bubbles in the arteries

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beche de mer once bubbled...
I haven't had much personal experience of this type of situation, but could a PFO result in the catastropic type of event described by Nan?

(Note to self: keep away from medical thread after second glass of wine.)
Hi again BdM,

For the non medical readers, could I reply to Dr Vikingo's question to start? Most shunts in the circulation are from the high pressure arterial side to the lower pressure venous side. In the case of a patent ductus arteriosus, very simply, the anatomical defect allows the passage of high pressure blood from the origins of the aorta to pass into the origins of the much-lower pressure pulmonary artery. This left to right shunt is seldom, if ever, reversed because the pressure differential is so great.

Whether a PFO is a specific anatomical entity and whether this is strictly an "atrial septal defect", it is most certainly a defect in the septal wall separating the two atria. These are both low pressure collecting chambers for the heart and the pressure differential between them is not great. I am sure someone could quote the figures.

To my mind the important thing for DCI is that, under certain circumstances, the shunting of blood across this defect in the inter-atrial wall can be reversed from the normal left-to-right situation. The circumstances require a transient increase in intrathoracic pressure followed by the release of this pressure which allows a slug of blood to "rebound" from the great veins into the right atrium, with an associated rise in its internal pressure, which may momentarily exceed the pressure within the left atrium (previously relatively starved of blood), thus causing a reversal of the shunt.

If the blood within the great veins contains bubbles, a slug of supersaturated blood containing these bubbles may cross into the left atrium, mix with arterial blood and thence reach the vital organs. The question is whether these bubbles are stable enough to remain intact when they find themselves in the arteries (where there is no supersaturation).

This is pure conjecture, but I imagine these bubbles only need to remain in existence for a matter of seconds before they reach the periphery, where they once more find themselves in a supersaturated environment to staibilse and grow.

As for Nan's question, I believe this could have been caused by a PFO. Having said that, an arterial gas embolism is commonly seen after pulmonary barotrauma. Again put simply, the gas trapped in the bulla (or pleural space), like all gas, will seek out the route of least resistance, which is often the pulmonary venous system.

(Thanks Dr Vikingo for not highlighting my earlier faux pas!):)
 
... the "non medical readers."

Even more simply, only a tiny fraction of persons with patent ductus arteriosus (PDA) reach adulthood without any signs or symptoms of the abnormality. More importantly, given that it is essentially an extra-cardiac shunting of blood from the aorta to the lungs under high pressure it is difficult to descry any ready mechanism for the movement of gas bubbles from venous to arterial circulation.

On the other hand, one quarter of all adults have a patent foramen ovale (PFO) that is asymptomatic. And, being an
intra-cardiac abnormality with the potential for right-to-left shunting under pressure changes occasioned by equalization techniques such as the Valsalva maneuver, it presents a very plausible mechanism for the arterialization of decompression-related gas bubbles.

Best regards.

DocVikingo
 
The Iceni once bubbled...


... whether this is strictly an "atrial septal defect", it is most certainly a defect in the septal wall separating the two atria. These are both low pressure collecting chambers for the heart and the pressure differential between them is not great. I am sure someone could quote the figures.


I looked up these figures when I was grappling with the concept last week.

Mean right atrial pressure is 6 mm Hg.
Mean left atrial pressure is 12 mm Hg.

So the pressure differential is only 6 mm Hg. It wouldn't take much to reverse flow.
 
Nan once bubbled...
I should think a tear would not necessarily introduce enough air into the bloodstream, since you'd have to pressurize bubbles into little teeny capillaries that were oozing blood back-at-ya at the same time.

I've been trying to visualise what would happen at parenchymal level in the event of a tear. A bubble would be delivered into the injured tissues and during ascent it would tend to enlarge. It would seek the area of lowest pressure, and that would be the venous side of the pulmonary circulation. I envisage it getting drawn in to the capillaries and thence into the pulmonary veins.
 
tends to be a pretty catastrophic injury.

Not only does gas find its way into the pulmonary veins it also tends to find its way into the mediastinum where an increase in pressure will compress the heart. (an external sign being surgical emphysema in the head and neck.)

In addition, of course, the presence of high pressure gas within the chest itself could be more than enough to stop all venous return to the heart.

Moral of the story: -

Do not hold your breath during any ascent.:eek:
 
No, it doesn't take much to induce a reversal of the normal interatrial pressure gradient--a sneeze or a good cough can do it.

To expand on Paul's last remarks, gas finding its way into the pleural sac can result in pneumothorax of varying degrees of severity. Partial collapse of a lung often does not result in significant compression of the heart/associated vasculature, and may present with shortness of breath, limited chest movement, chest pain & a dry cough.

With tension pneumothorax such as Paul is describing, signs can include subcutaneous surgical emphysema, decreased breath sounds on the side of the collapse, a weak pulse, enlarged neck veins & displacement of the trachea to one side. Complaints may include extreme anxiety.

Best regards.

DocVikingo
 

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