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The anatomic location of the neural elements involved in the control of breathing and ventilation reside primarily in medullary and pontine structures of the brainstem. In the medulla, two groups exist: a dorsal respiratory group lying in close proximity to the nucleus tractus solitarius and the fourth ventricle, and a ventral respiratory group located in the ventral medullary reticular formation, each richly cross-innervated. The dorsal respiratory group is involved mainly with timing and initiation of the respiratory cycle and can be thought of as the pacemaker for breathing, while the ventral group modulates the function of breathing, such as modulating and inhibiting pacemaker signaling to allow for cessation of inspiratory effort and eventual exhalation, controlling the force of contraction of inspiratory muscles, and dilator functions of the larynx and pharynx. Of note, generation of the medullary drive requires no afferent input from other parts of the body, be it lungs or otherwise. In the pons, neural activity can be thought of as processing medullary afferents involved in both inspiratory and expiratory activities. The pneumotaxic respiratory center of the rostral pons is not, as was earlier thought, involved with respiratory rhythmicity but with limiting inspiratory lung volumes, or apneusis (cessation of ventilation effort at TLC).


Other brain and/or neural structures contribute to ventilatory control. Stimulation of the reticular activating system will increase the frequency and depth of breathing. The cerebral cortex can interrupt and modulate ventilator effort required for such actions as talking, singing, coughing, and various expulsive efforts. Stimulation of carotid sinus will decrease both vascular tone and respiratory effort, while carotid body activation will have the opposite effect. A variety of above-brainstem structures will also assist and inhibit medullary output in the performance of sneezing, coughing, and swallowing, but these mechanisms are poorly defined.


Chemical control of breathing and ventilation occurs at both the peripheral and central nervous system levels via peripheral and central chemoreceptors (Figure 143-1). Central chemoreceptors can be thought mainly to be responsive to changes in Pco2, pH, and acid–base parameters. Around 80%-85% of the ventilatory response to inhaled carbon dioxide originates within the central medullary chemoreceptors. These receptors lie very close to the anterolateral surface of the medulla close to both the glossopharyngeal and vagus nerves, and are overlaid by the anterior inferior cerebellar arteries, allowing CO2 to diffuse rapidly across the blood–brain barrier at this location. The rise in brain tissue and CSF CO2 will lead to a corresponding increase in carbonic acid, whose ionization will then increase H+ ion concentration, and decrease pH. It is the resulting change in pH that stimulates the firing rate of the medullary ventilation pacemaker neurons. As a result, increases in ventilatory rates are more responsive to respiratory acidosis than metabolic acidosis at similar blood pH, and for several reasons. First, changes in blood pH will be counteracted rapidly by multiple buffering mechanisms, whereas ...

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