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
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.