Diving, Patent Foramen Ovale

Article Author:
Eric Hexdall
Article Editor:
Jeffrey Cooper
Updated:
11/16/2017 12:58:08 AM
PubMed Link:
Diving, Patent Foramen Ovale

Introduction

Patent foramen ovale (PFO) is a condition in which the foramen ovale, present in the atrial septum of the developing fetus, fails to close after birth. In divers, it has been associated with severe neurological decompression sickness, inner ear decompression sickness, and cutis marmorata.

Etiology

The foramen ovale is present in utero and allows blood to pass from the right atrium to the left atrium, bypassing the fetal lungs. It normally closes within a few years after birth; however, if it fails to close, it may continue to allow shunting of venous blood into the left heart.

Epidemiology

The foramen ovale remains open, or patent, in 25% to 34% of the adult population, with detectable shunting in 8% to 10%. 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 (Vann et al.). In relatively small cohorts of divers with a known patent foramen ovale, the incidence of decompression sickness ranges from 0.5% (Torti, Billinger, and Schwerzmann) to 1.8% (Liou et al.).

Pathophysiology

Seawater weighs approximately 64 pounds per cubic foot/1024 kilograms per cubic meter. Fresh water weighs slightly less, but the two are considered equivalent when determining diving depth and calculating decompression schedules. When a diver descends in the water, the pressure around him or her increases as a function of the weight of the surrounding water. For example, at 33 feet of seawater (FSW)/10 meters of seawater (MSW), the pressure is twice atmospheric pressure (2 atmospheres absolute, or ATA, 1 ATA = 1.01325 bar = 760 mmHg); at 66 fsw/20 MSW, three times atmospheric pressure (3 ATA); at 99 fsw/30 MSW, four times (4 ATA), and so on. In order for the diver to inflate his or her lungs, breathing gas must be supplied at a pressure equivalent to the ambient water pressure. This is the function of diving equipment, whether it is self-contained underwater breathing apparatus (SCUBA) or surface-supplied.

Most divers breathe compressed air, which is 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. Dives deeper than that are typically made using a mixture of helium and oxygen since helium has almost no narcotic properties. Many technical divers use a combination of helium, nitrogen, and oxygen (“trimix”) at shallower depths to help offset the effects of nitrogen narcosis.  Of note, though nitrogen is not chemically inert, it is often referred to by divers 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 rises as well. This 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 become dissolved in the body as a function of partial pressure and time. In other words, the farther a diver descends and the longer he or she stays at depth, the more inert gas becomes dissolved in the blood and body tissues.

As a diver ascends toward the surface, the inert gas pressure in the lungs decreases and the pressure gradient between the lungs and the body equilibrates and then reverses. When the partial pressure of dissolved inert gas in the body is higher than the partial pressure of inert gas in the lungs, the tissues become supersaturated. The gas molecules in the body then pass through the alveolar-capillary membrane into the lungs and are exhaled. This is a simplified description of the process known as decompression. There are detailed decompression algorithms designed to control this process and allow the diver to return safely to the surface.

Bubbles may form in supersaturated body tissues. The physical process by which these bubbles form is the same as that which occurs 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 normally travel through the right heart and lodge in the pulmonary circulation, where they are slowly eliminated.

Bubbles in the venous circulation which are present after decompression may be shunted through a patent foramen ovale when they reach 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 the two remains unclear. Also, intrapulmonary shunts are present in most of the population at rest and are even more prevalent during vigorous exercise, so patent foramen ovale is not the only mechanism of arteriovenous shunting in divers without other abnormalities of the cardiac septum.

History and Physical

Patent foramen ovale is asymptomatic. It has been associated with migraine with aura and cryptogenic stroke, though the evidence for this is conflicting.

The dive profile in which right-to-left shunt is most likely to be implicated in decompression sickness is one that 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 such episode increases the likelihood that 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 AV shunting, as noted above. Patent foramen ovale testing is not indicated in divers who have suffered from only minor decompression sickness symptoms, for example, joint pain, swelling, and type 1 skin rash.

*Long, deep dives, aggressive decompression protocols, omitted decompression, rapid ascent, heavy work at depth, cold on decompression, and repetitive dives (especially over multiple days) are risk factors for decompression sickness.

Evaluation

Routine screening for patent foramen ovale in divers is not recommended; however, it is reasonable to screen high-risk individuals such as those who suffer from a migraine with aura or congenital heart disease, or who have a family history of patent foramen ovale (Smart et al. judgment).

Echocardiography with bubble contrast is the standard detection method for patent foramen ovale. Studies should be performed at rest and with provocative maneuvers, e.g., Valsalva. Transcranial Doppler is an inexpensive and non-invasive screening tool for patients with a suspected right-to-left shunt, but it cannot determine intracardiac shunt morphology. Transthoracic echocardiography (TTE) with bubble contrast is sensitive enough to detect a clinically significant patent foramen ovale (Smart et al. judgment), but some practitioners may choose to perform transesophageal echocardiography (TEE) with bubble contrast.

Treatment / Management

Divers who present with acute decompression sickness should be treated with hyperbaric oxygen therapy by established protocols, for example, the United States Navy's treatment tables found in the U.S. Navy Diving Manual, available for download here: www.navsea.navy.mil/Home/SUPSALV/00C3-Diving/Diving-Publications/

Divers who have suffered from unexplained severe sudden-onset neurological decompression sickness, inner ear decompression sickness and/or cutis marmorata and are subsequently found to have a patent foramen ovale should be cautioned against returning to diving. More than one such decompression sickness incident increases the gravity of this recommendation. However, clearance to dive is based partly on the judgment of the trained, experienced practitioner. Some of these divers may safely return to diving provided they exercise caution, which can mean diving with nitrox using air tables or using the "air" setting on a dive computer, avoiding decompression diving, and not diving to the limits of their computer's tables or decompression algorithms. Military and commercial divers are usually 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 is an individual decision that should be made in consultation with a cardiologist and a physician trained in diving medicine. PFO closure is not without risk, and this risk must be balanced against the individual risk of decompression sickness when evaluating divers with PFO. Mas et al. (2017) reported a major device and procedural complication rate of 5.9% using eleven different devices (N=238), and Saver et al. (2017) report a combined procedural (2.4%) and device-related (2.6%) complication rate of 5.0% using the Amplatzer PFO occluder (N=499). Pearman et al. (2015) reported a serious complication rate of 2.9% in 105 divers who had a PFO closure performed by a single cardiologist. Verna & Tobis (2011) cite a closure device explantation rate of 0.28% (N=13,736).

Torti et al. (2004) reported an incidence of serious DCS of 5 per 10,000 dives (.05%) in divers with PFO (N=63). Liou et al. (2015) reported an incidence of serious DCS of 18/1000 (1.8%) in divers with PFO (N=39); however, their incidence of serious DCS in divers without PFO was 1.3% (N=36), which is significantly higher than the .01% to .095% cited by other authorities based on much larger cohorts (Vann et al. 2011). Some evidence suggests that size matters; in one retrospective study, the mean PFO size in divers who had experienced DCS was 5 mm larger than the mean PFO size in the general population (Wilmshurst et al., 2015).

PFO closure should not be routinely considered in divers with asymptomatic patent foramen ovale who have not suffered from decompression sickness. These divers should instead be counseled to dive conservatively, as outlined above. Rarely, a diver with a known patent foramen ovale and no history of DCS who plans to participate in expedition-level dives involving extensive decompression may request closure in advance of these dives. Again, the risk of device and procedural complications must be weighed against the best estimate of the individual diver's risk of DCS.

A diver who has undergone patent foramen ovale closure may return to diving after he or she is cleared for full activity by the cardiologist and a physician 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 (Smart et al.). Evidence suggests that closure of patent foramen ovale may decrease the risk of decompression illness in divers with patent foramen ovale who have previously suffered from decompression sickness (Billinger et al., Henzel et al.).