TY - JOUR
T1 - Chemoreflex physiology and implications for sleep apnoea
T2 - Insights from studies in humans
AU - Mansukhani, Meghna P.
AU - Wang, Shihan
AU - Somers, Virend K.
N1 - Publisher Copyright:
© 2014 The Physiological Society.
PY - 2015/2/1
Y1 - 2015/2/1
N2 - New Findings: What is the topic of this review? This review summarizes chemoreflex physiology in health and disease, with specific focus on chemoreflex-mediated pathophysiology in obstructive and central sleep apnoea. What advances does it highlight? Chemoreflex mechanisms are thought to contribute significantly to the pathophysiology and adverse outcomes seen in sleep apnoea. Clinical implications of altered chemoreflex function in sleep apnoea from recent studies in humans, including cardiac arrhythmias, coronary artery disease, systolic/diastolic heart failure and sudden cardiac death are highlighted. Activation of the chemoreflex in response to hypoxaemia results in an increase in sympathetic neural outflow. This process is predominantly mediated by the peripheral chemoreceptors in the carotid bodies and is potentiated by the absence of the sympatho-inhibitory influence of ventilation during apnoea, as is seen in patients with sleep apnoea. In these patients, repetitive nocturnal hypoxaemia and apnoea elicit sympathetic activation, which may persist into wakefulness and is thought to contribute to the development of systemic hypertension and cardiac and vascular dysfunction. Chemoreflex activation could possibly lead to adverse cardiovascular outcomes, such as nocturnal myocardial infarction, systolic and/or diastolic heart failure, cardiac arrhythmias and sudden death in patients with sleep apnoea. This review summarizes chemoreflex physiology in health and disease, with specific focus on chemoreflex-mediated pathophysiology in obstructive and central sleep apnoea. Measurement of the chemoreflex response may serve as a potential avenue for individualized screening for cardiovascular disease. Whether modulation of this response in sleep apnoea may aid in the prevention and treatment of adverse cardiovascular consequences will require further study.
AB - New Findings: What is the topic of this review? This review summarizes chemoreflex physiology in health and disease, with specific focus on chemoreflex-mediated pathophysiology in obstructive and central sleep apnoea. What advances does it highlight? Chemoreflex mechanisms are thought to contribute significantly to the pathophysiology and adverse outcomes seen in sleep apnoea. Clinical implications of altered chemoreflex function in sleep apnoea from recent studies in humans, including cardiac arrhythmias, coronary artery disease, systolic/diastolic heart failure and sudden cardiac death are highlighted. Activation of the chemoreflex in response to hypoxaemia results in an increase in sympathetic neural outflow. This process is predominantly mediated by the peripheral chemoreceptors in the carotid bodies and is potentiated by the absence of the sympatho-inhibitory influence of ventilation during apnoea, as is seen in patients with sleep apnoea. In these patients, repetitive nocturnal hypoxaemia and apnoea elicit sympathetic activation, which may persist into wakefulness and is thought to contribute to the development of systemic hypertension and cardiac and vascular dysfunction. Chemoreflex activation could possibly lead to adverse cardiovascular outcomes, such as nocturnal myocardial infarction, systolic and/or diastolic heart failure, cardiac arrhythmias and sudden death in patients with sleep apnoea. This review summarizes chemoreflex physiology in health and disease, with specific focus on chemoreflex-mediated pathophysiology in obstructive and central sleep apnoea. Measurement of the chemoreflex response may serve as a potential avenue for individualized screening for cardiovascular disease. Whether modulation of this response in sleep apnoea may aid in the prevention and treatment of adverse cardiovascular consequences will require further study.
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U2 - 10.1113/expphysiol.2014.082826
DO - 10.1113/expphysiol.2014.082826
M3 - Article
C2 - 25398715
AN - SCOPUS:84921885975
SN - 0958-0670
VL - 100
SP - 130
EP - 135
JO - Experimental physiology
JF - Experimental physiology
IS - 2
ER -