Torsades de Pointes Ventricular Tachycardia

TdeP VT results from any disorder of cardiac ion channel function or regulation that prolongs ventricular myocyte action potential duration as evidenced by prolongation of the rate-corrected QT interval on the ECG (QTc, typically calculated using Bazett's formula). The risk of TdeP VT is dependent on the degree of QTc prolongation, particularly if it is > 0.50 seconds.

TdeP VT may result from

• Loss of function of repolarizing potassium current channels OR

• Gain of function of depolarizing sodium or depolarizing calcium current channels

Each of these factors predisposes to TdeP VT by prolonging repolarization, which induces early after-depolarizations (secondary depolarization events during the plateau of the action potential) and spatial dispersion of ventricular refractoriness. The dispersion of refractoriness permits propagation of the early after-depolarizations and initiation of torsade de pointes ventricular tachycardia.

TdeP VT often causes syncope because the underlying rate (200 to 250 beats/minute) is nonperfusing. Palpitations are common among conscious patients. Because the QT interval shortens with increased ventricular rates TdeP VT is often self-terminating. However, it instead may degenerate into ventricular fibrillation and cause sudden death. Sometimes the long QT interval is detected after resuscitation.

• Electrocardiography (ECG)

Diagnosis is by ECG showing an undulating QRS axis, with the polarity of complexes shifting around the baseline (see figure Torsades de pointes ventricular tachycardia). ECG between episodes shows a long QT interval after correction for heart rate (QTc). Normal QTc values are about 0.40 second for men and 0.41 second for women and are considered prolonged when > 0.47 second for men or > 0.48 second for women. A family history may suggest a congenital syndrome.

ECG warning signs of impending TdeP VT other than prolongation of the QT interval include

• T-wave and U-wave fusion (sometimes with giant TU waves)

• Post-extrasystolic changes in repolarization pattern

• Macroscopic T-wave alternans (visible alternation of two different appearing T-waves)

• Frequent polymorphic ventricular premature beats representing single beats of TdeP (often in bigeminy)

• Repetitive short runs of polymorphic ventricular tachycardia

The TdeP VT itself is a rapid, polymorphic VT that tends to self-terminate. Onset typically follows a short-long-short RR interval initiation sequence (although this sequence is not specific for TdeP VT): The first short RR interval is between a baseline beat (usually a normal beat) and a premature beat (usually a premature ventricular beat). The long RR interval is the post-extrasystolic pause and ends with a baseline beat (usually a normal beat). The pause further prolongs the QT interval of this baseline beat and it is followed by a short RR interval when the TdeP VT begins. Although patients may have a normal QTc at other times, the QTc is usually substantially prolonged around the time of TdeP VT and the QT interval of the last QRS complex prior to TdeP VT must be long (often with a giant TU wave).

Torsades de pointes ventricular tachycardia

• Unsynchronized direct current cardioversion for ventricular fibrillation

• Correction of electrolyte abnormalities, especially hypokalemia

• Magnesium sulfate (MgSO4) IV

• Treatment of cause

An acute episode prolonged enough to cause hemodynamic compromise is treated with unsynchronized cardioversion, beginning with 100 joules. Nevertheless, early recurrence is the rule. Electrolyte abnormalities (eg, hypokalemiaantiarrhythmic drug) shortens the QT interval and may be effective especially for drug-induced torsades de pointes. Class Ia, Ic, and III antiarrhythmics are avoided.

Long-term treatment is avoidance of conditions that prolong the QT interval. Some patients with an acquired long QT-interval syndrome have an underlying subclinical congenital long QT-interval syndrome suggested by persistent QTc interval prolongation after removal of exogenous QTc prolonging influences.