Hemodynamic functions and blood viscosity in surface hypothermia.
Hemodynamic functions and blood viscosity changes in hypothermia (core approximately 25 degrees C) were studied in 14 pentobarbital-anesthetized dogs subjected to surface cooling. The viscosity of blood (eta B) increased progressively to 173% of that at 37 degrees C when body temperature was lowered to 25 degrees C. The increase in blood viscosity was caused by: a) the direct effect of low temperature on plasma viscosity, b) hemoconcentration as a result of plasma loss, and c) the low-flow (low-shear) state induced by hypothermia. A larger portion of the increased viscosity was caused by the low-flow state in hypothermia. The systemic flow resistance (SFR) increased to 271% of control, and this was attributable about equally to the increases in blood viscosity and systemic vascular hindrance (SFR/eta B). Similarly, the viscosity of blood contributed significantly to raising the pulmonary flow resistance. The relative constancy of mixed venous O2 saturation suggests that the cardiac output at low body temperature is generally adequate to meet the metabolic needs.
D000818:Animals; D001783:Blood Flow Velocity; D001794:Blood Pressure; D001809:Blood Viscosity; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output; D002496:Central Venous Pressure; D004285:Dogs; D006339:Heart Rate; D006439:Hemodynamics; D006863:Hydrogen-Ion Concentration; D007035:Hypothermia / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D012212:Rheology
D002245:Carbon Dioxide; D010100:Oxygen