Lactic Acidosis and the Cardiovascular System in the Dog

Abstract

Lactic acidosis is a clinical syndrome characterized by metabolic acidemia (pH < 7.25) and hyperlactemia (lactate > 5 mmol/l). Many patients with type B lactic acidosis have no evidence of tissue hypoxia or myocardial dysfunction when 1st evaluated. Although it is considered that cardiac dysfunction is secondary to the systemic effects of lactic acidosis, the reverse may sometimes be true. To evaluate this possibility, studies were carried out in 43 dogs consisting of a control group and 3 groups which had hyperlactatemia and metabolic acidemia related to either: phenformin infusion; hepatectomy; lactic acid infusion. Serial studies of cardiac function, as well as measurements of GFR (glomerular filtration rate) and hepatic portal vein (HPV) blood flow, were carried out. In dogs infused with phenformin for 99 min, the arterial pH, lactate, bicarbonate, heart rate and mean blood pressure (BP) were normal. However, there was significant deterioration (P < 0.01) in several indices of cardiac function, including the peak positive dP/dt [change in pressure with time], cardiac output, LVEDP (left ventricular end-diastolic pressure) and percentage extraction of O2 and lactate by the heart. After 3 h of phenformin, the blood lactate exceeded 5 mmol/l and there were further significant decrements (P < 0.01) in cardiac output, LVEDP and dP/dt, as well as BP and heart rate. In dogs subjected to hepatectomy, the decrement in cardiac output was similar to that with phenformin infusion. However, in animals infused with lactic acid, despite a similar blood pH and lactate, cardiac output was unaffected. Although percentage myocardial O2 extraction declined in phenformin-infused animals, there was a concomitant increase in coronary sinus blood flow such that myocardial O2 utilization was probably unaltered. Thus, in certain types of experimental type B lactic acidosis, myocardial dysfunction may be a primary event, with other associated systemic manifestations being secondary.