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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
There are three types of receptors in the lungs. Two types, the slowly adapting pulmonary stretch receptors and the rapidly adapting (irritant) receptors, send nerve impulses to the brain in myelinated nerve fibres in the vagi, while the third, C-fibres, send information in unmyelinated fibres. Slow adapting pulmonary stretch receptors. The slow adapting fibres of the Hering–Breuer reflexes are located in the smooth muscles of the trachea and bronchi. In the Hering–Breuer inflation reflex, the stretch receptors of these muscles during steady inflation of the lung are activated and results in an increase in the duration of expiration. A Hering–Breuer deflation reflex results in a decrease in the duration of expiration produced by marked deflation of the lung.Rapidly adapting stretch receptors. The rapidly adapting stretch receptors are found in the epithelial cells of large airways such as the carina. They increase their firing rate in response to the rate of change in lung volume and cause rapid shallow breathing. They were formerly known as irritant receptors because they respond to chemical stimuli such as cigarette smoke. The sigh or augmented breath we take every 15 minutes originates from the rapidly adapting receptors stimulated by atelectasis. This action is implicated in the first few breaths of the newborn.
Afferent Innervation of Lungs, Airways, and Pulmonary Artery
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
Hazel M. Coleridge, John C.G. Coleridge
Reflexes arising from the lower respiratory tract can conveniently be divided into two categories, regulatory and defensive, and the sensory nerves mediating these reflexes can, in general, be considered under similar headings. Afferent nerve endings subserving regulatory reflexes are active under normal circumstances, their impulse frequencies increasing or decreasing as their stimuli vary around the normal set points. Their function is to supply the necessary information to preserve the status quo and their sensitivities are appropriate to the signalling of on-going physiologic events. Information from endings of this type is conducted rapidly to the central nervous system in myelinated fibers that can transmit high-frequency trains of impulses, allowing the encoding of precise temporal information about mechanical changes. Slowly adapting pulmonary stretch receptors clearly fall into this category.
Physiology of the Airways
Published in Anthony J. Hickey, Sandro R.P. da Rocha, Pharmaceutical Inhalation Aerosol Technology, 2019
Anthony J. Hickey, David C. Thompson
In the central nervous system regulation of airway function, afferent and efferent nerves serving sensory and effector functions, respectively, innervate the airways (Table 2.2, Figure 2.3) (Widdicombe, 2001). Slowly adapting receptors (or pulmonary stretch receptors) are located in the smooth muscle of the central airways (trachea to larger bronchi), respond to airway stretch, and are thought to be involved in the reflex control of ventilatory drive. Rapidly adapting receptors (or irritant receptors) ramify within the epithelium of the central airways and are sensitive to chemical or irritant stimuli (e.g. inflammatory mediators), mechanical stimuli, and interstitial edema. Activation of these receptors results in an increase in the rate or depth of breathing and in bronchoconstriction mediated through a central nervous system reflex in efferent cholinergic nerve activity. Inhalation of foreign substances, such as particulates, can activate these receptors to elicit reflex bronchoconstriction. Afferent C-fibers are tachykinin-containing nerves that ramify within the epithelium and between smooth muscle cells (Lundberg et al., 1984). Chemical (e.g. inflammatory mediators), particulate, and mechanical stimuli activate afferent C-fibers to cause rapid, shallow breathing or apnoea and to evoke central reflex bronchoconstriction through increased efferent cholinergic nerve activity (Coleridge and Coleridge, 1984; Widdicombe, 2001).
Acute respiratory distress syndrome (ARDS) caused by the novel coronavirus disease (COVID-19): a practical comprehensive literature review
Published in Expert Review of Respiratory Medicine, 2021
Francisco Montenegro, Luis Unigarro, Gustavo Paredes, Tatiana Moya, Ana Romero, Liliana Torres, Juan Carlos López, Fernando Esteban Jara González, Gustavo Del Pozo, Andrés López-Cortés, Ana M Diaz, Eduardo Vasconez, Doménica Cevallos-Robalino, Alex Lister, Esteban Ortiz-Prado
A second possibility is related to self-inflicted patient lung injury (P-SILI) caused by the respiratory effort made by patients with respiratory failure when breathing spontaneously or with the support of noninvasive mechanical ventilation (NIMV), since the high respiratory impulse generates large tidal volumes (VT) with potential to cause transpulmonary pressure changes. Zones closed by lung damage are temporarily opened and closed again, generating stress injury (pressure changes) and strain injury (changes by deformation), which is known as a ‘Pendelluft phenomenon’ [33]. The different forces generated by muscular work cause damage to already injured lungs, increasing vascular leakage by increasing transmural pulmonary vascular pressure. The high respiratory drive may be due to increased stimulation of juxtacapillary receptors or inhibition of slowly adapting pulmonary stretch receptors (Hering-Breuer reflex) [34].
Dyspnea in Parkinson’s disease: an approach to diagnosis and management
Published in Expert Review of Neurotherapeutics, 2020
Srimathy Vijayan, Bhajan Singh, Soumya Ghosh, Rick Stell, Frank L. Mastaglia
The subconscious physiological occurrence of involuntary breathing originates within the brainstem, with the rhythmicity of breathing being controlled by key structures in the medulla oblongata [10–13]. Carbon dioxide and oxygen tension are key drivers of output from the brainstem. Awareness and adjustment of breathing is thought to occur via feedback through a number of sensory inputs to the brainstem and cerebral cortex which results in increased ventilatory drive. While this can occur appropriately, as during exercise, in some pathological states this feedback mechanism may indeed be functioning inappropriately or even excessively. When considering the sensory basis for dyspnea, a number of physiological mechanisms are noteworthy. Afferent impulses from vagal receptors, pulmonary stretch receptors, irritant receptors and C fibers located within the airways provide direct feedback to central structures to influence the pattern and level of breathing. The respiratory muscles themselves also contain sensory receptors and parasympathetic innervation which, via afferent nerve terminals, provide information via the spinal cord to the brainstem and cortex. Chest wall mechanoreceptors provide feedback regarding mechanical efforts of the lung and therefore provide conscious awareness of motor drive during periods of increased ventilatory effort [8,14,15]. It is important to understand these neuroanatomical and physiological pathways to fully appreciate the diversity of potential mechanisms that may contribute to dyspnea. The complex interplay of a number of networks gives rise to the symptom and explains the heterogenous clinical and symptomatic presentations [16].
Pathophysiology and clinical evaluation of the patient with unexplained persistent dyspnea
Published in Expert Review of Respiratory Medicine, 2022
Andi Hudler, Fernando Holguin, Meghan Althoff, Anne Fuhlbrigge, Sunita Sharma
While this is not intended to be a comprehensive review of the pathophysiology of dyspnea, it is important to highlight key concepts to understand diagnostic approaches. The control of breathing and its perception depend on a complex interplay of signals arising from within the central nervous system, both from the automatic centers in the brain stem and from the motor cortex (efferent), as well as from a variety of receptors in the upper airway, lungs, and chest wall (afferent) [7,8]. For most patients, dyspnea begins with a physiologic impairment that stimulates afferent receptors, which is perceived as an unpleasant sensation when this information is transmitted to the cerebral cortex. There are multiple afferent pathways sending information from mechanical, neurological, and metabolic sensors. These can be divided into central nervous system (medullary, cortical, and limbic), metabolic (carotid/aortic bodies, medullary chemoreceptors), and respiratory sensors (pulmonary stretch receptors, J-receptors, airway C-fibers, upper airway receptors, muscle spindles and tendon receptors, and chest wall joint receptors) etiologies [9]. Information from these sources is transmitted to and processed by the medullary respiratory center which sends efferent commands to the ventilatory muscles. During this process, a neurological copy of the command is simultaneously sent to the sensory cortex. This exchange between motor and sensory cortex is called a corollary discharge and is thought to be the mechanism by which conscious awareness of breathing effort occurs [10]. If the efferent ventilatory muscle response is appropriately responsive to the afferent input signals, respiration mostly occurs without conscious awareness. However, respiration can come into awareness at any moment either voluntarily or automatically if breathing needs to be attended to [10]. This process is also known as ‘gating’ [11] and is the basis of monitoring essential physiological functions and adopting appropriate behavior [12]. When ventilation needs are physiologically increased, afferent stimuli direct the respiratory muscles to increase ventilation in tandem with the perception of dyspnea via inspiratory neural drive (IND). However, this process is hindered by mechanical limitations in some disease processes, resulting in an inability to translate these afferent inputs into efferent output. This disconnect results in a pathologic process known as neuromechanical dissociation, which causes increased IND and subsequently results in the perception of dyspnea to increase rapidly [5]. While this imbalance in respiratory afferent/efferent signals contributes to the feeling of dyspnea, its perception is ultimately influenced by culture, environment, and affective processing [13].