Abnormal left ventricular (LV) diastolic function has frequently been reported in patients with chronic obstructive pulmonary disease (COPD). In the present work, diastolic function was studied by a combined analysis of pulmonary venous and mitral blood flow velocities in 34 patients with COPD clinically stable and without history of heart disease, and 20 control subjects. We confirmed the increased contribution of the atrial contraction to the LV filling in COPD patients in comparison with control subjects; furthermore, a decreased left atrial (LA) filling during the ventricular systole was observed. Changes in LV filling were not the consequence of a systolic dysfunction, because LV systolic function was normal. Doppler indices indicated that LA pressure was below 15 cm H(2)O in all the patients with COPD and control subjects. Several factors can be put forward to explain these changes; the first one is tachycardia. In addition to hypoxemia and medications, echocardiography suggested that a decreased LV preload participated in increased heart rate. Analysis of Doppler transmitral and pulmonary venous flows demonstrated the role of the ventricular interdependence because a correlation existed between LA and LV filling pattern and right ventricle pressure and diameter.

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 (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. 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.

In the present study, we observed the haemodynamic changes, using echocardiography and Doppler, in ten healthy volunteers during 6 h of compression in a hyperbaric chamber with a protocol designed to reproduce the conditions as near as possible to a real dive. Ambient pressure varied from 1.6 to 3 atm (1 atm=101.325 kPa) and partial pressure of inspired O2 from 1.2 to 2.8 atm. Subjects performed periods of exercise with breathing through a closed-circuit self-contained underwater breathing apparatus (SCUBA). Subjects did not eat or drink during the study. Examinations were performed after 15 min and 5 h. After 15 min, stroke volume (SV), left atrial (LA) diameter and left ventricular (LV) end-diastolic diameter (LVEDD) decreased. Heart rate (HR) and cardiac output (CO) did not vary, but indices of the LV systolic performance decreased by 10% and the LV meridional wall stress increased by 17%. After 5 h, although weight decreased, the serum protein concentration increased. Compared with values obtained after 15 min, SV and CO decreased, but LV systolic performance, LA diameter, LVEDD and LV meridional wall stress remained unchanged. Compared with the reference values obtained at sea level, total arterial compliance decreased, HR remained unchanged and CO decreased. In conclusion, hyperbaric hyperoxia results in significant haemodynamic changes. Initially, hyperoxia and the SCUBA system are responsible for reducing LV preload, increasing LV afterload and decreasing LV systolic performance, although CO did not change. Prolonged exposure resulted in a further decrease in LV preload, because of dehydration, and in a further increase in LV afterload, due to systemic vasoconstriction, with the consequence of decreasing CO.