, drug induced syncope,
metabolic and endocrine disorders, hypovolemia, hypoglycemia, hyperventilation.
SYNCOPE- CARDIAC SYNCOPE:
The most common cause of obstructive stenosis is aortic valvular stenosis. However, other
causes would include hypertrophic cardiomyopathy which is typically exertional, but can be due to
arrhythmia or conduction system disease. Primary pulmonary hypertension and severe
pulmonic stenosis are occasionally associated with effort syncope. Tetralogy of Fallot and other
cyanotic congenital heart defects with right to left shunting and pulmonary hypertension and/or
right ventricular outflow obstruction also can cause exertional syncope. Left atrial myxomas may
occur with change of position secondary to obstruction of the mitral orifice by the mass. Thrombosis
of a prosthetic valve may cause sudden obstruction and syncope. Arrhythmic syncope should be a
concern if there are palpitations, and underlying cardiac disease. Advanced or high degree AV block
is the most common arrhythmia causing syncope as the Stokes-Adams syndrome.
Most of these defects involve the His-Purkinje system post MI or in the elderly. The ECG may
demonstrate various combinations of fascicular block. Heart block may also be caused by drugs
such as digitalis, calcium blockers and beta blockers. Ventricular tachycardia and fibrillation, and
prolonged QT interval may degenerate into torsades de pointes causing syncope.
The Romano-Ward syndrome is associated with a prolonged QT interval, as well as the JervellLange-Nielsen syndrome which also has associated congenital deafness. Supraventricular
arrhythmias may be associated with the sick sinus syndrome that is prevalent postoperatively in
congenital heart diseases or the elderly. Paroxysmal atrial tachyarrhythmias may cause syncope,
particularly in the elderly with associated cerebrovascular disease. Occasionally, young patients
without structural heart disease will develop syncope due to polymorphic ventricular
tachycardia. Patients with acute myocardial infarction present with syncope in about 5-10% of
patients, usually with Q wave inferior infarctions.
EVALUATION: The resting ECG may provide clues to the cause of the syncope. A prolonged QT
interval may be associated with polymorphic ventricular tachycardia. Q waves may represent an
old MI with related ventricular arrhythmias or hypertrophic cardiomyopathy that may also cause
ventricular arrhythmias. A bifascicular block might indicate the patient has developed
bradycardic syncope. Other findings as Wolff-Parkinson-White, atrial and ventricular ectopy
may be a clue. Cardiac monitoring will only reveal the cause in about 15% of cases. Patient
activated recorders may be helpful. Echocardiography can diagnose aortic stenosis, hypertrophic
cardiomyopathy and atrial myxoma. Exercise testing for exertional syncope may uncover exercise
induced ischemia or arrhythmias. Invasive electrophysiologic studies are important for arrhythmic
syncope and can diagnose the mechanism of syncope in about 66% of patients. It can elicit
ventricular and supraventricular tachycardia and the response to pacing and pharmacologic
interventions. Neurally mediated syncope may be diagnosed with a positive response to tilt testing
with or without isoproterenol provocation. The signal averaged ECG is important for defining post
MI after potentials that are associated with sudden death and arrhythmias.
Electrophysiologic testing is important in elucidating a bradyarrhythmia or heart block as the cause
of syncope. For example a prolonged HV interval longer than 100 milliseconds, a prolonged
sinus node recovery time, or a pacing induced infranodal block would all be helpful. If the patient
has a negative electrophysiologic study there is only a 20% likelihood of recurrent syncope and a low
mortality risk. Other tests that may be needed to rule out non-cardiac causes would include serum
glucose, electrolytes, hematocrit, toxicology screen for alcohol and drugs, head CT, EEG,
hyperventilation testing, cough, micturition, and pain syncope, orthostatic testing, and testing for
carotid sinus syncope. This type of syncope usually occurs from pressure to the neck as tight
139
collars, trauma and tumors. Autonomic dysfunction syncope can be caused by Parkinson's
disease, Shy-Drager syndrome or Wernicke's encephalopathy. In about 35% of patients with
recurrent syncope, no cause can be found. They have a 6% 1 year mortality.
Syncope due to cardiac etiologies have a 20-30% 1 year mortality. Patients with bradyarrhythmias
due to diffuse conduction system disease can be treated with the appropriate type of pacemaker.
DDD or DVI pacemakers may be indicated in these patients with sinus rhythm and primary
conduction system disease. Pacemaker + pharmacologic therapy is needed in the tachycardiabradycardia syndrome. Radiofrequency ablation, antitachycardia pacemakers, implantable AICDS,
and revascularization may be needed.
SYNCOPE (Neurocardiogenic)Head up tilt testing includes continuous monitoring of arterial pressure by an intra-arterial cannula
place in the brachial or femoral artery. Initially, the test is carried out for 20 minutes at 70
degrees in a drug free state. If the test does not show hypotension with or without
bradycardia, the patient is place in the supine position and IV isoproterenol is started at 1 ug/min.
The infusion is increased gradually until there is a 20% elevation in the heart rate. At this point the
test is repeated at 60 degrees for 20 min. The treatment of choice is a beta blocker. Some
patients do not respond to a beta blocker and in some the patient's symptoms are aggravated.
Prediction of long term efficacy for a beta blocker can be achieved by a negative tilt test with
esmolol infusion. Disopyramide, theophylline, ephedrine, fludrocortisone and scopolamine patches
have all been used with varying degrees of success.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Current Concepts: Management of Chronic Obstructive Pulmonary Disease The New England
Journal of Medicine -- April 8, 1993 -- Vol. 328, No. 14 Gary T. Ferguson, Reuben M. Cherniack:
Table 1: Risk Factors for COPD.
140
Figure 1: Typical Regimen for Treating COPD.
141
Outcome was measured in terms of improvement in the FEV1, FEV1:FVC, and peak flow; improvement in the distance covered in a 6or 12-minute walk; and objectively observed reduction in dyspnea, medication use, and nocturnal symptoms. MDI denotes metereddose inhaler.
Table 2: Characteristics of Bronchodilators Delivered by Metered-Dose Inhalers.
142
Table 3: Indications for Supplemental Oxygen for COPD.
143
(COPD)
A. Symptoms
1. Definition: Chronic cough for >3 consecutive months in two consecutive years
2. Production of sputum (usually thick, white-yellow, yellow-green)
3. Other symptoms include: shortness of breath, tachypnea, right heart (RV) failure
4. Chronic airflow obstruction is underlying defect
B. Occurrence
1. Smokers - current or previous; account for >90% of cases of COPD
2. Elderly (progressive loss of lung function with aging)
3. Alpha1-Antitrypsin Deficiency – homozygous only
C. Pathophysiology [7]
1. Chronic inflammation of airways due to irritations
2. Cigarette smoke, including second hand smoke, is major irritant
3. Destruction of normal lung tissue is chronic process, accelerated by irritants
a. Non-smokers lose FEV1 at ~10-15cc/year after age 35
b. Smokers lose FEV1 at 25-30cc/year
4. Mechanisms of Lung Tissue Destruction
a. Thought to be due to neutrophil proteases released during inflammation
b. Alpha-1 antitrypsin is a protease inhibitor essential for protection of lung tissue
c. A1-antitrypsin deficiency causes pan-alveolar destruction, pan-lobular emphysema
d. Smokers typically develop centrilobular fibrosis
e. Proteases destroy alveoli as well as cilia
5. Causes of Inflammation
a. May be related to inability to clear organisms efficiently from lungs
b. Pollutants and cigarette smoke inhibit alveolar macrophage function and ciliary motion
c. Result is increased bacterial load which leads to chronic inflammation
d. The inflammation in bronchitis is characterized by sputum overproduction and fibrosis
144
e. Contrast with asthma, where inflammation causes airway constriction
6. Net Result is Hypoxemia
a. Several mechanisms of hypoxemia exist
b. Mucus plugging with shunting and V/Q mismatch appears to make major contribution
c. Destruction of lung tissue prevents O2 exchange
7. Response to Hypoxemia [9]
a. Increased ventilatory drive – decreases pCO2, increases pO2 and work of breathing
b. Non-pulmonary vascular beds dilate - decreased systemic vascular resistance (SVR)
c. Decreased SVR induces tachycardia and increased stroke volume (cardiac output up)
d. Pulmonary vascular resistance (PVR) increases to improve ventilation perfusion matches
e. This increase in PVR leads to pulmonary hypertension and right heart failure
f. Hypoxia also leads to increased erythropoietin production, increased red cell mass
g. The increased RBC mass increases cardiac work
h. Supplemental oxygen, particularly at night, may slow or prevent progression [8]
8. Etiology of CO2 retention in COPD is controversial
a. Appears to be mainly due to mucus plugging with V/Q mismatch
b. Increasing O2 in patients with COPD may increase CO2 retention
c. Likely due to increased V/Q mismatch and hypoventilation due to reduced hypoxic drive
d. Respiratory drive in CO2 retainers is most pH (not CO2 level) dependent
9. Emphysema
a. Emphysema is a pathologic diagnosis with destruction of lung tissue
b. Centriacinar, panacinar and distal acinar pathologies are seen
c. Patients are typically hypoxic and hypocarbic, late stage O2 dependent with tachypnea
d. Cor pulmonale (R heart failure) may occur due to pulmonary hypertension
e. Often referred to as "pink puffer" (pink because CO2 level is low with low normal O2)
f. PFTs show markedly reduced DLCO, increased residual volume and reduced FEV1/FVC
10. Chronic Bronchitis
a. Clinical diagnosis with definition of cough and sputum production as for COPD
b. Specifically refers to chronic inflammation of the bronchial tubes
c. Patients with prominent bronchitis are borderline hypoxic but retain CO2 (hypercarbic)
d. They typically have a compensated respiratory acidosis (ie. with high bicarbonate)
e. Often referred to as "blue bloaters" (blue because of high CO2 levels)
f. Cor pulmonale often occurs due to pulmonary hypertension
g. Polycythemia is common due to chronic hypoxemia
h. High dose O2 administration (>2-4L/min may exacerbate CO2 retention (see above)
i. PFTs show nearly normal DLCO, increased total lung capacity, reduced FEV1/FVC
D. Common Organisms Found in COPD Patients
1. Streptococcus pneumoniae
2. Haemophilus influenza
3. Moraxella catarrhalis (Branhamella): G- diplococci
4. Other gram-negative organisms
5. Thus, antibiotic use in COPD should cover the above organisms
6. In general, TMP/SFX, second (or third) generation cephalosporin, AugmentinВ®, are useful
E. Treatment of Chronic Disease
1. Stop smoking
2. Bronchodilators
a. Ipratropium (AtroventВ®): 2-4 puffs po qid; anti-cholinergic, preferred for chronic disease
b. Гџ2 agonists, eg. Albuterol (VentolinВ®), also effective; more so in acute exacerbations
c. In chronic COPD treatment, efficacy of ipratropium is better than Гџ2-agonists
3. Theophylline may increase respiratory muscle strength mildly (~10%) [3]
a. Use in difficult / severe cases is strongly recommended
b. May prevent overnight attacks
c. Improvement in exercise tolerance in moderate to severe COPD cases
d. Improvement often seen on patients on ventilator with low tidal volume, apnea, etc.
4. Antibiotic Therapy
a. In most patients, there is no benefit to chronic suppressive therapy with antibiotics
b. In general, antibiotics should be reserved for mild to moderate exacerbations
5. Decongestants
a. Pseudoephedrine
b. EntexВ® or DeconsalВ® (Pseudoephedrine with Gauifenesin)
c. Anti-histamines are not recommended (dry up secretions)
6. Glucocorticoids
a. Inhaled agents of clear benefit in COPD (not in exacerbations)
b. Use high dose (eg. 80mg iv q8- Solu-MedrolВ®) in COPD exacerbations (see below)
7. BronkosolВ®: to thin out thick secretions, make easier to clear
8. Organidin: iodinated mucolytic, thins mucus, easier to clear.
9. Supplemental Oxygen [ 8, 9]
a. Usually for patients with pO2 at rest of <55mm
b. Clear benefits in exercise tolerance when given over long term
c. Improvement in cardiac function (including right heart pressures)
145
d. Unclear effect on mortality
e. Some patients do not respond at all, and there are currently no predictors of response
F. Inhaled Glucocorticoids in COPD
1. Recent study of all comers with obstructive airway disease (COPD / Asthma)
a. Patients given baseline Гџ2-agonist; randomized to second therapy:
b. Inhaled steroid (beclomethasone) vs. inhaled anti-cholinergic (Ipratropium Bromide)
2. Results show much greater efficacy of inhaled steroid
a. No difference between placebo and AtroventВ®
b. Note that all patients were on Гџ2-agonists, however
3. Strongly indicate that patients with COPD (and asthma) should be treated with inhaled
glucocorticoids
4. Oral Glucocorticoids [5]
a. In stable disease will benefit only ~10% of patients
b. Not usually indicated in stable disease due to high side effect profile
G. Treatment of COPD Exacerbations
1. Low dose Oxygen (concern about CO2 retention with higher levels O2)
2. Rule out CHF contribution (wheezing may be cardiac vs. bronchospastic)
3. Chest Radiograph - rule out frank pneumonia
4. Nebulizers
a. Гџ2 agonists
b. May add MucomystВ® (N-acetyl cysteine to loosen secretions)
c. Ipratropium 500µg + albuterol – more effective for FEV1 increase than ß2-agonist alone
d. Consider also for patients on home nebulizer therapy
5. Steroids iv - may be most important therapy (eg. 80-100mg iv Solu-MedrolВ® q8-)
6. Antibiotics
a. No frank pneumonia - still need to cover H. influenza, Moraxella, Pneumococcus, etc.
b. Ceftriaxone or Cefuroxime iv
c. Oral: BactrimВ® good initial choice; Cefuroxime or Cefixime (SupraxВ®) if allergic
d. Other excellent po antibiotics include Ofloxacin, Clarithromycin and AugmentinВ®
e. Ampicillin out of favor due to increased resistance of H. influenza and M. catarrhalis.
f. Patients treated with antibiotics recover more rapidly and have less deterioration [ 4, 6]
7. Ipratropium bromide
a. Adjunct to Гџ2-agonist therapy; combination more effective than Гџ2-agonist alone
b. Available for combination nebulizer treatment with Гџ2-agonists
c. Only mild cardiac effects.
8. Theophylline See Card "Theophylline Toxicity"
a. Mild bronchodilator See Card "Asthma"
b. Increases Respiratory muscle (diaphragmatic) strength
c. Mild diuretic
d. Intubated patients who fail to wean due to poor muscle strength may benefit greatly
e. IV aminophylline load is usually preferred (~5mg/kg slow bolus, then 0.5mg/kg/hr iv)
f. Tachycardia, tremors, palpitations, and hypertension may occur
9. Diuretics - may improve oxygen transit if pulmonary edema is present
10. Mechanical Ventilation
a. Endotracheal Intubation is usually used
b. Positive pressure, non-invasive ventilation is very effective in some patients [10]
c. In general, non-invasive methods should be considered
11. Prognosis [11]
a. In hospital mortality was 24% for patients in intensive care for COPD exacerbation
b. Most in hospital mortality was associated with non-respiratory organ dysfunction
c. For >65 year old patients, 1 year after hospital discharge, mortality was 60%
H. Surgical Treatment of COPD [12]
1. Indications
a. Incapacitating dyspnea
b. Compression of relatively normal lung parenchyma by diseased lung tissue
2. First performed by Brantigan in 1957
3. Bullectomy and volume reduction pneumoplasty are performed
4. 30% of lung is excised with aim to reduce total lung capacity and residual volume
5. Allows diaphragmatic contour to return to baseline, thus improving respiratory mechanics
6. Variable Success
a. No definite predictors of successful outcome with respect to PFTs or imaging
b. Poor six minute walk test pre-operatively may predict good outcome
c. Improved lung function, reduction in pCO2, and increased RV function was seen [12]
DIFFERENTIAL DIAGNOSES OF PULMONARY ABNORMALITIES
A. Lung Cavitation
1. Tuberculosis
146
2. Fungus Histoplasmosis, Nocardia, Actinomyces, Aspergillus
3. Lung Cancer: usually non-small cell carcinoma
4. Pulmonary infarction
5. Aspiration Pneumonia with Abscess formation
6. Lymphoma - usually non-Hodgkin's
7. Bacterial Abscess: anaerobic / mixed
8. Inflammatory: Wegener's Granulomatosis, Rheumatoid Arthritis (necrobiotic), sarcoidosis
9. Cystic Bronchiectasis
10. Developmental Cysts
11. Parasitic Disease - hydatid, paragonimiasis
12. Silicosis - very rarely cavitary
B. Hemoptysis
1. Diseases
a. Pulmonary Embolus
b. Arterio-venous malformation (AVM)
c. Goodpasture's (anti-basement membrane Antibodies) Syndrome
d. Vasculitis
e. Sarcoidosis
f. Mitral Stenosis - with high pulmonary pressures; called "cardiac apoplexy"
2. Infection (Bronchiectasis, bronchitis)
a. Bacterial pneumonia
b. Tuberculosis (most common world-wide)
c. Nocardia
d. Lung abscess
e. Unusual: fungal balls, fungal infection (aspergillosis), parasitic infections
3. Neoplastic
a. Lung Carcinoma
b. Lymphoma (unusual)
c. Carcinoid Tumors Syndrome"
C. Pulmonary Edema
1. Etiology
a. Acute Cardiac Decompensation
• Mitral Regurgitation
• Ischemia
• Arrhythmia
• Infarction
• Heart Failure (Left Sided)
b. ARDS
c. Hypoproteinemia
• Liver Failure
• Nephrotic Syndrome
d. Inflammatory Response
e. Pulmonary Embolism and Infarction
2. Symptoms
a. Hypoxia due to poor gas exchange
b. Shortness of Breath (including "cardiac asthma")
c. Pain, usually over the lower lung fields
d. Paroxysmal Nocturnal Dyspnea, Orthopnea
D. Interstitial Lung Disease (ILD)
1. Hypersensitivity Pneumonitis
2. Atypical pneumonia: Mycoplasma, Legionella, Pneumocystis, Viral, Chlamydia
3. Granulomatous Diseases
a. Sarcoidosis
b. Wegener's Granulomatosis
c. Tuberculosis - unusual
4. Interstitial pulmonary fibrosis (IPF)
a. Usual interstitial pneumonitis (UIP)
b. Desquamative interstitial pneumonitis (DIP)
5. Connective Tissue Disease
a. Usually lower lobes: Rheumatoid Arthritis
(RA), Scleroderma, SLE, Myositis
b. RA: HLA linked, often with pleural involvement
c. Usually upper lobes: ankylosing spondylitis
6. Asbestosis (pleural involvement)
7. Silicosis, Berylliosis
8. Radiation pneumonitis: >4000 R total dose; Fibrosis
9. Metastatic Infiltration: lymphangitic spread (breast CA, lymphoma, etc)
10. Drug Reaction: bleomycin, nitrofurantoin, ?methotrexate
11. Others
a. Idiopathic pulmonary hemosiderosis
147
b. Eosinophilic granuloma
c. Lymphangioleiomyomatosis (LAM)
E. Solitary Pulmonary Nodule
1. Usually defined as < 3 - 4cm opacity without atelectasis or hilar adenopathy
2. Etiology
a. Bronchogenic Ca (35-50%): non-small cell cancers were more common than SCLC
b. Metastatic Cancer (breast, colon, renal, Kaposi's Sarcoma)
c. Carcinoid Tumor (total 10%)
d. Granulomatous Process: TB, Histoplasma, Coccidiomycosis, Cryptococcus, Aspergillus
e. Other: Bronchial Cyst, AV Fistula, Fibroma, Rheumatoid Nodule, Hematoma, Sarcoid
f. Rounded Atelectasis, Hamartoma
g. Resolving pneumonia, infarction
3. Factors Favoring Malignancy
a. Older age of patient
b. Smoker
c. Margins Not Sharp
d. Uncalcified, or Calcification NOT laminated, homogeneous or popcorn
e. Change in size on Chest Radiograph over 2 years
f. A very rapid doubling in size (<7 days) favors benign histology
g. Size >2cm
4. Evaluation
a. Chest radiography is most common initial test
b. Nodules <2cm require thin section CT study
c. >2cm is nearly always a bronchogenic CA; staging with chest and abdominal CT
d. Sputum Cytology: diagnostic 20% of malignancies (endobronchial tumors often exfoliate)
e. Fiberoptic Bronchoscopy: Diagnostic yields 50-75%; drops off for lesions <2cm
f. Transthoracic Aspiration: Diagnostic <2cm ~60%, >2cm ~85%
5. Chest Radiographic (CXR) Results of Benign Lesions
a. Calcification usually means benign (<1% malignancies appear calcified on CXR)
b. Benign Calcifications: laminated (granuloma), popcorn (hamartoma), homogeneous
c. No change in size over 2 years
d. CT scan gives better assessment of size and calcification
Pulmonary Function Testing PFT
PULMONARY EMBOLI:
Origin of Emboli:
-(80-90%) large lower extremity & pelvic veins
-Rt Atrium (CHF, A-Fib, indwell cath)
148
-Hepatic & Renal Veins
-Tricuspid Endocarditis or upper extremity thrombi in IV drug abusers
Predisposing Pathology:
1) Stasis,
2) Endothelial Damage
3) Hypercoagagulable State
Predisposing factors:
immobility BCP's,
IBD, shock, CHF
pregnancy, stroke, neoplasm, obesity, SLE, nephrotic syndrome, polycythemia,
-HIP & Knee surgery/any surgery
-Any pt in Hosp approx 30% will have
DVT
PROPHYLAXIS:
low dose heparin: decr risk fro 30-5
Adj Dose Heparin: PTT in high nml range
-effective 24h prior to surg
Coumadin 2mg/d 1-2d prior to surg
-followed by full Tx post-op
Pressure compression device: cause sys
-anticoagulation
Venous Thrombi(Red): Fibrin & RBC's
Art Thrombi (white): Plt dense
Etiologic Factors:
1. Lack of Endogenous Anticoag Factors
a) antithrombin III
b) protien C
c) protein S
2. TPA - impaired synth & release
3. Plasminogen - abnml fxn or quantity
4. Antiphospholipid Atibodies - in SLE cause of Art & Venous thrombi
5. Exogenous Estrogen: dose related
hypercoagulable state
(risk unrelated to duration of use)
Presentation:
-uncomplicated embolus w/dyspnea
-pulm infarct syndrome(pleuritc CP
+/- hemotysis
-circulatory collapse (<10%)
RISK:
-compounded w/age, obesity, CHF, presence of CA, acute MI, prior
DVT or PE & immobilization
1. Low: age<40 w/uncomplicated surg
age>40 w/minor surg
2. Moderate: age >40 w/gen surg>30min
3. High: major orthoSurg on low limbs
or age>40 w/extensive abd/
pelvic surg for malignant dz
(fatal PE in 1-5%)
SX:
1.Common: Most common Tachypnea
(>50%): Dyspnea, tachypnea,
tachycardia, cough, rales,
pleuritic CP, angina
2. Less Common(10-40%): hemoptysis,
low fever, JVD, DVT signs
syncope, altered MS
3. Rare(<10%) weezing, DIC, abd pain
EKG Signs:
Sinus Tachycardia
S1 Q3 T3 (40% w/nonspec T wave changes)
149
S-T wave abnormalities
PACs, PVC’s, atrial tach
Rt atrial strain, RBBB, RAD(or LAD)
CXR:
Atelectasis
elevation of hemidiaphragm (lost volume)
pleural effusion
"knuckle sign" PA tapers abruptly
pulm infarction: pre-existing CV dz
LAB Signs:
-98% of all PE Pts w/abnml A-a grad or
w/ PaCO2 <36 (sens not specific)
V/Q scan:
inj radiolabeled albumin &
- inhaled inert hot xenon
** (Pos: 50% false + rate) **
1. Nml: reliably excludes PE
2. Low Prob: 20-40% are pos
(same for intermit & matched result)
3. Int Scan: abnml perf + infl on CXR
4. Matched defect: due to bronchoconstriction
5. High Prob: 86% accuracy if large
perfusion defect or segmental
-only 37% if sub segmental
(confirmed by pulm angio)
PAgram:Pulm Arteriogram:
definitive Dx
- Morbidity: 4-6%- increased in Pts w/
RV-EDP > 20mmHg
- must do prior to thrombolysis,
embolectomy, or anticoag in Pt w/
bleeding risk
FX of PE on Right Ventricle:
- Massive PE leads to increased RV
afterload- enlarged RV, shifts vent
septum to Lt & decreased LV preload
- leading to decreased CO
- leads to RV dilation & ischemia
from reduced coronary flow in systol
-----------------------------------TREATMENTS:
Heparin: indicated in PE, suspected PE
& DVT
- 1/2 life=60-90 min
- Bolus dose: give prior to definitive
*** Dx to prevent early mediatorinduced pulm vasoconstriction
& bronchoconstriction by thrombin
activation & PLT aggregation
- Acts by binding Antithrombin III
which inactivates Thrombin
& inhibits coagulation
- Duration of TX: gen continued 7-10d
- Early Ambulation is Discouraged since
fresh thrombi may embolize prior to
adherence to vein wall (7-10 days)
- Maintainance Drip or Sq post bolus
- IV 12,000 - 18,000 IU/hour
- SQ 12,000 - 14,000 IU q12 hour
(test PTT midway between sq inj)
--------------------------------
150
Coumadin: for long term maintainance
- antagonist of Vit K - depleates clot
factors II, VII, IX, X
- Effectivenes depends on depletion of
clotting factors - FacII(Prothrombin)
1/2 life =60 hours- no use in rushing
- Give 10mg PO x 3d, get PT on 1st &
3rd day
- To prevent recurrent PE: 6mo of TX
unless definitive studies show
cleared DVT & PE (IPG & Lung Scan)
---------------------------THROMBOLYTIC TX:
1. hemodynamically unstable Pts
2. rTPA within 3 days of surgery
Streptokinase, Urokinase, & TPA
- act to facilitate fibrinolysis by
converting plasminogen to PLASMIN
which hydrolyses fibrin,fibrinogen &
blood coag factors
- TRIALS show thrombolytic Tx superior
to heparin in improving PAgrams,
hemodynamic indices, & perf scans
***-particularly in massive PE's
- F/U TRIALS: thrombolysis w/<longTerm
residual pulm clots & pulmonary
diffusion capacity than w/Heparin
(seen @ 2weeks, 1yr, & 7yrs)
- NO dif w/TPA by IV or intrapulm Cath
- UROKINASE: direct act of plasminogen
(isolated from human urine)
- STREPTOKINASE: must bind plasminogen
& then become plasmin activator
(isolated from grpC B-hem Strep)
- rTPA: "CLOT SPECIFIC" thrombolysis
Activates Plasminogen-plasmin
only significantly inpresence
of fibrin which facilitates
conversion of plasminogen,
**** thus producing localized FCTs
- 100mg infusion x 7 hours
may be superior to 50 mgX 2hrs
---------------------------CONTRAINDICATIONS to THROMBOLYSIS:
Absolute Contraindications:
-active internal bleeding
-recent surgery
-? aortic aneurysm
-recent head trauma/CNS TUMOR/CVA
-Ophthal bleed--?DM
-BP> 200/120
-------------------Relative Contraindications
-recent minor trauma
-Hx: chronic severe HTN
-active PUD /bact endocarditis
-Bleeding diathesis/Anticoag Tx
-sig Liver/ kidney Dysfxn
-age > 75
-prior streptokinase (particularly
-within initial 6-9mo period)
Complication of thrombolysis:
- bleeding (1% intracraneal)
- antibody formation (w/SK)
- allergic Rxn (w/SK)
151
- fever (w/SK)
- resistance to thrombolysis
ISOPROTERONOL: beta agonist:
bronchodil, pulm/syst vasodilator,
& +inotrope
- in Pt w/ MILD PE & cardiac failure
- lowers pulm HTN & increases CO
TX FOR UNSTABLE PT w/PE
1. Thrombolysis
2. Embolectomy(only for central emboli)
3. Tranvenous Catheter Embolectomy
4. IVC Filter
Recurrent PE: may lead to pulm HTN
and Cor Pulmonale
REF: Biebuyck JF: PulmThromboembolism:
Dz Recog. & Pt Mgt.Anesthesiology
73:146-64,1990
Pulmonary Embolism Lecture Slides(Dr. Goff)
152
153
154
155
156
157
158
159
160
161
Anticoagulation
162
163
TB Mycobacterium Tuberculosis
SOURCE: human transmission especially pulm TB pt
=pts w/tubercle bacilli in sputum are most infectious)
=pt in whom are TB+ by sputum cult alone are much < infectious
=transmitted by aerosol drops & penetrate bronchi & lungs
---------------------------------------Pathophysiology.....................
PRIMARY INFECTION: usually latent but
sometimes w/clin signs: either skin,
fever, nodes, or x-ray focus
SKIN RESPONSE/PPD: + after few weeks of
exposure to tuberculin
EARLY POST PRIMARY RESPONSE: miliary TB,
meningitis or pleuricy
LATE POST PRIMARY TB: lesions in
lymph nodes, joints, bones or abd
REAACTIVATION OF PRIMARY TB FOCUS:
usually following wakening of immune
fxn or exogenous reinfection -->
leads to caseous focus in lung that
liquifys & proliferates microbes.
-once drained via bronchi-> the focus
remains as a TB pulm cavity
---------------------------------------DIAGNOSIS:
SITE: Most often lungs but 30% extrapulm
**Pulmonary TB**:
164
AGE: all ages >>in 20-35 year old males
Sx: persistant cough +/- fever, anorexia
hemoptysis.
TUBERCULIN TEST: neg result r/o dz unless
pt is moribund/cachectic, has
measles/pertussis virus, on steroids
or in 3rd trimester of pregnancy
**POSITIVE RESULT:Little Dx value
since could mean either past BCG vac
or old primary inf w/o active dz.
SPUTUM: Imperitive to get 2 sputum smpls
2cc/each for micro smear exam
**Extrapulmonary TB**
TEN RULES FOR READING CHEST X-RAYS
(http://www.mtsinai.org/pulmonary/books/house/rules-a.html)
(Especially for House Officers in Clinical Specialties)
1. The only way to learn to read chest x-rays is to read chest x-rays. Daily.
2. Always check the name and date on the film. Five percent of
the time the film will be of someone else.
3. When confronted with an abnormal chest x-ray, always seek
out prior films for comparison. Unless absolutely, positively
certain, always assume that old films are available
somewhere.
4. Don't ignore the lateral film. It can often clarify the presence
or absence of lower lobe disease.
5. "Technique" accounts for much of the variation in serial chest
x-rays. Don't confuse this change (e.g., the amount of x-ray
penetration, or rotation of the patient) with change in disease.
6. Consider everything on the film that might provide some
potentially useful information: endotracheal tube? (respiratory
failure); surgical clips? (thoracotomy); absent breast shadow?
(mastectomy); chest leads? (AP film); large amount of soft
tissue? (obesity); etc.
7. The presence of clear lung fields (no infiltrate, no vascular
redistribution) and normal-sized heart rules out left-sided
congestive heart failure as a cause of the patient's symptoms.
8. Lung fields can never be called clear on a portable chest x-ray
until you've identified the left hemi-diaphragm and lack of
infiltrate behind the heart.
9. The chest x-ray never lies.
10. Ask for help. Help is always available.
165
Chest Radiography Lecture by Dr. Goff
166
167
168
169
170
171
172
173
174
175
176
177
178
179
180
181
Rules on Oxygen Therapy -- What Every House Officer
Should Know
(http://www.mtsinai.org/pulmonary/books/house/rules-a.html)
Physiology
1. PO2, SaO2, CaO2 are all related but different.
2. PaO2 is a sensitive and non-specific indicator of the
lungs' ability to exchange gases with the atmosphere.
3. FIO2 is the same at all altitudes.
4. Normal PaO2 decreases with age.
5. Oxygen from the wall outlet is always 100%.
6. The body does not store oxygen.
Therapy & Diagnosis
7. Supplemental O2 is an FIO2 > 21%.
8. Supplemental O2 is a drug.
9. Supplemental O2 is the most commonly-prescribed
drug in hospitals.
10. A reduced PaO2 is a non-specific finding.
11. A normal PaO2 and alveolar-arterial PO2
difference (A-a gradient) do not rule out
pulmonary embolism.
12. High FIO2 doesn't affect COPD hypoxic drive.
13. A given liter flow rate of nasal O2 does not
= any specific FIO2.
14. Face masks cannot deliver 100% oxygen unless
there is a tight seal.
15. Oxygen masks migrate.
182
SIGNS OF OBVIOUS BREATHING (WOB)
(http://www.mtsinai.org/pulmonary/books/house/rules-a.html)
If a patient's breathing is obvious on initial contact (for example, when you first see the patient on
walking into the room) it is abnormal. Normal breathing at rest is simply not obvious; one has to look
very closely for chest movement to
appreciate breathing. Six signs that may make someone's breathing obvious to the observer - all
abnormal - are listed below.
flaring of nostrils with breathing
tachypnea (generally, to be obvious, respiratory
rate is > 24 breaths/min)
noisy breathing (wheezing, stridor, moaning, etc.)
use of accessory breathing muscles (neck muscles,
intercostal muscles, etc.)
pursed lip breathing (often seen in severe COPD)
Cheyne-Stokes breathing (alternating periods of apnea with
tachypnea; apnea periods may last up to 30 seconds)
THE FOUR MOST IMPORTANT EQUATIONS IN CLINICAL PRACTICE
(http://www.mtsinai.org/pulmonary/books/house/rules-a.html)
Pulmonary, Acid Base, ABG
1. The PaCO2 equation
PaCO2 = CO2 produced by metabolism (ml/min) x k/alveolar ventilation (L/min)
where
alveolar ventilation = minute ventilation minus dead space
ventilation
k = 0.863.
REASON IMPORTANT: This equation explains why one cannot assess PaCO2 clinically, i.e., with
only bedside observations such as respiratory rate, depth of breathing, level of discomfort, breath
sounds, etc. There are no clinical variables in this equation. For example, a patient with fast and/or
deep breathing can still be retaining CO2 if most of the air goes to dead space (either because of
shallow tidal volumes or ventilation-perfusion mismatch). Since there is nothing clinical in this
equation, one cannot use clinical criteria to assess PaCO2 (i.e., adequacy of alveolar ventilation). A
patient may appear to be "hyper-ventilating" but in fact be hypoventilating, i.e., have a high PaCO2.
2. The alveolar gas equation
PAO2 = FIO2 (B.P. - 47) - 1.2 PaCO2
where
PAO2 = alveolar PO2
FIO2 = fraction of inspired oxygen
B.P. = barometric pressure
47 = water vapor pressure in airway in mm Hg
Alveolar-arterial PO2 difference [A-a gradient] =
calculated PAO2 - measured PaO2
REASON IMPORTANT: You need the calculated PAO2 to know if arterial PO2 (PaO2) is abnormal or
not. Specifically, the variables in this equation (B.P., FIO2 and PaCO2) must be known to properly
interpret any PaO2 value. Is a PaO 2 of 28 mm Hg normal? (Yes, if breathing mountain air at the
summit of Mt. Everest, where B.P. is only 253 mm Hg). Is a PaO2 of 100 mm Hg abnormal? (Yes, if
the patient is breathing 100% oxygen). Does a PaO2 of 50 mm Hg indicate a problem of ventilationperfusion mismatch? (Yes, if the A-a gradient is increased; no, if the A-a gradient is normal, in which
case the low PaO2 may be solely from elevated PaCO2).
3. The Henderson Hasselbalch equation
pH = pK + log HCO3/.03(PaCO2)
183
REASON IMPORTANT: Helps diagnose presence and type of acid-base disorder, and the body's
compensation for it. The abbreviated version is adequate in most clinical situations. Equation shows
there are only four primary acid-base disorders: two where the first change is in HCO3- (metabolic
alkalosis and acidosis) and two where the first change is PaCO2 (respiratory alkalosis and acidosis).
4. The arterial oxygen content (CaO2 ) equation
CaO2 content = amount O2 bound to hgb + amt.O2
dissolved
= (1.34 x hgb x SaO2) + (.003 x PaO2)
where
O2 content = ml O2 /100 ml blood
1.34 = ml O2 that can maximally bind to a gram of hgb
hgb = hemoglobin content, in grams/dl
SaO2 = saturation of hemoglobin with oxygen in arterial
blood
.003 = ml O2 that can dissolve in plasma per mm Hg PaO2
per 100 ml blood
REASON IMPORTANT: Incorporates factors for adequate arterial oxygen content, most important of
which is hemoglobin; over 97% of arterial oxygen content is normally carried by hgb. Note that oxygen
content is the only readily available value that directly reflects the number of oxygen molecules in the
blood. In assessing degree of hypoxemia (as opposed to the cause), CaO2 is more useful than either
PaO2 or SaO2. A patient can be profoundly hypoxemic with a normal PaO2 (for example, from severe
anemia or carbon monoxide intoxication) or with a normal SaO2 (from severe anemia).
5. And the fifth most important equation?
(http://www.mtsinai.org/pulmonary/books/house/rules-a.html)
Anion gap equation
Fick equation for oxygen uptake
Equation for oxygen delivery
Conversion equations for: centigrade to Fahrenheit;
cm H2O to mm Hg; kg to lbs.
Resistance equation (for blood flow or air flow)
Compliance equation for a solid organ (heart, lungs)
Harris-Benedict nutrition equations
Creatinine clearance equation
Equation for fractional excretion of sodium
Equation for calculating serum osmolality
184
185
PAO2 = FIO2(PBO2-47) - 1.2(PaCO2)
ALT. = altitude in feet
PB = barometric pressure
FIO2 = fraction of inspired oxygen
PIO2 = pressure of inspired oxygen in the trachea
PaCO2 = arterial PCO2, assumed to = alveolar
PCO2
PAO2 = alveolar PO2, PAO2 is calculated using an
assumed R value of 0.8 except for the summit of
Mt. Everest, where 0.85 is used 24
PaO2 = arterial PO2, assuming a P(A-a)O2 of 7
mm Hg at each altitude; each PaO2 value is normal
for its respective altitude
CaO2 = (SaO2 x Hb x 1.34) + .003(PaO2)
186
Figure 1. PaCO2 vs. alveolar ventilation (VA). The relationship is shown for carbon dioxide
production rates of 200 ml/min and 300 ml/min. Changes in PaCO2 are shown for a one liter
decrease (short horizontal lines) in VA starting at two different PaCO2 values, 30 and 60 mm Hg. A
decrease in alveolar ventilation in the hypercapnic patient will result in a greater rise in PaCO2 than
will the same V.A change when PaCO2 is low or normal. Also, note that an increase in carbon dioxide
production when VA is fixed will result in an increase in PaCO2
.
187
Figure 2. Normal range of P(A-a)O2 from FIO2 of .21 to 1.00, based on data obtained from 16 healthy
subjects aged 40 to 50 years.23 Lines represent mean values and + or - 2 standard deviations. The
P(A-a)O2 increases up to an FIO2 of 0.6, then plateaus with further increases in FIO2. Note that P(Aa)O2 may normally exceed 100 mm Hg on an FIO2 of 1.00.
Figure 3. PaO2 vs. SaO2 and oxygen content. The oxygen dissociation curve relates PaO2 to SaO2. The shape and
position of the curve are the same regardless of hemoglobin content. The right ordinates show arterial oxygen contents for
two different concentrations of hemoglobin: 15 gm% and 10 gm%. Normal P50 (the PaO2 at which hemoglobin is 50%
saturated with oxygen) is approximately 27 mm Hg. "X" represents measured PaO2 and oxygen saturation of Case 4.
188
Shunt Equation
Normal Ranges for Ventilatory Values
Respiratory Rate (RR)= 8-16 b/m (*<=38)
Core Temperature = 36-38 C (96.8-100.4 F)
Esophageal Pressure
(Pes=PESmax-PESmin)=< 15 cmH2O
Airway Pressure (Paw) <= 40 cmH2O
Tidal Volume (Vt)= 7-10 cc/kg (*>=325)
Tidal Volume(cc)/Weight(kg) *>=4
Work of Breathing (WOBp)= .05 J/L (<= .8
J/L max sustained)
TransPulmonary Pressure (PTP)= 6-8 cm
H2O
Respiratory Time Fraction (Ti/Ttot)= .3-.4
(abn if >.4 or > .1 increase)
Mean Inspiratory Flow (VT/Ti)<= .4
VT/RR= .05-.075 L/s (*<= 105 b/m/l)
Airway Resistance (Raw)= 2-5 cmH2O/L/s
Dynamic Compliance (Cdyn)= 50-100
cc/cmH2O (*>=22)
Static Compliance (Cstat)= *>=33 cc/cmH2O
Respiratory Drive (P0.1)= 3-4.5 cm H2O (<=
6 cm H20)
PTP/Pmax <= .4 (sustained)
Pressure Time Index (PTI)<= .15 (sustained)
Minute Ventilation (Ve)= 7-10 l/m (*<=15)
Maximal Inspiratory Pressure (Pmax, NIF,
MIP) *<= -15 cm H2O
PaO2/PAO2 ratio *>=.35
CROP index** *>=13
* Threshold Values of Indexes Used to Predict
Weaning Outcome
** CROP Index=(Cdyn*Pimax*[PaO2/PAO2])/R
Tobin et al, NEJM 1991; 324: 1445-50
189
Pleural Effusions
Pathophysiology of Pleural Effusion
Starling Equation:
F = K((Pcap - Pif) - (Ocap - Oif))
F = Flow in cc/sec
K = Permeability Constant cc/sec/cmH2O/cm^2
P = Hydrostatic Pressure in cmH2O/cm^2
O = Oncotic Pressure in "
cap = capillary
if = Interstitial Fluid
Pd = (Pcap - Pif) - (Ocap - Oif)
Pd = Driving Pressure
= 8 - 9 cm H2O favoring fluid movement
from parietal capillaries
into pleural space
= 10 -11 cmH2O favoring flux from pleural
space into visceral pleural
capillaries (Reabsorption)
Therefore Increased Flow & Pl Ef :
1. Increased K (Capillary Permeability)
a. eg. pneumonia; inflammation; PE; Empyema; CVD
Uremia, pancreatitis, Subphrenic abscess
Whipple, hepatic abscess, Dresslers, XRT,
Vasculitis, Chronic Hemothorax
b. w/ Decreased Lymphatic Flow --> exudate
CA, TB
2. Increased Pcap (Hydrostatic Pressure)
a. With decreased Oncotic------> transudative
eg. CHF, cirrhosis, nephrosis, myexedema (rarely
exudative), peritoneal dialysis, hypoprotein,
Meig's (left eff, benign ovarian fibroma w/
ascites rarely exudative)
3. Decreased Pif (Increased Negative Intrapleural Pressure)
-eg. Atelectasis----->transudate early
4. Decreased Ocap (Oncotic capillary Pressure)
-eg. Nephrotic Syndrome, hypoalbuminemia
5. Increased Oif (Oncotic Pleural Fluid)
-eg. Pleural tumor, inflammation, infection
6. Decreased Lymphatic Flow / Exudative
-Chylothorax, Sarcoid, Yellow Nail, Milroy's Ds
7. Other: CVP catheter, Postpartum pl ef
8. Drug & Hypersensitivity ----> exudate
-Macrodantin, Methylsergide, Nitrogen mustard, Quinicr,
Sclerotherapy for esoph varices
-HALF OF ALL PLEURAL EFFUSIONS ARE CAUSED BY CANCER; WHILE THE MOST COMMON
CAUSE IS CHF...
-2/3 OF ALL MALIGNANT EFFUSIONS ARE FROM LUNG, BREAST OR LYMPHOMA
ANY TUMOR CAN CAUSE IT; GU / REPRODUCTIVE / GI ---> 15%
15% OF ALL EFFUSIONS ARE FROM UNKNOWN CA ORIGIN.
-50% OF PATIENTS W/ BREAST OR LUNG CA WILL DEVELOP
PLEURAL EFFUSION
Symptoms
190
Dyspnea, Cough & Chest Pain are the commonest symptoms (especially w/
CA.)
The cough may be positional.
Physical Signs:
Amount of P.E. Resp Rate Expansion Fremitus Sounds Tracheal Shift
Small (< 300cc) n-^ n n vesc none
Moderate (300-1500) n, ^^ n-lo n-lo lo-vesc "
Large (>1500) ^^^ lo lo lo lo lo BV none maybe
Less than 300 cc's usually not found on Physical Exam; may here a rub
though.
Greater than 10 cm layering free flowing fluid on decubitus CXR OK to TAP.
With > 1500 cc; there is usually mediastinal shift away. If this does not
occur r/o:
a. Obstruction of Main Stem Bronchus w/ Volume loss
b. Trapped Lung (As in Mesothelioma)
c. Fixation of Mediastinum (Tumor, Nodes Lymphoma)
Sometimes Large ( >1000cc ) of Subpulmonic Fluid can be Occult on CXR
Causes of Pleural Effusion
TRANSUDATES
Increased Hydrostatic Pressure
---------------------------
Miscellaneous
-------------
CHF
Acute Atelectasis
Constrictive Pericarditis
Subclavian Catheter misplaced
SVC obstruction
Idiopathic
Urinary Obstruction
Decreased Oncotic Pressure
-------------------------Cirrhosis w / Ascites
Nephrotic Syndrome
Hypoalbuminemia
Peritoneal Dialysis
Acute Glomerulonephritis
Myxedema
USUALLY BILATERAL EFFUSIONS
EXUDATES
191
Pulmonary Embolism (30-50%)
Infectious Drug Induced
------------------------------
Pleural Disease
----------------------------
Bacteria, TB, Fungi, parasites
Virus, mycoplasmal
Hepatitis
Pulmonary Infarction
---------------------------Neoplastic
Chylo / Pseudochylothorax
--------------------------------------------------------Metastatic, Bronchogenic, lymphoma,
leukemia, mesothelioma, chest wall
Miscellaneous
tumor
---------------------------Esophageal rupture,
Sarcoidosis
Collagen Vascular Diseases
Chronic Atelectasis, Trapped
-----------------------------lung, Uremia, Asbestos,
RA, SLE, Drug-Induced SLE, Sjogren's Familial Mediterranean Fever
Wegners, etc
PostMI, Lyphedema (Yellow Nail
Syndrome), Obstructive Uropathy
Intra-abdominal Diseases
(urinoma), XRT, Myxedema,
----------------------------Immunoblastic Lymphadenopathy
Abd Sx, Pancreatitis, Subdiaph Abscess,
Incarcerated diaphr hernia, Intrahepatic Idiopathic
Abscess Meig's Syndrome
Thoracentesis
1. Safe & simple Dx'tic & Tx'tic procedure. Made even safer by Ultrasonic
localization. Rarely severe bradycardia & hypotension as needle passes
parietal pleura (PLEURAL SHOCK): Vasovagal rxn...may pretx w/ atropine.
Can get Reexpansion Pulmonary Edema if > 1000-1500 cc 's removed too
quickly (based on pleural pressure and if kept <= 20 cm H2O unlimited
volume can be removed...manometry).
Pleural Effusion
GROUP 1
Pts w/ previously dx'ed New Pl Ef & No Dx Pl Ef w/ Asbestos
GROUP 2
CA & Pl Ef exposure &/or Hx PE
GROUP 3
Tcentesis Or Xray like Mesothel
+
Pleural bx
GROUP 4
Undx'ed Effusions After Conventional
methods have failed.
-cytogenetics
-Pleuroscopy
-Thoracotomy
Multiple thoracenteses may be needed to dx a Malignancy:
#1 ----> 53% yield
#2 ----> 64%
#3 ----> 69%
#4 ----> 72%
Some Ca have a lower yield on thoracentesis:
-Hogdkin's only 23% yield
-Lung, Breast, Ovary & Lymphosarcoma 63-73%
When Pleural Bx is combined with Thoracentesis the yield is increase
to 81-90%. [ COPE or ABRAHAMS NEEDLE ]
Coupling Cytology & Cytogenetic analysis yields a 92% positive dx'tic
192
yield for malignancy (perform after 2 negative thora's and pleural bx).
Pleuroscopy has a 93-96% yield for malignant Pl Ef.
In 10-20% of exudative effusions are enigmatic.
Malignant Pleural Mesothelioma
Dull aching non-pleuritic chest pain, dyspnea & cough of
insidious nature. Very difficult Dx. Hemoptysis, fever,
weight loss, hypertrophic pulmonary osteoarthropathy and
hypoglycemia (the latter 2 are w/ benign mesothelioma).
Hx asbestos exposure in only 50% - 70%. Peak age 50-70
with male : female 2:1 to 5:1. 80-90% of pts will have
xray evidence of Pl Ef, often with scoliosis and shift of
the mediastinum toward the effusion. Associated rib destruction, pleural plaquesor calcifications, intrapulmonary
nodules, pleural thickening or rind in fissures & paramediastinal structures; most often in the lung bases &
posteriorly.
Pleural Fluid Analysis
TEST
EXUDATE
VALUE
Specific Gravity
>
1.016
<=
Protein pleural
>
3 g/dl
<=
>
0.5
Pleural/Serum Protein
LDH pleural
>
or
>
2/3 upper
normal
Pleural/Serum LDH >
0.6
Glucose
<
60
Pleural/Serum Glucose
<
Prostaglandin E
TRANSUDATE
<=
200 IU/L <=
<=
<=
>=
.5
>=
280 pg/ml <----------> 27 pg/ml
Bedside Refractometer as Poor Man's Test of SG & Total Protein
---------------------------------------------------------
Lipid Profiles:
Milky or opalescent persisting after centrifuge
Chylous Effusions: > 400 mg Total Lipids / dl
65 - 220 mg Cholesterol / dl
Triglyceride > 110 mg/dl & > 2 x serum
SUDAN III is +
+ Chylomicrons on Lipoprotein electro
is dx'tic of CHYLOTHORAX
Chyliform Effusions : (Pseudochylous Effusion) has
Increased Lipids with
Triglycerides < 50 mg / dl
- SUDAN III
Elevated Cholesterol
No chylomicrons
(Chronic Fluid usually 5 yrs old)
193
Other Pleural Fluid Tests
- pl CEA : > 2.5 - 12.5 ng/ mL is malignant adeno CA (poor screening test)
- Gm Stain; Aerobic & Anaerobic Cultures; AFB; Fungal; Silver Stain
- Counterimmune electrophoresis (CIE)
- Directogens
- Increased Pleural Creatinine : Urinothorax (from Urinary Tract
Obstruction)
- Hyaluronic Acid > 0.8 mg/ml ------> Mesothelioma
- Adenosine Deaminase (ADA) > 30 IU/L in all with TB (lower in all w/
parapneum / CA)
- Pleural Bx: In TB & CA will be + in 50% of Exudates
In TB > 80% will be + for AFB or Granulomata & TB c/s 75% of pt
In CA w/ fluid & Bx 90% yield
Low yield in Mesothelioma
- Pleuroscopy
- Cytogenetic (Chromosomal Studies)
- Bronchoscopy: Epecially with Parenchymal Abnormalities
R/O Obstructing Lesion with will cause fistula w/ Chest Tube
Pleural Fluid
Descriptions:
C = Clear ..............Most Transudates &
SC = Straw Colored....... some Exudates
T = Turbid ............. Infectious
P = Pus................. Empyema
Y = Yellow.............. & turbid = infection
SS = Serosanguineous
G = Green...............& turbid rheumatoid Pleurisy
B = Bloody..............Trauma, Tumor, Pulm Infarct
Cloudy Milky White......Chylothorax (chylous effusion)
Thoracic duct trauma, tumor, lymphangio
Lymphoma, Surgical
Thick yellow metallic...Pseudo-chylothorax = chyliform effusion
Sheen................as in chronic tb, ra, trapped lung
Viscous Hemorrhagic.....Malignant Mesothelioma
Anchovy Color...........Amebic Liver Abscess ruptured into
Pleural Cavity
Cellular Descriptions:
Small Lymphocytes (>50% of Cells) r/o CANCER!!!
Eosinophilia : pneumothorax or air; benign asbestos pleurisy
< 5% CA Exudates & is good Px
Disease States w/ Pleural Fluid
Transudative Diseases:
Congestive Heart Failure: C,SC; <1000 RBC & WBC; Mononuclear; Normal GLUC,pH &
Amylase....With Tx of CHF may become exudative!!!
Cirrhosis w/ Ascites : C,SC; < 1000rbc <500wbc; mono; normal G,Ph,Am
Exudative Diseases:
Malignancy : T,B; 5000-100,000RBC 100-10000wbc; Mononuclear; gluc
< 60 to normal; maybe < 7.3; Variable amylase
Uncomplicated Parapneum : T; 5000-100000rbc&wbc; pmn; >40 gluc; >7.2; nor am
Complicated Parapneum : T,P; " ; pmn; < 40 ; <7.2; "
Chest Tube especially if Glu < 40 or pH < 7.00!!!!!
Pulmonary Embolism : SC,B; 100-200000rbc, 100-50,000wbc; pmn/mono; norm
Pancreatitis : SS,B; 1000-100000rbc, 1000-50000wbc;pmn; p/s amy >2
194
or > 160 U; pseudocyst, CA, esoph rupture
Rheumatoid Pleuritis : T,Y; <1000rbc, 1000-20000wbc; pmn/mono; g<25; ph<7.2 80% men; subq
nodules; pleural RF >= 1:320
Low Complement & Immune Complexes
Systemic Lupus : " ; except normal glucose & pH; ANA LE cells
ANA >= 1:160 or p/sANA >1
Tuberculosis : SC,SS; <10000rbc <5000wbc; PMN early, MONO late; <60; >=7.3; < 5% mesothelial
cells; pleural bx 90% dx
Treatment of Pleural Effusions
A. Malignant Effusions:
-Some tumors are amenable to chemotherapy and can be used
as a therapeutic index (eg. Germ Cell tumor, Hodgkin’s,
Lymphoma, small cell lung ca, Breast Ca {hormone responsive},)
-Treatment depends on the condition & life expectancy as to
how aggressive one should be and how symptomatic the patient
is. Most malignant effusions will reaccumulate rapidly w/out
treatment.
-Thoracentesis alone: Mean time for re-accumulation was 4.2 days
with most recurring in 1-3 days & by 1 month 97% were back.
Repeated thoracentesis carries increased risk of pneumothorax,
bleeding, empyema, fluid loculation & HYPOPROTEINEMIA (which
favors transudation and more fluid.) Effective immediate symptom
relief by effecting pressure - volume curves & length-tension
relationship of the diaphragm.
-Tube Drainage: closed drainage is inefficacious; but Denver
pleuroperitoneal shunt a good alternative(?). Tube drainage is
a necessary prelude to pleurodesis (the drainage should be
less than 50-100 cc/24 prior to instillation therapy.)
Pleurodesis:
Tetracycline: (No longer available) 1500 mg +/lidocaine in 50-100 cc. 15mg/kg
70% pts free of Pl Ef @ 1 month.
Bleomycin : 40 IU / m^2 90 IU intracavitary
dose... 78-85% success rate 1.24 U/kg 1.25 milligrams per kilogram (not to exceed 40 milligrams per
square meter in elderly patients)
Doxycycline : 500 mg
Talc : By slurry or Poudrage via Pleuroscopy.5 grams of talc via insufflation during thoracoscopy or as
a slurry via chest tube
Quinacrine : Not used
The presence of Hilar or mediastinal masses, atelectasis or
endobronchial lesions are associated with an increased failure
rate of sclerosing agent.
-Pleurectomy: Major operative procedure with 23% complication
rate (air leaks, bleeding, pneumonia, empyema,
chf, pe, resp insuf.) High morbidity & mortality
w/ 90-100% response rate.
-External Beam Radiation: is of limited use in malignant eff.
1400-2300 rads. effective in lymphomatous effusions
195
ABDOMINAL PAIN
Immediate Questions
(Determine whether the patient has an acute "surgical" [i.e.,
requiring surgery] abdomen):
A. What are the patient's vital signs? Orthostatic blood pressure and pulse changes help ascertain the
patient's volume status. Fever occurs in inflammatory conditions. Tachycardia and hypotension would
suggest circulatory or septic shock from perforation, hemorrhage, or fluid loss into the intestinal lumen
or peritoneal cavity.
B. Where is the pain located? When did the pain begin? Sudden onset suggests perforated ulcer,
mesenteric occlusion, ruptured aneurysm or ruptured ectopic pregnancy. What is the quality of pain?
Intestinal colic occurs as cramping abdominal pain interspersed with pain-free intervals.
C. Are there any associated symptoms? Vomiting may result from intestinal obstruction or could result
from a visceral reflex caused by pain.
D. If the patient is a woman, what is her menstrual history?
CHARACTERISTIC PHYSICAL FINDINGS IN THE ACUTE ABDOMEN
Peritonitis
Generalized guarding, tenderness, rebound
tenderness, hypoactive or absent bowel sounds
Appendicitis
Right lower quadrant tenderness, guarding and
rebound, discrete tenderness at McBurney's point,
peak age 10-20.
Acute cholecystitis
Right upper quadrant tenderness and guarding,
positive Murphy's sign, may radiate to right scapula.
High Small Bowel obstruction
Severe vomiting, dehydration, no distention
Low Small Bowel obstruction
Distention, hyperactive and high pitched bowel
sounds, vomiting.
Bowel Infarction
Pain out of proportion to tenderness, rectal bleeding
if venous infarction.
Ruptured aortic aneurism
Pulsatile tender mass, hypotension, back pain
Pancreatitis
Steady, severe, LUQ and epigastric pain radiating
to the back; pain less when sits forward; decreased
BS; diffuse tenderness.
Plan:
The initial goal in evaluating a patient with abdominal pain is to determine whether or not surgical
treatment is indicated to prevent further morbidity.
A. The abdominal films can help differentiate between:
1. Several diagnoses can cause a surgical abdomen,
the most life-threatening considerations are
perforated or ruptured viscus, intraabdominal
hemorrhage, and necrosis of a viscus, (e.g., necrosis
of an intraabdominal viscus due to intussusception,
volvulus, strangulated hernia, or ischemic colitis).
Other specific conditions that may not cause an
acute "surgical" abdomen should be considered:
pancreatitis, intraabdominal abscess, peptic ulcer
disease or gastritis, pyelonephritis, renal stones,
infectious gastroenteritis, ovarian cyst, tumor and
salpingitis.
196
2. Among the elderly and those on steroids,
abdominal pain may be mild despite the presence of
an acute abdomen. One should not underestimate
the seriousness of mild abdominal pain in the
elderly, especially if it is associated with acute
confusion, fever, an elevated WBC or a metabolic
acidemia.
B. Laboratory tests to consider are a CBC with a
differential, amylase, liver function, urinalysis, and
pregnancy test.
C. Flat and upright abdominal films. These films can be
readily obtained and may provide important information.
Observe for the following: gas pattern, evidence of bowel
dilation, air-fluid levels, presence or absence of air in the
rectum, pancreatic calcifications, biliary and renal
calcifications, aortic calcifications, loss of psoas margin.
D. Observation. With the exception of those conditions
that require urgent surgical exploration, most cases of
abdominal pain can be initially managed with close
observation, correction of any fluid or electrolyte
disturbances, and judicious use of analgesics.
In general, any patient on a medical service
developing acute abdominal pain should receive an
evaluation by a general surgeon. In those cases in
which mechanical obstruction is suspected or
vomiting is present, nasogastric decompression
should be initiated. Patients who appear in septic or
circulatory shock should receive vigorous
intravenous volume replacement, cultures, empiric
antibiotics and be in an ICU setting.
GASTROINTESTINAL BLEEDING (Acute upper)The mortality for acute upper gastrointestinal bleeding is about 8-10% and in part is due to underlying
diseases of the liver, kidney, CNS, pulmonary and neoplastic disease.
CLINICAL: The most common presentation is that of hematemesis and melena. Hematemesis
is suggestive of bleeding that is proximal to the ligament of Treitz. Hematemesis may be either
frank bright red blood or "coffee ground". Bright red blood infers that the hematemesis occurred
immediately after bleeding, whereas coffee ground emesis is due to blood that has interacted with
hydrochloric acid. Patients may also have melena (black, tarry, foul smelling stools). Melena must
be differentiated from those patients that are taking iron, licorice or bismuth. Melena is due to
degradation of the hemoglobin in the GI tract by bacteria to hematin or other homeochrome. Melena
can takes several days to clear after there has been cessation of the upper GI bleeding.
Approximately 50-100 ml of blood is needed in order to produce melena.
PHYSICAL: Physical examination is important, for it can provide a clue as to the etiology of the
bleeding. For example, if the patient has spider angiomas, splenomegaly, asterixis, ascites,
testicular atrophy, jaundice and gynecomastia, the possibility of esophageal varices or alcoholic
gastritis arises. Abdominal tenderness in the epigastric area is suggestive of peptic ulcer disease.
Hyperactive bowel sounds may indicate that the bleeding is in the upper GI tract. If
hyperpigmented macules are seen on the lips this would suggest the Peutz-Jeghers
syndrome. Soft tissue masses may be associated with Gardner's syndrome. Lymphadenopathy,
abdominal masses and Kaposi's sarcoma lesions would be suggestive of a malignant process
as the etiology. Perioral telangiectasias would point toward hereditary hemorrhagic telangiectasia,
whereas blue subcutaneous nodules can be associated with blue rubber bleb nevus syndrome.
History is also important in providing clues as to the cause of the bleeding. Inquire as to the use of
NSAIDS, and if the patient is being treated for peptic ulcer disease. If the patient had violent
coughing or retching prior to the GI bleeding, Mallory-Weiss syndrome would be in the differential
diagnosis. Mallory-Weiss tears are lacerations that occur in the gastric cardia or the
gastroesophageal junction. They are usually about 1-2 cm in length. They typically occur with
persistent vomiting or wrenching, but have been seen following heavy lifting, hiccups, straining at
the stool, trauma, asthma, cardiopulmonary resuscitation, childbirth, and endoscopy. In about
50% of cases no etiology can be found. Mallory-Weiss tears account for about 15% of all upper GI
197
bleeding. Mallory-Weiss bleeding usually stops spontaneously in greater than 90% of cases. If
bleeding does not stop, epinephrine injection and thermal therapy may be effective. In patients
who fail endoscopic therapy, angiographic embolization or intra-arterial vasopressin can be
used, which is effective in 70%. Also, inquire about the patient's alcohol use and if there has been
liver disease in the past, as this would indicate that the bleeding originated from esophageal
variceal bleeding.
A history of previous aortic graft surgery indicates the possibility of an aortoenteric fistula.
Aortoenteric fistulas are rare, with most of these occurring in the third portion of the duodenum. Most
of the patients have had Dacron graft surgery. The fistula may occur at the suture line or into the
graft. There may be associated sepsis and positive blood cultures. The first bleed from an
aortoenteric fistula is known as the herald bleed, usually is brief, and usually stops spontaneously.
However, this is deceiving, as the bleeding resumes in a few hours or days and can be massive.
CT scanning can show air bubbles in the wall of the aorta, or evidence of perigraft infection.
Angiography may not demonstrate the fistula unless there is active bleeding. Upper endoscopy
should be done in all patients that have had an aortic graft placed and GI bleeding, to rule out other
potential causes for the bleeding.
LABORATORY: Serial CBCs should be done. The initial Hct may be deceiving because it does not
accurately reflect the degree of blood loss. However, as the intravascular volume is restored, the
hematocrit will drop. This may take up to 3 days. Platelets should be assessed as
thrombocytopenia may be due to portal hypertension. If patients are actively bleeding, and the
platelet count is less than 70,000/ul, platelet transfusions should be given. Prolongation of the
prothrombin time is compatible with liver disease and is treated with subcutaneous vitamin K and
fresh frozen plasma if the patient is actively bleeding. Elevated BUNs are commonly found in
upper GI bleeding, due to absorption of blood proteins and intravascular volume depletion.
Patients needing multiple blood transfusions should have frequent calcium and potassium
determinations.
DIFFERENTIAL DIAGNOSIS: Most cases of upper GI bleeding are due to peptic ulcer disease,
with duodenal ulcers more common than gastric ulcers. The remaining causes consist mostly of
varices, Mallory-Weiss lacerations and gastric erosions.
TREATMENT: The first step in treatment is a rapid assessment of the urgency of the bleed. A
patient that presents with a BP of 95-100 systolic, and tachycardia suggests that the patient has
lost 50% of blood volume. If the patient is not in shock, BPs should be checked in the supine and
upright positions. A systolic blood pressure that drops to less than 90 mm Hg on standing
suggests a loss of 25-40% of the blood volume. If there is a decrease of 10 mm Hg or more in the
systolic blood pressure, or an increase in heart rate above 120, a loss of 20% of the blood volume
is probable. Patients that have active bleeding should be immediately treated with IV normal
saline or Ringer's solution administered through two large bore 14 to 18 gauge peripheral
catheters. Blood should be obtained for immediate type and cross match, CBC, platelet count, PT,
PTT and chemistries. EKGs should be done in patients over the age of 40, those with chest pain,
or a history of coronary artery disease. Oxygen should be given if large amounts of blood have
been lost. Some patients will need endotracheal intubation to prevent aspiration, particularly
those with esophageal variceal bleeding. In some emergencies, non-crossed matched O negative
blood may be necessary. Patients with questionable bleeding sites will need a nasogastric tube
inserted. A return of bright red blood indicates active, recent upper GI bleeding. However, the
absence of a bloody return does not rule out upper GI bleeding, for the bleeding may be coming
from the duodenum, or the nasogastric tube may be curled in the fundus of the stomach.
Likewise, bile stained aspirates do not rule out an upper source. Following the assessment, the
nasogastric tube can be removed.
GASTRIC LAVAGE: In the past, iced saline has been used extensively. Recently, however,
the effectiveness of this has been questioned, and studies have shown increases in
bleeding times, and prothrombin times. Therefore, iced saline is probably of no proven benefit, and,
in fact, may be detrimental. Likewise, the addition of epinephrine to the lavage fluid, is of no
benefit.
ACID REDUCERS: There has been no single trial that has shown consistent, overall benefit of
H2 antagonists in stopping acute GI bleeding. Omeprazole, which is a proton pump inhibitor, has
been shown in some reports to be successful in stopping GI bleeding. Other reports have shown
no significant differences between placebo and omeprazole in terms of rebleeding, transfusion
requirements, morbidity, and the need for surgery. Tranexamic acid has also been used in
upper GI bleeding with inconsistent data. Furthermore, the side effects associated with the use of
tranexamic acid, has limited its use. Somatostatin and octreotide (its analogue) have no
proven benefit in active upper GI non-variceal bleeding. The benefits of sucralfate is also
questionable at the present time. Vasopressin has not shown any particular benefit in stopping
acute non-variceal upper GI bleeding.
198
ENDOSCOPIC THERAPY: There are 2 types of endoscopic therapy; the thermal method, such as
heater probe, electrocoagulation, laser therapy, AND the injection therapy. Studies have found that
thermal methods and injection therapy can reduce the need for emergency surgery by 60-80%,
and reduce recurrent bleeding when used in patients with active hemorrhage or visible vessels
seen at endoscopy. Laser therapy is not used much because of its high cost, lack of portability, and
associated technical problems. Monopolar electrocoagulation has been used for coagulation of
blood vessels, but there is the potential for sparking, deep tissue destruction and perforation. The
use of multipolar coagulation , however, results in more controlled tissue destruction. The degree of
tissue destruction is determined by the amount of pressure that is placed on the tissue by the
multipolar probe. The heater probe, like the multipolar coagulation system, controls the amount of
destruction by the amount of probe pressure applied to the tissue. Endoscopic injection therapy
can achieve hemostasis by using 98% alcohol, epinephrine, sclerosant and saline. Epinephrine
functions by constricting the blood vessels, and producing edema in the surrounding tissues.
Sclerosant and 98% alcohol cause inflammation in the blood vessels with shrinkage of the
surrounding tissues which leads to vessel thrombosis. Most GI specialists would recommend
multipolar electrocoagulation, heater probe or injection therapy because of their low cost, efficacy,
safety and ease of use. Most series show a perforation rate of less than 1%.
SURGERY AND ANGIOGRAPHY: Patients that fail endoscopic hemostasis will need surgery.
Patients that are not good candidates for surgery and fail endoscopic therapy can be treated
with angiographic embolization or intra-arterial vasopressin.
ALCOHOLISM
A. History: "CAGE"
1. Have you ever tried to Cut Down on your drinking?
2. Do you get Angry when people talk to you about your drinking?
3. Have you ever felt Guilty about drinking?
4. Do you ever have an "Eye Opener" in the morning?
B. Diseases Associated with Alcoholism
1. Gastrointestinal Irritation
a. Gastritis and Gastric Ulcers
b. Esophagitis
2. Pancreatitis
a. Acute Pancreatitis
b. Chronic pancreatitis with complications
c. Pancreatic carcinoma
3. Metabolic Abnormalities
a. Increased NADH/NAD ratio causes:
• increased conversion of acetaldehyde to beta-hydroxybutyrate (BHB)
• lactic acidosis - increased lactate synthesis from reduction of pyruvate
b. Folate Deficiency: Mean Corpuscular Volume (MCV) >105 fl
c. Iron Deficiency (may be due to gastrointestinal bleed)
d. Thiamin Deficiency - may be exacerbated by glucose therapy (ie. give thiamine first)
e. Note that chronic liver disease may also cause an increased MCV
f. Alcoholic Ketoacidosis
g. Decreased urinary excretion of uric acid (due to lactate inhibition)
h. ETOH Anemia: slightly increased MCV (~103 fl)
4. Hepatitis
a. Fatty Liver (enlarged)
b. Cirrhosis (Micronodular or Laennec’s)
5. Buccal Hyperplasia
6. Neurologic Disease
a. Encephalopathy: Wernicke type, Hepatic encephalopathy (usually cirrhotic)
b. Cerebellar Degeneration
c. Nutritional polyneuropathy (peripheral)
d. Seizures
7. Wernicke's Encephalopathy
a. Due to Thiamine (Vitamin B1) deficiency
b. Mental Confusion, nystagmus, ophthalmoplegia, gait ataxia
c. Medical Emergency
d. Requires immediate thiamin 50mg iv (or im) to prevent further brain damage
e. Thiamine should be given before other iv infusions (or Wernicke's may be exacerbated)
f. Often with Korsakoff's syndrome – gross disturbance in recent memory
8. Seizures
a. Alcoholic (during intake)
b. Withdrawal (24-60 hours after intake)
c. Delirium Tremens (usually 48-96 hours post intake)
d. Trauma (focus)
199
9. Myopathy [1]
a. Skeletal muscle weakness and atrophy
b. Dilated cardiomyopathy - women appear more susceptible than men [4]
c. Usually requires >10 years of heavy drinking
10. Other
a. Poor Dentition
b. Trauma
c. Internal Bleeding
d. Increased risk of serious infection - pneumonia, aspiration, tuberculosis [5]
e. Increased risk (>2 fold) of developing ARDS with chronic alcohol abuse vs. none [8]
f. Low level alcohol ingestion appears to reduce cholesterol and may be cardioprotective
g. Depression [10]
11. Fetal Alcohol Syndrome [2]
a. Exposure to EtOH during pregnancy
b. First trimester exposure probably: bland face, microcephaly, retardation
c. Later exposure probably: behavioral abnormalities
d. Timing and peak level of EtOH most important
e. Newborns with syndrome may have withdrawal symptoms, tremors, hypotonia
f. Neuroligc abnormalities, Septal defects, Renal hypoplasia also occur
g. Complete abstinance from EtOH recommended during pregnancy
C. Metabolism of Ethanol [7]
1. Ethanol is oxidized by alcohol dehydrogenase producing acetaldehyde
2. This is converted to acetate, and 2 NAD molecules are reduced to NADH
3. High NADH levels favor conversion of pyruvate to lactate leading to lactic acidosis
a. High lactic acid levels inhibit renal urate excretion leading to hyperuricemia
b. High NADH levels also oppose gluconeogenesis, Krebs cycle, and fatty acid oxidation
c. Inhibition of gluconeogenesis predisposes to hypoglycemia and seizures
4. Acetaldehyde
a. Inhibits repair of alkylated nucleoproteins
b. Promotes cell death by depleting cells of glutathione (an anti-oxidant)
c. Binds tubulin leading to inhibition of protein secretion and hepatocyte ballooning
d. Crosses placenta, impairs fetal fetal DNA methylation, leads to fetal alcohol syndrome
5. Induction of microsomal ethanol-oxidizing system (MEOS)
a. Long term ethanol consumption induces MEOS
b. This permits metabolic tolerance to alcohol
c. This oxidizing system can convert many substances to very toxic agents
d. Acetaminophen (TylenolВ®), isoniazid, cocaine are converted to toxic molecules
e. The MEOS also generates toxic oxygen species
f. Depletion of reduced glutathione and anti-oxidant vitamins contributes to toxicity
g. Short term alcohol consumption competes with other drugs for MEOS
D. ETOH Withdrawal
1. Minor symptoms occur 1-2 days after withdrawal, usually after stopping chronic EtOH use
2. Major symptoms: 1-2% of ETOH abusers. Cannot predict which ones
3. Pathophysiologic and Symptomatic Changes
a. Autonomic Nervous System Dysfunction: nausea and vomiting
b. Increased sympathetic outflow: Locus ceruleus (norepinephrine) activation
c. Neuronal Excitation: Seizures
d. Mental Clouding: hallucinations, delirium
4. Mnemonic for withdrawal: "THE DTs"
a. Tremulousness - 8-12 hours
b. Hallucinations - 24-48 hours
c. Epilepsy (Seizures) - 8-24 hours
d. Delirium
e. Tremors with Delirium - >48 hours after ETOH stopped
f. Note that ETOH level is not necessarily zero (0) during withdrawal
5. Delirium Tremens
a. Medical Emergency
b. ICU Monitoring
c. Adequate sedation
d. Control of cardiovascular system
E. Therapy for Withdrawal
1. Block sympathetic discharge
a. Clonidine 0.2mg po or patch as needed; excellent for hypertension, tachycardia
b. Benzodiazepines - will reduce sympathetic discharge
c. Гџ-Blockers - especially with esophageal varices. Proprandol qid or Atenolol qd
2. Prevent (Reduce) Withdrawal [ 3, 9]
a. Benzodiazepines are first line and may also prevent or reduce seizures
b. Lorazepam (AtivanВ® 1-2mg q2-4 hrs) IM or IV; avoid diazepam (ValiumВ®, long half life)
c. Oxazepam (SeraxВ® 15-30mg q4-6-), Chlordiazepoxide (LibriumВ® 25-50mg q8-), others
d. Originally recommended standing dose with taper over 3-7 days
200
e. Suggest prn dosing, fairly liberally, for inpatients, as effective, decreased side effects
f. Benzodiazepines have never been prevent to prevent DTs
3. Fluid resuscitation - most alcoholics are dehydrated
4. Nutritional Supplementation
a. Thiamine 100mg iv - give first; prior to any glucose to prevent acute Wernicke Syndrome
b. Glucose 1 Amp D50 - give after thiamine as glycogen stores are depleted
c. Folate 1mg iv qd
d. Multivitamins
F. Alcoholic Liver Disease
1. Pathophysiology
a. Metabolism via alcohol dehydrogenase (ADH) and MEOS (induced by EtOH)
b. Toxic effects of metabolites (eg. acetaldehyde), highly reactive with biomolecules
c. Acetaldehyde (CH3CHO) is made from ETOH oxidation (CH3CH2OH)
2. Pathology
a. Fatty Liver - can begin within days of heavy drinking
b. Alcohol induced cirrhosis - often occurs in absence of hepatitis intermediate
c. Cirrhosis results from reduction in collagen degradation
d. Fibrosis results from necrosis of liver cells with inflammation
3. Symptoms
a. Hepatomegaly, Jaundice
b. Ascites, Encephalopathy
4. Effects on liver
a. AST mildly increased; ALT may not be increased
b. Typically AST:ALT > 2 (ETOH induces AST)
c. Jaundice may occur in early moderate or severe disease
d. Fatty liver change leads to hepatomegaly and eventually liver failure
e. Micronodular cirrhosis and fatty liver may be seen on biopsy specimens
G. Abstinence
1. Difficult for most persons
2. Family history of alcoholism predicts recurrent alcoholism
3. Social reinforcement of abstinence, usually with Alcoholics Anonymous, is critical
4. Disulfiram (AntabuseВ®) - causes a severe reaction when taken with alcohol
5. Naltrexone (ReViaВ®)
a. An opioid receptor antagonist, recently FDA approved for treating alcohol dependence
b. Reduces craving in abstinent patients
c. Blocks reinforcing effects of alcohol in patients who do drink
d. Dose is 50mg po qd and acts for ~24 hours; duration of treatment usually 12 weeks
e. Adverse effects - mild nausea, mild sedation, may cause mild hepatitis
f. Drug interactions - with thioridazine can increase sedation; avoid hepatotoxic drugs
g. Agent should not be started until patient is alcohol (and opiate) free
h. Long term trials are lacking but may prevent relapses
6. Desipramine [10]
a. High rates of depression in alcoholics suggest use of anti-depressants
b. In alcoholics without depression, desipramine did not reduce alcohol abuse
c. In alcoholics with depression, desipramine increased abstinence from alcohol
ALCOHOLIC WITHDRAWALThiamine 100 mg IV or IM prior to glucose then 50 mg qid x 5-10 days.
Magnesium sulfate 50% soln 2 ml IM q12h x1 day then once daily x 3 days.
Lorazepam 1-4 mg po or IV q4h OR
Librium 25-100 mg po or IV q4-6h the first day then reduce by 100 mg each following day.
Tenormin 50-100 mg daily for tachycardia, increased BP and tremors.
Folic acid 1 mg po daily.
Hydrate.
For seizures use valium, dilantin.
ALCOHOLSEIZURES: Withdrawal from acute alcohol intoxication may cause seizures. Most occur 12-48
hrs after a drinking binge, but may occur at any time. Dilantin 1 gram IV over 30 minutes with
continuous monitoring ECG and BP. Renal and liver function studies should be obtained. CT of
head is considered. Lumbar puncture should be seriously considered in patients with sepsis or
persistent fever in whom a readily evident cause for the temperature elevation cannot be found.
201
DELIRIUM TREMENS: This is the most serious complication of alcohol withdrawal. Usually starts a
day or so after drinking is stopped and may last for 1-2 days. Characterized by agitated,
confusional state, tremulousness and autonomic hyperactivity. Need hydration and sedation.
WERNICKE'S ENCEPHALOPAHTY AND KORSAKOFF'S PSYCHOSIS: Wernicke’s encephalopathy
usually manifests as a triad of encephalopathy, ophthalmoplegia and ataxia due to thiamine
deficiency. Neuropathologic changes are seen in the tissues surrounding the 3rd and 4th ventricles,
most prominently in the mamillary bodies and may be seen on MRI or CT. Korsakoff’s psychosis is a
disabling memory disorder related to Wernicke’s encephalopathy and may result from thiamine
deficiency. Patients should be given 100 mg of thiamine hydrochloride (Betalin S) IV daily for 5
days.
CEREBELLAR DEGENERATION: is seen in long term alcoholics. Clinical manifestations include
gait ataxia and dysarthria. Treatment is supportive. Abstention from alcohol and improvement in
nutrition have reduced the rate of progression and in some cases even reversed symptoms.
MARCHIAFAVA-BIGNAMI DISEASE: is rare and may be acute, subacute or chronic in nature.
Clinically it results in dementia, dysarthria, spasticity and gait apraxia and may progress to coma.
Neuropathologic cause is necrosis of the corpus callosum and subadjacent cortical white matter.
MRI may visualize.
CENTRAL PONTINE MYELINOLYSIS: There may be an aberrant mental state, quadriparesis,
paraparesis, and lower cranial nerve dysfunction. The syndrome occurs following the rapid
reversal of chronic and subacute hyponatremic states, and may result from conditions other than
alcoholics such as chronic liver disease, and burns. In severe cases it may result in a locked in
syndrome (complete paralysis except for the eyes). Neuroanatomically there is demyelination of
the base of the pons. Treatment is non-specific. Slow correction of sodium deficiency by means
of restriction of water consumption or closely monitored administration of small amounts of
hypertonic saline solution should be carried out.
FETAL ALCOHOL SYNDROME: Features include cranial-facial dysmorphisms, systemic and
mental retardation and developmental anomalies of several organ systems. Occurs in about .1.3% of live births in the USA and accounts for about 5% of congenital abnormalities. Partial
expressions of full blown clinical syndrome have been described. PERIPHERAL NERVOUS
SYSTEM EFFECTS: They may correlate with the extent and length of alcohol use, and are most
often those of a symmetric, distal polyneuropathy involving sensory, motor, and autonomic
nerves. Paresthesia, dysesthesia, numbness and ataxia are common as are symptomatic
mononeuropathies resulting from local trauma or compression of larger peripheral nerves.
MYOPATHIES: affect about 50% of chronic alcohol abusers. May occur shortly after a drinking
binge, manifested clinically by pain and tenderness of an affected muscle, usually a proximal
skeletal muscle. Lab reveals myoglobulinuria and an elevation of serum CPK-MM. EMG may
show myopathy and muscle biopsies often demonstrate involvement of type I fibers. Complications
may include cardiac dysrhythmias, renal failure and electrolyte abnormalities. A chronic state of
alcoholic myopathy, evidenced by muscle cramping and atrophic changes particularly of the hip and
shoulder girdles is even more common. Involvement of type II fibers is often seen on muscle
biopsy in patients with chronic myopathy.
VIOLENT PATIENTSThe violent patient is usually calmed by using either a benzodiazepine or haloperidol. If the patient
is not psychotic, lorazepam is usually used. Patients that have psychotic episodes such as
schizophrenia or bipolar affective disorders, haloperidol or droperidol are the best drugs. In some
patients, both of these drugs may be used. This combination is usually composed of 5 mg of
haloperidol and 2 mg of lorazepam given IM every 2-3 hours until sedation. This combination
should not be given IV. Lorazepam is preferred over diazepam because it has a faster onset of
action and shorter duration of action. Do not use oral lorazepam. IV lorazepam should be used
judiciously because of vein irritation. Lorazepam given sublingually has been effective and works
just as fast as IM injection. If both lorazepam and haloperidol are being given, the two can be
mixed in the same syringe and given IM. Lorazepam is given at 1-2 mg every 1-2 hours, either
sublingually or IM until the patient is sedated or up to a maximum of 4 mg. For patients with renal,
or COPD or the elderly, downward adjustments will have to be made. In these patients you should
start with .5 mg. Haloperidol is given in small intramuscular boluses to treat schizophrenia and
other psychoses. Extrapyramidal complications are side effects. IV haloperidol is not routine even
though the literature supports its safety and efficacy. It can be used if a violent patient needs
alleviation of agitation immediately. Sedation usually reaches its peak at about 20 minutes after
an IM dose and 5-10 minutes after IV. Start with 5-10 mg of Haloperidol as a slow IV push, which
may be repeated every 10 minutes until calm is established. Elderly patients are only given 1-2 mg
IV every 10 minutes for 3 doses, and then the dose may be escalated to 5 mg every 10 minutes if it
202
is tolerated. Patients that are severely agitated may need up to 50-75 mg IV every 30-60 minutes.
Use caution in patients that are ethanol intoxicated or other drug intoxications. Haloperidol may also
lower the seizure threshold. Haloperidol usually doesn't impact on the patient's vital signs or
respiratory function when given IV. Extrapyramidal reactions are rare and tend to be milder with IV
Haloperidol use, and usually do not occur during the first 24 hours. Diphenhydramine is used to
reverse the symptoms. A very rare side effect is neuroleptic malignant syndrome. Droperidol,
may have fewer side effects than haloperidol. The dosage is 2.5 to 5.0 mg via IV push.
RANSON'S CRITERIA: For Determining Prognosis of Acute Pancreatitis
UPON ADMISSION:
1.Age > 55
2.Blood Glucose > 200 mg/dl
3.WBC count > 16,000 / cu mm
4.Serum LDH > 700 IU%
5.SGOT > 250 SF units % (56 units/dl)
AFTER 48 HOURS:
1.HCT decrease > 10%
2.Serum Ca2+ < 8mg % (mg/dl)
3.Base Deficit > 4 mEq/l
4.BUN increase > 5mg % (mg/dl)
5.est. fluid retention > 6L
6.Arterial 02 tension < 60 mm/dg
< 3 signs - better prognosis, < 1% mortality.
> 3 signs - serious acute pancreatitis - may be 25% mortality.
Modified Child's Index for Grading Severity of Liver Dz
Clinical or Lab
Feature
123
Encephalopathy
None
Mild-moder Severe
Ascites
None
Slight Moderate
Bilirubin
< 2mg/dl 2-3 mg/dl > 3 mg/dl
Albumin
> 35 g/l 28-34 g/l < 28 g/l
Prothrombin time
<4 sec 4*6 sec > 6 sec
(prolonged)
5-6 points: good operative risks
7-9 points: moderate operative risks
10-15 points: poor operative risks
ACUTE BLINDNESS
Immediate Questions:
A. What is extent of visual loss?
Monocular? Visual Field, hemianopsia (one-half visual
field), homonymous (same half), bitemporal (pituitary
tumor) or binasal (rare)?
B. Prior symptoms? Eye pain?
Differential Diagnosis of Acute
Monocular Blindness:
A. Retinal detachment.
Often preceded by floaters or flashing lights; painless;
detachment visible on funduscopic exam. Risks are
extreme myopia and trauma. Emergency ophthalmologic
consult is needed for urgent reattachment.
203
B. Central retinal vein occlusion.
No prodrome; painless. Funduscopic shows edema,
hemorrhages and dilated veins. Associated with
hypertension. Requires emergent ophthalmologic consult.
C. Central retinal artery occlusion.
Acute onset; painless; may be history other thromboembolic disease, atrial fibrillation or carotid
disease. Funduscopic reveals pale disc and cherry red spot in the macula. Requires emergent
ophthalmologic evaluation.
D. Acute (narrow angle) glaucoma.
E. Ischemic optic neuritis: Temporal arteritis.
Elderly white woman; may be history of headache;
elevated ESR. Abrupt onset blindness. Begin empiric high
dose steroids, if diagnosis is suspected.
F. Trauma.
G. Optic Neuritis.
Decreasing vision over several days; associated with
multiple sclerosis.
H. Infiltrate or compression due to tumor or aneurysm.
Data to Document Eye Findings:
A. Inspection
B. Extraocular muscle movement
C. Pupil response direct and consensual
D. Visual acuity and fields
E. Funduscopic
F. Obtain emergent ophthalmologic exam
ACUTE DYSTONIC REACTION
Immediate Questions:
A. What are the vital signs?
B. What medications is the patient receiving?
C. Is IV Benadryl (diphenhydramine) available on the
floor?
Diagnosis and Management:
A. Dystonias are idiosyncratic drug reactions that involve acute
involuntary muscle movements and spasms. Although any muscle
group in the body can be involved, the commonest manifestations
are torticollis, facial grimacing, and opisthotonos.
B. Because of their antidopaminergic properties, anti-psychotic
agents often are associated with a variety of motor disorders. The
use of drugs of this class, Compazine for example, can cause an
acute dystonic reaction.
C. Treatment is diphenhydramine 50 mg IM or IV, or
benztropine 2 mg IM or IV; improvement generally occurs within
seconds or within 15 to 30 minutes. These doses can be
repeated in 30 minutes. Even if the agent is discontinued, oral
treatment with either agent may be helpful for the next 3 to 21
days, since symptoms can recur.
204
SEIZURES
A. Definitions and Background
1. Seizures are abnormal spontaneous firing of nerve tissue
2. May affect part (focal) or all (general) of the brain
3. Over 2 million patients with seizure disorder (epilepsy) in USA
4. Medications control ~80% of these patients very well
5. Thus, over 400,000 patients with intractable or poorly controlled seizures
B. Causes in Infants
1. Trauma
2. Infection / Fever
3. Tumor
4. Degenerative
5. Aminoaciduria
6. Metabolic
a. Hypoglycemia
b. Hyponatremia
c. Hypocalcemia
7. Developmental
a. Arteriovenous Malformation (AVM)
b. Hyperactive focus - usually a scar
8. Idiopathic
C. Causes in Children
1. Hemorrhage
2. Toxins - drugs
3. Renal Failure
4. Cerebrovascular Abnormalities
5. Metabolic
6. Infection / Abscess
7. Fever
D. Causes in Adults
1. Idiopathic
2. Post-Traumatic
3. Post- or peri-stroke
4. Tumor - ~10% of new onset seizures
5. Alcohol - withdrawal seizures more common than during use
6. Eclampsia
7. Vasculitis
8. Medial Temporal Sclerosis
9. Metabolic - As above
10. Abscess / Encephalitis / Meningitis
11. Medications
a. Anti-psychotics - lower seizure threshhold
b. Lidocaine
c. Гџ-Lactams - especially imipenem, high dose penicillin
d. Meperidine (Demerol(r)) - metabolites are epileptogenic
12. Multiple Sclerosis - very rare cause
E. Differential Diagnosis
1. Syncope, Presyncope
2. Transient ischemic attack
3. Transient global amnesia
4. Cardiac Arrhythmia
5. Migraine (atypical)
6. Vertigo
7. Tremor
8. Breath-Holding / Functional
F. Types of Seizures and Therapy [ 1, 6]
1. Level of Consciousness
a. Simple: no loss of consciousness
b. Complex: impairment or alteration of consciousness
2. Focus of Seizure activity
a. Partial: begins at specific focus (may be idiopathic or structural or due to injury)
b. Generalized: appear to begin diffusely in large part of the brain, loss of consciousness
3. Tonic Clonic: grand mal. Entire body is involved
4. Absence Seizures (Petit mal)
a. 1-2 minute staring episodes
b. Infrequent patient with very short (1-10 second) "spells" who have absence seziures
5. Complex Partial: lip smacking, fumbling, staring, guttural vocalization, confusion
6. Myoclonic Seizures: associated with anoxia, ischemia, drug overdose, idiopathic
205
7. Treating Symptomatic Partial Epilepsy [7]
a. Simple partial seizures: cbz > pht=vpa
b. Complex partial seizures: cbz > pht and/or gaba > vpa > pb = prim
c. Evolution to Generalized (tonic-clonic) seizures: cbz > pht > pb > vpa
8. Treating Idiopathic Generalized Epilepsy (mainly children)
a. Absence seizures: esm = vpa > clonazepate
b. Myoclonic seizures: vpa > clonazepate
c. Generalized tonic-clonic seizures: vpa > cbz > pht > pb = prim
9. Surgery for Seizures
G. International Classification of Epileptic Seizures
1. Partial Seizures
a. Simple Partial Seizures (no impaired consciousness)
b. Complex Partial Seizures (impaired consciousness)
c. Partial Seizures evolving into secondary generalized seizures
2. Generalized Seizures
a. Absence Seizures
b. Myoclonic Seizures
c. Clonic Seizures
d. Tonic Seizures
e. Tonic-Clonic Seizures
f. Atonic Seizures
3. Unclassified Seizures
H. Specific Anti-Convulsant Agents [7]
1. Acute Therapy for Generalized Seizures
a. Dilantin 1gm load iv (hypotension common side effect)
b. Phenobarbital 30-60mg iv repeated every 5-10 minutes
c. Benzodiazepine
• Diazepam (Valium(r)) more effective than lorazepam (Ativan(r))
• Especially useful for alcoholic and alcohol withdrawal seizures
d. Pentobarbital: status epilepticus; induce coma
2. Benzodiazepines
a. Diazepam (Valium(r)): grand mal (tonic-clonic), alcoholic related seizures; 5mg iv/im
b. Lorazepam (Ativan(r)): shorter t1/2 than diazepam; easier to use for withdrawal
c. Clonazepam (Klonopin(r)): myoclonic seizures, also useful for anxiety
3. Phenytoin (pht; Dilantin(r))
a. Use: Partial Epilepsy, Generalized Tonic-Clonic seizures
b. Side Effects: cognitive changes, gum hyperplasia, hirsutism, nystagmus
c. Hypotension often occurs with intravenous loading (usually 50mg per minute to 1gm)
d. Overdose: ataxia, nystagmus (especially vertical), induction of seizures, lethargy
e. Note that phenytoin overdose usually occurs when patients on drug are given iv loading
4. Carbamazepine (cbz; Tegretol(r))
a. Use: Complex-partial seizures, Generalized Seizures, Second Line Myoclonic Seizures
b. Side Effects: Drowsiness, diplopia, GI upset, low WBC (5-10%), Rash, allergy
c. Severe Side Effects: Agranulocytosis, platelet decrease, aplastic anemia (1/20,000)
d. WBC and Platelets should be monitored each week initially, then each month
e. Drug Interactions (hepatic metabolism): warfarin, estrogens, theophylline, alcohol
5. Valproic Acid / Valproate (vpa; Depakene(r), Depakote(r)):
a. Use: All seizure types, especially generalized epilepsy
b. Side Effects: gastrointestinal upset, weight and apetite increase, fatigue, tremor, hair loss (510%;
reversible)
c. Severe: hepatotoxic reactions (usually on other drugs). Monitor liver function tests.
d. Fatal Hemorrhagic Pancreatitis.
6. Phenobarbital (pb) or Primidone (prim; Mysoline(r))
a. Second line therapy in adults with resistant seizures
b. Side Effects: Sleepiness, depression, personality changes
c. Encephalopathy and hyperammonemia can also occur in adults
7. Ethosuximide: petit mal only (without other seizure types)
8. Phenyl Dicarbamates
a. Meprobamate (Equanil(r))
b. Felbamate (Felbatol(r)): Oral only; approved for partial seizures В± generalization
c. May block sodium channels, enhance g-aminobutyric acid (GABA)
d. Less behavior and other side effects than earlier agents
e. Side Effects: mild to moderate, HA, insomnia, fatigue, A/N/V, aplastic anemia, hepatitis
f. Aplastic anemia risk high enough with Felbamate to warrant close monitoring [5]
9. Gabapentin (GABA, Neurontin(r))
a. Efficacy for partial and secondary generalized seizures, as add on agent
b. Decrease incidence in secondary generalized seizures
c. Enhances activity of GABA neurotransmission, inhibits sodium channels
d. Drug interactions: does not alter plasma concentrations of other agents
206
e. Side Effects: mild in general; somnolence, dizziness, ataxia, fatigue, nystagmus, nausea
10. Lamotrigine (lamo, Lamictal(r))
a. Approved in USA for use in partial seizures in adults
b. Blocks voltage dependent sodium channels
c. Metabolism by glucuronidation, does not induce P450 enzymes, few drug interactions
d. Valproate inhibits metabolism of lamotrigine, and lamotrigine decrease valproate levels
e. Generally very well tolerated when added to other drugs or used alone
f. Most patients begin at 50mg po qd x 2 weeks, increase slowly to 300-500mg/day
g. Effective in children with the Lennox-Gastaut Syndrome
11. Other Agents (not yet available in USA) [9]
a. Oxcarbazepine: analog of carbamazepine, pro-drug requires liver metabolism
b. Clobazam: benzodiazepine with reduced cognitive effects, used in refractory seizures
c. Tiagabine: blocks GABA reuptake, refractory epilepsy
d. Topiramate: blocks sodium channels, attenuates kainite responses, enhances GABA effect
e. Vigabatrin: inhibits GABA breakdown, effective in resistant and new epilepsy
f. Zonisamide: blocks sodium and calcium channels, effective in partial seizures
12. Experimental Agents
a. Losigamone
b. Remacemide
c. Levetiracetam
d. Fosphenytoin
13. All of the studied agents cause birth defects with
1% Risk of spina bifida (see below)
14. Choice of agent
a. Use of single agent recommended whenever possible (~65% of patients)
b. Above section (E) outlines preferred agents
c. Surgical evaluation may be considered if drug combinations fail
15. Discontinuing Agents
a. >60% of persons who remain free of seizures can have medications discontinued
b. Most physicians wait 2-5 yearsof seizure-free time before slow reductions in dose
I. Summary Of Uses Of Anti-Convulsive Agents
Drug
Generalized
Absence
Myoclonic
Phenobarbital
++
+
Phenytoin(Dilantin(r))
++
Carbamazepine(Tegretol(r)) ++
Valproate (Depakote(r))
+++
++
++
Ethosuximide
++
Clonazepam(Klonopin(r))
+
+
+
Diazepam(Valium(r))
+
+
Felbamate(Felbatol(r))
++
Clonazepate
+
++
J. Drug Treatment During Pregnancy [7]
1. Seizures are generally well controlled during pregnancy
2. Phenytoin levels may fall during pregnancy
3. Small increase in serious fetal malformations (~3% vs. 2% for average pregnancy)
4. Women on valproate or carbamazepine should take folic acid 5mg po qd during pregnancy
5. Slight increase in risk of Vitamin K depletion on cbz, pht, pb, and prim
6. Recommend 20mg vitamin K during last few weeks of pregnancy if on these medications
K. Temporal Lobe Epilepsy
1. Arise in:
a. Medial temporal lobe
b. Amygdaloid Nucleus
c. Hippocampus
2. Propagation to amygdala
3. Symptoms
a. Feelings of depersonalization
b. Emotionality
c. Automatic Behavior
d. Loss of memory during bizarre behavior
4. Cannot distinguish from partial complex seizures arising from frontal lobes without EEG
5. Treatment
a. Carbamazepine
b. Dilantin
c. Valproate
d. Phenobarbital
207
Status Epilepticus
Definition: According to the International Classification of Seizures, it is ''a condition characterized by
an epileptic seizure that is so frequent or so prolonged as to create a fixed and lasting condition".
From a practical standpoint, continuous, generalized, tonic-clonic seizure activity lasting 30 minutes
or longer, i.e., grand mal status epilepticus, is most worrisome and represents a life threatening
emergency.
Diagnostic evaluation:
Immediately send off a CBC, a serum chemistry
profile, and drug screen.
Assess for
possible drug intoxication or drug
withdrawal as effectively as possible. Keep in
mind that
anticonvulsant drug withdrawal is a
common cause of status epilepticus.
Obtain an arterial
blood gas if there is evidence
of respiratory compromise.
Obtain a brain scan (CT or MRI), with
and
without contrast as quickly as feasible to assess
for a possible mass lesion.
Evaluate
for lumbar puncture, especially if there
is clinical evidence of an infectious process and
there is
no contraindication by brain scan and
bleeding studies.
An EEG, on an emergency basis, may
be
indicated if there is an atypical presentation or a
suboptimal response to medical
intervention.
Management: It is important to establish that there is no respiratory compromise and no evidence of
cardiovascular collapse. Preparation for possible intubation and respiratory support should be made.
Correction for metabolic disturbance, if present, is clearly indicated. Low serum Na+, glucose, Ca++,
or Mg++ can result in recurrent seizure activity. Drug or alcohol withdrawal, or certain drug
intoxication, can be precipitating factors. It is important to recognize that withdrawal from
phenobarbital generally requires resumption of phenobarbital with a loading dose which will
necessitate intubation with respiratory support.
An intravenous line is mandatory. Initial, i.e., short-term, control of generalized seizure activity can
often be obtained with either intravenous lorazepam, at a dose of 0.1 mg/kg, or diazepam at 0.2
mg/kg. Either agent is infused over two minutes. It is important to recognize that these agents can
promote respiratory depression at relatively small doses in certain individuals. If either of these agents
is used, it is with the understanding that longer term, i.e., maintenance, therapy must also be initiated
unless there is a recognized metabolic derangement that can be rapidly corrected.
Fosphenytoin is now available as the replacement for parenteral phenytoin. Each fosphenytoin vial
contains 75 mg/ml which is equivalent to 50 mg/ml of phenytoin ( 1.5 equivalents). Its primary
advantages over phenytoin include: significantly reduced risk of cardiovascular depression, markedly
improved local infusion tolerance, and the ability to give it intramuscularly. Its dosing is expressed as
phenytoin equivalents (PE). The loading dose in status epilepticus is 15 to 20 mg PE/kg at a
maximum intravenous infusion rate of 150 PE/min. (For example the order for a 67 kg man would be:
"Fosphenytoin 1000mg PE to be infused IV over 10 minutes". In such a circumstance, intravenous
administration is preferred to intramuscular because the intravenous route allows less time to achieve
a therapeutic plasma concentration. Fosphenytoin is converted to phenytoin after parenteral
administration. It is recommended that phenytoin blood levels not be measured until the conversion of
fosphenytoin to phenytoin is complete. This occurs approximately two hours after completion of the
intravenous infusion.
If the patient continues to have seizure activity despite adequate intravenous loading with
fosphenytoin, then phenobarbital loading is indicated. Phenobarbital is given at an intravenous dose
of approximately 20 mg/kg at an infusion rate of no more than 1.5 mg/kg/min. This translates into
approximately 100 mg/min in adults. If this is unsuccessful, then intravenous pentothal is given at a
loading dose of 3 to 4 mg/kg over two minutes followed by a continuous infusion at a rate of 0.2
mg/kg/min. The dose is then adjusted upward, every 3 to 5 minutes by 0.1 mg/kg/min, until the EEG
becomes isoelectric.
LUMBAR PUNCTURE TESTS
1.Cell Count
2.Gram Stain, AFB, KOH, Bacteria and Fungal
208
Cultures (CIE)
3.Glucose, Protein, LDH, VDRL
4.Cell Count, RBC, WBC
5.Viral Culture - CIE
Indications:
1.CNS infection
2.Determine CNS Bleeding
Contraindications:
1.Infection at site
2.Any Bleeding Disorder
3.Mass Lesion
4.Papilledema
CSF ANALYSIS
PRESSURE: 75-150mmH2O in lat decub pos
PROTIEN: 15-45 mg/dl
LD: 1/10 of serum
GLUCOSE: 45-85 (60-70% of blood)
COLOR: if yellow (xanthochromic) may
indicate subarach bleed(previus
bleed) or dark yellow indicating
subarach block.
-abnml color seen w/prot >100
CELLS:
total cell CT: 0-5/cu. mm
2-10=borderline pleocytosis
25-50=elevated pleocytosis
>50=severe pleocytosis
(>500 usually purulent meningitis w/
predominant granulocytes)
(300-500 w/predom lymph or monos
-viral, syphilis, TB, lyme, partially
tx'd bact inf, MS in 50%, sarcoid)
(>40% MONOs c/w subarachnoid bleed)
Stroke Risk Factors and Prevention Therapy
Stroke Prevention Therapy for Patients with Atrial Fibrillation
Age < 65 - Risk factors Present: Warfarin (maintain INR at 2-3)
Age < 65 - Risk factors Absent: Aspirin
Age 65 to 75 - Risk factors Present: Warfarin (maintain INR at 2-3)
Age 65 to 75 - Risk factors Absent: Warfarin or aspirin
Age > 75 - Risk factors Present or Absent: Warfarin (maintain INR at 2-3)
(INR = international normalized ratio)
Risk Factors for Stroke
hypertension
diabetes mellitus
CHF
coronary artery disease
mitral stenosis
prosthetic heart valves
209
left atrial enlargement
global left ventricular dysfunction
thyrotoxicosis
history of TIA or stroke
COMA (Common Causes)INFECTION: Meningitis, subdural empyema, encephalitis, and brain abscess.
TUMORS: Primary tumors with gliomas being the most common. Metastatic disease most
commonly from breasts, lungs, GI, and kidney.
VASCULAR DISEASE: Subdural hematoma, epidural hematoma, subarachnoid hemorrhage
and intracerebral hemorrhage.
DRUGS AND TOXINS: Heavy metals, alcohol, salicylates, barbiturates, opiates, tranquilizers,
sedatives.
FLUID, ELECTROLYTE AND ACID BASE DISORDERS: All are capable of causing coma if
severe.
HYPOXIA: Anemia, hypo and hypertension, respiratory failure, decreased cardiac output.
ENDOCRINE DISEASE: Hypo and hyperglycemia. Hypo and hyperthyroidism, hypo and
hyperadrenalism, hypo and hyperparathyroidism, hypo and hyperpituitarism.
OTHER: Uremia, heat stroke and hypothermia, Vitamin deficiencies as thiamine which can cause
Wernicke's encephalopathy, seizures, concussion, status epilepticus.
COMA CAUSESINFECTION: Sepsis, encephalitis, meningitis, abscess, granulomatous, viral encephalitis.
TRAUMA: concussion, contusion, laceration, subdural and epidural hematoma.
NEOPLASTIC: metastatic and primary.
TOXIC: antidepressants, ethanol, tranquilizers, barbiturates, narcotics, anticonvulsants,
anticholinergics, cimetidine, bromides, cyanide, carbon monoxide, cyanide, heavy metals,
digoxin, lithium, methemoglobinemia, phenothiazine, organophosphates, salicylates, radiation.
SYSTEMIC: renal failure, hypoventilation, hepatic failure.
HYPOPERFUSION AND HYPOXEMIA: respiratory failure, status epilepticus, post cardiac arrest,
severe anemia, aortic stenosis, altitude edema, arrhythmias, DIC, carotid sinus
hypersensitivity, fat and post bypass emboli, pulmonary emboli, hyperventilation,
hypertensive encephalopathy, hyperviscosity, malaria, hypovolemia, malaria, syncope, SBE,
vasculitis and autoimmune disease.
METABOLIC: increased or decreased glucose, calcium and sodium, hyperosmolar state, severe
acidosis and alkalosis, Addison's or Cushing’s syndrome, hyper and hypothermia, carcinomatosis,
hypopituitarism, increased and decreased magnesium, decreased phosphorous, superior vena
cava syndrome, acute porphyria, toxic shock syndrome, increased and decreased thyroid,
thiamine, niacin, B6 and B12 deficiency.
ANTIBIOTICS & Infectious Disease
1. Aerobic GNR:
1)Aminoglycosides
2)Cephalosporins 2-3rd gen
3)TMP/SMX
2. Anaerobes:
1)PCN, Amp,tetra,cephI-III,
Clinda.
2)Chloramphenicol
3) Metronidazole
(only Chlor/Flagyl cross BBB)
3. GPC/GPR:
1)PCN
2)PCN Resistant AbTx/
Extended Spectrum:
a)IV: ox,naf,meth
b)PO: clox, diclox
3)Meth Resistant Organisms:
(S.Aureus, St.Epi, S.Fecalis)
a)S.Epi: vanco +/- gent
b)MRSA: Vanco
4)ENTEROCOCCUS:
210
a)non SBE: AMP
b)SBE: PCN/VANCO + AMINO
4. H FLU: (Assume Amp Resistance)
1)Chloramphenicol
2)TMP/SMX
3)3rd Gen Cepahalosporin
4)Amox + Clauvulanic Acid
5)Erythro + sulfa
5. Neisseria:
1) PCN, Chlor, Erythro, CephIII.
6. Pseudomonas:
1)Tobra, Amakacin, Gent
2)Ceftazidime
3)Imipenem-Cilastatin
4)Cipro
5)Cefipine
. Cellulitis
(usually due to grpA strep)
1. PCN VK 0.5-1gm PO QID
2. Erythro 500 mg po qid
. Diabetic Cellulitis
1. Cefoxiten 1-2g IV q8
(good anaerobic coverage)
. Meningitis:
(most commonly S.Pneum or N.Mening)
1. For S. Pneumonia
PCN 2million U IV q2 x 10-14d
2. For N. Meningitis: same as above
3. for H. Flu:
Cefuroxime 3g IV q8
TMP/SMX
4. Gram - Rods= 3rd Gen Ceph w/
. UTI
1. Amp 500mg po qid
2. TMP/SMX DS one PO BID
3. cephalixin 500mg po
qid
C-DIF COLITIS:
May suggest lactobaccili by
yogurt ingestion
caused partic by macrolides
but any ABX
TX: Flagyl, Vanco po, Bacitracin po
HIV & AIDS Stats, etc
RISK: Needlestick 0.3%
infected male to female < 50%
STAGING: majority pt ASx
LABS
Absolute CD4(helper) #
(nml=350-1200)
PERSISTANCE STAGE: low viral product
w/ seroconversion CD4 to 200 range
plateau for to several years
CD4 > 500 low risk for opp infection
CD4 <50: High risk for opp inf
211
(follow trend since labs vary by
20-30%)
HIV Viral Burden
B2 microglobulin level
-sm mw prot synth & secreted by cell
involved w/ HLA I maj histocomp Ag's
(by interferon and infections)
-HIV+ & +B2MG = inc risk of AIDS
(>5mg/dL)
HIV p24 level: Eliza for p24 Ag
(not fed licensed)
In late Dz pt may make more P24Ag
HIV Ag & P24 may be detected prior
to seroconversion
Plasma HIV co-culture
LABS: ELIZA & Western Blot
ELIZA: Tests for HIV Ab:
(tests against HIV Ag)
False +'s occur partic if
+ANA,RF,cryoglobs,or PREGNANT
False -'s in early HIV <12mo
due to lack of Ab production
High + pred value in high
incidence population
inexpensive & widely available
(high index of suspicion makes +result
not repeated due to impr ELIZA)
(if low seroprevalence group :+ is
likely false lab error)
WB: IMMUNOBLOT: viral Ag
4% false pos (usually screened out by
eliza)
High + pred value in high incidence
population
More Expensive Than ELIZA
variable reproducibility
indeterminate either:
-early disease or cross Rx AB
re check at 3months
PT EVAL:
? VD hepatitis, toxoplasma,
? where do they live, ?pets
1st tests:
PPD, toxo serology, Hep screen, VDRL
CD4 T4 helper cell count
if >500 check q6months
if 200-500 begin AZT & check q6mo
if close to 200 check q3months
if <200 begin PCP prophylaxis &
re-check q3-6 months
(infection risk @ CD4 < 200)
TX: TX for CD4 < 500
AZT: well tol if used early
DATA: improves survival
decreases opp infections
increases CD4 transiently
Decreases progression to AIDS
Dose:500mg qd in 100mg po q4
212
TOXICITY: incr MCV in everyone
anemia, leukopenia
DDI: didanosine VIDEX
-raises CD4 count
-survival studies not in yet
-thus only for those who cant
take AZT
TOXICITY:-pancreatitis (9%) can be
fatal
-priph neuropathy (34%)
DOSE: must chew tabs
>75kg 300bid
<50kg 125bid
50-74kg 200bid
PCP DZ TX:
-Bactrim: 15-20mg/kg/d x 3wks
-pentamidine: 3-4mg/kg/d x 3wks
For mild to mod DZ:
-Dapsone/TMP: 100mg qd & 20/mg/kg/d
Experimental tx: clinda / primaquine
trimetrexate/leucovorin
STEROIDS: for po2<75 on RA
PCP PROPHYLAXIS:(for all w/CD4<200
or if pt has had PCP)
BACTRIM: 1 ds po qd
PENTAMIDINE AERO: 300mg q month
CRYPTOCOCCAL MENINGITIS:
Ampho B:in initial episode
FLUCONOZOLE: for chronic suppression
(200mg qd)
TB: if HIV+ - 10% chance of
reactivation each year
-if PPD+ >5mm INH prophylaxis
TOXOPLASMA: 95% is recrudescence
80% relapse if not tx
Typically: focal brain lesion
(50-70% are toxo - others are:
lymphoma, PML, herpes, TB, Kaposi’s
-lesion typically by basal ganglia
.5-11.6cm vs 30cm for lymphoma)
TOXO TX:
- Sulfadiazine/PYM/folinic Acid
- Clinda/PYM
- Azithromycin/clarithromycin/????
HIV PNEUMONIA
MALIGNANCY: lymphoma
CVD
AdenoCA
SARCOID
PROTAZOA: PCP
VIRAL: Influenza
RSV,Adenovirus
EBV, Hsv, VSV,
FUNGAL:Crypto
Histo
Blasto
Aspergillis
BACTERIA:
Mycoplasma
Legionella
213
HFlu, Pneomcoccus,
TWAR & other Chlamydia
Psitticosis
MAI/TB
PARASITES: strongaloidies
DX: cults, cold agglut, legionella,
CMV/viral studies, CD4
(majority of PCP w/CD4<200)
Broch Specimen: for silver stain
AFB, Viral, Fungal
TX For PCP:
sulfa better than pentamidine since faster acting than pentamidine & less expensive.
--------------------------------------DIARRHEA
bacteria: salmonella, shigella, camplyo,
yersinia, C-dif, listeria, MTB/MAI
protozoa: entamebae histolytica
cryptosporidium, microsporidiosis
isospora(tx w/bactrim), giardia,
strongoloides
virus: CMV, Adenovirus
malignancy: lymphoma (sm bowel), KS
drugs: ddi, megase,
fungal: candida, histo(if from midwest)
--------------------------------------Antiretroviral (AIDS) Agents, Daily Dosage and Major Toxicities Nucleoside analogs
Zidovudine, AZT (Retrovir)
500-600 mg po (typically 200 mg po tid)
Children 3 mo- 1 2 yr:180 mg/M2 q6h, not
to exceed 200 mg q6h
Bone marrow suppression, Severe anemia,
Granulocytopenia, Symptomatic myopathy,
myositis (with prolonged use)
Didanosine, ddl, (Videx)
Two 100 mg tablets bid (> =60 kg), One
100 mg tab Plus one 25 mg tab bid (< 60
kg) Powder: 250 mg bid (> =60 kg)
Pancreatitis, Peripheral neuropathy, Liver
failure, Retinal depigmentation and change in
vision (in children)
Zalcitabine, ddc (Hivid)
0.75 mg po tid (0.375 mg po tid for patients
<30 kg), 0.75 mg po tid
Severe peripheral neuropathy, Pancreatitis,
Esophageal ulcers,
Cardiomyopathy/congestive heart failure,
Anaphylactoid reaction
Stavudine, d4T (Zerit)
40 mg po bid (>=60 kg), 30 mg po bid (<60
kg)
Delayed peripheral neuropathy,
Hepatotoxicity, Anemia (but decreased bone
marrow toxicity in comparison to zidovudine)
Lamivudine, 3TC (Epivir)
150 mg po bid (>50 kg) with AZT, 2 mg/kg
po bid (<50 kg) with AZT
Headache, insomnia, fatigue, peripheral
neuropathy, myalgia
Protease inhibitors
214
Saquinavir mesylate (Invirase)
600 mg po tid
Generally well tolerated.
Ritonavir (Norvir)
600 mg bid
Generally well tolerated.
Indinavir (Crixivan)
800 mg tid
Generally well tolerated.
Prophylaxis of opportunistic infections AIDS
215
CDC Recommendations for Reducing Perinatal HIV Transmission
1. At 14 to 34 weeks of gestation, a CD4 count above 200 per uL and no previous antiretroviral
therapy: three-phase zidovudine (Retrovir) therapy should be offered to the pregnant woman and to
the infant after birth.
2. At more than 34 weeks of gestation: three-phase zidovudine therapy should be offered to the
pregnant woman and to the infant after birth.
3. With a CD4 counts below 200 per uL: three-phase zidovudine should be offered for the woman's
benefit.
4. With more than six months of any antiretroviral therapy before pregnancy: three-phase zidovudine
therapy should be offered on a case-by-case basis.
5. For women who received no antiretroviral therapy during pregnancy and present in labor:
zidovudine therapy should be offered intrapartum to the mother and to the infant after delivery as the
clinical situation permits.
6. For infants born after no zidovudine prophylaxis: zidovudine therapy should be offered for the infant
if therapy can be initiated within 24hours of birth.
CDC = Centers for Disease Control and Prevention; HIV = human immunodeficiency virus.
*_Implies no previous antiviral therapy has been used.
Adapted from Recommendations of the U.S. Public Health Service Task Force on the use of
zidovudine to reduce perinatal transmission of human immunodeficiency virus. MMWR Morb Mortal
Wkly Rep 1994;43(RR-11):1-20.
Perinatal Care of HIV-Infected Mothers and Their Infants
Antenatal surveillance
216
1. Perform standard prenatal baseline laboratory tests and Papanicolaou smears, plus CD4 counts,
toxoplasmosis and cytomegalovirus titers, liver enzyme levels, a tuberculin test (purified protein
derivative) and a glucose-6-phosphate dehydrogenase (G6PD) level.7
2. Offer zidovudine (Retrovir) prophylaxis according to the guidelines formulated by the Centers for
Disease Control and Prevention (see Table 4).37
3. Consider antenatal influenza, pneumococcal and hepatitis B immunizations (may wait until after the
first trimester). 4 7
4. Perform a complete physical examination and a review. of systems during each trimester. 7 27
5. Maintain surveillance for HIV-related opportunistic infections based on CD4 staging; initiate
prophylaxis as indicated. 7
6. Repeat sexually transmitted disease screening tests (rapid plasmin reagin test/VDRL test,
gonorrhea culture and Chlamydia assay) and group B streptococcal culture in the third trimesters
7. If the pregnant woman is receiving zidovudine therapy, monitor the complete blood count and liver
enzyme levels each month.37
8. Obtain a CD4 count each trimester if the count is under 600 per uL; repeat the CD4 count at six
weeks and six months postpartum. 37
9. Discuss postpartum contraception and safe sexual practices. 7
Intrapartum management
1. Minimize internal fetal monitoring and fetal scalp sampling; fetal scalp lesions increase the risk of
exposure to maternal blood. 7 27 36
2. Wear double gloves and eye shields to protect against exposure to body fluids. 4 4, 7
3. Avoid episiotomy, vacuum extraction and the use of forceps. 7,27
4. At this time, cesarean sections have no specific HIV-related indications. 7,27
5. To avoid needle sticks, repair of all lacerations and episiotomies should be performed by the most
experienced personnel available.
Postpartum management
1. Counsel the mother about the proper disposal of sanitary pads and the need for careful hand
washing before she handles the infant.7
2. Circumcision is not specifically contraindicated.
3. Breast feeding should be discouraged in developed countries. 4,7 36
4. Provide routine postpartum and HIV-related care to the mother as indicated. 7
5. The child may require referral to a specialist familiar with the care of infants at risk for HIV infection.
37
HIV = human immunodeficiency virus.
FEVER CLUES- DIAGNOSTIC SIGNIFICANCE BY MAGNITUDE OF THE TEMPERATURE:
Extreme pyrexia > 106 F includes CNS fevers (hemorrhagic, neoplastic, trauma or infection), drug
fever, heat stroke, HIV infection and malignant hyperthemia.
FEVER WITH RELATIVE BRADYCARDIA: CNS lesions, Dengue, drug fever, Epidemic typhus,
Legionnaires disease, Leptospirosis, lymphomas, malaria, psittacosis, typhoid fever, and yellow fever.
To find out if there is a relative bradycardia take the last digit of the temperature in Fahrenheit and
decrease this by one and then multiply that number by 10 and then add it to 100. For example if the
temperature is 104, the pulse rate is calculated as 4-1=3x10 + 100=130. Therefore, if a patient
has a temperature of 104, then a pulse lower than 130 constitutes relative bradycardia. This works
best if the temperature is 102 or above.
217
DIAGNOSTIC SIGNIFICANCE OF DURATION AND DEGREE OF FEVER: Prolonged obscure
fevers less than 102 include any malignancy, cirrhosis, CMV infection, hepatitis (B or non Anon B), infectious mononucleosis (Epstein Barr), SBE, TB, untreated legionnaires disease,
Mycoplasma pneumonia, and Zoonoses. Prolonged obscure fevers greater than 102 include drug
fever, hypernephroma, intraabdominal, renal-perinephric or pelvic abscess, Kawasaki disease,
lymphoma, metastasizing carcinoma to the liver or CNS, pulmonary hypersensitivity diseases,
SBE, TB (especially disseminated or extrapulmonary).
DIAGNOSTIC SIGNIFICANCE OF FEVER IN THE HOSPITAL PATIENT WITHOUT LOCALIZING
SIGNS AND TEMP < 102: Catheter associated bacteriuria, hepatitis B and non A non B,
dehydration, delirium tremens, nonspecific inflammation, resolving hematomas, postoperative
anesthesia related fever, and thyroid storm.
DIAGNOSTIC SIGNIFICANCE OF FEVER IN THE HOSPITAL PATIENT WITHOUT LOCALIZING
SIGNS AND TEMP > 102: Anesthetic induced hepatitis, intraabdominal or pelvic peritonitis or
abscess, IV line sepsis, prosthetic valve endocarditis, urosepsis, adrenal insufficiency, CNS fever,
drug fever, malignant hyperthermia secondary to anesthesia, transfusion reactions, and vasculitis.
DIAGNOSTIC SIGNIFICANCE OF FEVER IN THE HOSPITAL PATIENT WITH LOCALIZING
SIGNS AND TEMP < 102: Cholecystitis, Clostridium difficile diarrhea, decubitus ulcers,
pharyngitis, postperfusion syndrome, pyelonephritis, uncomplicated wound infection, atelectasis,
gout, myocardial infarction, pancreatitis, phlebitis, post pericardiotomy syndrome, and pulmonary
emboli.
DIAGNOSTIC SIGNIFICANCE OF FEVER IN THE HOSPITAL PATIENT WITH LOCALIZING
SIGNS AND TEMP > 102: Clostridium difficile colitis, cholangitis, intraabdominal or pelvic
peritonitis or abscess, IV line sepsis, nosocomial pneumonia, procedure related bacteremias,
suppurative thrombophlebitis, pancreatic abscess, infected pseudocyst, and vasculitis.
FEVER OF UNKNOWN ORIGIN- FUO
INFECTION: pulmonary abscess, empyema, pneumonia, bronchiectasis, endocarditis,
sinusitis, dental abscess, pharyngeal abscess, brain abscess, epidural abscess,
meningoencephalitis, abdominal or hepatic abscess, cholangitis, hepatitis, peritonitis, diverticulitis,
perinephric or cortical abscess, pyelonephritis, prostatitis, septic arthritis, osteomyelitis,
decubitus ulcer.
AUTOIMMUNE CAUSES: Giant cell arteritis, Goodpasture's disease, Crohn's disease, ulcerative
colitis, Adult Still's disease, polyarteritis, relapsing polychondritis, sarcoidosis, rheumatic fever,
SLE, Wegener's granulomatosis, vasculitis.
ONCOLOGIC CAUSES: cancer of the lung, pleura, GI tract, renal cell carcinoma, hepatocellular
cancer.
HEMATOLOGIC: cyclic neutropenia, hemolytic disease, leukemia, lymphoma, pernicious anemia.
ALLERGIC: drug reaction to antibiotics, iodides, phenobarbital, methyldopa, streptokinase,
quinidine, cimetidine, phenytoin, insect bites and horse serum.
METABOLIC: alcoholic hepatitis and cirrhosis, alcohol withdrawal and DTs, Fabry's disease, gout,
familial Mediterranean fever, recurrent acute porphyria, hyperthyroidism, hyperlipidemia type I,
hypothalamic damage secondary to infection, infarct, tumor, trauma, hyperthermic damage,
neuroleptic malignant syndrome.
TISSUE PRODUCTS: gangrene, blood collection in the gut or cavities, portal vein thrombosis,
myocardial infarction, toxic shock syndrome, venous thrombosis, pulmonary embolism or
infarction.
UNCOMMON BACTERIA: Listerosis, brucellosis, salmonellosis, tularemia, plague.
FUNGAL: as coccidioidomycosis, histoplasmosis.
RICKETTSIAL:
SPIROCHETAL: Leptospira, Borrelia, syphilis.
VIRAL: as infectious mononucleosis, HIV, CMV. PARASITIC: as amoeba, malaria, filaria,
toxoplasma.
218
MYCOBACTERIAL: TB.
FEVER WITH RELATIVE BRADYCARDIA- The pulse should rise approximately 10 beats/minute
for each degree F increase in temperature. Exclude patients that take beta blockers,
verapamil, hypothyroidism and adrenal insufficiency. The following infectious disease will
produce a fever with a low pulse: Legionellosis, Leptospirosis, Brucellosis, Dengue fever,
Psittacosis, Rocky mountain spotted fever, Typhoid fever, tuberculosis, yellow fever. Also,
consider non-infectious causes as drug fever, factitious fever, lymphoma, CNS tumor or trauma
causing increased intracranial pressure.
HEAT STROKE
A. Types [1]
1. Exertional
a. Young People
b. Sporadic
c. Common: Rhabdomyolysis, Lactic Acidosis, Renal Failure
d. Severe: Disseminated Intravascular
Coagulopathy (DIC)
2. Classic
a. Elderly
b. Heat Waves [2]
c. No sweating
d. Acute renal failure and Rhabdomyolysis are rare
e. Social isolation and lack of air conditioning are risk factors [2]
f. Increased Risk: Heart Failure, Diabetes, ETOH intoxication, severe Scleroderma
3. Heat stroke definition requires >40.5-C (105-F)
B. Signs an Symptoms
1. Loss of Consciousness may be presenting symptom
2. CNS
a. Headache, Vertigo, Faintness,
b. Confusion / Coma
c. Seizures
d. Stroke (Focal Deficit)
3. Abdominal Distress
4. Temp >41- common (106-F): Pyrexia and Prostration
5. Skin Hot and Dry
6. Hyperpnea, Rapid pulse, BP usually low
7. Flaccid muscles, decreased deep tendon reflexes
8. Cardiovascular
a. Hypotension
b. CHF
C. Laboratory
1. Leukocytoses and Hemoconcentration
2. Proteinuria
3. BUN elevation - probably due to increased tissue destruction at high temperatures
4. Respiratory alkalosis and Metabolic Acidosis
5. Common - lactic acidosis
6. DIC may occur - petechiae, purpura, hematemesis, epistaxis
7. Liver damage can occur 24-36- post-admission
8. Renal failure - myoglobulinuria, oliguria, anuria
D. Therapy
1. Remove all clothing
2. Immediate shower, lukewarm water recommended
3. Fan (cool air) to dissipate heat
4. Lower rectal temperature to 100-102- within 1 hour
5. Ice bath not effective
6. Good fluid resuscitation
7. Watch for electrolyte imbalance and arrhythmias
8. May need Central Venous or Pulmonary Artery Measurements
9. Avoid large doses of tylenol and NSAIDs
E. Differential of Very High Fever
1. Malignant Hyperthermia (Heat Stroke)
2. Neuroleptic Malignant Syndrome
3. Severe Hyperthyroidism
4. Meningitis (sepsis occasionally gives very high fevers)
219
5. Rocky Mountain Spotted Fever
6. Drug Reaction
7. Cerebral Malaria
8. Heat Stroke
9. Still's Disease
NEUROLEPTIC MALIGNANT SYNDROMEThe neuroleptic malignant syndrome (NMS) is a potentially fatal syndrome, characterized by
fever, muscle rigidity, autonomic instability, and an altered sensorium caused by neuroleptic
drugs as phenothiazines, thioxanthenes, butyrophenones, loxapine and clozapine.
There is no relation to the duration or dose of the medications, but there appears to be an
increased incidence of the syndrome when the dosage is suddenly increased from a previously
stable level. The incidence of the syndrome in patients taking neuroleptic drugs is .5 - 1%. Many
of these neuroleptic drugs are used to treated conditions such as Tourette's syndrome, Huntington's
chorea, Sydenham's chorea, emesis and in managing dissociative anesthesia.
The syndrome appears to be more common in young men who have disorders as depression,
mania and schizoaffective disorders. At particular risk are those taking lithium along with
neuroleptic medications. Also, any person taking the very potent drugs, haloperidol (Haldol), and
trifluoperazine (Stelazine) and fluphenazine (Permitil, Prolixin) are at increased risk. There seems
to be an increased incidence of neuroleptic malignant syndrome in those in whom the dose of
neuroleptic has recently been increased, and in patients that are using the depot preparations of
fluphenazine decanoate (Prolixin).
The major criteria of NMS includes fever, rigidity and elevated creatine phosphokinase. The
minor criteria consist of tachycardia, blood pressure alteration, diaphoresis, tachypnea,
leukocytosis and an altered state of consciousness as excitement, coma and stupor. To make a
diagnosis of NMS requires 3 major criteria or two major criteria and four minor criteria. The
temperature usually is between 101 and 104 F, but higher temperatures have been seen. The
rigidity may be associated with dysarthria, dysphagia, tremors, opisthotonos, blinking eyes and a
positive Babinski. The tempo of the evolution of the disease may be characterized as being fairly
swift, usually developing over 24-72 hours unless treatment is instituted.
Once treated, the syndrome slowly subsides over about 10 days, unless there is intervening
complications. Those patients that have received depot medications as Prolixin may take 10-30
days to recover.
COMPLICATIONS: There may be 20-30% mortality over a 3-30 day period. Complications that
may be life threatening include acute renal failure developing from myolytic heme pigment tubular
necrosis, dehydration, decreased renal perfusion from autonomic instability. There may be
cardiovascular collapse which can be due to rhythm disturbances and electrolyte alterations.
Disseminated intravascular coagulation may develop as well as thromboembolism. The
decreased level of consciousness may result in dysphagia and aspiration. The rigidity may cause
decreased chest compliance with its attendant complications.
LABORATORY: The creatine phosphokinase levels are extremely high, being reported up to
100,000 IU/L, but more typically between 2000 and 15000. The aldolase may be elevated. There is a
leukocytosis usually in the range of 15,000 to 30,000 with a leftward shift. UA may reveal hematuria
due rhabdomyolysis. Liver function tests may be elevated. CSF sometimes shows increased
protein but otherwise is benign. At autopsy there has been no specific findings. The EEG
may reveal only non-specific changes.
DIFFERENTIAL DIAGNOSIS: Several other diseases may be simulated, but usually can be
distinguished by subtle differences. For example, patients that are taking MAO inhibitors may
develop hypertension if exposed to tyramine, which can cause rigidity and hyperthermia. The
distinction between NMS and the MAO syndrome is extremely important, because treating the
MAO syndrome with levodopa and bromocriptine (drugs used in treating NMS), may augment the
hypertensive hyperthermic crisis of the MAO syndrome. Infections of the central nervous system
are differentiated by changes in the CSF. Phenothiazine induced heat stroke may be confusing,
but in this disorder there is no diaphoresis or rigidity. Malignant hyperthermia is an autosomal
dominant condition which is associated with anesthetic exposure. In the so-called anticholinergic
crisis there is dry skin, no rigidity or diaphoresis, but there are dilated pupils. In lethal
catatonia there is a history of schizophrenia and an absence of neuroleptic medication. Any
hypertonic state as tetany, strychnine poisoning and stiffman syndrome must be ruled out. CNS
AIDS, viral encephalitis and Wilson's disease may also be considered in the differential.
220
TREATMENT: Treatment starts with stopping the offending neuroleptic. Dialysis is of no help
because of high protein binding and lipid solubility. The patient should be hydrated to help prevent
and control myoglobinuric renal failure. Control of fever with cooling blankets and adequate
nutrition is essential. Prevention therapy with subcutaneous Heparin should be given to avert
pulmonary thromboembolic disease. Measures should be taken to keep the lungs clear of
secretions, prevent pulmonary aspiration, use antibiotic therapy as needed, and provide ventilatory
support as needed. Bromocriptine 2.5-10 mg po tid and amantadine 100-200 mg po bid have been
used. Dantrolene can be given as 50 mg IV, as needed to help the rigidity, but 10 mg/kg/day
should not be exceeded. Dantrolene may also be given orally 50-200 mg qd. Monitor liver function
tests when using Dantrolene. l-DOPA and electroshock therapy have been used as well as
Nitroprusside IV and minoxidil when Dantrolene failed.
Any patient after recovering from NMS, must be evaluated individually for re-institution of
neuroleptics in order to control their underlying disease. Several points should be mentioned. It is
critical that informed consent be obtained, and that from 10-30 days elapse after remission from the
syndrome. The dopamine agonist used in treatment should be continued for at least 10 days
following remission of NMS, and even longer, if depot drugs were involved. Try to use low
potency neuroleptics at low dosages, and titrate very slowly. Creatine phosphokinase levels should
be monitored frequently. It is estimated that about 25% of patients will re-develop the NMS after the
original episode and another 25 % will develop at least one feature of the neuroleptic malignant
syndrome. The other 50% of patients must be watched indefinitely, because re-development is
always a possibility.
MENINGITIS- Common causes of meningitis by age:
Neonatal: E coli 50-60%; Group B streptococcus 20-40%; Listeria monocytogenes 2-10%.
Children: Haemophilus influenzae 40-60%, Neisseria meningitidis 10-35% S. Pneumoniae 1020%;
Adults: S pneumoniae 30-50%, N. meningitidis 10-35%, Gram negative bacilli 10-20%, Listeria 510%.
Patients with otitis/sinusitis / mastoiditis are prone to S. pneumoniae, H. influenzae.
With CSF rhinorrhea S. pneumoniae is common.
Closed head trauma may lead to S. pneumoniae, H. influenzae meningitis.
Penetrating head trauma can cause S. aureus, Gram negative bacilli meningitis.
Asplenic patients are susceptible to S. pneumoniae, N. meningitidis, H. influenzae,
Sickle cell anemia patients are more prone to Salmonella, H. influenzae, S. pneumoniae.
Alcoholic patients are susceptible to Klebsiella and S. pneumoniae.
HIV infection can cause meningitis by C. neoformans, Toxoplasma, L. monocytogenes,
Cytomegalovirus. (Immunosuppressed patients are subject to L. monocytogenes and C.
neoformans.
Neurosurgical procedure can be complicated by S. aureus, and gram negative bacilli meningitis.
Differential:
Herpes encephalitis is nonseasonal, may have a focal neurologic defect, seizures and temporal
lobe lesions on MRI/CT scan.
Sarcoid meningitis causes cranial nerves palsies and there will be evidence of systemic disease.
Viral meningitis may produce a maculopapular rash, diarrhea and is seasonal.
Chemical meningitis will have a history of spinal anesthesia or tap.
Bacterial endocarditis have septic emboli, positive blood cultures and heart murmur.
Early TB meningitis shows a preponderance of PMN leukocytes initially followed by lymphocytes,
cranial nerve abnormalities and the chest x-ray is abnormal in 50%.
Amebic meningoencephalitis gives a history of freshwater swimming.
Parameningeal infection will show the lesions on MRI/CT imaging.
Carcinomatous meningitis usually has no fever, but cranial nerve involvement common, and patient
has known cancer.
Lyme disease is seasonal, history of tick bite, cranial nerve 7 palsy and flulike symptoms.
MENINGITIS (Causes)- CAUSES:
Haemophilus is the leading cause in children.
Pneumococcus is the top cause in adults.
Occurs suddenly, and frequently presents with seizures or coma. Meningococcus patients present
with a characteristic rash, but the rash may be seen with ECHO and staphylococcus. Listeria is
usually seen in immunosuppressed patients. Tuberculosis usually presents as a smoldering
subacute or chronic disease. Cranial nerve involvement is common.
221
Viral patients usually have a viral syndrome. Most will have a short and uncomplicated course.
Most are caused by enteroviruses as ECHO and Coxsackie.
Gram negative meningitis is usually associated with trauma or following surgery. Klebsiella, E. coli
and Pseudomonas are the most common.
Cryptococcus is seen in immunosuppressed patients.
Coccidiodes is present in the southwest USA.
Candida may also cause.
Neoplastic disease can result from metastases to the CNS or leukemia.
Sarcoid and SLE meningitis are not common.
MENINGITIS (CSF Profiles)BACTERIAL: The leukocyte count is >500 with a predominance of PMNs. The protein is
increased. The glucose is decreased while the pressure is increased. Gram stain will be
positive in 80%.
FUNGAL, TB AND PARTIALLY TREATED BACTERIAL: The leukocyte is < 500 with a predominance
of lymphocytes. The protein is normal or slightly increased. The glucose is decreased. The pressure
is normal or increased. Mycobacteria are rarely seen. India Ink is positive for cryptococcus.
VIRAL: The leukocyte count is <500 with a predominance of lymphocytes. The protein is
normal or slightly decreased. The glucose is normal, while the pressure is normal or
increased. Microscopic exam is negative.
Elevated protein with no other CSF abnormalities, including a normal cell count can be seen in
stroke patients, diabetics, chronic alcoholics and uremic patients.
MENINGITIS CSF TESTSBacterial: cell count usually 1000-5000 with > 80% granulocytes. Protein 100-500.
Glucose < 40.
Gram stain positive 75-80%.
Culture 70-85%.
Acid fast,
India ink,
cytology,
wet mount negative.
Counterimmunoelectrophoresis positive.
Lactate positive at > 35 mg/dl.
Limulus lysate positive in gram negative meningitis > 90%.
Cryptococcal antigen negative.
Adenosine deaminase negative.
Cyclic adenosine monophosphate decreased.
LDH often elevated.
Aseptic meningitis:
Cell count usually 100-500 with less than 50% granulocytes, but may be > 50% in early tuberculous,
amebic, fungal, viral or spirochetal meningitis.
Protein 100-500.
Glucose is normal but may be low in meningitis secondary to M. tuberculosis, C. neoformans, and
other fungi, chemicals, sarcoidosis, neoplasms, syphilis, and subarachnoid hemorrhage.
In viral meningitis it is < 40 in less than 5% of viral cases, especially mumps and lymphocytic
choriomeningitis.
Gram stain is negative, but may be positive in fungal meningitis (40% with Candida species).
Culture is negative, but is positive in > 80% in tuberculosis and cryptococcal (50%), and rarely with
viral.
The acid fast stain is positive in TB in 15 to > 60%.
The India ink is positive in cryptococcal meningitis in 50-75%.
Wet mount is positive in amebic meningitis.
CIE, Limulus lysate, and lactate are negative.
Cryptococcal antigen is positive in cryptococcal (>95%).
Adenosine deaminase is positive in TB (>80%).
LDH is often elevated.
222
MENINGITIS (Meningococcal)Meningococcal meningitis (MM) can be a severe illness, with uncomplicated meningococcal
meningitis causing death in about 10-20%. If the disease is fulminant the mortality may reach
over 50%. The incidence in the USA is about 1.2 cases /100,000. MM is caused by Neisseria
meningitidis, a gram negative, oxidase positive, nonmotile, non spore forming organism that
contains endotoxin in the cell wall. The organism will grow well on chocolate agar with 2-5%
carbon dioxide. It is distinguished by metabolizing glucose, and usually maltose but not lactose.
Group B now is the most important serogroup which accounts for approximately 40% of cases.
Group C accounts for 30%, group Y for 20% and Group A 2%. The peak incidence of
meningococcal disease is late winter and early spring and is spread by droplet contamination.
The risk is highest in crowded areas such as day care centers, school classrooms and army camps.
Most of the cases involve children or adolescents. About 40% of the population are
nasopharyngeal carriers of meningococci, but fewer than 1% of carriers will develop the disease.
Meningococcal infection may take on several presentations. Meningococcemia is a fulminant
form of septicemia and may occur with or without meningitis. There may also be chronic
meningococcemia, septic arthritis, pneumonia, pericarditis, otitis media, vaginitis, and
conjunctivitis.
CLINICAL: MENINGOCOCCEMIA: Meningococcemia usually starts with an upper respiratory
infection and is then followed by headache, hypotension and fever. Petechiae, and purpura
develop over the trunk, palms, soles and extremities very rapidly.
CHRONIC MENINGOCOCCEMIA: Patients with chronic meningococcemia have episodic fever,
headaches, arthritis and arthralgia, and bouts of petechiae. Between these episodes the patient
may have no symptoms and appear non-toxic. Splenomegaly may be present. The mean duration
of this disease is about 6-8 weeks.
FULMINANT MENINGOCOCCEMIA: Fulminant meningococcemia, also known as the
Waterhouse-Friderichsen syndrome, occurs in 10-20% of patients with meningococcemia, has a
high fatality rate and is characterized by shock, disseminated intravascular coagulation and
extensive mucosal and skin hemorrhage.
MENINGOCOCCAL MENINGITIS: Meningococcal meningitis is the second most common cause
of bacterial meningitis after the neonatal period. In childhood it is second to H. influenza and in the
adult it is second to pneumococcus. The patient usually presents with chills, headache, high
fever, abdominal and back pain, and vomiting. There is nuchal rigidity with a positive Brudzinski and
Kernig signs. Cranial nerve palsies, especially the third, fourth, sixth, seventh and eighth cranial
nerves are common complications which usually resolve with treatment, but hearing deficits may not
resolve. The skin rash consists of patches of ecchymosis, petechiae and purpura.
DIFFERENTIAL DIAGNOSIS:
HENOCH-SCHONLEIN PURPURA: Henoch-Schönlein purpura (HSP) is an immune vasculitis
that also presents with purpura. It is usually seen in children but may be seen in adults. HSP will
often follow a viral infection. There is microscopic hematuria, fever, abdominal pain and
polyarthralgia. The purpuric skin rash characteristically affects the extensor surfaces of the feet and
legs, buttocks and the extensor surfaces of the arms. There also may be swelling of the ankles,
hands, knees, wrists and elbows.
SYSTEMIC LUPUS ERYTHEMATOSUS WITH LUPUS ANTICOAGULANT: Some lupus patients
are very ill when first seen and may have purpura. There may be widespread skin necrosis with
secondary hemorrhage.
GONOCOCCEMIA: One shouldn't have too much difficulty in diagnosing gonococcemia because
the characteristic skin lesions are scattered pustulo-papules rather than extensive hemorrhagic
purpura.
ROCKY MOUNTAIN SPOTTED FEVER AND ENTEROVIRUS INFECTION These two diseases
may simulate meningococcemia and would be included in the differential diagnosis.
LABORATORY: The patient will need a lumbar puncture which will show the CSF to be cloudy or
purulent with increased protein, decreased glucose and elevated pressure. The cell count is
usually greater than 1000 cells/uL with a predominance of polymorphonuclear cells with gram
negative intracellular diplococci. Latex agglutination for the capsular polysaccharide antigen is
positive in about 60-80%. This antigen may be detected in the CSF, urine or serum. The
organism may be seen by smear or culture of the CSF, blood or aspirated petechiae. Blood culture is
positive in about 2/3 of the cases of meningococcemia with or without meningitis. Gram stain of
the buffy coat may show the gram negative cocci if there is fulminant meningitis. Isolation of N.
meningitidis from the nasopharynx is not helpful because of the high incidence of colonization. Any
adult patient that develops invasive meningococcal disease should be suspected of having an
immunoglobulin defect or abnormality of the complement system. Total immunoglobulins, IgG2
subclass, C3, and total hemolytic complement (CH50) should be done. If DIC is present the
prothrombin time is prolonged, the platelets are decreased and the fibrinogen levels are low.
223
TREATMENT: Treatment is with IV aqueous penicillin G 2 million units every 2 hours, given until
the patient has been afebrile for about 5-7 days. If the patient is allergic to penicillin, chloramphenicol
should be used at 1-1.5 grams IV every 6 hours. Patients should be in isolation for the first 24
hours of treatment.
PROPHYLAXIS: Close contacts and family members should receive prophylaxis with rifampin for 2
days. In the adult use 600 mg po bid. For children from 5-12 years give 10 mg/kg bid and for
neonates 3-12 months use 5 mg/kg bid. Meningococcal vaccine is used to control epidemics or
for travelers to epidemic areas.
MENINGITIS (Treatment)- The following is the IV empiric therapy of meningitis directed at various
levels of age and special situations: In all of the following situations, ceftriaxone may be
substituted for cefotaxime, with the exception of neonates < 1 month, in which ceftriaxone is not
recommended because it can displace bilirubin from albumin binding sites. The pediatric dose for
ceftriaxone is 100 mg/kg in divided doses q12h. The adult dose of ceftriaxone is 2 grams given in
divided doses q12h.
NEONATAL (< 1 month): Ampicillin is given at 200 mg/kg in divided doses every 4 hours +
gentamicin 7.5 mg in divided doses q8h (or tobramycin 6 mg/kg in divided doses q8h or amikacin
20 mg/kg in divided doses q8h). Alternatively, cefotaxime given at 200 mg/kg in divided doses q4h
+ aminoglycoside can be given. This treatment will cover Group B streptococcus, Listeria
monocytogenes, and Escherichia coli.
INFANTS (1-3 months): Ampicillin 200 mg/kg in divided doses q4h + cefotaxime given at 200 mg/kg
in divided doses q4h OR alternatively ampicillin 200 mg/kg in divided doses q4h + aminoglycoside
(amikacin 20 mg/kg in divided doses q8h, or gentamicin 7.5 mg in divided doses q8h, or
tobramycin 6 mg/kg in divided doses q8h). These antibiotics will cover Haemophilus
influenzae, Streptococcus pneumoniae, Listeria monocytogenes, Neisseria meningitidis, and Group B
streptococci.
CHILDREN 3 months- 7 years: Cefotaxime 200 mg/kg in divided doses q4h, OR alternatively
ampicillin 200 mg/kg in divided doses q4h + chloramphenicol 75 mg/kg in divided doses q6h
(monitor serum levels of chloramphenicol). These antibiotics will cover Haemophilus influenzae,
Neisseria meningitidis, and Streptococcus pneumoniae.
OLDER CHILDREN (> 7 years) AND ADULTS: Penicillin G 250,000 U/kg in divided doses q4h
(Pediatric) or 24 million U given as divided doses q4h (ADULT), OR alternatively, cefotaxime 200
mg/kg given in divided doses q4h (Pediatric) or 12 grams given in divided doses q4h (ADULT).
This will cover Neisseria meningitidis and Streptococcus pneumoniae.
CSF SHUNTS: Vancomycin 10 mg/kg q8h + ceftazidime 150 mg/kg given in divided doses q8h
(Pediatric) or 6 grams in divided doses q8h (Adults). This will cover Staphylococcus aureus and
epidermidis and Gram negative bacilli. Consideration must be given for shunt removal and
intraventricular vancomycin).
ASPLENIA: Cefotaxime 200 mg/kg in divided doses q4h (Pediatric), or ceftazidime 12 grams in
divided doses q4h (Adult). This will cover Neisseria meningitidis, Haemophilus influenzae, and
Streptococcus pneumoniae.
POST NEUROSURGICAL PROCEDURES: Nafcillin 200 mg/kg in divided doses q4h (Pediatric) or
Nafcillin 12 grams in divided doses q4h (Adults) + ceftazidime 150 mg/kg in divided doses q8h
(Pediatric), or ceftazidime 6 grams in divided doses q8h (Adult). This will cover Pseudomonas
aeruginosa, Staph aureus and epidermidis, and Gram negative bacilli.
CLOSED HEAD TRAUMA: Penicillin G 250,000 U/kg in divided doses q4h (Pediatric), or Penicillin G
24 million U in divided doses q4h (Adult). This will cover Streptococcus pneumoniae.
TRANSPLANT PATIENTS: Ampicillin 200 mg/kg in divided doses q4h (Pediatric), or Ampicillin 12
grams given in divided doses q4h (Adult) + aminoglycoside (Amikacin 20 mg/kg in divided doses
q8h (Pediatric) or Amikacin 15 mg/kg in divided doses q8h (Adult), OR Gentamicin 7.5 mg/kg in
divided doses q8h (Pediatric) or Gentamicin 5 mg/kg in divided doses q8h (Adult), OR Tobramycin
6 mg/kg in divided doses q8h (Pediatric), or tobramycin 5 mg/kg in divided doses q8h (Adult). This
will cover Listeria monocytogenes.
ALCOHOLIC PATIENTS: Penicillin G 24 million units in divided doses q4h + cefotaxime 200 mg/kg in
divided doses q4h. This will cover Streptococcus pneumoniae and Gram negative bacilli.
RECURRENT MENINGITIS: Penicillin G 250,000 U given in divided doses q4h (Pediatric), or
Penicillin G 24 million U in divided doses q4h (Adult). This will cover Streptococcus pneumoniae.
ELDERLY PATIENTS: Penicillin g 24 million U in divided doses q4h. This will cover
Streptococcus pneumoniae.
TERMINAL COMPLEMENT DEFICIENCY: Penicillin G 250,000 U in divided doses q4h
(Pediatric), or Penicillin G 24 million U in divided doses q4h (Adults). This will cover Neisseria
meningitidis.
TREATMENT BASED ON MORPHOLOGY BY GRAM STAIN: Gram positive bacilli could represent
Listeria monocytogenes and is treated with ampicillin +/- aminoglycoside, or alternatively
trimethoprim-sulfamethoxazole. Gram negative cocci could represent Neisseria meningitidis, and is
treated with Penicillin G or alternatively cefotaxime, ceftriaxone or chloramphenicol. Gram positive
cocci in short chains and pairs could represent Streptococcus pneumoniae, or Group B
streptococci, and is treated with Penicillin G, or alternatively with cefotaxime, ceftriaxone, or
224
chloramphenicol. Gram positive cocci in clusters could represent Staphylococcus aureus, and
is treated with nafcillin or alternatively with vancomycin (has variable CSF penetration). Gram
negative coccobacilli represents Haemophilus influenzae, and is treated with cefotaxime or
ceftriaxone, or alternatively with ampicillin + chloramphenicol. Gram negative bacilli could
represent Pseudomonas aeruginosa or Klebsiella (treated with ceftazidime + aminoglycoside),
or Escherichia coli (treated with cefotaxime or alternatively with Trimethoprim-sulfamethoxazole). If
no Gram stain organisms are seen, treat empirically with ampicillin + cefotaxime or ceftriaxone.
DIABETIC KETOACIDOSIS DKA
Presentation
1. DKA often presents as anorexia, N/V, and abdominal pain.
a. Abdominal pain be sufficiently severe to suggest an acute surgical abdomen.
b. Abdominal tenderness, guarding, decreased bowel sounds, and
increased WBC may be present.
c. Abdominal pain from DKA almost always subsides in 6-8 hours after
institution of therapy.
2. DKA is often proceeded by a period of polydipsia, polyphagia, polyuria,
weight loss, increasing weakness, and mental obtundation.
3. The onset is usually gradual over several days.
4. Hypothermia is the rule and does not preclude infection.
DIFFERENTIAL DIAGNOSIS DKA HNKC
Onset
DKA
Gradual
HYPOGLYCEMIA
Sudden
Skin
Warm, dry
Cool, clammy
Respirations
Rapid and deep
(Kussmaul)
not as profound
Breath Odor
Sweet, fruity
Ketosis
Blood sugar
Osmolarity
Na+
Metabolic
acidosis
DKA
Present
Not deep, but
may be rapid
Very profound
MNKC
Absent
Usually < 600
Usually > 900
Never < 600
Usually < 350
Usually > 350
~ 28
~ 80
Usually low
Usually high
Usually severe
Usually not severe
( acidosis < 7.35 )
PRECIPITATING FACTORS (There is always a precipitating factor)
1. Infection - most common
- usually UTI, URI, infected decubitus
2. Silent MI
3. Non-compliance is taking Meds
4. Intraabdominal catastrophes
5. Pancreatitis (Note increased amylase seen in 2/3 of patients
with DKA)
6. Stroke
7. Trauma, surgery, psychological stress
MANAGEMENT
225
ALWAYS MAKE A FLOW SHEET!
Initial labs:
1. SMA-7
a. Glucose - use Dextrostix initially and PRN.
b. Bun - often increase d/t dehydration.
c. Creatinine - may be increased out of proportion to BUN 2o
interference by acetoacetate with picric acid
in assay.
2. Acetone
- Bedside: Dilute plasma 1:1 with NS or water and test with
crushed Acetest tablet; > 2+ reaction = significant
ketosis (may use undiluted serum instead).
3. CBC
a. HCT - often increase d/t dehydration.
b. WBC - leukocytosis is common even without infections and may
be masked.
4. ABG's
5. Calcium and Phosphorus - baseline
6. Lactate
- Not increased in ordinary DKA; acidosis not accounted for by
ketoacidosis may be 2o lactic acidosis, especially in elderly,
hypotensive patients.
7. U/A - glucose, ketones, UTI
Calculate:
1. Correct the Na+ for glucose
For every 100 mg/dl increase in glucose > 100, add 2.5 mEq/l
to the measured serum Na+.
2. Fluid deficit
a. Normal TBW - 0.6 x IBW (kg)
b. Current TBW - Normal serum Na+ (Normal IBW)
Corrected serum Na+
c. Body water deficit - Nl TBW - Current TBW
d. Correct half the deficit in the first 8 hours
and the rest over the next 16-24 hours.
3. Serum Osmolarity
2 (corrected Na+) + (glucose) + (BUN)
18
2.8
- A patient in coma with osmolarity < 340 is probably not in DKA;
look for stroke or severely decreased phosphate.
Treatment:
1. FLUIDS - use NS or 1/2NS
a. Use 1/2NS if: Corrected serum Na+ > 150
Bicarb is being given.
Otherwise use NS initially.
b. Usually give 1-2 liters over the first hour.
c. Severe hypotension: may need albumin, whole blood,
or continuous NS.
d. Monitor CVP if: heart disease, renal disease, hypotension,
elderly, susceptible to overload.
e. Swan-Ganz catheter preferred if: severe shock, pulmonary
hypertension, MI.
f. Follow initial rapid hydration with 1/2NS at 300-500 cc/hr.
2. Insulin:
a. Peak action of regular insulin: IV - 5-10 mins.
IM - 1-2 hours
SQ - 4 hours
b. Two routes preferred: continuous IV or IM.
c. Dose: 0.1 unit/kg/hr IV
0.1 unit/kg/dose IM 7 units/hour
d. Give IV bolus of 10 - 20 units (0.33 units/kg)
first (both routes)
e. Continuous IV: 50 units in 250 cc 1/2NS 1 unit/5cc via infusion pump at 35 cc/hour
- (addition of albumin to set-up is not necessary)
f. Measure glucose, acetone, electrolytes and ABG's every hour.
g. Blood sugar should decrease 10% per hour or 100 mg/dl per hr.
- if not, increase (double) the infusion rate or repeat the
loading dose.
226
h. At blood sugar = 250: switch to 5 units of insulin
250 cc D51/2NS, and continue the infusion
until the plasma is cleared of ketones.
- (Average dose is 50 units over 5 hours
to decrease blood sugar to 250).
i. Maintain the blood sugar at 250 and continue the infusion
until the acidosis is corrected (pH normal, HCO3, AG).
j. Criteria for stopping insulin infusion:
(1) Normal pH (acidosis corrected)
(2) Negative serum and urine acetone
(3) Eating
(4) Looks good and feels good
k. The patient should be out of DKA in 10 - 16 hours.
If not out of DKA in 16 hours there is an increased
incidence of mucormycosis (headache, drainage of pink
nasal secretions)
l. To establish the insulin regimen:
(1) Usually the patient will be clear by the next morning
(2) If the infusion is still running give half of the previous
insulin dose as NPH or give 0.1 units/kg of NPH
as the a.m. dose
(3) If the infusion is discontinued:
(a) Begin sliding scale regular insulin
SQ every 4 hours.
OR:
(b) Give 10 units NPH empirically as the AM dose.
(most people will tolerate this dose).
(c) Get 7 AM and 4 PM blood sugars daily.
Regulate the insulin dose if the 4 PM blood
Sugar is > 200.
(d) When 4 PM blood sugar is < 200,
get qid blood sugars (7 AM, 11 AM, 4 PM, and 10 PM)
to refine dosage.
3. BICARBONATE
a. Indications:
(1) pH < 7.1
(2) Hypotension, shock or both when pH < 7.2
(3) Consider bicarbonate when low pCO2
(already maximally compensated)
or lung disease (can't compensate)
b. Dose: 2 amps (88 mEq) diluted in 1 liter of l/2NS given
over 1 - 2 hours. Repeat dose until pH > 7.2
c. Do not give as bolus unless in resuscitation, shock
or if initial pH <7.0.
4. POTASSIUM
a. Monitor q 1 hour.
b. Make sure there is urine output.
c. If K is normal or low, start K at once;
if increased, give when K+ reaches 5.5
d. Give 40 mEq in the first liter and 20 - 40 mEq/L thereafter.
5. PHOSPHATE
a. If possible, get an initial phosphate (and calcium)
as a baseline and monitor every 4 - 6 hours.
b. Decrease in phosphate will usually not be seen until
8 - 12 hours; replace phosphate if and when it falls
to low levels.
c. Prevention of hypophosphatemia in DKA
(1) 20 mEq/L of K+ replacement may be given as K Phosphate.
(2) K Phosphate = 4.4 mEq K+ + 3mmole phosphate/ cc
(3) 5 cc of K phosphate/L = 22 mEq K+ + 15mmole
(466 mg P) phosphate/L
(4) Rate of K phosphate solution must not exceed 10mmole/hr.
(5) Some authorities should give the first 10 - 30 mEq of
K+ replacement as K phosphate.
d. Danger of phosphate therapy is that too much phosphate
binds calcium leading to hypocalcemia.
e. Low phosphate leads to deficiency of ATP and 2.3 DPG which
shifts the Hb dissociation to the left and impairs oxygen
delivery to the tissues.
227
6. ADDITION MEASURES
a. If obtunded: Endotracheal intubation prior to NGT to prevent
aspiration
b. Foley catheter if obtunded, urinary outlet obstruction, or
oliguria after several hours of treatment.
c. Tagamet 300 mg. IVPB every 8 hours to prevent stress
ulcerations.
d. Search for precipitating factors
(1) Cultures
(2) Spinal Tap
(3) Serial EKG's and cardiac enzymes
e. Cerebral Edema is a risk if fluid deficit is corrected too fast
or if markedly hypotonic fluids are used.
-Usually seen in adolescent diabetics.
-S/S: progressive obtundation, increased ICP (papilledema,
blown pupil), and hypothalamic dysfunction (hyperpyrexia,
diabetes insipidus)
f. Diet
(1) Liquids when PO fluids tolerated
(2) Regular ADA diet in 24 - 48 hours
g. Monitor Calcium and Phosphate daily
h. Unexplained or refractory shock: think of MI, sepsis,
bowel infarction, or lactic acidosis.
i. Remember that patients with lousy kidneys do not spill glucose!
j. Sliding scale for glucometer:
Blood sugar: > 400
Regular insulin SQ: 20 units
> 300
15 units
> 200
10 units
Hemoglobin A1c [Glycohemoglobin] and Blood Glucose
Approximate Relationship
Between HbA1c and Average
Blood Glucose
-----------------------Average
HbAlc
Glucose (mg/dl) (%)
-----------------------360
14
330
13
300
12
270
11
240
10
210
9
180
8
150
7
120
6
90
5
------------------------
Diabetic Glucose Target Goals:
Pre-meal glucose-- 80-120 mg/dl
Bedtime glucose--- 100-140 mg/dl
Hb1c-------------- < 7%
228
THYROID DISEASE INTRODUCTION
A. Occurrence
1. Thyroid problems are extremely common
2. ~5% of population has palpable thyroid abnormality
3. More common in women than men (10:1)
4. Anomalies ~2X more likely to be carcinoma in men than in women
B. Disease Entities
1. Hyperthyroidism
a. Subtle in elderly, often presents with atrial fibrillation or CHF
b. In young persons, often presents as resting tachycardia, weight loss, heat intolerance
c. Graves' Disease: autoimmune stimulation of TSH receptor (anti-TSH-R antibodies)
2. Hypothyroidism
a. Commonly caused by drugs: lithium, sulfonylureas, amiodarone
b. Hashimoto's Thyroiditis: autoimmune destruction of thyroid follicles
c. Common complication of treatment for hyperthyroidism
3. Thyroid Inflammation - thyroiditis
a. Diffuse enlargement is most common
b. Painful or painless helps with differential diagnosis
4. Subclinical Thyroid Disease [9]
a. Increased use of TSH as screening has increased number of cases
b. Subclinical disease implies normal thyroid hormones (T4, T3) with abnormal TSH
c. Low TSH (eg. <0.5) with normal T4 and T3 is subclinical hyperthyroidism
d. High TSH (eg. >5.0) with normal T4 and T3 is subclinical hypothyroidism
e. However, patients may have subtle symptoms from these thyroid abnormalities
5. Drug Induced Thyroid Disease
a. Decrease TSH Secretion: dopamine, glucocorticoids, octreotide
b. Decrease T4 Secretion: lithium, iodide, amiodarone
c. Increase T4 Secretion: iodide, amiodarone
d. Decrease T4 Adsorption: colestipol, cholestyramine, aluminum, iron, sucralfate
e. Increase Serum TBG: estrogen, tamoxifen, heroin, methadone, mitotane, fluorouracil
f. Decrease Serum TBG: androgens, danazol, slow release niacin, glucocorticoids
g. Displace T4 from Binding Sites: furosemide, salicylates
h. Increase Hepatic T4 Metabolism: phenobarbital, rifampin, phenytoin, carbamazepine
i. Decrease T4 to T3 Conversion: propylthiouracil, amiodarone, Гџ-blockers, glucocorticoids
6. Thyroid Mass (Thyroid Nodule)
a. Multinodular vs. Solitary Nodule
b. Previous head and neck irradiation has 5-10% risk of developing nodule over 20 years
c. Diagnosis is usually made by needle biopsy
C. Evaluation of Goiter (Thyroid Enlargement)
1. Consider endemic causes - deficiency or adverse drug effects
2. History
a. Symptoms of hypo- or hyperthyroidism
b. Medication History
c. Symptoms of mechanical obstruction: airway problems, dysphagia
3. Physical Exam
a. Observation of gland size is very important; normal gland rarely visible
b. Palpation should be performed from behind the patient
c. Characterize the enlargement: Single Nodule, Multinodular, Diffuse
d. Prominent glands should be measured with a ruler
4. Fine Needle Aspiration of Thyroid Nodule(s)
D. Causes of Diffuse Thyroid Enlargement
1. Hyperthyroidism
a. 95% Graves' Disease
b. 5% Hashimoto's or other type of thyroiditis
c. Evaluation: eye findings, Thyroid Stimulating Antibodies, TSH, T4 index
d. Radioiodide uptake: determine if condition is transient (eg. thyroiditis) vs. longer term
2. Euthyroid: usually preclinical stage of either Graves' or Hashimoto's Disease
3. Hypothyroid - Usually Hashimoto's Thyroiditis
E. Multinodular Goiter
1. Hyperthyroidism
a. Plummer's Disease
229
b. Foci of functional autonomy develop within simple goiter (?)
c. Ablative Therapy (radioactive iodine)
2. Euthyroid
a. Most patients are women
b. Autonomously functioning nodules more common
c. Hormone suppression
3. Hypothyroid
a. Unclear etiology (? Hashimoto's disease)
b. Hormone replacement therapy is indicated
F. Causes of Solitary / Dominant Nodules
1. Classification
a. Previously classified by ability of nodule to take up radio-isotope ("hot" nodule)
b. However, nearly all nodules are initially evaluated by fine-needle aspiration (FNA)
c. Main issue is to rule out presence of carcinoma in the nodule
d. Thyroid Function Tests are generally only useful in patients with systemic symptoms
2. Benign FNA Results
a. Hashimoto's Thyroiditis is most common
b. Colloid only may be seen - usually patient is observed
3. Follicular Neoplasm
a. Most are adenomas; size is crucial determinant
b. In elderly 25% >4cm present with T3 Thyrotoxicosis
c. Radionucleotide scanning will help delineate hot from cold nodules
d. Carcinoma is major concern here, but hot nodules are usually benign
e. Full TFTs including T3 levels should be obtained
4. Frank Malignancy
a. Consider ultrasound, CT or MRI of neck for more extensive evaluation
b. Papillary, Follicular, and Medullary (~5%) Carcinomas are found
5. Some specialists prefer initial radio-iodine scan to classify "hot" vs. "cold" nodules
a. ~5% of all thyroid nodules are hyperfunctioning ("hot")
b. The remainder are "cold" or "warm" and these are most suspicious for carcinoma
6. Causes of Solitary Nonfunctional ("Cold") Thyroid Nodules
a. Adenoma (~75-80%)
b. Carcinoma (~15%)
c. Cyst (simple and other)
d. Multinodular goiter
e. Inflammatory diseases, Abscess, Dermoid, Teratoma (all rare)
7. Causes of "Hot" Nodules
a. Hot nodules are far more common in woman than men (F:M 13:1)
b. Patient may be euthyroid or hyperthyroid ("toxic")
G. Evaluation of Thyroid Nodules [ 1, 3]
1. Fine Needle Aspiration (FNA) [ 1, 2, 6]
a. Most effective method for diagnosing malignancy
b. Overall yield is: Benign 69%; Suspicious 10%; Malignant 4%; Non-Diagnostic 17%
c. Yield of non-diagnostic is extremely operator dependent
d. False negative ~5%, False positive ~5%; Sensitivity 68-98%; Specificity 72-100%
e. Non-diagnostic FNAs should be repeated with ultrasound guidance
f. If FNAs are non-diagnostic twice, surgical biopsy and/or resection should be considered
2. Thyroid Function Tests (TFTs)
a. For evaluation of thyroid hormone levels (usually done, but rarely useful)
b. Majority of the nodules are "cold" - that is, do not produce T4 hormone
c. Even some "hot" nodules will release near-normal amounts of thyroid hormone
3. Ultrasound
a. Mainly done to ascertain gland size, number and size of nodules
b. Detection of cysts (>2mm) or nodules (>3mm) and calcifications
c. May delineate extra-thyroid from intra-thyroid masses
d. Evaluate lymph nodes in patients with thyroid cancer
e. Useful for aiding fine needle aspiration (biopsy)
4. Radio-iodine scan (123-I)
a. Assesses organification and uptake
b. Thus, will determine "hot" vs.” cold" nodules; diffuse vs. local uptake
c. Generally, these are preferred over technetium scans
5. Technetium scan
a. Assesses blood supply and uptake of gland (not organification)
b. Useful for determining anatomy of gland and in patients allergic to iodine
6. MRI and CT Scanning
a. Mainly for evaluation of complicated cases, particularly with carcinoma
b. Evaluate Masses for regional extension and symptoms due to local effects
H. Treatment of Thyroid Nodules
1. Carcinomas should generally be resected followed by T4 suppressive/replacement therapy
2. Adenomas causing symptoms (local compression, T4 production) should usually be resected
230
3. Cold Nodules
a. Suppression therapy is often very effective
b. Both Levothyroxine and iodine are both effective [7]
4. Hot (Hyperfunctioning) Nodules
a. Ablative therapy with iodine is one option
b. Surgical resection can be performed
THYROTOXIC CRISISCLINICAL: Patients present with exaggerated symptoms of hyperthyroidism. The precipitating factor
usually is a pulmonary infection, diabetic complications, pulmonary embolism, or myocardial
infarction. The use of haloperidol, recent iodine or surgical therapy, cessation of antithyroid
drugs may also be causative. There may be diarrhea and altered mental state, and young females
are commonly involved. There may be atrial fibrillation, elevated temperature, increased pulse
pressure, goiter, exophthalmopathy, lid lag, arthritis, pretibial myxedema, tender hepatomegaly,
gynecomastia, lymphadenopathy, fine tremor, galactorrhea, and delirium.
LAB: There may be increase glucose unless there is adrenal insufficiency, increased calcium
normocytic normochromic anemia, increased transaminases, BUN and bilirubin. The ECG shows
sinus tachycardia or supraventricular arrhythmias. A T4 should be done (the T4 may be decreased
to normal in the acutely ill). Also obtain a thyroid panel, TSH, cultures, chemistries and CBC.
TREATMENT: Cooling blankets and acetaminophen may be used for hyperthermia >104 F.
Salicylates should not be given because they will displace thyroid hormones from binding protein,
exacerbating the condition. Cardiac monitoring should be carried out. Use B-complex and IV fluid
maintenance. CHF should be treated and small doses of propranolol may be beneficial by slowing
the heart rate. Propranolol is given at 2-5 mg IV at 1 mg/min or 40-80 mg PO q6h.
Propranolol will block peripheral conversion of T4 to T3 and decrease the hyperadrenergic effects.
It should not be used in asthma or CHF that is not due to tachyarrhythmia. Sodium iodide 1 gm IV
q8h or Lugol's solution 30 cc po daily is started 2 hours after Propylthiouracil is given. Iodine will
block thyroid hormone release. Propylthiouracil is given at 1 gm through a nasogastric tube or by
rectum as a loading dose, then 400 mg PO daily for 3-6 weeks. Dexamethasone is given at 2 mg
q6h until patient is stable. Dexamethasone will block the peripheral conversion of T4 to T3 and
correct any relative adrenal insufficiency.
Thyroid Storm
SX: HTN, Palpitations, febrile, Tachy
High suspicion if pt is FEBRILE
other SX: n/v/
:due to stress infection
-Tx
Lugol's Soln: K+ Iodide: prevents
iodine metab of thy hormones
propylthiouracil:
?Steroids: usually must give in
myxedema coma due to immune
syndrome(Schmidt’s) from co-antibody
against thyroid & adrenals
(so must give steroid w/Synthroid
since Synthroid will stim adrenals)
ADRENAL INSUFFICIENCYAdrenal insufficiency (AI) can be a medical emergency and the failure to recognize it could have
catastrophic consequences. The incidence of AI may be rising with AIDS and the increasing use of
steroids. CAUSES: The causes can be divided into two categories: primary adrenal disease and
secondary. PRIMARY can be caused by the following: Granulomatous disease (TB,
Histoplasmosis and other fungal infections, and sarcoidosis), Neoplastic infiltration, Amyloidosis,
Hemochromatosis, Drugs (ketoconazole, mifepristone, anticoagulants), meningococcemia with
Friderichsen-Waterhouse syndrome, adrenal hemorrhage, adrenoleukodystrophy in boys,
autoimmune adrenalitis, and acquired immunodeficiency syndrome. SECONDARY hypothalamic
and or pituitary disorders can be caused by pituitary and hypothalamic tumors, lymphocytic
hypophysitis, and withdrawal from glucocorticoid therapy. Idiopathic autoimmune adrenalitis is the
most common cause accounting for 80% of adrenocortical insufficiency. There are several
231
endocrine disorders associated with this disease: (diabetes mellitus, thyrotoxicosis, thyroiditis,
alopecia, vitiligo, myasthenia gravis, hypoparathyroidism, pernicious anemia, ovarian failure,
hypercalcemia, chronic moniliasis, and Schmidt's syndrome). Several antibodies are often
found as; gastric antibodies (20%), parathyroid antibodies (20%), adrenal antibodies (60%) and
thyroid antibodies (40%). Metastatic disease involves the adrenal glands in 25% of oncologic
patients. Ninety percent of the adrenal gland has to be destroyed before a patient is symptomatic.
Most cancer patients don't have this amount of involvement. AIDS can cause adrenocortical
insufficiency by infiltration with Mycobacterium avium-intracellulare, Cytomegalovirus, Kaposi's
sarcoma, and Cryptococcus. Ketoconazole can also cause AI. CLINICAL DIAGNOSIS:
Weakness and fatigue are the most frequent findings (94%) followed by the following in decreasing
frequency: Skin hyperpigmentation manifested as tanning, freckles, vitiligo, blue-black discoloration
of the areolas and mucous membranes (91%), Anorexia and weight loss (88%), Postural hypotension
(81%), Hyponatremia (67%), Nausea and vomiting (66%), Hyperkalemia (55%), Azotemia
(52%), Diarrhea and abdominal pain (23%) and hypoglycemia (19%. Dermal hyperpigmentation
is seen in primary adrenocortical insufficiency, but is not seen in secondary insufficiency. Look
especially at the palmar creases and in scars where there is increased pigmentation. The entire
body can be affected but look especially at the face, neck, upper extremities, scrotum, penis,
axillary areas and the periumbilical area. Dilutional hyponatremia is more common in secondary
insufficiency than primary. It is caused by increased arginine vasopressin secretion and reduced
free water elimination by the kidneys. Hyperkalemia only occurs in primary adrenocortical
insufficiency because of the aldosterone deficiency. LABORATORY: RAPID ACTH TEST- Give
cosyntropin 250 ug IV and measure plasma cortisol and aldosterone levels at baseline and after 30
min. The normal response at 30 min should be an increase of > 7 ug/dL of cortisol and aldosterone
OR double the baseline value OR an absolute value of 20 ug/dL of cortisol and aldosterone. In
primary AI there is a decreased cortisol and aldosterone level. In secondary, there is a decreased
cortisol level and increased aldosterone level. PLASMA ACTH- Measure the ACTH at baseline
before the rapid ACTH test is done. The normal diurnal plasma ACTH level is 0-70 pg/ml. In
primary AI there is increased ACTH level and in secondary AI there is decreased ACTH levels. If
you suspect acute adrenal insufficiency, baseline levels of cortisol, aldosterone and ACTH should
be done along with routine blood chemistries. Give 5% dextrose in normal saline, about 2 liters
in the first 6 hours. Give dexamethasone, 4 mg IV initially then 4 mg every 6 hours. Next, for
diagnosis, give cosyntropin, 250 ug IV and determine the plasma cortisol after 30 minutes.
Investigate the possible causes, get TB skin test and cultures and MRI of the adrenals.
TREATMENT: Give 20 to 30 mg of hydrocortisone daily, 2/3 in the early AM and the remainder in
the early afternoon. If there is primary insufficiency give .05 to .3 mg of fludrocortisone daily to
maintain fluid and electrolyte balance. Before surgery and major stress give hydrocortisone 100
mg IV followed by 10 mg/hour during the procedure and postoperatively give 100 mg of
hydrocortisone every 8 hours until the patient is stable; then taper the dose over 3-5 days.
ANTICOAGULATION TREATMENT
General Treatment with Heparin
1.Baseline Study
2.Loading Dose 80U/Kg (Range = 5000-10,000U)
Heparin IVPB
3.Follow immediately by constant IV infusion
1000-1500 units/hour or 18U/Kg/Hr not to
exceed 1500U/Hr.
4.4 hours later get PTT
5.Aim = 1 1/2 - 2 x control, or 15 - 30 sec over
control.
IF:
1.< 5 seconds above normal - reload with
10,000 units and increase transfusion rate
by 200 units/hr.
2.5-20 seconds above normal - reload at
5000 units (1/2 dose) and increase
transfusion rate by 100 units/hr.
3.10-15 seconds above normal - increase
infusion rate by 100 units/hr.
4.15-30 seconds above normal - maintain at
same rate
5.> 30 seconds above normal -hold IV 1-1
1/2 hours (decrease PTT rise by 1/2) and
restart infusion decrease by 200-300
units/hr.
Recheck PTT in 4-6 hours!
232
Notes:
1.Adjust dose according to PTT, continue
until coag. rate as measured by PTT
stabilizes within the desired range, then may
extend interval between PTT's to 12 hours
then 24 hours.
2.CBC with platelet count after 3 days of
treatment and on the 7th day.
CONVERSION GUIDELINES
Heparin ---> Coumadin
Day 1 - Baseline PT ----> Begin (at 10 mg/day)
Day 2 - Draw PT ----> Give 10 mg Coumadin - if PT >
1 1/2 control or INR > 2.5 decrease by 5mg
Day 3 - Draw PT ----> Give 10 mg Coumadin - if PT >
1 1/2 control or INR > 2.5 decrease by 2.5 mg
Day 4 - Draw PT ----> Give 5mg Coumadin - if PT > 2
x control or INR > 3 decrease by 1-2 mg
Day 5 - Draw PT ----> Give 5 mg if PT > 2 x control or
INR > 3 decrease 1-2 mg
Day 6 and on: Draw PT
&LT1 1/2 control (INR &LT1 2)
1 1/2 - 2 Control (INR 2-3) > 2 control (INR > 3)
inc 1-2mg/day No Changes
dec dose 1-2mg/day
|
|
|
|
\|/
|
------------------> Draw PT 5-7 days later <---------------Once a stable PT of 1 1/2 - 2 x control or INR of 2 to 3
is established, PT's may be obtained every 2 weeks,
then 3 weeks, then monthly.
Notes:
1.Baseline PT taken on day 1 (after 4-5 days of
Heparin) is necessary to ID a patient who is
debilitated or malnourished and who as a result
may have low clotting factors and prolonged PT.
This patient may be sensitive to effects of
Coumadin.
2.Before 2nd dose, have PT drawn to check for
sensitivity.
ALTERNATIVE
CONVERSIONS
Start Coumadin 15 mg/day. When PT starts to move
out, give 2.5 (times number of days to move out) for
daily dose.
Minidose Heparin
5000 units SQ Bid
ANTICOAGULANT INR RECOMMENDATIONS FOR VARIOUS SITUATIONSProphylaxis of venous thrombosis in high risk surgical procedures: 2-3
INR.
Treatment of pulmonary embolism: 2-3 INR.
233
Prevention of venous thrombosis: 2-3 INR.
Mechanical prosthetic heart valves at high risk: 2.5-3.5 INR:
Prevention of embolization in acute myocardial infarction: 2-3 INR.
Prevention of embolization in tissue heart valves: 2-3.
Prevention of embolization in valvular heart disease: 2-3 INR.
Prevention of embolization in atrial fibrillation: 2-3 INR.
Prevention of embolization in patients with recurrent systemic embolism: 23 INR.
BLEEDING DISORDERSKEY QUESTIONS IN HISTORY TAKING:
1....Have you ever had excessive bleeding during surgery?
2....Have you ever had excessive bleeding during dental extractions?
3....Have you had excessive menstrual bleeding?
4....Do you get spontaneous bruises or nose bleeds?
5....Do you have a family history of bleeding problems?
6....Have you had liver disease, renal disease, collagen vascular disease, cancer, nutritional
deficiencies, Cushing's disease or dysproteinemias?
7....Have you ever taken anticoagulant drugs?
Normal PT, PTT and bleeding time do not eliminate the possibility of a significant bleeding
disorder. Von Willebrand's disease is the disorder found most commonly in combination with
normal results on screening. Diagnosis requires von Willebrand's factor antigen assay and ristocetin
cofactor assay. In some cases electrophoretic analyses of the multimer, that constitute Von
Willebrand's factor proteins, is also needed. Initial diagnosis of Von Willebrand's disease in
adulthood is not uncommon, especially if the patient has not undergone any surgical procedures in
the past. MILD Hemophilia A or B may also present in adulthood. Mild cases may not adversely
affect the PTT. In fact, a PTT may be normal even in some patients who have factor VIII or IX levels
as low as 20% of normal.
Less common conditions that may be missed when screening tests are normal are
afibrinogenemia, hypofibrinogenemia, dysfibrinogenemia, factor XIII deficiency and inherited
qualitative platelet defects.
ISOLATED PTT ELEVATION:
A....Poor collection of venous blood with some clotting present.
B....Lupus anticoagulant. (Mixing the patients plasma with normal plasma doesn't correct the
prolonged PTT in patients with lupus inhibitors. Patients with lupus anticoagulant usually do not
experience bleeding complications, but one of the most common clinical manifestations is
thrombosis.
C....Factor XII deficiency, high molecular weight kininogen, or prekallikrein can cause PTT
prolongation, but these patients do not have a significant hemostatic defect.
D....Hemophilia A & B
E....Von Willebrand's disease
F....Acquired Factor VIII inhibition, and circulating anticoagulants may cause significant bleeding
problems.
ISOLATED BLEEDING TIME ELEVATION:
A....Thrombocytopenia
B....Von Willebrand's disease
C....Medications such as alcohol, antihistamines, beta lactam antibiotics, cardiovascular agents as
calcium channel blockers, disopyridamole, quinidine and NSAIDS.
D....Faulty testing technique.
ISOLATED PT PROLONGATION:
A....Deficiency of vitamin K-dependent factors (factors II, VII, IX, and X, which result from poor
nutrition, therapy with warfarin or liver disorders).
B....Acquired coagulation factor inhibitors are seen rarely in patients with lymphoma or collagen
vascular disease and can lead to prolongation of the PT.
BLOOD TRANSFUSION COMPLICATIONSBlood transfusion complications can be due to hemolytic reactions, non hemolytic reactions,
transfusion reactions associated with anti IgA antibodies, delayed hemolytic transfusion
234
reactions, febrile transfusion reactions, urticarial transfusion reactions, circulatory overload, and
infectious contamination of donor blood.
ACUTE HEMOLYTIC REACTIONS: These are usually due to ABO incompatibility. These may
occur after infusion of RBCs, white cells, platelets or fresh frozen plasma. In most cases, the
donor will have an A or B antigen on the RBCs. Other hemolytic causes include patient
antibodies to donor Duffy, Kidd, and Kell RBC antigens which will cause a hemolytic anemia.
Females are more at risk for transfusions reactions since they become sensitized through
pregnancy and blood transfusions secondary to obstetrical complications. Age also is a risk
factor because older patients receive more transfusions. Hemolytic transfusion reactions
include pain at the site of infusion, fever, chills, chest, back and abdominal pain, apprehension,
nausea, flushing and dyspnea. The patient may develop hypotension, hemoglobinuria, renal
failure, and bleeding secondary to DIC. The severity of the reaction is proportional to the amount of
blood the patient has received. Therefore, the transfusion should be stopped immediately when
suspected. The patient should be given generous amounts of IV normal saline and furosemide
to increase renal cortical blood flow, keeping the urine output at 100 ml/hour. If hypotension does not
respond to hydration, dopamine may be started at a low dose of less than 2ug/kg/min in an attempt
to increase renal blood flow. The use of heparin for DIC is controversial. The blood bank
should be notified immediately. Blood samples are drawn from the recipient and the serum is
checked for a pinkish or red color which would indicate hemoglobin, and a direct Coomb's test.
DELAYED HEMOLYTIC REACTIONS: Usually occur about 5-7 days after transfusion, but
occasionally may be seen up to 3 weeks after transfusion. These are usually asymptomatic, but
can be quite severe with the symptoms resembling acute hemolytic reactions. Most of these are
due to exposure to a previous antigen from pregnancy or transfusion. The antibody that is produced
is usually below detectible limits. These antibodies include anti-Fy, anti-E, anti-Jk, anti-C, antiD and anti-K. No specific treatment is usually needed for delayed hemolytic disease.
URTICARIAL REACTIONS: Occurs in about 2% of transfused patients. These patients are treated
by stopping the transfusion. There is no evidence of acute hemolysis and the urticaria are due to a
reaction to plasma proteins. For prevention, these patients are treated with antihistamines and
washed RBCs.
ANAPHYLACTIC IGA DEFICIENT REACTIONS: These produce sudden onset respiratory distress,
shock and urticaria. They may also develop flushing, back pain, hypotension, chest and abdominal
pain, hives, and nausea. They are rare and are usually found in patients who are IgA deficient and
have formed anti-IgA antibodies during prior transfusion or pregnancy. The anaphylaxis usually
begins before the patient has received 10 ml of blood. These patients are treated with IV
epinephrine .5 mg 1:10,000 every 5-10 minutes as needed, fluids, steroids and dopamine if shock is
present. To prevent future episodes, autologous blood, washed RBCs or RBCs from an IgA deficient
donor should be given.
TRANSFUSION ASSOCIATED ADULT RESPIRATORY DISTRESS SYNDROME: This disorder is
clinically similar to fluid overload, but occurs less commonly. It causes dyspnea by 6 hours,
hypotension, normal pulmonary capillary wedge pressure, bilateral pulmonary infiltrates and
fever. The patients usually recovers rapidly within 24-48 hours. It is usually due to an anti white
cell antibody in the donor blood of a multiparous female. This antibody reacts with an antigen on the
patient's white cells with subsequent leukoagglutination and obstruction of blood flow. There also
is a release of toxic granulocyte products that can cause capillary vasoconstriction producing
increased pulmonary vascular resistance. Confirmation of this disorder requires a search of the
donor plasma for antigranulocyte and/or antilymphocyte antibodies which is time consuming. The
treatment is supportive, with many patients needing a ventilator with positive end expiratory
pressure, furosemide and dopamine. Some patients may also need large doses of
methylprednisolone sodium succinate 30 mg/kg given once or twice. Prevention is with leukocyte
filters and washed RBCs. FLUID
OVERLOAD: Fluid or circulatory overload can cause a dry cough, tightness of the chest and acute
pulmonary edema. It is fairly common, especially in infants and the elderly. Treatment
includes pretreatment with furosemide and slowing the transfusion to about 1/2 unit of packed RBCs
given over 4 hours or about 100 ml/hour. BACTERIAL
CONTAMINATION OF THE DONOR BLOOD: This is a serious consequence of blood transfusions
that can have a high mortality with death occurring within 6-12 hours. The patient presents with fever,
chills, dyspnea, nausea, vomiting and hemoglobinuria. Gram negative rods are commonly involved,
since they can grow at cold temperatures. Yersinia enterocolitica has been very common, but
clinically is rare. It can be diagnosed by obtaining a gram stain of the donor blood obtained from the
blood bag.
FEBRILE TRANSFUSION REACTIONS: Febrile reactions are characterized by chills, fever,
flushing, tachycardia, and headache that starts within one hour after transfusion begins, and may last
235
for 8-10 hours. It has a frequency of about 1% of all transfusions. Febrile reactions are usually due
to antibodies toward donor white cells, with a history of previous transfusion or pregnancy. The
blood should be stopped immediately, because acute hemolytic transfusions reactions can also
produce fever. In febrile reactions there is no hemolysis. If no hemolysis is found, the treatment
is supportive with antipyretics and use of leukocytic filters and washed RBCs.
VIRAL HEPATITIS: NON-A, NON-B HEPATITIS: Less than 1% of transfused patients will develop
viral hepatitis with a risk of infection of 0.1%/unit transfused. Non-A, Non-B is the most common
cause of post transfusion hepatitis (90%). The duration from exposure to seroconversion varies
between 6 weeks to 1 year. Clinically, the patient has elevation of liver enzymes and a positive
hepatitis C antibody. Other causes of hepatitis must be ruled out as alcoholic hepatitis, hepatitis
A, B, and D, and Epstein-Barr and CMV hepatitis. Chronic hepatitis secondary to non-A, non-B
hepatitis develops in 50%, cirrhosis (20%), and hepatocellular cancer in 5%. If a patient has been
accidentally exposed to a blood transfusion with a test suggestive of non-A, non-B hepatitis, immune
serum globulin should be given as some studies have suggested protection.
HEPATITIS B: Hepatitis B causes about 10% of post-transfusion hepatitis. The incubation period
is about 3 months. The sequelae are similar to non-A, non-B hepatitis. Treatment is with hepatitis
B immune globulin, 5 ml, + hepatitis B vaccine given IM in the deltoid at 0, 1, and 6 months.
CMV INFECTION: This infection occurs when there is infusion of infected white cells (usually B
lymphocytes). The primary risk is when immunosuppressed transplant patients and premature
neonates are infected. The mortality in transplant patients is about 60-85%, while neonates may
have a mortality of 40% and a morbidity of 50%. Because of this high morbidity and mortality, all
CMV negative transplant patients, and all CMV negative premature neonates weighing less than 1250
grams, should only be given CMV negative blood if needed. The clinical symptoms consist of
hepatitis, pneumonia, hepatosplenomegaly and production of cytopenias. Adults can develop
colitis, esophagitis, gastritis, arthritis, retinitis and encephalitis.
OTHER TRANSFUSIONS COMPLICATIONS: Other rare post transfusion complications include
malaria, post-transfusion purpura, Graft-versus-host disease, leukemia (HTLV I) and paroxysmal
nocturnal hemoglobinuria.
Medical Evaluation of Surgical Risk
Operative Risk Profiles
Typical: 0 - 0.01%
Low but increased: 0.01 - 0.9%
Significant: 1 - 5%
Moderate: 5 - 10%
High: 10 - 20%
Very high: >20%
Periop deaths = .3%
10% during induction of anesthesia
35% intraop
55% within 48 hrs after surgery
Causes of periop deaths:
1. Inadeq ventilation
2. Aspiration
3. Arrythmias
4. Drug-related myocardial depression
5. Refractory hypotension
Causes of postop deaths:
1. Pneumonia (20%)
2. Non-pulm infections (peritonitis, G sepsis)
3. Cardiac arrest
4. Pulmonary embolism
5. Renal failure
6. Hypovolemic shock
7. Inoperable cancer
8. Stroke
Increased risk for periop mortality:
1. Age
2. Emergency surgery
3. Cancer
236
Anesthesia:
spinal -> wide fluctuations in blood pressure,
greater anxiety, less airway and ventilatory
control, peripheral vasodilatation
ASA Classification of Periop Morbidity
and Mortality:
I - normal
II - mild disease
III - severe disease limiting activity but not
incapacitating
IV - severe incapacitating, a constant threat
to life
V - expected to die in 24 hours
Periop Morbidity & Mortality
Detsky Modified Multifactorial Index
Variable Points
------------Coronary artery disease
MI within 6 mos
10
MI >6 mos
5
Canadian Cardiovascular Society angina
Class III
10
Class IV
20
Unstable angina within 6 mos
10
Alveolar Pulmonary Edema
within 1 week
10
ever
5
Valvular disease
suspected critical aortic
stenosis
20
Arrhythmias
Rhythm other than sinus or
sinus+APC's on last
5
pre-op EKG
More than 5 VPB's at any
time prior
to surgery
5
Poor medical status
5
Age over 70
5
Emergency operation
10
Detsky Modified MFI
Pulmonary Risk:
Less than cardiovascular risks.
Primary risk is COPD.
Restrictive disease much less worrisome.
Need to produce a good cough.
Factors that increase risk of postop pulmonary complic:
1) smoking hx
2) obesity
3) age>60 years
4) length of anesthesia > 3 hours
5) type of surgery (upper abdominal and thoracic greatest
risks)
PFT are most reliable predictor of operative risk.
Obtain on pts with pulmonary symptoms (dyspnea,
chronic cough) and those undergoing thoracic operations.
Low risk: FEV1 > 2,000 ml
Medium risk: FEV1 1,000 ml to 2,000 ml
High risk: FEV1 < 1,000 ml (might require prolonged
respiratory support postop)
FEV1 (% of pred) < 75% assoc w/ incr rate of pulm
complic
MVV (maximal voluntary ventilation) < 50% pred -
237
serious operative risk
On ABG an incr pCO2 may indicate a pt who will be
difficult to wean off a ventilator
Preop Preparation:
Stop smoking at least 1 week prior to operation (2 months is
better)
If signs of reversible airway disease (15% improvement in
FEV1 after bronchodilators) then consider theophylline or
aerosilized bronchodilator
Postop:
Incentive spirometry every few hours
Early mobilization
Peak incidence of post-op MIs: 3rd day postop - can
be silent secondary to analgesics
Surgery post-MI:
3 months - risk=30%
>=6 months - risk=5%
Risk factors for CAD:
age>70, DM, HTN, LVH, PVD,
carotid artery disease
CHF:
2% in pt with no prior hx of CHF
6% in pt with h/o CHF but no current evidence of
CHF (on CXR or exam)
>30% in pts with preop S3 gallop or JVD
2 peaks of occurrence:
1) immediately post-op
2) 24-48 hours later (secondary to fluid mobilization)
Arrhythmias:
Generally do not pose a significant hazard for periop morbidity or mortality.
SVT occurs in about 4% of postop patients - has a high
morbidity - should search for CHF, MI, pericarditis, infection, hypoxemia, acidosis, hypokalemia,
anemia or aggravating meds (ie. epinephrine). Resolves spont in 40%, responds to meds in 47%,
needs electr CV in 6%.
Valvular Heart Disease:
Most murmurs benign. Greatest risk with AS.
Significant stenosis or regurgitation of mitral or aortic
valves are each associated with a 20% incidence of new
or worsening CHF in the postop period.
If not sure can treat with antibiotics for endocarditis
prophylaxis and w/u valves afterwards.
HTN:
mild is not a surgical risk factor. Risk only increases with
diastolic bp>110. Can exhibit exaggerated fluctuations in bp
(hyper and hypo) periop.
Continue anti-HTN meds until AM of surgery - should be
restarted postop. Can use IV, IM or SQ forms if pt can't take
pos (hydralazine, labetalol, Inderal, Procardia, Vasotec,
Cardizem). IV nitroprusside for control of severely elevated bp.
Dental:
238
if anticoag then keep PT<20 sec - can continue AC. Can use
local epinephrine and atropine in small quantities. Endocarditis
prophylaxis in patients with valve disease.
Anemia:
usually treat to Hct >= 30 (unless chronic - then >=20) transfuse at least 24 hrs prior to surgery
Platelets:
>=100,000 for major surgical procedures
>=30,000 for minor operations
Can transfuse - each unit will raise platelet count by about
10,000
Platelets can also be dysfunctional with a normal count - can
see this by prolonged bleeding time (but may not correlate with
surgical blood loss). Common causes are drugs (ie. ASA,
NSAIDS) and von Willebrand's disease. Should D/C ASA 5-7
days prior to surgery and NSAIDS 1-2 days prior.
PT/PTT:
if elevated are the result of a drug or disease
PT - elev by coumadin - need to stop 3-4 days prior to the
surgery (if elective). If urgent can give Vit K (10 mg SQ &
repeat 12 hrs later) &/or transfuse with FFP. Vit K will interfere
with coumadin for days afterwards where FFP will not.
- also elevated by chronic liver disease, malabsorb of Vit K and
DIC.
PTT - elev by heparin - short half life. If need to reverse effects
immed then can use protamine.
- also elevated by hemophilia and lupus anticoagulant
Tight AC control: for pts with MV prosthesis, dialysis pts with
shunts prone to clot off and pts prone to embolization. Stop
Coumadin 3-4 days preop - start full-dose heparin - stop
heparin 6-12 hrs pre-op and restart postop when bleeding risk
is minimal (can also start at half-dose and then increase to
full-dose several days later).
Loose AC control: for pts with AoV prosthesis, remote history
of TIA or DVT. Stop Coumadin 3-4 days preop and restart
several days postop.
Thromboembolism Prophylaxis in Surgical Procedures
-------------------------------------------------Type of Surgery Prophylaxis Regimen*
--------------------------------------------------------General Low dose heparin 5,000u sq bid-tid
Urology** Low dose heparin 5,000u sq bid-tid
Gynecology** Low dose heparin 5,000u sq bid-tid
Neurosurgery
Extracranial Low dose heparin 5,000u sq bid-tid
Intracranial Pneumatic compression
239
Orthopedic (hip Two step warfarin Begin 10 d before
surgery and knee surgery - keep PT
reconstruction) 2-3 sec prolonged
Give twice preop
dose postop- keep
PT 1.5x control
Adjusted dose Begin 2 d before
heparin surgery at 3,500
units sq tid.
Check PTT 6 hrs
after AM dose and
incr or decr by
500-1000 units to
keep PTT 30-40 s.
Dihydroergotamine- 2 hrs preop and
heparin (Embolex) bid postop
Dextran-40 Give 10 ml/kg as 12 hr infusion on day of surgery,
followed by 7 ml/kg/d as constant infusion x 5 days
Use cautiously w/ h/o CHF
Pneumatic compression
* duration of prophylaxis should be 5-7 days or until pt is
ambulatory
** for open prostatectomies and for gyn cancer
operations consider stronger prophylaxis (ie one of the
orthopedic regimens)
Postop DVT occurs in about 25% of above operations.
Incidence of fatal pulmonary embolism 1-5%:
Diabetes:
most common postop complication besides hyperglycemia is
infection (wound or UTI) and cardiovascular events (MI or
CHF).
Pts on insulin as outpts should receive some insulin preop but
at a reduced dose. One regimen is giving half the pts normal
intermediate acting insulin preop and supplementing with short
acting insulin postop. If insulin is given preop then pt should be
on a glucose containing infusion (ie D5W at 125 ml/hr).
If on oral agents then can be maintained with possible periop
insulin if glucose is >250-300. Long acting oral agents should
be stopped 3 days preop to prevent intraop or periop
hypoglycemia and shorter acting agents should be stopped the
day before surgery.
Greatest risk occurs in pts with chronic liver
dysfunction, especially those with progressive hepatic
failure.
Antibiotics for Endocarditis Prophylaxis
Site Std Regimen Reg for PCN allergy
--------------------------------------------------------Dental and oral/ PCN V 2.0gm po
Erythromycin 1.0g
respir tract 1 hr before then po 1 hr before
1.0gm 6 hrs after then 500mg 6 hrs
after
GI and GU tract Ampicillin 2.0gm
240
Vancomycin 1.0gm
IM or IV + Gent IV over 1 hr +
1.5 mg/kg IM or Gent 1.5 mg/kg IM
IV given .5-1 hr or IV given 1 hr
before then 8 hrs before then 8 hrs
after after
POISONING
[Initial management] Provide airway, ventilation and vital signs. Protect yourself from
organophosphate & carbamate insecticides and cyanide. If the patient is unconscious and
convulsing, give Dextrose, and naloxone (2 mg in child or adult. If there is ingestion of
propoxyphene, pentazocine or butorphanol then more than 2 mg may be required), and Oxygen. If
the patient is alcoholic, give Thiamine 100 mg IV or IM before dextrose. If unable to give drug IV
then may give atropine, epinephrine, lidocaine and naloxone through an endotracheal tube.
Diazepam can be given rectally. SEIZURES: If the seizures are due to theophylline then they may
be refractory to usual therapeutic medications, and the patient may need general anesthesia.
Seizures due to hypoglycemia must be treated immediately with glucose. Seizures due to
isoniazid will respond to pyridoxine. Seizures related to anticholinergic agents may respond to
physostigmine, if the usual anticonvulsants are not effective. Hemodialysis may be needed for
seizures due to salicylates or lithium. Be aware that alcoholic withdrawal may cause seizures.
Tricyclic seizures may need bicarbonate. INVESTIGATIONS: EKG (for dysrhythmias or conduction
defects from tricyclics). Chest x-ray (for aspirations & non cardiogenic pulmonary edema).
Measure the anion gap and electrolytes (salicylates, methanol, ethylene glycol, carbon
monoxide, toluene, cyanide, and hydrogen sulfide). Get serum osmolality & calculate the osmolality
(2x sodium) + (glucose/18) + (BUN/2.8). The difference between these two is the osmolar gap.
If more than 10 mOsm/liter then think methanol, ethylene glycol, or isopropanol poisoning. UA (for
crystals of ethylene glycol) Qualitative drug screening of urine, serum & possibly gastric
contents). Specific drug levels are useful in acetaminophen, anticonvulsants, digoxin, aspirin,
ethanol, methanol, ethylene glycol, iron, isopropyl alcohol, lithium & theophylline overdoses.
Contact the poison center. For salicylates & ethanol treat with urine alkalinization &
hemodialysis. For methanol & ethylene glycol treat with hemodialysis. Breath analysis will
reveal clues. Petroleum distillates have a characteristic odor, fruity odor (ketoacidosis &
ketones of ethanol and isopropyl alcohol), almond odor (cyanide), garlic odor (arsenic or
organophosphates), glue odor (chronic toluene abuse) and rotten egg odor (hydrogen sulfide or
disulfiram). Do a physical exam to look for focal neurological signs (CVA, subdural hematoma),
nuchal rigidity (meningitis), needle tracts (arms, feet, groin, under the tongue, neck,
supraclavicular), drugs in the rectum, vagina & swallowed drug packets, and cardiac arrest
(cocaine). Get family members to bring in prescription bottles and call the pharmacy to get a list of
drugs. Search the clothing, home & garbage. Look for drug paraphernalia. ANTIDOTES:
1....Benzodiazepines [Flumazenil] 0.2 mg over 30 seconds. If ineffective after 30 seconds give .3 mg
over 30 seconds. If no response after 30 seconds give .5 mg over 30 seconds at 1 minute
intervals up to a total dose of 3 mg. Flumazenil should not be given if benzodiazepines are being
given for convulsions or there is simultaneous ingestion of tricyclics. 2....Tricyclics
antidepressants [Bicarbonate] 3....Digitalis [Digoxin specific antibody fragments] If the amount
ingested and the serum digoxin concentration are both unknown then given 10-20 vials IV if there is
a life threatening dysrhythmia. If the number of milligrams is known then divide that by 0.6 to
ascertain the number of vials to give OR if the serum digoxin concentration is known, the number
of vials = the digoxin concentration in ng/ml x 5.6 x weight in kg/600. 4....Opiates [Naloxone]
Start at 2 mg IV. Less may be needed to prevent withdrawal symptoms. More may be needed
if synthetic narcotics have been taken as propoxyphene, pentazocine & butorphanol.
5....Anticholinergic agents [Physostigmine] 1-2 mg IV over 5 minutes. May be useful to treat
tachydysrhythmia or seizures. Should only be used for severe delirium. 6....Methanol, ethylene
glycol [Ethanol] Give loading dose of 10 ml of 10% solution /kg of body weight. Maintenance dose
0.15 ml/kg/hr. If the patient is on dialysis, double the maintenance dose. Titrate to blood ethanol
level of 100 mg/dl. 7....Calcium channel blockers, hydrofluoric acid, and fluorides [Calcium] 1 g
calcium chloride given over 5 min by IV infusion with cardiac monitoring. Monitor the calcium level.
8....Organophosphate or carbamate insecticides [Atropine] Give an initial test dose of 2 mg IV.
Repeat in larger doses until there is drying of pulmonary secretions. 9....Isoniazid, hydrazine,
monomethylhydrazine in Gyromitra species mushrooms [Pyridoxine]. If the amount of ingestion is
unknown, start with 5 g IV. Overdose can cause neuropathy. If amount ingested is known then
given gram per gram equivalent of pyridoxine. 10....Beta blockers [Glucagon] Start with 5-10 mg IV.
ACETAMINOPHEN TOXICITYIf the patient is seen within 12 hrs of ingestion and is alert, ipecac 30 ml with fluids is given. Repeat
in 15 minutes or gastric lavage. Do not give charcoal or cathartics.
LAB: acetaminophen level 4 hrs post ingestion, liver tests, BUN, creatinine, glucose, PT.
241
THERAPY: Within 24 hrs of ingestion give Mucomyst loading dose of 140 mg/kg PO, diluted 3:1
in juice, soda or water, then maintenance of 70 mg/kg PO q4h for 17 doses. Beyond 24 hrs of
ingestion supportive therapy is indicated without Mucomyst. Avoid diuresis, sedatives and drugs that
are metabolized in the liver. Obtain daily labs for at least 4 days. For a prolonged PT give vitamin
K 10 mg IM. Refractory bleeding may require fresh frozen plasma. The toxic dose in adults is > 7.5
grams, with hepatic damage > 10 grams. The symptoms are malaise, nausea, vomiting and
sweating.
Use Rumack-Matthew Nomogram For Acetaminophen Overdose
CARBON MONOXIDE POISONINGCarbon monoxide is a colorless, odorless gas that is produced by the combustion an any type of
carbon containing material. It may be found in automobile exhaust, coal and gas heaters, and as a
toxin in smoke inhalation patients from fires. As many as 40% of smoke inhalation victims die of
carbon monoxide poisoning. The most common sources for exposure include automobile
exhausts, faulty space heaters and furnaces, fires, improperly vented wood stoves and
fireplaces, and engines used without ventilation in enclosed spaces. Cigarette smokers are
constantly exposed to CO and can reach a COHb level as high as 10% in chronic smokers. The
242
severity of carbon monoxide (CO) varies depending on the ambient CO concentration, the minute
ventilation of the individual, the health status of the individual, and the duration of exposure.
Equilibrium is reached much more rapidly in individuals who engage in vigorous physical
activity. Patients with underlying heart and lung disease cannot tolerate hypoxia produced by
even small or moderate CO levels. Infants are even more at risk to CO poisoning, because
fetal hemoglobin has a very high affinity for CO. CO poisoning occurs as a metabolic
breakdown product of methylene chloride. Fumes from paint strippers that contain methylene
chloride which are metabolized to CO. CO is rapidly absorbed through the lungs and is
eliminated by the lungs. It produces toxicity by hypoxemia, cellular asphyxia and ischemia. It
combines with hemoglobin with an affinity that is about 250 times that of oxygen. Therefore, even at
low levels of CO, there can be excessive saturation of hemoglobin binding sites, severely limiting the
blood's oxygen carrying capacity. As little as 0.1% CO (1000 ppm) can produce potentially fatal
50% saturation of hemoglobin at equilibrium. Exposure at workplaces is restricted to 50 ppm as
an eight hour average. Levels approaching 1500 ppm are considered dangerous to life. CO binding
to hemoglobin changes the shape of the oxygen hemoglobin dissociation curve, which causes a
left shift, resulting in further decreases of intracellular oxygen concentrations. Decreased cardiac
output occurs, probably due to intracellular binding of CO with myoglobin, causing decreased
output and hypotension. CO may also bind to intracellular cytochromes, which negates oxygen
utilization. The consequent tissue hypoxia results in ischemic and cellular damage, a
conversion to anaerobic metabolism, a reactive hyperglycemia secondary to liver glycogen
breakdown, and a severe metabolic acidosis. CO poisoning accounts for almost 50% of all fatal
poisoning occurring yearly in the USA.
CLINICAL: The symptoms depend on the carbon monoxide hemoglobin levels. Individuals with 010% usually have no symptoms. Levels of 10-20% will cause complaints of headache, tightness
across the forehead, dilation of cutaneous vessels, dyspnea with minor exertion and angina in
coronary artery patients. Patients with levels between 20-30% have throbbing headaches, dyspnea,
nausea, and dizziness. Levels between 30-40% have vomiting, very severe headaches, and poor
judgment. Levels between 40-50% have syncope, confusion, tachycardia, and tachypnea. Levels
between 50-60% have seizures, syncope and coma. Levels between 60-70 present in coma,
hypotension, arrhythmias or death. Levels greater than 70% usually leads to respiratory failure and
death. The diagnosis cannot be made unless you suspect exposure. If the patient is found in a
car with the engine running, your suspicion should be heightened, just as in finding multiple victims
in a common room. Cans of paint strippers and solvents that contain methylene chloride found with
the victim in a poorly ventilated room should also arouse your suspicion. Carbon monoxide may
commonly be diagnosed as influenza with headache, nausea and vomiting. Most textbooks stress
the cherry red coloration of the skin, but in reality this is very rare, and cannot be relied upon for
diagnosis. Sometimes retinal hemorrhages may be seen. Arterial blood gases usually show a
metabolic acidosis, due to the tissue hypoxia and ischemia. The arterial PO2 and the
calculated oxygen saturation is typically normal because dissolved oxygen in the serum is not
affected by CO. Pulse oximetry oxygen saturation usually remains normal despite severe CO
poisoning. The diagnosis is confirmed by the laboratory measurement of COHB levels in the blood.
High COHb levels greater than 20% indicate a dangerous exposure. Patients that seemingly
recover from CO poisoning may not recover fully. CO poisoning can produces a
neuropsychiatric syndrome days to weeks following recovery consisting of dull mentation, behavioral
changes, loss of memory, cognitive changes and garrulousness. Complications include
blindness, deafness, parkinsonism, seizures, incontinence, cortical blindness, aphasia, apraxia,
psychosis, cogwheel rigidity, rhabdomyolysis, myoglobinuria and renal failure.
DIFFERENTIAL DIAGNOSIS should include head trauma, hypoglycemia, meningitis, alcohol and
drug intoxication. Cyanide, hydrogen sulfide and other toxic gases should also be considered in
the differential.
TREATMENT: Treatment begins with the administration of 100% oxygen provided with a tight fitting
mask or a non-re breather mask with oxygen reservoir, or by an endotracheal tube at a flow of 10
liters/min. Hypotension is treated with 1-2 liters of crystalloid solution. Low potassium is frequently
seen and should be treated in order to avert cardiac arrhythmias. Patients with mild to moderate
metabolic acidosis (pH 7.2-7.3) should not be treated because the acidosis can facilitate oxygen
deliver to the tissues by moving the oxygen hemoglobin dissociation curve to the right.
Administration of 100% oxygen will also shorten the CO half life from 5 hours in room air to 40-80
minutes. With hyperbaric oxygen at 2-3 atmospheres, the arterial pO2 is raised as high as 2000
mm Hg and the COHb half life can be further reduced to 23 minutes. The indications for hyperbaric
oxygen include any one who has lost consciousness due to CO exposure or a symptomatic patient
with a COHb level extrapolated to 25% at the time of the initial exposure. Children with COHb levels
of 20% or higher at the time of exposure can be candidates. Pregnant patients exposed to COHb
levels as low as 20% are also candidates. If patients are treated by hyperbaric oxygen, urgency is the
key. Patients that were treated within 6 hours had a 13.5% mortality, while 30.1% died if treated later
than 6 hours.
243
CIGUATERA FISH POISONINGMany patients with Ciguatera fish poisoning that seek medical attention from symptoms of
gastroenteritis are missed. A patient that presents with nausea, vomiting, diarrhea, diaphoresis and
numbness and tingling, particularly around the mouth, may be mis-diagnosed as hyperventilation
syndrome plus viral gastroenteritis. Key points to differentiate Ciguatera fish poisoning from the
garden variety gastroenteritis are: Ciguatera fish poisoning produces a phenomenon known as
sensory reversal dysesthesia, whereby a patient perceives cold objects as warm and vice versa.
The second key point is that alcohol will produce a return of the symptoms or a worsening of the
symptoms. The third point is that Ciguatera fish poisoning will last for about 1-2 weeks and about
50% of patients will still have symptoms at 2 months. The neurologic symptoms persist
much longer than the gastrointestinal symptoms. Ciguatera poisoning is contracted by eating fish
that harbor the single cell toxic producing parasite, Gambierdiscus toxicus. There are more than 400
fish species that live around coral reefs and harbor the parasite. Gambierdiscus toxicus attaches
itself to marine algae, and small fish will eat the algae. Larger fish will eat the smaller fish and
thus a poisoning chain is set up. In particular, grouper, red snapper, amberjack, barracuda,
sturgeon fish, jack tuna, sea bass, moray eels and king mackerel are the common fish involved with
this infestation. The larger the fish, the larger the concentration of the poisonous toxin, and the
greater the magnitude of the symptoms. Fish under 5 pounds are relatively safer to eat than those
over 25 pounds. Ciguatoxin cannot be deactivated by cooking, freezing, drying, smoking,
marinating, salting, or pickling, and gastric enzymes and acids will not inactivate it. The toxin is
tasteless and odorless. The toxin doesn't cause any ill affects in the fish, even though there are
high concentration in the viscera such as the gonads and liver. Florida and Hawaii are common
states that have a higher incidence, but with modern transportation any state can be affected.
Ciguatera fish poisoning is endemic in tropical regions as the Caribbean and the Indo-Pacific
islands.
CLINICAL: Approximately 2-24 hours after ingesting the affected fish, nausea, vomiting, watery
diarrhea, abdominal cramps, myalgias and diaphoresis will begin. The abdominal symptoms usually
last about 3 days but can be longer. Eighty percent of patients will develop paresthesias of the
extremities, numbness and tingling around the mouth and hot and cold reversal as mentioned above.
The patient may also have dizziness, ataxia, pruritus, facial pain, rash, tremors, nuchal rigidity,
and rarely audio and visual perturbations, confusion and coma.
TREATMENT: Treatment is mainly supportive with IV fluids and electrolyte replacement. The
pruritus may be managed with terfenadine 60 mg bid. Amitriptyline, 25 mg bid may help the
pruritus and the dysesthesias. Mannitol 20%, 1 gram/kg given over 30 minutes may help in the
severe cases. The patient should be told to avoid alcohol and further fish ingestion.
Anaphylaxis
-Anaphylactic -- IgE-mediated
-Anaphylactoid -- not IgE-mediated
prob Complement mediated
Presentation
Airway: wheezing, stridor, laryngeal edema
Cardiac: incr vasc perm, circulatory collapse, hypotension
GI:incr motility from histamine, diarrhea
Skin: urticaria, flushing
Treatment
Airway -- intubate prn
Breathing -- ventilate prn, consider breathing treatments
Circulation - epinephrine
1:1000 1cc SQ or .3cc q5min
1:10,000 10cc IV .3-5cc
Antihistamines
H1 blockers -- 50-100mg diphenhydramine
H2 blockers -- cimetidine
Steroids
200 mg of Solu-Cortef
100 mg of Solu-Medrol
Consider
Phenylephrine drip
Levo drip
Epinephrine drip
DYE RXN: high prob of having another
reaction
244
SCABIESScabies is caused by a small female itch mite Sarcoptes var. hominis. The adult female measures
about 400 microns and is extremely difficult to see. It causes a significant amount of morbidity in the
family and also in nursing homes. The most frequent location of the rash is on the wrists and
hands followed by the extensor elbows, feet, ankles, penis, scrotum buttocks and axillae. Scabies
is usually acquired by sleeping with a person who is infested, or in the bed of an infested person.
The entire family can be affected. The mite is incapable of jumping or flying but can cover about
2.5 cm of warm skin per minute. The mite seems to be attracted to the skin by host odor and body
heat. The mite is transferred between hosts by direct contact, infested clothing and linens. Live
mites can be found from the dust of bedroom floors, mattresses, chairs, floors, curtains and dirty
laundry of nursing homes.
CLINICAL: The eruption consists of burrows, pustules, papules, nodules and occasionally
urticaria. Itching is extreme and usually occurs at night. The onset of symptoms usually are delayed
for several weeks after the first infestation. The pruritus is caused by sensitization to the mite.
Usually only a few mites are present with most patients having around 10. There are epidemics of
scabies which occur in cycles. The lesions are typically seen on the volar aspect of the wrists,
breasts, axillae, interdigital webs of the hands and genitalia. Females may have lesions around
the areolae of the nipples and male patients may have the lesions on the penis. In young
children, the palms and soles may be involved with vesicular and pustular lesions. In
immunosuppressed patients the lesions may occur on the face and scalp which are usually
spared except possibly in infants. The burrow is a 2-3 mm track, but may be difficult to see in about
a quarter of the patients. The mite, eggs and stool reside in this track which is formed by the
female mite tunneling under the stratum corneum epidermidis. The female mite in the burrow lays
eggs at about 2-3 per day for up to 2 months. The egg hatches in about 3-4 days. Only about
10% of the eggs will eventually become adults. As the larvae emerge after a few days from the
burrow, papules are formed around hair follicles which become pruritic. The larvae become adults
in about 10-14 days. The adult female burrows into the skin and is eventually fertilized starting the
entire cycle again. Continuous scratching can lead to thickening of the skin and nodule formation.
with hyperpigmentation. Some of these lesions become infected with group A beta-hemolytic
Streptococcus pyogenes or coagulase positive Staphylococcus aureus. Atypical presentations may
occur in two different forms: Scabies incognito and Norwegian scabies. Scabies incognito causes
a widespread non-inflammatory distribution due to previous use of topical corticosteroid
preparations. Norwegian scabies or crusted scabies is a rare presentation seen in
immunocompromised or neurologically impaired patients. Typical patient populations would
include the malnourished, mentally retarded, AIDS patients, leukemia, diabetes mellitus or those
receiving immunosuppressive therapy. In this form there is crusting of the face, scalp, hands, feet
and pressure bearing areas. Generalized body distribution may occur affecting even the nails. The
pruritus is minimal.
DIAGNOSIS: Diagnosis is made from the history of contact with an infested person along with the
typical presentation of lesions in the interdigital web spaces, axillae and genitalia. The patient
should be asked if anyone else in the household or nursing home is itching and scratching.
The definitive diagnosis depends on microscopic identification of the mite. Several non excoriated
lesions should be chosen and scraped with an #15 mineral oil impregnated scalpel. This debris is
then transferred to a slide with cover and viewed under the microscope. The mite, larvae, eggs and
excrement all may be seen.
TREATMENT: LINDANE: Lindane should not be used in pregnant patients, infants and those that
have excoriations. It is relatively safe when used appropriately. In older patients lindane is no
longer considered the first line treatment. Rare cases of seizures in neonates has occurred.
Lindane (1% gamma benzene hexachloride) is available as Kwell, G-well and Scabene. It should
not be applied to damp skin which will increase the absorption. Typically, 1 oz of lotion or cream
is applied from the chin down to the toes and is then showered off 8-12 hours later. This should
be repeated in one week in order to eliminate late hatching larvae. Lindane does not kill the eggs.
PERMETHRIN: Permethrin 5% cream is now considered the treatment of choice. It is available
as a 5% cream base known as Elimite. It was originally marketed as Nix, a 1% cream rinse.
Permethrin is often times effective when lindane fails. It is poorly absorbed and is rapidly
metabolized and excreted making it safer than lindane. It may safely be used in infants aged 2
months to 5 years of age. Permethrin 5% cream is probably the drug of choice if the patent is
pregnant. The cream is massaged into the skin from head to toe and left on the body for 8-12 hours.
A repeat application is given in one week. CROTAMITON: Crotamiton (Eurax) 10% cream or lotion
is applied from chin to toes for 8-12 hours for 5 nights. It is far less effective than the above two.
The cure rate is only about 50-66% that of lindane. It may used in children and pregnant or
lactating women. For itching, topical .1% fluorinated corticosteroid ointment may be used BID. The
pruritus often takes about 2 weeks to subside after the patient is treated with lindane or
permethrin. In severe cases a short course of prednisone, 40 mg daily, and tapered over 2-3
weeks may be necessary for refractory pruritus. All clothes that have been worn within 48 hours of
treatment along with bedclothes and towels must be machined-washed in hot water or dry cleaned.
Shoes should be placed in plastic bags for 1 week before these are worn again. Floors should be
swept, chairs and mattresses should also be cleansed, as it has been shown that the mite can live
245
for more than 2 days on floors and furniture. There should be simultaneous treatment of all members
of the household, sexual contacts and household guests that frequent the domicile.
ACUTE ARTHRITIS
Immediate Questions:
1. Is it really arthritis? When examining an individual with
"joint" pain, you will ask yourself a series of questions. First, does
the patient have arthritis, or some other form of musculoskeletal
pain? There are four categories of etiologies for "joint" pain.
A. Arthritis:
Hx- pain in the joint, or in the reference area of the joint;
pain will increase with any joint movement; that is, all
ranges of motion will cause pain.
PE- tenderness over "entire" joint, especially joint line;
swelling of "entire" joint, either soft tissue or bony; joint
effusion; limitation of and pain in range motion in all
directions.
B. Periarticular: (e.g., tendinitis, bursitis, ligamentous)
Hx- pain in or near the joint; usually localized to one
aspect of the joint; pain with certain movements of the
joint.
PE- localized tenderness and swelling, often along the
outline of the involved structures; no joint effusion; usually
normal passive range of motion, but decreased active
range of motion when the involved structure is moved.
C. Nonarticular: (e.g., fibrositis, endocrine/metabolic, myalgia)
Hx- pain unrelated to joint or joint movement; atypical
pain pattern.
PE- usually normal articular exam; often with relatively
normal physical exam.
D. Referred: (e.g., visceral, neurogenic, psychogenic)
Hx- pain following a dermatome or peripheral nerve
distribution; neurological symptoms; non-musculoskeletal
symptoms.
PE- neurological abnormalities: strength, sensation,
reflexes; non-musculoskeletal abnormalities.
Joint Aspiration:
Joint tap is needed to determine the etiology of acute arthritis. An
infection can destroy a joint, so treatment must be initiated
rapidly. future link to See pages (?) for information on joint
aspiration techniques.
Diagnostic Considerations for Acute Arthritis:
Acute arthritis is a serious condition. Failure to recognize and
treat an infection can lead to rapid joint destruction. The
disorders that require prompt, specific treatment are infectious
and crystal-induced arthritis. Pyogenic infections of the joints in
adults are seen primarily in the debilitated, the elderly and those
who are parenteral drug abusers. Among healthy adults with
acute monarthritis, the probability of nongonococcal joint sepsis
is estimated to be less than 10%. That is, other than GC
246
arthritis, infections are infrequent. Findings that suggest
gonococcal disease include a prodromal of myalgias, migratory
arthralgias, fever, dermatitis or tenosynovitis. These associated
findings occur in about 65% of patients.
Gram-positive organisms account for 80 to 90 percent of acute
nongonococcal infectious arthritis, and staphylococci are
responsible for the majority of those cases. Such infections
especially occur in rheumatoid joints, those patients
receiving corticosteroids and individuals with a prosthetic joint.
Gout
typically presents among men over age 45, (women usually do
not have gout until postmenopausal). Acute gouty arthritis is
typically an episodic, monarticular arthritis that develops rapidly
to exquisite pain, heat, erythema and swelling. Severe first
metatarsophalangeal arthritis (podagra) is common. The onset is
abrupt and may follow trauma, surgery or no discernible stimulus.
Fever (101 to 103deg.F) can be present.
Pseudogout
is a microcrystalline synovitis induced by crystals of calcium
pyrophosphate dihydrate and associated with calcification of
hyaline and fibrocartilage (chondrocalcinosis). More properly,
this disorder is named calcium pyrophosphate dihydrate (CPPD)
crystal deposition disease. Unlike gout, the large joints are
preferentially involved in CPPD crystal deposition disease,
especially the knee, (found in over half the cases). Involvement of
the shoulder, hip, wrist, elbow, and MCP joints also occurs.
Generally, episodes of pseudogout are less intense and more
protracted than those of gout. However, they also may mimic
gout in intensity, duration and joint involvement.
Pressure Ulcers in Adults:
Prediction and Prevention
The staging of pressure ulcers
recommended for use by this panel is
consistent with the recommendations of the
National Pressure Ulcer Advisory Panel
(NPUAP):
Stage I: Nonblanchable erythema of
intact skin; the heralding lesion of
skin ulceration. Note: Reactive
hyperemia can normally be expected to
be present for one-half to
three-fourths as long as the pressure
occluded blood flow to the area; it
should not be confused with a Stage I
pressure ulcer.
Stage II: Partial thickness skin loss
involving epidermis and/or dermis.
The ulcer is superficial and presents
clinically as an abrasion, blister,
or shallow crater.
Stage III: Full thickness skin loss
involving damage or necrosis of
subcutaneous tissue that may extend
down to, but not through, underlying
fascia. The ulcer presents clinically
as a deep crater with or without
undermining of adjacent tissue.
Stage IV: Full thickness skin loss
with extensive destruction, tissue
necrosis or damage to muscle, bone,
247
or supporting structures (for
example, tendon or joint capsule).
Note: Undermining and sinus tracts
may also be associated with Stage IV
pressure ulcers.
Staging definitions recognize these
limitations:
Assessment of Stage I pressure ulcers
may be difficult in patients with
darkly pigmented skin.
When eschar is present, accurate
staging of the pressure ulcer is not
possible until the eschar has
sloughed or the wound has been
dГ©brided.
The guideline is intended for clinicians
who examine and treat persons at risk of
developing pressure ulcers. These
clinicians include family physicians,
internists, geriatricians, dietitians,
occupational and physical therapists,
nurses, and nurse practitioners working in
a variety of health care settings such as
acute care, rehabilitation, geriatric
care, and home- and community-based
settings.
After an extensive review of the
scientific literature, the panel used the
following criteria to grade the evidence
supporting each recommendation:
A There is good research-based
evidence to support the recommendation.
B There is fair research-based
evidence to support the recommendation.
C The recommendation is based on
expert opinion and panel consensus.
Risk Assessment Tools and Risk Factors
Goal: Identify at-risk individuals needing
prevention and the specific factors
placing them at risk.
Bed- and chair-bound individuals or those
with impaired ability to reposition should
be assessed for additional factors that
increase risk for developing pressure
ulcers. These factors include immobility,
incontinence, nutritional factors such as
inadequate dietary intake and impaired
nutritional status, and altered level of
consciousness. Individuals should be
assessed on admission to acute care and
rehabilitation hospitals, nursing homes,
home care programs, and other health care
facilities. A systematic risk assessment
can be accomplished by using a validated
risk assessment tool such as the Braden
Scale or Norton Scale (reproduced here).
Pressure ulcer risk should be reassessed
periodically. (Strength of Evidence = A.)
All assessments of risk should be
documented. (Strength of Evidence = C.)
248
249
250
Pulmonary Bedside Reference
251
Central Line Placement
Site
252
cm insertion
.
Right IJ
Right SC
Left IJ
Left SC
(Ht (cm)/10) - 1 ~ 15 cm
(Ht (cm)/10) - 2 ~ 14 cm
(Ht (cm)/10)+2 ~ 18 cm
(Ht (cm)/10)+4 ~ 20 cm
Endotracheal Tube Placement
Lip Line @
23 cm in MEN
21 cm in WOMEN
Check CXR
Massive Hemoptysis (any of the below)
Massive Hemoptysis
200 - 300 cc in 12 hrs
400 - 600 cc in 24 hrs
16 - 25 cc/hr or
>= 100 cc in any 4 hr time period
Respiratory Distress associated with any volume of Hemoptysis
'7-3' - Rule for fluid monitoring
Initial PCWP Fluid
< 10 mmHg 200 ml in 10 minutes
10-15 mmHg 100 ml in 10 minutes
> 15 mmHg 50 ml in 10 minutes
Reaction Therapy
PCWP increases > 7 mmHg Stop
PCWP increases 3 - 7 mmHg Wait 10 minutes
Always > 3 mmHg Stop
PCWP increases < 3 mmHg More fluid
253
254
Guidelines For Fluid Challenges By CVP or PCWP
PCWP
PCWP
PCWP
PCWP
255
< 10 mmHg
10 - 15 mmHg
16 - 20 mmHg
> 20 mmHg
250 cc/hr
150 cc/hr
60 cc/hr
Reseal IV
Evidence Based Medicine Lectures
256
257
258
259
260
261
262
263
264
265
266
267
268
269
270
271
272
273
Worksheet for Using an Article About Therapy or Prevention
Citation:
_______________________________________________
_______________________________________________
_______________________________________________
Guide
Comment
s
п‚· Are the Results of the Study Valid?
1. Was the assignment of patients to treatment randomized?
[ ] Yes
[ ] No
[ ] Can't Tell
- was follow-up complete?
- were patients analyzed in the groups to
2. Were all patients who entered the trial properly
which they were randomized
accounted for and attributed at its conclusion?
(intention to treat analysis)?
[ ] Yes
[ ] No
[ ] Can't Tell
3. Were patients, their clinicians, and study personnel 'blind' to treatment?
[ ] Yes
[ ] No
274
[ ] Can't Tell
4. Were the groups similar at
the start of the trial?
- Baseline prognostic factors (demographics, co-morditity, disease
severity, other known confounders) balanced?
- If different, were these adjusted for?
[ ] Yes
[ ] No
[ ] Can't Tell
Cointervention?
Contamination?
Compliance?
5. Aside from the experimental intervention, were the groups treated
equally?
[ ] Yes
[ ] No
[ ] Can't Tell
6. Overall, are the results of the study valid?
[ ] Yes
[ ] No
[ ] Can't Tell
п‚· What are the Results
1. How large was the treatment
effect?
Absolute risk
reduction?
Relative risk reduction?
2.How precise was the estimate of the treatment
effect?
Confidence
intervals?
п‚· Will the Results Help Me in Caring for My Patients?
1. Can the results be applied to my
patient care?
Patients similar for demographics, severity, co-morbidity and other
prognostic factors?
Compelling reason why the results should not be applied?
[ ] Yes
[ ] No
[ ] Can't Tell
2. Were all clinically important outcomes
considered?
[ ] Yes
[ ] No
[ ] Can't Tell
Are substitute endpoints
valid?
3. Are the likely treatment benefits worth the potential harms and
costs?
[ ] Yes
[ ] No
[ ] Can't Tell
275
NNT for different
outcomes?
276
277
278
279
280
281
282
283
284
285
286
287
288
289
290
Worksheet for Using an Article About Assessing Diagnostic Tests
Citation:
_______________________________________________
_______________________________________________
_______________________________________________
Guide
Comment
s
п‚· Are the Results of the Study Valid
1. Was there an independent, blind comparison with a
reference standard?
Is reference standard used acceptable?
Were both reference standard and test applied
to all patients?
[ ] Yes
[ ] No
[ ] Can't Tell
2. Did the patient sample include an appropriate spectrum of
patients to whom the diagnostic test will be applied in clinical
practice?
[ ] Yes
[ ] No
[ ] Can't Tell
3. Did the results of the test being evaluated influence the decision to
291
"Verification" or "work-
up" bias?
perform the reference standard?
[ ] Yes
[ ] No
[ ] Can't Tell
4. Were the methods for performing the test described in sufficient
detail to permit replication?
Preparation of patient?
Performance of test?
Analysis and interpretation of
results?
[ ] Yes
[ ] No
[ ] Can't Tell
5. Overall, are the results of the study valid?
[ ] Yes
[ ] No
[ ] Can't Tell
п‚· What Were the Results?
How big or small is this LR?
Magnitude of charge from
pre-to post-test probability
1. Are likelihood ratios for the test results presented or
data necessary for their calculation provided?
Size of L.R
п‚· 0.1 or 10
large/conclusive
0.1-0.2 or 5п‚· moderate
10
0.2-0.5 or 2-5
small but sometimes
0.5-1 or 1-2
NB
small, rarely NB
[ ] Yes
[ ] No
[ ] Can't Tell
п‚· Will the results Help Me in Caring for My Patients?
1. Will the reproducibility of the test result and its interpretation be satisfactory in my
setting?
[ ] Yes
[ ] No
[ ] Can't Tell
2. Are the results applicable to my
patient?
Similar distribution of disease severity?
Similar distribution of competing diseases?
Compelling reasons why the results should not be
applied?
[ ] Yes
[ ] No
[ ] Can't Tell
3.Will the results change my
management?
292
Test and treatment
thresholds?
High or low LR's?
[ ] Yes
[ ] No
[ ] Can't Tell
Is target disorder dangerous if left undiagnosed?
Is test risk acceptable?
4. Will patients be better off as a result
Does effective treatment exist?
of the test?
Information from test will lead to change of Management
beneficial to patient?
[ ] Yes
[ ] No
[ ] Can't Tell
Worksheet for Using an Article About Prognosis
Citation:
_______________________________________________
_______________________________________________
_______________________________________________
Guide
Comment
s
п‚· Are the Results of the Study Valid?
1. Was there a representative and well-defined sample
of
patients at a similar point in the course of the disease?
Inclusion and exclusion
criteria?
Selection biases?
Stage of disease?
[ ] Yes
[ ] No
[ ] Can't Tell
2.Was follow-up sufficiently long and
complete?
Reasons for incomplete follow-up?
Prognostic factors similar for patients lost- and not lost-tofollow-up?
[ ] Yes
[ ] No
[ ] Can't Tell
3. Were objective and unbiased outcome criteria
used?
Outcomes defined at start of study?
Investigaotors 'blind to prognostic
factors?
[ ] Yes
[ ] No
[ ] Can't Tell
4. Was there adjustment for important prognostic factors?
[ ] Yes
[ ] No
[ ] Can't Tell
5. Overall, are the results of the study valid?
293
[ ] Yes
[ ] No
[ ] Can't Tell
п‚· What are the Results
1. How large is the likelihood of the outcome event(s) in a specified period of
time?
Survival
curves?
Confidence
intervals?
2. How precise are the estimates of
likelihood?
п‚· Will the Results Help Me in Caring for My Patients?
1. Were the study patients similar
to my own?
Patients similar for demographics, severity, co-morbidity, and other
prognostic factors?
Compelling reason why the results should not be applied?
[ ] Yes
[ ] No
[ ] Can't Tell
2. Will the results lead directly to selecting or avoiding therapy?
[ ] Yes
[ ] No
[ ] Can't Tell
3. Are the results useful for reassuring or counselling patients?
[ ] Yes
[ ] No
[ ] Can't Tell
Worksheet for Using an Article About Causation of Harm
Citation:
_______________________________________________
_______________________________________________
_______________________________________________
Guide
Comment
s
п‚· Are the Results of the Study Valid?
RCT, cohort, base-control?
1.Were there clearly identified comparison groups that were similar with
Other known prognosis
respect to important determinants of outcome, other than the one of
factors similar or adjusted
interest?
for?
[ ] Yes
[ ] No
[ ] Can't Tell
2. Were the outcomes and exposures measured in the same way in the
groups being compared?
294
Recall bias? Interviewer
bias?
Exposure opportunity
similar?
[ ] Yes
[ ] No
[ ] Can't Tell
3.Was follow-up sufficiently long and
complete?
Reasons for incomplete follow-up?
Risk factors similar in those lost and not lost to followup?
[ ] Yes
[ ] No
[ ] Can't Tell
4. Is the temporal relationship
correct?
[ ] Yes
[ ] No
[ ] Can't Tell
5. Is there a dose-reponse
gradient?
[ ] Yes
[ ] No
[ ] Can't Tell
Exposure preceded
outcome?
Risk of outcome increases with quantity or duration of
exposure?
6. Overall, are the results of the study valid?
[ ] Yes
[ ] No
[ ] Can't Tell
п‚· What are the Results?
1. How strong is the association between exposure and
outcome?
2. How precise is the estimate of
risk?
RR's or
OR's?
Confidence
intervals?
п‚· Will the Results Help Me in caring for My Patients?
1. Are the results applicable to my
practice?
Patients similar for demographics, morbidity and other
prognostic factors?
Are treatments and exposures similar?
[ ] Yes
[ ] No
[ ] Can't Tell
2.What is the magnitude of the
risk?
[ ] Yes
[ ] No
[ ] Can't Tell
295
Absolute rsk increase (and its
reciprocal)?
3.Should I attempt to stop the
exposure?
Strength of evidence?
Magnitude of risk?
Adverse effects of reducing
exposure?
[ ] Yes
[ ] No
[ ] Can't Tell
Worksheet for Using
Clinical Practice Guidelines
Citation:
_______________________________________________
_______________________________________________
_______________________________________________
Guide
Comment
s
п‚· Are the Recommendations Valid?
1. Were all important options and outcomes clearly specified?
[ ] Yes
[ ] No
[ ] Can't Tell
2. Was an explicit and sensible process used to identify, select, and combine evidence?
[ ] Yes
[ ] No
[ ] Can't Tell
п‚· 3. Was an explicit and sensible process used to consider the relative value of different outcomes?
[ ] Yes
[ ] No
[ ] Can't Tell
4. Is the guideline likely to account for important recent developments?
[ ] Yes
[ ] No
[ ] Can't Tell
5. Has the guideline been subject to peer review and testing?
[ ] Yes
[ ] No
[ ] Can't Tell
6. Overall, is the guideline valid?
[ ] Yes
[ ] No
[ ] Can't Tell
п‚· What are the Recommendations?
1. Are practical, clinically important, recommendations made?
[ ] Yes
296
[ ] No
[ ] Can't Tell
2. How strong are the recommendations?
[ ] Yes
[ ] No
[ ] Can't Tell
3. What is the impact of uncertainty associated with the evidence and values used in the
guidelines?
[ ] Yes
[ ] No
[ ] Can't Tell
п‚· Will The Recommendations Help You in caring for Patients?
1. Is the primary objective of the guideline consistent with your objective?
[ ] Yes
[ ] No
[ ] Can't Tell
2. Are the recommendations applicable to your patients?
[ ] Yes
[ ] No
[ ] Can't Tell
Worksheet for Using a Systematic Review
Citation:
_______________________________________________
_______________________________________________
_______________________________________________
Guide
Comment
s
п‚· Are the Results of the Study Valid?
1. Did the overview address a focused clinical question?
[ ] Yes
[ ] No
[ ] Can't Tell
2. Were the criteria used to select articles for inclusion appropriate?
[ ] Yes
[ ] No
[ ] Can't Tell
3. Is it unlikely that important, relevant studies were missed?
[ ] Yes
[ ] No
[ ] Can't Tell
297
4. Was the validity of the included studies appraised?
[ ] Yes
[ ] No
[ ] Can't Tell
5. Were assessments of studies reproducible?
[ ] Yes
[ ] No
[ ] Can't Tell
6. Were the results similar from study to study?
[ ] Yes
[ ] No
[ ] Can't Tell
п‚· What are the Results?
1. What are the overall results of the review?
2. How precise were the results?
п‚· Will the Results Help Me in Caring for My Patients?
1. Can the results be applied to my patient care?
[ ] Yes
[ ] No
[ ] Can't Tell
2. Were all clinically important outcomes considered?
[ ] Yes
[ ] No
[ ] Can't Tell
3. Are the benefits worth the harms and costs?
[ ] Yes
[ ] No
[ ] Can't Tell
Worksheet for Using an Article About An Economic Analysis
Citation:
_______________________________________________
_______________________________________________
_______________________________________________
Guide
298
Comment
s
п‚· Are the Results of the Study Valid?
Costs and outcomes for each
strategy?
1. Did the analysis provide a full economic comparison of health
Whose viewpoint?
care stragegies?
Cost-effectiveness/benefit/utility
study?
[ ] Yes
[ ] No
[ ] Can't Tell
Clinical effectiveness established?
2. Were the costs and outcomes properly measured and Costs measured accurately?
Data on costs and outcomes appropriately
valued?
integrated?
[ ] Yes
[ ] No
[ ] Can't Tell
3. Was appropriate allowance made for uncertainties in the
analysis?
Sensitivity analysis?
Statistical
significance?
[ ] Yes
[ ] No
[ ] Can't Tell
4. Are estimates of costs and outcomes related to the baseline risk in the
treatment population?
[ ] Yes
[ ] No
[ ] Can't Tell
What are the Results?
1. What were the incremental costs and outcomes of each strategy?
2. Do incremental costs and outcomes differ between sub-groups?
[ ] Yes
[ ] No
[ ] Can't Tell
3. How much does allowance for uncertainty change the results?
п‚· Will the Results Help in Caring for My Patients?
1. Are the treatment benfits worth the harms and
costs?
[ ] Yes
[ ] No
299
Strong dominance?
Weak dominace?
Non-dominance?
Incremental costeffectiveness?
Sub-group analyses by
risk?
[ ] Can't Tell
2. Could my patients expect similar health
outcomes?
Study patients similar to my patients?
Study clinical management similar to my local
practice?
[ ] Yes
[ ] No
[ ] Can't Tell
3. Could I expect similar
costs?
Study/local resource consumption
similar?
Study/local prices similar?
[ ] Yes
[ ] No
[ ] Can't Tell
Worksheet for Using an Article Reporting Variations in the Outcomes of Health Services
Citation:
_______________________________________________
_______________________________________________
_______________________________________________
Guide
Comment
s
п‚· Are the Results of the Study Valid?
1. Are the outcome measures accurate and comprehensive?
[ ] Yes
[ ] No
[ ] Can't Tell
2. Were there clearly identified sensible comparison groups?
[ ] Yes
[ ] No
[ ] Can't Tell
3. Were the comparison groups similar with respect to important
determinants of outcomes, other than the one of interest?
- Important factors
measured?
- Measures reproducible
and accurate?
- Groups similar for
important factors?
[ ] Yes
[ ] No
[ ] Can't Tell
4. Were appropriate analyses undertaken to reduce the effect of
dissimilarities between comparison groups?
[ ] Yes
300
- Multivariate analyses?
- Low risk sub-group
analyses
[ ] No
[ ] Can't Tell
5. Overall, are the results of the study valid?
п‚· What are the Results
1. How strong is the association between exposure and outcome?
2. How precise is the estimate of risk?
п‚· Will the Results Help Me in Caring for My Patients
1. Are the results applicable to my practice?
[ ] Yes
[ ] No
[ ] Can't Tell
2. What is the magnitude of the risk?
[ ] Yes
[ ] No
[ ] Can't Tell
3. Should I attempt to stop the exposure?
[ ] Yes
[ ] No
[ ] Can't Tell
301
Index (I/O’s ........................................................................... 42
'7-3' - Rule for fluid monitoring ............................ 24, 255
Abciximab ................................................................. 113
ABDOMINAL PAIN ................................................... 198
ABG ................................ 34, 66, 67, 101, 185, 228, 240
ABG’s in Pulmonary Embolism ................................... 66
ABORTION ................................................................. 35
abscess............................. 103, 148, 192, 199, 212, 220
Abscess .................................... 148, 194, 196, 207, 232
Accuracy of Pulse Oximetry........................................ 65
ACE.... 98, 105, 106, 107, 110, 111, 114, 120, 121, 122,
131, 138
ACE inhibitors ................................... 106, 110, 111, 121
acetaminophen ......................................... 233, 243, 244
ACETAMINOPHEN TOXICITY ................................. 244
Acid Base............................................................ 76, 185
Acid Base Algorithm.................................................... 76
Acid-Base........................................................ 57, 62, 81
acid-base disorders........................................... 101, 186
Acidosis................... 23, 81, 98, 105, 106, 107, 109, 221
ACIDOSIS............................................................. 13, 14
ACLS........................................................................... 13
Acquired Factor VIII inhibition ................................... 236
ACTH ........................................................................ 234
Actinomyces.............................................................. 148
ACUTE ABDOMEN................................................... 198
Acute arthritis ............................................................ 249
ACUTE ARTHRITIS.................................................. 248
ACUTE BLINDNESS ................................................ 205
ACUTE DYSTONIC REACTION............................... 206
ACUTE HEMOLYTIC REACTIONS .......................... 237
Acute Lung Injury ........................................................ 71
acute myocardial infarction ....................................... 236
Acute renal failure ..................................................... 221
Acute Renal Failure .................................................. 124
ACUTE RENAL FAILURE......................................... 104
ACUTE RENAL INSUFFICIENCY ............................ 131
Acute Respiratory Distress Syndrome ........................ 71
Acute Respiratory Failure ........................................... 82
acute tubular necrosis............................................... 107
ACUTE TUBULAR NECROSIS ................................ 108
Addison's ............................................................ 98, 212
adrenal ...................................................... 220, 221, 233
Adrenal insufficiency ......................................... 138, 233
ADRENAL INSUFFICIENCY .................................... 233
Advanced Cardiac Life Support .................................. 13
afterload ............ 106, 114, 118, 121, 122, 123, 131, 151
Afterload.................................... 118, 120, 121, 122, 123
AIDS.... 12, 135, 213, 214, 215, 216, 217, 222, 233, 247
Albumin ..................................................... 105, 107, 205
Albuterol.............................................................. 99, 146
Alcohol .............................................. 116, 202, 203, 207
Alcoholic............................ 119, 138, 201, 202, 203, 223
alcoholic withdrawal .................................................. 243
ALCOHOLIC WITHDRAWAL.................................... 203
Alcoholism......................................................... 101, 201
ALCOHOLISM .......................................................... 201
Algorithm..................................................................... 76
ALI............................................................................... 71
Allergic ........................................................................ 28
Alpha-1 antitrypsin .................................................... 145
Alpha1-Antitrypsin Deficiency ................................... 145
alpha-tocopherol ....................................................... 113
Alteplase ................................................................... 118
alveolar gas equation................................................ 185
alveolar ventilation ............................................ 185, 189
302
aminoglycosides ................................. 98, 101, 107, 226
Aminoglycosides....................................... 105, 108, 212
Aminophylline ............................................................. 22
amiodarone............................................................... 231
Amphotericin..................................................... 105, 108
amphotericin B.................................................. 101, 107
amyloidosis....................................................... 109, 135
Amyloidosis .............................................. 119, 138, 233
Anaphylactic ............................................................. 246
ANAPHYLACTIC IGA DEFICIENT REACTIONS ..... 237
Anaphylactoid ................................................... 216, 246
Anaphylaxis .............................................................. 246
anemia26, 110, 111, 116, 137, 186, 208, 209, 212, 215,
216, 220, 223, 233, 234, 237, 240
Anemia ............................... 28, 110, 201, 212, 217, 241
anesthesia ..... 28, 34, 35, 107, 220, 222, 223, 238, 239,
243
aneurysm.......................... 105, 108, 131, 152, 198, 206
ANF .................................................................. 107, 109
angina 24, 112, 113, 114, 115, 116, 119, 129, 130, 150,
239, 245
Angina ...................................................... 112, 113, 114
ANGIOGRAPHY....................................................... 201
Angioplasty ....................................................... 113, 121
anion gap...................................................... 62, 63, 109
Anion Gap................................................. 62, 74, 77, 81
Anion Gap Acidosis .................................................... 62
Anion Gap Gap..................................................... 75, 78
Anti-Arrhythmic Drugs ................................................ 14
ANTIBIOTICS ........................................................... 212
anticholinergic................................................... 222, 243
anticoagulant .................................................... 236, 241
ANTICOAGULANT INR RECOMMENDATIONS FOR
VARIOUS SITUATIONS- ..................................... 236
Anticoagulation ......................................................... 164
Anti-Coagulation ....................................................... 121
ANTICOAGULATION TREATMENT ........................ 234
Anti-Convulsant Agents ............................................ 208
anticonvulsants......................................... 132, 212, 243
ANTIDOTES ............................................................. 243
Anti-hypertensives .................................................... 111
Anti-Oxidants ............................................................ 116
Antiretroviral ............................................................. 216
anuria.......................................................... 26, 108, 221
AORTIC DISSECTION ..................................... 131, 136
Aortic stenosis .......................................................... 138
Aortic Stenosis.......................................................... 119
AORTOGRAPHY...................................................... 137
APGAR ................................................................. 35, 36
ARDS.................................................. 71, 124, 148, 202
ARF .............................................................. 82, 95, 105
Argyle-Robinson ......................................................... 33
Arrhythmia ................................ 121, 125, 138, 148, 207
Arrhythmias ...................................... 120, 124, 239, 240
Arterial Blood Gas Diagnostic Worksheet .................. 81
Arterio-venous malformation .................................... 148
Arthrocentesis............................................................. 54
ASA ............................ 62, 113, 114, 116, 135, 239, 241
asbestos ........................................................... 195, 196
Ascites .............................................. 193, 196, 203, 205
Aspergillus ........................................................ 148, 149
Aspirin............................................... 113, 114, 116, 211
asthma.... 26, 28, 35, 117, 138, 146, 147, 148, 200, 233
asthmatics .................................................................. 11
atenolol ..................................................... 113, 117, 138
Atenolol..................................................... 113, 114, 203
Ativan ................................................................ 203, 208
AtivanВ® ..................................................................... 203
ATN........................................................................... 108
atrial fibrillation .......... 101, 121, 122, 206, 231, 233, 236
Atrial Fibrillation .................................................. 18, 211
Atrial Flutter................................................................. 18
Atrial natriuretic factor ............................................... 107
Atrioventricular (AV) Heart Block during Anesthesia .. 22
Atropine............................... 13, 14, 18, 22, 23, 112, 243
AtroventВ® .......................................................... 146, 147
AuriculinВ® ......................................................... 107, 109
autoimmune ................................ 62, 135, 212, 231, 233
AVM .................................................................. 148, 207
azotemia ................................... 105, 107, 108, 110, 111
Azotemia ........................................................... 109, 234
AZT ................................................... 214, 215, 216, 217
Babinski .............................................................. 39, 222
balloon pump ............................................................ 121
Bartter’s....................................................................... 62
belladonna .................................................................. 51
Benzodiazepine ........................................................ 208
Benzodiazepines....................................... 203, 208, 243
Beta Blocker................................................................ 18
Beta-Blockers................................................ 14, 22, 117
Bicarbonate................................................... 75, 78, 243
Bicarbonate Gap ................................................... 75, 78
Bicitra .................................................................. 35, 106
BLEEDING DISORDERS ......................................... 236
Bleomycin ................................................................. 197
BLOOD ............................................................... 52, 237
blood pressure ... 26, 112, 113, 117, 118, 121, 130, 131,
137, 198, 200, 222, 239
BLOOD TRANSFUSION COMPLICATIONS-........... 237
Blood Tube Type......................................................... 53
blue bloaters ............................................................. 146
BODY FLUIDS ............................................................ 52
bradyarrhythmia ........................................................ 141
Breasts............................................................ 26, 28, 29
Bretylium ..................................................................... 13
Brevibloc ........................................................... 117, 140
Bronchiectasis........................................................... 148
Bronchodilators ................................................. 144, 146
Bronchogenic Ca ...................................................... 149
bruises ...................................................................... 236
bumetanide ....................................................... 121, 122
Bumetanide......................................................... 99, 122
bypass surgery.......................................................... 121
CAD .................. 111, 112, 113, 114, 115, 116, 121, 240
CAGE........................................................................ 201
Calcitonin .................................................................... 98
Calcium ...... 14, 22, 23, 98, 99, 104, 105, 106, 110, 113,
114, 121, 139, 228, 230, 243
Calcium Antagonists ........................................... 14, 114
calcium channel blockers.................. 107, 131, 138, 236
Calculated Na Deficit ................................................ 103
Calorics ....................................................................... 33
captopril ............................................................ 114, 120
CAPTOPRIL.............................................................. 130
Carbamazepine......................................... 208, 209, 210
carbon monoxide .............................. 186, 212, 243, 245
Carbon monoxide...................................................... 245
CARBON MONOXIDE .............................................. 245
Carcinoid........................................................... 148, 149
Carcinoma......................................... 103, 105, 148, 232
Cardiac. 13, 14, 18, 28, 29, 56, 101, 112, 116, 117, 118,
119, 121, 124, 125, 129, 135, 138, 139, 140, 148,
207, 233, 238, 246
Cardiac Arrest ....................................................... 13, 14
Cardiac Dysrhythmias................................................. 18
303
cardiac output .. 106, 107, 117, 118, 121, 124, 129, 146,
212
cardiac tamponade ............................................. 51, 140
CARDIAC TAMPONADE.................................... 13, 135
Cardiogenic Shock ................................................... 124
cardiomyopathy ... 30, 31, 114, 119, 121, 122, 123, 138,
140, 202
Cardiomyopathy ................................. 31, 124, 127, 216
Cardiomyoplasty....................................................... 121
Cardiovascular...................... 28, 97, 116, 140, 221, 239
Cardioversion ....................................................... 18, 22
Carotid ................................................................ 22, 138
Carvedilol.................................................................. 120
Central Line Placement ............................................ 254
CENTRAL LINES ....................................................... 49
CENTRAL PONTINE MYELINOLYSIS..................... 204
Central retinal artery occlusion ................................. 206
Central retinal vein occlusion ................................... 206
Cerebellar ..................................................... 30, 39, 201
CEREBELLAR DEGENERATION ............................ 204
Chest Radiograph..................................... 111, 147, 149
Chest radiography .................................................... 149
chest x-ray .......................................... 49, 137, 167, 223
CHF ... 31, 105, 107, 117, 118, 119, 120, 121, 122, 123,
124, 129, 130, 147, 150, 192, 193, 196, 212, 221,
231, 233, 240, 242
Chloramphenicol............................................... 212, 213
Chlordiazepoxide...................................................... 203
Chloride responsive.................................................... 62
Chloride unresponsive................................................ 62
cholesterol ........................ 105, 108, 114, 115, 116, 202
Cholesterol ....................................... 112, 114, 195, 196
cholesterol embolization ........................................... 108
Chronic Bronchitis .................................................... 146
CHRONIC RENAL FAILURE.................................... 109
Chyliform Effusions................................................... 195
Chylous Effusions..................................................... 195
Cigarette ........................................................... 145, 245
CIGUATERA............................................................. 246
Ciguatera fish poisoning ........................................... 246
Cirrhosis ................................... 124, 193, 196, 201, 203
cisplatin............................................................. 101, 107
CLASSIFICATIONS OF DISSECTIONS .................. 136
Clonazepam ..................................................... 208, 209
Clonidine........................................... 130, 132, 139, 203
CLONIDINE .............................................................. 130
CMV INFECTION ..................................................... 238
CO poisoning............................................................ 245
Coagulopathy ........................................................... 221
cocaine ............................................. 130, 131, 202, 243
Cocaine .............................................................. 28, 115
COHb.......................................................... 81, 245, 246
collagen vascular disease ................................ 106, 236
Coma .................................................................. 38, 221
COMA................................................................. 33, 212
Confusion ......................................................... 201, 221
CONGESTIVE HEART FAILURE............................. 118
Contraindications to Thrombolysis ........................... 118
CONVERSIONS Equations ...................................... 104
COPD 31, 108, 114, 142, 143, 145, 146, 147, 184, 185,
204, 239
Cor pulmonale .......................................................... 146
coronary artery disease ... 112, 113, 114, 115, 139, 200,
212
Coronary Artery Disease .................................. 111, 116
cosyntropin ............................................................... 234
cough..... 26, 28, 32, 141, 145, 146, 150, 167, 193, 195,
237, 239
coumadin .................................................... 11, 113, 241
CPR .............................................................. 13, 14, 118
Cranial Nerves ................................................ 28, 30, 39
Creatine Kinase ........................................................ 116
creatinine clearance.................................................. 110
CREATININE CLEARANCE ..................................... 104
CRF................................................................... 109, 110
Cryptococcus ............................................ 149, 224, 234
CSF ANALYSIS ........................................................ 211
CT ...... 42, 110, 131, 135, 137, 141, 149, 200, 204, 210,
211, 223, 232
CVP............................... 49, 56, 126, 127, 192, 228, 257
CXR ........................ 33, 42, 50, 149, 151, 193, 240, 255
cyanide...................................................... 129, 212, 243
cyclosporin ........................................................ 101, 107
Cyclosporin ....................................................... 107, 108
Cytomegalovirus ............................................... 223, 234
DDAVP.............................................................. 110, 111
DDI............................................................................ 215
decubitus ulcers .......................................................... 34
Defibrillate ................................................................... 13
Defibrillation .......................................................... 18, 22
DELAYED HEMOLYTIC REACTIONS ..................... 237
delirium ............................... 45, 107, 202, 220, 233, 243
Delirium Tremens...................................................... 202
DELIRIUM TREMENS .............................................. 204
Delta Gap.............................................................. 75, 78
Depakote........................................................... 208, 209
Dermatomes ......................................................... 40, 41
Desipramine.............................................................. 203
Dexamethasone........................................................ 233
Dextran ..................................................................... 242
diabetes ..... 26, 108, 109, 110, 114, 115, 138, 212, 230,
234, 247
Diabetes...................... 28, 109, 112, 113, 115, 221, 242
DIABETIC KETOACIDOSIS ..................................... 227
diabetics............ 107, 111, 114, 116, 119, 121, 224, 230
dialysis ................ 99, 107, 110, 111, 136, 192, 241, 243
Dialysis...................................... 107, 109, 110, 193, 222
Diarrhea .................................................................... 234
Diastolic Dysfunction......................................... 119, 123
DIASTOLIC HEART FAILURE (DHF)....................... 122
Diazepam.................................................. 208, 209, 243
DIAZOXIDE............................................................... 130
DIC............................ 108, 151, 212, 221, 225, 237, 241
DIFFERENTIAL DIAGNOSES OF PULMONARY
ABNORMALITIES ................................................ 148
DIFFERENTIAL DIAGNOSIS DKA HNKC................ 227
Digibind ....................................................................... 23
Digitalis ................................... 18, 22, 23, 120, 121, 243
Digoxin .................................................. 18, 23, 122, 243
Dilantin .............................................. 204, 208, 209, 210
Dipstick ....................................................................... 54
Ditropan ...................................................................... 51
Diuretic................................................................ 97, 106
diuretics 97, 98, 101, 103, 107, 109, 120, 121, 122, 123,
130, 131
Diuretics ...... 62, 107, 110, 120, 121, 122, 129, 139, 147
DKA............................................. 62, 103, 227, 228, 229
DNR ................................................................ 11, 12, 43
Dobutamine............................................... 112, 113, 121
Dopamine............................................ 21, 107, 108, 109
Doxycycline............................................................... 197
DRAIN......................................................................... 50
DRESSLER'S SYNDROME...................................... 135
DRUG OVERDOSE .............................................. 13, 14
DTs ........................................................... 202, 203, 220
Dyspnea........................................ 11, 28, 148, 150, 193
EC-ASA..................................................................... 113
ECG ..... 98, 99, 101, 111, 112, 113, 114, 136, 140, 204,
233
echocardiogram ........................................................ 112
304
Eclampsia ......................................... 124, 132, 134, 207
ECLAMPSIA ............................................................. 131
EKG ........ 12, 42, 97, 129, 137, 139, 151, 230, 239, 243
elderly 45, 116, 120, 140, 197, 199, 204, 228, 231, 232,
237, 249
Elderly................................. 45, 104, 145, 205, 206, 221
ELECTROPHYSIOLOGIC STUDY.......................... 139
Emboli....................................................................... 150
Emphysema.............................................................. 146
Enalapril............................................................ 120, 121
ENALAPRILAT ......................................................... 129
Encephalopathy................................ 201, 203, 205, 208
Endocarditis.............................................. 150, 241, 243
Endocrine ............................................................. 26, 28
ENDOSCOPIC THERAPY ....................................... 201
Endotracheal Tube Placement ................................. 255
Epinephrine .......................................... 13, 14, 201, 247
equation............................................................ 185, 186
ergometry ................................................................. 112
Erythropoietin ................................................... 110, 111
Esmolol....................................................... 22, 117, 140
Esophageal Pressure ............................................... 191
Esophagitis ............................................................... 201
Estrogen ........................................................... 116, 150
ethanol........................................ 54, 202, 205, 212, 243
Ethanol ....................................................... 63, 202, 243
Ethosuximide .................................................... 208, 209
ethylene glycol.......................................... 107, 111, 243
Etidronate ................................................................... 97
ETOH...................... 36, 37, 81, 120, 201, 202, 203, 221
ETOH Withdrawal..................................................... 202
ETT............................................... 34, 36, 112, 113, 114
euvolemic ................................................................. 102
Evidence Based.......................................................... 47
Evidence Based Medicine Lectures ......................... 258
Evisceration ................................................................ 53
exacerbations ........................................................... 146
Exercise.............................. 28, 112, 113, 116, 117, 140
EXUDATES .............................................................. 194
EYE SIGNS ................................................................ 33
family .......... 11, 25, 26, 37, 44, 226, 236, 243, 247, 250
Family History..................................................... 26, 115
fax................................................................... 11, 24, 25
FEBRILE TRANSFUSION REACTIONS.................. 238
Femoral lines .............................................................. 50
FEna ......................................................................... 107
FETAL ALCOHOL SYNDROME .............................. 204
FEV1 ......................................... 143, 145, 146, 147, 240
fever..... 11, 26, 28, 34, 35, 36, 108, 130, 135, 138, 151,
153, 166, 167, 195, 199, 204, 219, 220, 221, 222,
223, 225, 237, 238, 249
Fever ................................ 110, 194, 198, 207, 221, 249
FEVER.............................................. 219, 220, 221, 225
Fick Method .............................................................. 125
Fine Needle Aspiration ..................................... 231, 232
Fish Oil ..................................................................... 116
Fluids & Electrolytes ................................................... 55
Flumazenil ................................................................ 243
Folate................................................................ 201, 203
Folate Deficiency ...................................................... 201
FOLEY........................................................................ 51
Folic acid .......................................................... 115, 203
fractional excretion of sodium........................... 108, 186
Friderichsen-Waterhouse syndrome ........................ 233
fungal.......................... 53, 108, 135, 148, 216, 224, 233
FUO .......................................................................... 220
furosemide.......... 97, 100, 109, 110, 121, 122, 231, 237
Furosemide........................................... 97, 99, 109, 122
Gabapentin ............................................................... 209
galactorrhea.............................................................. 233
Gallium nitrate............................................................. 98
Gambierdiscus toxicus.............................................. 246
GASTRIC LAVAGE.................................................. 200
Gastric Ulcers ........................................................... 201
Gastritis..................................................................... 201
Gastrointestinal ............................................. 28, 97, 201
GASTROINTESTINAL BLEEDING........................... 199
Genitalia................................................................ 27, 30
Genitourinary .............................................................. 28
GFR .................................................. 104, 106, 109, 110
GI bleeding.................................................. 52, 199, 200
Glasgow Coma Scale ................................................. 38
glaucoma .................................................................. 206
Glomerulonephritis.................................... 106, 109, 193
Glomerulosclerosis ................................................... 106
Glucagon............................................................. 22, 244
glucocorticoids .................................. 105, 106, 147, 231
Glucocorticoids ................................................. 146, 147
Glycohemoglobin ...................................................... 230
Goodpasture's................................................... 148, 220
Gout .......................................................................... 249
Gram Stain.......................................................... 54, 211
grand mal .................................................................. 208
Graves ...................................................................... 231
Guidelines For Fluid Challenges............................... 257
gynecomastia.............................................. 28, 199, 233
Haemophilus influenza.............................................. 146
Hashimoto's ...................................................... 231, 232
HbA1c ....................................................................... 230
HDL................................................................... 115, 116
heart block ................................................ 104, 125, 141
Heart Failure ......................... 18, 30, 120, 148, 196, 221
HEART SOUNDS ....................................................... 31
Heart Transplant ....................................................... 121
heart transplants ....................................................... 111
HEAT STROKE......................................................... 221
Hematopoietic System ................................................ 28
Hemochromatosis ............................................. 119, 233
Hemodialysis............................... 99, 110, 111, 136, 243
hemodynamic................................ 18, 52, 113, 135, 152
Hemodynamic ............................................................. 55
Hemodynamic Examples .......................................... 127
Hemoglobin A1c........................................................ 230
Hemolysis ................................................................... 98
hemolytic................... 108, 116, 220, 225, 237, 238, 247
Hemolytic transfusion reactions ................................ 237
Hemophilia ................................................................ 236
Hemoptysis ............................................... 148, 195, 255
hemothorax ................................................................. 50
Henderson Hasselbalch equation ............................. 186
Henoch-Schönlein Purpura....................................... 106
Heparin ............. 113, 114, 150, 151, 152, 223, 234, 235
Hepatitis .................................................... 194, 201, 238
hepatomegaly ................................................... 203, 233
Hirudin............................................................... 113, 114
Hirulog............................................................... 113, 114
Histoplasmosis.................................................. 148, 233
history 11, 12, 24, 25, 26, 27, 28, 34, 35, 36, 37, 43, 44,
101, 102, 107, 112, 113, 116, 139, 198, 200, 203,
206, 212, 222, 223, 236, 238, 241, 247
HISTORY ................................................ 24, 25, 27, 236
HIV ........ 36, 52, 106, 213, 214, 215, 218, 219, 220, 223
Homocysteine ........................................................... 115
hydralazine........................ 120, 129, 130, 131, 135, 241
Hydralazine ....... 106, 120, 121, 122, 129, 131, 132, 138
HYDRALAZINE......................................................... 129
hydrocortisone .................................................... 98, 234
hydrothorax ................................................................. 50
hypercalcemia......................................... 96, 97, 98, 234
Hypercalcemia ............................................................ 97
305
HYPERCALCEMIA............................................... 96, 97
Hypercapnia ............................................................... 22
Hypercholesterolemia............................................... 115
Hyperhomocystinemia .............................................. 115
hyperkalemia ........................................ 98, 99, 101, 107
Hyperkalemia.............................. 98, 105, 107, 111, 234
HYPERKALEMIA............................................ 13, 14, 99
hypermagnesemia ............................................ 104, 110
Hypernatremia .......................................................... 100
HYPERNATREMIA..................................................... 99
hyperparathyroidism ....................... 62, 96, 97, 110, 212
Hyperphosphatemia ................................................. 110
hyperpigmentation ............................................ 234, 247
Hypersensitivity Pneumonitis.................................... 148
hypertension ...... 24, 26, 28, 30, 97, 106, 108, 114, 118,
121, 122, 124, 129, 130, 131, 136, 138, 139, 140,
146, 147, 200, 203, 206, 212, 222, 228
Hypertension ... 105, 106, 109, 110, 111, 112, 115, 119,
136
HYPERTENSIVE CRISIS AND SPECIFIC DRUG
THERAPY ............................................................ 130
hyperthyroidism .......................... 97, 212, 220, 231, 233
Hyperthyroidism................................................ 221, 231
hypertrophic pulmonary osteoarthropathy ................ 195
Hyperuricemia .................................................. 106, 110
hypervolemic ............................................................ 102
Hypoalbuminemia..................................................... 193
hypocalcemia............................................ 101, 109, 229
Hypocalcemia ........................................................... 207
Hypoglycemia ........................................................... 207
hypokalemia ..................................................... 101, 240
HYPOKALEMIA.................................................. 14, 101
hypomagnesemia ..................................................... 101
Hypomagnesemia..................................................... 101
hyponatremia.................................................... 102, 234
Hyponatremia ................................................... 207, 234
HYPONATREMIA............................................. 102, 103
hypoparathyroidism ............................................ 97, 234
HYPOPHOSPHATEMIA........................................... 103
Hypotension. 22, 50, 108, 119, 129, 137, 208, 221, 229,
246
HYPOTHERMIA ................................................... 13, 14
Hypothyroidism........................................... 23, 103, 231
HYPOVOLEMIA ......................................................... 13
hypovolemic.............................................................. 102
hypoxemia ................................ 108, 146, 186, 240, 245
Hypoxemia.......................................................... 22, 146
Hypoxia..................................... 23, 62, 81, 87, 146, 148
HYPOXIA...................................................... 13, 14, 212
ICU ................................. 13, 33, 52, 101, 121, 199, 202
IgA nephropathy ....................................................... 106
IIb/IIIa........................................................................ 113
IJ lines ........................................................................ 50
Imipramine................................................................ 114
Infected catheter......................................................... 49
Infectious Disease .................................................... 212
Infectious Diseases .................................................... 27
Inotropic............................................................ 120, 121
Intensive Care .......................................................... 122
Intern ............................................................................ 1
Internal Jugular................................................... 50, 124
Intoxication ........................................................... 22, 23
INTRACEREBRAL HEMORRHAGE ........................ 131
INTRINSIC RENAL DISEASE .................................. 107
ipecac ....................................................................... 244
Ipratropium ....................................................... 146, 147
ischemic..... 31, 108, 114, 117, 121, 122, 123, 131, 135,
137, 199, 207, 245
ISCHEMIC STROKE ................................................ 131
ISOLATED BLEEDING TIME ELEVATION.............. 236
ISOLATED PT PROLONGATION............................. 236
ISOLATED PTT ELEVATION ................................... 236
Isoprenaline .......................................................... 18, 22
isopropanol ............................................................... 243
IsordilВ®...................................................... 113, 114, 120
Isosorbide Dinitrate ................................................... 114
Jervell-Lange-Nielsen syndrome .............................. 140
joint sepsis ................................................................ 249
Kaposi's sarcoma...................................................... 234
Kayexalate .................................................................. 99
KCl ...................................................................... 42, 101
ketoacidosis ................................................ 63, 228, 243
Ketoconazole ............................................................ 234
Klonopin ............................................................ 208, 209
Korsakoff's ........................................................ 202, 204
LAB ............................................... 11, 63, 151, 233, 244
labetalol............................. 111, 129, 130, 131, 138, 241
Labetalol ................................................... 106, 129, 131
LABETALOL ............................................................. 129
Labor and Delivery...................................................... 35
LAEDP ...................................................................... 124
Lamifiban .................................................................. 115
LAWS OF HOSPITAL PRACTICE.............................. 11
LEFT VENTRICULAR FAILURE............................. 131
Left Sided Failure...................................................... 119
left ventricular end diastolic volume.......................... 118
Left Ventricular Hypertrophy ..................................... 115
Legionella.................................................. 135, 148, 216
LibriumВ®.................................................................... 203
Lidocaine................................................. 13, 22, 23, 207
Lindane ..................................................................... 247
Lipid .................................................................. 115, 195
lithium.................................... 62, 97, 212, 222, 231, 243
lorazepam ......................................................... 204, 208
Lorazepam ................................................ 203, 204, 208
low molecular weight heparin.................................... 113
Low urine output ......................................................... 51
LOWN Classification ................................................... 23
Lugol's....................................................................... 233
Lugol's solution ......................................................... 233
Lumbar Puncture ........................................................ 53
LUMBAR PUNCTURE .............................................. 211
Lung Cancer ............................................................. 148
Lung Cavitation ......................................................... 148
Lupus ........................................................ 106, 197, 236
lupus anticoagulant ................................................... 236
LV dysfunction .................................................. 119, 121
LVEDP .............................................................. 124, 125
LVEDV ...................................................................... 118
LVH ................................................... 115, 119, 122, 240
Lymphangioleiomyomatosis...................................... 149
lymphoma ... 98, 136, 149, 194, 215, 216, 220, 221, 236
Lymphoma ................................ 103, 148, 193, 196, 197
magnesium ....... 101, 103, 104, 110, 123, 131, 139, 212
Magnesium ................... 22, 23, 101, 104, 121, 132, 203
MAGNESIUM TOXICITY .......................................... 103
MAGNETIC RESONANCE IMAGING....................... 137
malignancy.................. 96, 107, 135, 195, 216, 220, 232
MALIGNANT ............................................. 135, 192, 222
malignant hyperthemia.............................................. 219
Malignant Hyperthermia............................................ 221
Mallory-Weiss ........................................................... 200
mannitol .................................................................... 107
MARCHIAFAVA-BIGNAMI DISEASE ....................... 204
Marfan's .................................................................... 136
Massive Hemoptysis ................................................. 255
maximal voluntary ventilation.................................... 240
MB isozyme .............................................................. 116
Mechanical Ventilation ........................................ 95, 147
Medications. 25, 27, 35, 36, 43, 105, 109, 111, 207, 236
306
MENINGITIS............................. 215, 223, 224, 225, 226
meningococcemia............................................. 225, 233
Mental Status Exam ............................................. 37, 38
Meperidine................................................................ 207
Mesothelioma ........................................... 193, 195, 196
Metabolic Acidosis........................................ 62, 81, 221
Metabolic Alkalosis ............................................... 62, 81
methanol................................................................... 243
metoprolol................................................. 117, 120, 138
Metoprolol................................................. 113, 114, 117
Metronidazole ........................................................... 212
Milk alkali .................................................................... 97
Milrinone ................................................................... 120
MINI-MENTAL STATUS EXAM.................................. 32
MINOXIDIL ............................................................... 130
Mithramycin ................................................................ 97
Mitral Regurgitation .................................. 119, 124, 148
mitral stenosis................................................... 123, 212
Mitral Stenosis .......................................................... 148
Mnemonic ................................................... 63, 122, 202
Modified Child's Index for Grading Severity of Liver Dz
............................................................................. 205
MODS................................................................. 84, 124
moniliasis.................................................................. 234
Moraxella catarrhalis ................................................ 146
Morbidity ........................................................... 151, 239
Morphine........................................................... 113, 122
Mortality .................................................... 120, 121, 239
MRI ....... 33, 42, 131, 135, 137, 204, 210, 223, 232, 234
mucolytic................................................................... 146
Mucomyst ................................................................. 244
MucomystВ®............................................................... 147
Multinodular Goiter ................................................... 231
Multiorgan Dysfunction Syndrome.............................. 84
Multiple Sclerosis ..................................................... 207
MURMERS ................................................................. 31
mushrooms............................................................... 243
MVV.......................................................................... 240
myalgias ........................................................... 246, 249
myasthenia gravis..................................................... 234
Mycobacterium ................................................. 166, 234
Mycoplasma ............................................. 148, 216, 220
myeloma ....................................................... 97, 98, 108
Myeloma ..................................................................... 96
Myocardial depression................................................ 22
myocardial infarction... 24, 114, 136, 137, 139, 140, 220
Myocardial Infarction ........................................ 115, 117
MYOCARDIAL INFARCTION ............................. 13, 131
MYOCARDIAL ISCHEMIA ....................................... 111
Myxedema ........................................................ 193, 194
myxoma ............................................................ 138, 140
Na+ ..................................... 99, 100, 105, 109, 227, 228
N-acetyl cysteine ...................................................... 147
Naloxone .................................................................. 243
NASOGASTRIC TUBE............................................... 52
Nebulizers................................................................. 147
NEEDLE STICKS ....................................................... 52
neoplasia .................................................................. 103
nephrotic........................................... 107, 108, 109, 150
Nephrotic Syndrome......................... 105, 148, 192, 193
Nervous System ................................................. 28, 202
neurocardiogenic .............................................. 139, 140
Neurocardiogenic ............................................. 140, 141
neuroleptic malignant syndrome............................. 222
Neuroleptic Malignant Syndrome ............................. 221
Neurologic .................................................. 30, 140, 201
Neurological.................................................... 26, 27, 37
NEUROLOGICAL EXAM............................................ 38
NIFEDEDPINE ......................................................... 130
nifedipine .......................... 106, 113, 118, 121, 130, 138
Nifedipine .................................................. 114, 122, 130
nitrates ...................................................... 112, 113, 122
Nitrates.............................. 113, 114, 121, 122, 123, 139
Nitroglycerin ...................................... 114, 122, 130, 132
NITROGLYCERIN .................................................... 130
Nitroglycerine .................................................... 130, 131
Nitroprusside..................... 122, 129, 130, 131, 138, 223
NITROPRUSSIDE .................................................... 129
NMS .................................................................. 222, 223
Nocardia.................................................................... 148
Non-steroidal anti-inflammatory drugs .............. 105, 108
Normal ABG Ranges .................................................. 67
Normal Gap Acidosis .................................................. 62
Normal Lab Values ..................................................... 58
Normal Ranges for Ventilatory Values...................... 191
Norwegian scabies.................................................... 247
nose bleeds............................................................... 236
NSAIDS. 45, 98, 105, 106, 107, 108, 110, 135, 236, 241
nuchal rigidity .................................................... 225, 243
Nucleoside analogs................................................... 216
nystagmus............................... 26, 33, 39, 201, 208, 209
Obesity...................................................................... 115
occupational........................................................ 25, 250
Oliguria........................................................ 51, 104, 108
OLIGURIA................................................................. 107
Oncotic Pressure .............................................. 192, 193
Operative ............................................................ 34, 238
opium .......................................................................... 51
optic neuritis.............................................................. 206
Optic Neuritis ............................................................ 206
Optokinetic Reflex....................................................... 33
Oral Contraceptives .................................................. 115
Orders ................................................................... 42, 43
ORTHOSTATIC HYPOTENSION ............................. 138
osmolar gap .............................................................. 243
OUTPATIENT ............................................................. 11
overdose ........................................... 107, 111, 131, 208
Oxazepam................................................................. 203
oxybutynin................................................................... 51
Oxygen..... 29, 56, 69, 70, 120, 122, 127, 145, 146, 147,
184, 185, 200, 243
Oxygen Dosing ........................................................... 70
oxygen saturation.............................................. 190, 245
Oxygen Transport System .......................................... 69
Oxyhemoglobin ........................................................... 68
PA Catheter .............................................................. 124
Pacemaker.................................................... 18, 22, 141
PaCO2 .............. 56, 62, 63, 81, 151, 185, 186, 188, 189
Pain..................................... 45, 111, 114, 148, 193, 198
palmar creases ......................................................... 234
Pamidronate................................................................ 97
Pancreatic carcinoma ............................................... 201
Pancreatitis124, 194, 197, 198, 201, 205, 208, 216, 227
Paracentesis ............................................................... 53
Past Medical History ............................................. 25, 27
Pathophysiology of MI............................................... 116
PCWP .... 24, 55, 56, 118, 124, 125, 126, 127, 129, 130,
255, 257
pericarditis......................... 119, 123, 127, 135, 225, 240
Pericarditis ................................ 105, 107, 127, 135, 193
PERICARDITIS......................................................... 135
Peritonitis .................................................................. 198
Permethrin ................................................................ 247
pernicious.......................................................... 220, 234
PFT ................................................................... 146, 149
Phenobarbital............................................ 208, 209, 210
Phenothiazine ................................................... 139, 222
PHENTOLAMINE...................................................... 129
Phenytoin .................................................... 23, 208, 209
Phosphate................................. 105, 106, 111, 229, 230
307
PHYSICAL...................................... 25, 29, 31, 198, 199
Physical Examination ................................................. 26
physostigmine........................................................... 243
Physostigmine .......................................................... 243
pink puffer................................................................. 146
plaques ..................................................................... 112
platelet ........ 63, 111, 113, 115, 200, 208, 235, 236, 241
pleural effusion ........................................... 50, 137, 151
Pleural Effusions............................................... 192, 197
Pleurodesis............................................................... 197
Pleuroscopy...................................... 194, 195, 196, 197
Plicamycin .................................................................. 98
PMH................................................................ 24, 25, 36
Pneumocystis ........................................................... 148
Pneumonia ................................. 28, 103, 148, 213, 238
pneumothorax............................................. 50, 196, 197
poisoning .......................... 111, 129, 222, 243, 245, 246
POISONING ............................................. 243, 245, 246
Polycythemia ............................................................ 146
Polymorphic VT ........................................................ 123
Postrenal azotemia................................................... 109
POSTRENAL AZOTEMIA ........................................ 107
potassium ...... 62, 98, 99, 101, 106, 107, 110, 111, 139,
200, 246
Potassium............................................... 22, 23, 99, 110
Prazosin.................................................................... 120
Prednisone ......................................................... 97, 107
Preexcitation-Syndrome ............................................. 22
Pregnancy ............................................ 28, 62, 118, 209
PREGNANCY............................................................. 36
preload.............. 118, 119, 120, 121, 122, 123, 131, 151
Preload ..................................................... 118, 122, 123
Prerenal azotemia .................................................... 109
Pre-renal azotemia ........................................... 105, 108
PRERENAL AZOTEMIA........................................... 107
Pressure Ulcers ........................................................ 249
Presyncope............................................................... 207
Prinzmetal's .............................................................. 112
Pro-Banthine............................................................... 51
Procainamide...................................................... 22, 135
Prognosis.................................. 114, 117, 147, 205, 295
prolonged QT............................................................ 140
Prolonged QT-Interval ................................................ 22
Propafenone ......................................................... 18, 22
propantheline.............................................................. 51
Propranolol ................................. 22, 117, 131, 138, 233
propylthiouracil ................................................. 231, 233
prosthetic heart valves...................................... 212, 236
protease.................................................................... 145
Protease inhibitors.................................................... 217
protein intake ............................................................ 110
Proteinuria ........................................................ 110, 221
pruritus................................................ 27, 246, 247, 248
Pseudochylous ......................................................... 195
Pseudoephedrine ..................................................... 146
Pseudogout .............................................................. 249
Pseudohyperkalemia .................................................. 98
Psych.......................................................................... 37
Psychiatric .................................................... 26, 28, 140
psychiatry ................................................................... 12
PTH .................................................................... 96, 110
Pulmonary ..... 56, 62, 66, 103, 120, 122, 123, 124, 125,
126, 137, 138, 141, 146, 148, 149, 153, 167, 185,
193, 194, 197, 221, 238, 239, 253
pulmonary artery catheter......................................... 136
PULMONARY ARTERY CATHETERIZATION......... 123
pulmonary capillary wedge pressure ................ 118, 129
pulmonary edema.... 107, 111, 119, 121, 124, 137, 147,
237, 243
PULMONARY EMBOLI ............................................ 150
pulmonary embolism. 107, 124, 140, 184, 233, 236, 242
Pulmonary Embolism ........................ 124, 148, 193, 197
PULMONARY EMBOLISM ......................................... 13
Pulmonary Embolus.................................................. 148
Pulmonary Function Testing ..................................... 149
Pulmonary infarction ................................................. 148
Pulmonary vascular resistance ................................. 146
Pulse Oximetry............................................................ 64
Pulseless Electrical Activity ........................................ 13
Pulseless VT ............................................................... 13
PULSES...................................................................... 31
PUPILS ....................................................................... 33
PVR............................................. 56, 125, 126, 130, 146
pyrexia ...................................................................... 219
Pyridoxine ................................................................. 243
Quinidine......................................................... 18, 22, 23
RANSON'S CRITERIA.............................................. 205
Rate Pressure product .............................................. 112
Reflexes ................................................................ 36, 39
Renal biopsy ............................................................. 110
Renal Failure..................................................... 207, 221
Renovascular ............................................................ 108
ReoProВ® ................................................................... 113
Respiratory Acidosis ............................................. 62, 81
Respiratory Alkalosis ............................................ 62, 81
Respiratory System..................................................... 28
Retinal detachment ................................................... 206
Review of Systems ............................................... 26, 27
Rhabdomyolysis.......................................... 98, 108, 221
Rheumatoid............................................... 148, 149, 197
Rhogam ...................................................................... 35
Right Sided Failure ................................................... 119
Rinne Test................................................................... 29
Risk .. 112, 113, 115, 116, 121, 124, 129, 142, 209, 211,
212, 221, 238, 239, 240, 250, 297
risk factors................................... 27, 111, 112, 115, 221
Romano-Ward syndrome.......................................... 140
salicylates ................................................. 212, 231, 243
Sarcoid........................................ 96, 149, 192, 223, 224
sarcoidosis ................................ 135, 148, 220, 224, 233
Sarcoidosis ......................................... 97, 119, 148, 194
Sarcoptes var. hominis ............................................. 247
Scabies ..................................................................... 247
SCABIES .................................................................. 247
Scoring for Acute Lung Injury and Acute Respiratory
Distress Syndrome ................................................. 71
Seizure...................................................................... 208
Seizures .................... 201, 202, 207, 208, 209, 221, 243
SEIZURES ................................................ 204, 207, 243
sensory reversal dysesthesia.................................... 246
Sepsis ....................................................... 108, 124, 212
Septic Shock ............................................................. 124
SeraxВ® ...................................................................... 203
serum osmolality ............................................... 186, 243
Shunt Equation ......................................................... 191
Shy-Drager........................................................ 138, 141
SIADH ....................................................................... 103
SIGN-OUT Note.......................................................... 43
Signs ............... 26, 30, 42, 107, 108, 119, 151, 193, 221
SIGNS OF OBVIOUS BREATHING (WOB) ............. 185
Silent Ischemia.......................................................... 111
Silicosis ..................................................................... 148
Sinus Bradycardia................................................. 18, 23
sinus tachycardia ...................................................... 233
Sinus Tachycardia ........................................ 18, 23, 151
SIRS............................................................................ 83
SLE ........................... 107, 135, 148, 150, 194, 220, 224
smoke ......................................................... 38, 145, 245
Smokers.................................................................... 145
smoking............. 26, 28, 36, 37, 115, 146, 239, 240, 246
308
Smoking.................................................................... 115
SOAP.......................................................................... 33
Social History.............................................................. 26
Sodium iodide........................................................... 233
Solu-MedrolВ®.................................................... 146, 147
sputum.................................. 26, 28, 145, 146, 166, 167
Sputum Cytology ...................................................... 149
Гџ-blockers......................................... 113, 114, 121, 231
Гџ-Blockers ................................ 113, 114, 121, 122, 203
Гџ-carotene ........................................................ 113, 116
ST depressions................................................. 112, 114
ST segment ...................................................... 111, 112
Starling Curve........................................................... 118
Starling Equation ...................................................... 192
Status Epilepticus ..................................................... 210
Steroids .............................................. 98, 147, 233, 247
Streptococcus pneumoniae .............................. 146, 226
Streptokinase............................................ 117, 118, 152
stroke. 31, 111, 115, 116, 118, 130, 131, 136, 138, 146,
150, 207, 212, 219, 221, 222, 224, 228
Stroke ....... 103, 116, 126, 211, 212, 221, 222, 227, 238
SUBARACHNOID HEMORRHAGE ......................... 131
Subclavian .................................................. 50, 124, 193
Suicide........................................................................ 12
Sulfinpyrazone.......................................................... 114
Supplemental Oxygen for COPD.............................. 145
supraventricular ................................ 101, 139, 140, 233
Supraventricular (SV) Tachycardia............................. 22
Supraventricular Extrasystole..................................... 18
surgery24, 34, 51, 52, 53, 107, 109, 112, 118, 121, 135,
136, 137, 138, 150, 152, 198, 200, 201, 224, 227,
234, 236, 238, 239, 241, 242, 249
Surgery Prophylaxis ................................................. 241
SVT........................................................................... 240
SWAN GANZ.............................................................. 24
Swan Ganz Catheter Wave Forms........................... 128
Swan-Ganz....................................................... 125, 228
Symptoms.... 27, 37, 101, 103, 104, 108, 111, 116, 119,
145, 148, 193, 203, 209, 221, 231
syncope ........................ 26, 28, 139, 140, 141, 212, 245
SYNCOPE ........................................ 138, 139, 140, 141
Syndrome X...................................................... 112, 114
systemic embolism ................................................... 236
Systemic Inflammatory Response Syndrome............. 83
Systolic Dysfunction ......................................... 119, 121
T4 214, 231, 232, 233
tachypnea .. 50, 105, 122, 136, 145, 146, 150, 185, 222,
245
Tamponade ........................................ 31, 124, 135, 136
TB 12, 28, 135, 149, 166, 167, 192, 194, 196, 211, 215,
216, 220, 223, 224, 233
TEE........................................................................... 137
Tegretol ............................................................ 208, 209
TEN RULES FOR READING CHEST X-RAYS ........ 167
TENSION PNEUMOTHORAX.................................... 13
thallium ..................................................... 112, 116, 117
THE LECTURER ........................................................ 12
theophylline ................ 11, 111, 140, 141, 208, 240, 243
Theophylline ..................................................... 146, 147
Therapy of Systolic Failure ....................................... 120
thiamin ...................................................................... 201
thiamine .................................... 121, 201, 203, 204, 212
Thiamine........................................... 201, 202, 203, 243
thiazide ............................................................... 97, 103
thoracentesis .............................................. 50, 194, 197
Thoracentesis ............................................. 53, 194, 197
Thromboembolism Prophylaxis in Surgical Procedures
............................................................................. 241
THROMBOLYSIS ..................................................... 152
thrombolytic .............................................. 113, 137, 152
Thrombolytic ............................................................. 117
Thyroid .......................................... 28, 29, 231, 232, 233
THYROID DISEASE ................................................. 231
thyroiditis........................................................... 231, 234
THYROTOXIC CRISIS ............................................. 233
thyrotoxicosis .............................................. 97, 212, 234
TIA .................................................................... 212, 241
ticarcillin .................................................................... 101
TiclidВ® ....................................................................... 113
ticlopidine .................................................................. 113
Ticlopidine................................................. 113, 114, 115
TILT TABLE TESTING.............................................. 139
Tobacco .................................................................... 113
Torsades Des Pointes............................................... 123
tPA ............................................................................ 118
Transderm-Scop ....................................................... 140
TRANSESOPHAGEAL ECHOCARDIOGRAPHY..... 137
Transfusion ................................................................. 27
TRANSFUSION ASSOCIATED ADULT
RESPIRATORY DISTRESS SYNDROME ........... 237
TRANSUDATES ....................................................... 193
Travel .......................................................................... 36
Treadmill ................................................................... 112
Trendelenburg............................................... 49, 50, 130
Tricyclic ............................................................. 114, 243
TRIMETHAPHAN CAMSYLATE............................... 130
TSH................................................................... 231, 233
Tuberculosis........................ 12, 103, 148, 166, 197, 223
Tuberculous .............................................................. 135
Tubular Necrosis....................................................... 106
tubulointerstitial ......................................................... 109
Tumor lysis syndrome................................................. 98
Ultrasound................................... 13, 105, 110, 112, 232
universal precautions .................................................. 52
Uremia .......... 62, 63, 105, 107, 108, 111, 192, 194, 212
Uremic Syndrome ..................................................... 110
Urinalysis ...................................................... 54, 63, 110
URTICARIAL REACTIONS....................................... 237
Use Rumack-Matthew Nomogram For Acetaminophen
Overdose.............................................................. 244
Valium ....................................................... 203, 208, 209
309
Valproic Acid............................................................. 208
Valsalva ................................................................ 22, 31
Valvular............................................................. 239, 240
Vascular Disease................................................ 30, 109
vasculitis ........................................... 107, 212, 220, 225
Vasospasm............................................... 112, 113, 114
Vasotec............................................................. 129, 241
venous thrombosis ................................................... 236
ventilators ................................................................. 103
VentolinВ® .................................................................. 146
Ventricular Dysrhythmia ............................................. 22
ventricular fibrillation................................................. 101
ventricular tachycardia.............................. 101, 139, 140
Verapamil ............................... 18, 22, 23, 114, 122, 138
Vertigo .............................................................. 207, 221
vesnarinone .............................................................. 121
Vesnarinone ............................................................. 120
VF ....................................................................... 13, 120
VIOLENT PATIENTS................................................ 204
Vitamin.. 96, 97, 110, 111, 113, 114, 116, 201, 209, 212
vitamin D....................................... 97, 98, 106, 109, 110
Vitamin D .................................................... 96, 110, 111
vitamin K........................................... 200, 209, 236, 244
Von Willebrand's....................................................... 236
warfarin............................................. 114, 208, 236, 242
Water depletion ........................................................ 100
Weber Test ................................................................. 29
Wegener's ........................................................ 148, 220
Wernicke's ................................ 141, 201, 202, 204, 212
WERNICKE'S ENCEPHALOPAHTY AND
KORSAKOFF'S PSYCHOSIS .............................. 204
women ..... 111, 112, 115, 116, 202, 218, 231, 232, 248,
249
Worksheet for Using an Article About Therapy or
Prevention............................................................ 276
Worksheet for Using an Article About Assessing
Diagnostic Tests .................................................. 293
WOUND COMPLICATIONS....................................... 53
WPW ............................................................ 22, 23, 139
x 147, 244
Document
Category
Infarction
Views
1 067
File Size
10 096 KB
Tags
1/--pages
Report inappropriate content