Introduction: During cardiac arrest (CA), a major goal of responders is to ascertain the likelihood of successful cardiopulmonary resuscitation (CPR) and optimize efforts accordingly to achieve return of spontaneous circulation (ROSC). Pulseless electrical activity (PEA), a common form of CA in inpatient settings, often allows monitoring of heart rate (HR) immediately preceding cardiopulmonary resuscitation (CPR). We were interested in assessing the role of HR during PEA in outcome of CPR. To evaluate this in a controlled setting, we used a rodent model of asphyxial CA with electrocardiogram (ECG) recordings and neurological testing. We hypothesized that more severe bradycardia may be associated with failure to achieve ROSC and worse neurological outcome if ROSC is achieved.
Methods: Adult male Wistar rats (n=25) were anesthetized, intubated, and placed under mechanical ventilation. Needle electrodes were inserted into the rats to obtain continuous ECG data. Rats then underwent 8 minutes of asphyxial CA followed by CPR accompanied with intravenous epinephrine and bicarbonate injections. Neurological deficit scale (NDS) testing was conducted at 24hrs post-ROSC.
Results: Of 25 rats that underwent CA, 4 failed to achieve ROSC. HR was measured after 7.5 minutes of asphyxia (i.e. 30 sec. prior to CPR), when the systolic blood pressure was <10-20mmHg, which is presumed to be a “pulseless” equivalent in humans. Rats failing to achieve ROSC had a significantly lower HR in comparison to rats achieving ROSC (26.6±8.4 vs. 46.2±16.9; p< 0.05). Interestingly, among survivors, HR immediately pre-CPR was inversely correlated with NDS scores (r=-0.655, p< 0.05). No association was found between groups in pre-CA arterial blood gas measurements (e.g. pH, CO2, electrolytes).
Conclusions: In a rodent asphyxial model of CA mimicking a PEA state, rats failing to achieve ROSC had lower HR immediately prior to CPR. However, in rats achieving ROSC, slower pre-CPR HR is associated with better neurological outcome. These findings appear to be independent of respiratory acidosis. We propose a model and future experimentation that may help define underlying mechanisms. Validation is needed in human studies to assess potential translational implications in a clinical setting.