PFO in freediving – relevant or not?
- Michael Mutter
- vor 11 Minuten
- 7 Min. Lesezeit
In scuba diving, the link between a patent foramen ovale (PFO) and decompression sickness is fairly well established. In freediving, however, we know surprisingly little. Nevertheless, there are intriguing indications that a PFO could play a role, particularly during deep and repetitive dives.
But the picture is more complicated: perhaps some of what we have so far referred to as ‘cerebral DCS’ in freediving is not actually classic decompression sickness at all. And that is precisely what makes the question of the significance of the PFO particularly interesting.
More than half of freedivers have a PFO?
In 2022, Kelly and colleagues examined a total of 36 recreational to elite freedivers using contrast echocardiography and compared them with 36 controls. The result was astonishing: a PFO was found in 19 out of 36 freedivers (53 per cent), compared with just 9 out of 36 individuals (25 per cent) in the control group. The difference was statistically significant. In the general population, a PFO is found in approximately 20–30 per cent of adults. So why was it found in more than half of the freedivers examined?
There is no answer to this as yet. The study is small and does not allow conclusions to be drawn about cause and effect. Freediving does not, of course, cause a PFO. A selection effect is therefore conceivable: perhaps people with a PFO have a certain physiological advantage under extreme freediving conditions and are therefore found disproportionately often amongst successful freedivers. However, this is purely a hypothesis.
Could a PFO actually be beneficial for deep freediving?
As depth increases, the lungs become compressed and large volumes of blood are displaced into the thoracic cavity. During ascent, this is compounded by increasing hypoxaemia. This can trigger hypoxic pulmonary vasoconstriction: the pulmonary vessels narrow, and the right ventricle has to pump against greater resistance. As a result, pulmonary arterial and right atrial pressures may rise. A PFO can then, in a sense, act like a small door between the atria, allowing a right-to-left shunt.
Kelly et al. therefore discuss an interesting possibility: under extreme conditions, a PFO could act as a sort of pressure relief valve for the right heart. Blood would be partially diverted past the lungs, reducing the pressure load on the right side and potentially better maintaining left ventricular filling. This sounds appealing – but so far it remains merely a physiological hypothesis.
Is it even possible to develop decompression sickness whilst freediving?
The old belief that a freediver cannot develop decompression sickness because they take only a single breath down into the depths is probably incorrect. During deep dives, and particularly during repetitive dives with short surface intervals, significant amounts of nitrogen can accumulate in the tissues.
A systematic review by Blogg, Tillmans and Lindholm in 2023 identified a total of 44 episodes of decompression sickness following freediving sessions. A more recent review by Schipke, Limper and Tetzlaff found even more than 244 cases in the literature published over several decades. Neurological symptoms, and cerebral symptoms in particular, were strikingly common. And this is precisely where the PFO becomes interesting.
The classic PFO hypothesis
When venous nitrogen bubbles form following repetitive deep dives, they normally enter the lungs. The pulmonary capillaries act as a highly efficient bubble filter in this process. However, if the PFO is large enough, there is a possible shortcut:
venous bubbles → right atrium → PFO → left atrium → arterial circulation → brain
This would constitute a paradoxical gas embolism. We are familiar with this mechanism from scuba diving. In that context, large PFOs in particular – or pronounced right-to-left shunts – increase the risk of decompression sickness. In a prospective cohort study, a high-risk PFO was associated with an approximately nine-fold increased risk of PFO-associated decompression sickness. It would therefore seem reasonable to assume that the same occurs in freediving. However, it is not quite that simple.
A neurological episode in a freediver with a large right-to-left shunt
Gempp and Blatteau described a freediver who developed transient neurological symptoms following repetitive freediving. A contrast-enhanced transcranial Doppler scan subsequently revealed a large right-to-left shunt.
The authors considered paradoxical embolisation via a PFO to be a possible mechanism. This is an interesting case – but it is, after all, merely a case report. It does not prove that the PFO caused the neurological symptoms. And this is precisely where the central problem of the whole discussion lies:
To date, there is no prospective study showing that freedivers with a PFO actually develop decompression sickness more frequently than freedivers without a PFO.
Valsalva-manoeuvre: potentially of particular interest in freediving
During descent, freedivers must repeatedly equalise pressure. In the classic Valsalva manoeuvre, intrathoracic pressure – and thus also right atrial pressure – rises briefly. In the case of a PFO, this can result in a temporary right-to-left shunt.
This is unlikely to be relevant during a single initial descent: at this stage, there should be virtually no decompression bubbles circulating. However, the situation could be different during a repetitive freediving session:
After several deep dives, venous bubbles may already be present. During the next descent, a vigorous Valsalva manoeuvre is performed once more. Right atrial pressure rises – and any venous bubbles present could, in theory, be forced through the PFO into the left atrium. This results, at least physiologically, in a potentially unfavourable combination:
Deep repetitive dives + short surface intervals + circulating venous bubbles + large PFO + vigorous Valsalva manoeuvre. This mechanism has not been proven in freediving either.
Is ‘cerebral DCS’ in freediving actually a form of DCS at all?
This is precisely where the story becomes particularly interesting. Neurological incidents during repetitive apnea diving are frequently referred to as decompression sickness or, historically, as Taravana syndrome. But perhaps, at least in some of these cases, there is something entirely different at play.
A recent study raises the question of whether these events might correspond more to Posterior Reversible Encephalopathy Syndrome (PRES) than to classic embolic decompression sickness. This alternative interpretation is also explicitly discussed in the existing literature. More on this fascinating line of thought in a future article.
So what do we actually know?
Freediving can lead to significant nitrogen absorption, particularly during deep, repetitive dives, and neurological incidents following such dive profiles have been documented. A PFO could, in principle, play a role here, as venous gas bubbles can enter the arterial circulation via a right-to-left shunt – a mechanism well known from scuba diving.
Particularly striking is the small study in which 53 per cent of the freedivers examined had a PFO, compared with 25 per cent of the control subjects. However, it is unclear why PFOs were found so frequently in freedivers.
What is crucial, therefore, is what we do not know: to date, it has not been demonstrated that freedivers with a PFO actually suffer neurological decompression events more frequently than freedivers without a PFO. It is also unclear whether the size of the PFO or the extent of the right-to-left shunt influences the risk.
And the situation may be even more complicated. Recent MRI findings suggest that at least some cases of supposed ‘cerebral DCS’ in freediving may in fact represent PRES or a PRES-like syndrome with vasogenic cerebral oedema. In such a mechanism, a PFO might not be necessary at all for the development of neurological symptoms.
Thus, whilst paradoxical embolisation via a PFO remains physiologically plausible – ‘plausible’ does not mean ‘proven’.
A PFO is therefore a potential risk modifier in freediving, but so far it is not a proven independent risk factor. Before we can truly assess its significance, we must first gain a better understanding of the various mechanisms underlying neurological incidents in freediving.
Should freedivers be screened for a PFO?
Based on current knowledge: no, at least not as a matter of routine. There is currently no scientific basis for general PFO screening of asymptomatic freedivers.
Even in scuba diving, where the association between PFO and decompression sickness is much better established, the current SPUMS/UKDMC guidelines do not recommend general screening of all divers.
The situation is different for a freediver who develops unexplained neurological symptoms following deep or repetitive apnea dives. In such cases, investigating the presence of a right-to-left shunt may well form part of the diagnostic work-up. However, the detection of a PFO is by no means proof that it was the cause of the incident. The more recent PRES observations, in particular, call for caution here.
My conclusion is therefore a cautious one:
A PFO is a plausible risk modifier in freediving – but has not yet been proven to be a risk factor.
further reading on dekoblog:
Literature
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