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Chest, Vol 95, 525-529, Copyright © 1989 by American College of Chest Physicians
ARTICLES |
SS Maze, MN Kotler and WR Parry
Division of Cardiovascular Disease, Albert Einstein Medical Center, Temple University School of Medicine, Philadelphia 19141.
For the purpose of elucidating the mechanisms and/or effects of the cardiovascular changes occurring during Cheyne-Stokes respiration, we utilized Doppler echocardiography to determine intracardiac flow velocity profiles during the changing phases. Left ventricular inflow (LVI) and outflow (LVO) were examined in ten patients, nine with heart failure and one with a cerebrovascular accident. The mean LVI, peak early (E) and late diastolic (A) and LVO velocities were measured at the end of both the hyperpneic and apneic phases. The phasic hemodynamic changes observed during Cheyne-Stokes respiration by Doppler profile could be explained by the development of LV diastolic dysfunction and a decrease in LV stroke volume during the apneic phase of Cheyne-Stokes respiration. Alternatively, an increase in PCO2 during the apneic phase may increase pulmonary vascular resistance lowering preload and stroke volume, whereas during the hyperpneic phase, pulmonary vascular resistance is reduced with resultant increase in left ventricular preload and increase in stroke volume. Both theories are speculative and the precise hemodynamic changes associated with Cheyne-Stokes respiration requires further investigation.
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