The long QT interval responsible for torsades de pointes ventricular tachycardia (TdeP VT) can be acquired, congenital or a combination.
QT-interval prolongation predisposes to early after-depolarizations and spatial dispersion of ventricular refractoriness, which can lead to arrhythmias. (For discussion of congenital causes, see Long QT Interval Syndromes Long QT Interval Syndromes The long QT interval syndromes (LQTS) result from any congenital or acquired disorder of cardiac ion channel function or regulation (channelopathy) that prolongs ventricular myocyte action potential... read more , and see also Overview of Arrhythmias Overview of Arrhythmias The normal heart beats in a regular, coordinated way because electrical impulses generated and spread by myocytes with unique electrical properties trigger a sequence of organized myocardial... read more ).
Pathophysiology of 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.
The most common factor in acquired TdeP VT is a
QT interval–prolonging drug, especially Class Ia, Ic, or Class III antiarrhythmic drugs Medications for Arrhythmias The need for treatment of arrhythmias depends on the symptoms and the seriousness of the arrhythmia. Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic... read more
Other drugs that can induce TdeP VT include tricyclic antidepressants, phenothiazines, and certain antivirals and antifungals (see CredibleMeds for up-to-date information).
In most cases, there are several predisposing causes, which may include: female sex, older age, hypokalemia Hypokalemia Hypokalemia is serum potassium concentration < 3.5 mEq/L (< 3.5 mmol/L) caused by a deficit in total body potassium stores or abnormal movement of potassium into cells. The most common... read more , hypomagnesemia Hypomagnesemia Hypomagnesemia is serum magnesium concentration < 1.8 mg/dL (< 0.70 mmol/L). Causes include inadequate magnesium intake and absorption or increased excretion due to hypercalcemia or drugs... read more , hypothyroidism Hypothyroidism Hypothyroidism is thyroid hormone deficiency. Symptoms include cold intolerance, fatigue, and weight gain. Signs may include a typical facial appearance, hoarse slow speech, and dry skin. Diagnosis... read more , slow ventricular rate, irregular ventricular rate, acute intracranial disasters (eg, bleeding, stroke Overview of Stroke Strokes are a heterogeneous group of disorders involving sudden, focal interruption of cerebral blood flow that causes neurologic deficit. Strokes can be Ischemic (80%), typically resulting... read more , traumatic brain injury Traumatic Brain Injury (TBI) Traumatic brain injury (TBI) is physical injury to brain tissue that temporarily or permanently impairs brain function. Diagnosis is suspected clinically and confirmed by imaging (primarily... read more ), eating disorders Introduction to Eating Disorders Eating disorders involve a persistent disturbance of eating or of behavior related to eating that Alters consumption or absorption of food Significantly impairs physical health and/or psychosocial... read more , organophosphate poisoning Organophosphate Poisoning and Carbamate Poisoning Organophosphates and carbamates are common insecticide ingredients that inhibit cholinesterase activity, causing acute muscarinic manifestations (eg, salivation, lacrimation, urination, diarrhea... read more , and structural heart disease (especially acute ischemia, myocarditis, and ventricular hypertrophy).
Symptoms and Signs of Torsades 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 Ventricular Fibrillation (VF) Ventricular fibrillation causes uncoordinated quivering of the ventricle with no useful contractions. It causes immediate syncope and death within minutes. Treatment is with cardiopulmonary... read more and cause sudden death. Sometimes the long QT interval is detected after resuscitation.
Diagnosis of Torsades de Pointes Ventricular Tachycardia
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 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).
Pearls & Pitfalls
Torsades de pointes ventricular tachycardia
Treatment of Torsades de Pointes Ventricular Tachycardia
Unsynchronized direct current cardioversion for ventricular fibrillation
Correction of electrolyte abnormalities, especially hypokalemia
Magnesium sulfate (MgSO4) IV
Treatments to increase basal heart rate, including pacing or IV isoproterenol
Treatment of cause
An acute episode prolonged enough to cause hemodynamic compromise is treated with unsynchronized cardioversion Defibrillation Cardiopulmonary resuscitation (CPR) is an organized, sequential response to cardiac arrest, including Recognition of absent breathing and circulation Basic life support with chest compressions... read more , beginning with 100 joules. Nevertheless, early recurrence is the rule. Electrolyte abnormalities (eg, hypokalemia Hypokalemia Hypokalemia is serum potassium concentration < 3.5 mEq/L (< 3.5 mmol/L) caused by a deficit in total body potassium stores or abnormal movement of potassium into cells. The most common... read more ), 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 2nd 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. Lidocaine (a class Ib antiarrhythmic drug Class Ib antiarrhythmic drugs The need for treatment of arrhythmias depends on the symptoms and the seriousness of the arrhythmia. Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic... read more ) shortens the QT interval and may be effective especially for drug-induced torsades de pointes. Class Ia, Ic, and III antiarrhythmics are avoided.
If a drug is the cause, it is stopped, but until drug clearance is complete, patients with frequent or long runs of torsades de pointes ventricular tachycardia require treatment to shorten the QT interval. Because increasing the heart rate shortens the QT interval, temporary pacing, IV isoproterenol, or both are often effective. Increasing heart rate will also shorten the “long” in the “short-long-short” initiation sequences of TdeP VT.
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.
The long QT interval responsible for torsades de pointes ventricular tachycardia can be congenital or acquired.
Torsades de pointes runs are usually self-terminating but frequently recurrent.
Unsynchronized defibrillation is required if a torsades induces ventricular fibrillation.
The torsades rhythm is treated with magnesium sulfate 2 g IV over 1 to 2 minutes, correction of hypokalemia, pacing or isoproterenol to increase heart rate, and correction of the cause.
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