VENTILATORY AND PULMONARY VASCULAR-RESPONSE TO HYPOXIA AND SUSCEPTIBILITY TO HIGH-ALTITUDE PULMONARY-EDEMA

Citation
E. Hohenhaus et al., VENTILATORY AND PULMONARY VASCULAR-RESPONSE TO HYPOXIA AND SUSCEPTIBILITY TO HIGH-ALTITUDE PULMONARY-EDEMA, The European respiratory journal, 8(11), 1995, pp. 1825-1833
Citations number
32
Categorie Soggetti
Respiratory System
ISSN journal
09031936
Volume
8
Issue
11
Year of publication
1995
Pages
1825 - 1833
Database
ISI
SICI code
0903-1936(1995)8:11<1825:VAPVTH>2.0.ZU;2-0
Abstract
Reduced tolerance to high altitude may be associated with a low ventil atory and an increased pulmonary vascular response to hypoxia We there fore, examined whether individuals susceptible to acute mountain sickn ess (AMS) or high altitude pulmonary oedema (HAPE) could be identified by noninvasive measurements of these parameters at low altitude. Vent ilatory response to hypoxia (HVR) and hypercapnia (HCVR) at rest and d uring exercise, as well as hypoxic pulmonary vascular response (HPVR) at rest, were examined in 30 mountaineers whose susceptibility was kno wn from previous identical exposures to high altitude. Isocapnic HVR e xpressed as difference in minute ventilation related to difference in arterial oxygen saturation (Delta V'E/Delta Sa,O2) (L-min(-1)/%) was s ignificantly lower in subjects susceptible to HAPE (mean+/-SEM 0.8+/-0 .1; n=10) compared to nonsusceptible controls (1.5+/-0.2; n=10), but w as not significantly different from subjects susceptible to AMS (1.2+/ -0.2; n=10), Hypercapnic ventilatory response was not significantly di fferent between the three groups, Discrimination between groups could not be improved by measurements of HVR during exercise (50% maximum ox ygen consumption (V'O-2,max)), or by assessing ventilation and oxygen saturation during a 15 min steady-state exercise (35% V'O-2,max) at fr actional inspiratory oxygen (FI,O-2) of 0.14, Pulmonary artery pressur e (Ppa) estimated by Doppler measurements of tricuspid valve pressure at an FI,O-2 of 0.21 and 0.12 (10 min) did not lead to a further discr imination between subjects susceptible to RARE and AMS with the except ion of three subjects susceptible to RAPE who showed an exaggerated HP VR. It is concluded that a low ventilatory response to hypoxia is asso ciated with an increased risk for high altitude pulmonary oedema, whil st susceptibility to acute mountain sickness may be associated with a high or low ventilatory response to hypoxia. A reliable discrimination between subjects susceptible to high altitude pulmonary oedema and ac ute mountain sickness with a low ventilatory response to hypoxia is no t possible by Doppler echocardiographic estimations of hypoxic pulmona ry vascular response.