Commentaries on Viewpoint: Why predominantly neurological DCS in breath-hold divers?

TO THE EDITOR: Schipke and Tetzlaff (5) suggest breath-hold diving may recruit intrapulmonary arteriovenous anastomoses (IPAVA), providing a pathway for venous gas emboli to become arterialized leading to transient neurological injury consistent with transient ischemic attacks. To be a valid hypothesis there must be evidence of microbubbles in the right ventricle, left ventricle, carotid, or cerebral arteries of breath-hold divers after a typical dive profile with common dive times and surface intervals. Only one study could find evidence of microbubbles in the pulmonary infundibulum in a single subject (2) who had never even had symptoms of decompression sickness! With no evidence of arterialized microbubbles, the suggestion of IPAVA recruitment is premature. The recruitment of IPAVA by hypoxia is equally controversial, owing in part to an invalidated measurement technique that lacks a quantifiable assessment of IPAVA blood flow and involves a contrast agent that is susceptible to changes in transit time, blood gases, barometric pressure, and blood viscosity (1). Alternatively, we wondered if the dive profile of commercial breath-hold divers could be a sufficient intermittent hypoxic stimulus predisposing divers to the same cerebrovascular dysfunction observed in obstructive sleep apnea patients with similar presentations on neuroimaging studies (4). Progressive cerebrovascular dysfunction may underlie acute neurological injury, particularly if breath-hold diving acutely increases cerebrovascular transmural wall stress (through increased cerebral blood volume). The presence of vasogenic edema in breath-hold divers with neurological injury (3) supports a role for the breakdown of the blood-brain barrier, rather than gas emboli from IPAVA recruitment.