Lung injury related to extreme environments

Hydrostatic lung injuries

The evolution of fish to amphibians, reptiles to endothermic birds and mammals has been accompanied by a progressively thinner pulmonary blood gas barrier, to accommodate the constraint of increased oxygen uptake and carbon dioxide output [1]. Accordingly, pulmonary circulation has evolved as a separate high flow–low pressure system. In humans, mean pulmonary artery pressures (PAP) are 8–20 mmHg, pulmonary wedge pressures are 5–14 mmHg and pulmonary capillary pressures are 8–12 mmHg [2]. A low-pressure regimen preserves the integrity of an alveolar capillary membrane only 0.3 μm thick. However, this structure is vulnerable to increased pressures during strenuous exercise or environmental hypoxic exposure as a cause of stress failure of the pulmonary capillaries and accumulation of extravascular lung water [3]. Reports of lung injury related to extremes of exercise and variations in ambient pressure and altitude confirm this vulnerability. The resulting lung injury takes the form of noncardiogenic pulmonary oedema.

The occurrence of noncardiogenic pulmonary oedema and pulmonary haemorrhage has been described in relation to a variety of disorders related to auto- and exogenous immunological reactions, infections and certain inhalants. However, numerous reports of lung injury manifesting as pulmonary oedema with associated haemorrhage have been described more recently in relation to immersion underwater, swimming, extreme exercise and exposure to altitude. In addition, pulmonary oedema resulting from negative intra-alveolar pressure has been described in the anaesthesia literature and may play a role in exercise- and immersion-induced pulmonary oedema.

Haemodynamically induced pulmonary oedema

A single mechanism responsible for production of noncardiogenic pulmonary oedema related to immersion, altitude and exercise has not …