Respiratory-Related Reflexes and the Cerebellum
Alan D. Miller, Armand L. Bianchi, Beverly P. Bishop in Neural Control of the Respiratory Muscles, 2019
Respiratory drive is regulated by information emanating from sensory receptors within the airway/lungs and respiratory muscles as well as central and peripheral chemoreceptors. In this chapter we will only review and update information concerning respiratory reflexes elicited by activation of vagal and phrenic afferents, which have been the major research focus of our laboratories. Because of space limitations only representative references can be included and their selection in no way diminishes the importance of the contributions made by others in establishing current concepts. Central modulation of these reflexes is well appreciated but controversy exists as to the role, if any, the cerebellum plays. This is somewhat surprising since the cerebellum’s involvement in the reflex regulation of the motor drive to other skeletal muscles is well established. This chapter will examine recent findings suggesting that the cerebellum plays a significant role in the regulation of breathing when greater demands are made on the system than exist during resting ventilation.
Special environments
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2015
The mechanisms responsible for the continued increase in respiratory drive are as follows: The pH of the CSF bathing the central chemoreceptors is restored to normal by choroid plexus active transport of bicarbonate ions out of the CSF to the blood.Renal excretion of the excess bicarbonate in blood to restore arterial pH to normal.The respiratory centre is reset to function at a lower arterial Pco2, so that the carbon dioxide response curve is shifted to the left with an increased slope, and the apnoeic threshold is decreased.
Physiology Related to Special Environments
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
The mechanisms responsible for the continued increase in respiratory drive or ‘secondary hyperventilation’ are as follows: The pH of the CSF bathing the central chemoreceptors is restored to normal by choroid plexus active transport of bicarbonate ions out of the CSF to the blood.Renal excretion of the excess bicarbonate in blood to restore arterial pH to normal.The respiratory centre is reset to function at a lower arterial Pco2, so that the carbon dioxide response curve is shifted to the left with an increased slope, and the apnoeic threshold is decreased.
Mouth occlusion pressure at 100ms (P0.1) as a respiratory biomarker in amyotrophic lateral sclerosis
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2021
Susana Pinto, Michael Swash, Mamede De Carvalho
Currently, as there is no method to directly measure the activity of the respiratory center, the respiratory drive is inferred based on its output. P0.1 values are already available in most modern ventilators used in intensive care units, where they are used to adjust for possible patient-ventilator asynchronies, either when there is high or low respiratory drive activity (18). P0.1 has three determinants (18): the neural command, nerve conduction to the respiratory muscles, and the pressure-generating capacity of the inspiratory muscles. It remains uncertain why our patients with inspiratory muscle weakness and high values of pCO2 included in SG0 cannot increase the activity of the respiratory drive. However, patients with higher or lower P0.1, with very different phenotypes, but predominantly elderly-women with bulbar-onset and faster functional decline in SG1, and also men with higher BMI in SG0, have similar survival rates. We suggest, as described elsewhere (48) that upper motor neuron burden is increased in patients with lower P0.1, and that higher P0.1 is related to increased bulbar respiratory neuron excitability in ALS with predominantly bulbar phenotype. Further studies are necessary to clarify these issues and to determine if this additional information is relevant to categorize patients and improve their respiratory management. Surprisingly, both abnormally weak and strong responses of the respiratory drive to poor ventilation are observed in ALS, and functional progression is faster in the latter group, perhaps implying more severe peripheral abnormality in the ventilatory system.
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].
Endothelialitis plays a central role in the pathophysiology of severe COVID-19 and its cardiovascular complications
Published in Acta Cardiologica, 2021
Christiaan J. M. Vrints, Konstantin A. Krychtiuk, Emeline M. Van Craenenbroeck, Vincent F. Segers, Susanna Price, Hein Heidbuchel
Several factors besides expansion of the viral pneumonia and its immune response may contribute to the pathogenesis of the worsening respiratory failure. The intravascular micro- and macro-thrombosis within the pulmonary circulation will lead to increased dead-space ventilation [33]. This, combined with increased metabolic demand may result in a marked increase of the respiratory drive during spontaneous breathing increased rate and augmented transpulmonary pressure and strain. The combination of high negative inspiratory intrathoracic pressures and increased lung permeability can exacerbate interstitial and pulmonary edema leading to worsening of pulmonary infiltrates and respiratory failure. The consequent in part patient self inflicted lung injury that may occur during high-flow oxygen therapy or non-invasive ventilation, may be attenuated by intubation, potentially indicated once deep negative swings in intra-esophageal pressure are observed [34,35], but has to be balanced against the risks of intubation and ventilation, as well as ventilator-induced lung injury. At a later stage, dense consolidation and progressive fibroproliferation will result in decreased recruitability by positive end-expiratory pressure (PEEP) ventilation or positioning of the patient in a prone position [36].
Related Knowledge Centers
- Breathing
- Carbon Dioxide
- Cellular Respiration
- Oxygen
- Peripheral Chemoreceptors
- Physiology
- Artery
- Pco2
- Respiratory Rate
- Blood Gas Tension