The various forms of pulmonary barotrauma (interstitial emphysema, pneumomediastinum, pneumoperitoneum, subcutaneous emphysema, lung cyst formation, and pneumothorax) are prominent among the iatrogenic causes of critical illness. Patients with acute respiratory distress syndrome appear to be at highest risk. Although direct rupture of the visceral pleura occasionally occurs, the barotrauma that complicates mechanical ventilation most frequently develops more circuitously. Alveolar rupture is most likely to occur in 'non-partitional' or 'marginal' alveoli, which have bases contiguous with relatively immobile structures (vessels, bronchioles, or fibrous septae). Once excessive pressure gradients between marginal alveoli and contiguous perivascular connective tissues have caused alveolar rupture, extra-alveolar gas follows a pressure gradient along the perivascular sheaths toward the hilum.
In the absence of mediastinal pathology, gas usually dissects along fascial planes into the mediastinum and soft tissues of the neck (subcutaneous emphysema) or retroperitoneum (pneumoperitoneum). Pneumothorax develops in a minority of such cases (perhaps 20-30 per cent) when soft tissue gas ruptures into the pleural space via an interrupted or weakened mediastinal pleural membrane. Unlike pneumothorax, interstitial emphysema, pneumomediastinum, and subcutaneous emphysema have little hemodynamic significance and seldom influence gas exchange in adult patients.
Until recently, ventilator-induced bronchial damage was thought to occur only rarely in adults. However, in the heterogeneously injured lung, high airway pressures can inflict considerable damage in small airways unsupported by cartilage. Airway distortion predisposes to cystic parenchymal damage, disordered gas exchange, and impaired secretion clearance.
When normal bronchovascular channels are blocked, gas accumulates locally or migrates distally to produce subpleural air cysts. It is not uncommon for a cyst created by positive airway pressure to enlarge quickly, even to a diameter exceeding 10 cm. These cysts compress normal lung tissue, increasing the airway pressure needed for effective ventilation and creating dead-space that raises the ventilatory requirement and mean alveolar pressure. Once under way, cystic barotrauma tends to be self-reinforcing. The rapid development of cystic barotrauma usually presages the occurrence of tension pneumothorax. Effective secretion clearance, treatment of infection, and, most importantly, reduction of airway pressure are fundamental to management.
In patients with acute respiratory distress syndrome ventilated with high tidal pressures and maintained with low left ventricular filling pressures, alveolar pressures may exceed those in the pulmonary veins. If alveolar rupture opens a communication pathway to the vascular system, this pressure gradient may drive air into the systemic circulation. Irritating microbubbles can then cause vasospasm, with resulting neurological damage or myocardial infarction.
A sustained increase of pleural pressure ('tension') often complicates a pneumothorax arising during mechanical ventilation. A tension component occasionally develops when a ball-valve mechanism pumps air into the pleural cavity during spontaneous breathing, but is much more common when positive pressure provides the ventilatory power. Positive intrapleural pressure expands the ipsilateral chest cage, impairing inspiratory muscular efficiency. Contralateral pleural pressure tends to be maintained at near-normal levels until late in the process. However, a shifting mediastinum may encroach upon the contralateral hemithorax, compromising lung expansion. Eventually, rising pleural and central venous pressures impede venous return sufficiently to cause hemodynamic deterioration. Vigorous inspiratory efforts tend to maintain intrapleural pressure (averaged for both lungs over the entire respiratory cycle) at near-normal levels until the patient fatigues, is sedated, or receives ventilator assistance. Abrupt hemodynamic deterioration may then occur as the mean pleural pressure rises. Ventilated patients with pneumothorax frequently experience abrupt hemodynamic deterioration immediately after receiving sedating or paralytic drugs. Tension can develop without lung collapse or even major volume loss when the lung is heavily infiltrated, or when air is trapped or bound locally by pleural adhesions.
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