Doppler Assessment of Pulmonary Hypertension Induced by Hypoxic Breathing in Subjects Susceptible to High Altitude Pulmonary Edema

Abstract

To verify the abnormal pulmonary vascular response implicated in the pathogenesis of high altitude pulmonary edema (HAPE), we examined the hemodynamic responses to hypoxia in HAPE-susceptible subjects (HAPE-S) by means of both right heart catheterization and pulsed Doppler echocardiography. The HAPE-S were seven men and one woman with a history of HAPE. Six healthy volunteers who had repeated experiences of mountain climbing without any history of altitude-related problems served as control subjects. The HAPE-S showed much greater increase in pulmonary vascular resistance (PVR) than did the control subjects, resulting in a much higher level of pulmonary arterial pressure (Ppa) under acute hypoxia both of 15% O2 and 10% O2. We then evaluated the usefulness of pulsed Doppler echocardiography in the prediction of pulmonary hypertension. Acceleration time (AcT) and right ventricular ejection time (RVET) were measured from the flow velocity pattern in the right ventricular outflow tract. The ratio of AcT to RVET was correlated to invasively determined mean Ppa (Ppa) and PVR. The results were as follows: (1) AcT/RVET = 0.52 to 0.0047 (Ppa), r = -0.93, SEE = 0.017, p less than 0.001 (HAPE-S); (2) AcT/RVET = 0.55 to 0.0055 (Ppa), r = -0.70, SEE = 0.030, p less than 0.001 (HAPE-S); (4) AcT/RVET = 0.52 to 0.00077 (PVR), r = -0.91, SEE = 0.016, p less than 0.001 (control subjects). We conclude that HAPE-S have a constitutional abnormality in the pulmonary vascular response to hypoxia, which is a possible causative factor of HAPE, and that pulsed Doppler echocardiography may be supportive to assess the pulmonary vascular pressor response in the HAPE-S.

Identification of individuals susceptible to high-altitude pulmonary oedema at low altitude

“…PASP measurements during hypoxic exposure showed a significantly greater increase in HAPE-susceptible subjects consistent with previous studies in which PASP was obtained either by echocardiography [7,21,22] or by right-heart catheterisation [5,6,9,15]. However, in a previous study with a similar design, there was a large overlap between HAPEsusceptible and nonsusceptible subjects in PASP during hypoxia [8].…”

“…The current upper limit of normal values (PASP 41 mmHg) agrees well with a study establishing normal values in a large number of subjects when one considers that these investigators assumed the right atrial pressure to be 10 mmHg [20]. Furthermore, the current measurements are in agreement with other studies assessing PASP at rest and during exercise [20][21][22][23][24].…”

“…These values are almost identical to the cut-off values used in a previous study [7], which were based on the upper limit of normal values reported in the literature for exercise in normoxia [23,24] or hypoxic exposure [21]. These results suggest that the limit of normal pulmonary vascular response for normoxic exercise and for acute exposure to hypoxia equivalent to an altitude of 4,500 m is ,40 mmHg for systolic PASP.…”

Acute Hypoxic Pulmonary Vascular Response Does Not Accompany Plasma Endothelin-1 Elevation in Subjects Susceptible to High Altitude Pulmonary Edema.

“…Wefound a small but significant difference in AcT/RVETafter hypoxic exposure between HAPE-S and control subjects, which was consistent with our previous results (1 , 5). Wepreviously evaluated the pulmonary vascular response to hypoxia in HAPE-Sby using right heart catheterization and echocardiogram, and found that AcT/RVETwas a good index to evaluate the pulmonary artery pressure (1,5). According to Tramarin et al (10) and Chan et al (1 1), tricuspid regurgitation velocity obtained by echocardiogram demonstrates the highest correlation with meanpulmonary artery pressure (r=0.72).…”

“…As previously shown, pulsed Doppler echocardiography is a useful method to evaluate pulmonary artery pressure noninvasively (5). In the present study, we investigated the difference in pulmonary vascular response to acute hypoxia between HAPE-S and control subjects by using pulsed Doppler echocardiography, and we also measured the plasma ET-1 levels before and after hypoxic exposure, in order to evaluate the role of ET-1 in the acute hypoxic pulmonary vascular response in HAPE-S.…”