Citation

Fitz-Clarke JR. Eur. J. Appl. Physiol. 2007; 100(2): 207-224.

Affiliation

Department of Physiology and Biophysics, Dalhousie University, 5849 University Avenue, Halifax, NS, Canada, B3H 4H7. jfitzclarke@eastlink.ca

Copyright

(Copyright © 2007, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/s00421-007-0421-z

PMID

17323072

Abstract

The world record for a sled-assisted human breath-hold dive has surpassed 200 m. Lung compression during descent draws blood from the peripheral circulation into the thorax causing engorgement of pulmonary vessels that might impose a physiological limitation due to capillary stress failure. A computer model was developed to investigate cardiopulmonary interactions during immersion, apnea, and compression to elucidate hemodynamic responses and estimate vascular stresses in deep human breath-hold diving. The model simulates active and passive cardiovascular adjustments involving blood volumes, flows, and pressures during apnea at diving depths up to 200 m. Redistribution of blood volume from peripheral to central compartments increases with depth. Pulmonary capillary transmural pressures in the model exceed 50 mm Hg at record depth, producing stresses in the range known to cause alveolar capillary damage in animals. Capillary pressures are partially attenuated by blood redistribution to compliant extra-pulmonary vascular compartments. The capillary pressure differential is due mainly to a large drop in alveolar air pressure from outward elastic chest wall recoil. Autonomic diving reflexes are shown to influence systemic blood pressures, but have relatively little effect on pulmonary vascular pressures. Increases in pulmonary capillary stresses are gradual beyond record depth.

Language: en