Normal Rat Lungs and Rat Lungs after Receiving High-Pressure Mechanical Ventilation at a Peak Airway Pressure of 45 cm of WaterĪfter 5 minutes of ventilation, focal zones of atelectasis were evident, in particular at the left lung apex. 8, 10 – 13 Some evidence suggests that the inflammatory response induced during ventilator-induced lung injury has systemic consequences, contributing to the pathogenesis of multisystem organ failure in patients with ARDS. 9 The consequences of lung overdistention include direct physical damage, with disruption of the alveolar epithelium and capillary endothelium, as well as the induction of an inflammatory response, with the release of cytokines and other mediators. In addition, the inflation of normal alveoli adjacent to noninflated, abnormal alveoli may create high shear forces that can contribute to injury of the lung parenchyma, even at modest applied pressures. Excessive volume and pressure, with correspondingly high transpulmonary pressure (the difference in pressure between the airway and the pleural space), contribute to ventilator-induced lung injury. Since nonaerated lung tissue is stiffer than normal lung tissue, compliance is reduced and airway pressure is increased. As a result, ventilation with the use of high tidal volumes may cause hyperinflation of relatively normal regions of aerated lung. The volume of aerated lung in patients with ARDS is considerably reduced because of edema and atelectasis. This phenomenon is called ventilator-induced lung injury ( Fig. More recently, it has been recognized that mechanical ventilation, although potentially lifesaving, can contribute to the worsening of lung injury. 6, 7 The concept of “recruitment” (i.e., the opening of previously collapsed alveoli) was thought to provide a justification for such high-volume ventilation. Although the practice was variable, tidal volumes of 10 to 15 ml per kilogram of body weight (as compared with a normal tidal volume of 5 to 7 ml per kilogram for spontaneously breathing controls at rest) were commonly used. This objective was usually met with the use of a high FiO 2 and a high minute ventilation. In the past, the primary goal of ventilation had been to increase arterial oxygenation to an acceptable range (principally, an arterial oxyhemoglobin saturation of 88 to 95%, but also normal partial pressure of carbon dioxide and pH). 4, 5 The efficiency of gas exchange deteriorates precipitously.Įndotracheal intubation and mechanical ventilation are almost always necessary to manage the severe hypoxemia of ARDS. The chemical composition and functional activity of surfactant can be altered in patients with ARDS, resulting in an elevation in surface tension, which tends to promote regional alveolar collapse. Macrophages and neutrophils accumulate in the interstitium, and proinflammatory cytokines are released into the lungs. Edema fluid and plasma proteins leak from the vasculature into the alveolar spaces. The syndrome is characterized by diffuse alveolar damage associated with increased permeability of the alveolar–capillary membrane. PATHOPHYSIOLOGICAL CHARACTERISTICS AND EFFECT OF THERAPYĪcute lung injury can be defined physiologically as acute respiratory failure due to pulmonary edema in the absence of an elevation in the hydrostatic pressure in the pulmonary veins. Common causes of ARDS are sepsis (with or without a pulmonary source), trauma, aspiration, multiple blood transfusions, pancreatitis, inhalation injury, and certain types of drug toxicity. 1 The incidence of ARDS is 64 cases per 100,000 person-years, and the mortality rate is 40 to 50%. 2 ARDS is a more severe form of lung injury, defined by a ratio of the partial pressure of arterial oxygen to FiO 2 of less than 200. In the United States, there are an estimated 190,600 cases annually, leading to 74,500 deaths and 3.6 million hospital days. 1 Acute lung injury has an incidence of 86 cases per 100,000 person-years and a mortality rate of 39%. Acute lung injury is defined by the American–European Consensus Conference as the acute onset of impaired gas exchange (the ratio of the partial pressure of arterial oxygen in millimeters of mercury to the FiO 2 of <300) and the presence of bilateral alveolar or interstitial infiltrates in the absence of congestive heart failure.
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