Hyperlactatemia due to arterial hypoxemia or reduced cardiac output, or both

Publisher Website
Google Scholar
Abstract
Thirty-four anesthetized dogs were mechanically ventilated with 21, 14, 12, 10, and 8% inspired O2, both with and without simultaneous reduction in cardiac output (.ovrhdot.Qt) of 25 or 50% (electromagnetic flowmeter) induced by inflating a balloon surgically placed in the main pulmonary artery. The dogs were paralyzed to prevent effects of variable muscle activity on lactate accumulation. Arterial and mixed venous blood gases and whole blood lactate concentration were measured directly and O2 delivery (.ovrhdot.Qt .times. arterial oxygen content) was calculated. There was no significant change in arterial pH or partial CO2 pressure except as a result of lactic acidemia. Hyperlactatemia occurred only with severe hypoxemia (8% inspired O2) and 50% reduction in .ovrhdot.Qt combined with hypoxemia (14% O2). The rise in blood lactate concentration occurred with arterial O2 partial pressure (PaO2) below a threshold value of 34 Torr for hypoxemia alone and 40 for combined hypoxemia and reduced .ovrhdot.Qt. There was a mixed venous O2 partial pressure (P.hivin.VO2) threshold of 27 Torr below which hyperlactatemia always occurred, regardless of the method of lowering. When compared with PaO2, .ovrhdot.Qt, or O2 delivery, P.hivin.VO2 was statistically the best predictor of anaerobiosis, as indicated by hyperlactatemia, during hypoxemia and/or reduced .ovrhdot.Qt under the conditions of this study. Venous O2 partial pressure is related specifically to the state of intracellular oxygenation, whether it be affected by changes in PaO2 or blood flow.