Water immersion promotes a redistribution of blood volume with a relative increase in central blood volume. The relative hypervolemia lead to the release of atrial natriuretic peptide and the lowering of noradrenaline, arginine vasopressin, aldosterone, and plasma rennin activity. The changes in neuroendocrine activities produce a marked diuresis. Body fluid loss is increased by exercise (swimming) during scuba diving. Consequently, dehydration is frequently observed after cessation of immersion.
Furthermore, experimental studies have demonstrated that during the decompression, circulating bubbles activate leukocytes and platelets, adversely affect blood rheology, and induce an activation of the complement system and a release of kinines. Endothelial transformations seem to be due to the mechanical effects of the circulating bubbles as well as the activation of leukocytes.
An increased hematocrit and a loss of plasma volume have been observed in both animals and male victims of decompression sickness.- Furthermore, venous gas emboli may damage the pulmonary vascular endothelium, causing permeability pulmonary edema in man. Consequently, the extravasation of plasma through injured endothelium might play a part in the hemoconcentration observed after the dive.
In our population, a significantly increase in HR was found after diving. Reduction in cardiac preload and pulmonary gas emboli could be responsible for the tachycardia. The decrease in SV was offset by the increase in HR such that CO remained unchanged.
LV filling profile was also modified after diving. A decrease in E/A ratio with a decrease in early transmitral velocity were observed. This filling pattern demonstrated a contribution of the atrial contraction to LV filling that became more important after diving. This LV filling profile modification has been previously observed by Marabotti et al. Several factors as variations of cardiac loading, ventricular interdependence, or LV relaxation alteration may be responsible for this modification. During the dive, subjects undergo respiratory constraints such as increased ambient pressure and ventilation through the scuba gear. An increase in Po2 can induce an impairment in cardiac relaxation. However, the duration of the myocardial effect after the end of hyperoxia exposure and inhalation of room air is unknown. The time course of vascular changes during systemic hyperoxic stress has been well studied on retinal vasculature. The latency for recovery from vasoconstriction was approximately 5 min after a normobaric hyperoxic exposure and 10 min after an hyperbaric oxygen expo-sure.