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Collapse on the cardiology ward

The case

68-year-old woman. Collapse on the cardiology ward

Admitted twelve days ago with an inferior STEMI treated with primary PCI to the right coronary artery. Started on sotalol 80 mg twice daily five days ago for recurrent non-sustained VT. Potassium was 4.1 mmol/L this morning. The nurse called the cardiac arrest team after the patient collapsed on the ward.

On arrival

HR
48
Spo2Percent
94
Respiratory rate
18
Temperature (°C)
36.4
Systolic BP (mmHg)
92
Diastolic BP (mmHg)
54

Stage 1 of 1

A 68-year-old woman is twelve days into her admission following an inferior STEMI. She was started on sotalol five days ago for recurrent non-sustained VT. Her potassium this morning was 4.1 mmol/L. The nurse calls the arrest team after the patient collapses. A twelve-lead ECG is recorded as the team arrives.

The tracing for the quiz “Collapse on the cardiology ward”.
Twelve-lead ECG recorded as the cardiac arrest team arrives Open this tracing in the studio
In the seconds before the collapse, the tracing shows sinus bradycardia. What interval abnormality is visible?

The sinus beats before the polymorphic tachycardia show a visibly prolonged QT interval, with the T wave extending well beyond the halfway point between successive QRS complexes at a rate of about 48. The QTc is prolonged at 520 ms in the context of sotalol and bradycardia. The PR interval and QRS duration in the sinus beats are within normal limits, and there is no shortened QT.

At the onset of the polymorphic ventricular tachycardia, a premature ventricular complex falls on the T wave of the preceding beat. What is this trigger mechanism called?

A premature ventricular complex firing during the vulnerable repolarisation period represented by the preceding T wave is the R-on-T phenomenon, the classic trigger for torsades de pointes in the setting of a prolonged QT. The Ashman phenomenon describes aberrant conduction after a long-short cycle in atrial fibrillation, which is not present here. The Wenckebach phenomenon is progressive PR prolongation, and the Brugada sign is an ECG pattern, neither of which describes this trigger.

Which drug on this patient's prescription prolongs the QT interval and is the most likely precipitant of the torsades?

Sotalol is a class III antiarrhythmic that prolongs repolarisation by blocking the delayed rectifier potassium current, directly prolonging the QT interval. This effect is amplified by the bradycardia it also causes through beta-blockade. The combination of QT prolongation and slow rate creates the ideal substrate for torsades de pointes. Atorvastatin, ticagrelor and aspirin do not meaningfully prolong the QT interval.

Diagnosis

Sotalol-induced torsades de pointes after inferior STEMI

Sotalol was started for a good reason, recurrent non-sustained ventricular tachycardia after an inferior infarct, but its class III action prolongs the QT interval and its beta-blocking effect slows the rate. Together these create the substrate for torsades de pointes, which is exactly what this tracing captures: a prolonged QT, a bradycardic pause, an R-on-T ectopic and then the twisting polymorphic tachycardia.

The immediate treatment is intravenous magnesium and overdrive pacing or isoprenaline to raise the rate. Sotalol must be stopped. The lesson is that the drug prescribed for one arrhythmia has caused another, and the ECG showed the warning before the arrest.

References

  1. Drew BJ, Ackerman MJ, Funk M, et al. Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation. Circulation. 2010;121(8):1047-1060.
  2. Roden DM. Drug-induced prolongation of the QT interval. N Engl J Med. 2004;350(10):1013-1022.
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This tracing was generated, not recorded. It opens in the studio with every dial live.

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Discussion

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