Source: Annual Congress 2002 - High altitude and hypoxia
Disease area: Pulmonary vascular diseases

Abstract

A number of authors have demonstrated a fall in forced vital capacity (FVC) on ascent to high altitude (HA) which has been suggested to be due to sub-clinical pulmonary edema. The etiology of this possible increase in extra vascular water remains obscure, although there is increasing evidence that high altitude pulmonary edema is of hydrostatic origin. Therefore the aim of the study was to investigate changes in forced vital capacity (FVC) in healthy subjects during adaptation to the HA of 3800m according to their pulmonary vascular reactivity. Twenty apparently healthy male lowlanders (mean age 21,1±]0,9 years) were studied. Pulmonary hemodynamics were assessed using two dimensional and Doppler echocardiography. All investigations were made at baseline before ascent to HA, during HA adaptation and after descent. According to the increase in their mean pulmonary artery pressure (MPAP) on ascent to HA all subjects were divided into two groups: hyperresponders (HR) (2 fold and more increase of MPAP compared to low altitude values, dMPAP>100%) and normoresponders (NR) (dMPAP<100%). Results are presented in the table. Thus, in healthy subjects with hypoxic pulmonary vascular hyperreactivity a tendency to more pronounced decrease in FVC is observed during high altitude adaptation.

	HR (n=9)	NR (n=11)	p
dMPAP (%)	123.9±]8.0	50.9±]0.2	0.001
dFVC (%)	8.2±]2.1	3.3±]2.2	0.05

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A. S. Sarybaev, B. Imanov, N. P. Mason, R. Naeije, F. du Toit, H. Le Roux, I. S. Sabirov, A. A. Aldashev, M. M. Mirrakhimov (Bishkek, Kyrgyzstan; Brussels, Belgium). Pulmonary vascular hyperresponses during acute induction to high altitude hypoxia are associated with more pronounced changes of forced vital capacity in healthy subjects. Eur Respir J 2002; 20: Suppl. 38, 698

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