Abstract
Epinephrine is recommended during cardiopulmonary resuscitation, but amplifies cardiac depression following ventricular fibrillation. In pediatric practice, cardiac arrest is almost always due to asphyxia, and while the effects of catecholamines are unknown, their use is ubiquitous.
[1] to characterize the myocardial effects of epinephrine following asphyxial cardiac arrest; and [2] to investigate the physiologic/biochemical mechanisms of dysfunction.
Sprague-Dawley rats (350–400 g) were anaesthetized and exposed to one-minute asphyxial cardiac arrest. Standardized resuscitation was attempted with mechanical ventilation (FiO2 1.0), chest compressions and intravenous medication. Three experimental series were completed. The effects of epinephrine (10 or 30 μg/kg) vs. control (saline) were examined using non-invasive ECHO (Series #1), and by direct (open chest) measurement of left atrial pressure (PLA) (Series #2). The impact of calcium channel blockade (verapamil 0.1 mg/kg) on epinephrine induced effects (30 μg/kg) was also evaluated by ECHO (Series #3). Monitoring comprised serial transthoracic echocardiography (shortening fraction-LVSF; end-diastolic diameter-LVEDD), invasive systemic arterial pressure and blood gas analysis at baseline and up to 2 h post-resuscitation.
Epinephrine increased mortality, and caused a dose-dependent decrease in diastolic function (reduced LVEDD; Fig. 1). The diastolic dysfunction was associated with increased PLA (P<0.05) and myocardial hypercontraction. Finally, verapamil eliminated epinephrine-induced mortality (P<0.002), and attenuated the diastolic dysfunction (P<0.05).
Epinephrine administration for CPR following asphyxial cardiac arrest is associated with dose-dependent diastolic dysfunction, left atrial hypertension and increased mortality. These effects are attenuated by calcium channel blockade. This data provides mechanistic insight and points to potential therapeutic approaches in pediatric cardiac arrest.
