Effect of positive end-expiratory pressure on alveolar capillary perfusion

Positive end-expiratory pressure (PEEP) increases arterial carbon dioxide tension and alveolar dead space by reducing alveolar capillary perfusion. The two likely mechanisms by which PEEP reduces alveolar capillary perfusion are reduction of cardiac output or compression of pulmonary capillaries within interalveolar septa, or both mechanisms. This study attempts to quantitate the impact of each of these mechanisms on alveolar capillary perfusion in anesthetized dogs by restoring cardiac output to baseline values with dextran 70 infusion after application of 15 cm H2O PEEP. Alveolar capillary perfusion was assessed directly through the visceral pleura by in vivo photomicroscopy. PEEP resulted in a fall in cardiac output and alveolar capillary perfusion with a concomitant rise in alveolar dead space-tidal volume ratio and arterial carbon dioxide tension. Infusion of dextran 70 returned the cardiac output to baseline levels but only slightly increased alveolar capillary perfusion. Both dead space/tidal volume ratio and arterial carbon dioxide tension remained significantly elevated with PEEP even with normal cardiac output. Microscopically, alveolar capillaries appeared compressed and flattened by PEEP, which indicated a mechanical interruption of blood flow. Extra-alveolar vessels remained perfused with PEEP. PEEP increased dead space/tidal volume ratio 36%; restoration of cardiac output reduced dead space/tidal volume ratio only 7% and did not return alveolar capillary perfusion to baseline levels. These data indicate that most of the reduced alveolar perfusion with PEEP results from direct compression of alveolar capillaries and not from reduced cardiac output.