Tension Pneumothorax Causes and Management

Pathophysiology and Clinical Presentation

Tension pneumothorax occurs when intrapleural pressure exceeds atmospheric pressure throughout the respiratory cycle, creating a one-way valve effect that draws air into the pleural space during inspiration but prevents its escape during expiration 1
The one-way valve mechanism leads to progressive air accumulation in the pleural space, causing mediastinal shift, decreased venous return, reduced cardiac output, and hypoxemia 2
The development of tension in a pneumothorax is not dependent on the size of the pneumothorax, and clinical presentation may correlate poorly with radiographic findings 2
The clinical presentation is striking: rapid labored respiration, cyanosis, sweating, tachycardia, and progressive respiratory distress 2
Tension pneumothorax should be particularly suspected in patients on mechanical ventilators or non-invasive ventilation who suddenly deteriorate or develop PEA arrest 2, 1

Invasive procedures account for the majority of cases, with transthoracic needle aspiration (24%), subclavian vessel puncture (22%), thoracocentesis (22%), and pleural biopsy (8%) being the most common 3
The risk of pneumothorax during transthoracic needle aspiration increases with deeper lesions and in patients with underlying COPD 3
COPD patients who develop iatrogenic pneumothorax are more likely to require tube drainage 4
Immediate needle decompression with a cannula of adequate length (at least 4.5 cm) should be performed, followed by chest tube placement 2, 1
The cannula should be inserted into the second intercostal space in the mid-clavicular line and left in place until a functioning intercostal tube is positioned 2
Patients on positive pressure ventilation who develop pneumothorax should always receive tube thoracostomy as positive pressure maintains the air leak 1
In mechanically ventilated patients with asthma, tension pneumothorax is a rare but life-threatening complication that should be considered when there is sudden deterioration 5

PEEP raises pleural pressure, which elevates right‑atrial back pressure and narrows the venous‑return gradient (normally 4–8 mmHg), leading to marked reductions in cardiac output; this reduction persists throughout the entire respiratory cycle, not only during inspiration. 6, 7
The European Society of Cardiology advises that the intrathoracic pressure elevation caused by PEEP can diminish venous return and exacerbate right‑ventricular failure in patients with massive pulmonary embolism or other conditions that increase pulmonary vascular resistance. 8, 9

PEEP increases pulmonary vascular resistance in direct proportion to the rise in mean alveolar pressure, adding afterload to an already compromised right ventricle; when pleural and interstitial pressures exceed pulmonary arterial pressure (West zone 1), pulmonary blood flow is largely obstructed and alveolar pressure becomes the outflow pressure for the right ventricle, substantially raising right‑ventricular afterload. 10

In patients with severe asthma who require mechanical ventilation, a protective strategy of low respiratory rate and tidal volume (≈6–8 mL/kg), a short inspiratory time and a prolonged expiratory time (I:E ratio 1:4–1:5) is recommended to limit auto‑PEEP and barotrauma risk. 11
If auto‑PEEP develops and produces significant hypotension, immediate disconnection of the ventilator circuit to allow passive exhalation, combined with manual chest‑wall compression, is advised to relieve intrathoracic pressure. 11
During cardiac arrest in any patient with difficult ventilation, clinicians should strongly consider tension pneumothorax as a reversible cause and may empirically treat it (e.g., needle decompression) while continuing resuscitation efforts. 11