Increased cardiac output increases lung water in canine permeability pulmonary edema

Abstract

We investigated the effects of increased cardiac output (CO) on oleic acid pulmonary edema in 14 open-chest, anesthetized, mechanically ventilated dogs. Pulmonary artery wedge pressure (Pawp) was adjusted to approximately 9 mm Hg via a left atrial balloon and CO to 1.7 L · m −1 via systemic arteriovenous fistulas (AVF); five minutes after oleic acid (0.08 mL · kg −1), dogs were randomly divided into two groups, high CO and low CO. In the high CO group, CO was increased by opening the AVFs. Pawp was maintained at 9 mm Hg for four hours in all dogs. The average CO time in the high CO group was 3.9 L · min −1 and 1.3 L · min −1 in the low CO group ( P < .01). Lung water accumulation was significantly increased in the high CO group with a wet weight/ body weight ratio of 29 g ò kg −1 v 21 g · kg −1 in the low CO group ( P < .004). With time, mean pulmonary artery pressure increased significantly ( P < .05) in both groups, but was not different between groups at any time. While pulmonary vascular resistance remained constant in the high CO group, it increased markedly ( P < .05) in the low CO group, possibly due to a decrease in pulmonary vascular surface area. The increase in lung water accumulation in the high CO group is probably due to prevention of pulmonary vascular derecruitment and therefore a greater perfused pulmonary vascular surface area.