Arterial and Mixed Venous Blood Acid-Base Balance During Hypoperfusion With Incremental Positive End-Expiratory Pressure in the Pig

The authors sought to determine how hypoperfusion influences acid-base balance in arterial and mixed venous blood. In anesthetized, ventilated pigs (n = 12), we determined hemodynamics, O2 uptake, CO, output, dead-space ventilation, arterial and mixed venous blood acid-base balances, and lactate concentrations during graded reductions in cardiac output by incremental positive end-expiratory pressure (PEEP, 0–20 cm H2O). Cardiac output decreased from 3.2 ± 0.2 (mean ± sem) to 1.2 ± 0.1 L/min at 20 cm H2O PEEP. Oxygen delivery declined more than O2 uptake did by 60% ± 2% and 27% ± 2%, respectively. The decrease in CO2 output (by 21% ± 2%) was less than that in O2 uptake. Fractional dead-space ventilation increased. At a slight increase in carbon dioxide tension (Pco2) of 4 ± 1 mm Hg, pH decreased in arterial blood from 7.54 plusmn; 0.01 to 7.47 ± 0.02 mmol/L, and standard bicarbonate decreased from 30.3 ± 0.5 to 27.5 ± 0.6 mmol/L. The decrease in standard bicarbonate exceeded the increase in blood lactate concentrations. At a similar decrease in standard bicarbonate, the decrease in pH was larger (P < 0.005) in mixed venous blood than in arterial blood owing to a larger increase in Pco2 (from 40 ± 2 to 50 ± 2 mm Hg, P < 0.005). The changes were reversed after discontinuing PEEP. The authors conclude that ischemia after incremental PEEP results in tissue metabolic acidosis with superimposed respiratory acidosis. This is not caused by increased tissue production or by impaired pulmonary excretion of CO2 but by a larger decrease in blood flow than in CO2 production in the tissues, so that CO2 stores increase. Decreased pulmonary blood flow and increased dead-space ventilation prevent a decrease in arterial Pco2 by diminished CO2 production. A smaller reduction in CO2 production than in O2 uptake is only partly explained by bicarbonate buffering of lactic acid.