It has been shown that hypothermia induced after successful resuscitation of comatose survivors of ventricular fibrillation cardiac arrest improves survival and neurologic function. Recent studies also suggest that earlier induction of hypothermia may yield even more improvement. We sought to determine if a new pump system, in addition to vigorous external chest compression, could rapidly induce hypothermia during cardiopulmonary resuscitation in a porcine model of cardiac arrest.
Nine pigs (25–37 kg) were instrumented with micromanometers and thermocouple probes. Two 8-Fr catheters were placed into the femoral veins. Cardiac arrest was induced with 60-Hz current. After 5 mins of no support, chest compression was performed by a circumferential pneumatic bladder (vest-cardiopulmonary resuscitation). Blood was withdrawn from one catheter by a pump system that maximized flow by servo-control of inlet pressure, was cooled, and was returned through the other catheter. Four dogs were instrumented similarly, and cooling was performed during normal circulation.
In the pigs, baseline temperatures were (mean ± sem) 37 ± 1°C. With blood cooling in the external chiller to 10°C, cerebral and right atrial temperatures were reduced by 0.49 ± 0.09 and 0.67 ± 0.21°C/min, respectively, for 10 mins. With blood cooling in the external chiller to 4°C, cerebral and right atrial temperatures were reduced by 0.61 ± 0.18 and 1.56 ± 0.33°C/min, respectively. Cerebral cooling lagged behind right atrial cooling. There was a strong correlation between coronary perfusion pressure (aortic to right atrial mean decompression-phase pressure) and cerebral cooling rate (r = .79; p < .022). Rates of cooling during normal circulation in dogs were similar.
Rapid induction of mild hypothermia is feasible with a system that uses venous access, standard access techniques, and external chest compression. Induction of mild hypothermia during cardiac arrest in the field appears feasible and may allow the benefit of very early induction of hypothermia to be determined in patients.
From the Departments of Medicine (MMZ, AR, AJ, KR, AL, HRH), Radiology (HRH), and Biomedical Engineering (AL, HRH), The Johns Hopkins University School of Medicine, Baltimore, MD.
Address for Correspondence: Henry Halperin, MD, MAP, FAHA, Johns Hopkins Hospital, Blalock 524, 600 N Wolfe Street, Baltimore, MD 21287. Tel: 410 955–2412, Fax : 410 955–0223, Email: firstname.lastname@example.org