Role of Carotid Body Chemoreflex Function in the Development of Cheyne‐Stokes Respiration During Progression of Congestive Heart Failure

Cheyne‐Stokes respiration (CSR) is associated with increased morbidity and mortality in patients with congestive heart failure (CHF). In this study we sought to determine whether augmented carotid body chemoreflex (CBC) sensitivity is responsible for enhancing central chemoreflex (CC) sensitivity and the development of CSR in an animal model of CHF. Telemetry transmitters were used to chronically measure diaphragm EMG (dEMG). Additionally, acute ventilatory responses to hyperoxia (HYPER), isocapnic hypoxia (IsoH), and hyperoxic hypercapnia (HH), were measured in order to assess CBC and CC sensitivity. Left ventricular (LV) function was quantified via echocardiography, and CSR was quantified as the apnea‐hypopnea index (AHI) from the dEMG tracings. We found that AHI was negatively correlated with LV function, and increased above baseline after 2 weeks of pacing. The HYPER evoked decrease in ventilation was positively correlated with LV function and progressed successively after 1 week of pacing. Similarly, ventilatory responses to IsoH and HH were both augmented during the course of pacing, however IsoH responses were augmented earlier than HH responses. Our findings suggest that CHF increases CBC control of eupneic ventilation, and that changes in CC sensitivity which follow those in the CBC coincide with development of CSR in this experimental model. This work was funded by NIH PO1 HL06222212.