Citation

Schipke JD, Tetzlaff K. J. Appl. Physiol. (APS Bethesda) 2016; 120(12): 1474-1477.

Affiliation

University of Tübingen, Germany.

Copyright

(Copyright © 2016, American Physiological Society)

DOI

10.1152/japplphysiol.00840.2015

PMID

26796755

Abstract

This viewpoint proposes the hypothesis that the hypoxia of breath-hold diving recruits pulmonary shunts and may lead to the arterialisation of venous gas emboli (VGE). The resulting arterial gas emboli (AGE) might seed the cerebral circulation causing the growth of nitrogen bubbles and manifestation of cerebral decompression sickness (DCS). The literature suggesting clinical signs and symptoms consistent with DCS in breath-hold divers is being reviewed, and mechanisms that may cause neurological DCS-like clinical features, including transient ischemic attacks and stroke, are discussed. This article points at an important physiological difference between breath-hold and compressed gas (scuba) diving: While pulmonary barotrauma or cardiac right-to-left shunts have been shown to be associated with AGE in scuba diving, hypoxia and opening of intrapulmonary shunts may play a key role in neurological injury from breath-hold diving. It is suggested that intrapulmonary arteriovenous anastomoses may open during hypoxia and represent breaches in the pulmonary filter providing a route for right-to-left shunting of VGE. Such mechanism might explain stroke-like clinical phenomena that have been reported after breath-hold dives.

Language: en