Theoretical analysis of oxygen transport during hypothermia

Abstract
Oxygen transport and delivery to peripheral tissues during hypothermia are analyzed theoretically, taking into consideration various conditions observed both in nature and clinically. With decreasing temperature, P50 (the oxygen tension [Po 2] at 50% hemoglobin saturation with oxygen) decreases, thereby leading to low mixed venous oxygen tension ( \(P\bar vO_2 \) ) and thus low tissuePo 2 values. On cooling from 37°C to 25°C at pH 7.4, the P50 decreases from a normal 26.8 mm Hg to 13.2 mm Hg. In the intact animal, as well as in a patient on cardiopulmonary bypass, oxygen consumption ( \(\dot V_{O_2 } \) ) and cardiac output ( \(\dot Q\) , or recommended pump flow rate) decrease. If the ratio of \(\dot Vo_2 /\dot Q_T \) remains constant, then the arteriovenous O2 content difference, \(C(a - \bar v)O_2 \) , must remain constant. If \(C(a - \bar v)O_2 \) is 5 ml/dl, we calculate that the \(C(a - \bar v)O_2 \) must decrease from a normal 40 mm Hg to 26.8 mm Hg at 25°C. Clinically induced hypothermia is usually accompanied by hemodilution of the patient's blood to 50% normal hematocrit, which would reduce \(C(a - \bar v)O_2 \) to 13.7 mm Hg. Use of constant relative alkalinity (pH=7.58 at 25°C) further reduces the P50 to 10.8 mm Hg and the \(C(a - \bar v)O_2 \) to 10.9 mm Hg. Other clinical situations are also discussed. Sensitivity analysis predicts that during hypothermia \(C(a - \bar v)O_2 \) (and thus tissuePo 2) is very dependent on P50, hemoglobin concentration, and \(\dot Q_T \) , and less dependent on oxygen solubility and arterialPo 2. We conclude that monitoring of mixed venous or tissuePo 2 might be advisable, and that blood flow is the component of oxygen transport most amenable to manipulation by the clinician to ensure adequate tissue oxygenation during induced hypothermia.