Doppler Evaluation of Changing Cardiac Dynamics during Cheyne-Stokes Respiration: Conclusion
Although there is no obviously apparent physiologic reason for there to be a spontaneous cyclic variation of cardiac flow, it would seem unreasonable in the light of our inadequate understanding of the pathophysiology of Cheyne-Stokes respiration, to toally discount the cardiac events as being primary rather than secondary to the ventilatory cycle. Respiratory control is regulated by a chemostatic feedback system under the influence of three basic components. These are the respiratory chemoreceptors (controlling system), the arterial, venous and cerebrospinal fluid pH, Po2 and Pco2 (controlled system) and the “loop,” with an inherent time delay, being the circulation transferring information from the lungs to the brain. The controlling system regulates the amount of ventilation depending on the strengths of the various chemical stimuli. An alteration of either one or varying combinations of these components may upset respiratory control. Prolongation of the circulation time is probably the major factor responsible for Cheyne-Stokes respiration in patients with heart failure, although other factors affecting the gas tensions as well as respiratory center sensitivity may also be involved.- The cyclic reductions in cardiac output observed may be a consequence of disturbed left ventricular filling. Fluctuations in cerebral perfusion may follow alterations in cardiac output, and upset an already precariously balanced respiratory control system. Abnormal ventilatory patterns which are clinically manifested as Cheyne-Stokes respiration may occur as a result of this impaired respiratory control. other
This report highlights an obvious association between the respiratory cycle of Cheyne-Stokes respiration and a periodic alteration of cardiac function, characterized by variations in left ventricular filling pattern and left ventricular stroke volume. Although the study group consists predominantly of a heart failure patient population, the similar velocity changes observed in the patient with neurologic Cheyne-Stokes respiration and normal left ventricular function would suggest that, at the very least, there is a common pathophysiologic basis. We can only speculate on the association of respiratory and cardiac events and on the precise pathophysiology of Cheyne-Stokes respiration. Further hemodynamic evaluation of patients with Cheyne-Stokes respiration will yield valuable information and provide insight into the cardiac effects and/or pathophysiology of this important physical finding.