BICARBONATE DOES NOT INCREASE LEFT-VENTRICULAR CONTRACTILITY DURING L-LACTIC ACIDEMIA IN PIGS

Lactic acidosis decreases left ventricular contractility, but whether bicarbonate increases left ventricular contractility during lactic aci dosis in vivo is controversial. Therefore, we measured hemodynamics an d left ventricular mechanics before and after bicarbonate administrati on during L-lactic acid infusion in 15 anesthetized pigs. The pigs wer e beta-blocked and atrially paced to minimize indirect effects of acid osis on contractility. We measured mean arterial pressure, left ventri cular end-diastolic pressure, thermodilution cardiac output, left vent ricular pressure (Millar catheter), and left ventricular volume (three orthogonal pairs of ultrasonic crystals). Left ventricular contractil ity was assessed primarily using the slope (E(max) of the end-systolic pressure-volume relationship. While PCO2 was kept constant, 0.2 M L-l actic acid was infused, which reduced arterial pH to 7.05 +/- 0.06. An imals were then randomized to receive either 1 M NaHCO3 (n = 8), which increased pH to 7.45 +/- 0.11, or an equivalent amount of 1 M NaCl (n = 7). Bicarbonate decreased mean arterial pressure (105 +/- 20 to 95 +/- 39 mm Hg, p < 0.05) but did not increase cardiac output. These eff ects were not significantly different from the effects of saline. Bica rbonate did not significantly increase E(max) (4.2 +/- 0.8 to 4.9 +/- 0.8 mm Hg/ml) and was indistinguishable from saline (5.0 +/- 0.7 to 5. 2 +/- 0.7 mm Hg/ml). We conclude that bicarbonate infusion does not di rectly increase left ventricular contractility during lactic acidemia in pigs within this pH range.