Mechanisms of Hypoxemia in Decompression Sickness
Hypoxemia in decompression sickness occurs primarily through two mechanisms: ventilation-perfusion (V/Q) mismatch when bubbles obstruct pulmonary capillaries, and right-to-left shunting when large bubble volumes overwhelm the pulmonary circulation or traverse intracardiac defects. 1
Primary Pulmonary Mechanisms
Pulmonary Capillary Obstruction and V/Q Mismatch
Bubbles forming during decompression are transported through the venous circulation to the lungs, where they are normally filtered at the pulmonary capillary level if the lung circulation is intact. 1
When a large volume of bubbles forms, the pulmonary circulation itself becomes compromised, leading to pulmonary decompression illness ("the chokes"), which presents with chest tightness, cough, dyspnea, and falling systemic blood pressure. 1
This bubble obstruction creates areas of lung that are perfused but poorly ventilated, resulting in V/Q mismatch—the most common and easily treatable cause of hypoxemia with supplemental oxygen. 1
Intrapulmonary and Intracardiac Shunting
If there is any anatomical shunt (atrial septal defect, patent foramen ovale, or intrapulmonary shunt), or a physiological shunt occurring when bubble volume is large, bubbles may bypass the pulmonary filter and access the systemic circulation. 1
Physiological shunting can occur even without pre-existing cardiac defects when the sheer volume of bubbles overwhelms the pulmonary circulation's filtering capacity. 1
In one study of amateur divers with neurological symptoms within 5 minutes of surfacing, 50% of those without intracardiac shunts had abnormalities of the flow-volume loop suggesting small airway disease, indicating that pulmonary structural abnormalities contribute to bubble passage and subsequent hypoxemia. 1
Secondary Inflammatory Mechanisms
Bubble-Induced Vascular Injury
Bubble formation within the circulation triggers complement and platelet activation, leading to formation of microemboli and altered endothelial function, which further compromises gas exchange. 1
These secondary phenomena cause capillary leakage and endothelial dysfunction, worsening V/Q matching and potentially contributing to pulmonary edema. 1, 2
Clinical Presentation Pattern
The falling oxygen tension in breathing gas during ascent exacerbates symptoms, as hypoxemia becomes more marked during the ascent phase when bubbles are actively forming and pulmonary compromise is developing. 1
Symptoms may progress from relatively trivial manifestations to severe cardiopulmonary collapse depending on the volume and location of bubbles. 1
Important Clinical Caveat
Normal oxygen saturation does not exclude tissue hypoxia in decompression sickness—patients may have adequate arterial oxygenation but still suffer from stagnant hypoxia due to bubble-induced circulatory obstruction at the tissue level. 3 This distinction is critical because while supplemental oxygen treats hypoxemic hypoxia from V/Q mismatch, it does not address the mechanical obstruction of tissue perfusion by bubbles, which requires definitive hyperbaric oxygen therapy to reduce bubble size and restore tissue perfusion. 3, 2