Faulty PADI Question

[The Iceni]

Hi madmole!

Talk about not seeing the wood for the trees! I had always wondered why on earth divers talked about the Valsalva manoeuvre since I though it very unlikely to be something divers did voluntarily.

You are, of course, quite right in that the act of clearing the ears or lifting a heavy object constitutes a valsalva manoeuvre.

On occassion I have had to clear my ears on the way down, but never on the way up and I suspect this is pretty universal. It leads one to speculate as to whether micronuclei generated by a leaky valve or a shunt and moved into the arterial tree on clearing the ears during the descent are implicated in in-table DCI hits.

Seems unlikely to me.

On the other hand, I have been asked about the practicalities of a screening programme for PFO.

In my opinion, whatever method of detection is used it requires a skilled cardiologist who will charge the order of £600 ($1,000) for the procedure which is not guaranteed to detect all significant shunts.

I therefore suspect the vast majority of trainee divers would find the costs prohibitive.

 

[Dr Deco]

Dear Madmole and Readers:

This aspect of arterialization of gas bubbles is a fascinating area in barophysiology. Others have checked this also. ( Germonpré P, P Dendale, P Unger, and C Balestra (1998). Patent foramen ovale and decompression sickness in sports divers. J. Appl. Physiol., 84 (5), 1622 - 1626. )

There is no question that pressure changes in the thorax can influence arterialization through a patent foramen ovale (PFO). This does not need to be a Valsalva maneuver. Other similar staining maneuvers (coughing, sneezing, etc.) can also effect an atrial pressure reversal. (Balestra C; Germonpré P; Marroni A (1998). Intrathoracic pressure changes after Valsalva strain and other maneuvers: implications for divers with patent foramen ovale. Undersea Hyperb Med; 25(3): 171-4).

Others have also found this with respect to straining and (paradoxical) stroke. Klotzsch, Sliwka, et al. (1996) (An increased frequency of patent foramen ovale in patients with transient global amnesia. Analysis of 53 consecutive patients. Arch Neurol 53(6): 504-8) studied patients with global amnesia (TGA) in whom Valsalva-like activities immediately preceded the onset of TGA as well as the frequency of PFO as the prerequisite for paradoxical embolism. Using contrast TCD sonography, they observed a PFO in 55% of the patients with TGA, and 47% of these reported a precipitating activity (e.g., lifting heavy furniture, digging out roots of a tree, strenuous defecation, filling a concrete mixer, and pumping bicycle tires) immediately before the TGA occurred.

This is a topic I have followed closely since it would be a big problem for astronauts during extravehicular activity (space walks). We looked at this during one of our NASA studies and found the results to be variable. (Powell, M. R., K. V. Kumar, W. Norfleet, and J. Waligora, B. Butler (1995). Patent foramen ovale and hypobaric decompression. Aviat Space Environ Med. 66(3): 273-5) It was not clear that a PFO per se (and bubbles, of course) was all that was necessary for arterializations.

The techniques that we employed was both echocardiography as well as transcranial Doppler (TCD) ultrasound. (Albert A, Muller HR, Hetzel A (1997). Optimized transcranial Doppler technique for the diagnosis of cardiac right-to-left shunts. J Neuroimaging; 7(3): 159-63). This later techniques is what I would recommend as it gives evidence of hemodynamically significant lesions.

Dr Deco :doctor:

 

[WreckWriter]

To my thinking you legitimately missed both questions.

Tom

 

[Dr Deco]

Dear WreckWriter:

Missed - - - Sometimes happens. What did you have in mind?

Dr Deco

 

[canuckton]

But you anwered mine...thanks.

Here in Canada, I was told by one doctor that he could do a test for PFO, and his method was to inject Argon gas and then use Doppler Sonar Imaging to detect bubbles. He admitted that the tests were inconclusive, and suggested that the test might be done with the client on a treadmill.

I had my doubts and did not undergo the test.

What do you think of this? Pretty fly by night? It was in 1993.

 

[madmole]

Dr Peter Wilmshurst in the UK has been doing a lot of PFO testing on UK divers who have been bent. So far he has found around 80% of in table bends cases had a PFO. Thats some correlation!!!. This research has been runnimng since the mid 80's and is well known in Europe (PFO's are part of normal BSAC training)

Also about 25% of the poulation have a PFO, and that includes folks on this forum

The test is done by injecting a little O2 gas in aquious solution into the venal blood flow near the heart, while the victim perfoms a forceval valsalva movement and the buddles are doppler monitored in the arterial side. Its almost proceedure now in the UK for all in table bends victims to be sent for PFO testing.

I can speak from experiance the test is uncomfortable and does carry a small risk. (I was part of a group of normal divers tested to see if we followed the 25% rule). I tested negative fortunately, but some of my senior instructors with over 1000 dives tested positive

Forcefull ear clearing on the descent may be a factor, (Especially on repeat dives, when microbubble nuclei are around) but more likely its being bounced or armstrains during the hang time, straining while climbing up the boat ladder with twin sets and stages, coughing, or sneezing that is the insult. In other words all the stuff you should normally avoid anyway

In a perfect world there would be an easy and quick non invasive test for PFO and 2 sets of tables, one for those without (like the current tables) and a more conservative set for those with, to manage the microbubbles so they would be smal;l and not cause problems if they did shunt

An area where lots more reseach is needed

 

[The Iceni]

Hi madmole,

I can understand the attractiveness of a screening programme for PFO but feel this may be quite impractical with our current state of knowledge and resources-to-treat.

For a screening programme to be effective the statisticians will tell you that the test must be specific and sensitive. It must also be cheap and readily available. In addition, to my mind, one needs an effective treatment for all those positives.

The various tests currently available appear to be specific but are they sufficiently sensitive? You say you tested negative. Does this mean you do not have a PFO or do you think this could possibly represent a false negative? - The incidence of PFO at post mortem is higher than those found by doppler.

A special set of tables for those testing positive? What do you think the threshold size will be?

As you say our knowledge base is sadly lacking.

 

[madmole]

As you qute rightly say, even though I tested negative doesn't meant I dont have one. We do need a better test, Post Mortem testing is not a very approproate one (actually I would assume a 100% PFO detection rate post mortem. After all you've just cut the heart UP!!!!!)

The more we learn, the more we realise what we dont know. The trouble is what we dont know might hurt us in this case

Roll on the real time blood and tissue microbubble analyser, that just straps on

 

[Dr Deco]

Dear Readers:

To have problems with DCS and a PFO, it is necessary that two conditions be present. You must have

• a hemodynamically significant PFO,
• a certain number of gas bubbles in the venous return,
• passage of bubbles from right to left in the heart circulation.

All of these conditions must be met, and, fortunately, it appears that they seldom are.

Not all PFOs are “hemodynamically significant.” Work has been done on this in Europe in connection with “paradoxical stroke.” This is sometimes referred to as vein-to-artery stroke. Almost nothing has been done in the United States and most researchers and physicians do not have any real idea of the meaning of the term “PFO shunt volume.” Utilization of concepts such as “increase of rebound flow during recumbency” are virtually nonexistent in the USA in my circle of barophysiologists (ugh!). Some certainly do know these concepts in conjunction with PFOs when it is explained to them.

Until we have a better appreciation of these conditions and the PFO, we will continue to have a poor understanding of what should be done. Please check my reply in the thread on 6-27-2002.

Dr Deco :doctor:

 

[The Iceni]

Originally posted by Dr Deco on 27th June
Others have also found this with respect to straining and (paradoxical) stroke. Klotzsch, Sliwka, et al. (1996) (An increased frequency of patent foramen ovale in patients with transient global amnesia. Analysis of 53 consecutive patients. Arch Neurol 53(6): 504-8) studied patients with global amnesia (TGA) in whom Valsalva-like activities immediately preceded the onset of TGA as well as the frequency of PFO as the prerequisite for paradoxical embolism.

An explanation for non-medical reader;

The above research suggests a powerful relationship between right-to-left shunts and the prevalence of stroke in the non-diving community where few, if any, bubbles are found in the veins. So what is there to emobolise?

The answer is small blood clots, which are thought to break away from the walls of the larger veins and atrial walls. There is an stiking parallel between the clinical features of arterial gas emboli and a thromboembolism causing such strokes. It would seem that few blood clots (thrombi) develop in the ateries but they are commonly seen in the veins, the type in the news at present, caused by "ecomomy class syndrome", is deep vein thromboses, which can break off and embolise to the lungs. These clots can be extremely large sufficent to cause severe, even fatal, damage to the lungs - a pulmonary embolus.

However it is quite possible that the veins of adults normally contain a large number of very small thrombi that are mopped up by the lungs, as are the small bubbles generated during a diver's ascent.

With a significant PFO these minute clots can arterialise and find their way to the brain causing such mini stokes or "transient ischaemic attacks". One form of which is transient global amnesia another is an intense form of migraine with aura. I suppose a haemodynmically significant shunt could also lead to coronary embolism and be one cause of a heart attack.

As an aside, this why aspirin is recommended almost as a panacea against heart attack and stroke since it reduces the formation of venous thromboemboli. I suppose this is of particular of significance in the 30% of the population with a PFO.

Unfortunatley, I do not believe there is any evidence to show that aspirin reduces the incidence of DCI!