Heart rate response to transient hypoxia in patients with heart failure and Cheyne–Stokes respiration

Abstract

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.