Influence of changes in cardiac output on the acid-base status of arterial and mixed venous blood.
While maintaining the arterial CO2 tension constant near the normal level of the dog (4.3 kPa), we studied the influence of decreasing cardiac output on both the arterial and mixed-venous blood acid-base status in anaesthetized, artificially ventilated dogs. Cardiac output was manipulated by applying positive end-expiratory pressure (PEEP), and by beta-adrenergic blockade to suppress a compensatory heart rate response. The systemic vascular response was attenuated by alpha-adrenergic blockade. Metabolic rate remained virtually unchanged when cardiac output decreased. Under these conditions a fall in cardiac output led to a shift of the arterial acid-base status in the direction of a metabolic acidosis. The changes occurring in the mixed-venous blood resembled those of an in-vivo CO2 bufferline, with the shift being such as if a respiratory acidosis was developing.
D000137:Acid-Base Imbalance / Q000209:etiology*; D000138:Acidosis / Q000209:etiology; D000142:Acidosis, Respiratory / Q000209:etiology; D000818:Animals; D001158:Arteries; D001769:Blood; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D005260:Female; D006863:Hydrogen-Ion Concentration; D008297:Male; D010643:Phenoxybenzamine / Q000494:pharmacology; D011175:Positive-Pressure Respiration; D011433:Propranolol / Q000494:pharmacology; D014680:Veins
D010643:Phenoxybenzamine; D002245:Carbon Dioxide; D011433:Propranolol