Haute Ecole Paul-Henri Spaak
ISEK (catégorie paramédicale - paramedics department)
PURPOSE: Previous studies have shown that bubble formation induced endothelial damage on conduit arteries. We aim to evaluate the effect of diving on microvascular and macrovascular function. METHODS: Nine divers took part in a SCUBA dive... more
PURPOSE: Previous studies have shown that bubble formation induced endothelial damage on conduit arteries. We aim to evaluate the effect of diving on microvascular and macrovascular function. METHODS: Nine divers took part in a SCUBA dive at 30 msw (400 kPa), for 30 min of bottom time. Pre- and post-dive, they underwent an assessment of endothelial-dependent (acetylcholine) and endothelial-independent (sodium
This study investigated the influence of a far infrared-ray dry sauna-induced heat exposure before a simulated dive on bubble formation, and examined the concomitant adjustments in hemodynamic parameters. There were 16 divers who were... more
This study investigated the influence of a far infrared-ray dry sauna-induced heat exposure before a simulated dive on bubble formation, and examined the concomitant adjustments in hemodynamic parameters. There were 16 divers who were compressed in a hyperbaric chamber to 400 kPa (30 msw) for 25 min and decompressed at 100 kPa x min(-1) with a 4-min stop at 130 kPa. Each diver performed two dives 5 d apart, one with and one without a predive sauna session for 30 min at 65 degrees C ending 1 h prior to the dive. Circulating venous bubbles were detected with a precordial Doppler 20, 40, and 60 min after surfacing, at rest, and after flexions. Brachial artery flow mediated dilation (FMD), blood pressure, and bodyweight measurements were taken before and after the sauna session along with blood samples for analysis of plasma volume (PV), protein concentrations, plasma osmolality, and plasma HSP70. A single session of sauna ending 1 h prior to a simulated dive significantly reduced bubble formation [-27.2% (at rest) to 35.4% (after flexions)]. The sauna session led to an extracellular dehydration, resulting in hypovolemia (-2.7% PV) and -0.6% bodyweight loss. A significant rise of FMD and a reduction in systolic blood pressure and pulse pressure were observed. Plasma HSP70 significantly increased 2 h after sauna completion. A single predive sauna session significantly decreases circulating bubbles after a chamber dive. This may reduce the risk of decompression sickness. Sweat dehydration, HSP, and the NO pathway could be involved in this protective effect.
- by Costantino Balestra and +1
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- Risk assessment, Diving, Prospective studies, Humans
The current practice of mechanical ventilation comprises the use of the least inspiratory O2 fraction associated with an arterial O2 tension of 55 to 80 mm Hg or an arterial hemoglobin O2 saturation of 88% to 95%. Early goal-directed... more
The current practice of mechanical ventilation comprises the use of the least inspiratory O2 fraction associated with an arterial O2 tension of 55 to 80 mm Hg or an arterial hemoglobin O2 saturation of 88% to 95%. Early goal-directed therapy for septic shock, however, attempts to balance O2 delivery and demand by optimizing cardiac function and hemoglobin concentration, without making use of hyperoxia. Clearly, it has been well-established for more than a century that long-term exposure to pure O2 results in pulmonary and, under hyperbaric conditions, central nervous O2 toxicity. Nevertheless, several arguments support the use of ventilation with 100% O2 as a supportive measure during the first 12 to 24 hrs of septic shock. In contrast to patients without lung disease undergoing anesthesia, ventilation with 100% O2 does not worsen intrapulmonary shunt under conditions of hyperinflammation, particularly when low tidal volume-high positive end-expiratory pressure ventilation is used. In healthy volunteers and experimental animals, exposure to hyperoxia may cause pulmonary inflammation, enhanced oxidative stress, and tissue apoptosis. This, however, requires long-term exposure or injurious tidal volumes. In contrast, within the timeframe of a perioperative administration, direct O2 toxicity only plays a negligible role. Pure O2 ventilation induces peripheral vasoconstriction and thus may counteract shock-induced hypotension and reduce vasopressor requirements. Furthermore, in experimental animals, a redistribution of cardiac output toward the kidney and the hepato-splanchnic organs was observed. Hyperoxia not only reverses the anesthesia-related impairment of the host defense but also is an antibiotic. In fact, perioperative hyperoxia significantly reduced wound infections, and this effect was directly related to the tissue O2 tension. Therefore, we advocate mechanical ventilation with 100% O2 during the first 12 to 24 hrs of septic shock. However, controlled clinical trials are mandatory to test the safety and efficacy of this approach.