OXYGEN DELIVERY AND CONSUMPTION DURING HYPOTHERMIA AND REWARMING IN THE DOG

Changes in oxygen consumption V̇(O2)) and oxygen delivery (D(O2)) were compared in three groups of paralyzed, sedated dogs: 1) a group (n = 5) cooled to 29°C and immediately rewarmed to 37°C; 2) a group (n = 5) cooled to and maintained at 29°C for 24 h, and then rewarmed; and 3) a group (n = 5) maintained at 37°C for 24 h. During the cooling phase, in both the acute and prolonged hypothermia animals, V̇(O2) and D(O2) decreased significantly from control values (P < 0.05). The decrease in D(O2) occurred as a result of a similar decrease in cardiac index (CI; P < 0.05) that was associated with a significant increase in systemic vascular resistance index (SVRI; P < 0.05). Arteriovenous oxygen content difference (C(a-v)(O2)), O2 extraction ratio, mixed venous oxygen tension (Pv̄(O2)), pH, and base deficit (BD) were not different from control values even during prolonged hypothermia. Normothermic control dogs also demonstrated a significant decrease in CI (P < 0.05) at 24 h. Surface rewarming increased V̇(O2) back to control values in the acute hypothermia group and to values above control (P < 0.05) in the prolonged hypothermia group. D(O2) remained below control in both groups, resulting in a significant increase in O2 extraction (P < 0.05) and a decrease in Pv̄(O2) (P < 0.05) in the prolonged hypothermia animals. Following rewarming administration of sodium nitroprusside returned D(O2), CI, and SVRI to control values but did not increase V̇(O2). All animals survived the study without need for inotropic support. The heart and peripheral vasculature appear to be responsive to direct vasodilation when, with rewarming, residual excess afterload prevents oxygen delivery from matching oxygen requirement.