What is tension physiology?

Tension Physiology

Tension physiology occurs when intrapleural pressure exceeds atmospheric pressure throughout the entire respiratory cycle due to a one-way valve mechanism, causing progressive air accumulation that impairs venous return, reduces cardiac output, and leads to cardiovascular collapse. 1

Core Pathophysiologic Mechanism

• Air enters the pleural space during inspiration but cannot escape during expiration, creating progressive pressure buildup through a one-way valve effect 1
• The mechanism causes mediastinal shift, reduced venous return, and kinking of great vessels leading to hemodynamic instability 1
• Intrapleural pressure rises progressively with each respiratory cycle, eventually exceeding atmospheric pressure and compressing mediastinal structures 2

Cardiovascular Consequences

• Major cardiovascular instability occurs when mean insufflation pressures reach approximately 10 mmHg, associated with a 67% decrease in cardiac output (from 6.6 L/min to 2.2 L/min) 2
• Further pressure increases to 15 mmHg produce an 82% decrease in cardiac output from baseline (6.8 L/min to 1.2 L/min), progressing to pulseless electrical activity arrest at approximately 20 mmHg 2
• Central venous pressure rises (from 7.6 mmHg to 15.2 mmHg) while pulmonary artery diastolic pressure falls (from 15 mmHg to 12 mmHg), with equalization of these pressures occurring immediately before major hemodynamic decline 2

Temporal Sequence of Physiologic Derangement

• Significant hypoxemia occurs early and precedes hypotension in ventilated patients with tension physiology 3
• Oxygen saturation decreases immediately and continues to decline throughout progression, falling below 50% prior to cardiovascular collapse 3
• Mean arterial pressure and heart rate remain relatively stable until approximately 57% total lung capacity pneumothorax is reached, at which point significant decline in blood pressure and increase in heart rate indicate established tension physiology 3
• Cardiac output shows a small but significant decrease after initial air accumulation, with progressive decline thereafter 3

Critical Distinction from Simple Pneumothorax

• Tension development is NOT dependent on pneumothorax size—small pneumothoraces can become immediately life-threatening 1
• The defining feature is the one-way valve mechanism that prevents air egress, not the absolute volume of intrapleural air 1
• All pneumothoraces have pressures greater than atmospheric during expiration (which is why conventional intercostal tube drainage works), but tension physiology requires sustained supraatmospheric pressure throughout the respiratory cycle 4

Mechanical Versus Hypoxemic Mechanisms

• The cardiovascular collapse in tension physiology results from both early severe hypoxemia and late mechanical compression 3
• Occlusive mechanical compression, evidenced by equalization of mean intrapleural pressure with central venous pressure, is a late event occurring at the point of cardiovascular collapse 3
• In spontaneously breathing patients with intact mediastinal pleura, tension is transmitted incompletely to the mediastinum and contralateral hemithorax, with marked respiratory intrathoracic pressure swings and compensatory tachycardia initially preventing cardiovascular collapse 5

Positive Pressure Ventilation Context

• In mechanically ventilated patients, decreased cardiac index is the most consistently detected abnormality indicating tension physiology 6
• Expected increases in central venous pressure and heart rate may not occur in patients receiving inotropic therapy, making cardiac output monitoring critical 6
• Positive pressure ventilation accelerates tension development by maintaining the air leak and preventing spontaneous respiratory compensation 7, 8

Clinical Recognition Parameters

• Rapid labored respiration with progressive respiratory distress distinguishes tension from simple pneumothorax 1, 8
• Attenuated or absent breath sounds on the affected side are the most common bedside finding 1
• Patients develop cyanosis, profuse sweating, and tachycardia as tension progresses 1, 8
• Sudden deterioration or pulseless electrical activity arrest in patients on mechanical or non-invasive ventilation should prompt immediate presumption of tension physiology 1, 8