All gas-filled spaces within the body are potentially subject to volume change as ambient pressure changes. For highly compliant organs such as those of gastrointestinal tract, the contraction and expansion of gases with descent and ascent are accommodated with ease. The lungs are less compliant, however, and if gas breathed at depth is not adequately vented during ascent, transmural pressure gradients sufficient to cause injury may result. This disorder is known as PBT of ascent.
The pathophysiology of PBT is complex and poorly understood. Injury appears dependent to some extent on both volume distension of lung tissue and development of a harmful transmural pressure gradient. Thus, not surprisingly, there is evidence that the degree of overpressure required to cause lung tissue injury depends on the extent to which the lung is splinted by its surrounding structures2. Experimentally, cadaver lungs have been shown to rupture with a positive inflation pressure of 70 mm Hg, but if the thorax is prevented from expanding (e.g. by thoracic binding), pressures up to 110 mm Hg are tolerated before rupture occurs. It seems that a distended lung is damaged by a lower transmural pressure, whereas a higher transmural pressure is required to cause injury when the lung is prevented from distending2. It is notable that a transmural pressure of 70 mm Hg, shown to be harmful in cadaver studies, can be generated by an ascent from only 1 metre if the lungs are near total lung capacity (TLC) before ascent.
It is also possible that lung ‘injuries’ that are benign, unnoticed and possibly frequent at the surface may be unmasked and clinically relevant in diving. Denison3 reported cases of pulmonary rupture occurring with deep inspiration and suggested that this may be an asymptomatic yet frequent event. In addition, he postulated that when the lungs are close to TLC, sneezing or coughing generates enough pressure to exceed the elastic limits of the lung, thus possibly resulting in damage. Although this damage may remain asymptomatic and go unreported at 1 ATA, the leakage of gas from the lung into the mediastinum or chest cavity and its subsequent expansion with ascent in a diver may be symptomatic or even life-threatening. Novice divers, because of inexperience with their equipment and the environment, tend to swim with lung volumes close to TLC. Skip breathing, a procedure used by many divers in an attempt to conserve air, is a voluntary reduction in breathing rate, but it is usually associated with close to maximal lung volumes. Both these situations, in which the lungs are held close to TLC, may predispose the individual to PBT.
Scarring within the lung parenchyma has long been considered to increase risk of PBT. However, Calder4 reported that the site of injury was inconsistently related to the site of the scar. This finding may be explained by differing compliance in the scar and surrounding tissue. If gas begins to expand in both sites, the more compliant healthy tissue will expand more, creating a shear stress between the two zones. This shear stress may result in an injury to the adjacent healthy tissue.
When alveoli rupture, the escaping gas can either enter any blood vessels that are injured simultaneously or escape into the lung interstitium. The former process will cause alveolar gas to enter the arterial circulation, commonly referred to as ‘arterial gas embolism’. Escape into the interstitium allows gas to track along the outside of the pulmonary airways and blood vessels toward the hilum of the lung where the pleura is discontinuous. Its subsequent escape into the mediastinum gives rise to mediastinal emphysema. From there, gas can track upward along the trachea to lie subcutaneously at the base of the neck, thus giving rise to ‘subcutaneous emphysema’. Finally, if there is rupture of alveoli adjacent to the visceral pleura, then gas may enter the pleural cavity and produce a pneumothorax (Figure 6.1).
These events may occur singly or in combination. In a Royal Navy series5 of 109 non-fatal cases of PBT submarine escape training accidents, the disorder in the majority of the cases was cerebral arterial gas embolus (CAGE). However, 15 divers with arterial gas emboli also had mediastinal emphysema, 7 with arterial gas embolism also had pneumothorax (3 bilateral, 4 unilateral), 4 had only mediastinal and cervical subcutaneous emphysema, and 1 had only unilateral pneumothorax.
The most feared (and probably the most common) of these events is arterial gas embolism. During overdistension of the lung, the capillaries and small vessels are stretched and may tear, along with other lung tissue. Because these vessels are small and often compressed by distended air sacs, air embolism may not result until overdistension is relieved by exhalation. Gas from ruptured alveoli is introduced to the pulmonary veins and carried back to the heart. Rarely, the volumes of gas are so great that the left ventricle can become air-locked and the diver will die instantly. More commonly, smaller and variable amounts of gas are entrained into the arterial circulation. The bubbles tend to distribute with flow; thus, those organs receiving a significant proportion of the cardiac output, particularly the brain, are likely to suffer the greatest exposure to bubbles. There is also some evidence that the distribution of bubbles in large blood vessels, particularly larger bubbles, can also be influenced by buoyancy. Therefore, in an upright diver (e.g. during ascent, when PBT is most likely to occur), larger bubbles tend to track around the roof of the aortic arch and are more likely to enter the vessels supplying the upper body and brain.
Passage of these bubbles through the circulation is interrupted by the systemic capillary beds. Bubble behaviour and effects at this point are largely influenced by their size. Bubbles that are large enough that their leading end occupies several generations of branching arterioles may stick and cause obstruction to flow. Smaller bubbles can redistribute through the microcirculation and thus cause minimal obstruction. Even larger bubbles redistribute in this way as the gas inside them is absorbed and they shrink. Clearly, however, even transient obstruction to flow in a tissue sensitive to hypoxia (e.g. the brain) may result in damage before bubble redistribution occurs. Loss of oxygen supply impairs neuronal ability to regulate intracellular ionic homeostasis because of breakdown in the sodium-potassium pump. Uncorrected inward leak of sodium is followed by cellular oedema and depolarization, the latter resulting in release of excitotoxins (e.g. glutamate) and a cascade of injurious events that may lead to early neuronal death or delayed apoptosis. The resulting cerebral dysfunction manifests most commonly as sudden-onset unconsciousness and/or multifocal stroke-like events (see later).
Even the redistribution of bubbles is not a benign event. Bubbles may cause endothelial disruption as they pass through small arterioles and capillaries, and white blood cells adhere to the damaged vessel walls. Their activation leads to release of inflammatory cytokines which can also cause tissue oedema and other forms of secondary damage. There is clear evidence from animal studies that shows a secondary decline in blood flow and neuronal function in cerebral tissue following redistribution of small aliquots of gas; this decline is caused by these processes and does not take place if the animal is depleted of white blood cells before the bubble exposure. This sort of inflammatory sequel to arterial gas embolism is thought to explain the frequent observation of initial improvement in early symptoms (which may reflect bubble redistribution) followed by a secondary deterioration (caused by the inflammatory events).
Secondary deterioration may also be caused by re-embolization by further bubbles that have been trapped in the pulmonary veins and heart chambers. Although there is little proof that this process is materially affected by postural changes, this possibility underpins the frequent advice to keep an apparent victim of arterial gas embolism in a supine position, even in the presence of apparent recovery, until the diver is seen at a hyperbaric chamber.
The understandable focus on cerebral effects of arterial gas embolism should not be allowed to obscure the potential for effects on other organs. It has already been suggested that large amounts of gas can cause early cardiac arrest by air locking the heart. It is also possible for bubbles to enter the coronary arteries and cause myocardial ischaemia and arrhythmias. The heart may also be affected indirectly by disturbance in function of the brainstem cardiovascular centres by cerebral arterial emboli. It is likely that many other tissues are affected by arterial bubbles without necessarily producing symptoms. For example, creatinine kinase levels (skeletal muscle fraction) and some liver enzymes are commonly elevated after arterial gas embolism, a finding suggesting that subclinical injury has occurred in these organs.