Pathophysiology of Surgical Pneumothorax in the Awake Patient

Surgical pneumothorax makes awake thoracic surgery procedures feasible. This iatrogenic event is followed by a complex cascade of physiologic changes in both lung ventilation and perfusion, as well as in mechanical interaction between lungs, pleural cavity, diaphragm and mediastinum.

In most instances, the newly developed intrapleural atmospheric pressure environment leads to a drop in lung volume, thus assuring an adequate space for easy surgical maneuvering. The extent of this effect, however, varies considerably and is related to the conditions of lung tissue, airways and pleural cavity.

During surgical pneumothorax, ventilation-to-perfusion mismatch increases shunt fraction. Mechanical changes may include mediastinal shifting towards the dependent ventilated lung, and paradoxical respiration with collapse of non-dependent lung during inspiration and expansion during exhalation, leading to alveolar hypoventilation and hypoxemia. Mediastinal shift and paradoxical respiration decrease the efficiency of spontaneous ventilation with re-breathing of exhaled gases. Hemodynamic changes include an increase in vascular resistance due to mechanical limitation to flow and hypoxemia, which accompanies collapse of the lung and may enhance this effect by inducing pulmonary vasoconstriction. Administration of oxygen can usually prevent hypoxemia but permissive hypercapnia can develop, particularly in patients with severe emphysema.

Hence, though well tolerated by the majority of patients, hypoxemia, hypercapnia and hypoventilation are all common findings during awake thoracic surgery and need to be carefully taken into account by physicians who decide to be involved in this novel surgical field.

Keywords: Open pneumothorax, awake thoracic surgery, VATS, ventilation, paradoxical respiration.