Abstract
Oscillatory breathing (OB) patterns are observed in pre-term infants, patients with cardio-renal impairment, and in otherwise healthy humans exposed to high altitude. Enhanced carotid body (CB) chemoreflex sensitivity is common to all of these populations and is thought to contribute to these abnormal patterns by destabilizing the respiratory control system. OB patterns in chronic heart failure (CHF) patients are associated with greater levels of tonic and chemoreflex-evoked sympathetic nerve activity (SNA), which is associated with greater morbidity and poor prognosis. Enhanced chemoreflex drive may contribute to tonic elevations in SNA by strengthening the relationship between respiratory and sympathetic neural outflow. Elimination of CB afferents in experimental models of CHF has been shown to reduce OB, respiratory-sympathetic coupling, and renal SNA, and to improve autonomic balance in the heart. The CB chemoreceptors may play an important role in progression of CHF by contributing to respiratory instability and OB, which in turn further exacerbates tonic and chemoreflex-evoked increases in SNA to the heart and kidney.
Highlights
Abnormal oscillatory breathing (OB) patterns are frequently observed in diverse populations, including infants born prematurely (Copeman et al, 1964), patients with heart failure (Ponikowski et al, 1999), or end stage renal disease (Hanly and Pierrato, 2001), and in otherwise healthy humans who travel to high altitude (Lahiri et al, 1983)
CHEMOREFLEX SENSITIVITY AND DISORDERED BREATHING IN HEART FAILURE Cheyne–Stokes respiration (CSR), a form of OB in which oscillations in tidal volume are separated by apneic episodes, is highly prevalent in patients with chronic heart failure (CHF) (Mortara et al, 1997; Ponikowski et al, 1999; Giannoni et al, 2008)
Our preliminary findings indicate that the reduction in renal blood flow to carotid body (CB) chemoreflex activation is markedly accentuated in CHF animals
Summary
Abnormal oscillatory breathing (OB) patterns are frequently observed in diverse populations, including infants born prematurely (Copeman et al, 1964), patients with heart failure (Ponikowski et al, 1999), or end stage renal disease (Hanly and Pierrato, 2001), and in otherwise healthy humans who travel to high altitude (Lahiri et al, 1983). Studies from our laboratory have demonstrated enhanced ventilatory, sympathetic nerve, and carotid sinus nerve responses to isocapnic hypoxia as well as a tonic increase in resting afferent chemoreceptor discharge during normoxia in both rabbit and rat models of heart failure (Sun et al, 1999a,b; Li et al, 2005; Del Rio et al, 2013b; Haack et al, 2014; Marcus et al, 2014a).
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