Symptomless post-dive bubbles have an easily detectable pathogenetic potentsal.+

[DocVikingo]

[NOTE: Some earlier discussion of this general topic can be found at --> http://forums.scubadiving.com/showth...ht=endothelial]


Respir Med. 2013 Jan 30. pii: S0954-6111(13)00007-3. doi: 10.1016/j.rmed.2013.01.002. [Epub ahead of print]

Increase of pulmonary arterial pressure in subjects with venous gas emboli after uncomplicated recreational SCUBA diving.

Marabotti C, Scalzini A, Chiesa F.

Extreme Centre, Scuola Superiore Sant'Anna, Pisa, Italy; CNR Institute of Clinical Physiology, Pisa, Italy. Electronic address: c.marabotti@alice.it.

Abstract

The presence of circulating gas bubbles has been repeatedly reported after uncomplicated SCUBA dives. The clinical and pathophysiological relevance of this phenomenon is still under debate but some experimental data suggest that silent bubbles may have a damaging potential on pulmonary endothelial cells. The aim of the present study was to evaluate the possible hemodynamic effect on pulmonary circulation of post-dive circulating gas bubbles. To this aim, 16 experienced divers were studied by Doppler-echocardiography in basal conditions and 2.0 ± 0.15 h after an uncomplicated, unrestricted recreational SCUBA dive. At the post-dive examination, circulating bubbles were present in 10/16 subjects (62.5%). Divers with circulating bubbles showed a significant post-dive increase of pulmonary systolic arterial pressure (evaluated by the maximal velocity of the physiological tricuspid regurgitation; P < 0.01)) and right ventricular internal dimension (P < 0.05). Divers without circulating bubbles showed no significant change in cardiac anatomy and pulmonary arterial pressure. Both groups showed a significant post-dive decrease of transmitral E/A ratio (index of left ventricular diastolic function: subjects with bubbles P < 0.01; subjects without bubbles P < 0.05). These results seem to indicate that circulating gas bubbles may lead to a hemodynamically relevant increase of pulmonary arterial pressure, able to induce an acute right ventricular dilation. Post-dive diastolic function changes, observed in both groups, may be explained by a preload reduction due to immersion natriuresis. The results of the present study add some evidence that post-dive circulating bubbles, although symptomless, have an easily detectable pathogenetic potential, inducing unfavorable hemodynamic changes in the lesser circulation."

[fugu]

So, evidence that peeing in your wetsuit is beneficial ?
prudent ascent rates, half-stops, safety stops - keep those bubbles tiny.

[Travis]

Doc, now will you stop chiding people for missing prior posts with the same information, even with different headings or sources? http://forums.scubadiving.com/showth...-about-fitness

I still think this study would be more helpful if the baseline fitness of the participants was factored into the results.

[DocVikingo]

Doc, now will you stop chiding people for missing prior posts with the same information, even with different headings or sources? http://forums.scubadiving.com/showth...-about-fitness.

No ; )

[aviddiver.her]

I recall a study several years ago that demonstrated vitamins C and E taken before dives maybe helpful in preventing some cardiac changes. If I recall correctly, it had something to do with pulmonary hypertension and/or cardiac output.

Does anyone have access to a link to that research/article?

[Travis]

I recall a study several years ago that demonstrated vitamins C and E taken before dives maybe helpful in preventing some cardiac changes. If I recall correctly, it had something to do with pulmonary hypertension and/or cardiac output.

Does anyone have access to a link to that research/article?

This may be the study you are thinking of. It shows predive dosing with C and E can reduce endothelial dysfunction as assessed by flow mediated dilitation, but does not have an immediate effect on acute changes in cardiac function.

J Physiol. 2007 Feb 1;578(Pt 3):859-70. Epub 2006 Nov 16.
The effects of acute oral antioxidants on diving-induced alterations in human cardiovascular function.

Obad A, Palada I, Valic Z, Ivancev V, Baković D, Wisløff U, Brubakk AO, Dujić Z.
Source

Department of Physiology, University of Split School of Medicine, Soltanska 2, 21000 Split, Croatia.

Abstract

Diving-induced acute alterations in cardiovascular function such as arterial endothelial dysfunction, increased pulmonary artery pressure (PAP) and reduced heart function have been recently reported. We tested the effects of acute antioxidants on arterial endothelial function, PAP and heart function before and after a field dive. Vitamins C (2 g) and E (400 IU) were given to subjects 2 h before a second dive (protocol 1) and in a placebo-controlled crossover study design (protocol 2). Seven experienced divers performed open sea dives to 30 msw with standard decompression in a non-randomized protocol, and six of them participated in a randomized trial. Before and after the dives ventricular volumes and function and pulmonary and brachial artery function were assessed by ultrasound. The control dive resulted in a significant reduction in flow-mediated dilatation (FMD) and heart function with increased mean PAP. Twenty-four hours after the control dive FMD was still reduced 37% below baseline (8.1 versus 5.1%, P = 0.005), while right ventricle ejection fraction (RV-EF), left ventricle EF and endocardial fractional shortening were reduced much less (approximately 2-3%). At the same time RV end-systolic volume was increased by 9% and mean PAP by 5%. Acute antioxidants significantly attenuated only the reduction in FMD post-dive (P < 0.001), while changes in pulmonary artery and heart function were unaffected by antioxidant ingestion. These findings were confirmed by repeating the experiments in a randomized study design. FMD returned to baseline values 72 h after the dive with pre-dive placebo, whereas for most cardiovascular parameters this occurred earlier (24-48 h). Right ventricular dysfunction and increased PAP lasted longer. Acute antioxidants attenuated arterial endothelial dysfunction after diving, while reduction in heart and pulmonary artery function were unchanged. Cardiovascular changes after diving are not fully reversed up to 3 days after a dive, suggesting longer lasting negative effects.

[aviddiver.her]

Thanks Travis, that looks like it.

[Lepomis]

I wonder if this is perhaps a factor in the dive-related afib that some of us get? The apparent increased pressure/stress on the pulmonary side might extend into the pulmonary veins and left atrium, but (I don't think) that was addressed in this study.

The pulmonary veins at their entrance to the left atrium, primarily, plus occasionally additionally in the left atrium itself, are the usual sites for the extra impulses that lead to afib.

DSAO -- with attention to the "side-effects" (pun intended)
Jim

[Travis]

I wonder if this is perhaps a factor in the dive-related afib that some of us get? The apparent increased pressure/stress on the pulmonary side might extend into the pulmonary veins and left atrium, but (I don't think) that was addressed in this study.

The pulmonary veins at their entrance to the left atrium, primarily, plus occasionally additionally in the left atrium itself, are the usual sites for the extra impulses that lead to afib.
DSAO -- with attention to the "side-effects" (pun intended)
Jim

I've wondered about that since there is definitely mechanical stretching of the heart chambers and great vessels from the increased fluid load. Seems possible that it might contribute to greater excitability of the pulmonary vein tissues. But I've also become interested in the notion of "vagally-mediated" AF which according to some researchers tends to follow a significant instance of increased vagal innervation. There appears to be a range of time to onset, but I've noticed mine now tend to happend quite soon after ascending from a dive. But even the nighttime onset is consistent with increased vagal tone. I became more interested in this idea after I experienced a very rare non-dive related episode following a sustained period of nausea which is a vagal response. Maybe the combination of mechanical stimulation and increased vagal tone from diving conspires to flip those of us prone to this annoying feature. FWIW, check out "heat shock protein" and "atrial fibrillation" at Medline. Since HSP's are generated by exercise as well as heat stress, I'm wondering if the fact that my conditioning falls off during prolonged dive trips may make me more susceptible to the triggers for AF? In any case, I notice that ectopic beats increase whenever my exercise program falters for a week or so and then drop off dramatically when I return to training.