Fitz-Clarke John R
Department of Physiology and Biophysics, Dalhousie University, 5849 University Avenue, Halifax, NS, Canada, B3H 4H7.
Eur J Appl Physiol. 2007 May;100(2):207-24. doi: 10.1007/s00421-007-0421-z. Epub 2007 Feb 24.
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.
借助雪橇辅助的人类屏气潜水世界纪录已超过200米。下潜过程中肺部受到压缩,致使血液从外周循环流入胸腔,导致肺血管充血,这可能因毛细血管应力衰竭而造成生理限制。开发了一个计算机模型来研究浸入、屏气和压缩过程中的心肺相互作用,以阐明血液动力学反应并估计深度人类屏气潜水中的血管应力。该模型模拟了在高达200米的潜水深度屏气期间涉及血容量、血流和压力的主动和被动心血管调节。血容量从外周腔室向中心腔室的重新分布随深度增加。在记录深度时,模型中的肺毛细血管跨壁压力超过50毫米汞柱,产生的应力在已知会导致动物肺泡毛细血管损伤的范围内。通过将血液重新分布到顺应性肺外血管腔室,毛细血管压力会部分减弱。毛细血管压力差主要是由于向外的弹性胸壁反冲导致肺泡气压大幅下降。自主潜水反射被证明会影响全身血压,但对肺血管压力的影响相对较小。超过记录深度后,肺毛细血管应力的增加是渐进的。