DESCRIPTION

• Torsade de pointes (translated from French as "twisting of the pointes") ventricular tachycardia (TdP) is a polymorphic ventricular tachycardia that occurs in the setting of a prolonged QT interval.
• It is recognized by the EKG appearance of nonuniform but organized rotation, or twisting, of the peaks of the QRS around the central axis of the EKG baseline.
• Although polymorphic, there is a distinct progressive increase and decrease in the amplitude of the QRS within each burst.
• The arrhythmia may occur in the congenital long QT syndrome, as an idiosyncratic response to a variety of drugs, as well as in bradycardia and electrolyte abnormalities, specifically hypokalemia and hypomagnesemia.
• The congenital variety is discussed in the topic on Long QT Syndrome. The short-term management of the acquired and congenital syndromes has many similarities, but the long-term management and prognosis are different.
• Synonym(s): Torsades; Polymorphic ventricular tachycardia with QT prolongation; Atypical ventricular tachycardia; Ventricular fibrillo-flutter; Paroxysmal ventricular fibrillation; Transient ventricular fibrillation

Pregnancy Considerations

Not a contraindication to pregnancy. However, arrhythmias are sometimes exacerbated by pregnancy, especially if electrolyte disturbances develop.

EPIDEMIOLOGY

Prevalence depends on population studied, especially on what drugs are used in the population. All age groups can be affected, although presentation of the congenital form occurs more often in the younger age group and presentation of the acquired form in older patients after drug administration.

RISK FACTORS

• Female gender
• Length of QT interval

ETIOLOGY

OTHER

• At least 6 genes have been identified, as discussed in the topic on the Long QT Syndrome.
• When TdP occurs independently of the congenital form, it is unknown whether there is genetic predisposition that becomes manifest when a precipitating stimulus is present (ie, drugs listed below, hypokalemia, hypomagnesemia).
• Conditions that prolong repolarization:
  • Hypokalemia
  • Hypomagnesemia
  • Hypocalcemia
  • Bradycardia
  • Hypothyroidism
• Altered nutritional states (liquid protein diet, anorexia nervosa)
• Neurologic catastrophes, such as subarachnoid hemorrhage, that alter myocardial repolarization.

COMMONLY ASSOCIATED CONDITIONS

None are known in the congenital form. For the acquired form, patients are usually treated with a QT-prolonging drug for a specific medical problem.

Outline

• Description
  • Pregnancy Considerations
• Epidemiology
• Risk Factors
• Etiology
  • Other
• Commonly Associated Conditions

Signs and symptoms:

• Syncope and presyncope
• Palpitations

DIAGNOSTIC TESTS & INTERPRETATION

• The EKG is the diagnostic test and shows:
• Polymorphic ventricular tachycardia that varies from beat to beat and appears to rotate around the central axis of the EKG
• Rate variable, usually 160–250 bpm
• Long QT interval, initiated by long-short coupling interval [eg, premature ventricular complex (PVC) followed by pause, sinus beat, and late cycle PVC (after peak of T wave)]
• EKG may show T-wave alternans, or variability of T wave amplitude and/or morphology before TdP onset.
• Often multiple nonsustained bursts

Lab

None for general use, although genetic screening is done in a research context

DIFFERENTIAL DIAGNOSIS

• Recognition of the characteristic pattern in the setting of a prolonged QT interval on the ECG is the foundation of the diagnosis.
• Polymorphic ventricular tachycardia caused by ischemia in the setting of acute MI, or as an idiopathic arrhythmia, Brugada syndrome, central nervous system injury; that is, disease states that can alter cardiac repolarization, and therefore the QT interval

Outline

• Information
• Diagnostic Tests & Interpretation
  • Lab
• Differential Diagnosis

• Defibrillation if sustained (cardiac arrest)
• IV magnesium (1–2 g acutely)
• Isoproterenol can be used in the acute setting for drug-induced TdP. This is less frequently done today when TdP is acquired because it is frequently ineffective and temporary pacing is so successful.
• Alternatively to isoproterenol, atropine can be used.
• -Blockers are the pharmacologic mainstay of therapy in the congenital form (see topic on Long QT syndrome).
• Antiarrhythmic drugs, such as lidocaine, bretylium, and phenytoin, yield inconsistent benefit.

ADDITIONAL TREATMENT

General Measures

• see topic on long QT syndrome for management of TdP in that setting.
• For the idiopathic variety, avoidance and withdrawal of drugs that cause the syndrome are the mainstays of therapy.
• Correction of hypokalemia, hypomagnesemia, and hypocalcemia is essential.
• Pacing can be used to prevent TdP in the acute setting, especially when it occurs in the setting of bradycardia.
• Treat hypothyroidism, if present.

SURGERY

see topic on Long QT syndrome for congenital variety.

IN-PATIENT CONSIDERATIONS

Admission Criteria

• Admission is virtually always indicated when this arrhythmia is recorded because it can lead to cardiac arrest.
• Discharge is dictated by resolution/removal of the precipitating cause or appropriate medical management of the congenital long QT syndrome.

Outline

• Additional Treatment
  • General Measures
• Surgery
• In-Patient Considerations
  • Admission Criteria

FOLLOW-UP RECOMMENDATIONS

Patient Monitoring

• see topic on Long QT syndrome for follow-up monitoring in the congenital form.
• For acquired TdP, avoidance of precipitating causes is essential.
• If antiarrhythmic treatment is necessary, use drugs that shorten QT (mexiletine, phenytoin). Note that amiodarone can uncommonly cause TdP.
• When in response to precipitating cause, it is often idiosyncratic and therefore cannot be predicted.
• Avoid and prevent bradycardia, hypokalemia, hypomagnesemia, hypocalcemia, hypothyroidism, and drugs described in this topic.

PATIENT EDUCATION

• Avoid contraindicated drugs, hypokalemia, hypomagnesemia, and hypocalcemia.
• Learn contraindicated drugs.
• see the Appendix for the table on list of QT-prolonging drugs.

PROGNOSIS

In the acquired form, outcome is generally good if precipitating causes are avoided. see topic on Long QT syndrome regarding congenital form.

Outline

• Follow-Up Recommendations
  • Patient Monitoring
• Patient Education
• Prognosis

CODES

ICD9

427.1Paroxysmal ventricular tachycardia

SNOMED

• 31722008 Torsades de pointes (disorder)
• 66657009 paroxysmal ventricular tachycardia (disorder)

ADDITIONAL READING

• Dessertenne F. La tachycardie ventriculaire á deux foyers opposé variables. Arch Mal Coeur. 1966;59:263–272.
• Haverkamp W, Shenasa M, Borggrefe M, et al. Torsades de pointes. In: Zipes DP, Jalife J, eds., Cardiac Electrophysiology: From Cell to Bedside. Philadelphia: WB Saunders, 1995:885–899.

Peter Ott

Andrew E. Epstein