Blood Lactate Accumulation: Hemodynamics and Acid Base Status

Abstract

The authors evaluated the relationship between blood lactate accumulation and hemodynamics in a prospective controlled animal study. Seven healthy pigs were anesthetized and mechanically ventilated with a 0.6 fraction of inspired oxygen to achieve a normal PaCO2. Catheters for blood sampling, lactate infusion, and hemodynamic assessment were inserted into the femoral vein and femoral artery. Bolus infusions (466 µmol • kg— 1 over 1 minute) of a neutral solution of sodium lactate were given at 0, 30, 60, and 90 minutes. Each bolus was followed by continuous infusion of the same lactate solution (31.7 µmol • kg— 1 • min—1 after the first, with the rate doubled after each subsequent bolus). Arterial blood samples were drawn at baseline and at 30, 60, 90, and 120 minutes, with simultaneous hemodynamic assessment. Significant increases were seen in blood lactate (from 1.6 ± 0.4 mmol/L at baseline to 4.4 ± 0.8 at 30 minutes, 8.0 ± 1.0 at 60 minutes, and 14.4 ± 2.1 at 90 minutes), pH (from 7.40 ± 0.03 to 7.44 ± 0.05 at 30 minutes, 7.50 ± 0.05 at 60 minutes, and 7.56 ± 0.04 at 90 minutes), and HCO3 — (from 28 ± 1.4 mmol/L to 30 ± 0.7 at 30 minutes, 34 ± 0.9 at 60 minutes, and 37 ± 1.2 at 90 minutes). PaCO2 decreased significantly from 44 ± 3 torr at baseline to 40 ± 4.7 torr at 90 minutes. Blood pressure decreased after each lactate bolus, recovering within 2 minutes initially but not after later injections. Cardiac output, heart rate, and glucose increased significantly, mean arterial pressure and systemic vascular resistance decreased, and stroke volume did not change. Thus, the accumulation of blood lactate due to exogenous administration of a neutral solution of sodium lactate was associated with significant systemic vasodilation, increased cardiac output, increased heart rate, and metabolic alkalosis.