QTprolonging

QT prolonging refers to properties of certain drugs, toxins, or physiological conditions that lengthen the QT interval on the surface electrocardiogram, indicating delayed ventricular repolarization. Prolongation can be congenital, as in congenital long QT syndrome, or acquired, commonly due to medications, electrolyte disturbances, bradycardia, or other illnesses.

Most acquired QT prolongation results from blockade of the cardiac hERG potassium channels, reducing the IKr current and slowing repolarization. This shifts the balance of the cardiac action potential and prolongs the QT interval. Contributing factors can include low potassium or magnesium, low calcium, hypothermia, and interactions among multiple QT-prolonging drugs.

Clinically, prolonged QT increases the risk of torsades de pointes, a polymorphic ventricular tachycardia that can degenerate into ventricular fibrillation and sudden death. Risk is higher with longer QTc, female sex, older age, electrolyte abnormalities, bradycardia, heart disease, and recent initiation or combination of QT-prolonging drugs.

Diagnosis relies on accurate measurement of the QT interval and its heart-rate–corrected value (QTc). A QTc above about 450 ms in men and 470 ms in women is typically considered prolonged, with values above 500 ms associated with a higher risk of torsades de pointes.

Management focuses on removing or reducing exposure to offending agents, correcting electrolytes, and monitoring. In acute torsades, intravenous magnesium sulfate is standard, with copper-fastened correction of electrolytes and, if needed, temporary pacing or pharmacologic strategies to increase heart rate. Prevention includes careful drug selection, baseline and follow-up ECGs in at-risk individuals, and evaluation for congenital long QT syndrome when indicated.