Pulmonary edema does/does not occur in human athletes performing heavy sea-level exercise

PULMONARY EDEMA DURING BREATH-HOLD DIVING IMMERSION TO THE EDITOR: It has been demonstrated several years ago that the strength of the alveolar-capillary membrane is high and that the stress failure of the wall may occur when the pulmonary capillary pressure is raised to abnormal levels as it may happen during heavy exercise. If this stimulus is associated with changes on thoracic geometry and modifications of lung gas volume, the final result is the increase in the transpulmonary pressure, which acts on the alveolar-capillary wall with the common consensus on these issues (1, 5). One model accounting entirely for this scenario is breath-hold diving. During breath-hold immersion it is common to have decrease in thoracic elasticity, increase in the airway resistance, severe reduction of inspired gas volume to the value of residual volume, increase in the pulmonary capillary pressure due to increase in pulmonary capillary blood volume. All these factors contribute to mechanically stimulate the alveolar-capillary barrier to its progressive weakness to the breaking point with the dramatic consequences of shortness of breath, cough productive of blood tinged and/or pink frothy sputum, crepitations on auscultation, and chest radiograph findings of pulmonary edema. A recent observation study on pulmonary diffusion capacity following sea diving up to 30-m depths got results compatible with the occurrence of pulmonary injury in 16% of our breath-hold diver population. This proportion could be even higher if one considers that the increase in pulmonary capillary blood volume, consistently observed early in the post-diving period, can mask short-lived alterations at the level of the alveolar-endothelial membrane.