Cardiovascular changes induced by cold water immersion during hyperbaric hyperoxic exposure.

The present study was designed to assess the cardiac changes induced by cold water immersion compared with dry conditions during a prolonged hyperbaric and hyperoxic exposure (ambient pressure between 1.6 and 3 ATA and PiO(2) between 1.2 and 2.8 ATA). Ten healthy volunteers were studied during a 6 h compression in a hyperbaric chamber with immersion up to the neck in cold water while wearing wet suits. Results were compared with measurements obtained in dry conditions. Echocardiography and Doppler examinations were performed after 15 min and 5 h. Stroke volume, left atrial and left ventricular (LV) diameters remained unchanged during immersion, whereas they significantly fell during the dry session. As an index of LV contractility, percentage fractional shortening remained unchanged, in contrast to a decrease during dry experiment. Heart rate (HR) significantly decreased after 5 h, although it had not changed during the dry session. The changes in the total arterial compliance were similar during the immersed and dry sessions, with a significant decrease after 5 h. In immersed and dry conditions, cardiac output was unchanged after 15 min but decreased by almost 20% after 5 h. This decrease was related to a decrease in HR during immersion and to a decrease in stroke volume in dry conditions. The hydrostatic pressure exerted by water immersion on the systemic vessels could explain these differences. Indeed, the redistribution of blood volume towards the compliant thoracic bed may conceal a part of hypovolaemia that developed in the course of the session.

Haemodynamic changes induced by submaximal exercise before a dive and its consequences on bubble formation.

OBJECTIVES: To evaluate the effects of a submaximal exercise performed 2 h before a simulated dive on bubble formation and to observe the haemodynamic changes and their influence on bubble formation. PARTICIPANTS AND METHODS: 16 trained divers were compressed in a hyperbaric chamber to 400 kPa for 30 min and decompressed at a rate of 100 kPa/min with a 9 min stop at 130 kPa (French Navy MN90 procedure). Each diver performed two dives 3 days apart, one without exercise and one with exercise before the dive. All participants performed a 40 min constant-load submaximal and calibrated exercise, which consisted of outdoor running 2 h before the dive. Circulating bubbles were detected with a precordial Doppler at 30, 60 and 90 min after surfacing. Haemodynamic changes were evaluated with Doppler echocardiography. RESULTS: A single bout of strenuous exercise 2 h before a simulated dive significantly reduced circulating bubbles. Post-exercise hypotension (PEH) was observed after exercise with reductions in diastolic and mean blood pressure (DBP and MBP), but total peripheral resistance was unchanged. Stroke volume was reduced, whereas cardiac output was unchanged. Simulated diving caused a similar reduction in cardiac output independent of pre-dive exercise, suggesting that pre-dive exercise only changed DBP and MBP caused by reduced stroke volume. CONCLUSION: A single bout of strenuous exercise 2 h before a dive significantly reduced the number of bubbles in the right heart of divers and protected them from decompression sickness. Declining stroke volume and moderate dehydration induced by a pre-dive exercise might influence inert gas load and bubble formation.

Haemodynamic effects of hyperbaric hyperoxia in healthy volunteers: an echocardiographic and Doppler study.

In the present study, we observed the haemodynamic changes, using echocardiography and Doppler, in ten healthy volunteers during 6 h of compression in a hyperbaric chamber with a protocol designed to reproduce the conditions as near as possible to a real dive. Ambient pressure varied from 1.6 to 3 atm (1 atm=101.325 kPa) and partial pressure of inspired O2 from 1.2 to 2.8 atm. Subjects performed periods of exercise with breathing through a closed-circuit self-contained underwater breathing apparatus (SCUBA). Subjects did not eat or drink during the study. Examinations were performed after 15 min and 5 h. After 15 min, stroke volume (SV), left atrial (LA) diameter and left ventricular (LV) end-diastolic diameter (LVEDD) decreased. Heart rate (HR) and cardiac output (CO) did not vary, but indices of the LV systolic performance decreased by 10% and the LV meridional wall stress increased by 17%. After 5 h, although weight decreased, the serum protein concentration increased. Compared with values obtained after 15 min, SV and CO decreased, but LV systolic performance, LA diameter, LVEDD and LV meridional wall stress remained unchanged. Compared with the reference values obtained at sea level, total arterial compliance decreased, HR remained unchanged and CO decreased. In conclusion, hyperbaric hyperoxia results in significant haemodynamic changes. Initially, hyperoxia and the SCUBA system are responsible for reducing LV preload, increasing LV afterload and decreasing LV systolic performance, although CO did not change. Prolonged exposure resulted in a further decrease in LV preload, because of dehydration, and in a further increase in LV afterload, due to systemic vasoconstriction, with the consequence of decreasing CO.

Hyperbaric hyperoxia induces a neuromuscular hyperexcitability: assessment of a reduced response in elite oxygen divers.

We compared the changes in compound muscle mass action potential (M-wave) recorded in vastus lateralis in response to hyperbaric hyperoxia (HBO) in nine combat divers who dived daily while breathing 100% O2 or O2-enriched mixture (O2 divers) to those measured in eight recreational divers who dived occasionally using compressed air/21% O2 (air divers). The O2 divers completed a 6-h HBO exposure in which the inspired oxygen pressure (PiO2) varied from 1.15 to 2.7 absolute atmospheres (ATA), PiO2 being maintained at 1.15 ATA throughout the first 2-h period, whereas the air divers only completed a 2-h HBO exposure with PiO2 constant at 1.15 ATA. Before HBO exposure, there were no intergroup differences between baseline M-wave characteristics (amplitude and duration), but the conduction time was significantly shorter in O2 divers compared with air divers. After 90 min of HBO (1.15 ATA) the air divers demonstrated neuromuscular hyperexcitability, as evidenced by an increased M-wave amplitude (13%, P<0.01 versus baseline), shortened M-wave duration (5%, P<0.05 versus baseline), and reduced conduction time (5%, P<0.01 versus baseline). In O2 divers, similar HBO-induced M-wave changes were only observed when PiO2 was greater than 1.50 ATA. We conclude that HBO elicites neuromuscular hyperexcitability, attenuated in elite O2 divers.