Chest
ReviewThe Control of Breathing in Clinical Practice
Section snippets
Respiratory Sensors
The afferent input into the central system is provided primarily by four groups of neural receptors: (1) peripheral arterial chemoreceptors; (2) central (brainstem) chemoreceptors; (3) intrapulmonary receptors; and (4) chest wall and muscle mechanoreceptors.
Integrated Responses of the Ventilatory Control System
The categorization of the respiratory control system employed above is a useful means of organizing and outlining the anatomic and physiologic information available regarding its various components. However, all normal physiologic functions and derangements of respiratory control must consider the integrated function of the entire system. Considerable information of clinical significance is best understood as it relates to the integrated ventilatory response to the various chemical stimuli.
Sleep
At sleep onset, the behavioral and cognitive influences on ventilatory control are largely eliminated. e and respiratory responses to exogenous (and presumably endogenous) stimuli such as the response to hypoxia and hypercapnia are generally reduced.53, 54 In addition, an increase in airflow resistance typically occurs at sleep onset because of relative hypotonia of the upper airway dilatory muscles.55 Ventilatory compensation to both added and intrinsic resistance to breathing is also severely
Asthma
Symptomatic asthmatics normally breathe at a normal or increased frequency.78 Their ventilatory drive (as measured by mouth occlusion pressure) increases during exacerbations, probably in response to the resistive load imposed by increased airflow resistance.79 This compensation is usually excellent, as most asthmatics hyperventilate during an episode of wheezing with dyspnea. Although asthmatics are usually hypoxemic during attacks, supplemental oxygen does not significantly raise the low Paco2
Drugs and the Control of Breathing
From a clinical standpoint, the most important classes of drugs that influence ventilatory control are the inhalational anesthetics, narcotics, and minor tranquilizers. Inhalational anesthetics such as halothane, ether, and nitrous oxide cause respiratory depression in normal subjects by decreasing resting e and the response to increasing Paco2 or hypoxemia.119 In patients with severe COPD but without CO2 retention, there is substantially more hypoventilation during light halothane anesthesia
Conclusion
Our knowledge of the control of ventilation is constantly evolving through continued clinical and basic research. Abnormalities of respiratory drive are often overlooked in clinical practice. They should be considered whenever the level of respiratory muscle weakness, intrapulmonary gas exchange abnormalities, or lung mechanical dysfunction cannot explain deranged blood gases. Breathing abnormalities tend to be more severe during sleep than during wakefulness, and they have serious
ACKNOWLEDGMENTS
The authors would like to gratefully acknowledge Kathryn Caruana-Montaldo for the preparation of this manuscript.
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