100 QUESTIONS IN CARDIOLOGY

82 How do I treat torsade de pointes at a cardiac

arrest?

Simon Sporton

Consideration of the electrophysiological disturbances pre-

disposing to the development of torsade de pointes provides a logical

approach to management. Experimental and clinical evidence impli-

cates abnormal prolongation of cardiac action potential as a critical

factor. Under these conditions early after-depolarisations may occur

and lead to repetitive discharges (“triggered activity”).

Drugs that prolong cardiac action potential and are associated

with torsade include antiarrhythmic agents of class Ia and III,

tricyclic antidepressants, phenothiazines, macrolide antibiotics,

certain antihistamines and cisapride. Hypokalaemia and hypo-

magnesaemia are well recognised causes of torsade although the

evidence for hypocalcaemia is less convincing. Bradycardia –

either sinus or due to atrioventricular block – is an important

contributory factor.

In the setting of cardiac arrest torsade should be managed with

synchronised DC cardioversion which is almost always

successful in restoring sinus rhythm. However, additional

measures will be necessary to prevent recurrence. These measures

are aimed at shortening cardiac action potential duration. The

heart rate should be increased. Atropine has the advantage of

rapid availability and ease of administration. Where the brady-

cardia is due to atrioventricular block atropine is unlikely to

increase the ventricular rate. Transvenous ventricular pacing

should be established rapidly although it is almost certainly wise

to stabilise the patient first with an isoprenaline infusion (at a

rate of 1-10micrograms/min, titrated against the heart rate) or

external cardiac pacing. There is experimental and clinical

evidence to support the use of intravenous magnesium in the

acute treatment of torsade. A dose of 8mmol (administered over

10-15 minutes) has been shown to abolish torsade in the majority

of patients although a second dose may be necessary. There is no

evidence to support the use of either intravenous potassium or

calcium. The serum concentration of these electrolytes is

frequently disturbed as a result of cardiac arrest per se and a

reasonable strategy would be to obtain a formal laboratory meas-

urement after a period of haemodynamic stability and to correct as