Breath-hold diving allows many recreational swimmers to explore shallow areas of clear water. Even in a swimming pool the duration of a dive depends on the elapsed time until Paco2 reaches a level that stimulates inhalation (Chap. 11). Duration also depends on a diver's TLC and RV. Trained breath-hold divers typically hyperventilate before submerging, employing a VT that is nearly equal to vital capacity. After 10 seconds of such deep hyperventilation, Paco2 can decline by 15-20 mm Hg while putting perhaps a liter of O2 within the alveoli. With practice, as much as 650 mL of this O2 can be consumed before Pao2 declines and Paco2 rises sufficiently to stimulate breathing. There are risks to such hyperventilation before a breath-hold dive. First, reducing Paco2 by hyperventilation causes alkalosis with unpredictable systemic consequences. Second, a rapid decline in Paco2 reduces cerebral blood flow and can elicit vertigo or loss of consciousness even before the dive begins. With practice, breath-hold diving probably adjusts chemoreceptor sensitivity to tolerate alkalosis as well as a higher Paco2, a lower pHa and Pao2, or a higher [lactate] before breathing is stimulated.
Such respiratory system adaptations are common among marine mammals, and are augmented by a fully developed diving reflex (Chap. 39) that induces not just apnea but an abrupt bradycardia and profound vasoconstriction to all tissues except heart and brain. Some have suggested that respiration among Japan's Ama pearl divers has acclimatized or adapted to the daily repetitive dives that this population has performed over many centuries. However, more objective evidence indicates that these individuals rely instead on accrued cultural knowledge of how to economize energy expenditures during such dives. From a very young age, the Ama are taught to grasp a heavy rock to descend with less effort, to plug their nares and ear canals hands-free with balls of waxed fibers, and to coat their skin with animal fat that retards heat loss. The Ama also employ mostly shallow water dives, rarely to depths of more than 20 m and never approaching the impressively deep and prolonged dives of seals and whales.
Snorkeling with face mask and breathing tube facilitates diving farther from shore, but physiologically it resembles breath-hold diving. Some inventive practitioners of the sport have attempted to use a longer snorkeling tube, reasoning that they could submerge to greater depths for longer times. Unfortunately this logic fails for several reasons. First, inflating the lungs is more difficult at greater depth because of the increased trans-thoracic pressure exerted on the chest wall by the water (Table 13.3). The lungs, airways, and even the snorkel tube are prone to collapse as water depth increases. Second, adding airway resistance in the form of a longer "trachea" increases the work of breathing (Chap. 6). Third, a tube increases "anatomical" dead space, remembering that VD is already ~2 mL/kg at the surface (Chap. 4). Thus, insufficient fresh air would enter the lungs through a long snorkel tube unless a subject's VT is very large, and that would require enormous effort to expand the chest against the water pressure.
Table 13.3Effect of water depth on pressure exerted on adjacent gas volumes ||Download (.pdf) Table 13.3 Effect of water depth on pressure exerted on adjacent gas volumes
|Water Depth ||Barometric Pressure ||PIo2 ||PIn2 ||Lung Volume |
|(m) ||(ft) ||(atm) ||(mm Hg) ||(mm Hg) ||(mm Hg) ||(mL) |
|0 ||0 ||1 ||760 ||150 ||600 ||6,000 |
|10 ||33 ||2 ||1,520 ||300 ||1,200 ||3,000 |
|20 ||66 ||3 ||2,280 ||450 ||1,800 ||2,000 |
|30 ||99 ||4 ||3,040 ||600 ||2,400 ||1,500 |
|40 ||132 ||5 ||3,800 ||750 ||3,000 ||1,200 |
|50 ||165 ||6 ||4,560 ||900 ||3,600 ||1,000 |
|60 ||198 ||7 ||5,320 ||1,050 ||4,200 ||857 |
|180 ||594 ||19 ||14,440 ||2,850 ||11,400 ||316 |
During submersion, gas pressures within any body cavities must continually equalize with the surrounding external hydrostatic pressure to prevent barotrauma. Air trapped within a nasal sinus or the middle ear by inflammation and mucus can create tissue injury and pain when compressed, even at shallow depths. Indeed, patients afflicted with poorly drained sinuses experience pain even with small changes in ambient pressure, like those felt in an airplane or elevator, or with approaching weather fronts. Fortunately for swimmers, the normally compliant chest wall allows for at least partial equilibration during submersion, compressing the air that is within the lungs when the dive begins (Table 13.3). Then as the breath-holding diver ascends toward the surface, air within lung spaces re-expands to its original volume, minus O2 that was absorbed and displaced only with highly soluble CO2. Not unexpectedly, many marine mammals tolerate extremely long and deep dives precisely because their entire respiratory system (including the trachea) readily accommodates compression by external water pressure.
A self-contained underwater breathing apparatus (scuba) permits much longer submersions and to greater water depths, but such gear creates new problems for the lungs and chest. As reviewed in Chap. 1, Boyle's law specifies that the volume of a gas varies inversely with its pressure. Water exerts one atmosphere of pressure (1 atm = 760 mm Hg ≅ 14.2 lbs/inch2) for every 10 m of depth. The effects of these laws on actual lung volume during deep breath-hold diving are impressive (Table 13.3). For example, the lungs of a diver who inhales 5 L at the surface contain only 2.5 L of gas at a depth of 10 m, as lungs and trachea are compressed by water surrounding the thorax.
The challenges faced by the lungs of a scuba diver are complex. First, as they prepare for descent, air from their storage tank enters the face mask at a regulated manifold "head" pressure that only slightly exceeds the 1 atm of PB at sea level. With descent this regulated manifold pressure must increase to prevent collapse of the mask against the face by the same water weight that would collapse the diver's chest, trachea, and lungs. Breathing in this manner resembles the use of continuous positive airway pressure (CPAP) masks to treat obstructive sleep apnea (Chap. 25) or intubation to apply positive end-expiratory pressure (PEEP) during mechanical ventilation (Chap. 30). Both strategies provide an air stent that maintains airway patency, albeit at much lower values of PAW than would develop during scuba diving. The student should also recall the negative effect that high airway pressures have on alveolar blood flow (Chap. 7). At a moderate diving depth of 40 m (132 ft), the regulated manifold pressure must be at least 5 atm in order to stent the mask, airways, and thorax open (Table 13.3).
The manifold pressure at this dive depth presents the lungs with an effective PIo2 of 750 mm Hg, equivalent to breathing pure O2 at the surface. Prolonged exposure to such a high PIo2 causes hyperoxic lung injury of the type that critical care physicians try to avoid by reducing a patient's FIo2 in the ICU to the lowest value consistent with good oxygenation (Chap. 28). During ascent, a scuba diver who has maintained nearly sea-level lung volumes while under water by breathing pressurized air must stop inhaling and continuously exhale to expel the expanding gas in their lungs. Surfacing too quickly to allow pressure equilibration through the mouth and nose may rupture lung tissues and airways due to the force of gas re-expansion.
More subtle than this effect of scuba breathing on the gas-containing spaces within the lungs is the dissolution during the dive of inhaled air into body tissues, notably as O2 and N2 diffuse down their potentially enormous partial pressure gradients (Table 13.3). Because of its relatively low aqueous solubility, N2 may continue to dissolve in tissues throughout a dive's duration. Thus, ascent after prolonged dives can cause decompression sickness (or the bends), as dissolved tissue N2 coalesces into bubbles throughout the body. Such bubbles continue to merge and enlarge as they enter the vascular system, where the risks of air emboli and tissue infarctions are high (Chap. 27). Decompression sickness is most commonly reported today among inexperienced divers. However, it also can occur in persons working underwater beneath an inverted bell (caisson) that is continuously ventilated with sufficient amounts of pressurized air to exclude water (Fig. 13.3). Indeed, decompression sickness was first identified in the medical literature as caisson disease for this reason.
Schematic of a pneumatic caisson as used for underwater ship repair or construction of a bridge pier or dam. The internal air pressure needed to exclude water and keep a dry environment depends upon its working depth.
The potential severity of decompression sickness is such that scuba divers use depth tables and dive computers to limit both their time under pressure and their ascent speed. The effects of too rapid decompression range from joint pain and rashes to paralysis and death. When feasible, decompression sickness is treated by hyperbaric oxygen therapy in a hyperbaric chamber to maximize the partial pressure gradient that favors N2 excretion. If treated early, there is a significantly greater likelihood of minimizing permanent injury. Mild interstitial edema is common in the respiratory parenchyma of decompression victims but it usually resolves within 2-3 hours of surfacing. Spirometric lung volumes and DLCO have been reported to be normal within the same recovery period after dives to 65 m in depth that lasted 60-80 minutes.
CLINICAL CORRELATION 13.2
Nitrogen narcosis (also termed inert gas narcosis, raptures of the deep, Martini effect) is a reversible alteration in mental status that occurs while scuba diving at depth. This narcosis resembles alcohol intoxication or nitrous oxide inhalation, but impairment is not usually noticeable above 30 m (100 ft). The most dangerous aspects of nitrogen narcosis are impaired decision-making ability, loss of focus, poor judgment, failure at multi-tasking, and reduced musculoskeletal coordination. Affected divers complain of vertigo, exhaustion, and tingling or numbness of the lips, mouth and fingers, while their dive companions note exhilaration, giddiness, extreme anxiety, depression, or paranoia. While narcosis affects all divers, predicting the depth when impairment becomes serious is difficult; susceptibility varies from dive to dive and among individuals. The condition is reversed by ascent and appears to have no long-term effects.
Diving beyond 40 m (130 ft) is considered non-recreational, and carries very substantial risks for nitrogen narcosis, oxygen toxicity, and decompression sickness. Such deep dives require specialized gas manifold regulators, advanced conditioning and training, and comprehensive dive management by a medically qualified team at the surface. One important aspect of such specialist training is the use of various gas mixtures such as heliox that consist of O2 blended with inert gases like helium instead of N2 to reduce the total amount of dissolved gases in the tissues.