Azithromycin induced torsade de pointes image

Acute management

Treatment can be divided into short-term and long-term management. Short-term management of torsade is the same in image 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.

In an otherwise stable patient, direct current (DC) cardioversion is kept as a last resort, because torsade is paroxysmal in nature and is characterized by its frequent recurrences following cardioversion. Although torsade frequently is self-terminating, it may degenerate into ventricular fibrillation, which requires DC defibrillation.

Any offending agent should be withdrawn. Predisposing conditions such as hypokalemia, hypomagnesemia, and bradycardia should be identified and corrected.

Pharmacologic therapy

Magnesium is the drug of choice for suppressing early afterdepolarizations (EADs) and terminating the arrhythmia. Magnesium achieves this by decreasing the influx of calcium, thus lowering the amplitude of EADs. [19]

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. Because of the danger of hypermagnesemia (depression of neuromuscular function), the patient requires close monitoring.

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.

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 experiences breakthrough torsade, a short-acting beta-blocker, such as esmolol, can be tried. [20]

Isoproterenol 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 above 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 such as isoproterenol 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. This is dependent on intact atrial-to-ventricular conduction at the pacing rate found necessary.

Pacing azithromycin induced torsade de pointes image should be instituted at a rate of 90-110 bpm until the QT interval is normalized. Overdrive pacing may be necessary at a rate of up to 140 bpm to control the rhythm.

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. 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.

Long-term treatment

Beta-adrenergic antagonists at maximally tolerated 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 should be avoided in those congenital cases in which bradycardia is a prominent feature. Beta-blockers are contraindicated in acquired long QT syndrome because bradycardia produced by these agents can precipitate torsade. One approach to assess the adequacy of beta-blockade is by exercise testing. One investigator recommends aiming for at least a 20% reduction in maximum heart rate compared to that of the baseline (pre-beta blocker therapy). Another approach is to check the blood levels of beta blockers (eg, propranolol) when possible. [21]

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 with 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.

Long-term treatment in acquired long QT syndrome 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.


Immediate cardiology evaluation and follow-up are required. Other possible consultations include the following:

  • Electrophysiologist

  • Cardiologist

  • Geneticist (in cases of familial or congenital long QT syndrome)


Competitive sports are prohibited in patients with congenital long QT syndrome.


Complications may include the following:

  • Monomorphic ventricular tachycardia

  • Ventricular fibrillation

  • Sudden cardiac death


In congenital long QT syndrome, the mortality rate for untreated patients is 50% in 10 years, which can be reduced to 3-4% with therapeutic intervention.

In acquired long QT syndrome, the prognosis is excellent once the inciting factor has been identified and reliably withheld.

Patient education

Instruct patients to use medications only with the approval of a physician. Instruct patients to avoid competitive sports (in cases of congenital long QT syndrome).

Close follow-up is needed because of a risk of sudden cardiac death. Offer emotional support; suggest attending a cardiac support group.

Patients should be taught how to monitor their pulse and recognize adverse drug effects. Families should undergo training for basic life support.



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