Diving physiopathology: the end of certainties? Food for thought

Abstract

our understanding of decompression physiopathology has slowly improved during this last decade and some uncertainties have disappeared. a better understanding of anatomy and functional aspects of patent foramen ovale (PFo) have slowly resulted in a more liberal approach toward the medical fitness to dive for those bearing a PFO. Circulating vascular gas emboli (Vge) are considered the key actors in development of decompression sickness and can be considered as markers of decompression stress indicating induction of pathophysiological processes not necessarily leading to occurrence of disease symptoms. During the last decade, it has appeared possible to influence post-dive VGE by a so-called "preconditioning" as a pre-dive denitrogenation, exercise or some pharmacological agents. in the text we have deeply examined all the scientific evidence about this complicated but challenging theme. Finally, the role of the "normobaric oxygen paradox" has been clarified and it is not surprising that it could be involved in neuroprotection and cardioprotection. However, the best level of inspired oxygen and the exact time frame to achieve optimal effect is still not known. The aim of this paper was to reflect upon the most actual uncertainties and distil out of them a coherent, balanced advice towards the researchers involved in gas-bubbles-related pathologies.

Vascular dysfunction following breath-hold diving

“…Decompression sickness (DCS) in SCUBA diving was related to gas bubbles created in tissues, in venous blood (venous gas emboli (VGE) or arterialized gas emboli (AGE)), arising from the decrease of inert gas solubility with the decrease of ambient pressure during ascent (Ljubkovic et al 2011(Ljubkovic et al , 2012Balestra et al 2019). DCS in breath-hold diving (BHD) was only anecdotal until recently because it was thought that the only inert gas added during these dives was nitrogen that remained in the lungs (Schipke and Tetzlaff 2016).…”

Decompression Illness in Repetitive Breath-Hold Diving: Why Ischemic Lesions Involve the Brain?

“…Gas embolization alone may not be sufficient to cause DCI. Repeated bubble insults and involvement of other processes may be necessary (Thalmann, 2003;Balestra et al, 2019;Barak et al, 2020).…”

“…A rapid increase in blood pressure, endothelial dysfunction, a transitory cerebral vascular autoregulation dysfunction, and blood-brain barrier breakdown in BH diving (Barak et al, 2015;Balestra et al, 2019;Patrician et al, 2021) may play a similar role as in a reversible cerebral vasoconstriction syndrome (RCVS) and posterior reversible encephalopathy syndrome (PRES) resulting from a cerebral arterial constriction in a context of major inflammatory diseases or injuries (Ducros, 2012;Pilato et al, 2020). However, clinical presentation and imaging in BHDND is different.…”

“…The formation of cerebral ischemic lesions in BH divers probably requires gas bubble emboli in the main arteries of the brain. In addition, DCS appears a systemic disease that is related to gas bubbles, but its manifestations depend on multiple factors and individual response of the diver (Balestra et al, 2019).…”

Livedo Racemosa – The Pathophysiology of Decompression-Associated Cutis Marmorata and Right/Left Shunt

“…However, this aspect has to be investigated in further studies. Therefore, the dive profile (low bubble diving) and behavior before and after surfacing is all the more important (Balestra et al, 2019). Especially heavy lifting and exertion after the dive can cause arterialization of VGEs.…”