• Conán L McCaul, Patrick McNamara, Doreen Engelberts, Cameron Slorach, Lisa K Hornberger, and Brian P Kavanagh.
• The Lung Biology Program, The Research Institute, The Hospital for Sick Children, 555 University Ave., Toronto, Ont., Canada M5G 1X8.
• Resuscitation. 2006 Feb 1;68(2):267-75.

AbstractMost laboratory studies of cardiac arrest use models of ventricular fibrillation, but in the emergency room, operating room or intensive care unit, cardiac arrest frequently results from asphyxia. We sought to investigate the effect of different durations of asystole secondary to asphyxia on myocardial function after resuscitation. In a laboratory based experimental series, anaesthetized rats received either 4 or 8 min of asphyxial cardiac arrest, and following standardized resuscitation, serial transthoracic echocardiography was performed. Severe depression of left ventricular fractional shortening occurred in both groups with partial recovery only in the 4-min arrest group, while left ventricular end-diastolic diameter was increased in the 4-min group. The pH, HCO3(-) and SBE were reduced in both groups after resuscitation, but the degree of acidosis was greater in the 8-min group. In this model, transthoracic echocardiography demonstrated both systolic and diastolic impairment following asphyxial cardiac arrest, and a clear dose-effect relationship between duration of asphyxia and degree of impairment. A shorter duration of asphyxia was associated with a lesser increase in left ventricular end-diastolic dimension, compared with more protracted asphyxia; the shorter arrest was associated with better recovery of contractile function and acidosis. Increased duration of asphyxia causes increased systolic and diastolic dysfunction. These findings may have significant implications for resuscitative therapeutics. ECHO assessment may permit specific targeting of therapy directed towards systolic or diastolic function during CPR.

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