eMedicine Specialties > Emergency Medicine > Cardiovascular
Torsade de Pointes: Treatment & Medication
Updated: Aug 4, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
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Treatment
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.
Medication
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.
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.
Magnesium sulfate
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.
Adult
1-2 g IV diluted in 100 mL of D5W over 1-2 min; may repeat q4h with close monitoring of deep tendon reflexes
Pediatric
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
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; 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 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
Potassium chloride (Klor-Con, K-Dur, Micro-K)
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.
Adult
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
Pediatric
1 mEq/kg IV over 1-2 h prn based on frequently obtained lab values
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
Documented hypersensitivity; hyperkalemia, renal failure, conditions in which potassium is retained, oliguria, azotemia, crush syndrome, severe hemolytic reactions, anuria, adrenocortical insufficiency
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
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
Adrenergic agonist
These agents alter the electrophysiologic mechanisms responsible for arrhythmic disturbances.
Isoproterenol (Isuprel)
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.
Adult
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
Pediatric
Not established
AHA recommends initial infusion rate of 0.1 mcg/kg/min IV; titrate to HR effect
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
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, 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
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.
Esmolol (Brevibloc)
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.
Adult
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
Pediatric
Not established; suggested dose 100-500 mcg/kg administered IV over 1 min
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
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 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
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 |
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Further Reading
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
