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A tension pneumothorax is present when the intrapleural pressure exceeds the atmospheric
pressure throughout expiration and often during inspiration as well.[1] Most patients who develop
a tension pneumothorax are receiving positive pressure to their airways, either during mechanical
ventilation or during resuscitation.[1] For a tension pneumothorax to develop in a spontaneously
breathing person, some type of one-way valve mechanism must be present so more air enters the
pleural space on inspiration than leaves the pleural space on expiration, so air accumulates in the
pleural space under positive pressure.[1]
Pathophysiology
The development of a tension pneumothorax is usually heralded by a sudden deterioration in the
cardiopulmonary status of the patient. The explanation for this sudden deterioration is probably
related to the combination of a decreased cardiac output due to impaired venous return and
profound hypoxia due to ventilation-perfusion mismatches. In mechanically ventilated sheep, an
induced tension pneumothorax (mean pleural pressure of +25 cm H2O) reduced the cardiac
output from 3.5 to 1.1 L/min.[78] The arterial PO2 also fell from a baseline value of 159 to
59 mm Hg. Comparable reductions in cardiac output and oxygen saturation were seen in pigs[79]
and in dogs[80] following induction of tension pneumothoraces. Similarly, in patients on
mechanical ventilation who develop tension pneumothorax, there is a large drop in the cardiac
output.[81]
Clinical Manifestations
Patients most commonly have a tension pneumothorax while they are receiving positive-pressure
mechanical ventilation, during cardiopulmonary resuscitation,[82] or as a complication of
hyperbaric oxygen therapy.[1] Occasionally, a tension pneumothorax will evolve during the
course of a spontaneous pneumothorax. Tension pneumothorax can develop from improper
connection of one-way flutter valves with small-caliber chest tubes.[83]
The clinical picture associated with the development of a tension pneumothorax is striking. The
patient appears distressed, with rapid labored respirations, cyanosis, marked tachycardia, and
profuse diaphoresis. The physical findings are those of a very large pneumothorax. Arterial
blood gases reveal marked hypoxemia and sometimes respiratory acidosis.
If the procedure just described confirms the diagnosis of a tension pneumothorax, the catheter
should be left in place and in communication with the atmosphere until air ceases to exit through
the syringe. Additional air can be withdrawn from the pleural space with the syringe and the
three-way stopcock. The patient should be prepared for immediate tube thoracostomy