From the Wilderness Medicine Newsletter

Patent Foramen Ovale | The Hidden Danger
An Altitude and Depth Perspective

Jeff Toorish
18 May 2015

The foramen ovale is a small orifice located in the atrial septum. Its purpose is to enhance the circulation of blood during fetal development. A fetus in the womb does not use its own lungs to oxygenate blood because its lungs are not yet developed having had no exposure to air. Instead the fetus relies on oxygen from the mother via the umbilical cord. For this reason, blood must travel directly from the right atrium of the fetal heart to the left atrium of the fetal heart through the foramen ovale, bypassing a trip to the right ventricle and, ultimately, the undeveloped fetal lungs.

Increased blood pressure at birth normally closes the foramen ovale and it normally becomes permanently sealed during the first months of life in most people. If this hole in the atrial septum does not close properly it retains patency and is called a patent foramen ovale (PFO), which normally presents as a flap-valve that only opens during certain conditions. If the pressure is great enough, oxygen poor blood will travel directly

from the right atrium of the heart to the left atrium. This is also a gateway for clots to travel more easily through the heart.
Approximately 25 percent of people in the general population have PFO, although many will never know it. That number increases in specific population cohorts and PFO is linked to stroke, seizure, migraine headaches, increased decompression sickness in divers, and increased diagnoses of HAPE in climbers. Remarkably, many front line and pre-hospital providers have never heard of PFO and even in hospital settings it is often overlooked. In this report I will explore these hidden dangers and its potential impact in the pre-hospital setting.
Adult autopsy studies have shown that between 20 and 34% of adults from the third to ninth decades of life have at least a small PFO (Hagen, Scholz, Edwards, 1984). Research has failed to determine specific risk factors for patent foramen ovale but transesophageal echocardiology findings in the setting of cryptogenic stroke in adults indicate black patients are about half as likely to have PFO as white patients (Kizer, Silvestry et al, 2002).
Patent foramen ovale can shunt blood from left to right or right to left, but patients with left to right shunting are generally asymptomatic. In right to left shunting, patients are more likely to experience cyanosis, both acute and chronic. Cyanosis is made worse during activities that increase pulmonary vascular resistance such as breath holding, crying, or coughing. During the Valsalva maneuver, patients are also likely to experience increased shunting as well.

This is important in the pre-hospital setting because EMS providers sometimes
attempt vagal maneuvers in patients with supraventricular tachycardia (SVT). Often the first vagal maneuver attempted is the Valsalva maneuver. But in patients with PFO, this may create unwanted shunting of under oxygenated blood to the left atria and subsequently to the left ventricle and ultimately to the body and brain.
The relationship between PFO and neurocardiogenic syncope (seizures) and migraines is poorly understood. Most likely a PFO exacerbates these conditions but it is unclear if it actually causes them. What is clear is that PFO can lead to TIA/CVA which can later be a factor in seizures, including epilepsy and migraine headaches.
This is significant in the EMS setting because pre-hospital providers often see patients with stroke or stroke like symptoms, seizure activity and migraine headache sufferers.

For scuba divers, PFO presents a unique danger. In the 1990s, doctors in Belgium conducted a case study of PFO in sport divers who were treated for decompression sickness (DCS). They concluded that divers with PFO are more likely to experience an episode of DCS than divers without PFO. These researchers concluded that PFO can be a cause of DCS by paradoxical embolism of nitrogen bubbles that would otherwise have been filtered out via the lungs and vasculature (Germonpre, et al. 1998). It is worthwhile noting that many cases of DCS are unexplained, referred to as “undeserved hits” by the diving community. But it is likely that at least a sizable percentage of these “undeserved hits” are actually related to undiagnosed PFO in divers.
In controlled studies, the number of divers who experienced an episode of DCS who also had PFO was 22 out of 37 (Germonpre, et al, 1998) a significantly higher prevalence of DCS than in divers who do not have PFO. In general decompression sickness is relatively rare in diving even among divers with PFO. However, while not the focus of this report, this does beg the question; should divers be screened for PFO prior to undertaking diving instruction?
Doctors can detect a Patent foramen ovale using a variety of tests including the transthoracic echocardiogram; color flow Doppler; and saline contrast (bubble) study. The gold standard for PFO diagnosis is the transesophageal echocardiogram. This test uses a small transducer inserted on a tube into the esophagus. The esophagus is adjacent to the heart which gives doctors a clear view of both the structure of the heart and blood flow through the organ making it easier to see a PFO using color-flow doppler or saline contrast.

While divers and diving doctors have been aware of the dangers of patients with PFO and many divers have had (somewhat controversial) corrective surgery to close the opening, climbers seem less aware of the dramatic increase in HAPE diagnoses related to PFO.
According to a report in the Journal of the American Medical Association, PFO is dramatically linked to increased cases of HAPE (Alleman, et al, 2006). In that report the authors concluded, “(i)ndividuals susceptible to high-altitude pulmonary edema (HAPE) are characterized by exaggerated pulmonary hypertension and arterial hypoxemia at high altitude, but the underlying mechanism is incompletely understood. Anecdotal evidence suggests that shunting across a patent foramen ovale (PFO) may exacerbate hypoxemia in HAPE.”
The report also states that a PFO was approximately four times more common in mountaineers who were deemed HAPE-susceptible than in climbers who were considered resistant to HAPE. As further evidence of the HAPE/PFO connection, the JAMA report noted that HAPE-susceptible climbers with a large PFO were even more likely to suffer from extreme hypoxemia.

Research shows patients with PFO are at much higher risk for ischemic cerebrovascular events, particularly cryptogenic strokes (Carlos, et al. 2007). This is caused by the direct link from the right atrium to the left atrium. In addition to being deoxygenated, the blood in the right atrium also carries various waste products, including clumps of cells and chemicals such as serotonin that are normally filtered in the lungs before they pass into the left atrium. These waste products are potent building blocks for potential strokes. This link poses an even greater risk for older patients (Handke, 2007).
But the PFO itself may play a specific role in the formation of the clots. The flap of the PFO can create turbulence, creating a powerful environment for a blood clot to form and eventually move directly from the left atrium to the left ventricle and on to the carotid arteries where it disrupts blood flow to the brain.
While treatment related to PFO is not possible in the pre-hospital setting, being aware of this additional factor is useful to EMS providers because often PFO is often overlooked in post CVA/TIA treatment. Checking for and properly treating a PFO can decrease the potential for future ischemic attacks.

In addition to stroke, there are other physical maladies that can be clues to the presence of PFO in a patient. There is considerable evidence to suggest that patients who experience migraines with an aura are twice as likely to have a PFO. The evidence also indicates that these patients likely have a relatively large PFO when compared to migraine patients who do not experience aura or people who do not have migraines.
While it is not clear what links PFO and migraines with aura, there are a variety of theories. There may be a genetic origins link between the two. Researchers are also exploring the notion that tiny metabolic waste particles and clumps of cells in the blood reach the brain with the potential to trigger a wave of electrical activity in the brain’s cortex which is the basis for a migraine aura.
In clinical studies in Scandinavia, patients who had their PFOs closed had a decrease in the frequency of migraines (Martin, et al. 2004). It is important to note that there is no causal link at this point but there is a growing body of evidence linking migraine with aura and PFO.
For EMS providers, this is an additional assessment tool that may provide doctors with data to help prevent a more serious stroke.

Most people with patent foramen ovale will never know they have it because the condition remains asymptomatic. For those who are diagnosed with PFO the question arises, should they treat the condition or let it be? Many scuba divers, for example, choose to have their PFO surgically closed via a relatively simple surgical procedure to reduce their chances of developing decompression sickness.

That is a decision left to the patient and doctor. But as evidence grows that PFOs may be a factor is more serious illness, often resulting is severe disability or even death, more patients may decide closing the PFO is a more prudent prophylactic measure. What is clear is that continuing research on PFO and its potential negative impact on patients may well become another assessment tool for both pre-hospital care and medical treatment.






Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc. Jan 1984;59(1):17-20.

Kizer JR, Silvestry FE, Kimmel SE, Kasner SE, Wiegers SE, Erwin MB. Racial differences in the prevalence of cardiac sources of embolism in subjects with unexplained stroke or transient ischemic attack evaluated by transesophageal echocardiography. Am J Cardiol. Aug 15 2002;90(4):395-400.

P. Germonpré, P. Dendale, P. Unger and C. Balestra, Patent foramen ovale and decompression sickness in sports divers. Journal of Applied Physiology, May 1, 1998, vol. 84 no. 5 1622-1626

Handke M, Harloff A, Olschewski M, Hetzel A, Geibel A, Patent foramen ovale and cryptic stroke in older patients. New England Journal of Medicine 2007; 22: 2262-2268

Post, Martjin C.; Thijs, Vincent; Herroelen, Luc; Budts, Werner I.H.L. "Closure of a patent foramen ovale is associated with a decrease in prevalence of migraine."Neurology April, 2004:62:1439–1440.

Allemann Y, Gytter D, Lipp E, Sartori C, Duplain H, Egli M, Cook S,
Scherer U, Seiler C, Patent Foramen Ovale and High-Altitude Pulmonary Edema Journal of the American Medical Association 2006



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