Lung Distention, Barotrauma and Mechanical Ventilation
Mechanical ventilation usually entails the application of varying amounts of positive airway pressure in a cyclic fashion to force tidal breaths into the lungs and maintain distending pressure. The addition of supplemental O2 to enrich the ventilating gas is universal, and is itself a separate factor of artificial ventilation. Positive-pressure ventilation supplies a force necessary to overcome elastic and resistive forces of the entire ventilatory apparatus. Only a portion of this force is actually directed at alveolar distention, and in subjects with severe bronchospasm or asynchrony of spontaneous ventilatory efforts with those of the ventilator, very little of the distended pressure may be sensed by the alveoli. However, if positive-pressure ventilation grossly overdistends the alveoli even once or induces repetitive degrees of lesser overdistention of the lungs because either the overall tidal volume is too high or the distribution of the delivered gas is such that only certain regions of the lung are distended, then alveolar injury may occur. These injuries are collectively referred to as barotrauma. Such injury actually reflects over-distention of the alveoli rather than over-pressure of the airways. Accordingly, the term “volutrauma” has been suggested to reflect this process . Although overdistention of the lung at end-inspiration is a major cause of barotrauma, changes in end-expiratory volume also play a major role, especially if fixed tidal volumes are used to ventilate a subject.
KeywordsContinuous Positive Airway Pressure Tidal Volume Acute Lung Injury Airway Pressure Functional Residual Capacity
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Dreyfuss D, Soler P, Basset G et al (1988) High inflation pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure. Am Rev Respir Dis 137:1159–1164PubMedCrossRefGoogle Scholar
Romand J, Shi W, Pinsky MR (1995) Cardiopulmonary effects of positive-pressure ventilation during acute lung injury. Chest 108:1041–1048PubMedCrossRefGoogle Scholar
Dreyfuss D, Soler P, Saumon G (1992) Spontaneous resolution of pulmonary edema caused by short periods of cyclic overinflation. J Appl Physiol 72:2081–2089PubMedGoogle Scholar
Fu Z, Costello ML, Tsukimoto K et al (1992) High lung volume increases stress failure in pulmonary capillaries. J Appl Physiol 73:123–133PubMedGoogle Scholar
Omlor G, Niehaus GD, Maron MB (1993) Effect of peak inspiratory pressure on the filtration coefficient in the isolated perfused rat lung. J Appl Physiol 74:3068–3072PubMedGoogle Scholar
Kolobow T, Moretti MP, Fumagalli R et al (1987) Severe impairment in lung function induced by high peak airway pressure during mechanical ventilation. An experimental study. Am Rev Respir Dis 135:312–315PubMedGoogle Scholar
Gattinoni L, Pesenti A, Caspani ML et al (1984) The role of total static lung compliance in the management of severe ARDS unresponsive to conventional ventilation. Intensive Care Med 10:121–126PubMedCrossRefGoogle Scholar
Maunder RJ, Shuman WP, McHugh JW et al (1986) Preservation of normal lung region in the adult respiratory distress syndrome. Analysis by computed tomography. JAMA 255: 2463–2465PubMedCrossRefGoogle Scholar
Gattinoni L, Pesenti A, Avalli L et al (1987) Pressure-volume curve of total respiratory system in acute respiratory failure. Am Rev Respir Dis 136:730–736PubMedCrossRefGoogle Scholar
Loick HM, Wendt M, Rötker J et al (1993) Ventilation with positive end-expiratory airway pressure causes leukocyte retention in human lung. J Appl Physiol 75:301–306PubMedGoogle Scholar
Zapol WA (1992) Volutrauma and the intravenous oxygenator in patients with adult respiratory distress syndrome (editorial). Anesthesiology 77:847–849PubMedCrossRefGoogle Scholar
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