Venous Gas Emboli and Trimix diving

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muddiver

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The following summary was copied from the American Academy of Underwater Sciences new letter:

Ljubkovic M, Marinovic J, Obad A, Breskovic T,
Gaustad SE, Dujic Z. High incidence of venous and
arterial gas emboli at rest after trimix diving without
protocol violations. J Appl Physiol. 2010 Sep 2. [Epub
ahead of print].

Scuba diving is associated with generation of gas emboli
due to gas release from the supersaturated tissues during
decompression. Gas emboli arise mostly on the venous
side of circulation and they are usually eliminated as they
2010, volume 4, issue 10, page 5
pass through the lung vessels. Arterialization of venous
gas emboli (VGE) is seldom reported and it is potentially
related to neurological damage and development of
decompression sickness. The goal of the current study
was to evaluate the generation of VGE in a group of
divers using a mixture of compressed oxygen, helium and
nitrogen (trimix) and to probe for their potential
appearance in arterial circulation. Seven experienced male
divers performed three dives in consecutive days
according to trimix diving and decompression protocols
generated by V-planner, a software program based on the
Varying Permeability Model. The occurrence of VGE was
monitored ultrasonographically for up to 90 minutes after
surfacing and the images were graded on a scale from 0 to
5. The performed diving activities resulted in a substantial
amount of VGE detected in the right cardiac chambers
and their frequent passage to the arterial side: in 9 out of
21 total dives (42%) and in 5 out of 7 divers (71%).
Concomitant measurement of mean pulmonary artery
pressure revealed a nearly twofold augmentation, from
13.6±2.8, 19.2±9.2 and 14.7±3.3 mm Hg assessed before
the first, second and the third dive, respectively, to
26.1±5.4, 27.5±7.3 and 27.4±5.9 mm Hg detected after
surfacing. No acute decompression-related disorders were
identified. The observed high gas bubble loads and
repeated microemboli in systemic circulation raise
questions about the possibility of long-term adverse
effects and warrant further investigation.

Some food for thought.
 
Thanks, I'd like to read the entire article when it comes out. Certainly interesting stuff!
 
What he said. Will it be made generally available?
 
The published dives are ~64m (210ft) dives on ~17/46 for 15mins (plus minus a few meters and a few % helium depending on which of the 3 consecutive test days you're looking at, 3-4 mins of this Btime is descent). They used Yount's original published VPM-B model (which I don't have and can't replicate). But the profiles shown are close to or a bit more aggressive than V-planner running VPM-B at nominal conservatism. There is more time on deep stops in the 40-20m range than VPM planner wants and quite a bit less time at the shallower end like 6m. There's no O2 just EAN50 deco. Based on the pretty aggressive profiles, I'm surprised the test divers weren't more symptomatic.
 
Well VPM-B controls ascents by keeping gas volume below a critical value so finding bubbles is expected. So I am struggling with what was new here. Is it that some bubbles end up on the arterial side.
 
Well VPM-B controls ascents by keeping gas volume below a critical value so finding bubbles is expected. So I am struggling with what was new here. Is it that some bubbles end up on the arterial side.

They may be small, but there are ALOT of them. More than can be filtered by the lungs at 1ATA. They are apparently passing to the arterial side via pulmonary shunts and the concern is that they are lodging in brain tissues and creating ischemic areas. That said, the profiles were way more aggressive than I've ever done so these aren't unexpected findings IMHO.
 
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