Bubbles and hypovolemia, article

[pescador775]

June 2, 2006 — An echocardiographic study done on healthy volunteers in actual scuba diving conditions found an important bubble grade in all, according to a report in the May issue of Chest. The hemodynamic changes suggested that hypovolemia is an important factor and that restoration of fluid balance should be considered after all dives.

"During a scuba dive, subjects undergo environmental constraints such as immersion, exposure to cold, and increased ambient pressure," write Alain Boussuges, MD, PhD, from the Institut de Médecine Navale du Service de Santé des Armées in Marseille, France, and colleagues. "Intravascular gas bubbles are carried from the venous circulation to the pulmonary vessel, where they are eliminated through the lungs. The formation of bubbles is recognized as the basis for decompression illness, but such bubbles are also commonly detected in venous circulation of asymptomatic divers."

In this study, 10 healthy scuba divers dove to a mean depth of 34.3 ± 2.7 m of sea water (113 ± 9 feet). Mean duration of the dive was 25.3 ± 3.5 minutes.

One hour after the dive, microbubbles were detected in the right-heart chambers of all subjects, and left atrial and left ventricular diameters were significantly decreased. Cardiac output measured by aortic blood flow remained unchanged, but heart rate increased and stroke volume decreased after the dive. Left ventricular filling, which was assessed on transmitral profile, was partially increased by atrial contraction. Right cavity diameters were unchanged, but there was an increase of the right ventricular/right atrial gradient pressure.

"The diving profile studied promotes a rather important bubble grade in all volunteers," the authors write. "Two factors can explain these results: low volemia secondary to immersion, and venous gas embolism induced by nitrogen desaturation. Consequently, restoration of the water balance of the body should be considered in the recovery process after diving."

Chest. 2006;129:1337-1343

 

[Dr Deco]

Hello readers:

Dive Study

This is one of those studies when something can be found if you look hard enough. What surprises me is that a study reported a few years ago (see references below) with very high Doppler bubble grades did not find a change in pulmonary artery pressure. This is not at all the same as the study described by pescador 75, but it is somewhat surprising that one group found a large change in a cardiac parameter and the other found no change. This is especially true when the bubbles were much more plentiful in the “no-change” study.

Hydration

I do believe that hydration is important and would really like to see a study where water intake was measured in divers. A set of dives could be made where there was high intake and a set with low intake. This would best be a cross-over study with the same test subjects. Doppler bubble detection would be needed.

We would find if there was indeed a difference in bubble formation as a function of hydration.

Dr Deco :doctor:



References :book3:

Diesel DA, Ryles MT, Pilmanis AA, Balldin UI. Non-invasive measurement of pulmonary artery pressure in humans with simulated altitude-induced venous gas emboli. Aviat Space Environ Med. 2002 Feb;73(2):128-33.

BACKGROUND: Decompression to simulated altitude causes super-saturation of
Nitrogen dissolved in body tissues and can result in venous gas emboli (VGE),
which are usually "cleared" in the lung. Large intravenous boli of air administered to animals increase pulmonary artery pressure (PAP), and may induce cross-over of gas to the left side of the heart (creating dangerous arterial gas emboli). This study was conducted to determine whether high VGE grades induced at simulated altitude elevate PAP in humans. METHODS: Eight human subjects with subclinical tricuspid regurgitation were exposed to simulated altitude of > or = 24,000 ft for up to 4 h. Systolic PAP was derived from Doppler ultrasound echo imaging measurements of peak flow velocity of the regurgitant jet. VGE was rated using the Spencer scale. A technique of "bubble titration" was employed with changes in exercise and altitude to maintain sufficient bubbles without decompression sickness. RESULTS: All subjects developed grade III-IV VGE, but three developed decompression sickness, resulting in earlier termination. Pre-exposure systolic PAP averaged 24.4 mm Hg. After 1, 2, 3 and 4 h, systolic PAP was 23.7 (n = 8), 23.4 (n = 8), 23.3 (n = 6), and 25.9 (n = 5) mm Hg, respectively. Systolic PAP remained unchanged, in spite of bubble grades III-IV for up to 4 h. CONCLUSION: As systolic PAP did not increase with hypobaric exposures that created substantial VGE, the bubble loading was not sufficient to overwhelm the lung clearing capacity. The risk of high PAP resulting in VGE cross-over is low during typical operational altitude exposures.