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Control of Ventilation
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Stimulation of the central chemoreceptors increases their afferent output, increasing the activity of the medullary respiratory centre and the respiratory muscles. A rise in arterial will therefore produce a reflex increase in ventilation (Figure 21.3). Conversely, a reduction in hydrogen ion concentration inhibits the central chemoreceptors. Most of the ventilatory response to carbon dioxide is via the central, not the peripheral, chemoreceptors. The central chemoreceptors are responsible for about 60% of the ventilatory drive to carbon dioxide.
Fetal Circulation
Published in Miriam Katz, Israel Meizner, Vaclav Insler, Fetal Well-Being, 2019
Miriam Katz, Israel Meizner, Vaclav Insler
The effect of variations in blood chemistry on ventilation and blood circulation is mediated by the chemoreceptors. Chemoreceptor cells are located in the medulla oblongata, the aortic arch, and in the carotic sinus. The central chemoreceptors respond to changes in oxygen and carbon dioxide tension in the arterial blood or in the cerebrospinal fluid. In the adult a drop in oxygen concentration and/or rise in CO2 will trigger tachycardia and a increase in arterial blood pressure — both of them being protective mechanisms, attempting to increase blood circulation in order to improve oxygen supply.
Control of Respiration
Published in Lara Wijayasiri, Kate McCombe, Paul Hatton, David Bogod, The Primary FRCA Structured Oral Examination Study Guide 1, 2017
Lara Wijayasiri, Kate McCombe, Paul Hatton, David Bogod
Describe the ventilatory response to hypoxia. Hypoxaemia stimulates ventilation through its effects on the carotid and aortic bodies (peripheral chemoreceptors). Hypoxaemia is not a stimulus for the central chemoreceptors, although prolonged hypoxia will cause cerebral acidosis, which in turn can stimulate respiration.Isocapnic (holding CO2 constant) oxygen curves illustrate the effect of changing PaO2 on alveolar ventilation. The main stimulation of respiration through hypoxia occurs at PaO2 < 8 kPa. Hypercarbia augments the ventilatory response to hypoxia.Increasing PaCO2 by 0.1 kPa results in an increase in alveolar ventilation of approximately 1–2 L/min. In the same way a reduction in PaCO2 results in a reduction in alveolar ventilation up until a PaCO2 of 4 kPa below which there is no effect. Hypoxia produces a higher alveolar ventilation for any given PaCO2.
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).
Maternal protein restriction affects cardiovascular, but not respiratory response to L-glutamate microinjection into the NTS of conscious rats
Published in Nutritional Neuroscience, 2021
D. S. Alves, D. F. S. Barbosa, V. O. Nogueira, Y. Tourneur, D. A. F. Fontes, J. L. Brito-Alves, J. H. Costa-Silva
Modifications in the generation and modulation of basal respiratory rhythm and changes in the central and peripheral chemosensitivity to O2 and CO2 may trigger the overactivity of the sympathetic nervous system and, consequently, lead to hypertension in this experimental model [1]. The over-excitability of peripheral and central chemoreceptor might contribute to activation of the central regions of cardiorespiratory control, such as the nucleus of the solitary tract (NTS).The NTS is a region of the brainstem that receives the first synapses of the cardiovascular peripheral afferents and establishes communication with other central areas of generation and modulation of respiratory and sympathetic activity [2]. Also, the NTS is related to the regulation of baseline sympathetic and respiratory activities, as it receives the afferent information from arterial baroreceptors and pulmonary stretch receptors, and it hosts the respiratory neurons of the dorsal respiratory column [5,6]. The commissural NTS is the region where majority of the peripheral chemoreceptor synapses are established [7], where L-glutamate plays an important role in the modulation of the cardiovascular system (by the sympathetic and nervous system) and the respiratory system [3,8].
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].