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Review
. 2010 Mar 2;55(9):934-47.
doi: 10.1016/j.jacc.2010.01.001.

Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation

Barbara J Drew, Michael J Ackerman, Marjorie Funk, W Brian Gibler, Paul Kligfield, Venu Menon, George J Philippides, Dan M Roden, Wojciech Zareba; American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology; Council on Cardiovascular Nursing; American College of Cardiology Foundation
Collaborators
Review

Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation

Barbara J Drew et al. J Am Coll Cardiol. .
No abstract available

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Figures

Figure 1
Figure 1
Onset of TdP during the recording of a standard 12-lead ECG in a young male with a history of drug addiction treated with chronic methadone therapy who presented to a hospital emergency department after ingesting an overdose of prescription and over-the-counter drugs from his parent’s drug cabinet. Classic ECG features evident in this rhythm strip include a prolonged QT interval with distorted T-U complex, initiation of the arrhythmia after a short-long-short cycle sequence by a PVC that falls near the peak of the distorted T-U complex, “warm-up” phenomenon with initial R-R cycles longer than subsequent cycles, and abrupt switching of QRS morphology from predominately positive to predominately negative complexes (asterisk).
Figure 2
Figure 2
Top rhythm strip, TdP degenerating into ventricular fibrillation in an 83-year-old female hospitalized in the intensive care unit for pneumonia. She was started on intravenous erythromycin several hours before cardiac arrest. A ventricular couplet followed by a pause provided the short-long-short cycle sequence that triggered TdP. Bottom rhythm strip, ECG 1 hour before the onset of TdP shows extreme prolongation of the QT interval (QTc in cycles with larger T waves=730 ms), a ventricular couplet (asterisk), and macroscopic T-wave alternans (vertical arrows). If these signs of impending TdP had been recognized, discontinuation of the culprit drug and administration of magnesium most likely would have prevented the subsequent cardiac arrest.
Figure 3
Figure 3
QTc distribution curves in normal males and females and in a cohort of patients with congenital LQTS. Upper limits of normal (99th percentile) for QTc are 470 ms in males and 480 ms in females. For both males and females, a QTc >500 ms is considered dangerous. OR indicates odds ratio; RR, relative risk.
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