Cardiac Arrhythmias Part 3: Pharmacotherapy of Cardiac Arrhythmias 2015 Slides 95-99 summarize arrhythmia content from Part I & II but in a different format. Cardiac Arrhythmias Reviewed in Part I & II – 95 Background information 1. Definitions and classifications 2. EKG recognition 3. Re–entry 4. Vaughn-Williams Classification of anti-arrhythmic drugs (AAD) Classification – individual agents and digoxin Heart blocks – briefly discussed Atrial fibrillation/flutter Treatment of A-Fib 1. rate control 2. rhythm control 3. stroke prevention: warfarin, dabigatran, rivaroxaban, apixaban Proposed Treatment Model Based on Patient Presentation: A-Fib – 96 Slides 95-99 summarize arrhythmia content from Part I & II but in a different format. It presents it in terms of pt. presentation: 1. First episode; 2. Asymptomatic recurrence; or 3. Symptomatic recurrence First Episode Summary: A-Fib – 97 Pt. presentation: Hemodynamic instability→ DCC immediately Duration: < 2 days→ may cardiovert immediately Duration: >2 Days (hemodynamically stable) Anticoagulate x 3 weeks Rate control in weeks prior to cardioversion Attempts cardioversion Anticoagulate x 4 weeks post cardioversion If cardioversion is NOT attempted then: 1. chronic rate control therapy 2. chronic stroke prevention therapy Avoid use of chronic antiarrhythmic agent A-Fib Recurrence: minimally symptomatic/asymptomatic – 98 Chronic rate control (AFFIRM trial based) Chronic stroke prevention Tx IMPERATIVE: dabigatran, rivaroxaban, Apixaban, or ASA +/- Plavix based on age and risk factor assessment (CHADS2) A-Fib: recurrence symptomatic – 99 Recurrence in symptoms despite optimal rate “control” or inability to achieve optimal rate control → consider restoration and maintenance of NSR 1. rate control (@ minimum till pt. cardioverted) 2. cardioversion→ DCC or chemical 3. maintain NSR→ with antiarrhythmic agent(s) 4. stroke prevention TX → pre/post cardioversion 1 5592│Cardiac│ 2015 Cardiac Arrhythmias Part 3: Pharmacotherapy of Cardiac Arrhythmias 2015 Non-pharmacologic management A-Fib – 100 Growing management → successfully done with data to back up procedures 1. AV nodal ablation with pacemaker placement a. Renders AV node dysfunctional → pt. given a pacemaker b. Some pts. left in A-Fib and MUST be given lifelong anticoagulant 2. RF ablation for a flutter a. Find re-entrant circuit → ablate it → cures the arrhythmia 3. Surgery a. Types: Maze procedure pulmonary vein isolation b. 80% occurrence of NSR (normal sinus rhythm) with surgeries c. Pts. anti-coagulated for period of time to see if pt. goes back into A-Fib Drawing catheter placement for ablation – 101 See WPPD slides Catheter placement shown in this slide is for Left Accessory Pathway PSVT. Procedure is similarly done in A-Fib. Paroxysmal Supraventricular Tachycardia (PSVT) – 102 Rapid sinus rhythm associated with AV nodal re-entry or AV re-entrant tachycardia Mechanism causing PTSV Re-entrant mechanisms – usually seen age < 40 yrs. 1. Infra-nodal = inside AV Node → prominent 2. Extra-nodal = AV nodal re-entrant tachycardia i.e. Wolf Parkinson White Syndrome Rates range from 150 – 200/min Pts. can be QUITE symptomatic Non-drug TX sometimes to increase vagal tone can sometimes manage symptoms carotid massage Valsalva Ice water on face Anti-coagulation NOT generally needed in PSVT because there is viable, coordinated atrial contraction 2 5592│Cardiac│ 2015 Cardiac Arrhythmias Part 3: Pharmacotherapy of Cardiac Arrhythmias 2015 Treatment of acute PSVT (top): prevention of recurrences (bottom) – 103 Start by evaluating symptoms PSVT frequently associated with Panic Attack. Unclear if Panic Attack creates PSVT or vice versa. Symptoms: 1. Most mild PSVT → panic is a big part of presentation 2. Chest pain 3. Shortness of breath 4. Atrial and ventricular rates can be very high → pt. very symptomatic 5. Likelihood of clot = extremely low to non-extant. Remember, in PSVT there is viable, coordinated atrial contraction so blood is pumping. It is not stagnant which would enhance clot formation. Severe symptoms → go directly to DCC (do not pass go; do not collect $200 dollars as in Monopoly!) Mild symptoms → Evaluate ECG → most of the time easy to do. This stage done in ER. Look at the QRS complex. This is the electrical picture of ventricular depolarization. Assume ventricular contraction follows ventricular depolarization. Remember ECG, does not tell anything about the strength of contraction. 1. Is QRS complex wide? 2. Is QRS complexes occurring 1 after another or are they irregular in frequency i.e. rate varies. Irregular frequency suggests Wolf Parkinson White type of arrhythmia 3 5592│Cardiac│ 2015 Cardiac Arrhythmias Part 3: Pharmacotherapy of Cardiac Arrhythmias 2015 Treatment of acute PSVT (top): prevention of recurrences (bottom) – 103 Initial evaluation - basic ECG. Look at QRS interval Must diagnose these in electrophysiology lab, not ER. Treatments Evaluating ECG This stage of ECG evaluation cannot be done in ER → Must be done in electrophysiology Lab. ECG alone cannot diagnose: 1. AVNRT = AV Node Re-entrant Tachycardia 2. Orthodromic or Antidromic AV Node Tachycardia 3. A-Fib with accessory pathway All you know in the ER, is the basic ECG in the first step of evaluation looking at QRS complex. Treatment Evaluation of the basic ECG = not always reliable. As a result treatment determination can be challenging. See pt. presentation and scenarios below. 1. Mild symptoms – wide QRS; irregular rhythm Pt. administered verapamil or diltiazem→ you could make patient worse, much worse. Ventricular rate of 150 could easily go to 300 and pt. deteriorate profoundly. 2. Mild symptoms – narrow QRS, regular rate. Pt. administered procainamide. One of two things may happen: 1. Drug may not work; 2. Drug may make patient worse. Treatment approach→ assume worse arrhythmia possible i.e. accessory pathway → Wolf Parkinson White (WPW); wide QRS, irregular rate. 1. Administer test dose of adenosine→ not part of TX listed; safe; works well. 2. Possible outcomes: 1. arrhythmia worsens; atrial rate ↑; 2. nothing happens 3. T ½ adenosine = 7 seconds; very brief →it goes away almost immediately If atrial rate ↑ or patient worsens → can assume it is WPW or A-Fib with accessory pathway. TX= procainamide/amiodarone. If pts. rate changes → it should ↓ relatively quickly and be short-lived with T ½ = 7 secs. TX options then are: verapamil or procainamide. Pt. should do well. 4 5592│Cardiac│ 2015 Cardiac Arrhythmias Part 3: Pharmacotherapy of Cardiac Arrhythmias 2015 Later, patient will need other interventions i.e. AV nodal blockade Ventricular arrhythmias types – 104 1. Premature ventricular contractions (PVCs) 2. Ventricular tachycardia (VT) 3. Ventricular fibrillation (VF) 4. Torsades de Pointes http://www.rnceus.com/ekg/ekgtp.html Premature ventricular contractions (PVCs) – 105 Occurrence in healthy pt. → confers little risk. Most people have with varying frequency. Occurrence and absence of heart disease, even with symptoms, is benign. no drug TX needed if symptomatic→ TX = β-Blocker Often occur following AMI (acute myocardial infarction) ↑ risk sudden cardiac death (SCD); there is a statistical association antiarrhythmic drugs (AADs) – except Type II, should NOT be used to suppress PVCs use of β-Blocker ↓ risk of death and controls symptomatic PVCs, especially in acute phase indicated for prevention of recurrent MI and arrhythmias during/post infarction See CAST Trial next slide 5 5592│Cardiac│ 2015 Cardiac Arrhythmias Part 3: Pharmacotherapy of Cardiac Arrhythmias 2015 Cardiac Arrhythmia Suppression Trial (CAST) – 106 PVCs are associated with↑ mortality post-MI Fundamental study question: Does PVC suppression lead to mortality reduction in pts. post-MI? Inclusion: 1. Post-MI pts. 6 days – 2 yrs. 2. > 6 PVCs/hr. (6 /hr. = 1 PVC q 10 mins.) 3. randomized to: flecainide, encainide, moricizine, placebo (flecainide parent drug of encainide) Findings: 1. Class IC agents suppressed PVCs post-MI 2. HOWEVER, therapy resulted in a higher mortality rate compared to placebo 3. Treatment with class IC agents increase the risk of fatal ventricular arrhythmias 4. Likelihood of survival, better with placebo with P=0.0006 → highly statistically significant observation based on P value 5. Post-MI, occasional PVC should not receive treatment with 1C agents; probably not with class III agents either. Study did not address class III data. 6. TX for infrequent, asymptomatic PVCs with classical AAD is an appropriate. Study CAST Design RCT Treatments Inclusion Findings Flecainide (class IC) N=1,445 1. Class IC suppressed PVCs post-MI Encainide (class IC) 1. > 6 PVCs/min 2. ↑ Mortality rate compared to Moricizine (class IC) 2. Post MI 6 days Placebo Placebo To 2 yrs. 3. Class IC agents↑ risk of fatal Duration: ≈1.5 yrs. Ventricular arrhythmias CAST trial N Engl J Med 1991; 324:721 – 107; encainide removed from market after since this study It is okay to use β-Blocker to treat PVCs CAST trial graph - slide 108 Demonstrates likelihood of survival better with placebo Ventricular Tachycardia (VT) – 108 Definition: 1. Series of ≥ PVCs (nothing in between) 2. Rate > 100 BPM Determine if PVCs are sustained or non-sustained. Definition depends on duration. 1. Non-sustained = duration < 30 seconds; self terminates 2. Sustained: > 30 seconds or requires termination PVCs; > 3 consecutively; rate = 150 BPM http://www.practicalclinicalskills.com/ekg-reference-guide-details.aspx?lessonID=25 6 5592│Cardiac│ 2015 Cardiac Arrhythmias Part 3: Pharmacotherapy of Cardiac Arrhythmias 2015 Acute treatment: VT – 109 VT both sustained and non-sustained are associated with evolution of V-Fib which is uniformly fatal. Patient presentation/treatment: 1. Severe symptoms/unstable (no pulse) : DCC 2. Non-sustained asymptomatic: 1. called pulsatile→ a pulse is detectable so there is cardiac output 2. no TX required symptomatic: 1. β-Blockers 2. Amiodarone or sotalol if no response to β-Blocker AICD?→ Problematic in non-sustained VT 3. post-MI, TX with β-Blockers or auto reverts→ no AICD 4. heart failure with non-sustained VT→ yes AICD 3. Sustained VT may become ventricular fibrillation (VF) Unstable: DCC, right away. If unresponsive then amiodarone. Stable – treat with drug: IV amiodarone, lidocaine, procainamide, or DCC 1. stable = awake; pulsatile; conscious; has BP AICD? → Yes, especially post-MI. Virtual standard of care to have both drug and AICD Ventricular fibrillation (VF) – 110 Fibrillation is electrical anarchy whether in atria or ventricle Absence of organized ventricular rhythm; no coordinated muscular contractions; no cardiac output; BP effectively = 0 Ventricles contracting but it is individual myofibrils causing contractions VF is thought to be common cause of sudden cardiac death (SCD) in USA→ frequency = 500,000/yr. Treatment: DCC, only treatment that works reliably. DCC energy for V-Fib >> A-Fib 1. A-Fib = 50-100 up to 200 Joules 2. V-Fib = start @ 200, goes up to 400 Joules http://www.practicalclinicalskills.com/ekg-reference-guide-details.aspx?lessonID=26 Automatic implantable Cardioverter – defibrillator (AICD) – 111 See WPPD slide Effects on longevity well-documented with AICD Sophisticated devices that contain: defibrillator; pacemaker; overdrive pacemakers; detects tachycardia→ takes over rhythm and slows it down. If can’t slow rhythm → administers small jolts. If ineffective → administers larger jolt. Small impulse uncomfortable; larger jolt significant discomfort. Has psychological impact. 7 5592│Cardiac│ 2015 Cardiac Arrhythmias Part 3: Pharmacotherapy of Cardiac Arrhythmias 2015 AICD + antiarrhythmic Agent – 112 40 – 70% of patients with ICD require concurrent AAD therapy; very commonly patient receives amiodarone Purpose of adding an ADD: 1. ↓ number of inappropriate firings 2. ↓ number of high-voltage shocks, inappropriate shocks provoked by SVT arrhythmias 3. prolong battery life In practice it is common to see an AICD plus AAD (antiarrhythmic drug) possibly with β-Blocker / CCB Torsades de Pointes (TdP) – 113 Difficult to treat. Goal = prevention→ minimize agents/combo of QT prolonging drugs QTc usually > 500 milliseconds (?); ↑ associated risk of TdP Textbook has 560 msec→ presenter suspects it is a typo. That is the longest QTc he has seen Common causes of TdP myocardial ischemia/infarction heart failure severe bradycardia → < 50 beats/minute hypothermia electrolyte imbalance: ↓ K+, ↓ Mg++ keep K+ > 4; Mg++ > 2 Monitor patients on AAD, diuretics, other cardiac drugs for electrolyte imbalances Torsades de Pointes (“twisting of the points”) – 114 Describes electrophysiology phenomenon of the electrical axis of the myocardium actually turning about an electrical axis. It turns about this axis when you see: large depiction of QRS followed by small one. Suggests electrical axis relative to leads on the chest moving 1st towards electrodes then away from electrodes. in Gartner http://medlibes.com/uploads/Screen%20shot%202010-07-06%20at%209.39.21%20PM.png TdP risk factors: 1. heart disease heart disease 2. drugs 3. electrolyte abnormalities: ↓ K+; ↓ Mg++ 8 5592│Cardiac│ 2015 Cardiac Arrhythmias Part 3: Pharmacotherapy of Cardiac Arrhythmias 2015 Common QT prolonging drugs – 115 TdP associated with large # of drugs - not all archived cardiac drugs Drug Class Drug Name Antiarrhythmic drugs quinidine Procainamide Disopyramide Amiodarone (<1%)→ quite small risk Dofetilide Dronedarone (<1%)→ quite small risk Sotalol Ibutilide Psychotropics Haloperidol/droperidol Phenothiazines Tricyclic/tetracyclic Antidepressants Atypical antipsychotics i.e. quetiapine, ziprasidone Toxins Organophosphate insecticides Arsenic Antibiotics Pentamidine (Time-limited use) Macrolides i.e. erythromycin, clarithromycin Fluoroquinolones Trimethoprim – sulfamethoxazole Fluoroquinolones i.e. levofloxacin, moxifloxacin, gemifloxacin Voriconazole Pain Methadone Miscellaneous Liquid – protein diets Corticosteroids Diuretics Quinine Chloroquine Chloral hydrate Tacrolimus TdP treatment – 116 DCC with sedation to restore stable rhythm sedation preferred but not always done b/c of circumstances DOC (drug of choice) – IV Mg++ sulfate good but duration = short Pts. receiving Mg++ get DCC b/c of short duration of drug Pt. management: Correct/remove any precipitating causes remove QT prolonging drugs: get ECG→ note QTc; anything approaching 500→ too long use 440 msec is threshold; QTc > 440→ patient at risk for TdP target K+ > 4.0 mEq/L; target Mg++ greater > 2.0 mg/dL 9 5592│Cardiac│ 2015
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