Nonobstructive Sleep Patterns in Children
Mark A. Richardson, Norman R. Friedman in Clinician’s Guide to Pediatric Sleep Disorders, 2016
The act of breathing is a complex choreography involving the CNS, peripheral nervous system, and the respiratory muscles. While voluntary breathing is initiated from the cerebral cortex, the automatic breathing during sleep requires the body to first determine the need for a breath on the basis of input from peripheral and central chemoreceptors. The peripheral chemoreceptors lie primarily within the carotid bodies and respond to hypoxia and, to a lesser extent, to hypercapnia/acidosis. The central chemoreceptors appear to be widely distributed within the medulla and lower brain. These central chemoreceptors respond to the acidosis within the cerebrospinal fluid resulting from hypercapnia. Input from both the peripheral and central chemoreceptors feeds into the respiratory centers within the medulla (especially, the nucleus of the solitary tract) and influence the rhythm of the breathing pattern.
Control of breathing
Andrew M. Luks, Philip N. Ainslie, Justin S. Lawley, Robert C. Roach, Tatum S. Simonson in Ward, Milledge and West's High Altitude Medicine and Physiology, 2021
Dopamine is the most abundant transmitter found in the carotid body. Hypoxia increases the rate of release of dopamine from glomus cells. Norepinephrine (noradrenalin) and 5-hydroxytryptamine (i.e., serotonin) are next in abundance. There are also small quantities of acetylcholine, ATP, and enkephalin-like peptides in some glomus cells (Leonard et al. 2018). Substance P, endothelin-1, adenosine, angiotensin erythropoietin, and purinergic receptors are also present and may be involved in modulating the hypoxic response (Leonard et al. 2018; Wilson et al. 2005). It should be noted that, although in the context of high altitude, the most important function of the peripheral chemoreceptors (carotid and, to a lesser extent, aortic bodies) is to respond to hypoxia, they also respond to changes in pH and PaCO2 in dependent fashion through stimulus interaction; there is also growing consensus that the peripheral chemoreceptors also act as general metabolic sensors and, for example, are stimulated by changes in glucose and/or insulin (Conde et al. 2018). The greatest systemic response to PaCO2 is via the central chemoreceptors in the brainstem. As an example of the relative contribution of the chemoreceptors, a study by Fatemian et al. (2003) revealed that subjects who had had both carotid bodies removed had about 36% lower hypercapnic ventilatory response (HCVR) than normal subjects.
Pathogenesis of Sleep-Disordered Breathing in Adults
Susmita Chowdhuri, M Safwan Badr, James A Rowley in Control of Breathing during Sleep, 2022
Specialized structures called chemoreceptors monitor local O2 and CO2 partial pressures (PaO2 and PaCO2) and provide signals to the brainstem, which integrates these afferent inputs to determine output to the muscles of ventilation, including the respiratory pump (principally the diaphragm) and the muscles of the upper airway. Central chemoreceptors are located in the central nervous system, principally in the medulla, and are sensitive to changes in CO2 and pH. Peripheral chemoreceptors are components of the peripheral nervous system, located principally at the bifurcations of the carotid arteries (i.e. the carotid bodies) and in the aorta. They mainly respond to local hypoxia, but may also increase their activity in conditions of low pH, elevated PaCO2, or low blood flow (11).
Novel approaches: targeting sympathetic outflow in the carotid sinus
Published in Blood Pressure, 2023
Dagmara Hering, Krzysztof Narkiewicz
The peripheral arterial chemoreceptors are located in the carotid and aortic bodies, and respond primarily to changes in oxygen levels (hypoxia), while central chemoreceptors are located on the ventral surface of the medulla oblongata and primarily respond to changes in carbon dioxide (CO2) levels (hypercapnia) [10,12]. Activation of afferent impulses from the carotid chemoreceptors in response to hypoxia leads to simultaneous activation of the cardiorespiratory centre in the medulla oblongata (synapsing to neurons in the caudal, commissural nucleus tractus solitarius, NTS) resulting in simultaneous hyperventilation and selective peripheral vasoconstriction (increased sympathetic activity to blood vessels). At the same time, hyperventilation through a stretch of thoracic afferents elicits an inhibitory or buffering influence on the autonomic response to hypoxaemia resulting in bradycardia, mediated by increased cardiac vagal outflow (Figure 2).
Extra-pulmonary manifestations of COPD and the role of pulmonary rehabilitation: a symptom-centered approach
Published in Expert Review of Respiratory Medicine, 2021
Ana Machado, Alda Marques, Chris Burtin
Patients with COPD first perceive and report dyspnea during physical activity [52]. During exertion, there is an increase in metabolic carbon dioxide output, which stimulates peripheral and central chemoreceptors, leading to an increase in inspiratory neural drive and ventilation [51,52]. The known dynamic hyperinflation in COPD leads to a rapid and shallow breathing pattern, which results in functional limitation of inspiratory muscles, decreased dynamic lung compliance and inspiratory capacity, and worsening pulmonary gas exchange [49,51,52]. This constriction in tidal volume expansion, simultaneously with an increased/persistent chemostimulation, is perceived by patients as an unpleasant respiratory sensation, i.e., dyspnea [51]. Patients reduce their physical activity levels and adopt a sedentary lifestyle to avoid exertional dyspnea [49,51,52]. This leads to skeletal muscle deconditioning and deterioration of exercise capacity, which in turn lowers the threshold at which patients feel dyspnea during exertion (i.e., dyspnea appears at progressively lower exercise intensities), starting a vicious circle of dyspnea-inactivity [49,51,53]. The decline in physical activity is a strong predictor of mortality in patients with COPD [54]. Exertional dyspnea and the ventilatory limitations are key contributors to patients’ impaired exercise tolerance, which is further limited by muscle dysfunction, cardiovascular and nutritional imbalances, and psychological factors [55–57].
Spinal cord injury and diaphragm neuromotor control
Published in Expert Review of Respiratory Medicine, 2020
Matthew J. Fogarty, Gary C. Sieck
Peripheral and central chemoreceptors are found in the carotid bodies and brainstem, respectively, and increase ventilatory drive in response to hypoxia and/or hypercapnia, respectively [2]. Lung mechanoreceptors are sensitive to lung inflation and act to prevent airway over-inflation [2]. Local inhibition of phrenic motor neurons from interneurons within the spinal cord has also been characterized [57,58]. Additionally, there are direct corticospinal inputs [59,60] that allow for the voluntary control of ventilation or expulsive maneuvers, as well as during social and emotional activities [21,61].
Related Knowledge Centers
- Carbon Dioxide
- Carbonic Acid
- Cerebrospinal Fluid
- Peripheral Chemoreceptors
- Ph
- Medulla Oblongata
- Hypercapnia
- Blood Plasma
- Blood–Brain Barrier
- Sodium Cyanide