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REVIEW

HIGHLIGHTED TOPIC
The Physiology and Pathophysiology of the Hyperbaric and Diving Environments

The physiology and pathophysiology of human breath-hold diving

¹Department of Physiology and Pharmacology, Section for Anesthesiology and Intensive Care Medicine, Karolinska Insitutet, and Department of Radiology, Karolinska University Hospital, Stockholm, Sweden; and ²Center for Research and Education in Special Environments, and Department of Physiology and Biophysics, School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York

Submitted 31 July 2008 ; accepted in final form 24 October 2008

ABSTRACT

This is a brief overview of physiological reactions, limitations, and pathophysiological mechanisms associated with human breath-hold diving. Breath-hold duration and ability to withstand compression at depth are the two main challenges that have been overcome to an amazing degree as evidenced by the current world records in breath-hold duration at 10:12 min and depth of 214 m. The quest for even further performance enhancements continues among competitive breath-hold divers, even if absolute physiological limits are being approached as indicated by findings of pulmonary edema and alveolar hemorrhage postdive. However, a remarkable, and so far poorly understood, variation in individual disposition for such problems exists. Mortality connected with breath-hold diving is primarily concentrated to less well-trained recreational divers and competitive spearfishermen who fall victim to hypoxia. Particularly vulnerable are probably also individuals with preexisting cardiac problems and possibly, essentially healthy divers who may have suffered severe alternobaric vertigo as a complication to inadequate pressure equilibration of the middle ears. The specific topics discussed include the diving response and its expression by the cardiovascular system, which exhibits hypertension, bradycardia, oxygen conservation, arrhythmias, and contraction of the spleen. The respiratory system is challenged by compression of the lungs with barotrauma of descent, intrapulmonary hemorrhage, edema, and the effects of glossopharyngeal insufflation and exsufflation. Various mechanisms associated with hypoxia and loss of consciousness are discussed, including hyperventilation, ascent blackout, fasting, and excessive postexercise O₂ consumption. The potential for high nitrogen pressure in the lungs to cause decompression sickness and N₂ narcosis is also illuminated.

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