Control of Breathing

Objectives 1.Distinguish between the automatic and conscious/voluntary control of breathing. Identify the key structures involved in generation of the resting quiet breathing rhythm of inspiration followed by expiration. 2.Specify the key sources of sensory input to the rhythm generator that modify its output to the respiratory muscles. 3.Identify the location of the central & peripheral chemoreceptors and describe their effect (if any) on ventilation in response to changes in arterial PCO2, PO2 and pH. 4.Describe how a decrease in plasma pH regulates ventilation & partial pressures of oxygen and carbon dioxide in the blood. Provide examples of metabolic acids that have this effect in exercise and in diabetes.

Brain stem area involved in respiratory control

Excites the inspiratory center in the medulla, prolonging the period of action potentials in the phrenic nerve, and thereby prolonging the contraction of the diaphragm. The pneumotaxic center (location: upper pons) turns off inspiration, limiting the burst of action potentials in the phrenic nerve. Prolongs expiration

The phrenic nerve is formed by rootlets exiting the cervical spine C3,C4,C5. Two bilateral phrenic nerves supply the hemidiaphragms. ”C3,4,5 keep the diaphragm alive” Intercostal nerves exiting thoracic & lumbar spine provide input to nerves supplying the intercostal & abdominal muscles

Central Chemoreceptors

1. Changing carbon dioxide levels: Acute Ventilation increases linearly with any rise in PaCO2 above resting values, whereas ventilation decreases when PaCO2 falls below 40 mm Hg. Chronic Patients with chronic pulmonary disease may not be able to ventilate at levels required to hold PaCO2 at 40 mm Hg. Ventilation increases initially when PaCO2 begins to rise because the pH of the CSF falls, but the choroid plexus responds by se-creting HCO3- into the CSF, which, over a period of 8–24 hours, largely offsets the effect of the higher PaCO2 on plasma pH. Thus, although PaCO2 may remain high, the medullary chemorecep-tors no longer register the change, and the respiratory control system adapts to a new, higher PaCO2.

Effect of Low Arterial PO2 to Stimulate Alveolar Ventilation When Arterial Carbon Dioxide and Hydrogen Ion Concentrations Remain Normal

Ventilatory responses to changes in arterial PCO2 (PaCO2) and PO2 (PaO2).

2. Changing oxygen levels:

Composite Effects of P CO 2, pH, and P O 2 on Alveolar Ventilation

Acid–base Considerations When CO 2 dissolves in water, it forms carbonic acid. Although a relatively weak acid, it is produced in such prodigious quantities (>20 moles/day) that it could seriously interfere with normal tissue function if its levels were not closely monitored and regulated. In practice, the central nervous system (CNS) maintains plasma pH within an extremely tight range (pH 7.35–7.45), in part by adjusting ventilation to hold P a co 2 at around 40 mm Hg.

Causes of changes in extracellular fluid pH Changes in pH caused by the lungs are referred to as respiratory acidosis or respiratory alkalosis. Non respiratory changes are referred to as metabolic acidosis or metabolic alkalosis. – Respiratory acidosis: Increased P a co 2 results from hypoventilation, V̇ A /Q̇ mismatches, or an increase in the diffusional distance between the alveolar sac and pulmonary blood supply (due to pulmonary fibrosis or edema, for example). – Respiratory alkalosis: P a co 2 decreases with hyperventilation, typically because of anxiety or other emotional state. It can also result from hypoxemia precipitated by ascent to high altitude.

Decreases in arterial pH Decreases in arterial pH cause an increase in ventilation, mediated by peripheral chemoreceptors for H +. This effect is independent of changes in the arterial PCO 2 and is mediated only by chemoreceptors in the carotid bodies (not by those in the aortic bodies).

Decreases in arterial pH In metabolic acidosis, when there is decreased arterial pH, the peripheral chemoreceptors are stimulated directly to increase the ventilation rate (the respiratory compensation for metabolic acidosis)

Abnormal Breathing Patterns Apneustic breathing Biot’s breathing Cheyne-Stokes breathing