Chest ACCP Member Benefits
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Maze, S.
Right arrow Articles by Parry, W.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Maze, S.
Right arrow Articles by Parry, W.

Chest, Vol 95, 525-529, Copyright © 1989 by American College of Chest Physicians


ARTICLES

Doppler evaluation of changing cardiac dynamics during Cheyne-Stokes respiration

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.


This article has been cited by other articles:


Home page
ChestHome page
P. Solin, D. M. Kaye, P. J. Little, P. Bergin, M. Richardson, and M. T. Naughton
Impact of Sleep Apnea on Sympathetic Nervous System Activity in Heart Failure
Chest, April 1, 2003; 123(4): 1119 - 1126.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
G. D. Pinna, R. Maestri, A. Mortara, and M. T. L. Rovere
Cardiorespiratory interactions during periodic breathing in awake chronic heart failure patients
Am J Physiol Heart Circ Physiol, March 1, 2000; 278(3): H932 - H941.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
D. P. Francis, L. C. Davies, M. Piepoli, M. Rauchhaus, P. Ponikowski, and A. J. S. Coats
Origin of Oscillatory Kinetics of Respiratory Gas Exchange in Chronic Heart Failure
Circulation, September 7, 1999; 100(10): 1065 - 1070.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1989 by the American College of Chest Physicians.