Recreational scuba diving, patent foramen ovale and their associated risks

Scuba diving has become a popular leisure time activity with distinct risks to health owing to its physical characteristics. Knowledge of the behaviou r of any mixture of breathable gases under increased ambient pressure is cr ucial for safe diving and gives clues as to the pathopyhsiology of compress ion or decompression related disorders. Immersion in cold water augments cardiac pre- and afterload due to an incre ase of intrathoracic blood volume and peripheral vasoconstriction. In very rare cases, the vasoconstrictor response can lead to pulmonary oedema. Imme rsion of the face in cold water is associated with bradycardia mediated by increased vagal tone. In icy water, the bradycardia can be so pronounced, t hat syncope results. For recreational dives, compressed air (ie, 4 parts nitrogen and 1 part oxy gen) 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 dep ths of 60 to 70 m oxygen toxicity impairs respiration and at higher partial pressures also functioning of the central nervous system. The use of speci al nitrogen-oxygen mixtures ("nitrox", 60% nitrogen and 40% oxygen as the t ypical 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 du ring 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 predo minantly fatty tissue. Arterial gas embolism describes the penetration of s uch gas bubbles into the systemic circulation, either due to pulmonary baro trauma, transpulmonary passage after massive bubble formation ("chokes") or cardiac shunting. In recreational divers, neurological decompression events comprise 80% of r eported cases of major decompression problems, most of the time due to path ological effects of intravascular bubbles. In divers with a history of majo r neurological decompression symptoms without evident cause, transoesophage al 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-ima ging studies revealed an increased frequency of ischaemic brain lesions in divers, which do not correlate well with subtle functional neurological def icits 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 (ie, patent foramen ova le), arterialisation of gas bubbles might be more frequent than usually pre sumed.