Post-Dive Exercise Could Increase Risk Of Arterial Gas Embolism

[cdavis]

Check out the new study, listed on the front page. Its done on scuba divers, but probably has implications for freedivers. Something I never heard of, IPAVA, allows blood to shunt around the alveoli, possibly in response to high blood pressure. That seems highly likely to impact feedivers in things like BO and FRC diving. . Please, would some of you medical types look at this and give us a review.

Connor

 

[MarcinB]

I have read the above paper as well as several related ones. It seems that the bigest concern for freedivers is that intrapulmonary arteriovenous anastamoses (IPAVA) open in response to hypoxia. Since during deep diving hypoxia is most likely to occur at the final stage of ascent, the time when most nitrogen bubbles form, opening of IPAVA can contribute to DCS. It was found that IPAVA are present in ~90% of healthy people.

Theoretically opening of IPAVA can also increase the risk of BO during breath hold because they cause blood to bypass alveolar capillaries which results in decreased oxygen content in arterial blood. One study found that opening of IPAVA increased the alveolar-arterial pO2 difference by 4.5 mmHg, and that the admixture of venous blood to the arterial one increased from 2.8 to 3.8%. So it seems that only a minor portion of cardiac output can pass through IPAVA, therefore, it is unlikely that their opening can cause a sudden large drop in SaO2.

 

[cdavis]

Thanks MarcinB, I needed some help on this one. So the 2.8 percent figure represents a non breathhold or non exercise position?

"admixture of venous blood to the arterial one increased from 2.8 to 3.8%." Was this an average? Since the degree of IPAVA seems to vary quite a bit among people and since BO is often a very near thing, small differences might be important. Could this explain some of what looks like different susceptibility to BO?

 

[MarcinB]

These values are averages from three subjects. 2.8% represents basal normal conditions (resting and breathing subjects) 3.8% represents situation after IPAVA opening induced by epinephrine infusion. In most other studies I read the increase in the shunt after IPAVA opening was considered to be small as well. However, it's hard to tell to what extent this phenomenon increases one's susceptibility to BO because no studies were done during breath hold. Nevertheless, it definitely doesn't help.

Edit: http://jap.physiology.org/content/jap/109/4/1072.full.pdf
This is an interesting study, that was done on subjects breathing hypoxic gas mixtures. In general intrapulmonary shunt scores increased with the degree of hypoxia. Interestingly, there were large differences between individuals in the degree of the response. Moreover, arterial SpO2 variability among subjects increased with the degree of heterogeneity in shunt scores as hypoxia progressed. However, it's hard to tell to what extent it was related to differences in IPAVA opening since pulseoximeters are much less accurate at low SpO2 values.

In another study http://jap.physiology.org/content/jap/116/10/1324.full.pdf older subjects that had lower intrapulmonary shunt scores than the younger ones were characterized by higher arterial SpO2 (by 4%) while breathing hypoxic gas mixture. However, due to limitations of the above studies it's too soon to draw a conclusion that IPAVA opening directly contributes to a drop in SpO2. Nevertheless, it's an interest topic for further research and it cannot be excluded that IPAVA to some extent determine one's susceptibility to BO and/or lung squeeze.

 

[cdavis]

I've noticed that some people are much more suseptable to BO than others, always figured it was differences in co2 tolerance, maybe thats not the whole story. Sure looks like this could be part of the reason. Given the small sample sizes and observed variability, its pretty reasonable to suspect much larger variability in the general diver population.

Thanks for the research, fascinating stuff.