Olivier Castagna

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.

Peripheral arterial disease: an underestimated aetiology of exercise intolerance in chronic obstructive pulmonary disease patients:

Objective To assess the prevalence of peripheral arterial disease and its implications for exercise limitation in chronic obstructive pulmonary disease (COPD) patients. Method One hundred and fifty-one moderate-to-severe COPD patients (forced expiratory volume in 1s: 37 ± 6 SD% predicted) and 73 healthy age-matched control individuals (divided into 31 smokers and 42 nonsmokers) participated in this study. All COPD patients were either exsmokers or current smokers and their tobacco-smoking history was similar to that of healthy smokers. To evaluate the existence of arterial disease, lower limb perfusion pressure impairment was assessed using the ankle brachial index, whereas arterial stiffness was assessed by the pulse wave velocity (PWV). The definition of peripheral arterial disease required an ankle brachial index value of 0.90 or less, whereas the PWV increment was considered to be a direct witness of arterial stiffness increase. A 6-min walk test was performed to assess physical exercise capacity. Results Prevalence of peripheral arterial disease was higher in COPD patients than in healthy participants (81 ±3 SD; 49 ± 5 SD and 9 ± 2 SD%, respectively, in COPD, healthy smokers and nonsmokers). PWV mean values were significantly higher in COPD patients compared with healthy smokers and nonsmokers (10.3 ±2.1 SD m/s; 9.2 ±1.3 SD m/s and 8.7 ± 2.2 SD m/s, respectively). The distance covered during the 6-min-walk test was associated positively with the degree of peripheral arterial disease (r = 0.78; P = 0.05) and negatively with the PWV values (r = –0.74; P = 0.05). Not only tobacco-smoking history but also COPD severity was shown to influence these associations. Conclusion The effect of peripheral arterial disease on exercise intolerance in COPD seems to be considerable. Therefore, COPD patients participating in a pulmonary rehabilitation programme should profit from a systematic search for arterial disease. Arterial dysfunction has to be taken into account in the multidisciplinary treatment of these patients.

Postexercise cooling interventions and the effects on exercise-induced heat stress in a temperate environment

The aim of this study was to examine the effects of cool water immersion (20 °C; CWI) while wearing a cooling jacket (Cryovest;V) and a passive control (PAS) as recovery methods on physiological and thermoregulatory responses between 2 exercise bouts in temperate conditions. Nine well-trained male cyclists performed 2 successive bouts of 45 min of endurance cycling exercise in a temperate environment (20 °C) separated by 25 min of the respective recovery interventions. Capillary blood samples were obtained to measure lactate (La⁻), sodium (Na⁺), bicarbonate (HCO₃⁻) concentrations and pH, whilst body mass loss (BML), core temperature (T(core)), skin temperature (T(skin)), heart rate (HR), oxygen uptake , and minute ventilation were measured before (Pre), immediately after the first exercise bout (Ex1), the recovery (R), and after the second exercise bout (Ex2). V and CWI both resulted in a reduction of T(skin) at R (-2.1 ± 0.01 °C and -11.6 ± 0.01 °C, respectively, p < 0.01). Despite no difference in final values post-Ex2 (p > 0.05), V attenuated the rise in HR, minute ventilation, and oxygen uptake from Ex1 to Ex2, while T(core) and T(skin) were significantly lower following the second session (p < 0.05). Further, CWI was also beneficial in lowering T(core), T(skin), and BML, while a rise in Na⁺ was observed following Ex2 (p < 0.05). Overall results indicate that cooling interventions (V and CWI) following exercise in a temperate environment provide a reduction in thermal strain during ensuing exercise bouts.

Protective Effects of Fluoxetine on Decompression Sickness in Mice

Massive bubble formation after diving can lead to decompression sickness (DCS) that can result in central nervous system disorders or even death. Bubbles alter the vascular endothelium and activate blood cells and inflammatory pathways, leading to a systemic pathophysiological process that promotes ischemic damage. Fluoxetine, a well-known antidepressant, is recognized as having anti-inflammatory properties at the systemic level, as well as in the setting of cerebral ischemia. We report a beneficial clinical effect associated with fluoxetine in experimental DCS. 91 mice were subjected to a simulated dive at 90 msw for 45 min before rapid decompression. The experimental group received 50 mg/kg of fluoxetine 18 hours before hyperbaric exposure (n = 46) while controls were not treated (n = 45). Clinical assessment took place over a period of 30 min after surfacing. At the end, blood samples were collected for blood cells counts and cytokine IL-6 detection. There were significantly fewer manifestations of DCS in the fluoxetine group than in the controls (43.5% versus 75.5%, respectively; p = 0.004). Survivors showed a better and significant neurological recovery with fluoxetine. Platelets and red cells were significantly decreased after decompression in controls but not in the treated mice. Fluoxetine reduced circulating IL-6, a relevant marker of systemic inflammation in DCS. We concluded that fluoxetine decreased the incidence of DCS and improved motor recovery, by limiting inflammation processes.

Oxygen breathing or recompression during decompression from nitrox dives with a rebreather: effects on intravascular bubble burden and ramifications for decompression profiles

Preventive measures to reduce the risk of decompression sickness can involve several procedures such as oxygen breathing during in-water decompression. Theoretical predictions also suggest that brief periods of recompression during the course of decompression could be a method for controlling bubble formation. The aim of this study was to get clearer information about the effects of different experimental ascent profiles (EAPs) on bubble reduction, using pure oxygen or recompression during decompression for nitrox diving. Four EAPs were evaluated using bubble monitoring in a group of six military divers using Nitrox 40% O2 breathing with a rebreather. For EAP 1 and 2, 100% O2 was used for the end stage of decompression, with a 30% reduction of decompression time in EAP 1 and 50% in EAP 2, compared to the French navy standard schedule. For EAP 3 and 4, nitrox 40% O2 was maintained throughout the decompression stage. EAP 3 is based on an air standard decompression schedule, whereas EAP 4 involved a brief period of recompression at the end of the stop. We found that EAP 1 significantly reduced bubble formation, whereas high bubble grades occurred with other EAPs. No statistical differences were observed in bubbles scores between EAP 3 and 4. One diver developed mild neurological symptoms after EAP 3. These results tend to demonstrate that the “oxygen window” plays a key role in the reduction of bubble production and that breathing pure oxygen during decompression stops is an optimal strategy to prevent decompression sickness for nitrox diving.

Submarine Rescue Decompression Procedure from Hyperbaric Exposures up to 6 Bar of Absolute Pressure in Man: Effects on Bubble Formation and Pulmonary Function

Recent advances in submarine rescue systems have allowed a transfer under pressure of crew members being rescued from a disabled submarine. The choice of a safe decompression procedure for pressurised rescuees has been previously discussed, but no schedule has been validated when the internal submarine pressure is significantly increased i.e. exceeding 2.8 bar absolute pressure. This study tested a saturation decompression procedure from hyperbaric exposures up to 6 bar, the maximum operating pressure of the NATO submarine rescue system. The objective was to investigate the incidence of decompression sickness (DCS) and clinical and spirometric indices of pulmonary oxygen toxicity. Two groups were exposed to a Nitrogen-Oxygen atmosphere (pO2 = 0.5 bar) at either 5 bar (N = 14) or 6 bar (N = 12) for 12 h followed by 56 h 40 min resp. 60 h of decompression. When chamber pressure reached 2.5 bar, the subjects breathed oxygen intermittently, otherwise compressed air. Repeated clinical examinations, ultrasound monitoring of venous gas embolism and spirometry were performed during decompression. During exposures to 5 bar, 3 subjects had minor subjective symptoms i.e. sensation of joint discomfort, regressing spontaneously, and after surfacing 2 subjects also experienced joint discomfort disappearing without treatment. Only 3 subjects had detectable intravascular bubbles during decompression (low grades). No bubbles were detected after surfacing. About 40% of subjects felt chest tightness when inspiring deeply during the initial phase of decompression. Precordial burning sensations were reported during oxygen periods. During decompression, vital capacity decreased by about 8% and forced expiratory flow rates decreased significantly. After surfacing, changes in the peripheral airways were still noticed; Lung Diffusion for carbon monoxide was slightly reduced by 1% while vital capacity was normalized. The procedure did not result in serious symptoms of DCS or pulmonary oxygen toxicity and may be considered for use when the internal submarine pressure is significantly increased.

Immersion pulmonary oedema in a healthy diver not exposed to cold or strenuous exercise

In healthy divers, the occurrence of immersion pulmonary oedema (IPE) is commonly caused by contributory factors including strenuous exercise, cold water and negative-pressure breathing. Contrary to this established paradigm, this case reports on a 26-year-old, well-trained combat swimmer who succumbed to acute IPE during static immersion in temperate (21°C) water, while using a front-mounted counterlung rebreather. The incident occurred during repeated depth-controlled ascent practice at the French military diving school. It was discovered that the diver had attempted to stop any gas leakage into the system by over-tightening the automatic diluent valve (ADV) (25th notch of 27) during the dive, thus causing a high resistance to inspiratory flow. The ventilatory constraints imposed by this ADV setting were assessed as a 3.2 Joules·L⁻¹ inspiratory work of breathing and -5 kPa (-50 mbar) transpulmonary pressure. This report confirms the key role of negative pressure breathing in the development of interstitial pulmonary oedema. Such a breathing pattern can cause a lowering of thoracic, airway and interstitial lung pressure, leading to high capillary pressure during each inspiration. Repetition of the diving drills resulted in an accumulation of interstitial lung water extravasation, causing pathological decompensation and proven symptoms.