Of Deep Waters and Thin Air

With reported incidences typically ≈1%,1 swimming-induced pulmonary edema (SIPE) is increasingly recognized as a not uncommon syndrome that is triggered by strenuous swimming and characterized by dyspnea, cough, and hemoptysis. Interestingly, SIPE shares common features with another form of pulmonary edema that is caused by strenuous exercise in an evolutionary nonphysiological habitat, namely high-altitude pulmonary edema (HAPE): Both SIPE and HAPE typically affect young healthy individuals, are triggered by strenuous exercise in a cold environment, resolve spontaneously after return to physiological conditions, yet will recur on reexposure in prone individuals.2,3 At the pathological level, edema fluid in both SIPE and HAPE patients contains considerable amounts of red blood cells and high-molecular-weight proteins in the absence of markedly elevated inflammatory markers.4,5 The pathophysiology of both diseases has long puzzled the field and hampered the development of effective counterstrategies, because their features tend to evade the traditional classification of pulmonary edema.Article, see p 988 The classic Starling equation defines net fluid flow J v across the capillary barrier as![Formula][1] where L p is hydraulic conductivity (a measure of water permeability), A is the barrier surface area, σπ is the oncotic reflection coefficient (a measure of the barrier´s resistance to protein movement), and Pc, Pi, Πc, and Πi are the hydrostatic (P) and oncotic (Π) pressures in the capillary (c) or interstitial (i) compartment, respectively. Accordingly, we differentiate between 2 classes of pulmonary edema, namely hydrostatic edema caused by increased driving pressure (increased ΔP or reduced ΔΠ), and permeability-type edema caused by high L p or low σπ and traditionally considered a result of infectious or sterile inflammation. The dilemma emerges because the lack of inflammatory markers in SIPE or early HAPE argues against a classic … [1]: /embed/graphic-1.gif