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POLYMORPHIC VENTRICULAR TACHYCARDIA

Recommendations for Treatment of Adults With Polymorphic Ventricular Tachycardia COR LOE Recommendations

1 B-NR 1.  Immediate unsynchronized shock is recommended for adults with sustained polymorphic ventricular tachycardia.

2b C-LD 2.  Magnesium may be considered for treatment of adults with recurrences of polymorphic ventricular tachycardia associated with a long QT interval (torsades de pointes).

2b C-LD 3.  IV lidocaine, amiodarone, and measures to treat myocardial ischemia may be considered to treat recurrences of polymorphic VT in adults in the absence of a prolonged QT interval.

3: No Benefit C-LD 4.  Routine use of magnesium is not recommended for the treatment of polymorphic VT in adults with a normal QT interval.

Synopsis Polymorphic VT refers to a wide-complex tachycardia of ventricular origin with differing configurations of the QRS complex from beat to beat. However, the most critical feature in the diagnosis and treatment of polymorphic VT is not the morphology of the rhythm but rather what is known (or suspected) about the patient’s underlying QT interval. It is often difficult to know whether the tachycardia is pVT or ventricular fibrillation (VF). Most VF begins with pVT and if pVT is prolonged it will usually degenerate into VF (Figure 6). Torsades de pointes is a form of polymorphic VT that is associated with a prolonged heart rate–corrected QT interval when the rhythm is normal and VT is not present. The risk for developing torsades increases when the corrected QT interval is greater than 500 milliseconds and accompanied by bradycardia.1 Torsades can be due to an inherited genetic abnormality2 or can be caused by drugs and electrolyte imbalances that lengthen the QT interval.3 Conversely, polymorphic VT not associated with a long QT is most often due to acute myocardial ischemia.4,5 Other potential causes include catecholaminergic polymorphic VT, a genetic abnormality in which polymorphic VT is provoked by exercise or emotion6; “short QT” syndrome, a form of polymorphic VT associated with an unusually short QT interval (corrected QT interval less than 330–370 milliseconds)7,8; idiopathic right ventricular outflow tract polymorphic VT; and bidirectional VT seen in digitalis toxicity in which the axis of alternate QRS complexes shifts by 180°.9 There are no RCTs examining the acute pharmacological treatment of polymorphic VT. Supportive data, with and without long corrected QT interval, are largely based on case reports and case series. Recommendation-Specific Supportive Text

1 Regardless of the underlying QT interval, all forms of

polymorphic VT are considered hemodynamically and electrically unstable. Episodes of polymorphic VT may repeatedly recur and remit spontaneously, become sustained, or degenerate to VF. When the QRS complex of a VT is of uniform morphology, electric cardioversion synchronized to the QRS complex minimizes the risk of provoking VF during the vulnerable period of the cardiac cycle (T wave). In contrast, polymorphic VT cannot be synchronized reliably because of the differing characteristics of each QRS complex and requires high-energy (maximum manufacturer’s setting) unsynchronized shock. Assessment of a patient’s mental status is important when the appropriateness of sedation is considered before defibrillation. While effective in terminating polymorphic VT, defibrillation may not prevent its recurrence, for which pharmacological therapies are often required and the primary focus of subsequent recommendations. 2.	 Torsades de pointes typically presents in a recurring pattern of self-terminating, hemodynamically unstable polymorphic VT in context of a known or suspected long QT abnormality, often with an associated bradycardia. Termination of torsades by defibrillation may not prevent its recurrence, which requires additional pharmacological interventions. In small case series, IV magnesium has been effective in suppressing and preventing recurrences.10–13 Magnesium is believed to suppress fluctuations in the myocardial action potential that can trigger torsades.14 Correcting electrolyte abnormalities, particularly hypokalemia, is also advisable. Treatment of torsades with antiarrhythmic medications may prolong the QT interval and promote the arrhythmia. When given acutely, β-adrenergic blockers can also precipitate torsades by causing or worsening bradycardia. In patients with bradycardia or pause-precipitated torsades, expert consultation is best sought for additional measures such as overdrive pacing or isoproterenol.15 There is literature to support instances of medication induced torsades, so prevention of drug induced prolonged QT is an important priority for professionals. 3.	 Polymorphic VT that is clearly not associated with

QT prolongation, is most often triggered by acute myocardial ischemia or infarction and often rapidly degenerates into VF.3,5 Polymorphic VT may be difficult to differentiate from VF initially, but, as with other ventricular arrhythmias (VT and VF), is terminated with immediate defibrillation. However, termination of polymorphic VT with defibrillation may not prevent its recurrence, requiring additional pharmacological measures. No RCTs have been performed to determine the optimal pharmacological management of

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