Cardiorespiratory effects of hypothermia and bicarbonate alkalosis.
The cardiorespiratory effects of reducing body temperature to 30 degrees C (by packing in ice) and subsequent metabolic alkalosis (by infusion of NaHCO3) were studied in six anesthetized, paralyzed, and artificially ventilated (FIO2 = 0.4) dogs. Heart rate decreased from 135 +/- 6 beats/min (mean +/- S.E.) at 37 degrees C to 84 +/- 4 at 30 degrees C; it increased to 96 +/- 4 after 2 h alkalosis. Cardiac output decreased from 1.84 +/- 0.14 to 0.66 +/- 0.08 l/min and then increased to 0.83 +/- 0.07. pHa increased, as expected on cooling, from 7.41 +/- 0.07 to 7.49 +/- 0.03; with bicarbonate it increased to 7.79 +/- 0.03. PaCO2 decreased on cooling from 32.9 +/- 1.4 to 21.7 +/- 1.2 torr, increasing with bicarbonate to 27.9 +/- 1.4 torr. VO2 decreased from 104.9 +/- 5.1 ml . min-1 . m-2 at 37 degrees C to 51.3 +/- 2.0 at 30 degrees C; with alkalosis it increased by 16.2% to 59.6 +/- 3.3 ml . ml-1 . m-2, an increase identical to that seen in normothermic alkalosis. Thus, the mechanism of the alkalosis-induced increase in oxygen consumption is not suppressed by the decrease in VO2 seen in hypothermia, and the increase in VO2 appears to be a consequence of the change in relative alkalinity rather than the increase in pH.
D000471:Alkalosis / Q000503:physiopathology*; D000818:Animals; D001639:Bicarbonates / Q000494:pharmacology; D001784:Blood Gas Analysis; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D006439:Hemodynamics / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D007035:Hypothermia / Q000503:physiopathology*; D010101:Oxygen Consumption / Q000187:drug effects; D012119:Respiration / Q000187:drug effects
D001639:Bicarbonates; D002245:Carbon Dioxide