Circulatory defects during phenformin lactic acidosis.
Detailed hemodynamic and metabolic studies were performed during the course of phenformin related lactic acidosis in two patients. Arterial blood lactate was increased to 11.5 and 26.1 mM/L and arterial blood pH was reduced to 7.05 and 6.80 units, respectively. A marked reduction in cardiac indices (0.94 and 1.15 L/min/m2), stroke volume, and stroke work were observed, with either normal or increased arterial resistance. Mild increases in pulmonary artery systolic pressure (50/11), 45/25 mmHg) were observed, but necropsy in both cases disclosed no evidence of pulmonary vascular obstruction. In the absence of increases in central venous and pulmonary artery wedge pressure, a cardiac failure was excluded as primary cause of the low output state. Hypovolemia was excluded on the basis of radioisotope dilution measurements of plasma volume and red cell mass and no increase in cardiac output followed volume expansion. Oxygen extraction from blood was not grossly impaired. These observations indicate that phenformin-related lactic acidosis may evolve as a circulatory defect characteristic of shock in which oxygen delivery rather than oxygen utilization is impaired. The hemodynamic defect is best explained by a defect in the intravascular distribution of blood volume.
D000138:Acidosis / Q000139:chemically induced* / Q000503:physiopathology; D000368:Aged; D005260:Female; D006439:Hemodynamics; D006801:Humans; D007004:Hypoglycemic Agents / Q000009:adverse effects*; D007773:Lactates / Q000097:blood*; D010629:Phenformin / Q000009:adverse effects*
D007004:Hypoglycemic Agents; D007773:Lactates; D010629:Phenformin