Mechanisms of Pulmonary Gas Exchange Improvement during a Protective Ventilatory Strategy in Acute Respiratory Distress Syndrome

Publisher Website
Google Scholar
Abstract
To investigate the mechanisms underlying improvement of arterial oxygenation during a protective ventilatory strategy (PVS) in early acute respiratory distress syndrome (ARDS), we studied eight patients during volume-controlled mechanical ventilation, keeping respiratory rate and fraction of inspired oxygen (Fi O2 ) (0.82 ± 0.20) unchanged: (1) at baseline (tidal volume [Vt] 10 to 12 ml · kg− 1; positive end-expiratory pressure [PEEP] 8 to 10 cm H2O); (2) during PVS (PEEP 2 cm H2O above the low inflexion point (PFLEX) and Vt of 5 to 7 ml · kg− 1); and (3) post-PVS, back to baseline conditions. Inert gas measurements were done after 30 min in each ventilatory modality. During PVS, PaO2 increased significantly from 93 ± 27 to 166 ± 77 mm Hg (p < 0.008) and PaCO2 rose from 39 ± 7 to 57 ± 11 mm Hg (p < 0.0002) because of the decrease in minute ventilation (V˙ e) ( − 3.6 L · min− 1) (p < 0.005). Both heart rate (HR, + 13 min− 1) (p < 0.002) and cardiac output (Q˙, + 1.2 L · min− 1) (p < 0.05) increased. Static respiratory system linear compliance increased from 36 ± 14 to 44 ± 16 ml · cm H2O− 1 (p < 0.0002). PVS provoked recruitment of previously collapsed alveoli and redistribution of pulmonary blood flow from nonventilated alveoli to normal lung. Despite the increase in Q˙, intrapulmonary shunt fell from 39 ± 15% to 31 ± 11% (p < 0.04). We conclude that the decrease in intrapulmonary shunt owing to alveolar recruitment remains the pivotal mechanism to explain improvement of arterial oxygenation during this PVS.

This publication has 25 references indexed in Scilit: