Am. J. Respir. Crit. Care Med., Volume 161, Number 1, January 2000, 264-270

Operation Everest III (Comex '97): Modifications of Cardiac Function Secondary to Altitude-induced Hypoxia
An Echocardiographic and Doppler Study

ALAIN BOUSSUGES, FLORENCE MOLENAT, HENRI BURNET, EMMANUEL CAUCHY, BERNARD GARDETTE, JEAN-MARIE SAINTY, YVES JAMMES, and JEAN-PAUL RICHALET

Service de Réanimation Médicale et Hyperbarie, CHU Salvator, Marseille, France; CNRS, Laboratoire de Neurobiologie et Mouvement, Marseille, France; Département de Médecine de Montagne et de Traumatologie, Hôpital de Chamonix, France; COMEX SA, Marseille, France; Laboratoire de Physiopathologie Respiratoire et Intégrée, Faculté de Médecine Nord, Marseille, France; and Association pour la Recherche en Physiologie de l'Environnement (ARPE), UFR Médecine Bobigny, Bobigny, France

During Operation Everest III (Comex '97), to assess the consequences of altitude-induced hypoxia, eight volunteers were decompressed in a hypobaric chamber, with a decompression profile simulating the climb of Mount Everest. Cardiac function was assessed using a combination of M-mode and two-dimensional echocardiography, with continuous and pulsed Doppler at 5,000, 7,000, and 8,000 m as well as 2 d after return to sea level (RSL). On simulated ascent to altitude, aortic and left atrial diameters, left ventricular (LV) diameters, and right ventricular (RV) end-systolic diameter fell regularly. Heart rate (HR) increased at all altitudes accompanied by a decrease in stroke volume; in total, cardiac output () remained unchanged. LV filling was assessed on transmitral and pulmonary venous flow profiles. Mitral peak E velocity decreased, peak A velocity increased, and E/A ratio decreased. Pulmonary venous flow velocities showed a decreased peak D velocity, a decreased peak S velocity, and a reduction of the D/S ratio. Systolic pulmonary arterial pressure (Ppa) showed a progressive and constant increase, as seen on the elevation of the right ventricular/right atrial (RV/RA) gradient pressure from 19.0 ± 2.4 mm Hg at sea level up to 40.1 ± 3.3 mm Hg at 8,000 m (p < 0.05), and remained elevated 2 d after recompression to sea level (SL) (not significant). In conclusion, this study confirmed the elevation of pulmonary pressures and the preservation of LV contractility secondary to altitude-induced hypoxia. It demonstrated a modification of the LV filling pattern, with a decreased early filling and a greater contribution of the atrial contraction, without elevation of LV end-diastolic pressure. Boussuges A, Molenat F, Burnet H, Cauchy E, Gardette B, Sainty J-M, Jammes Y, Richalet J-P. Operation Everest III (Comex '97): modifications of cardiac function secondary to altitude-induced hypoxia. An echocardiographic and Doppler study.

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