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[Pathophysiology, prevention and therapy of altitude pulmonary edema].
Schweiz Med Wochenschr. 1992 Aug 04; 122(31-32):1151-8.SM

Abstract

Alveolar hypoxia and resulting tissue hypoxia initiates the pathophysiological sequence of high altitude pulmonary edema (HAPE). Very rapid ascent to high altitude without prior acclimatization results in HAPE, even in subjects with excellent tolerance to high altitude. Upon acute altitude exposure, HAPE-susceptible individuals react with increased secretion of norepinephrine, epinephrine, renin, angiotensin, aldosterone and atrial natriuretic peptide. In response to exercise at high altitude, subjects developing acute mountain sickness and HAPE secrete more aldosterone and antidiuretic hormone than subjects who remain well. This results in sodium and water retention, reduction of urine output, increase in body weight and development of peripheral edemas. The hypoxic pulmonary vascular response is enhanced in HAPE-susceptible subjects, thus favouring the development of severe pulmonary hypertension on exposure to high altitude. It has been postulated that uneven pulmonary vasoconstriction enhances filtration pressure in non-vasoconstricted lung areas, leading to interstitial and alveolar edema. The high protein content of the edema fluid in HAPE characterizes this edema as a permeability edema. The prophylactic administration of nifedipine prevents the exaggerated pulmonary hypertension of HAPE-susceptible subjects upon rapid ascent to 4559 m and thus prevents HAPE in most cases. This finding illustrates the crucial role of hypoxic pulmonary hypertension in the development of HAPE. The causal treatment of HAPE is descent, evacuation and administration of oxygen. Treatment of HAPE patients with nifedipine results in a reduction of pulmonary artery pressure, clinical improvement, increased oxygenation, decrease of the alveolar arterial oxygen gradient and progressive clearing of pulmonary edema on chest x-ray. Thus nifedipine offers a pharmacological tool for the treatment of HAPE.

Authors+Show Affiliations

Universitätsspital Zürich.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

ger

PubMed ID

1496342

Citation

Oelz, O, et al. "[Pathophysiology, Prevention and Therapy of Altitude Pulmonary Edema]." Schweizerische Medizinische Wochenschrift, vol. 122, no. 31-32, 1992, pp. 1151-8.
Oelz O, Maggiorini M, Ritter M, et al. [Pathophysiology, prevention and therapy of altitude pulmonary edema]. Schweiz Med Wochenschr. 1992;122(31-32):1151-8.
Oelz, O., Maggiorini, M., Ritter, M., Noti, C., Waber, U., Vock, P., & Bärtsch, P. (1992). [Pathophysiology, prevention and therapy of altitude pulmonary edema]. Schweizerische Medizinische Wochenschrift, 122(31-32), 1151-8.
Oelz O, et al. [Pathophysiology, Prevention and Therapy of Altitude Pulmonary Edema]. Schweiz Med Wochenschr. 1992 Aug 4;122(31-32):1151-8. PubMed PMID: 1496342.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Pathophysiology, prevention and therapy of altitude pulmonary edema]. AU - Oelz,O, AU - Maggiorini,M, AU - Ritter,M, AU - Noti,C, AU - Waber,U, AU - Vock,P, AU - Bärtsch,P, PY - 1992/8/4/pubmed PY - 1992/8/4/medline PY - 1992/8/4/entrez SP - 1151 EP - 8 JF - Schweizerische medizinische Wochenschrift JO - Schweiz Med Wochenschr VL - 122 IS - 31-32 N2 - Alveolar hypoxia and resulting tissue hypoxia initiates the pathophysiological sequence of high altitude pulmonary edema (HAPE). Very rapid ascent to high altitude without prior acclimatization results in HAPE, even in subjects with excellent tolerance to high altitude. Upon acute altitude exposure, HAPE-susceptible individuals react with increased secretion of norepinephrine, epinephrine, renin, angiotensin, aldosterone and atrial natriuretic peptide. In response to exercise at high altitude, subjects developing acute mountain sickness and HAPE secrete more aldosterone and antidiuretic hormone than subjects who remain well. This results in sodium and water retention, reduction of urine output, increase in body weight and development of peripheral edemas. The hypoxic pulmonary vascular response is enhanced in HAPE-susceptible subjects, thus favouring the development of severe pulmonary hypertension on exposure to high altitude. It has been postulated that uneven pulmonary vasoconstriction enhances filtration pressure in non-vasoconstricted lung areas, leading to interstitial and alveolar edema. The high protein content of the edema fluid in HAPE characterizes this edema as a permeability edema. The prophylactic administration of nifedipine prevents the exaggerated pulmonary hypertension of HAPE-susceptible subjects upon rapid ascent to 4559 m and thus prevents HAPE in most cases. This finding illustrates the crucial role of hypoxic pulmonary hypertension in the development of HAPE. The causal treatment of HAPE is descent, evacuation and administration of oxygen. Treatment of HAPE patients with nifedipine results in a reduction of pulmonary artery pressure, clinical improvement, increased oxygenation, decrease of the alveolar arterial oxygen gradient and progressive clearing of pulmonary edema on chest x-ray. Thus nifedipine offers a pharmacological tool for the treatment of HAPE. SN - 0036-7672 UR - https://www.unboundmedicine.com/medline/citation/1496342/[Pathophysiology_prevention_and_therapy_of_altitude_pulmonary_edema]_ L2 - http://www.diseaseinfosearch.org/result/2473 DB - PRIME DP - Unbound Medicine ER -