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), which is 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 patients who are conscious.

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 < 0.43 second for males and < 0.45 second for females. Values are considered prolonged when they are > 0.45 second for males or > 0.47 second for females (1). A family history may suggest a congenital syndrome.

ECG warning signs of impending TdeP VT in addition to 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

Warning Signs of Torsades de Pointes Ventricular Tachycardia

Image

Images courtesy of L. Brent Mitchell, MD.

The TdeP VT is suspected by recognizing a rapid, polymorphic VT, often that self-terminates. 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 ventricular premature 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

Clinical Calculators

QT Interval Correction (EKG)

• 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 biphasic 120 to 200 joules (or monophasic 360 joules). Nevertheless, early recurrence is the rule.

Electrolyte abnormalities (eg, hypokalemia), which can exacerbate the risk of ventricular arrhythmias, should be corrected. Patients often respond to magnesium, usually magnesium sulfate 2 g IV over 1 to 2 minutes. If this treatment is unsuccessful, a second bolus is given in 5 to 10 minutes, and a magnesium infusion of 3 to 20 mg/minute may be started in patients without renal insufficiency (1antiarrhythmic medication) shortens the QT interval and may be effective especially for medication-induced torsades de pointes (2). Class Ia, Ic, and III antiarrhythmics are avoided.

1).

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 (2).