Abstract
Severe neurological impairment was more prevalent in cardiac arrest survivors who were administered epinephrine than in those administered placebo in a randomized clinical trial; short-term reduction of brain tissue O2 tension (PbtO2) after epinephrine administration in swine following a short duration of untreated cardiac arrest has also been reported. We investigated the effects of epinephrine administered during cardiopulmonary resuscitation (CPR) on cerebral oxygenation after restoration of spontaneous circulation (ROSC) in a swine model with a clinically relevant duration of untreated cardiac arrest. After 7 min of ventricular fibrillation, 24 pigs randomly received either epinephrine or saline placebo during CPR. Parietal cortex measurements during 60-min post-resuscitation period showed that the area under the curve (AUC) for PbtO2 was smaller in the epinephrine group than in the placebo group during the initial 10-min period and subsequent 50-min period (both p < 0.05). The AUC for number of perfused cerebral capillaries was smaller in the epinephrine group during the initial 10-min period (p = 0.005), but not during the subsequent 50-min period. In conclusion, epinephrine administered during CPR reduced PbtO2 for longer than 10 min following ROSC in a swine model with a clinically relevant duration of untreated cardiac arrest.
Highlights
Of the 24 animals included in the present study, one animal in the epinephrine group was excluded from the analysis due to cardiopulmonary resuscitation (CPR)-related hemothorax, leaving 12 animals in the placebo group and 11 in the epinephrine group
The area under the curve (AUC) of coronary perfusion pressure (CPP) during CPR was significantly higher in the epinephrine group than in the placebo group
The restoration of spontaneous circulation (ROSC) rate was comparable between the placebo and epinephrine groups (8 [66.7%] versus 11 [100%], p = 0.093), but the epinephrine group required a shorter duration of CPR than the placebo group
Summary
Since Crile and Dolley first described the use of epinephrine as a treatment for cardiac arrest in 1906 [1], it has been the first-line drug used during cardiopulmonary resuscitation (CPR). The administration of epinephrine during CPR is primarily intended to increase coronary perfusion pressure (CPP) and myocardial blood flow, thereby facilitating the restoration of spontaneous circulation (ROSC). Multiple clinical studies have suggested that epinephrine increases the rate of ROSC but fails to improve neurologically favorable survival, the ultimate goal of resuscitation [2,3]. Despite these results, current CPR guidelines still recommend the administration of epinephrine in cardiac arrest patients [4].
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