Cardiovascular effects of induced hypercarbia during halothane-nitrous oxide anaesthesia.
The effect of induced hypercarbia on the cardiovascular system during steady-state halothane-nitrous oxide anaesthesia was investigated in 4 male patients without cardiac disease. Heart rate, cardiac index, systemic and pulmonary blood pressures rose as pCO2 was increased. Stroke volume, systemic and pulmonary vascular resistance remained unchanged. Oxygen consumption decreased and oxygen saturation of mixed venous blood increased. In conclusion the primary effect of hypercarbia was an increased heart rate and a resultant increase of cardiac output. The pressure changes merely reflect the effect on cardiac output. Under these circumstances a regulatory role of mixed venous pO2 on cardiac output is highly unlikely.
D000368:Aged; D000769:Anesthesia, Inhalation; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000097:blood; D006221:Halothane; D006339:Heart Rate; D006439:Hemodynamics; D006801:Humans; D006935:Hypercapnia / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009609:Nitrous Oxide; D010101:Oxygen Consumption; D010313:Partial Pressure; D014655:Vascular Resistance
D002245:Carbon Dioxide; D009609:Nitrous Oxide; D006221:Halothane