Thanks to Dr. Regan for preparing this edition of ICU Conference Wrap-up!
The Case: Syncope and Polymorphic Ventricular Tachycardia
San Francisco Syncope Rule
-CHESS (history of CHF, Hct<30%, EKG other than sinus or change from prior, c/o SOB, SBP<90)
-If ANY of these are present, pt is high risk for serious outcomes (PE, arrhythmia, CVA, SAH, other significant hemorrhage, MI, death) in 7 days
-The problems: poor specificity, not reproducible in follow up studies
-Conclusion: may be useful only AFTER physician’s initial eval identifies no cause of syncope
Ventricular Tachycardia
Classification:
1) Duration: sustainedàlasts >30 secs versus non-sustained
2) Morphology
-Monomorphic: originates from same focus, QRS complexes are identical
-Polymorphic: varying QRS amplitudes and morphology
*most common cause of polymorphic VT with normal QTc is myocardial ischemia
-Torsades de Pointes = polymorphic VT with prolonged (>0.44s) QTc
*causes: idiopathic, acquired (electrolyte disturbances, drugs, etc)
*most are acquired and pause-dependent (precipitated by slow HR)
Management of Polymorphic VT
-Unstable: defibrillation (in contrast to cardioversion for unstable VT)
-Stable: 1) Correct underlying causes-electrolytes, hypoxemia, myocardial ischemia
2) Medications
*Amiodarone (class IA, Na channel blocker): only if no prolongation of QTc (Level C evidence)
*Beta Blockers (class II): use in cases of myocardial ischemia (Level B)
*Lidocaine (class IB, Na channel blocker): use in cases of myocardial ischemia or infarction (Level C)
*Isoproterenol (nonselective beta agonist): when polymorphic VT is accompanied by bradycardia or appears precipitated by pauses in rhythm
3) Coronary angiography in cases of ischemia
Management of Torsades de Pointes (Polymorphic VT with long QTc)
-discontinue meds that prolong QTc
-correct electrolyte disturbances (K)
-magnesium sulfate 2g IV over 1 min, repeat in 10 mins prn then 1g/hr drip
-consider isoproterenol for refractory TdP associated w/bradycardia or drug-induced long QTc
-transvenous pacing
Procainamide
-class IA (Na channel blockade), also blocks potassium channels
-used in hemodynamically stable monomorphic VT
-contraindicated in prolonged QTc
Back to Our Case…
- Patient who presents with syncope, initial EKG reveals trifascicular block and prolonged QTc.
- Patient develops pulseless, wide complex tachycardia which is interpreted as VT and is defibrillated and started on procainamide drip
- Pt again develops unstable, wide complex tachycardia, this time interpreted to be polymorphic VT and is defibrillated. Initial EKG reviewed and in light of baseline long QTc, new rhythm interpreted further characterized as torsades de pointes. Pt given Magnesium sulfate
- Repeat EKG shows markedly prolonged QTc so procainamide is discontinued and the pt is started on lidocaine drip
- Transvenous pacemaker is placed as bridge to permanent PM/AICD
References:
- John Marx MD, Robert Hockberger MD, Ron Walls MD. Rosen’s Emergency Medicine, 7th edition. 2010.
- Neumar RW, et al. Part 8: Adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010 Nov 2; 122(18 suppl 3): S729-67.
- Zipes DP, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines. Circulation. 2006 Sep 5;114(10): e385-484.
Jay Khadpe MD
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