Pulmonary capillary pressure and gas exchange after E. coli bacteremia in pigs.

In 9 Goettingen minipigs we studied the effect of E. coli bacteremia on effective pulmonary capillary pressure and the longitudinal distribution of pulmonary vascular resistance. Precapillary pressure gradient (dPa) was calculated as the difference between mean pulmonary artery pressure (MPP) and effective pulmonary capillary pressure (Pc) (dPa = MPP-Pc), postcapillary pressure gradient (dPv) as the difference between Pc and left atrial pressure (dPv = Pc-LAP). The disturbance of pulmonary gas exchange was quantified by the AaDO2 quotient 1-PaO2/PAO2. Live E. coli infusion resulted in hypodynamic circulatory failure. Cardiac index fell from 3.7 +/- 0.81 . min-1.m-2 to 2.2 +/- 0.71 .min-1.m-2 after bacteremia lasting for 3.5 h. Simultaneously venous pulmonary vascular resistance rose from 25% of total pulmonary vascular resistance before to 32% after 3.5 h bacteremia, thus raising Pc from 11 mmHg to 16 mmHg. The degree of respiratory insufficiency was correlated with changes of MPP, dPa and dPv: 1-PaO2/PAO2 = 0.2 + 0.035.dPv (r = 0.829). Our results show, that the longitudinal distribution of pulmonary vascular resistance changes during septicemia, thus raising Pc. This may be an important factor in the genesis of septic pulmonary failure.