Page 1852 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 132: Diving Medicine and Drowning 1321

destruction, and release of inflammatory mediators. These events are decompression in divers during and after decompression. As in clinical
contributory, but their exact roles in DCS pathogenesis have not been settings, intravenous gas may be clinically silent, but VGE tend to cause
determined. injury in four situations: (1) obstruction of the heart or major vessels
If many bubbles are released into the venous system during decom- by gas, (2) arterialization of bubbles across the pulmonary vasculature,
pression, the pulmonary circulation may become obstructed, causing (3) arterialization of bubbles across a PFO, and (4) physical denatur-
the chokes. Chokes is characterized by sore throat, cough, chest pain, and ation of the blood by air. When venous gas bubbles enter the arterial
shortness of breath. This syndrome may lead to cardiovascular collapse system, even a small amount of gas can produce substantial morbidity
and death. Some bubbles may also cross-pulmonary capillaries as small or death. 15,16
gas emboli or pass into the arterial circulation through right-to-left The human lung is an effective filter for VGE larger than about 20 µm
cardiac shunts, for example, patent foramen ovale (PFO). Although in diameter ; this size barrier is not absolute because bubbles of 500 µm
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PFO is present in about 20% of normal individuals, its presence gener- may spillover through the pulmonary circulation as demonstrated
ally leads to more severe rather than more frequent episodes of DCS. 13 in experimental animals. The VGE crossover rate and passage size
15
The symptoms of chokes develop minutes to hours after decompres- increases in the setting of a large difference between pulmonary arte-
sion, and may be progressive. Physical examination reveals tachypnea, rial and pulmonary venous pressures. Pulmonary arterioles constrict in
tachycardia, crackles, wheezing, cyanosis, and gasping in severe response to VGE and pulmonary arterial pressure increases. As more
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cases. The chest radiograph may show diffuse pulmonary opacities VGE mechanically obstruct the vasculature, the gradient of pulmonary
similar to acute respiratory distress syndrome (ARDS). Should bubbles arterial versus venous pressure increases, thereby decreasing the filtering
pass into the arterial circulation, neurologic findings may appear, effectiveness of the pulmonary capillaries and allowing VGE to pass.
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primarily involving cerebral symptoms and signs. Arterial blood-gas The presence of anatomic intrapulmonary shunting also decreases the
determinations often show hypoxemia and respiratory alkalosis. filtering efficiency of the lungs.
■ PULMONARY BAROTRAUMA VGE disburse across a PFO into the arterial system. Detection of PFO
Paradoxical gas embolism may occur in divers (as in patients) when
Pulmonary barotrauma of ascent, also known as pulmonary overpressur- by echocardiography relies on gas microbubbles for ultrasonic contrast.
ization, is a potentially serious consequence of failure of expanding gas Right-to-left atrial crossover of these bubbles is variable and may require
in the lung to escape from alveoli. Overstretching of lung regions may Valsalva or other special maneuver to increase right atrial pressure.
rupture acini or alveoli and cause pulmonary interstitial emphysema. Bubble crossover also may occur spontaneously during some phases
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Disruption of the pulmonary parenchyma may cause mediastinal or of the cardiac cycle. The probability of paradoxical gas embolism
soft tissue emphysema, pneumopericardium, pneumothorax, or arterial increases in divers who have a resting PFO or who perform a Valsalva
gas emboli (AGE). Pulmonary overinflation occurs during ascent while during ascent or develop pulmonary hypertension and vascular obstruc-
diving with compressed breathing gases. It is most likely to occur with tion from overwhelming VGE. 8
breath-holding, loss of consciousness underwater, or airway obstruction VGE also become physiologically significant when a large quantity
that traps gas. Rarely, pulmonary over inflation may occur after explo- of gas obstructs major vessels of the pulmonary vasculature or the
sive decompression of aircraft at altitude. heart. In the heart, gas that obstructs the inflow and outflow of blood
Lung rupture during ascent also depends on physiologic factors such diminishes the cardiac output. In addition to obstructing the pulmonary
as pulmonary compliance, transpulmonary pressure, and lung volume. vasculature, venous gas triggers pulmonary arterial constriction, bron-
Airway closure and air trapping induced by immersion in the upright chospasm, dyspnea, and acute lung injury. 22
position may increase the risk of lung overstretching during ascent. If Physical interactions at the blood-bubble interface complicate
14
alveolar pressure becomes positive by about 100 cm H O relative to that mechanical obstruction of the circulation and amplify the physiologic
2
at the mouth, the lung will rupture. During breath-holding at total lung effects of small volumes of intravenous gas. The blood-bubble interface
capacity (TLC), the difference between alveolar and ambient pressure is stimulates biochemical events associated with release of multiple inflam-
approximately 50 cm H O. Thus, hydrostatic pressure outside the body matory mediators with subsequent damage to the vascular endothelium.
2
during ascent must decrease another 50 cm H O for the lung to rupture. Noncardiogenic pulmonary edema may develop quickly as extravasated
2
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Assuming a compliance of the lung and chest wall at a TLC of 15 mL/cm fluid floods alveoli and may progress to ARDS. Scuba divers have long
H O, lung volume during ascent must increase by 15 mL × 50 cm H O, recognized a similar sequence of events as the syndrome of chokes. 23
2
2
or 750 mL, before the lung ruptures. Using Boyle’s law (see Table 132-1), AGE in diving may occur from VGE that cross into the arterial circu-
an approximate depth can be determined from which a diver must lation or by gas entering the left heart after pulmonary overpressuriza-
ascend for pulmonary rupture during a breath-hold at TLC. At the tion. The occurrence of AGE by the latter mechanism may be associated
surface, P = 1.0 ATA; suppose the rupture volume V = 7000 mL. Then, with the entry of large amounts of gas into the pulmonary circulation,
1
1
the maximum allowed volume at depth V = 7000 − 750, or 6250 mL. and this disorder is second to drowning as the leading cause of fatal
2
The corresponding pressure is found as accidents. Indeed, the most common source of AGE in divers is pulmo-
nary barotrauma. Similar events may occur in patients who suffer direct
(1.0)(7000 mL) = P2(6250 mL) (132-2) pulmonary trauma, such as penetrating chest wounds, or after misad-
and ventures with transthoracic or transbronchial biopsies, or in patients on
mechanical ventilation who require high airway pressures. Pulmonary
P = (1.0)(7000/6250) = 1.12 ATA, or 4.0 ft (132-3)
2 over-distention may or may not produce other evidence of barotrauma
This calculation illustrates why pulmonary overinflation and AGE such as pneumothorax, pneumomediastinum, or pneumopericardium.
occur in shallow water during rapid ascent with full lungs. It also Intravascular gas is not reliably detected by brain CT or MRI, and the
indicates that relative volume changes are greatest at low hydrostatic diagnosis is suggested by the clinical setting and signs of end-organ
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pressures. damage, primarily brain or cardiac ischemia. Therefore, procedures to
document the presence of air should not delay the treatment of a criti-
VENOUS AND ARTERIAL GAS EMBOLISM cally ill patient unless there is a strong suspicion of a nondiving related
etiology such as cerebral hemorrhage. 8
Most intensive care specialists are familiar with venous gas emboli Like VGE, AGE obstruct, induce vasoconstriction, activate coagula-
(VGE), which occurs in a variety of clinical settings, often introduced by tion, complement, and neutrophils and aggregate platelets. This leads to
iatrogenic means, and not infrequently leading to serious consequences release of mediators of inflammation that activate and may subsequently
(see Chap. 39). However, VGE are also commonly detected during damage vascular endothelium. Even a minor episode of AGE has the

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