|Figure 1. X-rays showing patchy lung infiltrates, which rapidly resolve with descent to lower altitude (right) within 48 hrs2.|
...that rapid ascent to high altitude causes pulmonary edema in susceptible individuals?
In 1913, Thomas Ravenhill provided the first clinical description of high-altitude pulmonary edema (HAPE) in his landmark paper "Some experiences of mountain sickness in the Andes ." While serving as a medical officer in the mines of northern Chile at altitudes of 4,690-4,940 meters, Ravenhill's case reports described the patients' "slack and disinclined for exertion" shortly after arrival at high altitude from sea level, which progressed to cyanosis, acute dyspnea, air hunger and vomiting. He accurately describes "reduplication of the secondary heart sound," now known as a diagnostic indicator of pulmonary hypertension associated with alveolar hypoxia . When the patients returned to sea level, their condition rapidly resolved.
In the 1930s and ‘40s, several reports of HAPE emerged in the Spanish literature from studies in the Peruvian Andes not far from where Ravenhill had worked. HAPE would not be reported in the English literature again until 1960 when Charles Houston, an internist in Aspen, Colorado, reported a case of HAPE in the New England Journal of Medicine . Houston's most peculiar finding was that the patient's X-rays originally showed patchy infiltrates throughout the lung fields; however, two days later, the edema had resolved (Figure 1). He excluded pneumonia or cardiovascular disease as the cause of the edema and suggested a sum of three stresses brought on the condition: altitude, cold and heavy exertion. Houston confirmed Ravenhill's finding that descent promoted dramatic recovery. In the early 1960s, Fred  and Hultgren  independently performed hemodynamic studies on patients with acute high altitude pulmonary edema. These studies revealed that pulmonary hypertension, which responded to oxygen therapy, was associated with the patchy edema. This non-cardiogenic pulmonary hypertension was initially thought to be due to constriction of the pulmonary veins, but subsequent studies clearly demonstrated the vasoconstriction primarily occurs in pulmonary precapillary vessels in response to low oxygen tensions. Hultgren and Grover  proposed HAPE is due to non-uniform precapillary vasoconstriction, which redirects blood to unobstructed vessels. This regional over-perfusion induces high pressures within unobstructed portions of the pulmonary capillary bed, which in turn initiates a patchy hydrostatic edema.
Not everyone who rapidly ascends to high altitude is affected by HAPE . Susceptibility to HAPE is linked fto exaggerated hypoxia-induced vasoconstriction of the pulmonary circulation. Decreased bioavailability of vasodilators, such as nitric oxide, as well as an increase in vasoconstrictors, such as sympathetic activity and endothelin-1 release, contribute to the exaggerated hypoxic vasoconstriction. Certain risk factors increase an individual's susceptibility to HAPE, such as rapid ascent to an altitude greater than 2,500 meters, cold temperature, strenuous exercise, gender, age, recent or concurrent unrecognized underlying illness, congenital unilateral loss of pulmonary artery, and re-entry to altitude by high-altitude residents following a sojourn at a lower altitude . HAPE can be fatal if left untreated, but may be prevented by slow ascent. Rapid descent is the most important treatment method, while supplemental oxygen and vasodilators, such as nifedipine, may be used for immediate improvement to facilitate descent . Importantly, studies on HAPE have not only provided greater understanding of the disease itself, but have also provided insight into other pulmonary diseases associated with the lung's response to low oxygen tensions.
Author: Terrance Platt
Chief Editor: Sarah Sayner Ph.D., Jul. 2011
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