In addition to receiving a rapid infusion of intravenous fluids, hypotensive patients who have underlying airway disease should be allowed to deflate themselves by interrupting mechanical inflation, before ventilation is resumed at a reduced frequency. Failure to appreciate the importance of excessive hyperinflation in causing hypotension may lead to the eventual development of cardiac arrest and death. Although less common, ventilator-associated hypotension also occurs in ARDS at high levels of PEEP and when prolongation of the ratio of inspiration to expiration leads to excessive dynamic hyperinflation. Barotrauma may present as subcutaneous emphysema, pneumomediastinum, pulmonary interstitial emphysema, pneumoperitoneum, pneumopericardium, arterial gas embolism, or pneumothorax. Regardless of its ultimate pathway of dissection, extra-alveolar air usually originates from overdistended alveoli that rupture into the surrounding interstitial space.
Tension pneumothorax is the most common life-threatening manifestation of barotrauma.
The likelihood that a pneumothorax will be under tension depends not only on the volume of air in the pleural space but also on compressibility of the ipsilateral lung. When the lung resists collapse, as in ARDS or with gross hyperinflation, a relatively small amount of intrapleural air may produce positive intrapleural pressure. A tension pneumothorax leads to worsening hypoxemia and decreased venous return with hypotension. Hyperresonance and a reduction of breath sounds on the side of the pneumothorax are common, and inflation pressures are increased. Atelectasis is a common cause of severe hypoxemia that develops during mechanical ventilation.