Drugs associated with TdP vary greatly in their risk for arrhythmia; an updated list can be found at www.qtdrugs.org. Risk factors for drug-induced TdP include older age, female sex, heart disease, electrolyte disorders (especially hypokalemia and hypomagnesemia), renal or hepatic dysfunction, bradycardia or rhythms with long pauses, treatment with more than 1 QT-prolonging drug, and genetic predisposition. The risk-benefit ratio should be assessed for each individual to determine whether the potential therapeutic benefit of a drug outweighs the risk for TdP. After initiation of a drug associated with TdP, ECG signs indicative of risk for arrhythmia include an increase in QTc from predrug baseline of 60 ms, marked QTc interval prolongation >500 ms, T-U wave distortion that becomes more exaggerated in the beat after a pause, visible (macroscopic) T-wave alternans, new-onset ventricular ectopy, couplets and nonsustained polymorphic ventricular tachycardia initiated in the beat after a pause. In monitoring QT intervals in an individual before and after drug administration, a consistent method should be used (i.e., same recording device, ECG lead, measurement tool [automated or manual], and heart rate– correction formula). Recommended actions when ECG signs of impending TdP develop are to discontinue the offending drug, replace potassium, administer magnesium, consider temporary pacing to prevent bradycardia and long pauses, and transfer the patient to a hospital unit with the highest level of ECG monitoring surveillance where immediate defibrillation is available.
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