Haaheim, Brage

Diving under cold conditions may add an additional risk for bubble production and decompression sickness. Additionally, there is sparse information regarding hemodynamic changes occurring during a dive and its effects on the outcome of a dive. Thus, detailed recordings of cardiovascular changes at different core temperatures during diving were studied. Anesthetized rats were monitored with a pressure‐volume catheter in the left ventricle and the femoral artery. Rats were randomly assigned to be normothermic controls, to perform a dry hyberbaric dive at constant core temperature (37ºC) or a dry hyperbaric dive with a core temperature of 35ºC during decompression and the early post dive period. The rats were compressed to 600 kPa, maintained for 45 min breathing air, and decompressed linearly to the surface at a rate of 50 kPa·min −1 . Immediately after surfacing, right ventricle and pulmonary artery were insonated for bubble detection using ultrasound. Compression increased mean arterial pressure, pulse pressure, stroke volume, cardiac output, LV end‐systolic volume, LV end‐systolic pressure, LV dp/dt max, and total peripheral resistance in the rats. Most of these changes gradually declined and returned to baseline after decompression. However, rewarming to 37ºC after a 2ºC drop in core temperature caused a significant reduction in SV and CO, but this did not have an effect on bubble production and survival.

Abstract Background: We recently documented that cardiopulmonary resuscitation (CPR) for hypothermic cardiac arrest maintains cardiac output (CO) and mean arterial pressure (MAP) to the same reduced level during normothermia (38°C) vs. hypothermia (27°C). Furthermore, continuous CPR at 27°C maintains CO and MAP throughout a 3-h period, and provides O2 delivery to support aerobic metabolism. The aim of the present study was to investigate the effects of extracorporeal membrane oxygenation (ECMO) rewarming to restore O2 delivery and organ blood flow. Methods: Eight male pigs were anesthetized and immersion cooled to 27°C. After induction of hypothermic cardiac arrest, CPR was started and continued for a 3-h period. Thereafter, the animals were rewarmed with ECMO. Organ blood flow was measured using microspheres. Results: After cooling with spontaneous circulation to 27°C, MAP and CO were initially reduced to 66 and 44% of baseline, respectively. By 15 min after the onset of CPR, there was a further reduction in MAP and CO to 42 and 25% of baseline, respectively, which remained unchanged throughout the rest of 3-h CPR. During CPR, O2 delivery and O2 uptake (V̇O2) fell to critical low levels, but the simultaneous small increase in lactate and a modest reduction in pH, indicated the presence of maintained aerobic metabolism. Rewarming with ECMO restored MAP, CO, O2 delivery, and blood flow to the heart and to parts of the brain, whereas flow to kidneys, stomach, liver and spleen remained significantly reduced. Conclusions: CPR for 3-h at 27°C with sustained lower levels of CO and MAP and maintained aerobic metabolism sufficient to support O2 delivery. Rewarming with ECMO restores blood flow to the heart and brain, and creates a “shockable” cardiac rhythm. Thus, like continuous CPR, ECMO rewarming plays a crucial role in “the chain of survival” when resuscitating victims of hypothermic cardiac arrest.