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Emergency Medicine > CARDIOVASCULAR
Torsade de Pointes
Article Last Updated: Mar 27, 2008
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Michael J Bessette, MD, FACEP, Director of Emergency Medicine, Bayonne Medical Center
Michael J Bessette is a member of the following medical societies: American College of Emergency Physicians
Coauthor(s):
Sheldon Jacobson, MD, Chair, Professor, Department of Emergency Medicine, Mount Sinai Medical Center
Editors: Theodore J Gaeta, DO, MPH, FACEP, Clinical Associate Professor, Department of Emergency Medicine, Joan and Sanford Weill Medical College at Cornell University; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Gary Setnik, MD, Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School; John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center; Charles V Pollack, Jr, MD, MA, FACEP, Professor, Department of Emergency Medicine, University of Pennsylvania College of Medicine; Chairman, Department of Emergency Medicine, Pennsylvania Hospital
Author and Editor Disclosure
Synonyms and related keywords:
torsade de pointes, TDP, torsade, ventricular tachycardia, VT, polymorphous VT, twisting of the point, cardiac syncope, vasovagal syncope, QT syndrome, QT interval, sudden death, unstable heart beat rhythm, TDP rhythm, dysrhythmia, Brugada syndrome
Background
Torsade de pointes (TDP), often referred to as torsade, is an uncommon variant of ventricular tachycardia (VT). The underlying etiology and management of torsade are, in general, quite different from those of garden-variety VT. The management of torsade with group IA antidysrhythmic drugs can have disastrous consequences. Differentiating between these entities, therefore, is critically important.
For related CME activities, see Medscape's Cardiology CME.
Pathophysiology
Torsade is defined as a polymorphous VT in which the morphology of the QRS complexes varies from beat to beat. The ventricular rate can range from 150 beats per minute (bpm) to 250 bpm. The original report described regular variation of the morphology of the QRS vector from positive to net negative and back again. This was symbolically termed torsade de pointes, or "twisting of the point" about the isoelectric axis, because it reminded the original authors of the torsade de pointes movement in ballet. Most cases exhibit polymorphism, but the axis changes may not have regularity.
The definition also requires that the QT interval be increased markedly (usually to 600 msec or greater). Cases of polymorphous VT, which are not associated with a prolonged QT interval, are treated as generic VT. Torsade usually occurs in bursts that are not sustained; thus, the rhythm strip usually shows the patient's baseline QT prolongation.
The underlying basis for rhythm disturbance is delay in phase III of the action potential. The delay is mediated by the hERG potassium channel. This prolonged period of repolarization and the inhomogeneity of repolarization times among myocardial fibers allow the dysrhythmia to emerge. The initiating electrophysiologic mechanism may be triggered activity or reentry.
Six genetic variants currently are recognized. Genotypes LQT1 and LQT2 have slow potassium channels, while LQT3 shows defects in the sodium channels. Treatment modalities soon may be based on the genotype of the individual.
Frequency
United States
Prevalence of torsade is still unknown.
Mortality/Morbidity
In the United States, 300,000 sudden cardiac deaths occur per year. TDP probably accounts for fewer than 5%.
Race
Brugada syndrome is more frequent in Southeast Asians.1
Sex
Women are 2-3 times more likely to develop TDP than men.
- Women have more QT prolongation secondary to drug therapy.
- Congenital long QT syndrome is autosomal dominant but shows greater frequency of expression and a greater lengthening of the QT interval in women than in men.
Age
The highest frequency is in patients aged 35-50 years.
History
- Ask the patient about previous cardiac events or syncope and any medications that the patient is presently using.
- History of congenital deafness or family history of sudden death may indicate a long QT syndrome.
Physical
No physical findings are typical of torsade de pointes (TDP).
Causes
- Prolongation of the QT interval may be congenital, as seen in the Jervell and Lange-Nielsen syndrome (ie, congenitally long QT associated with congenital deafness) and the Romano Ward syndrome (ie, isolated prolongation of QT interval). Both of these syndromes are associated with sudden death due to either primary ventricular fibrillation or torsade that degenerates into ventricular fibrillation.
- Prolonged QT is found in only 0.25-0.3% of deaf-mute children.
- Brugada syndrome is characterized by a coved ST segment in the right precordial leads. The syndrome may cause sudden death due to polymorphic VT resembling TdP.
- The acquired conditions that predispose one to torsade either decrease the outward potassium current or interfere with the inward sodium and calcium currents, or fluxes.
- The electrolyte disturbances that have been reported to precipitate torsade include hypokalemia and hypomagnesemia. Close observation is required in predisposed patients, such as those with cirrhosis or hypothyroidism.
- Hypokalemia and hypomagnesemia, in turn, cause a delay in phase III (ie, reprolongation) and form the substrate for emergence of the dysrhythmia.
- Antiarrhythmic drugs reported to be etiologic include class IA agents (eg, quinidine, procainamide, disopyramide), class IC agents (eg, encainide, flecainide), and class III agents (eg, sotalol, amiodarone).
- Drug interactions with the antihistamines astemizole (recalled from US market) and terfenadine (recalled from US market) can precipitate torsade; these drugs should never be used with class IA, IC, or III agents.
- Astemizole and terfenadine, in high dosages or when used in combination with the azole antifungal drugs or the macrolide antibiotics, have been reported to precipitate torsade and sudden death.
- Grapefruit juice has been shown to slow the hepatic metabolism of these antihistamines as well as other drugs and to prolong the QT interval in patients taking astemizole or terfenadine (recently taken off the market by the US Food and Drug Administration [FDA]).
- Clinical implications of this interaction are unclear.
- Other drugs that prolong the QT interval and have been implicated in cases of torsade include phenothiazines, tricyclic antidepressants, lithium carbonate, cisapride, highly active antiretrovirals (HAARTs), high-methadone, anthracycline chemotherapeutic agents (eg, doxorubicin, daunomycin), some fluoroquinolones, and any other medication using the CYP3A metabolic pathway. Ranolazine, an antiangina agent, also prolongs the QTc, but torsade is a rare complication of this therapy.
- Risk factors
- Female gender
- History of syncope or resuscitated arrest
- Congenital deafness
- Family history of sudden death
Pediatrics, Tachycardia
Renal Failure, Chronic and Dialysis Complications
Toxicity, Antidysrhythmic
Toxicity, Antihistamine
Ventricular Fibrillation
Ventricular Tachycardia
Lab Studies
- Potassium, magnesium, and calcium levels
Other Tests
- Electrocardiogram (ECG): Once in sinus rhythm, examine the QT interval. See Media files 1-2 for typical examples.
- Frequent ECG monitoring is indicated for patients who are at risk due to chronic conditions or drug therapy.
Prehospital Care
- Institute immediate advanced cardiac life support (ACLS) protocol for VT.
- Overdrive pacing may be necessary at a rate of up to 140 bpm to control the rhythm.
Emergency Department Care
Torsade, an inherently unstable rhythm, is prone to revert to more stable rhythms spontaneously and prone to recurrences. Torsade also is subject to degeneration into ventricular fibrillation. Begin therapy as soon as the rhythm clearly fulfills the criteria for torsade.
- Treat hypokalemia if it is the precipitating factor and administer magnesium sulfate in a dose of 2-4 g intravenously (IV) initially.
- Magnesium is usually very effective, even in the patient with a normal magnesium level.
- If this fails, repeat the initial dose, but because of the danger of hypermagnesemia (depression of neuromuscular function) the patient requires close monitoring.
- Other therapies include overdrive pacing and isoproterenol infusion. Most (75-82%) torsade de pointes (TDP) rhythms are started by a pause. Pacing at rates up to 140 bpm may prevent the ventricular pauses that allow TDP to originate.
- The patient with torsade who is in extremis should be treated with electrical cardioversion or defibrillation. Anecdotal reports cite successful conversion with phenytoin (Dilantin) and lidocaine.
- Patients with congenital long QT syndromes are thought to have an abnormality of sympathetic balance or tone and are treated with beta-blockers. If the patient breaks through this therapy and enters the ED in torsade, a short-acting beta-blocker, such as esmolol, can be tried.
- A few cases of successful conversion using phenytoin and overdrive pacing have been reported.
- If patient is unresponsive to conversion with phenytoin and overdrive pacing, attempt electrical cardioversion.
- Cervical sympathectomy and implantable pacemakers/defibrillators have been used in some cases for long-term management.
- Shortening the action potential decreases the likelihood of immediate recurrence. Pacing or administration of isoproterenol to a rate of 90-100 bpm is effective.
- Withdraw all QT-prolonging drugs.
Consultations
Immediate cardiology evaluation and follow-up are required.
Magnesium and potassium are first-line therapies in the treatment of torsade de pointes (TDP). Isoproterenol and short-acting beta-blockers have also been used. For treatment of primary torsades associated with congenital prolonged QT syndromes, use a beta-blocker. In primary and secondary torsade, overdrive pacing is an appropriate secondary therapy. In treatment of recurrent torsade, implantable defibrillators are used as prophylaxis. If the patient is hemodynamically unstable, carry out electrical cardioversion or defibrillation at once.
Drug Category: Electrolytes
Therapeutic alternatives for the treatment of torsade de pointes. Assessment of patient for underlying electrolyte abnormalities that may cause refractory dysrhythmia is important. Some of the electrolyte abnormalities associated with torsade de pointes include hypokalemia and hypomagnesemia. Electrolytes also reduce the arrhythmic effects of offending drugs.
| Drug Name | Magnesium sulfate |
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| Description | DOC for treatment of torsade de pointes. Acts as antiarrhythmic agent and diminishes frequency of PVCs, particularly when secondary to acute ischemia. Deficiency in this electrolyte is associated with sudden cardiac death and can precipitate refractory VF. Magnesium supplementation is used for treatment of torsade de pointes, known or suspected hypomagnesemia, or severe refractory VF. |
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| Adult Dose | 1-2 g IV diluted in 100 mL of D5W over 1-2 min; may repeat q4h with close monitoring of deep tendon reflexes |
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| Pediatric Dose | Torsade de pointes: Not established
Hypomagnesemia: 25-50 mg/kg/dose IV q4-6h for 3-4 doses; single dose not to exceed 2 g also may be administered and repeated if hypomagnesemia persists |
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| Contraindications | Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis |
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| Interactions | 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 |
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| Pregnancy | A - Fetal risk not revealed in controlled studies in humans
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| Precautions | Magnesium may alter cardiac conduction, leading to heart block in digitalized patients; respiratory rate, deep tendon reflexes, and renal function should be monitored when administered parenterally; caution when administering since 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 |
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| Drug Name | Potassium chloride (Klor-Con, K-Dur, Micro-K) |
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| Description | First-line therapy in treatment of torsade de pointes. Essential for maintenance of intracellular tonicity, transmission of nerve impulses, contraction of cardiac, skeletal, and smooth muscles, and maintenance of normal renal function. Gradual potassium depletion occurs via renal excretion, through GI loss, or because of low intake. Depletion usually results from diuretic therapy, primary or secondary hyperaldosteronism, diabetic ketoacidosis, severe diarrhea (if associated with vomiting), or inadequate replacement during prolonged parenteral nutrition. Depletion sufficient to cause 1 mEq/L drop in serum potassium requires a loss of about 100-200 mEq of potassium from the total body store. |
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| Adult Dose | Serum levels >2.5 mEq/L: 10 mEq over 1 h prn based on frequently obtained lab values; not to exceed 200 mEq/d
Serum levels <2.5 mEq/L: 40 mEq over 1 h prn based on frequently obtained lab values; not to exceed 400 mEq/d |
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| Pediatric Dose | 1 mEq/kg IV over 1-2 h prn based on frequently obtained lab values |
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| Contraindications | Documented hypersensitivity; hyperkalemia, renal failure, conditions in which potassium is retained, oliguria, azotemia, crush syndrome, severe hemolytic reactions, anuria, adrenocortical insufficiency |
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| Interactions | ACE inhibitors may result in elevated serum potassium concentrations; potassium-sparing diuretics and potassium-containing salt substitutes can produce severe hyperkalemia; in patients taking digoxin, hypokalemia may result in digoxin toxicity; use caution if discontinuing a potassium preparation in patients maintained on digoxin |
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| Pregnancy | A - Fetal risk not revealed in controlled studies in humans
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| Precautions | Do not infuse rapidly; high plasma concentrations of potassium may cause death due to cardiac depression, arrhythmias, or arrest; plasma levels do not necessarily reflect tissue levels; monitor potassium replacement therapy whenever possible by continuous or serial ECG; when concentration >40 mEq/L infused, local pain and phlebitis may follow |
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Drug Category: Adrenergic agonist
These agents alter the electrophysiologic mechanisms responsible for arrhythmic disturbances.
| Drug Name | Isoproterenol (Isuprel) |
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| Description | Stimulates beta1- and beta2-adrenergic receptor activity. Binds beta-receptors of heart, smooth muscle of bronchi, skeletal muscle, skeletal vasculature, and alimentary tract. Positive inotropic and chronotropic actions. |
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| Adult Dose | 1 mL of 1:5000 solution (0.2 mg) diluted in 10 mL sodium chloride or 5% dextrose injection
0.02-0.06 mg IV (1-3 mL of diluted solution) initially
0.01-0.2 mg IV (0.5-10 mL of diluted solution) subsequent doses to achieve heart rate of 90-100 bpm
Alternatively, 10 mL of 1:5000 solution (2 mg) diluted in 500 mL of D5W, or 5 mL of 1:5000 solution (1 mg) diluted in 250 mL of D5W
5 mcg/min (1.25 mL/min of diluted solution) subsequent doses to achieve heart rate of 90-100 bpm |
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| Pediatric Dose | Not established
AHA recommends initial infusion rate of 0.1 mcg/kg/min IV; titrate to HR effect |
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| Contraindications | Documented hypersensitivity; tachyarrhythmias; tachycardia or heart block caused by digitalis intoxication; ventricular arrhythmias that require inotropic therapy; angina pectoris |
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| Interactions | Bretylium increases action of vasopressors on adrenergic receptors, which may, in turn, 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 |
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| 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
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| Precautions | By increasing myocardial oxygen requirements while decreasing effective coronary perfusion, isoproterenol may have deleterious effect on injured or failing heart; isoproterenol may worsen heart blocks or precipitate Adams-Stokes attacks in some patients, presumably with organic disease of AV node and its branches; caution with coronary artery disease, coronary insufficiency, diabetes, hyperthyroidism, patients sensitive to sympathomimetic amines; if HR exceeds 110 bpm, may be advisable to decrease infusion rate or temporarily discontinue infusion |
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Drug Category: Beta-adrenergic Blocker
Excellent for use in patients at risk for experiencing complications from beta-blockade, particularly with reactive airway disease, mild to moderately severe left ventricular dysfunction, and peripheral vascular disease. The short half-life of 8 min allows for titration to desired effect and ability to stop quickly if needed.
| Drug Name | Esmolol (Brevibloc) |
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| Description | Ideal for use in patients at risk for experiencing complications from beta-blockade, especially patients diagnosed with mild to moderately severe LV dysfunction and those with peripheral vascular disease. Has short half-life of 8 min; thus, easily titratable to desired effect. Therapy may be stopped quickly prn. |
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| Adult Dose | Initially, 500 mcg/kg/min IV infusion for 1 min followed by 4-min maintenance infusion of 50 mcg/kg/min; if adequate therapeutic effect not observed within 5 min, repeat loading dose and follow with maintenance infusion of 100 mcg/kg/min; continue titration procedure, repeating loading infusion and increasing maintenance infusion by increments of 50 mcg/kg/min for 4 min |
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| Pediatric Dose | Not established; suggested dose 100-500 mcg/kg administered IV over 1 min |
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| Contraindications | Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities |
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| Interactions | Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives may increase cardiotoxicity; digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents increase toxicity |
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| 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
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| Precautions | Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm, may worsen when medication withdrawn abruptly; withdraw drug slowly and monitor patient closely |
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Further Inpatient Care
- Admit patient to ICU for continued monitoring and withdrawal of offending drugs.
Transfer
- Since ICU care is warranted, transfer patient to a facility with acute cardiac care capabilities.
Deterrence/Prevention
- Avoid QT-prolonging medications.
- Patients with torsade de pointes (TDP) have a 50% chance of a recurrence even with therapy.
Medical/Legal Pitfalls
- Failure to recognize as separable from other forms of VT
- If one fails to differentiate this rhythm disturbance, the therapy of the dysrhythmia is likely to include a type IA antidysrhythmic agent, such as procainamide.
- Type IA agents perpetuate the rhythm disturbance in torsade de pointes (TDP).
| Media file 1:
A run of torsade de pointes in a 70-year-old man who developed QT prolongation (QTc = 0.61 sec) secondary to quinidine therapy. The bottom strip shows resolution with overdrive ventricular pacing. |
 |  View Full Size Image | |
Media type: Rhythm Strip
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| Media file 2:
A patient with prolonged QT and atrial ectopy. Strip shows premature beat that entrains and a run of torsade de pointes. |
 | View Full Size Image | |
Media type: Rhythm Strip
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Torsade de Pointes excerpt Article Last Updated: Mar 27, 2008
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