Tidal Hyperinflation during Low Tidal Volume Ventilation in Acute Respiratory Distress Syndrome

Università di Torino, Dipartimento di Anestesiologia e Rianimazione, Ospedale S. Giovanni Battista-Molinette, Corso Dogliotti 14, 10126 Turin, Italy.
American Journal of Respiratory and Critical Care Medicine (Impact Factor: 13). 02/2007; 175(2):160-6. DOI: 10.1164/rccm.200607-915OC
Source: PubMed


Tidal volume and plateau pressure limitation decreases mortality in acute respiratory distress syndrome. Computed tomography demonstrated a small, normally aerated compartment on the top of poorly aerated and nonaerated compartments that may be hyperinflated by tidal inflation.
We hypothesized that despite tidal volume and plateau pressure limitation, patients with a larger nonaerated compartment are exposed to tidal hyperinflation of the normally aerated compartment.
Pulmonary computed tomography at end-expiration and end-inspiration was obtained in 30 patients ventilated with a low tidal volume (6 ml/kg predicted body weight). Cluster analysis identified 20 patients in whom tidal inflation occurred largely in the normally aerated compartment (69.9 +/- 6.9%; "more protected"), and 10 patients in whom tidal inflation occurred largely within the hyperinflated compartments (63.0 +/- 12.7%; "less protected"). The nonaerated compartment was smaller and the normally aerated compartment was larger in the more protected patients than in the less protected patients (p = 0.01). Pulmonary cytokines were lower in the more protected patients than in the less protected patients (p < 0.05). Ventilator-free days were 7 +/- 8 and 1 +/- 2 d in the more protected and less protected patients, respectively (p = 0.01). Plateau pressure ranged between 25 and 26 cm H(2)O in the more protected patients and between 28 and 30 cm H(2)O in the less protected patients (p = 0.006).
Limiting tidal volume to 6 ml/kg predicted body weight and plateau pressure to 30 cm H(2)O may not be sufficient in patients characterized by a larger nonaerated compartment.

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    • "First, measures of lung injury will not perform well as prognostic measures because non-pulmonary factors including age, severity of sepsis, co-morbidities and non-pulmonary organ failure remain the most influential predictors of hospital mortality in ARDS, [25-39] and non-resolving respiratory failure accounts for less than 20% of ARDS deaths [34-36]. Also, although the finding that PaO2/FiO2 level is associated with mortality is consistent with the findings reported from cohorts used for empirical analysis in the development of the Berlin ARDS definition, [40-46] this has not been demonstrated consistently, a finding that may be attributable, in part, to practice variability in mechanical ventilation settings, which is known to have a large effect on PaO2/FiO2 levels [5,6,24,47,48]. Furthermore, post-mortem studies highlight the poor accuracy that clinical definitions such as the Berlin criteria have for histological definitions of diffuse alveolar damage, which are found in only a minority of patients with clinical ARDS [49,50]. "
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    • "Indeed, when large tidal volumes are delivered, this can lead to repeated over-distension of alveoli and further aggravate injury by volutrauma [6,35]. When lung protective ventilation is used, the aggravation of lung injury may depend on the degree of the reduction in aerated lung volume and the tidal volume used [36]. In the present study, the degree of the reduction in aerated lung volume following lung lavage was not severe as indicated by the mean P/F ratio above 400 on the high PEEP in experimental groups. "
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    BMC Anesthesiology 12/2013; 13(1):47. DOI:10.1186/1471-2253-13-47 · 1.38 Impact Factor
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    • "In acute respiratory distress syndrome (ARDS), aerated lung volume is diminished [1]. Regression of healthy lung parts and increased airway resistance results in overdistention of non-injured alveoli, even during lung protective ventilation with limited tidal volume and plateau pressures [2], thereby contributing to ventilator-induced lung injury (VILI). The only proven strategy aimed at limiting lung injury is low tidal volume ventilation [3]. "
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