Am. J. Respir. Crit. Care Med., Volume 164, Number 8, October 2001, 1448-1453

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

MARCO MANCINI, ELIZABETH ZAVALA, JORDI MANCEBO, CARLOS FERNANDEZ, JOAN ALBERT BARBERÀ, ANDREA ROSSI, JOSEP ROCA, and ROBERT RODRIGUEZ-ROISIN

Servei de Pneumologia (ICPCT); Unitat de Cures Intensives Quirúrgiques, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS); Unitat de Cures Intensives, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain; Unità Operativa Pneumologia, Ospedale Riuniti di Bergamo, Azienda Ospedaliera, di rilievo nazionale e di alta specializzazione, Bergamo, Italy

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 · kg¹; positive end-expiratory pressure [PEEP] 8 to 10 cm H₂O); (2) during PVS (PEEP 2 cm H₂O above the low inflexion point (P_FLEX) and VT of 5 to 7 ml · kg¹); and (3) post-PVS, back to baseline conditions. Inert gas measurements were done after 30 min in each ventilatory modality. During PVS, Pa_O2 increased significantly from 93 ± 27 to 166 ± 77 mm Hg (p < 0.008) and Pa_CO2 rose from 39 ± 7 to 57 ± 11 mm Hg (p < 0.0002) because of the decrease in minute ventilation ( E) (3.6 L · min¹) (p < 0.005). Both heart rate (HR, +13 min¹) (p < 0.002) and cardiac output (, +1.2 L · min¹) (p < 0.05) increased. Static respiratory system linear compliance increased from 36 ± 14 to 44 ± 16 ml · cm H₂O¹ (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 , 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.

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