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1 Swiss Cardiovascular Center Bern, University of Bern, 3010 Bern, Switzerland; 2 Department of Internal Medicine, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland; 3 Laboratory of Cardiovascular and Respiratory Physiology, Erasme University Hospital, 1070 Brussels, Belgium; and 4 Medical Intensive Care Unit of the Department of Internal Medicine, University Hospital Zürich, 8091 Zürich, Switzerland
Exaggerated hypoxia-induced pulmonary hypertension is a hallmark of high-altitude pulmonary edema (HAPE) and plays a major role in its pathogenesis. Many studies of HAPE have estimated systolic pulmonary arterial pressure (SPAP) with Doppler echocardiography. Whereas at low altitude, Doppler echocardiographic estimation of SPAP correlates closely with its invasive measurement, no such evidence exists for estimations obtained at high altitude, where alterations of blood viscosity may invalidate the simplified Bernoulli equation. We measured SPAP by Doppler echocardiography and invasively in 14 mountaineers prone to HAPE and in 14 mountaineers resistant to this condition at 4,559 m. Mountaineers prone to HAPE had more pronounced pulmonary hypertension (57 ± 12 and 58 ± 10 mmHg for noninvasive and invasive determination, respectively; means ± SD) than subjects resistant to HAPE (37 ± 8 and 37 ± 6 mmHg, respectively), and the values measured in the two groups as a whole covered a wide range of pulmonary arterial pressures (30-83 mmHg). Spearman test showed a highly significant correlation (r = 0.89, P < 0.0001) between estimated and invasively measured SPAP values. The mean difference between invasively measured and Doppler-estimated SPAP was 0.5 ± 8 mmHg. At high altitude, estimation of SPAP by Doppler echocardiography is an accurate and reproducible method that correlates closely with its invasive measurement.
Doppler echocardiography; right heart catheterization; high-altitude pulmonary edema
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