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The Journal of Thoracic and Cardiovascular Surgery, Vol 87, 386-393, Copyright © 1984 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association

ARTICLES

Traumatic myocardial dysfunction

DP Harley, I Mena, KA Narahara, R Miranda and RJ Nelson

Traumatic myocardial dysfunction is a frequently unsuspected, undiagnosed contributor to deaths from trauma. Electrocardiography, serum enzymes, and radionuclide myocardial scans are insensitive indicators of cardiac injury following blunt chest trauma. First-pass biventricular radionuclide angiography can accurately determine right and left ventricular ejection fractions and assess left ventricular segmental wall motion. Since August, 1980, we have evaluated 74 consecutive patients with blunt chest and multisystem trauma. Electrocardiograms and measurements of the myocardial band isoenzyme of creatine kinase were obtained at admission and repeated at 24 hour intervals for 3 days. Radionuclide angiography was performed 24 to 48 hours after admission. The electrocardiogram was abnormal in 21 patients (28%), levels of creatine kinase isoenzyme were elevated in six, and radionuclide angiographic abnormalities were present in 55 patients (74%). Electrocardiographic abnormalities correlated anatomically with angiographic abnormalities in 16 patients (76%). On follow-up radionuclide angiography, abnormalities had disappeared in nine of 12 patients restudied at 3 weeks. This study documents that the electrocardiogram and creatine kinase isoenzyme elevations are static, insensitive indicators of traumatic myocardial dysfunction. Radionuclide angiography with studies of left ventricular segmental wall motion demonstrate that traumatic myocardial dysfunction, although sometimes transitory, is a dynamic phenomenon that is more common than previously suspected. First-pass radionuclide angiography and wall motion studies are practical and valuable adjuncts to the management of the injured patient.

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