The respective roles of high pressure and high tidal volume to promote high airway pressure pulmonary edema are unclear. Positive end-expiratory pressure (PEEP) was shown to reduce lung water content in this type of edema, but its possible effects on cellular lesions were not documented. We compared the consequences of normal tidal volume ventilation in mechanically ventilated rats at a high airway pressure (HiP-LoV) with those of high tidal volume ventilation at a high (HiP-HiV) or low (LoP-HiV) airway pressure and the effects of PEEP (10 cm H2O) on both edema and lung ultrastructure. Pulmonary edema was assessed by extravascular lung water content and microvascular permeability by the drug lung weight and the distribution space of 125I-labeled albumin. HiP-LoV rat lungs were not different from those of controls (7 cm H2O peak pressure ventilation). By contrast, the lungs from the groups submitted to high volume ventilation had significant permeability type edema. This edema was more pronounced in LoP-HiV rats. It was markedly reduced by PEEP, which, in addition, preserved the normal ultrastructural aspect of the alveolar epithelium. This was in striking contrast to the diffuse alveolar damage usually encountered in this type of edema. To our knowledge, this constitutes the first example of a protective effect of PEEP during permeability edema.

The risk of lung injury due to alveolar overdistension during mechanical ventilation has been clearly delineated in healthy animals with intact lungs. In contrast, the effect of high-volume ventilation (HV) on previously injured lungs is less well documented: whether HV would simply add its own deleterious effects or act synergistically with previous injury has not been addressed. We compared the effect of 7 ml/kg body weight tidal volume mechanical ventilation for 2 min with that of 25 (HV25), 33(HV33), and 45(HV45) ml/kg body weight HV in anesthetized rats previously exposed or not exposed to alpha-naphthylthiourea (ANTU). ANTU alone produced moderate permeability edema with significant increases in extravascular lung water (Qwl), dry lung weight (DLW), and albumin distribution space in lungs (ASp). HV alone resulted in a permeability edema in which severity was dependent on the magnitude of the tidal volume. The effects of HV25 and HV33 and those of ANTU were only additive, as indicated by the absence of any significant two-factor (ANTU-HV) interaction by analysis of variance (ANOVA). In contrast, HV45 after ANTU produced significantly greater increases in Qwl, DLW, and ASp than expected from the sum of the effects of either insult alone. Two-way ANOVA disclosed two-factor interactions with p values < 0.001, < 0.02, and < 0.01 for Qwl, DLW, and ASp, respectively, indicating synergistic adverse effects on pulmonary edema.(ABSTRACT TRUNCATED AT 250 WORDS)

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Mechanical ventilation with high or even moderate peak inspiratory pressure produces pulmonary permeability edema. Besides the level of overinflation, duration may affect both severity and type of edema. We studied the effect of 2 min of 35-mmHg peak pressure mechanical ventilation (HV) on microvascular permeability and deep lung fluid balance in rats. It resulted in increased extravascular lung water (+50%), bloodless dry lung weight (+25%), and albumin uptake in lungs (+450%). The increase in dry lung weight and albumin uptake compared with that of lung water suggested major permeability alterations. Ultrastructural examination showed the presence of numerous endothelial blebs. Epithelial lining fluid (ELF) volume, its potassium and protein concentrations, and cellular composition were assessed by bronchoalveolar lavage. There was an increase in ELF volume (+180%), a decrease in ELF potassium concentration (-50%), and an increase in ELF protein content (+76%). A few blood cells were recovered, suggesting the presence of a few large epithelial breaks. Some animals were allowed to recover for periods less than or equal to 180 min after HV. Extravascular lung water, dry lung weight, and albumin distribution space returned to control levels within 45 min. ELF volume diminished but remained larger than in controls, and ELF protein concentration increased probably because of alveolar fluid resorption. No further hemorrhage was observed. These results indicate that periods of HV as short as 2 min transiently alter microvascular permeability in rats.

The identification of fat droplets within cells recovered by bronchoalveolar lavage in trauma patients may be a rapid and specific method for establishing the diagnosis of the fat embolism syndrome.