DESCRIPCIÓN DE LOS ALGORITMOS NO TRIVIALES A IMPLEMENTAR

Physicians should consider the conditions described in the following paragraphs when examining or treating breath-hold divers.

The pathophysiologic mechanisms of these conditions are described under Physiology of Breath-Hold Diving. It is also important to remember that there are forms of involun-tary breath holding, such as a person falling in water or the diver using an underwater breathing apparatus that suddenly malfunc-tions. Finally, some of the cardiovascular and respiratory physiology discussed earlier for breath holding at the surface may apply to the clinical situation in which a patient in acute respiratory failure (secondary, for example, to either an upper airway obstruc-tion or the use of neuromuscular blocking agents, commonly known as muscle relax-ants) cannot be adequately ventilated by the assisting physician or other medical personnel.

Cardiovascular Problems

Extreme levels of bradycardia have been reported during both simulated and actual breath-hold diving. In 1985, Arnold described R-R intervals as long as 10.8 sec, correspon-ding to a heart rate of 5.6 beats/min, induced by apneic face immersion in cold water⁸⁶; Ferrigno and associates²⁶recorded R-R inter-vals corresponding to heart rates of 8, 13, and 24 beats/min in three elite divers, respectively, during chamber dives to 55 m (180 ft) in cool water (Fig. 5–6). Heart rates as low as 20 to 24 beats/min were also recorded in the same three divers during ocean dives to 65 m (~213 ft).²⁹Interestingly, these divers reported no symptoms during these episodes of accentuated bradycardia, probably because the intense peripheral vasoconstriction of the diving response helped to maintain cerebral perfusion pres-sure during the prolonged diastolic periods.

A large number and variety of arrhythmias have been described in breath-hold divers³⁶; these rhythm disturbances are more fre-quent during dives in cold water³⁰and while the diver is at depth,²⁶and they are not only of the inhibitory type (to be expected from an increased vagal tone) but also include premature contractions (Fig. 5–7).²⁶ Despite the frequent arrhythmias recorded in three elite breath-hold divers during chamber dives to 55 m (180 ft) in cool water, these divers did not report any symptoms even during prolonged periods without any sinus beats (up to 45 sec; see Fig. 5–7), probably because many of the arrhythmic beats were hemodynamically effective.²⁶ The following

factors may contribute to the development of arrhythmias during diving:

• High vagal tone

• Distention of the heart from blood redis-tribution into the chest secondary to both immersion, particularly in cold water,¹² and to a drop in intrathoracic pressure during diving³¹

• Apneic face immersion in cold water⁸⁷

• Possible subendocardial ischemia⁸⁸from a large increase in blood pressure²⁶

In fact, as already described under Physiology of Breath-Hold Diving, arterial hypertension has been observed in breath-hold divers, with systolic values of approx-imately 300 mm Hg and diastolic values of approximately 200 mm Hg.²⁶

Arrhythmias and arterial hypertension appear to be rare in diving animals (P. Ponganis, personal communication), and they may represent maladaptations in human divers. These phenomena appear to be well tolerated by young and fit divers but may have more ominous consequences in older persons or in divers with preexisting cardiac disease. There is also the danger that the large intrathoracic blood pooling (more than 1.5 L of blood is redistributed from peripheral tissues into the heart and vessels in the chest during deep breath-hold dives)⁴⁹ that protects the diver from chest squeeze may cause rupture of pulmonary vessels and overdistention of the heart. In this regard, there are several anecdotal accounts of divers coughing up blood-tinged sputum after repetitive breath-hold dives to 30 m or more (L. Magno, personal communication).

Better documented is the case of an

unfortu-nate French diver who, after a series of dives to 25 m (82 ft) over 2 hours, experienced hemoptysis and died shortly thereafter.⁸⁹He had taken aspirin before diving, and he was found to have intraalveolar hemorrhage by radiography, bronchoscopy, and bron-choalveolar lavage.

Actually, even while a diver is swimming at the surface, approximately 700 mL of blood¹⁰ is already redistributed from the periphery into the chest. Cardiac diastolic filling may increase by 180 to 250 mL, and pulmonary capillary blood volume may increase by 51 to 200 mL.^90–93 These hemo-dynamic changes, which are enhanced by immersion in cold water, may contribute to pulmonary edema in swimmers and divers (see Chapter 25).^94–96 Typically, the symp-toms, including shortness of breath and coughing, resolve as soon as the diver gets out of water; symptoms may become more frequent with advanced age⁹⁷ and in swim-mers with subnormal baseline spirometry values.⁹⁸ Snorkeling between dives, allowing the chest to be submerged more deeply, results in a lower intrathoracic pressure, further increasing intrathoracic blood pool-ing and possibly contributpool-ing to deaths in elderly divers due to increased cardiac pre-and afterload or arrhythmias.^87,99

Problems in the Respiratory System

As mentioned before, immersion induces air trapping in the lungs; this phenome-non appears to be more pronounced in Figure 5–6.Electrocardiographic recordings in three

experienced breath-hold divers during chamber dives to 50 m (A and C) and 40 m (B) in 25°C water. (From Ferrigno M, Ferretti G, Ellis A, et al: Cardiovascular changes during deep breath-hold dives in a pressure chamber. J Appl Physiol 83:1282–1290, 1997.)

Figure 5–7.Relative occurrence of cardiac arrhythmias during submersed breath-hold dives to 40 and 50 m, performed by three experienced divers (EM, PM, RM) in a hyperbaric chamber. Measurements were averaged over 10-sec intervals. Arrhythmias were more frequent in cool (25°C) than in thermoneutral (35°C) water. EM, Enzo Maiorca; PM, Patrizia Maiorca; RM, Rossana Maiorca. (From Ferrigno M, Ferretti G, Ellis A, et al: Cardiovascular changes during deep breath-hold dives in a pressure chamber. J Appl Physiol 83:1282–1290, 1997.)

asthmatics, in whom reductions in pulmo-nary airflow have been observed during immersion after exercise.¹⁰⁰ Physicians should remember this phenomenon when evaluating divers with asthma. Pulmonary maneuvers, such as “buccal pumping” or

“lung packing,” are sometimes used by breath-hold divers to increase TLC and therefore the TLC/RV ratio at the beginning of a dive, potentially increasing the reach-able depth. These techniques consist of rapidly taking in mouthfuls of air after a maximal inhalation while performing maneu-vers similar to swallowing, which direct the additional air it into the lungs. By doing so, the divers can increase VC by up to about 40%,¹⁰¹ probably because blood is expelled out of the chest due to the increased inward recoil of the overexpanded chest and lungs.

In fact, the large increase in airway pressure resulting from these maneuvers could lead to lung rupture.¹⁰²These dangerous techniques can also cause substantial reductions in blood pressure and even fainting secondary to a decrease in venous return and, conse-quently, in cardiac output.¹⁰³

Although pulmonary barotrauma during ascent is typically a danger for divers who breathe a compressed gas underwater, this condition may affect a breath-hold diver, even though the total gas volume in the lungs at the end of a dive cannot be larger than the one present at the beginning of the dive.

What could happen in a breath-hold diver is that something would prevent escape of the expanding gas from one or more regions of the diver’s lungs during ascent, causing localized overdistention, rupture, and its clinical consequences, including pneumotho-rax, pneumomediastinum, and arterial gas embolism. Some cases of neurologic prob-lems and even death in breath-hold divers may have been caused by emboli secondary to pulmonary barotrauma of ascent.^104–106 Several mechanisms have been suggested for this condition. One possibility is related to very rapid ascents: Blood that had redistrib-uted into the pulmonary circulation during the descent may drain out of the pulmonary vessels more slowly than the rate at which alveolar air is expanding, causing blood engorgement of these vessels (L. Magno, per-sonal communication). This would lead to a decrease in lung compliance and an increase in airway closure,¹⁰⁷with the possibility that some regions of the diver’s lungs may not be able to safely accommodate the expanding

gas during ascent. Another possibility is related to differences in compliance between lung regions, particularly in divers with pre-existing lung disease or surgical scarring, causing tears in the lungs. Finally, as men-tioned earlier, lung-packing maneuvers or simply a very forceful inspiration could lead to lung rupture before the dive,¹⁰⁸making the diver more susceptible to pulmonary baro-trauma during ascent.

Neurologic Problems

Breath-hold divers can experience decreased levels or even loss of consciousness from hypoxia as a consequence of hyperventila-tion or hypoxia of ascent; when the diver is alone, this may lead to drowning. Craig¹⁰⁹ clearly explained the danger of a forceful hyperventilation when he cited 58 cases of loss of consciousness during underwater swimming. Spear fishermen face a similar danger,¹¹⁰ although loss of consciousness appears to be rare among Ama divers, who do not practice forceful hyperventilation.⁵⁶ As explained earlier, hypoxia of ascent results from the fall in alveolar PO₂ that is particularly rapid during the final part of ascent. At this dangerous time, there may be a paradoxical relief from air hunger due to expansion of the chest wall¹¹¹ and the con-comitant fall in alveolar PCO₂,⁴³ giving the diver a false sense of security.

Another condition that could lead to decreased levels of consciousness in breath-hold divers is CO₂ accumulation, which could occur if surface intervals between dives were very short in the absence of vig-orous hyperventilation. Paulev and Neraa described enough CO₂ retention to cause narcosis following a series of seven dives to 18.5 m (about 60 ft), separated by surface interval of only 1 to 2 min.¹¹² Linér and Linnarsson recommended surface intervals of at least 3 min between dives to avoid CO₂ accumulation.¹¹³

In 1965, Cross⁶⁴ suggested the possibility that repetitive breath-hold diving could cause decompression sickness: He described several neurologic symptoms, including partial or complete paralysis, vertigo, loss of consciousness, and even death, in pearl divers from the Tuamotu Archipelago, where these problems were called taravana (tara,

“to fall”; vana, “crazily”). These divers per-formed frequent dives to 100 fsw or more,

with bottom times of 30 to 60 sec, staying underwater for about a minute and a half;

they dived for about 6 hours a day with brief intervals between dives. In the same year, Paulev¹¹⁴ described similar neurologic prob-lems in four divers of the Danish Navy after repeated breath-hold dives to 15 to 20 m (49 to 65 ft); fortunately, these divers were successfully treated with recompression in a hyperbaric chamber. Theoretical calcula-tions by Lanphier indicated that enough nitrogen could be accumulated after repeated deep breath-hold dives separated by short surface intervals to cause decom-pression sickness.¹¹⁵ In fact, nitrogen accu-mulation with repetitive breath-hold diving has been described in venous blood of Korean female divers.¹¹⁶ A considerable amount of nitrogen can also accumulate during the course of a single deep breath-hold dive: In 1987, Olszowka¹¹⁷ calculated that an extra 700 mL of nitrogen would accu-mulate in the body of a diver after a single 220 sec dive to 90 m (295 ft).

Serious neurologic problems, including sensory, motor, visual, and speech distur-bances, have been reported more recently in breath-hold divers from Australia,¹¹⁸ Italy,¹¹⁹ Spain,^106,120 France,¹²¹ and Japan.^122,123 Fortu-nately, most of these neurologic problems either resolved spontaneously or were suc-cessfully treated with recompression. Some changes in diving techniques may have con-tributed to the reappearance of decompres-sion sickness among breath-hold divers: In the case of the Spanish divers, all of them had repeatedly dived to 40 m (131 ft) or more using electrically operated underwater scooters; in the case of the Ama divers from Japan, in whom decompression sickness was not a problem in the past,¹²⁴ the relatively recent introduction of wet suits has allowed longer daily diving sessions in recent decades. This new practice may be responsi-ble for the appearance of decompression sickness among the Amas,¹²⁵as confirmed by focal cerebral injuries detected with MRI in some Japanese divers.^122,126MRI presented a similar picture in a French diver¹²¹; the pos-sibility that emboli may be responsible for these lesions has been corroborated by detection of venous gas emboli with ultra-sound Doppler technique after repetitive breath-hold diving.^127,128

Neurologic problems suggestive of decom-pression sickness have also been reported in at least two cases of single deep breath-hold

dives.^106,119In one case, the diver was using a new and faster buoyancy device to ascend from about 120 m (almost 394 ft); his rate of ascent was about 4 m/sec (13 ft/sec) and, shortly after surfacing, he experienced paresthesias, quickly followed by right-sided hemiplegia.¹¹⁹ Fortunately, his symptoms resolved within about 30 min during recom-pression treatment. A possible explanation for these symptoms is bubble formation in the arterial blood during an extremely rapid ascent: In this situation, blood saturated with nitrogen at a given depth would reach the brain (and release bubbles) when the diver has arrived at a much shallower depth.⁴⁹Another possibility is that the diver suffered from a form of pulmonary baro-trauma leading to arterial gas embolism (see the earlier discussion, Problems in the Respiratory System).

Finally, even at depths at which scuba divers suffer from nitrogen narcosis, this condition does not appear to be a practical problem in deep breath-hold diving, proba-bly because exposure to high nitrogen pres-sures is very brief. It is also possible that nitrogen uptake is greatly reduced during a deep breath-hold dive because the alveolar area available for gas exchange is reduced by the extreme compression of the lungs at great depths.

Ear and Sinus Problems

Breath-hold divers may be particularly prone to ear and sinus barotrauma and related problems because of repeated exposures to rapid pressure changes, particularly at shal-lower depths. For a detailed discussion of these conditions, see Chapter 22.

CONCLUSIONS

Breath-hold diving to modest depths is a wonderful sport that can be done safely as long as divers understand the physiologic changes this activity produces and take appropriate precautions, such as limiting predive hyperventilation and never diving alone. On the other hand, deep breath-hold diving is much more dangerous, as demon-strated by the accidents involving spear fishermen and record divers as described under Clinical Aspects of Breath-Hold Diving.

Recently, a terrible accident claimed the young life of Audrey Mestre during her attempt to establish a new world depth record with totally assisted technique (also known as “no limit”).¹²⁹ This unfortunate event is a reminder of how dangerous this type of extreme breath-hold diving is and should lead to its abandonment.

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