High altitude pulmonary edema in the Karakorums

Seventy nine subjects who were acclimatised to a height of 7000 feet [average duration 4Ll months] were investigated. Out of these 12 were control subjects [Group 1] and 67 were those who had developed high altitude pulmonary oedema [Group 2]. Both groups were investigated at Rawalpindi [1500 feet] within three weeks of their arrival. Clinical examination, chest X-ray, ECG, 2D echocardiogram, haematological tests and pulmonary functions were normal. On exercise testing the blood pressure response was exaggerated in Group 2 compared to Group 1 [P <0.01]. Cardiac catheterisation [performed in 7 subjects in Group 1 and 22 subjects in Group 2] revealed no difference in the resting intracardiac pressures. With cold pressor test the pulmonary artery and aortic pressures rose significantly in Group 2 as compared to Group 1[P <0.01 for both pulmonary artery and aortic pressure]. Repeat exercise testing and right heart catheterisation [performed in 5 subjects in Group 1 and 12 subjects in Group 2] 10-12 weeks after the arrival to Rawalpindi showed similar blood pressure and pulmonary artery pressures. It is concluded therefore that [a] pulmonary and systemic vascular beds are hyperrespoasive to exercise and cold in susceptible subjects and [b] the effect of acclimatisation vanish in 10-12 weeks in the susceptible group

High altitude pulmonary oedema - response to exercise and cold on systemic and pulmonary vascular beds

Fourteen subjects who were acclimatised to a height of 7000 feet [average duration 3 +/- months] were investigated. Five were normal subjects [Group I] and 9 were those who developed high altitude pulmonary oedema [Group 2]. At the National Institute of Heart Diseases, Rawalpindi, clinical examination, chest X-ray, electrocardiogram, haematological tests, thyroid functions, echocardiography and lung function tests were normal. During exercise testing the blood pressure response was exaggerated in Group 2 compared to Group 1 [P < 0.01]. Cardiac catheterisation revealed no significant difference in the intracardiac pressures in the resting state in the two groups [P = NS]. With cold pressor test the pulmonary pressure and aortic pressure rose significantly in Group 2 as compared to Group 1 [P < 0.01]. It is suggested, therefore, that pulmonary and systemic vascular beds are hyper-responsive to cold in the susceptible subjects [Group 2]. This phenomenon may be further aggravated by exertion, hypoxia, and other undetermined factors in producing pulmonary oedema