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.
