Operation Everest III (Comex '97): Modifications of cardiac function secondary to altitude-induced hypoxia - An echocardiographic and Doppler study

During Operation Everest III (Comex '97), to assess the consequences of alt itude-induced hypoxia, eight volunteers were decompressed in a hypobaric ch amber, with a decompression profile simulating the climb of Mount Everest. Cardiac function was assessed using a combination of M-mode and two-dimensi onal 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 as cent to altitude, aortic and left atrial diameters, left ventricular (LV) d iameters, and right ventricular (RV) end-systolic diameter fell regularly. Heart rate (HR) increased at all altitudes accompanied by a decrease in str oke volume; in total, cardiac output (Q) 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. Pul monary venous flow velocities showed a decreased peak D velocity, a decreas ed peak S velocity, and a reduction of the D/S ratio. Systolic pulmonary ar terial pressure (Ppa) showed a progressive and constant increase, as seen o n the elevation of the right ventricular/right atrial (RV/RA) gradient pres sure 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 a trial contraction, without elevation of LV end-diastolic pressure.