Postresuscitation myocardial dysfunction is one of the leading causes of early death after successful resuscitation from sudden death. However, the diastolic characteristics of postresuscitation myocardial dysfunction are not well defined. We therefore investigated the postresuscitation left ventricular diastolic function following prolonged cardiac arrest and subsequent cardiopulmonary resuscitation.
Prospective, observational animal study.
Medical research laboratory in a university-affiliated research and educational institute.
Seven anesthetized pigs (40 ± 4 kg) were studied before and after 7 mins of untreated occlusive ventricular fibrillation induced cardiac arrest. Ejection fraction, early and atrial peak transmitral flow velocities, deceleration time of early transmitral flow velocity, myocardial performance index, peak Emax and Amax mitral annulus velocities by Doppler tissue imaging, and early diastolic left ventricular flow propagation velocity were measured at baseline; 60, 120, 180, and 240 mins; and 72 hrs after resuscitation.
Five animals were successfully resuscitated. Left ventricular ejection fraction, Em/Am ratio, and propagation velocity were significantly decreased, and myocardial performance index was significantly increased compared with baseline measurements. Left ventricular diastolic and systolic function returned to baseline level at 72 hrs postresuscitation.
Left ventricular systolic dysfunction was significantly impaired after cardiac arrest and cardiopulmonary resuscitation, as previously demonstrated. This was associated with a profound left ventricular diastolic dysfunction. However, this postresuscitation left ventricular systolic and diastolic myocardial dysfunction was reversible after 72 hrs in this experimental model of ventricular fibrillation cardiac arrest.
From the Weil Institute of Critical Care Medicine, Rancho Mirage, CA (TX, WT, GR, HW, SS, MHW); the Keck School of Medicine of the University of Southern California, Los Angeles, CA (WT, SS, MHW); and the Department of Cardiology, Renji Hospital, affiliated with Jiaotong University Medical School, Shanghai, China (TX, WT).
Supported, in part, by a grant from the American Heart Association, Dallas, TX (WT).
The authors have not disclosed any potential conflicts of interest.
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