Cheyne-Stokes Respiration

BackgroundPrevious studies showing a strong relationship between Cheyne-Stokes respiration and the severity of left ventricular systolic dysfunction have usually been done in selected patient populations with lower age and a higher proportion of males than the "typical" in-hospital patient with heart failure. The purpose of the present study was test the strength of this relationship in unselected patients admitted to hospital due to decompensated chronic heart failure.MethodsWe evaluated 191 patients (32% women), mean age 73 years, ready for discharge from the heart failure unit in the University Hospital of Malmo, Sweden. The patients underwent echocardiography for determination of left ventricular ejection fraction and left ventricular inner diastolic diameter. A respiratory investigation during sleep was performed the last night before discharge.ResultsWe found that 66% of the patients had Cheyne-Stokes respiration more than 10% of the total recording time. Only 7 (3.6%) of the patients had predominantly obstructive apnoeas. There was a significant but very weak relationship between left ventricular ejection fraction and left ventricular inner diastolic diameter on one hand and Cheyne-Stokes respiration on the other. Age was a stronger determinant of Cheyne-Stokes respiration than any of the cardiac or other clinical variables.ConclusionAlthough presence of Cheyne-Stokes respiration indicates left ventricular dysfunction, its severity seems only weakly related to the severity of heart failure. Age was found to be a stronger determinant, which may reflect the underlying age-dependency found also in healthy subjects. Due to age restrictions or other selection criteria, the importance of age may have been underestimated in many previous studies on factors associated with Cheyne-Stokes respiration.

In adults with heart failure, central sleep apnea (CSA), often manifested as Cheyne-Stokes respiration, is common, and has been associated with adverse outcome. Heart failure in children is commonly caused by dilated cardiomyopathy (DCM). It is unknown whether children with heart failure secondary to DCM have CSA, and whether CSA is related to the severity of heart failure. In this prospective observational study, 37 patients (<18 year) with heart failure secondary to DCM were included. They underwent polysomnography, clinical and laboratory evaluation and echocardiographic assessment. After a median follow-up time of 2 years, eight patients underwent heart transplantation. CSA (apnea-hypopnea index [AHI] ≥1) was found in 19 % of the patients. AHI ranged from 1.2 to 4.5/h. The occurrence of CSA was not related to the severity of heart failure. Three older patients showed a breathing pattern mimicking Cheyne-Stokes respiration, two of whom required heart transplantation. CSA was found in 19 % of the children with heart failure secondary to DCM. No relation was found with the severity of heart failure. In a small subset of children with severe DCM, a pattern mimicking Cheyne-Stokes respiration was registered.

BackgroundEchocardiography plays an integral role in the diagnosis of congestive heart failure including measurement of left heart pressure as well as mechanical dyssynchrony.MethodsIn this report we describe novel therapeutic uses of echo pulsed wave Doppler in atrioventricular pacemaker optimization in patients who had either not derived significant symptomatic benefit post biventricular pacemaker implantation or deteriorated after deriving initial benefit. In these patients atrioventricular optimization showed novel findings and improved cardiac output and symptoms.ResultsIn 3 patients with Cheyne Stokes pattern of respiration echo Doppler showed worsening of mitral regurgitation during hyperpneac phase in one patient, marked E and A fusion in another patient and exaggerated ventricular interdependence in a third patient thus highlighting mechanisms of adverse effects of Cheyne Stokes respiration in patients with heart failure. All 3 patients required a very short atrioventricular delay programming for best cardiac output. In one patient with recurrent congestive heart failure post cardiac resynchronization, mitral inflow pulse wave Doppler showed no A wave until a sensed atrioventricular delay of 190 ms was reached and showed progressive improvement in mitral inflow pattern until an atrioventricular delay of 290 ms. In 2 patients atrioventricular delay as short as 50 ms was required to allow E and A separation and prevent diastolic mitral regurgitation. All patients developed marked improvement in congestive heart failure symptoms post echo-guided biv pacemaker optimization.ConclusionThese findings highlight the value of echo-guided pacemaker optimization in symptomatic patients post cardiac resynchronization treatment.

Cheyne-Stokes respiration (CSR), a rhythmic rise and fall in ventilation often experienced by patients with heart failure during sleep, is typically accompanied by an oscillation in heart rate (HR) at the same frequency. The mechanisms responsible for this oscillation are still debated. In this study, we used the experimental model of the transient hypoxia test (i.e., a laboratory test that mimics the transient nature of the cyclic desaturations that occur during hyperpnoeic phases of CSR) to assess accurately the temporal relationship between the HR response to transient hypoxia and the tidal volume response in six heart failure patients. The same relationship was assessed during CSR using polysomnographic signals. We hypothesized that this relationship would provide important insights into the key mechanisms contributing to the HR response. During transient hypoxia, HR started to increase around the onset of tidal volume increase but continued to increase after the peak of the latter had been reached. The time delay between the two peaks (HR vs. tidal volume) was 7.9 ± 4.8 s. The same delay during hyperpnoeic phases of CSR was 1.0 ± 0.9 s. In addition, the increases in lung volume were much greater than those found in the laboratory tests. Based on the known dynamics of vagal and sympathetic control of HR, we speculate that the HR response to transient hypoxia might be attributable predominantly to the sympathetically mediated tachycardic effect of the increased central inspiratory drive, whereas the fast, vagally mediated pulmonary inflation reflex might be the predominant mechanism during CSR.