Pulmonary artery occlusion-left atrial pressure gradient: an important factor in determining pulmonary venous vascular resistance in acute pulmonary failure.

Abstract

To determine whether pulmonary artery occlusion pressure (PAOP) accurately reflects left atrial pressure (LAP) in acute pulmonary failure. Sham-controlled laboratory investigation on Goettingen minipigs. Induction of acute respiratory failure by a 4-hr infusion of live Escherichia coli bacteria in 11 animals; two animals served as the control group. Anesthesia was obtained with methohexital/piritramide and pancuronium bromide. Cardiac output and pressures were measured by means of femoral artery, pulmonary artery, and left atrial catheters. Arterial-alveolar Po2 ratio was calculated to evaluate pulmonary function. Measurements were obtained before and after 1 and 2 hr of the E. coli infusion. Statistical significance was tested with analysis of variance. E. coli infusion caused the hypodynamic shock and respiratory failure. The PAOP-LAP gradient was -0.3 +/- 1.6 mm Hg before bacteremia and increased significantly (p less than .001) to 2.9 +/- 1.8 and 3.4 +/- 2.0 mm Hg after 1 and 2 hr of bacteremia, respectively. No significant changes occurred in the sham group. A PAOP-LAP gradient may develop during acute respiratory failure. Therefore, pulmonary venous vascular resistance may be underestimated if its determination is based on PAOP. An increase in bronchial to pulmonary blood flow and pulmonary venoconstriction are discussed as hypothetical causes of a PAOP-LAP gradient during acute respiratory failure.