ABSTRACT
Many studies have described the physiology of water immersion (WI), whereas few have focused on post WI physiology, which faces the global water loss of the large WI diuresis. Therefore, we compared hemodynamics and vasomotor tone in 10 trained supine divers before and after two 6h sessions in dry (DY) and head out WI environments. During each exposure (DY and WI) two exercise periods (each one hour 75W ergometer cycling) started after the 3rd and 5th hours. Weight losses were significant (-2.24 +/- 0.13 kg and -2.38 +/- 0.19 kg, after DY and WI, respectively), but not different between the two conditions. Plasma volume was reduced at the end of the two conditions (-9.7 +/- 1.6% and -14.7 +/- 1.6%, respectively; p < 0.05). This post-WI decrease was deeper than post DY (p < 0.05). Cardiac output (CO) and mean arterial blood pressure were maintained after the two exposures. Plasma levels of noradrenaline, antidiuretic hormone and ANP were twofold higher after WI than after DY (p < 0.05). After DY total peripheral resistances (TPR) were increased (p < 0.05) and heart rate (HR) was reduced (p < 0.05). After WI there was a trend for a decrease in stroke volume (p = 0.07) with unchanged TPR and HR, despite more sizeable increases in plasma noradrenaline and vasopressin than after DY. We hypothesized that the higher levels of plasma natriuretic peptides after WI were likely counteracting the dehydration-required vasomotor adjustments.
Subject(s)
Dehydration/physiopathology , Immersion/physiopathology , Natriuretic Peptides/blood , Adult , Analysis of Variance , Blood Pressure/physiology , Dehydration/blood , Hemodynamics/physiology , Humans , Male , Plasma Volume/physiology , Statistics, Nonparametric , Time Factors , Vasomotor System/physiologySubject(s)
Barotrauma/etiology , Diving/adverse effects , Mediastinal Emphysema/etiology , Subcutaneous Emphysema/etiology , Adult , Barotrauma/diagnosis , Emergencies , Follow-Up Studies , Humans , Male , Mediastinal Emphysema/diagnostic imaging , Radiography, Thoracic , Subcutaneous Emphysema/diagnostic imaging , Time Factors , Tomography, Spiral ComputedABSTRACT
Underwater diving is a very closely medically managed activity. Performing it, the human organism is under the physical laws of pressure and following consequences. The expiratory flows are significatively reduced, enhancing the risk of alveolar hypoventilation at exertion, the central nervous system is the privileged target during inopportune tissue degassing related accidents (leaving 20% of sequellae), barotraumatic injuries threaten middle and inner ear or lung (pulmonary barotrauma is the most severe accident), the toxicity of gas under pressure (i.e. oxygen, nitrogen) exposes to specific risks of loss of consciousness. Lastly, the adaptative mechanisms to immersion can be overflown, leading to pulmonary oedema. Facing these constraints, the practitioner's role begins just before the diver's activity starts by looking for contraindications to diving. It continues during tuition time by teaching him the physiopathology of accidents, their prevention and first cares. Finally, in case of accident, a specialized medical team acts in diagnosis and treatment. From these points of view, diving medicine is a multispecialty medical matter.
Subject(s)
Diving/physiology , Accidents , Barotrauma/physiopathology , Barotrauma/therapy , Decompression Sickness/physiopathology , Decompression Sickness/therapy , Diving/adverse effects , Humans , Hyperbaric OxygenationABSTRACT
In hyperbaric environments, when inhaled inert gas composition is abruptly modified, the sum of the arterial inert gases partial pressures is different to the sum of these same gases in the inhaled mixture. While switching from a helium-oxygen to a nitrogen-oxygen mixture of same P1O2 and total pressure, the sum of the arterial inert gas partial pressure was transiently less than the one in the inspired gases: there was an arterial under-saturation: PaHe + PaN2 = 0.68 (P1He + P1N2). During the opposite switch (from nitrogen to helium), a reversed time course, namely a transient over saturation, was observed: PaHe + PaN2 = 1.31 (P1He + P1N2). Amongst the different possible explanatory hypotheses, the most probable is that inert gas partial pressure equilibrium through the alveolo-capillary membrane is not achieved when the blood leaves the pulmonary capillary.