Abstract
The QT interval represents the duration of ventricular depolarization and repolarization. It is measured from the beginning of the QRS complex to the end of the T wave. Prolongation of the QT interval may be congenital or acquired. This increases the risk of polymorphic ventricular tachycardia (i.e torsades de pointes) and cardiac arrest. To increase the awareness of this life-threatening phenomenon I outline an illustrative case in which acquired prolongation of the QT interval due to electrolyte derangement and administration of ciprofloxacin resulted in cardiac arrest due to torsade de pointes. Management of a patient with a long QT syndrome includes Immediate cessation of drugs that prolong the QT interval; cardiac monitoring, serial 12 lead ECGs and transthoracic echocardiography; measurement of serum electrolytes; intravenous potassium replacement; intravenous magnesium replacement; beta-blockade. Causes of acquired prolongation of the QT interval are common in critically ill patients. It is important to recognize this and consider screening with 12 lead ECG to reduce the risk of life-threatening ventricular arrhythmias.
Highlights
Prolongation of the QT interval may be congenital or acquired [1]
The QT interval represents the duration of ventricular depolarization and repolarization [3]
It is measured on the surface ECG from the beginning of the QRS complex to the end of the T wave [3,6]
Summary
Congenital long QT syndromes result from mutations in genes encoding for the sodium and potassium channels in cardiac cells [1,2]. Patients with drugassociated prolongation of the QT interval may have mutations in ion channel genes [4]. Illustrative Case A 30-year-old woman presented with a 3-day history of fever, dysuria, left flank pain, nausea, and vomiting She was diagnosed with pyelonephritis and admitted for treatment with intravenous ciprofloxacin and metoclopramide. Five days after re-admission a nurse witnessed the patient having a seizure whilst in bed. This was followed by cardiorespiratory arrest, and cardiopulmonary resuscitation (CPR) was started. The QTc returned to the pre-arrest duration of 0.38 seconds two days after electrolyte replacement, stopping the metoclopramide and changing ciprofloxacin to meropenem. There were no further convulsions or arrhythmias and the patient was discharged home
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