Effect of Epinephrine Administered during Cardiopulmonary Resuscitation on Cerebral Oxygenation after Restoration of Spontaneous Circulation in a Swine Model with a Clinically Relevant Duration of Untreated Cardiac Arrest

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.

Effects of Sodium Nitroprusside Administered Via a Subdural Intracranial Catheter on the Microcirculation, Oxygenation, and Electrocortical Activity of the Cerebral Cortex in a Pig Cardiac Arrest Model

“…Here, 66.7% of the animals in the IT‐saline group experienced cerebral cortical hypoxia, although the MAP and Pa o 2 clearly remained within the normal range throughout the 5‐hour observation period; multiple studies have reported similar findings. 27 , 28 , 40 In a clinical study including 14 patients comatose following cardiac arrest who underwent multimodal neuromonitoring, 7 (50%) experienced PctO 2 <20 mm Hg. 40 Microcirculation is dissociated from macrovascular circulation during the early post‐ROSC period.…”

“…The anesthesia, preparation, and data collection procedures have been previously described. 27 , 28 , 29 , 30 Briefly, following initial sedation with intramuscular administration of ketamine (20 mg/kg) and xylazine (2.2 mg/kg), the animals were tracheostomized and mechanically ventilated with a 70/30 mixture of N 2 O/O 2 and sevoflurane (titrated to maintain adequate anesthesia). An end‐tidal carbon dioxide sampling line was placed between the ventilator circuit and tracheal tube.…”

Assessment of the Effects of Sodium Nitroprusside Administered Via Intracranial Subdural Catheters on the Cerebral Blood Flow and Lactate Using Dynamic Susceptibility Contrast Magnetic Resonance Imaging and Proton Magnetic Resonance Spectroscopy in a Pig Cardiac Arrest Model

“…Postischemic cerebral hypoperfusion occurs within the first hour after ROSC and persists for at least several hours. 37 , 38 , 39 Therefore, it would be desirable to perform this treatment within the first hour after ROSC, preferably before or shortly after the onset of postischemic cerebral hypoperfusion, to minimize the detrimental effects of postischemic cerebral hypoperfusion. However, in real‐world clinical practice, it would be difficult to administer SNP intrathecally within the first few hours after ROSC as multiple life‐saving procedures, such as percutaneous coronary intervention, are performed during this period.…”