Patent Foramen Ovale (PFO)

More info on PFO

I have seen a little article and heard some information regarding with "Foramen ovale".
I personally have a little hole between both heart chambers which was detected a few years ago during a heart check-up. I am a keen diver, however, at present only dive during 1 or 2 dive holidays anually. I am a 34 year old female, non-smoker, good health and fitness level.
I wonder if you can inform me about any issues regarding diving with this condition or refer me to any publications on that subject.

I hope you will find the following information useful. Should you wish any further detail, do not hesitate to contact me or
Dr. Germonpre again.

Patent foramen ovale is not a true cardiac malformation, but the persistence of a fetal heart characteristic.

The foramen ovale is an oval shaped aperture, covered by a membranous tissue flap which rests on the left border of the foramen. The foramen ovale permits the passage of blood from the right atrium to the left atrium and the general arterial circulation, while inverse flow is prevented by the flap valve.

After birth, this membranous flap valve becomes adherent to the atrial septal wall and the passage of blood from the right atrium to the left one is prevented permanently.
In about 30% of the normal and healthy population, however, this bonding does not occur and the foramen ovale is kept closed by the pressure difference between the right and left atria which pushes the flap valve against the borders of the foramen. In particular situations, for example underwater (during a forced compensation manoeuvre, cough, vomiting or when wearing excessively tight divesuits and belts), the intrathoracic pressure may increase causing the opening of the foramen ovale. In the presence of a patent foramen ovale, the nitrogen bubbles, often present in venous blood after even modest dives, may pass directly into the arterial circulation and cause injuries typical of decompression illness and arterial gas embolism, without a dive profile justifying their appearance.

DAN Research
For a number of years DAN researchers have been focusing their attention on the number of incidents not justified by clear ascent or decompression errors, the so called "undeserved diving accidents".
It is possible that these incidents are favored by the presence of a patent foramen ovale. In order to investigate the true extent of the problem, DAN Europe, in collaboration with the University of Brussels, has launched and financed a study which includes the participation of volunteer divers.

The DAN Europe research group has, during the past year, conducted a standardised study on the incidence of foramen ovale in decompression accidents.
The aim of the study is to see if such a form of atrial septal structure may, in any way, imply an increased risk during recreational diving.
Actually, our research work compares two groups of divers of similar age, height, weight, body mass index, number of annual dives, habits etc.
One of the two groups consists of divers who have had at least one diving accident.
If we compare the data obtained from the two groups each of 37 divers, we obtain a 62% incidence of patent foramen ovale in the group of divers who had accidents (43.5% in the control group).
From the investigations carried out it results that patent foramen ovale is present in 88% of the divers with cerebral damage and 40% in those divers with peripheral neurological symptoms.
Our results show, therefore, a significantly higher incidence of patent foramen ovale in decompressin illness involving the brain.
Does this mean that it is necessary to investigate for the presence of cardiac malformations before certifying diving fitness?
Not necessarily, in fact, if we examine the patency of the foramen ovale at rest, we find that in 35% of our diving population who has suffered from a cerebral accident and 10% who has suffered from peripheral symptoms we have
to consider the type of patency and the morphology of the foramen ovale before we are able to discuss the risk during diving.
Accoring to present knowledge it is illogical to prohibit diving to divers having a patent foramen ovale because we do not know which type of foramen ovale is responsible for immobilization of arteries.
However, up to now we can state that any error or excessively fast ascent speed could, in these cases, involve a grater risk.
The results we will obtain with our continuing studies will be published in the following numbers of "DAN Europe News".
As the situation becomes particularly dangerous only in the presence of conspicuous bubbles it is reasonable to limit the immersions to depths and dive times which are associated with an absent or minimal production of bubbles during ascent and to avoid straining post dive.

My cardiologist diagnosted me of having a patent foramen ovale (PFO) .
He is not a diving medecine expert and is unable to advice me precisely on what I should do about my scuba diving !! Recent papers were quite alarming (Lancet March 1997)
Please could you send me some information on PFO and if I should stop diving or not ?
Are there any international recommandations ?

I don't know what theoretical knowledge you have on PFO, but is not to be considered as a disease. Therefore you can not have been "diagnosed with PFO", it can only have been "detected" during an echocardiography, maybe for other reasons (unless you specifically wanted the cardiologist to do an echocardiography for detecting PFO). Approx. 30% of all people - also divers- have PFO. The only issue we have to deal with is whether PFO constitutes a major risk factor for decompression sickness or not.
PFO is the remains of the opening in the septum between the right and left atrium or antechamber of the heart, that is present in 100% of unborn babies. This connection is necessary for the oxygenated blood to flow to the aorta during fetal life. Immediately after birth, this functional valve closes because the pressure in the left atrium becomes higher than in the right. In 60% of all people this closure is permanent. In 30% there remains a small to large channel that would allow passage of blood only from right
to left, when the right atrial pressure would become higher than the left atrial pressure.
This happens sometimes after a dive. When small microbubbles that circulate in the venous blood from the legs are exhaled in the lungs, this causes a retrograde pressure rise to the right ventricle of the heart, which in turn
causes a pressure rise in the right atrium. This pressure rise may be sufficient to cause bubbles to pass to the left (arterial) circulation and cause decompresison sickness (DCS). PFO has been found in many divers with DCS "of no apparent cause" (approx. 66%). This could mean that PFO is a cause of undeserved DCS, or at least one of the causes.
There has been considerable polemique about whether a diver with PFO has a great risk for DCS. We have conducted a large study on divers with deserved and undeserved DCS and compared these with divers ofthe same age and dive
experience (among other matched factors) and found that there was a significant difference (i.e. DCS divers had more and larger PFO) only in the group of divers with undeserved DCS that had symptoms related to the brain or ear or high spinal cord. This seems logical since arterial bubbles would go up, to the brain because of gravitational forces. All other forms
of DCS, deserved or undeserved, had a prevalence of PFO of about 35% which is the incidence in the normal population.
What does all this mean ?
To find out if PFO causes more DCS, you would have to do a prospective study. Test all divers for PFO, and over a number of years, you could then see if divers with PFO have more frequent DCS or not. For practical reasons this is at the moment not possible. The only reliable test for PFO is to do a transoesofageal echocardiography. If you had one, you will not this is not very pleasant. We cannot test 2000 divers like this just for science...
The study we did shows that the risk is probably not very high, except for this subgroup of divers. You must however know other statistics to interpret this. A european sports diver has a risk for DCS of about 1/6000 dives (DAN Europe statistics for dives deeper than 30m). If you have a large PFO, our data suggest that you may have a risk that is about 6 times higher, which means that statistically, if you make 1000 dives, you will have one DCS episode. Statistics mean that you can have this accident either tomorrow or never.
If you like I will send you the scientific report we published on this study. It would also interest me to know your personal situation, why you have been tested, how, and what size your PFO is. Lastly, it has also been shown by DAN statistics that is you do not descend deeper that 30m, your DCS risk falls to 1/40.000 dives. If you furthermore ascend slowly, perform a systematic safety stop and only dive when you are fit and feeling well, your risk should probably be much lower. A PFO would not matter so much then I guess.

I found your web site looking on internet for Patent Foramen Ovale.
Today, it is easy to close PFO by transcatheter procedure. I do that in my center near Paris for patient having experimented paradoxical embolism or becoming cyanotic after pneumonectomia for instance.
As about one quarter to one third on the population has a PFO, the risk for divers is very high.
What do you think anf know about that?

The answer to your question is not easy. Although the different studies we and others have conducted show that there is probably a significantly higher risk for (cerebral or high-spinal) DCS after dives within accepted diving decompression procedures, the overall absolute risk for DCS remains low.
Whereas the risk has been estimated at approx. 1/40000 dives for dives not deeper than 30m and 1/7000 for dives deeper than 30m, it seems that for divers with a large ("grade 2") PFO (more than 20 bubbles of contrast passage on TEE, either in spontaneous respiration or after Valsalva), this risk (retrospectively) can be estimated at 5 to 7 times higher, i.e. 1/6000 to 1/1000 dives respectively. This is in accordance with the simple observation that, although approximately 1/3 of all divers has a PFO, of which maybe 50% would have a PFO Grade 2, there are only so few decompression accidents. I have made a calculation for the Belgium diving population and have come up with approximately 800.000 man-dives per year, resulting in only 40 DCS AND EGA episodes per year ! And Belgian divers are not among the worlds' most prudent divers, I can assure you !

Transcatheter closure of PFO is a very elegant technique, comporting only a minimal risk. It is, at least here in Belgium, very expensive, and therefore we would not routinely recommend it for divers with PFO and no history of "undeserved" DCS. As for divers with a Grade 2 PFO and cerebral or high-spinal DCS symptoms after a "no-fault" dive, we tend to focus on preventive counselling, as to the mechanisms by which nitrogen bubbles are formed, where they go and how they can be "pushed" through a FO. Since it is evident that not the PFO, but the nitrogen bubble embolisation is the cause of the DCS episode, all this advice is aimed at reducing the number of circulating bubbles to a maximum. This advice consists among other in a reduction of diving depth (to less than 30m), a slow ascent, diving within the no-decompression limits and making a so-called "safety stop" at 3 to 5 m before surfacing. To these, we add for divers with PFO: to refrain from exercing isometric musle effort such as lifting of dive tanks, strenuous exercise, inflating the BCD by mouth, to even "pressing down" while defecating or urinating.
The decision whether to counsel a diver for transcatheter closure must depend on the severity of the symptoms and the results of the hyperbaric treatment after the DCS episode, the ability and will to return to diving, the level of diving that the diver usually practises (eg. professional diving vs. recreational diving) and the grading of the PFO using a well-established TEE technique. In certain selected cases, this procedure has become a valuable option. However, closure of the PFO will not eliminate the risk of DCS completely, since only approximately 50% of all DCS are
so-called "undeserved" DCS, and of these, only 50 to 80% appear to be related to PFO. Finally, a large-scale prospective study has not yet been done to evaluate the actual relative risk of diving with PFO. In view of the
high numbers of divers that would have to be involved and the cost and unpleasantness of the technique for diagnosing a PFO (contrast TEE), it is not ceratin that such a study will ever be undertaken.
For further reference, please see: P. Germonpré et al.: "Patent Foramen Ovale and decompression sickness in sports divers", J.Appl.Physiol. 84(5): 1622-1626, 1998. Likewise, don't hesitate to contact me if you have further questions or comments.

I have a question: in an article about PFO I read:
"The migration of these paradoxical embolisms to the cerebral circulation through the carotid and vertebral arteries (owing to the upright position of the diver during ascent and on the surface), causes the appearance of the serious symptoms of DCS type II."
Does decompression medicine return to the concept of the human body being a blood filled skin-bag without circulation? Will we consequently return to head-down position for DCS first aid?
Greetings from a confused member.

Not really a return to a simplistic anatomy! The fact is that the orientation of the carotid common arteries, as they detach from the aorta, is such that any gas bubble ejected from the left heart (and with PFO you can have a paradoxical embolism with a right-to-left passage), will find this path easier than reaching other areas. In fact the only statistically viable correlation between the presence of a PFO and DCI is the one with Cerebral DCI, especially in the case of an increased intrathoracic pressure, which makes the shunt more patent.


As for positioning the diver, this is a time-honored debate, but the Trendelenburg position has not yet been ruled out as an emergency and short-term patient positioning in AGE cases.