Cardiol Clin. 2005 Feb;23(1):97-104.
Patent foramen ovale and diving.
Centre for Hyperbaric Oxygen Therapy, Military Hospital Brussels, Bruynstraat 200, Brussels 1120, Belgium. email@example.com
Patency of the foramen ovale is a risk factor for DCS in SCUBA divers, even if they adhere to the currently accepted and used decompression tables. The primary cause of DCS, however, is the nitrogen bubble, not the PFO. There are a number of techniques any diver can use to minimize the occurrence of nitrogen bubbles after a dive.The authors current practice is to inform civilian sports divers of the increased risk and to advise them to adopt conservative dive profiles.This can be achieved by selecting a more conservative dive computer, performing only dives that do not require obligatory decompression stops, or using oxygen-enriched breathing gas mixtures("nitrox") while still diving on "air profiles" .Dive-safety organizations are currently under-taking studies aimed at proposing changes in the decompression algorithms to produce low-bubble dive tables . In the meantime, PFO remains a reason for caution.Whether all divers should be screened for PFOis an ongoing discussion  in view of methodologic and practical issues outlined in this article.Any definitive recommendations can be made only after a careful, prospective evaluation of the real relative risk for DCS and long-term cerebral damage.
Am J Cardiol. 2004 Jul 15;94(2):270-3.
Identification of professional scuba divers with patent foramen ovale at risk for decompression illness.
Cartoni D, De Castro S, Valente G, Costanzo C, Pelliccia A, Beni S, Di Angelantonio E, Papetti F, Vitali Serdoz L, Fedele F.
Department of Clinical Medicine, La Sapienza University, Rome, Italy.
Functional and anatomic characteristics of patent foramen ovale (PFO) were investigated in 66 professional scuba divers (41 with and 25 without decompression illness) using transthoracic and transesophageal echocardiography. PFO with right-to-left shunting at rest is associated with decompression illness, particularly the neurologic type. A wider patency diameter together with a higher membrane mobility are associated with the risk of developing the disease in divers with PFO.
Eur Heart J. 2004 Jun;25(12):1014-20.
Comment in: Eur Heart J. 2004 Dec;25(23):2173-4.
Risk of decompression illness among 230 divers in relation to the presence and size of patent foramen ovale.
Torti SR, Billinger M, Schwerzmann M, Vogel R, Zbinden R, Windecker S, Seiler C.
Department of Cardiology, University Hospital, CH-3010 Bern, Switzerland.
BACKGROUND: The risk of developing decompression illness (DCI) in divers with a patent foramen ovale (PFO) has not been directly determined so far; neither has it been assessed in relation to the PFO's size. METHODS: In 230 scuba divers (age 39+/-8 years), contrast trans-oesophageal echocardiography (TEE) was performed for the detection and size grading (0-3) of PFO. Prior to TEE, the study individuals answered a detailed questionnaire about their health status and about their diving habits and accidents. For inclusion into the study, > or =200 dives and strict adherence to decompression tables were required. RESULTS: Sixty-three divers (27%) had a PFO. Overall, the absolute risk of suffering a DCI event was 2.5 per 10(4) dives. There were 18 divers (29%) with, and 10 divers (6%) without, PFO who had experienced > or =1 major DCI events P=0.016. In the group with PFO, the incidence per 10(4) dives of a major DCI, a DCI lasting longer than 24 h and of being treated in a decompression chamber amounted to 5.1 (median 0, interquartile range [IQR] 0-10.0), 1.9 (median 0, IQR 0-4.0) and 3.6 (median 0, IQR 0-9.8), respectively and was 4.8-12.9-fold higher than in the group without PFO (P<0.001). The risk of suffering a major DCI, of a DCI lasting longer than 24 h and of being treated by recompression increased with rising PFO size. CONCLUSION: The presence of a PFO is related to a low absolute risk of suffering five major DCI events per 10(4) dives, the odds of which is five times as high as in divers without PFO. The risk of suffering a major DCI parallels PFO size.
Eur J Neurol. 2002 Jan;9(1):89-91.
Stroke in a scuba diver with patent foramen ovale.
Buttinelli C, Beccia M, Argentino C.
Dipartimento di Scienze Neurologiche, Universita degli Studi La Sapienza, viale dell'Universita no. 30, 00185 Rome, Italy.
Patent foramen ovale (PFO) is a frequent condition which carries a significant risk for stroke when associated with deep venous thrombosis and primary or secondary coagulation abnormalities. Here, we describe a patient in which scuba diving is thought to be associated with stroke in a subject with an otherwise clinically silent PFO.During a rapid ascent a 43-year-old-scuba diver reported weakness and paresthesias in the right arm which lasted about 10 min. He presented similar symptoms 2 days later 1 h after diving, and a third time on his flight back home.The MRI showed multiple hyperintense areas on T2-weighted images in the white matter. Transoesophageal echocardiography (TEE) showed a PFO, whilst all haematological and haemocoagulation tests were negative.Scuba diving may constitute a patho-physiological condition in the presence of PFO as breath-holding promotes right-to-left shunt and arterialization of venous bubbles.
Ann Intern Med. 2001 Jan 2;134(1):21-4.
Comment in: Ann Intern Med. 2001 Nov 20;135(10):928-9.
Ann Intern Med. 2001 Nov 20;135(10):928; author reply 929.
Relation between directly detected patent foramen ovale and ischemic brain lesions in sport divers.
Schwerzmann M, Seiler C, Lipp E, Guzman R, Lovblad KO, Kraus M, Kucher N.
Swiss Cardiovascular Center Bern and University Hospital.
BACKGROUND: In divers, the significance of a patent foramen ovale and its potential relation to paradoxical gas emboli remain uncertain. OBJECTIVE: To assess the prevalence of symptoms of decompression illness and ischemic brain lesions in divers with regard to the presence of a patent foramen ovale. DESIGN: Retrospective cohort study. SETTING: University hospital and three diving clubs in Switzerland. PARTICIPANTS: 52 sport divers and 52 nondiving controls. MEASUREMENTS: Prevalence of self-reported decompression events, patent foramen ovale on contrast transesophageal echocardiography, and ischemic brain lesions on magnetic resonance imaging. RESULTS: The risk for decompression illness events was 4.5-fold greater in divers with patent foramen ovale than in divers without patent foramen ovale (risk ratio, 4.5 [95% CI, 1.2 to 18.0]; P = 0.03). Among divers, 1.23 +/- 2.0 and 0.64 +/- 1.22 ischemic brain lesions per person (mean +/- SD) were detected in those with and those without patent foramen ovale, respectively. Among controls, 0.22 +/- 0.44 and 0.12 +/- 0.63 lesion per person were detected (P < 0.001 for all groups). CONCLUSIONS: Regardless of whether a diver has a patent foramen ovale, diving is associated with ischemic brain lesions.
Swiss Med Wkly. 2001 Jun 30;131(25-26):365-74.
Recreational scuba diving, patent foramen ovale and their associated risks.
Schwerzmann M, Seiler C.
Swiss Cardiovascular Center Bern, University Hospital, Inselspital, Bern, Switzerland. firstname.lastname@example.org
Scuba diving has become a popular leisure time activity with distinct risks to health owing to its physical characteristics. Knowledge of the behaviour of any mixture of breathable gases under increased ambient pressure is crucial for safe diving and gives clues as to the pathophysiology of compression or decompression related disorders. Immersion in cold water augments cardiac pre- and afterload due to an increase of intrathoracic blood volume and peripheral vasoconstriction. In very rare cases, the vasoconstrictor response can lead to pulmonary oedema. Immersion of the face in cold water is associated with bradycardia mediated by increased vagal tone. In icy water, the bradycardia can be so pronounced, that syncope results. For recreational dives, compressed air (i.e., 4 parts nitrogen and 1 part oxygen) is the preferred breathing gas. Its use is limited for diving to 40 to 50 m, otherwise nitrogen narcosis ("rapture of the deep") reduces a diver's cognitive function and increases the risk of inadequate reactions. At depths of 60 to 70 m oxygen toxicity impairs respiration and at higher partial pressures also functioning of the central nervous system. The use of special nitrogen-oxygen mixtures ("nitrox", 60% nitrogen and 40% oxygen as the typical example) decreases the probability of nitrogen narcosis and probably bubble formation, at the cost of increased risk of oxygen toxicity. Most of the health hazards during dives are consequences of changes in gas volume and formation of gas bubbles due to reduction of ambient pressure during a diver's ascent. The term barotrauma encompasses disorders related to over expansion of gas filled body cavities (mainly the lung and the inner ear). Decompression sickness results from the growth of gas nuclei in predominantly fatty tissue. Arterial gas embolism describes the penetration of such gas bubbles into the systemic circulation, either due to pulmonary barotrauma, transpulmonary passage after massive bubble formation ("chokes") or cardiac shunting. In recreational divers, neurological decompression events comprise 80% of reported cases of major decompression problems, most of the time due to pathological effects of intravascular bubbles. In divers with a history of major neurological decompression symptoms without evident cause, transoesophageal echocardiography must be performed to exclude a patent foramen ovale. If a cardiac right-to-left shunt is present, we advise divers with a history of severe decompression illness to stop diving. If they refuse to do so, it is crucial that they change their diving habits, minimising the amount of nitrogen load on the tissue. There is ongoing debate about the long term risk of scuba diving. Neuro-imaging studies revealed an increased frequency of ischaemic brain lesions in divers, which do not correlate well with subtle functional neurological deficits in experienced divers. In the light of the high prevalence of venous gas bubbles even after dives in shallow water and the presence of a cardiac right-to-left shunt in a quarter of the population (i.e., patent foramen ovale), arterialisation of gas bubbles might be more frequent than usually presumed.
Undersea Hyperb Med. 1998 Fall;25(3):175-8.
Comment in: Undersea Hyperb Med. 1999 Spring;26(1):49-50.
Risk of decompression sickness with patent foramen ovale.
Cardiology Section, Temple University Medical School, Philadelphia, Pennsylvania, USA.
Several reports have described populations of divers with decompression sickness (DCS) who have a patent foramen ovale (PFO). The presence of a PFO is known to occur in about 30% of the normal population, hence 30% of divers are likely to have a PFO. Although observations have been made on the presence of a PFO in divers with and without DCS, the risk of developing DCS when a diver has a PFO has not been determined. In this study, Logistic Regression and Bayes' theorem were used to calculate the risk of DCS from data of three studies that reported on echocardiographic analysis of PFO in a diving population, some of whom developed DCS. Overall incidence of DCS was obtained from the sport diving population, from the U.S. Navy diving population, and from a commercial population. The analysis indicates that the presence of a PFO produces a 2.5 time increase in the odds ratio for developing serious (type II) DCS in all three types of divers. Since the incidence of type II DCS in these three populations averages 2.28/10,000 dives, the risk of developing DCS in the presence of a PFO remains small, and does not warrant routine screening by echocardiography of sport, military, or commercial divers.
Undersea Hyperb Med. 1998 Fall;25(3):171-4.
Intrathoracic pressure changes after Valsalva strain and other maneuvers: implications for divers with patent foramen ovale. Balestra C, Germonpre P, Marroni A. Laboratory of General Biology, Universite Libre de Bruxelles, Belgium.
Scuba divers with patent foramen ovale (PFO) may be at risk for paradoxical nitrogen gas emboli when performing maneuvers that cause a rebound blood loading to the right atrium. We measured the rise and fall in intrathoracic pressure (ITP) during various maneuvers in 15 divers. The tests were standard isometric exercises (control), forceful coughing, knee bend (with and without respiration blocked), and Valsalva maneuver (maximal, gradually increased to reach control ITP, and as performed by divers to equalize middle ear pressure). All the maneuvers, as well as the downward slope of ITP at the release phase, were related to the control value. ITP levels were significantly higher than the standard isometric effort during a breath-hold knee bend (172%, P < 0.001), cough (133%, P < 0.05), and maximal Valsalva (136%, P < 0.05) whereas "usual" Valsalva maneuvers produced ITPs significantly lower than the standard (28%, P < 0.001). The downward slope of the pressure release curve was not significantly different among the different maneuvers (P < 0.1447). We conclude that maneuvers other than the usual divers' Valsalva are more likely to cause post-release central blood shift, both by the levels of ITP reached and by the time during which these ITPs are sustained. Divers (especially with PFO) should be advised to refrain from strenuous leg, arm, or abdominal exercise after decompression dives.
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