Claes E. G. Lundgren

The physiology and pathophysiology of human breath-hold diving

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 O(2) consumption. The potential for high nitrogen pressure in the lungs to cause decompression sickness and N(2) narcosis is also illuminated.

The underwater environment: cardiopulmonary, thermal, and energetic demands

Water covers over 75% of the earth, has a wide variety of depths and temperatures, and holds a great deal of the earths resources. The challenges of the underwater environment are underappreciated and more short term compared with those of space travel. Immersion in water alters the cardio-endocrine-renal axis as there is an immediate translocation of blood to the heart and a slower autotransfusion of fluid from the cells to the vascular compartment. Both of these changes result in an increase in stroke volume and cardiac output. The stretch of the atrium and transient increase in blood pressure cause both endocrine and autonomic changes, which in the short term return plasma volume to control levels and decrease total peripheral resistance and thus regulate blood pressure. The reduced sympathetic nerve activity has effects on arteriolar resistance, resulting in hyperperfusion of some tissues, which for specific tissues is time dependent. The increased central blood volume results in increased pulmonary artery pressure and a decline in vital capacity. The effect of increased hydrostatic pressure due to the depth of submersion does not affect stroke volume; however, a bradycardia results in decreased cardiac output, which is further reduced during breath holding. Hydrostatic compression, however, leads to elastic loading of the chest wall and negative pressure breathing. The depth-dependent increased work of breathing leads to augmented respiratory muscle blood flow. The blood flow is increased to all lung zones with some improvement in the ventilation-perfusion relationship. The cardiac-renal responses are time dependent; however, the increased stroke volume and cardiac output are, during head-out immersion, sustained for at least hours. Changes in water temperature do not affect resting cardiac output; however, maximal cardiac output is reduced, as is peripheral blood flow, which results in reduced maximal exercise performance. In the cold, maximal cardiac output is reduced and skin and muscle are vasoconstricted, resulting in a further reduction in exercise capacity.

Intravascular fluorocarbon-stabilized microbubbles protect against fatal anemia in rats.

It has earlier been hypothesized that intravascular microbubbles, derived from a dodecafluoropentane (DDFP) emulsion, can transport physiologically significant amounts of oxygen in the animal body. To test this notion, anesthetized oxygen breathing rats were rendered severely anemic by bleeding and volume replacement. Rats treated with 0.014 ml/kg of DDFP in a 2% emulsion had normal circulatory parameters and behaved normally when waking up from anesthesia while controls died during anesthesia. Oxygen-breathing intact rats given 0.01 ml/kg of DDFP had muscle oxygen tensions which, for about 2.5 hours, exceeded those of controls by 50–100%. It was further verified in vitro that DDFP-derived microbubbles can exchange oxygen with a surrounding aqueous medium. Extrapolation from these experiments indicates that less than 1 ml of DDFP, in emulsion-form, could provide for the resting oxygen consumption of an adult person. This suggests various therapeutic uses of the emulsion.

Maximal breath-holding time and immediate tissue CO2 storage capacity during head-out immersion in humans

AbstractThis study tested three possible mechanisms that could explain the prolonged breath-holds (BH) previously observed in humans during submersion in 35°C (thermoneutral) water, including a reduced metabolism, a decreased CO2 sensitivity, and an increased CO2 storage capacity. During immersed BH (n = 13), maximal BH time was prolonged by 20.3% (P < 0.05), the rate of rise of end tidal partial pressure of carbon dioxide (PETCO2) was slower (P < 0.05) by 31 % (compatible with increased CO2 storage capacity), but the breaking-pointPETCO2 (CO2 sensitivity) and the rate of decrease of end tidal partial pressure of oxygen (metabolism) were unchanged. During air breathing (n = 5), immersion resulted in a significant decrease in tidal volume (11%), but did not affect O2 uptake, CO2 elimination

Hypoxia Due to Shunts in Pig Lung Treated with O2 and Fluorocarbon-derived Intravascular Microbubbles

(\dot VCO_2 )

High blood pressure during breath-hold diving is not a physiological absurdity

, or respiratory exchange ratio (R). During a 4-min CO2-rebreathing (n = 9), the slope of the hypercapnic ventilatory response curve (CO2 sensitivity index) was unchanged by immersion, but the significantly decreased

Nitrogen washout during a fatty meal while breathing nitrogen-free gas at sea level.

\dot VCO_2