Scuba diving attracts more and more athletes … and less athletic.
However, it remains an activity at risk and if its practice is generally very well tolerated by the healthy heart, it is not necessarily the same for a cardiovascular system already tested.
Even if it is a sport without competition, the physical constraints are immediately present and the role of the training remains essentially technical.
Finally, the occurrence of a clinical failure in diving, even at shallow depth, can quickly become dramatic, such as a simple syncope that quickly evolves into a synonym for sudden death.
In this context, the cardiologist is more and more often confronted with demands from elderly subjects or perfectly maladjusted to the effort. The visit also occurs occasionally in emergency, the plane destined for heavenly waters being already retained for the day after tomorrow. Indeed, the medical certificate is sometimes considered by the diver as a mere formality, an opinion that does not share the doctor who fully engages his responsibility.
As in any sports practice, the aptitude visit must be complete before concluding a certificate of non-contraindication.
However, diving has some special features that must be taken into account.
Contrary to popular belief, scuba diving does not represent a simple health walk in the blue, with bottles on the back.Cardiovascular stresses are very present and sometimes unsuspected.
First of all, let us remember the physical effort inherent in any sporting practice and which can become very intense when diving conditions are unfavorable (cold, current, palmage efforts in a rough sea …) or in case of unforeseen events technical or physical incident in the palanque …). These efforts often occur in a context of high stress, which is an additional assault on the cardiovascular system.
Each candidate for scuba diving must therefore be able to develop a sustained physical effort.
Apart from these considerations, not surprising in sports medicine, scuba diving exposes to particular environmental constraints: immersion, cold, pressure, exposure to toxic gases and the gas embolism of the decompression .
All of them have cardiovascular consequences and we will outline the five main ones.
An increase in venous return:
It occurs as soon as it is launched, due to the redistribution of the blood mass that does not accumulate in the decline zones.
This redistribution of approximately 700 ml of blood recalls that of the decubitus and is accompanied by an increase in straight filling pressures (more than 15 mmHg) and cardiac output (about 20%) by placing of the phenomenon of Starling. This consequence is one of the factors which favors the occurrence of pulmonary edema.
The increase in cardiac work justifies that any symptomatic heart disease represents a definite contraindication to diving.
Moreover, the increase in the preload is accompanied by a secretion of atrial natriuretic factor, responsible for an increase in diuresis. Any diver is therefore a potential hypovolemic, with the consequences that this can represent in terms of blood hyperviscosity.
Peripheral and coronary vasoconstriction:
This effect is important and multifactorial.
It is initially related to immersion and its intensity is proportional to the temperature of the water. The immersion of the face is particularly important because of the large number of receptors in the trigeminal region, the stimulation of which leads to a “diving reflex”, where peripheral vasoconstriction predominates and the heart rate slows down.
Transient transient elevation is observed during immersion.
The partial pressure of O2:
The other important factor is the increase in the partial pressure of oxygen, which increases with the ambient pressure and thus with the depth.
If we recall that the pressure is reinforced by an atmosphere every 10 m, we understand that the PaO 2 doubles at 10 m depth and quadruple at 30 m. Beyond fifteen meters in air diving, the partial pressure of O 2 exceeds 0.3 atmosphere and it is considered that Man begins to be in a hyperoxic environment.
This hyperoxia, associated with cold, which also increases with depth, reinforces peripheral vasoconstriction and bradycardia. Oxygen is ultimately the most toxic gas for the cardiovascular system, due to the significant increase in post-charge it generates. At 5 atmospheres, it is responsible in the animal for a decrease in cardiac output and an increase in peripheral resistances in general and coronary resistances in particular. These effects have been found in humans from 2 atmospheres of oxygen.
Recall that a dive at 50 m in air represents an already high oxygen pressure at 1.26 atm.
Finally, the increase of the post-charge could be responsible for true hemodynamic decompensations, reproducible by the cold-hyperoxia association in some divers.
It is noteworthy that one study found that the majority of these divers, healthy up to that point, developed true arterial hypertension in their follow-up. Therefore, there appears to be a particular susceptibility to the hemodynamic consequences of diving in some subjects, in particular candidates with hypertension.
Hypertension is therefore considered a temporary contraindication until it is stabilized.
Finally, if vasoconstriction also concerns coronary arteries, it is reasonable to imagine that it is likely to favor a spasm or coronary flight phenomenon in patients with asymptomatic coronary artery disease. Very little work is available on this subject, little explored to date. However, it has been shown, for dummy dives at 30 m, an increase in peripheral resistances and a decrease in secondary cardiac output, not only at the slowing of the frequency but also at a decrease in the volume of systolic ejection.
This information demonstrates that hyperoxia, without consequence for short duration in the healthy subject, is perhaps not as innocuous in the atheromatous patient.
If coronary artery disease is of course a logical contraindication to diving, the “stable” coronary arises obviously a problem. In the United States, diving recovery is possible six months after a revascularization gesture, controlled by a maximum stress test without residual ischemia.
Immersion and cold:
As previously discussed, bradycardia depends initially on the immersion of the body, and in particular of the face, in a cold liquid. This is a direct effect of trigeminal receptor stimulation, which leads to a particularly intense vagal response. For this reason it is important to remember that the thermal conductivity of water is 25 times higher than that of air and that thermoneutrality is found only at temperatures of about 33 ° C, never the case in diving, even in the sunniest tropics. The cold is therefore a constant element to be taken into account.
This slowing of heart rate is, in a second step, reinforced by the direct effect of hyperoxia, which occurs with deep descent.
Moreover, it is traditional to consider that the pressure by itself favors the slowing of the heart rate, as has been demonstrated in vitro at 1500 m, on preparations of atrial tissue of several mammals. But under experimental conditions, this effect has never been objectified during experimental dives in humans, even for the deepest ones. The pressure per se, therefore, has in practice only negligible effects on the heart rate.
Nevertheless, bradycardia is real in diving and likely to favor the appearance of rhythm disorders dependent on the slowing of the heart rate.
This is why some bradycardiac molecules are not recommended in the diver, as ß-blockers are still currently contraindicated in the eyes of the French Federation of Underwater Studies and Sports (FFESSM). This attitude is probably to be qualified as we shall see again. In the same sense, and quite logically with respect to the syncopal risk, any notion of symptomatic or known rhythm disorder, as well as the prescription of an antiarrhythmic remain contraindications to diving.
Finally, the presence of a conduction disorder can be enhanced by the vagal hypertension of the dive and it is preferable to remain extremely cautious in this context. The presence of a pacemaker may not be a sufficient guarantee because they are not designed to withstand the pressure and the initial results of a study in progress in our center show that the deformations of boxes are frequent beyond 30 meters, but we will come back.
An alteration of the diastolic function:
This is an aspect that has not been approached until the last deep experimental dives. The principle is simple: the lower the depth, the more air that you breathe must be compressed since one must ventilate a gas whose pressure is identical to the ambient pressure. However, the density of the air increases with its compression, from about 1.15 g / l to about 7 g / l at 50 m. This increase in density has a direct effect on ventilatory work, which is multiplied by nearly 3.5 at this depth.
This generates heart-lung interactions, with effects that are similar to those observed in an asthma attack (such as the paradoxical pulse), and which indicate filling disorders associated with intra-thoracic pressure variations. These elements suggest that diving is not insignificant in terms of diastolic function.
The experimental data available in humans are rare, but they nevertheless show electrocardiographic modifications of the repolarization as a function of the density of the ventilated gases. Moreover, the only echocardiographic study carried out in deep-box divers at significant depths did not allow a significant alteration of the diastolic function to be detected at 350 m in Helium-Oxygen, ie for a gas density of approximately 7 g / l and therefore identical to that found at 50 m in air diving. This element is reassuring, but it concerns only 4 healthy and particularly trained subjects. These results can not be extrapolated to the whole diver and, in particular, to the hypertensive subject, confronted with the association of the post-load increase already described and an alteration of the diastolic function.
An increase in straight upward pressure:
Pulmonary gas embolism:
The ascent generates, in a quite physiological way, the appearance of bubbles in the venous circulation.
These are naturally eliminated by pulmonary route. This phenomenon, which is potentially responsible for an embolic accident in the event of a too rapid rise, remains almost without consequence during a slow ascent, respecting the decompression procedures.
However, in animals, there is tachycardia and increased right pulmonary and ventricular pressures in the aftermath of rapid decompression, due to pulmonary gas embolization of decompression.
Altered cardiac output:
This situation is liable to alter the cardiac output due to the discomfort of the left filling due to the phenomenon of ventricular interdependence. This pulmonary hypertension, which is perfectly tolerated in the healthy subject, can therefore be responsible for a sudden decompensation in a patient already suffering from chronic pulmonary hypertension or right heart failure.
All patients with pulmonary arterial hypertension or a right cardiac antecedent are therefore logically contraindicated for scuba diving.
The paradoxical embolism:
Moreover, the combination of venous bubbles and an increase in straight pressures can only favor the occurrence of a paradoxical embolism in case of shunt. This explains why the notion of heart disease with shunt is a definite contraindication to diving.
The permeable foramen ovale:
The case of the Foramen Ovale Permeable (FOP) is the subject of much controversy.
Indeed, if this particularity increases the risk of a decompression accident by a factor between 2.5 and 4.5 depending on the series, the probability remains sufficiently low (8 <10,000 dives) so that a screening policy system has not been deemed necessary to date. However, the occurrence of a decompression accident should cause a right-to-left shunt to be investigated and to counter the continuation of the dive in case of positivity.
In the present state of our knowledge, the establishment of a percutaneous device for the sole reason for pursuing recreational diving seems to us difficult to accept ethically and, in any case, totally incongruous in a based on solidarity.
Finally, in all cases it is useful to remind the divers that the ascent should be carried out according to the recommended procedures, but also that muscular efforts should be avoided and, in particular, those with abdomino-thoracic compression should be avoided. glottis, within two hours after a dive.
In summary, scuba diving is a definite constraint for the cardiovascular system with schematically:
– an increase in preload and post-load;
– predictable effects on diastolic function;
– a risk of sudden death in the event of rhythmic or conduction disturbance;
– embolic risk or right decompensation to the ascent.
The cardiological examination must therefore try to detect anomalies favoring these different risks.
Always fundamental, the interrogation must insist on any pathology potentially provoking malaise or heart failure.
As such, personal, but also family, histories are very informative
in terms of coronary artery disease or sudden death. Similarly, it is necessary to consider the pneumological, neurological, diabetic or ENT histological history which may represent temporary or definitive contraindications.
Arterial hypertension holds a special place, because of its frequency and its involvement in the pathology of diving.
Finally, as divers are willing to subscribe to the category of “living vouchers”, it is useful to insist on the various cardiovascular risk factors.
The interview must also take into account the diver’s motivations and technical skills, as the attitude will be different in the case of a diving candidate or experienced diver who is already heavily involved in this activity.
Finally, as we have seen, the treatment in progress may be of great importance in our decision.
Clinical examination and paraclinic:
* It must be strictly normal, any pathology is a priori a contraindication insofar as it would be symptomatic, including effort. A doubt must therefore prompt the use of the paraclinic.
* The voltage plug must not be neglected.
* The electrocardiogram remains of course fundamental. In addition to the problems of repolarization, he will seek to find a disturbance of rhythm or conduction, knowing that the block of the incomplete right branch, not necessarily pejorative, is not exceptional in the diver.
* Vagal maneuvers, seductive in a sport as vagotonic, are in fact little predictive of the conditions encountered in diving. The same goes for the traditional Ruffier-Dickson, which should not replace a good clinical examination and even less an effort test if it proves necessary.
* It would also seem reasonable to propose a routine exercise test in men over 40 years of age, or women aged 45 or 50 years, as well as echocardiography in all hypertensive patients severe or old.
To help us make our decisions, the FFESSM provides us with a list of cardiovascular contraindications to scuba diving.It is also on the back of the certificates of non-contraindication proposed by the Federation.
These cardiovascular contraindications are classified as “definitive” and “temporary”. This list is not exhaustive and can be commented on.
The concept of anticoagulant therapy, without being a contraindication per se, must be extremely careful because of the underlying pathology, which often represents a definite contraindication.
The presence of a pace-maker must, as has been pointed out, also render particularly circumspect and, in our opinion, a priori, to contradict diving. In addition to the risks of potential malfunctions linked to the pace, that of displacement of the probe due to the strains is not excluded. It therefore seems reasonable to forbid diving to a patient dependent on his pace and, in any case, to limit dives to 20 m for inveterate divers. The need for an anti-tachycardia device or a defibrillator in itself closes any discussion and represents a formal and definitive contradiction.
The contraindication associated with ß-blocking therapy may be a problem in hypertensive patients who are perfectly stabilized with their treatment and even more in the revascularized coronary artery and free from any ischemic anomaly during exercise at 6 months. This notion, rather French, deserves perhaps to be revisited in the era of the cardio-selective molecules, subject to a perfect pulmonary and hemodynamic tolerance to the effort.
Finally, in our opinion, the notion of a labyrinthine-type decompression accident justifies the same attitude as for that of a cerebral accident.
In this article, we have only discussed diving in the air, as dive techniques, derived from professional and military environments, are currently being developed using Nitrox sugars to reduce the nitrogen load, or containing helium (Trimix), to diminish the narcosis with nitrogen and thus open the way to greater depths.
Let us be pragmatic: apart from the asymptomatic FOP, where Nitrox diving can be discussed because it reduces the embolic risk, all these so-called “tech” (tek) dives are complex and do not provide any safety to our patients . It is in fact a semi-professional practice, intended for healthy and trained divers, supervised by people who must be perfectly trained in these specific techniques.
One might say that the role of the cardiologist is decisive for a certain number of cases, and that a good knowledge of the physiology of diving allows him to adopt the attitude most adapted to the situation.
Finally, it is useful to remind every “cardiac” diver some wise advice:
– gradual launching, especially in cold waters, in order to preserve the susceptibility of the post-load;
– avoid “physical” dives (current, cloudy water, prolonged palmage time …);
– avoid efforts, especially those with Valsalva, during the first two hours after exit;
– not to dive alone (it is obvious), but also to dive well accompanied: by people whose technical skills will allow them to help him if necessary;
– finally, advice to any diver, the “cardiac” as to others: do not dive if you do not feel in his “plate” …