Barotrauma key12/20/2023 At necropsy, there was severe pulmonary atelectasis, increased wet lung weight, and increased minimum surface tension of saline lung lavage fluid. In a sheep model of ARDS induced by moderately high airway pressures, Tsuno and colleagues 86 described progressive deterioration in total static lung compliance, functional residual capacity, and arterial blood gases, with radiologic abnormalities emerging over time. Large-animal models used by Tsuno and coworkers 86, 87 demonstrated that regional pressure–related overdistention results in a pattern of diffuse alveolar damage that is histologically similar to clinical ARDS, with similar pulmonary mechanics. Likewise, Dreyfuss and colleagues 26, 27 found that intermittent positive-pressure hyperventilation with high inflation pressures produced pulmonary microvascular injury and capillary permeability edema in a rodent model. Using geometric and mathematical modeling to evaluate mean airway pressure, Marini and Ravenscraft 56 found that, under conditions of passive inflation, mean arterial pressure correlated with arterial oxygenation, hemodynamic performance, and barotrauma.Įlevated PIP, high respiratory rates, oxygen toxicity, and alveolar overdistention combined account for ventilator-associated barotrauma. The high-PIP group had significant microvascular injuries. In an isolated perfused rabbit lung model, they ventilated four sets of lungs with either low or high rates of gas flow while holding the peak inspiratory pressure (PIP) either low (27 cm H 2O) or high (50 cm H 2O). Later, Peevy and coworkers 69 suggested that peak airway pressure was the most important mechanism of injury. Three of the main symptoms in ARDS are decreased lung compliance, alveolar edema, and hypoxemia, 82 all of which presented in the rats. This suggested that alveolar edema was caused by the depletion or inactivation of surfactant. 88 Rats ventilated with high airway pressure (45 cm H 2O) developed alveolar edema, hypoxemia (measured by the pressure/flow ratio 76), and decreased lung compliance they usually died within 1 hour. VILI was first recognized as a distinct type of barotrauma by Webb and Tierney. Parker and coworkers 68 reported that pressure- and volume-related alveolar rupture is the most common cause of pneumothorax in ventilated patients. A continuum of fascial planes connects the soft tissue compartments of the mediastinum, neck, and retroperitoneum, also allowing decompression of the pneumothorax into these compartments, with subsequent formation of dissecting air pockets. With subsequent rupture of the mediastinal pleura, air enters the pleural space, causing a pneumothorax. Because the mediastinal pleura is relatively weak and thin compared with the visceral pleura, air often dissects toward the hilum, where it can enter the mediastinum and form a pneumomediastinum. Once ventilator-applied pressure ruptures the alveoli, air dissects along the loose connective tissues of the bronchovascular bundle or the interlobular septa medially toward the hilum and peripherally toward the visceral pleura. Macklin 53 and Macklin and Macklin 54 reported, more than 60 years ago, that any sudden increase in alveolar pressure may result in a gradient sufficient to disrupt the alveolar wall. Pneumothoraces can cause significant impairment of ventilation, gas exchange, and cardiac function, requiring prompt diagnosis and treatment. Subcutaneous emphysema usually is not clinically significant itself but rather an indicator of airway injury that may have other manifestations and requires prompt evaluation. Common manifestations of extra-alveolar air include pneumothoraces and subcutaneous emphysema.
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