Intracellular and extracellular acid-base changes in hemorrhagic shock.

Each of 21 dogs was bled until mean arterial blood pressure fell to 50 torr; this hemorrhagic shock state was then maintained for two hours. During hemorrhagic shock, the blood lactate concentration increased sixfold. The severe metabolic acidosis in arterial blood was partially compensated by a decreased PCO2 caused by increased ventilation. However, in mixed venous blood, the metabolic acidosis was combined with a respiratory acidosis. This hypercapnia in venous blood was indicative of the increased PCO2 in tissues poorly perfused following hemorrhage. The increase in the PCO2 of the femoral venous blood was greater than that in mixed venous blood, suggesting that some tissue beds were better perfused than those of the hind limb during shock. The intracellular lactate concentration of hind limb skeletal muscle was greatly increased in the shock state, and tissue PCO2 rose. Intracellular pH of skeletal muscle was only slightly decreased and bicarbonate concentration was unchanged during this combined metabolic and respiratory acidosis. This capacity of skeletal muscle to maintain a high HCO-3 concentration in intracellular fluid during metabolic acidosis may be an enhanced response of the mechanism responsible for maintaining (HCO-3)i normally at a level approximately ten times that which would be expected if HCO-3 were distributed passively.