The significance of clinical characteristics such as Sao2, pulse rate, chest radiography, and pulmonary artery systolic pressure (PASP) between HAPE and high-altitude cerebral edema (HACE) was highlighted by Ghulam Mohammad, senior physician at SNM Hospital (G. Mohammad, personal communication). The relevance of Sao2 has long been established,12,46 and the patients were reported to have lower Sao2; interestingly, however, the latter inversely correlated with pulse rate more severely in HAPE (Fig 5). Because of its significance, Sao2 has been studied in relation to the ACE I/D polymorphism.30,47 Pulmonary hypertension is a necessary but insufficient feature to explain HAPE, and some drugs with vasodilator potential have efficacy in HAPE.48‐50 Although the PASP and severity of edema relate proportionately, a rise in PASP at HA does not necessarily mean that the patient has HAPE.48 The augmentation of PASP in HAPE corresponds to a dramatic fall in Sao2. Surprisingly, the older the patient, the higher the PASP, and HAPE occasionally is complicated by pulmonary thromboembolism, which further elevates pulmonary artery pressure. In some patients with HAPE, chest pain mimicking angina pectoris develops and then subsides as the PASP returns to normal. Unless taken in context of other abnormalities, HAPE can be confused with pneumonia, myocardial infarction, and pulmonary embolism. Elevated PASP alone is insufficient as a diagnosis, and chest radiographs may not be sensitive enough to detect it. These observations offer a rationale for further studies on the role of PASP in the pathophysiology of HAPE and in the differential diagnosis of HA respiratory symptoms. In distinction to HAPE, PASP is normal in HACE in this region, which is in agreement with earlier reports.51,52 Rarely do patients with HACE have a fall in Sao2 by > 50% without the anticipated rise in PASP, which is expected once Sao2 falls to < 60%.