DR ASEEM BHARDWAJ
MAHAVIR MEDICAL MISSION
PANGOLI CHOWK
PATHANKOT
BASIC CRITICAL CARE
CRITICAL CARE
 A FUSION OF DISPARTATE MEDICAL
SPECIALITIES APPLYING BEDSIDE
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PHYSIOLOGY TO IMPROVE MORBIDITY AND
MORTALITY
INTERDISCIPILANARY
TECHNICALLY COMPLEX
VERY LABOUR INTENSIVE
MOST EXPENSIVE PART OF HOSPITAL CARE
REQUIRES PROFESSSIONAL TRAINING
SIMPLY IN THE MIDDLE OF CHAOS
BASIC
CRITICAL CARE
 IDENTIFICATION AND MANAGEMENT OF
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EVENTS HAVING PROFOUND EFFECTS ON
PATIENT OUTCOME
DERTH OF TRAINED PROFESSIONALS
OVERALL
SMALLER CITIES COMPOUNDING EFFECT
PROFESSIONAL FREEDOM AT
LOGGERHEADS
ECONOMIC CONSTRAINTS
CRITICAL PATEINT
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THREATENED AIRWAY
UNEXPLAINED TACHYCARDIA(>130/MT)
UNEXPLAINED BRADYCARDIA(<50/MT)
RESPIATORY RATE>30 OR<8/MT
RECENT ONSET CHEST PAIN
ALTERED MENTAL STATUS
SEIZURES
HYPO OR HYPERTENSION(<90 SYSTOLIC OR>110 DIASTOLIC)
DYSPNOEA
ACUTE BLEEDING
ACUTE CHANGE IN URINE OUTPUT(<0.5ML/HR)
TEMPERATURE core >39* CELCIUS)
ANY DETERIORATION IN ONGOING STATUS EVEN WITHOUT ANY OF
THE ABOVE
CARDINAL RULES OF CRITICAL CARE
 INCREASE OXYGEN DELIVERY
 DECREASE OXYGEN DEMAND
 RESTORATION OF STANDARD STATUS
BASIC OF ALL CRITICAL CARE
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OXYGEN DELIVERY=OXYGEN DEMAND
OXYGEN DEMAND>OXYGEN SUPPLY
TISSUE HYPOXIA
ANAEROBIC
METABOLISM
LACTIC ACIDOSIS
CELLULAR
DYSFUNCTION
CELL INJURY
CELLULAR
APOPTOSIS
CELL DEATH
 ORGAN DYSFUNCTION
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MULTIORGAN SYSTEM FAILURE
OXYGEN DELIVERY
 CARDIAC OUTPUT AND MINUTE
VENTILATION
OXYGEN DELIVERY
CARDIAC OUTPUT
STROKE
VOLUME
• PRE LOAD
• AFTERLOAD
HEART RATE
• MYOCARDIAL
INTEGRITY
• CONDUCTION
MECHANISM
OXYGEN
DELIVERY
CAPACITY
• VASCULAR
STATUS
• HAEMOGLOBIN
OXYGEN CONSUMPTION
BMI
PHYSIOLOGICAL
STRESS
INFLAMMATORY
RESPONSE OF
BODY
OXYGEN DELIVERY
LUNGS
AIRWAY
LUNG
FUNCTIONS
COMPLIANCE
OXYGEN CONSUMPTION
 ARTERIAL OXYGEN DELIVERY MINUS
VENOUS OXYGEN DELIVERY
 NORMAL APPX 250 ML/MINUTE OR 5
ML/100ML OF BLOOD
 FICKS EQUATION
VO2=1.38Hb*10*CO*(SA O2-SV O2)
DETERMINANTS OF MIXED VENOUS
SATURATION
 ARTERIAL OXYGEN SATURATION (SaO2)
 OXYGEN CONSUMPTION (VO2)
 CARDIAC OUTPUT (CO)
 HAEMOGLOBIN
 MASTER EQUATION
SvO2=SaO2-(VO2/CO*Hb*1.34)
WHY MIXED VENOUS SATURATION
 NORMAL 60-80%
 EARLY INDICATOR OF PHYSIOLOGICAL
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STRESS
>75% NORMAL STATUS
50-75% INCREASED O2
DEMAND/DECREASED SUPPLY
30-50% LACTIC ACIDOSIS BEGINS
25-30%SEVERE LACTIC ACIDOSIS
<25% CELLULAR DEATH
MAXIMIZE O2 DELIVERY
ASSUME CONTROL • AIRWAY
OF VENTILATION • BREATHING AND FiO2 FACTORS
IMPROVE CARDIAC • PRELOAD OR DECREASE AFTERLOAD
PERFORMANCE
• IONOTROPES / VASOCONSTRICTORS
INCREASE OXYGEN • PACKED CEELS
CARRYING
• WHOLE BLOOD
CAPACITY
MINIMIZE OXYGEN COSUMPTION
WORK OF
BREATHING
CONTROL
INCREASED
DEMAND FACTORS
MYOCARDIAL
OXYGEN
CONSUMPTION
• SPONTANEOUS …BRONCHODILATORS,DIURESIS,O2
SUPPLEMENTATION
• ASSISTED….NIV,VENTILATION
• ANALGESIA,SEDATION,NORMOTHERMIA,HYPOTHERMIA
• ANTIBIOTICS,ANTINFLAMMATORY DRUGS METABOLIC
IMBALANCE
• CORONARY PERFUSION PRESSURE=AORTIC DIASTOLIC
PRESSURE-LVEDP
• EITHER INCREASE ADP OR DECREASE LVEDP
CAN WE PREDICT CRTICALITY
ROLE OF SEVERITY SCORES
 GENERAL AND ORGAN SPECIFIC INDICES
 OBJECTIVE ASSESSMENT AND INERNAL
AUDIT OF CRICAL CARE DELIVERY
 VALIDATION LARGER THE AREA UNDER ROC
CURVE(RECEIVER OPERATING
CHARACTERISTICS) MORE DISCRIMINANT IS
SCORE
 CALIBRATION GOODNESS OF FIT TEST
OBSERVER MORTALITY SHOULD NOT BE
STATISTICALLY DIFERRENT FOR POPULATION
DETAILS OF EQUAL PROBABILITY
SEVERITY SCORES
 APACHE(ACUTE PHYSIOLOGY AND CHRONIC
HEALTH SCORE)
 SAPS(SIMPLIFIED ACUTE PHYSIOLOGY
SCORE)
 MPM(MORTALITY PROBABILTY MODEL)
 APACHE III IS PAID LIMITING IT`S USE
 SAPS III IS THE LATEST AND FREE
 MPM HAS ADVANTAGE OF BEING APPLIED AT
ADMISSION(MPM110) AND AT 24
HRS(MPM1124)
WHEN PATIENT IS DECLARED NOT
CRITICAL FROM BEING CRITICAL
Blood
pressure and
cvp
Heart rate
respiration
Urine output
sensorium
MORE EFFECTIVE END POINTS
CONTINUOS CARDIAC
INDEX
SvO2/ScvO2
METABOLIC ACID BASE
STATUS
LACTATE LEVELS
REAL TIME
ECHOCARDIOGRAPHY
LESSER KNOWN BUT IMPORTANT
ASPECTS OF CRITICAL CARE
CARE OF INDWELLING TUBES
NUTRITIONAL SUPPORT
ENTERAL/PARENTRAL
COUNSELLING OF ATTENDANTS
ANTIBIOTICS IN CRITICAL CARE
 EMPERICAL USE SELECT ANTIBIOTIC AS
PER EXPECTED MICROBE,SITE OF
INFECTION,MODE OF CLEARANCE
 COMBINATION IS ALWAYS BETTER
 SPECIFIC ANTIBIOTICS AS PER
CULTURE/SENSTIVITY PATTERN
 PREVENTION OF SEPSIS BY CONTROLLING
MACRO AND MICRO ENVIRONMENT
WHAT FLUIDS TO BE USED
 CRYSTALLOIDS ARE EASY TO HANDLE FOR
PATIENT AND DOCTORS AS WELL
 A URINE OUTPUT OF 0.5ML/KG/HOUR IS
ACCEPTABLE.DO NOT CHASE THE URINE
OUTPUT
 COLLOIDS USE WITH CAUTION
 BLOOD PRODUCTS JUDICIOUS USE
IONOTROPES AND VASOACTIVE DRUGS
 USED WITH BASIC PHYSIOLOGICAL
AWARENESS THAT THEY CAN NOT ACT TO
GOOD EFFECT IN VOLUME DEPLETED
PATIENTS
 FLOW DIVERSION IS TACTICAL BUT NOT
LASTING .TREAT THE CAUSE IN THIS
WINDOW
PRACTICAL BASIC CRITICAL CARE
MONITORING
 SECURE AIRWAY AND Spo2 MONITORING
 IV LINE ACCESS
 CENTRAL LINE CVP MONITORING
 A GOOD WORKING 5 PARA MONITOR
 INDWELLING URINARY CATHETAR FOR UO
MONITORING
 ABG VERY PRACTICAL AND INFORMATIVE
ABSOLUTE INDICATIONS FOR
INTENSIVIST`S INTERVENTION
 PATIENT NEEDING VENTILATORY SUPPORT
 CARDIOGENIC SHOCK
 UNRESPONSIVE KIDNEYS
 TOTAL PARENTRAL NUTRITION
BASIC CRITICAL CARE IN
NUTSHELL
RAPID RESPONSE
TREAT THE CAUSE.PARAMETERS ARE MEANT
FOR MONITORING EFFICIENCY OF YOUR
TREATMENT
LOW THRESHOLD FOR INVOLVEMENT OF INTENSIVIST
BETTER TO BE SAFE THAN SORRY