Patent Foramen Ovale

By-Dr Simon Mitchell

Patent Foramen Ovale

Figure 1

Patent Foramen Ovale

Figure 2

Few diving medical issues have caused as much head scratching and angst among divers as the ‘patent foramen ovale’ (PFO). Few subjects get more attention on internet diving medicine discussion groups, but much of the commentary is poorly informed. This is an issue of very high contemporary relevance for reasons that I will come to below. In this article I will explain what a PFO is, and why it is important in diving medicine.

What is a PFO?

To appreciate the following explanation of a PFO, you should first look at the simplified diagram of the human circulation in Figure 1, and have a read of the explanatory caption. In the developing fetus (in the mother’s womb), oxygenation of the blood is achieved in the placenta, not the lungs. Indeed, not much blood needs to pass through the lungs at all, and it bypasses the lung circulation by several means, one of which is the foramen ovale. At this point, have a careful look at Figure 2 and read the caption.

When the baby is born and begins to breathe, the pressure is increased on the arterial (left) side of the heart relative to the venous (right) and the foramen ovale closes. As we would anticipate, blood is now pumped through the lungs for oxygenation. Initially the foramen ovale is closed by means of a ‘˜flap’ valve that seals against the wall of the left atrium. This remains closed under normal circumstances, as the pressure in the left atrium is slightly higher than that in the right atrium most of the time. In many people the valve eventually heals over and the foramen ovale disappears.

In some individuals, the foramen ovale fails to seal completely and they have what is known as a Patent Foramen Ovale (PFO). These lesions vary in their nature, size and significance. If the ‘flap valve’ is malformed or absent the foramen ovale may remain widely open and there can be spontaneous ‘shunting’ (movement of blood from one side to the other). However, most PFOs are smaller, the flap valves are at least partially effective, and so shunting does not occur constantly. Indeed, the PFO may be functionally closed most of the time. Not surprisingly, it is certainly possible for perfectly healthy individuals to have a PFO; more on this below.

A PFO can be detected using echocardiography, an ultrasound technique which provides images of the beating heart. The best views of the heart are obtained when an echocardiographic probe is ed into the oesophagus, and so images are obtained from behind the heart rather than through the chest wall from the front. This technique is referred to as ‘˜transoesophageal echocardiography’ (TOE).

Bubbles are highly reflective of ultrasound, and can be clearly seen during echocardiography. To test for blood shunting between the atria, a saline solution containing minute air bubbles (microbubbles) is injected into one of the subject’s peripheral veins. These will arrive first in the right atrium and can be clearly seen because of their high reflectivity. The left atrium is then carefully observed during a series of manoeuvres designed to raise right atrial pressure. If the bubbles can be seen passing across the atrial wall, this indicates the presence of a PFO.

Like all medical interventions, there are some risks in conducting these tests. Suffice to say it is not something you would have done for recreational pleasure.

Why might a PFO be important in diving medicine?

Bubbles form from dissolved gas in the venous blood (at Point 1 in Figure 1) after many dives, even those where there are no obvious problems. One advantage of the layout of our circulatory system is that the venous blood passes through the tiny capillary blood vessels of the lungs (follow this on Figure 1) before it returns to the left heart to be pumped into the arterial circulation (potentially, to places like the brain). This means that most of these bubbles that form in the veins get filtered out of circulation by the lungs. Unfortunately, a PFO provides a means by which blood could shunt from the right atrium to the left, thus allowing bubbles to bypass filtration in the lungs and directly enter the arterial circulation. In theory, bubbles are more dangerous once they get into the arteries.

Is a PFO important in diving medicine?

Well, let’s start with a couple unassailable facts:First, there are now quite a number of studies which show that if you test a group of divers who have suffered DCI, a higher proportion of these divers have a PFO than you will find in a similar group of divers who have never suffered DCI. This is particularly true for spinal DCI, cutaneous (skin) DCI, and possibly inner ear DCI.

Second, multiple studies have shown that the size of the PFO is important. Put simply, the larger the PFO, the larger the risk. Things start to get grey when you try to identify a’threshold size’ at which PFOs become significant. This type of data is not available. At this point, all it is possible to say is that large spontaneously shunting PFOs unequivocally increase risk, and small PFOs that shunt only with extreme provocation are probably of little or no importance.

So, PFOs appear associated with an increased risk of DCI, and the bigger they are the more true this becomes. At this point, the reader could be excused for interpreting this as building a strong argument for screening divers for a PFO before they learn to dive, and banning anyone with one, especially if it is big. Indeed, many divers have enthusiastically embraced this concept and failed to appreciate one or two vitally important issues.

The most striking of these issues is that PFO is remarkably prevalent in the general population (about 30%). We do not currently screen divers for PFO, and we would therefore expect that something like 30% of divers have one. Despite this, serious neurological DCI remains a rare event. Exact figures are not available, but there are published data that would support one in 100,000 dives as a reasonable estimate for serious DCI among non-technical recreational divers.

So, where does that leave us?

Well, first, I must highlight the illogical nature of the notion that a prevalent phenomenon is the explanation for a rare disease. Things don’t usually work this way. This is not to deny that PFO is a risk factor for serious neurological DCI, but since about 30% of dives are performed by divers with a PFO, and since serious DCI remains very rare despite this, PFO can only be part of the puzzle at best. What we have, in fact, is a complex state of affairs that should make us all very wary of expressing strong views without an intimate knowledge of the issues.

In the opinion of this author and the vast majority of my diving physician colleagues, the current data do not support screening every prospective diver for a PFO and eliminating or repairing those who have one. Any diver who advocates such a stance must be very careful what they wish for. If this view were ever to gain legislative momentum the recreational diving industry and its infrastructure would collapse virtually overnight. Obviously, this would not be a reason to avoid addressing the issue if it were warranted, but I reiterate that serious DCI is rare among mainstream recreational divers, and in fact is probably becoming rarer. Sure, the risk could be lowered even further by screening everyone for PFO, but it would destroy the industry. There are many similar opportunities in our society for invoking draconian measures to make safe activities even safer, but we choose not to do so because of the negative effects. Driving no faster than 50 kph on motorways is one example that springs to mind.

Having said all that, there are some situations in which screening divers for PFO is appropriate. One example arising from mainstream recreational diving is the diver who presents with serious or unusual DCI after a relatively unprovocative dive, or with multiple episodes of DCI. I might add, that PFO is not invariably the reason for such events, but nevertheless, they are an appropriate indication for screening.

Then we come to the thorny issue of technical diving. The circumstances are a little different here. It can be argued, though not on the basis of much hard data, that the risk of serious DCI, and of encountering the high venous bubble loads that could give rise to serious DCI, may be higher in technical diving, perhaps much more so, than in mainstream recreational diving. This may alter the motivation for wanting to be screened. Under these circumstances of uncertainty, I can appreciate the ‘sense’ in a technical diver wanting to be screened.

However, PFO testing should never be embarked upon without some rational notion of how to respond to the result. Those who advocate that everyone must be screened and that the finding of any PFO, no matter how small and irrespective of its shunting behaviour, should result in a ban from diving are not interpreting the literature correctly. However, in fairness, it would seem reasonable to decide against participation in technical diving if there were a PFO that could be provoked into shunting with moderate ease. The main point is that there should be some attempt at intelligent interpretation of the implications of the results. Even a negative test requires careful interpretation. For example, it may mean that the technique used was insensitive, and it does not mean that the diver is resistant to DCI (as some seem to think). Some of the most devastating cases of ‘˜undeserved’ DCI I have treated did not have a PFO.


Above all, we must realise that this is a complex issue, and for the good of the sport and industry, we must be very careful what we say on the matter. The diving medicine profession acknowledges a strong association between the presence of PFO and serious neurological DCI. However, the absolute risk of serious DCI remains small, even in the presence of a PFO, and a tiny or non-shunting PFO probably does not alter risk at all. The prevalence of PFO coupled with the rarity of serious DCI suggests that there remain other, perhaps more important risk factors for DCI that we are yet to unearth. With all of this in mind, routine screening of mainstream recreational divers for PFO is not supported. Under certain circumstances, it may be wise to screen divers who have suffered DCI. It is also acknowledged that divers performing more provocative technical dives may want to be pre-emptively tested, but they should carefully consider the implications of both a positive or ne

Figure 1

Simplified human circulation. Oxygenated blood (‘arterial blood’) (red vessels) leaves the lungs and is carried to the left side of the heart. It enters the left atrium (LA), then the left ventricle (LV), which pumps the blood through the arteries to all the various tissues of the head and body. In these tissues the blood flows through thin walled capillaries, and across these thin walls, oxygen in the blood is exchanged for carbon dioxide in the tissue. De-oxygenated blood (‘venous blood’) (blue vessels) passes back to the right side of the heart in the veins and is then pumped to the lungs. Once again, in the lungs the deoxygenated blood flows through thin walled capillaries where carbon dioxide in the blood is exchanged for oxygen in the tiny alveoli (air sacs) of the lung tissue. See text for explanation of point 1.

Figure 2

The human circulation showing a patent foramen ovale (PFO). Compare this to Figure 1. Here, we see a communication between the right and left atria of the heart. In the fetal circulation this causes blood to move from the venous side of the circulation to the arterial side (blue arrow) thereby bypassing the lungs.

© Copyright 2004

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