Patent Foramen Ovale in Diving

Etiology

During fetal development, the foramen ovale serves as a crucial passage, enabling blood flow from the right atrium to the left atrium, bypassing the fetal lungs during gestation. Typically, this opening naturally closes within a few years after birth. If it fails to close, it can result in the shunting of venous blood into the left heart.[4] However, the shunt is typically minuscule and not clinically significant due to the greater pressure in the systemic circulation.

Epidemiology

The foramen ovale remains open, or patent, in approximately 20% to 34% of adults, with detectable shunting occurring in 8% to 10% of cases.[5] The incidence of decompression sickness in the general diving population is relatively low, ranging from 0.01% to 0.095%, depending on the diving environment and type of diving performed.[6] In relatively small cohorts of divers with a known patent foramen ovale, the incidence of decompression sickness ranges from 0.5% to 1.8%.[7][8]

Pathophysiology

Seawater weighs approximately 64 lb/ft³ or 1024 kg/cm³. Freshwater weighs slightly less but is considered equivalent to seawater when determining the diving depth and calculating decompression schedules. When a diver descends into the water, the pressure around them increases as a function of the weight of the surrounding water. For example, at 33 feet of seawater (FSW) or 10 meters of seawater (MSW), the pressure is twice the atmospheric level (2 atmospheres absolute (ATA), where 1 ATA = 1.01325 bar = 760 mm Hg). At 66 FSW/20 MSW, the pressure is 3 times the atmospheric pressure (3 ATA), and at 99 FSW/30 MSW, it is 4 times (4 ATA), and so on. For the diver to inflate their lungs, breathing gas must be supplied at a pressure equivalent to the ambient water pressure. This function is fulfilled by diving equipment, whether self-contained underwater breathing apparatus (SCUBA) or surface-supplied.

Most divers breathe compressed air, comprising roughly 78% nitrogen. However, nitrogen produces measurable decrements in cognitive performance, beginning at a depth of about 3 ATA/3 bar/66 FSW/20 MSW. This effect, known as nitrogen narcosis, becomes debilitating beyond approximately 200 FSW/60 MSW.[9][10] Dives deeper than that are typically performed using a mixture of helium and oxygen, as helium exhibits minimal narcotic effects. Many technical divers use a combination of helium, nitrogen, and oxygen (trimix) at shallower depths to help offset the effects of nitrogen narcosis and the considerable cost of using helium alone as a diluent. Although nitrogen is not chemically inert, divers commonly label it as an inert gas.

At atmospheric pressure, the dissolved inert gas in the body is in equilibrium with that of the atmosphere. As the pressure of the diver's breathing gas increases with increasing depth, the partial pressure of inert gas in the breathing mix also rises. This elevation creates a positive pressure gradient between the inert gas in the lungs and the gas dissolved in the blood and body tissues. Inert gas molecules in the lungs then pass through the alveolar-capillary interface and dissolve in the body as a function of partial pressure and time. In other words, the farther a diver descends and the longer they stay at depth, the more inert gas dissolves in the blood and body tissues.

As a diver ascends towards the surface, the inert gas pressure in the lungs decreases, and the pressure gradient between the lungs and the body equilibrates and eventually reverses. When the partial pressure of dissolved inert gas in the body is higher compared to that in the lungs, the tissues become supersaturated. Gas molecules within the body then pass through the alveolar-capillary membrane into the lungs and are exhaled. This simplified overview of the process is known as decompression. Detailed decompression algorithms are designed to control this process and allow the diver to return safely to the surface.

Bubbles can form in supersaturated body tissues. The physical process of these bubbles forming is the same as in a carbonated beverage after the lid is removed. Decompression sickness occurs when these bubbles produce symptoms. Silent or asymptomatic bubbles may form in the venous blood even after normal, uneventful decompression. Silent venous bubbles typically travel through the right heart and lodge in the pulmonary circulation, where they are slowly eliminated.

Bubbles within the venous circulation present after decompression may be shunted through a patent foramen ovale upon reaching the right atrium. They subsequently become arterialized, where they may produce symptoms if they lodge in the arterial supply to the tissue. There is not a 1:1 correlation between patent foramen ovale and decompression sickness, and the exact relationship between them remains unclear. Furthermore, intrapulmonary shunts are commonly found in the general population at rest, particularly during vigorous exercise, suggesting that patent foramen ovale is not the only mechanism of arteriovenous shunting in divers without other abnormalities of the cardiac septum.[11][12]

History and Physical

Patent foramen ovale is typically asymptomatic and has been associated with migraine with aura and cryptogenic stroke, although the evidence supporting these associations is inconsistent.[13][14][15][16][17]

The dive profile in which a right-to-left shunt is most likely in decompression sickness is provocative enough to evoke silent venous gas emboli, uneventfully follows an established decompression protocol, is without other known risk factors, and produces sudden-onset severe decompression sickness symptoms. More than one episode increases the likelihood that a right-to-left shunt exists. When recommending patent foramen ovale testing and interpreting test results, the practitioner should remain mindful that patent foramen ovale is not the only source of arteriovenous shunting, as previously mentioned. Patent foramen ovale testing is not indicated in divers who have experienced only minor decompression sickness symptoms, for example, joint pain, swelling, and type 1 skin rash.

Risk factors for decompression sickness include long and deep dives, aggressive decompression protocols, omitted decompression, rapid ascent, heavy work at depth, exposure to cold during decompression, and repetitive dives, especially over multiple days.

Evaluation

Routine screening for patent foramen ovale in divers is not recommended; it is reasonable to screen high-risk individuals such as those who have experienced migraine with aura or congenital heart disease or who have a family history of patent foramen ovale.[2]

Echocardiography with bubble contrast is the standard method for detecting patent foramen ovale. Studies should be performed at rest and during provocative maneuvers, such as the Valsalva maneuver. Transcranial Doppler is an inexpensive and noninvasive screening tool for patients with a suspected right-to-left shunt, but it cannot determine intracardiac shunt morphology.[18][19][18] Transthoracic echocardiography with bubble contrast is sensitive enough to detect a clinically significant patent foramen ovale, but some practitioners may choose to perform transesophageal echocardiography with bubble contrast.[2][20]

Treatment / Management

Divers experiencing acute decompression sickness should undergo hyperbaric oxygen therapy following established protocols. The United States Navy's treatment tables in the U.S. Navy Diving Manual are available for download.

Divers who have experienced unexplained severe sudden-onset neurological decompression sickness, inner ear decompression sickness, or cutis marmorata and are subsequently found to have a patent foramen ovale should be cautioned against returning to diving. More than one decompression sickness incident increases the gravity of this recommendation. However, clearance to dive is based partly on the judgment of a qualified and experienced practitioner. Some of these divers may safely return to diving provided they exercise caution, which can mean diving using nitrox with air tables or the air setting on a dive computer, avoiding decompression diving, and not descending to the limits of their computer's tables or decompression algorithms.[2] Military and commercial divers are typically subject to more stringent requirements. Any diver with residual neurological symptoms should refrain from diving until those symptoms are fully resolved.

Divers with patent foramen ovale may inquire about percutaneous closure. This individual decision should be made in consultation with a cardiologist and a clinician trained in diving medicine. Patent foramen ovale closure is not without risk, and this risk must be balanced against the individual risk of decompression sickness when evaluating divers with patent foramen ovale. Mas et al (2017) reported a major device and procedural complication rate of 5.9% using 11 different devices (N=238), and Saver et al (2017) reported a combined procedural (2.4%) and device-related (2.6%) complication rate of 5.0% using the Amplatzer patent foramen ovale occluder (N=499).[21][22] Pearman et al (2015) reported a serious complication rate of 2.9% in 105 divers who had a patent foramen ovale closure performed by a single cardiologist.[23] Verna and Tobis (2011) cite a closure device explantation rate of 0.28% (N=13,736).[24]  Bissessor et al reported zero residual shunts at 1 year with only 1 in-hospital complication using both the available devices (N=70).[25] Lee et al (2018) reported closure complications in 2 of the 60 patients studied (3.3%).[26](B3)

Torti et al (2004) reported an incidence of serious decompression sickness of 5 per 10,000 dives (0.05%) in divers with patent foramen ovale (N=63).[7] Liou et al (2015) reported an incidence of serious decompression sickness of 18 per 1000 (1.8%) divers with patent foramen ovale (N=39); their incidence of serious decompression sickness in divers without patent foramen ovale was 1.3% (N=36), which is significantly higher compared to 0.01% to 0.095% cited by other authorities based on much larger cohorts.[8][6] Some evidence suggests a correlation between patent foramen ovale size and decompression sickness risk. A retrospective study found that the mean patent foramen ovale size in divers who had experienced decompression sickness was 5 mm larger compared to the mean patent foramen ovale size in the general population.[27](B2)

Patent foramen ovale closure should not be routinely considered in divers with asymptomatic patent foramen ovale who have not experienced decompression sickness. These divers should instead be counseled to dive conservatively, as previously discussed.[28] Rarely, a diver with a known patent foramen ovale and no history of decompression sickness who plans to participate in expedition-level dives involving extensive decompression may request closure before these dives. Furthermore, the risk of the device and procedural complications must be weighed against the best estimate of the individual diver's risk of decompression sickness.(B2)

A diver who has undergone patent foramen ovale closure may return to diving after they are cleared for full activity by the cardiologist and a clinician trained and experienced in the examination of divers. Post-closure echocardiography should show adequate reduction or abolition of the patent foramen ovale, and the diver should be off all anticoagulants other than aspirin.[2] Evidence suggests that closure of a patent foramen ovale may decrease the risk of decompression illness in divers with patent foramen ovale who have previously experienced decompression sickness.[20][29][30]

Differential Diagnosis

Differential diagnoses of patent foramen ovale include the following:

• Coronary sinus atrial septal defects 
• Ostium primum atrial septal defects
• Partial anomalous pulmonary venous connection 
• Sinus venosus atrial septal defect
• Total anomalous pulmonary venous connection