Key result
Asphyxial cardiac arrest resulted in significantly lesser impairment of postresuscitation myocardial function compared with cardiac arrest caused by ventricular fibrillation.
Why the study?
Does asphyxial cardiac arrest result in different postresuscitation myocardial function compared to primary cardiac arrest due to ventricular fibrillation in a rat model?
Does asphyxial cardiac arrest result in different postresuscitation myocardial function compared to primary cardiac arrest due to ventricular fibrillation in a rat model?
In a healthy rat model, asphyxial cardiac arrest results in significantly less postresuscitation myocardial impairment compared to ventricular fibrillation-induced cardiac arrest.
Should not alter clinical resuscitation protocols; leaves open etiology-specific myocardial recovery mechanisms for translational study.
Although myocardial dysfunction after resuscitation from ventricular fibrillation (VF) has been extensively investigated, less is known of the function of the myocardium after asphyxial cardiac arrest. The present experimental study was designed to compare postresuscitation left ventricular (LV) function after cardiac arrest caused by asphyxia with that of cardiac arrest induced by dysrhythmia. Four groups of Sprague-Dawley rats, which included eight animals in each group, were investigated. In the first two groups, cardiac arrest followed asphyxia produced by neuromuscular blockade with and without airway obstruction. In a third group, cardiac arrest was induced by electrical fibrillation of the ventricle. The fourth group represented animals in which the duration of asphyxial cardiac arrest was maintained for a time interval corresponding to that of the VF group. The fourth group received approximately the same number of electrical shocks as the third (VF) group. All animals were successfully resuscitated with precordial compression and mechanical ventilation. Postresuscitation measurements, including cardiac output, LV end-diastolic pressure (LVEDP), rate of pressure rise at LV pressure of 40 mm Hg (LV dP/dt40), and negative LV dP/dt, demonstrated decreased myocardial function in each group. No differences in cardiac function were observed between the animals with primary respiratory arrest whether or not the airway was obstructed. However, disproportionate and consistently greater impairment in myocardial function followed primary cardiac arrest due to VF when compared with equal duration of asphyxial cardiac arrest. We conclude that in this healthy animal model, asphyxial cardiac arrest resulted in significantly lesser impairment of postresuscitation myocardial function when compared with cardiac arrest caused by VF.
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Kamohara et al. (2001) studied Cardiac arrest (n=32). Asphyxial cardiac arrest vs. Ventricular fibrillation (VF) cardiac arrest was evaluated on Postresuscitation myocardial function (including cardiac output, LVEDP, LV dP/dt40, and negative LV dP/dt). Asphyxial cardiac arrest resulted in significantly lesser impairment of postresuscitation myocardial function compared with cardiac arrest caused by ventricular fibrillation.
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