Arterial and mixed venous PCO2 and hydrogen ion, bicarbonate and base excess concentrations in water-depleted dogs.
The arterial (a), mixed venous (v), and arterial-mixed venous differences (A-V) of hydrogen ion concentration ([H+]), PCO2, HCO-3 and base excess (BE) were measured during 3 h in control (C), water-depleted (WD) and water- and salt-depleted (WSD) dogs. In WD animals the difference in hydrogen ion concentration between venous and arterial blood increased because the [H+] increased more in venous than in arterial blood. In WSD animals (A-V) [H+] remained unchanged since both [H+]a and [H+]v increases were parallel. [H+] variations seem to represent the changes in fixed-acid concentration of blood. The difference between both groups of animals in (A-V) [H+] changes could be ascribed to PCO2 variations. [HCO-3] values changed inconsistently. Arterial samples from the experimental groups showed a continuous decrease at the same rate of change. The mean values in WSD were lower than in WD. [HCO-3]v of WSD decreased slowly during the experiment. The rate of decrease of (A-V) [HCO-3] was higher in WD than in WSD. The different behavior of of [HCO-3] between both arterial and mixed venous samples and among experimental groups disappeared if [HCO-3] changes were corrected for bicarbonate generation due to PCO2 variation (respiratory bicarbonate). Thus [HCO-3] corrected for PCO2 variation represents metabolic changes, in good agreement with both [H+] and BE variations. The metabolic acidosis cannot be explained only on the basis of the increase in blood lactate; it is suggested that other fixed acids might contribute to the decrease in blood bicarbonate. In both experimental groups PvCO2 increased continuously. The (A-V) PCO2 showed the same rate of change. There is a good relationship between this increase and the degree of plasma volume change. It therefore might be that PvCO2 increase is a direct consequence of hemodynamic impairment. In WD and WSD, BE decreased progressively in both arterial and mixed venous samples. BEa values were lower than BEv values after the experiment began. (A-V) BE decreased in an exponential manner in both experimental groups; this change could be ascribed to the increased level of deoxygenated hemoglobin in mixed venous blood, thus giving rise to a decrease in fixed acid concentration.
Arterial and mixed venous PCO2 and hydrogen ion, bicarbonate and base excess concentrations in water-depleted dogs. The arterial (a), mixed venous (v), and arterial-mixed venous differences (A-V) of hydrogen ion concentration ([H+]), PCO2, HCO-3 and base excess (BE) were measured during 3 h in control (C), water-depleted (WD) and water- and salt-depleted (WSD) dogs. In WD animals the difference in hydrogen ion concentration between venous and arterial blood increased because the [H+] increased more in venous than in arterial blood. In WSD animals (A-V) [H+] remained unchanged since both [H+]a and [H+]v increases were parallel. [H+] variations seem to represent the changes in fixed-acid concentration of blood. The difference between both groups of animals in (A-V) [H+] changes could be ascribed to PCO2 variations. [HCO-3] values changed inconsistently. Arterial samples from the experimental groups showed a continuous decrease at the same rate of change. The mean values in WSD were lower than in WD. [HCO-3]v of WSD decreased slowly during the experiment. The rate of decrease of (A-V) [HCO-3] was higher in WD than in WSD. The different behavior of of [HCO-3] between both arterial and mixed venous samples and among experimental groups disappeared if [HCO-3] changes were corrected for bicarbonate generation due to PCO2 variation (respiratory bicarbonate). Thus [HCO-3] corrected for PCO2 variation represents metabolic changes, in good agreement with both [H+] and BE variations. The metabolic acidosis cannot be explained only on the basis of the increase in blood lactate; it is suggested that other fixed acids might contribute to the decrease in blood bicarbonate. In both experimental groups PvCO2 increased continuously. The (A-V) PCO2 showed the same rate of change. There is a good relationship between this increase and the degree of plasma volume change. It therefore might be that PvCO2 increase is a direct consequence of hemodynamic impairment. In WD and WSD, BE decreased progressively in both arterial and mixed venous samples. BEa values were lower than BEv values after the experiment began. (A-V) BE decreased in an exponential manner in both experimental groups; this change could be ascribed to the increased level of deoxygenated hemoglobin in mixed venous blood, thus giving rise to a decrease in fixed acid concentration.