In our study, ultrasonographic investigations were performed 1 h after diving; consequently, the probability of an hyperoxia-induced cardiac relaxation impairment was low. Physiologically, the RV and LV are two distinct chambers that are anatomically and functionally bound: both share the interventricular septum and both are enclosed in the pericardium. As a consequence, alterations in RV size and function influence LV filling. In the present study, RV diameters were unchanged after the dive and no LV septal shift was observed. Consequently, the decrease of the cardiac preload demonstrated by cardiac diameters and SV decrease seemed to be the principal factor of the LV filling modification.
IVRT measurement confirms our hypothesis. The decreased LV preload, as seen previously, by reducing the pressure gradient from the LA to the LV may explain the increase in IVRT observed after diving (Table 4). An increase in maximal velocity of tricuspid regurgitation flow, suggesting an increase in the RV/RA gradient, was also observed.
A decrease in LV preload was demonstrated by LV study. Consequently, a decrease in RA pressure was very likely; however, an increase in pulmonary arterial pressure could be induced by pulmonary gas embolism. These two factors could explain an increase in RV/RA gradient.
RV diameters were unchanged after the dive. The association of an elevation in RV afterload and a reduction in RV preload may explain the lack of modification in RVEDD in our work.
In individuals with patent foramen ovale, circulating bubbles might cross over from the right side of the heart to the left side. An increase in right-sided cardiac pressures during decompression could promote the right-to-left shunt. Unfortunately, as we did not measure RA pressure, we could not estimate right cardiac pressures. Previous studies> have proved that the measurement of the inferior vena cava diameters provide a noninvasive estimation of the RA pressure. This method could be used in further studies to assess right-sided cardiac pressures during the decompression after a scuba dive.
Numerous hemodynamic changes were observed 1 h after an open-sea scuba dive. LA and LV diameters significantly decreased after the dive. CO remained unchanged but was the result of two opposite modifications: an increase in HR and a decrease in SV. Transmitral profile was modified with an increase of the contribution of the atrial contraction to LV filling. Right cavities diameters were unchanged, but an increase of the RV/RA pressure gradient was found.
Two factors can explain these results: low volemia secondary to immersion, and venous gas embolism induced by nitrogen desaturation. Lowering of plasma volume takes part in microcirculatory perfusion alterations observed during experimental decompression sickness. For recreational divers, hemoconcentration and reduction in plasma volume could interact with biological changes due to circulating bubbles and induce decompression sickness. Consequently, the restoration of the water balance of the body is an important part of the recovery process after diving. Oral hydration should be particularly important in case of repeated dives or during periods of daily diving. Further studies are needed to develop appropriate fluid-replacement strategies according to the diving procedure.