Both reduction in tidal volume (VT) and alveolar recruitment may be important to limit ventilator-associated lung injury during mechanical ventilation of patients with the acute respiratory distress syndrome (ARDS). The aim of this study was to assess the risk of alveolar derecruitment associated with VT reduction from 10 to 6 ml/kg. Whether this VT-related derecruitment could be reversed, either by a recruitment maneuver or by an increase in positive end-expiratory pressure (PEEP) level, was also investigated. Fifteen patients with ARDS were successively ventilated using conventional VT (CVT = 10 +/- 1 ml/kg) and low VT (LVT = 6 +/- 1 ml/kg); total PEEP (PEEPtot) was individually set at the lower inflection point (Plip) of the pressure-volume curve (PEEPtot = 11 +/- 4 cm H2O). Pressure-volume curves were recorded from zero PEEP (ZEEP) and from PEEP, and recruited volume (Vrec) was calculated as the volume difference between the two curves for a given pressure. Despite a similar PEEPtot, Vrec was significantly lower with LVT than with CVT, indicating low VT-induced alveolar derecruitment. Reduction in VT was associated with a reduced Sa(O2). In 10 patients, Vrec was also measured before and after a recruitment maneuver (two sustained inflations at 45 cm H2O), and after an increase in PEEP (by 4 cm H2O). Low VT-induced derecruitment was reversed by a recruitment maneuver and by increasing PEEP. We conclude that a reduction in VT could be responsible for alveolar derecruitment, which may be transiently reversed by a reexpansion maneuver or prevented by a PEEP increase above Flip.
Influence of tidal volume on alveolar recruitment. Respective role of PEEP and a recruitment maneuver
MAGGIORE, Salvatore Maurizio;
2001-01-01
Abstract
Both reduction in tidal volume (VT) and alveolar recruitment may be important to limit ventilator-associated lung injury during mechanical ventilation of patients with the acute respiratory distress syndrome (ARDS). The aim of this study was to assess the risk of alveolar derecruitment associated with VT reduction from 10 to 6 ml/kg. Whether this VT-related derecruitment could be reversed, either by a recruitment maneuver or by an increase in positive end-expiratory pressure (PEEP) level, was also investigated. Fifteen patients with ARDS were successively ventilated using conventional VT (CVT = 10 +/- 1 ml/kg) and low VT (LVT = 6 +/- 1 ml/kg); total PEEP (PEEPtot) was individually set at the lower inflection point (Plip) of the pressure-volume curve (PEEPtot = 11 +/- 4 cm H2O). Pressure-volume curves were recorded from zero PEEP (ZEEP) and from PEEP, and recruited volume (Vrec) was calculated as the volume difference between the two curves for a given pressure. Despite a similar PEEPtot, Vrec was significantly lower with LVT than with CVT, indicating low VT-induced alveolar derecruitment. Reduction in VT was associated with a reduced Sa(O2). In 10 patients, Vrec was also measured before and after a recruitment maneuver (two sustained inflations at 45 cm H2O), and after an increase in PEEP (by 4 cm H2O). Low VT-induced derecruitment was reversed by a recruitment maneuver and by increasing PEEP. We conclude that a reduction in VT could be responsible for alveolar derecruitment, which may be transiently reversed by a reexpansion maneuver or prevented by a PEEP increase above Flip.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.