Theoretical analysis of oxygen transport during hypothermia.

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 [PO2] at 50% hemoglobin saturation with oxygen) decreases, thereby leading to low mixed venous oxygen tension (PvO2) and thus low tissue PO2 values. On cooling from 37 degrees C to 25 degrees 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 (Vo2) and cardiac output (QT, or recommended pump flow rate) decrease. If the ratio of Vo2/QT remains constant, then the arteriovenous O2 content difference, C(a-v)O2, must remain constant. If C(a-v)O2 is 5 ml/dl, we calculate that the PvO2 must decrease from a normal 40 mm Hg to 26.8 mm Hg at 25 degrees C. Clinically induced hypothermia is usually accompanied by hemodilution of the patient's blood to 50% normal hematocrit, which would reduce PvO2 to 13.7 mm Hg. Use of constant relative alkalinity (pH = 7.58 at 25 degrees C) further reduces the P50 to 10.8 mm Hg and the PvO2 to 10.9 mm Hg. Other clinical situations are also discussed. Sensitivity analysis predicts that during hypothermia PvO2 (and thus tissue PO2) is very dependent on P50, hemoglobin concentration, and QT, and less dependent on oxygen solubility and arterial PO2. We conclude that monitoring of mixed venous or tissue PO2 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.