eMedicine Specialties > Cardiology > Arrhythmias
Torsade de Pointes: Treatment & Medication
Updated: Jul 30, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
Treatment can be divided into short-term and long-term management. Short-term management of torsade is the same in both acquired and congenital long QT syndrome except that beta1-adrenergic stimulation may be tried in the acquired form but is contraindicated in the congenital form.
- Short-term treatment
- Defibrillation
- Although torsade frequently is self-terminating, it may degenerate into ventricular fibrillation, which requires direct current (DC) defibrillation.
- In an otherwise stable patient, DC cardioversion is kept as a last resort because torsade is paroxysmal in nature and is characterized by its frequent recurrences following cardioversion.
- Discontinuation of the offending agent
- Any offending agent should be withdrawn.
- Predisposing conditions such as hypokalemia, hypomagnesemia, and bradycardia should be identified and corrected.
- Suppression of early afterdepolarizations (EADs)
- Magnesium is the drug of choice for suppressing EADs and terminating the arrhythmia.6,7 This is achieved by decreasing the influx of calcium, thus lowering the amplitude of EADs. Magnesium can be given at 1-2 g IV initially in 30-60 seconds, which then can be repeated in 5-15 minutes. Alternatively, a continuous infusion can be started at a rate of 3-10 mg/min. Magnesium is effective even in patients with normal magnesium levels.
- Some authorities recommend supplemental potassium to increase the potassium concentration to high normal, which increases the efflux of potassium from myocardial cells, thus causing rapid repolarization.
- Lidocaine usually has no effect in torsade. Occasionally, it can have an initial beneficial effect, but torsade recurs in all cases.
- Mexiletine also may be helpful in suppressing torsade. In one study, it was used in patients with HIV who had acquired long QT interval and torsade. It effectively suppressed the torsade on a long-term basis.8
- Acceleration of the heart rate can be achieved by using beta1-adrenergic agonists such as isoproterenol or overdrive electrical pacing.
- Isoproterenol
- This drug can be used in bradycardia-dependent torsade that usually is associated with acquired long QT syndrome (pause-dependent). It should be administered as a continuous IV infusion to keep the heart rate faster than 90 bpm.
- Isoproterenol accelerates AV conduction and decreases the QT interval by increasing the heart rate and reducing temporal dispersion of repolarization. Beta-adrenergic agonists are contraindicated in the congenital form of long QT syndrome (adrenergic-dependent).
- Because of precautions, contraindications, and adverse effects associated with its use, this drug is used as an interim agent until overdrive pacing can be started.
- Temporary transvenous pacing
- Based on the fact that the QT interval shortens with a faster heart rate, pacing can be effective in terminating torsade. It is effective in both forms of the long QT syndrome because it facilitates the repolarizing potassium currents and prevents long pauses, suppressing EADs and decreasing the QT interval.
- Atrial pacing is the preferred mode because it preserves the atrial contribution to ventricular filling and also results in a narrower QRS complex and hence a shorter QT.
- In patients with AV block, ventricular pacing can be used to suppress torsade.
- Pacing should be instituted at a rate of 90-110 bpm until the QT interval is normalized.
- Defibrillation
- Long-term treatment
- Congenital long QT syndrome
- Beta-adrenergic antagonists at maximally treated doses are used as a first-line long-term therapy in congenital long QT syndrome. Propranolol is used most extensively, but other agents such as esmolol or nadolol also can be used. Beta-blockers are contraindicated in acquired cases because bradycardia produced by these agents can precipitate torsade. Beta-blockers should be avoided in those congenital cases in which bradycardia is a prominent feature.
- Patients without syncope, ventricular tachyarrhythmia, or a family history of sudden cardiac death can be observed without starting any treatment.
- Permanent pacing benefits patients who remain symptomatic despite receiving the maximally tolerated dose of beta-blockers and can be used adjunctively to beta-blockers. It decreases the QT interval by enhancing the repolarizing potassium currents and suppressing EADs.
- High left thoracic sympathectomy, another antiadrenergic therapy, is effective in patients who remain refractory to beta-blockade and pacing. Accidental ablation of ocular efferent sympathetic nerves may result in Horner syndrome.
- Implantable cardioverter-defibrillators (ICDs) are useful in instances when torsade recurs despite treatment with beta-blockers, pacing, and possibly left thoracic sympathectomy. Beta-blockers should be used along with ICDs because shock can further precipitate torsade by adrenergic stimulation. In the United States, an ICD for refractory cases may often precede sympathectomy.
- Acquired long QT syndrome
- Long-term treatment in acquired cases usually is not required because the QT interval returns to normal once the inciting factor or predisposing condition has been corrected.
- Pacemaker implantation is effective in cases that are associated with heart block or bradycardia.
- ICDs are indicated in cases that cannot be managed by avoidance of the offending agent.
- The boundary between acquired and congenital may not always be clear. Additive factors are often present, and individuals may show increased susceptibility to QT effects.
- Congenital long QT syndrome
Consultations
- Electrophysiologist
- Cardiologist
- Geneticist (in cases of familial or congenital long QT syndrome)
Diet
No special dietary restrictions are necessary unless warranted by a predisposing condition, eg, low-cholesterol and low-salt diet for patients with coronary artery disease.
Activity
Competitive sports are prohibited in patients with congenital long QT syndrome.
Medication
IV magnesium sulfate is the drug of choice for suppressing torsade in an acute setting; however, it is not used for long-term management. In the case of acquired long QT syndrome, the QT interval normalizes once the etiological agent has been reliably withheld, and the condition usually does not require long-term therapy. Beta-adrenergic antagonists are the drug of choice for the long-term treatment of congenital long QT syndrome and are contraindicated in the acquired form of the syndrome.
Electrolytes
Decreases amplitude of EADs by blocking inward calcium current and thus effectively terminating torsade. Effectively controls torsade on short-term basis.
Magnesium sulfate
Nutritional supplement in hyperalimentation; cofactor in enzyme systems involved in neurochemical transmission and muscular excitability. In adults, 60-180 mEq of potassium, 10-30 mEq of magnesium, and 10-40 mmol of phosphate/d may be necessary for optimum metabolic response. Give IV for acute suppression of torsade. Repeat doses are dependent upon continuing presence of patellar reflex and adequate respiratory function.
Adult
1-2 g IV over 30-60 s, repeat in 5-15 min if necessary; alternatively, 3-10 mg/min IV infusion
Pediatric
Not established for torsade, but in preeclampsia or eclampsia dose is 20-100 mg/kg IV q4-6h prn; in severe cases, may use doses as high as 200 mg/kg/dose
Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade seen with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants and betamethasone and cardiotoxicity of ritodrine
Documented hypersensitivity; heart block, Addison disease, myocardial damage, or severe hepatitis
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Magnesium may alter cardiac conduction, leading to heart block in digitalized patients; respiratory rate, deep-tendon reflex, and renal function should be monitored when electrolyte is administered parenterally; caution when administering magnesium dose because may produce significant hypertension or asystole; in overdose, calcium gluconate, 10-20 mL IV of 10% solution, can be given as antidote for clinically significant hypermagnesemia
Beta-adrenergic antagonists
In congenital long QT syndrome, events of torsade are triggered by some form of adrenergic stimulation that can be blocked effectively by beta-adrenergic antagonists. Propranolol is the most extensively used drug in these cases.
Propranolol (Inderal)
Class II antiarrhythmic nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions
Adult
3-5 mg/kg/d PO in divided doses
Pediatric
1-2 mg/kg PO bid
Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase
Documented hypersensitivity; uncompensated congestive heart failure; bradycardia, cardiogenic shock; AV conduction abnormalities
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely
Antiarrhythmics
Mexiletine is structurally similar to lidocaine and is active orally. In one study in patients with HIV and acquired long QT interval, it effectively suppressed torsade on a long-term basis.
Mexiletine (Mexitil)
As a cardiac (class IB) antiarrhythmic, preferentially binds to open or inactivated calcium channels with rapid association rate. Binding to open channels effectively shortens action potential (particularly the third phase), and binding to inactivated channels maintains the inactivated (refractory) state. This slows the firing of the cells. Presumably, a similar effect may occur in skeletal muscle.
Adult
200 mg PO tid initially to control cardiac arrhythmia; may increase by 50 or 100 mg q2-3d until 300 mg tid reached; sometimes, as much as 400 mg tid used; not to exceed 1200 mg/d
Pediatric
Not established
Aluminum-magnesium hydroxide compounds, atropine, narcotics, hydantoins, rifampin, and urinary acidifiers decrease levels; metoclopramide and urinary alkalinizers may increase levels; cimetidine can either increase or decrease levels; caffeine and theophylline levels are increased
Documented hypersensitivity; cardiogenic shock or in those who have second-degree or third-degree AV block (without a pacemaker)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Second-degree or third-degree AV block (without a pacemaker) is a contraindication; can be used cautiously in patients with pacemakers and second-degree or third-degree block and in those with first-degree AV blocks, sinus node dysfunction, intraventricular conduction abnormalities, hypotension, or congestive heart failure (cardiology consultation recommended before use in any of these medical conditions); liver injury reported, particularly in conjunction with congestive heart failure or cardiac ischemia; monitor liver enzymes; rarely, leukopenia or agranulocytosis has been seen; CBC count should be monitored; convulsions have occurred in approximately 0.2% of patients, thus, caution is indicated if history of seizures is present; avoid other drugs that significantly modify the pH of urine
Beta-adrenergic agonists
Isoproterenol, which exerts its effect by stimulation of beta1 and beta2 receptors, is used in those acquired cases of torsade that are bradycardia-dependent. Accelerates AV conduction and reduces QT interval by reducing temporal dispersion repolarization.
Isoproterenol (Isuprel)
Has beta1-adrenergic and beta2-adrenergic receptor activity. Binds beta-receptors of heart, smooth muscle of bronchi, skeletal muscle, vasculature, and alimentary tract. Has positive inotropic and chronotropic actions. Should be used only in those cases of torsade associated with acquired long QT syndrome. Given as a bridging device when cardiac pacing cannot be instituted immediately and underlying bradycardia is present or torsade is pause-dependent.
Adult
Initially, 5 mcg/min IV titrated to keep heart rate approximately 100 bpm (1-20 mcg/min)
Pediatric
Not established
Bretylium increases action of vasopressors on adrenergic receptors, which, in turn, may result in arrhythmias; guanethidine may increase effect of direct-acting vasopressors, possibly resulting in severe hypertension; tricyclic antidepressants may potentiate pressor response of direct-acting vasopressors
Documented hypersensitivity; tachyarrhythmias, tachycardia, or heart block caused by digitalis intoxication; ventricular arrhythmias that require inotropic therapy; angina pectoris
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
By increasing myocardial oxygen requirements while decreasing effective coronary perfusion, may have a deleterious effect on the injured or failing heart; in some patients, presumably with organic disease of the AV node and its branches, may paradoxically worsen heart blocks or precipitate Adams-Stokes attacks; caution in coronary artery disease, coronary insufficiency, diabetes, or hyperthyroidism and sensitivity to sympathomimetic amines; if heart rate exceeds 110 bpm, may be advisable to decrease infusion rate or temporarily discontinue infusion
More on Torsade de Pointes |
| Overview: Torsade de Pointes |
| Differential Diagnoses & Workup: Torsade de Pointes |
 Treatment & Medication: Torsade de Pointes |
| Follow-up: Torsade de Pointes |
| Multimedia: Torsade de Pointes |
| References |
| Further Reading |
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References
Noda T, Shimizu W, Satomi K, Suyama K, Kurita T, Aihara N. Classification and mechanism of Torsade de Pointes initiation in patients with congenital long QT syndrome. Eur Heart J. Dec 2004;25(23):2149-54. [Medline].
Antzelevitch C, Sicouri S. Clinical relevance of cardiac arrhythmias generated by afterdepolarizations. Role of M cells in the generation of U waves, triggered activity and torsade de pointes. J Am Coll Cardiol. Jan 1994;23(1):259-77. [Medline].
Nikolic G, Bishop RL, Singh JB. Sudden death recorded during Holter monitoring. Circulation. Jul 1982;66(1):218-25. [Medline].
Lehmann MH, Timothy KW, Frankovich D, et al. Age-gender influence on the rate-corrected QT interval and the QT-heart rate relation in families with genotypically characterized long QT syndrome. J Am Coll Cardiol. Jan 1997;29(1):93-9. [Medline].
Nguyen PT, Scheinman MM, Seger J. Polymorphous ventricular tachycardia: clinical characterization, therapy, and the QT interval. Circulation. Aug 1986;74(2):340-9. [Medline].
Tzivoni D, Banai S, Schuger C, et al. Treatment of torsade de pointes with magnesium sulfate. Circulation. Feb 1988;77(2):392-7. [Medline].
Kurita T, Ohe T, Shimizu W, et al. Early afterdepolarization in a patient with complete atrioventricular block and torsades de pointes. Pacing Clin Electrophysiol. Jan 1993;16(1 Pt 1):33-8. [Medline].
Kocheril AG, Bokhari SA, Batsford WP, Sinusas AJ. Long QTc and torsades de pointes in human immunodeficiency virus disease. Pacing Clin Electrophysiol. Nov 1997;20(11):2810-6. [Medline].
Attwell D, Cohen I, Eisner D, et al. The steady state TTX-sensitive ("window") sodium current in cardiac Purkinje fibres. Pflugers Arch. Mar 16 1979;379(2):137-42. [Medline].
el-Sherif N, Caref EB, Yin H, Restivo M. The electrophysiological mechanism of ventricular arrhythmias in the long QT syndrome. Tridimensional mapping of activation and recovery patterns. Circ Res. Sep 1996;79(3):474-92. [Medline].
Gintant GA, Datyner NB, Cohen IS. Slow inactivation of a tetrodotoxin-sensitive current in canine cardiac Purkinje fibers. Biophys J. Mar 1984;45(3):509-12. [Medline].
Jackman WM, Friday KJ, Anderson JL, et al. The long QT syndromes: a critical review, new clinical observations and a unifying hypothesis. Prog Cardiovasc Dis. Sep-Oct 1988;31(2):115-72. [Medline].
Justo D, Prokhorov V, Heller K, Zeltser D. Torsade de pointes induced by psychotropic drugs and the prevalence of its risk factors. Acta Psychiatr Scand. Mar 2005;111(3):171-6. [Medline].
Kaplinsky E, Yahini JH, Barzilai J, Neufeld HN. Quinidine syncope; report of a case successfully treated with lidocaine. Chest. Dec 1972;62(6):764-6. [Medline].
Kay GN, Plumb VJ, Arciniegas JG, et al. Torsade de pointes: the long-short initiating sequence and other clinical features: observations in 32 patients. J Am Coll Cardiol. Nov 1983;2(5):806-17. [Medline].
Locati EH, Maison-Blanche P, Dejode P, et al. Spontaneous sequences of onset of torsade de pointes in patients with acquired prolonged repolarization: quantitative analysis of Holter recordings. J Am Coll Cardiol. Jun 1995;25(7):1564-75. [Medline].
Roden DM. Drug-induced prolongation of the QT interval. N Engl J Med. Mar 4 2004;350(10):1013-22. [Medline].
Roden DM, Lazzara R, Rosen M, et al. Multiple mechanisms in the long-QT syndrome. Current knowledge, gaps, and future directions. The SADS Foundation Task Force on LQTS. Circulation. Oct 15 1996;94(8):1996-2012. [Medline].
Salle P, Rey JL, Bernasconi P, et al. [Torsades de pointe. Apropos of 60 cases]. Ann Cardiol Angeiol (Paris). Jun 1985;34(6):381-8. [Medline].
Tan HL, Hou CJ, Lauer MR, Sung RJ. Electrophysiologic mechanisms of the long QT interval syndromes and torsade de pointes. Ann Intern Med. May 1 1995;122(9):701-14. [Medline].
Taylor D. Psychotropic drugs, torsade de pointes and sudden death. Acta Psychiatr Scand. Mar 2005;111(3):169-70. [Medline].
Vitelli LL, Crow RS, Shahar E, et al. Electrocardiographic findings in a healthy biracial population. Atherosclerosis Risk in Communities (ARIC) Study Investigators. Am J Cardiol. Feb 15 1998;81(4):453-9. [Medline].
Further Reading
Related guidelines
ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices).
(1) ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to revise the 1999 guidelines for the Management of Acute Myocardial Infarction). (2) 2007 focused update of the ACC/AHA 2004 guidelines for the management of patients with ST-elevation myocardial infarction. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.
Practice standards for electrocardiographic monitoring in hospital settings: an American Heart Association scientific statement from the Councils on Cardiovascular Nursing, Clinical Cardiology, and Cardiovascular Disease in the Young.
ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation).
Keywords
torsade de pointes, quinidine syncope, polymorphic ventricular tachycardia, VT, prolonged QT interval, arrhythmia, TdP, torsade de pointes ventricular tachycardia, TdPVT, ventricular fibrillation, early after depolarization, EAD, afterdepolarization, arrhythmia, torsades de pointes, torsades, torsade, sudden cardiac death, SCD, sudden death, ventricular fibrillation, tachyarrhythmia
