We thoroughly enjoyed the review of pulmonary edema associated with scuba diving by Slade et al, in the November issue of CHEST.1As they mentioned, capillary stress failure appears to be central to the pathophysiology of this disorder as well as of other disorders, like high-altitude pulmonary edema. This topic is of great interest to us at the Naval Medical Center San Diego, where > 20 cases per year of pulmonary edema associated with surface swimming are evaluated. Generally, this condition occurs in special forces combat swimmers during intense training. Recently, three combat swimmers between the ages of 22 years and 28 years, without previous medical problems, simultaneously presented with unilateral radiographic findings of pulmonary edema. These patients were participating in a two-mile surface swim in 17°C ocean water. All were wearing 5-mm-thick neoprene wet suits that fit comfortably, all denied aspiration, and all complained of severe dyspnea and a nonproductive cough. Varying degrees of hypoxemia, tachypnea, and unilateral crackles (two right-sided and one left-sided) were observed. Radiographic findings included unilateral Kerley-B lines, cephalization, airspace consolidation, and normal cardiac size. Treatment consisted of supplemental oxygen and inhaled β-agonists. In each patient, hypoxemia resolved within 12 h, and results of chest radiographs normalized in 24 to 48 h. Navy combat swimmers swim primarily in a lateral decubitus position to allow constant eye contact with a partner and to maintain a low surface profile in the water. The dependent submersed lung was the radiographically affected lung in each of our three patients. We believe that increased central vascular volume associated with immersion,2–3 along with elevation of pulmonary vascular resistance4and regional differences in perfusion secondary to the forces of gravity and high cardiac output,5–6 exposed regional capillaries to relatively high pressures. We believe that unilateral pulmonary edema, as observed in these combat swimmers, reflected global and regional pulmonary vascular changes that led to stress failure of the capillary bed.