Schwerzmann, M., & Seiler, C. (2001). Recreational scuba diving, patent foramen ovale and their associated risks. Swiss medical weekly, 131(25-26), 365-374.

" 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 pathopyhsiology 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 (ie, 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 (ie, patent foramen ovale), arterialisation of gas bubbles might be more frequent than usually presumed".

" Diving operations are technically complex, and the underwater environment poses a high risk of fatal or near miss accidents. Divers are exposed to increased ambient pressure, variable depths up to >150 m of sea water, sea states from calm to several metres high waves, gale force winds, currents and a wide range of temperatures. Short-term adverse cardiovascular effects of diving in humans have been shown [1], but there are no studies on the long-term effects.

Increased ambient pressure is associated with negative effects on endothelial function, possibly due to exposure to hyperoxia and the formation of vascular bubbles. In sea dives, this effect could be increased by the physiological stress of immersion [1]. Immersion alone leads to central blood pooling and increased cardiac preload, aggravated by cold water [2], an effect seen in humans at only 1–2°C below normal core temperature. This might explain the mechanism of pulmonary oedema in some ‘self-contained underwater breathing apparatus’ (SCUBA) divers [3].

Our results underline the importance of a dive-free day after strenuous diving and avoiding strenuous diving. We could not conclude from our findings whether symptoms and diseases reported by divers were due to diving per se or strenuous physical work. In exercise physiology, there is a hypothesis that excessive endurance exercise training can induce adverse cardiovascular effects in some individuals [20]. Other studies show no protection against, or even a higher risk of cardiovascular disease after strenuous physical work [21,22]. About 30% of athletes develop acute dilation of right-side cardiac chambers and right ventricle and ventricular septum dysfunction following a marathon. These cardiac changes restore in the post-race period. However, one hypothesis is that the risk of sudden cardiac death in extreme endurance athletes is related to repeated stretching of cardiac chambers, and some athletes might be prone to more chronic structural changes [23]. One can speculate that since the professional divers experience recurrent stretching of cardiovascular dimensions due to the effect of immersion, some of them might be prone to more chronic effects of these dimensional and structural changes of the heart. However, as far as we know, this has not been investigated and remains to be explored. Although diving is considered a physical activity, the symptoms and diseases reported by divers in this study could also be life-style related. We can only speculate on the mechanisms of our findings.

Further research into diving as a risk factor for cardiovascular disease is needed. It might be useful to study the time of onset of cardiovascular disease in former divers. Understanding the mechanisms of the cardiovascular effects of diving also requires further research"( Åsmul, K., Irgens, Å., Grønning, M., & Møllerløkken, A. (2017). Diving and long-term cardiovascular health. Occupational Medicine, 67(5), 371-376. )

Torti, S. R., Billinger, M., Schwerzmann, M., Vogel, R., Zbinden, R., Windecker, S., & Seiler, C. (2004). Risk of decompression illness among 230 divers in relation to the presence and size of patent foramen ovale. European heart journal, 25(12), 1014-1020.

Nazia,

Thank you for your response.

If we for a while go back to the question (instead of deep sea diving), we are talking of a right-to-left shunt due to rise in pressure in the right cardiac atrium in a person on land not performing any such extraordinary activities.

Thank you.

I also clarify my question further: will deep-sea-diving induce rise in right cardiac atrial pressure ALONE? Or raise the pressure of both cardiac atria? Will deep-sea- diving generate a right-to-left shunt shunt at the level of the cardiac atria?

This is a most fundamental issue.