• Medullary respiratory center
• Apneustic center
• Pneumotaxic center

• Inspiratory center:(Dorsal) Regulates rhythm of breathing
• Expiratory center:(Ventral) expiration

• Normally inactive
• Prolonged inspiration gasp followed by brief expiration.
• Located in lower pons

• Can turn off Medullary Inspiratory center.
• Located in upper pons.

• Can temporarily override the automatic brain stem centers
• Hyperventilation and Hypoventilation

Location: Near the Medullary inspiratory center(Dorsal)

Goal:

-Drive alveolar ventilation

-Control breathing rate

-Maintain arterial PCO₂ in normal range

Mechanism: Direct effect of the change in the pH of the CSF and indirect effect to change in arterial PCO₂.

↓pH of CSF→ Hypervetilation

↑pH of CSF→ Hypoventilation

The effect of the arterial PCO₂ and CSF(H+) on the central chemoreceptors.

Location: Carotid bodies and Aortic bodies. Always surrounded by arterial blood.

Goal:

-Control breathing rate and drive alveolar ventilation when PO₂< 60mmHg

Mechanism:

-Detect changes in PO₂, PCO₂ and pH.

-Send information to inspiratory center.

-Aortic bodies use Vagus nerve(CN X)

-Carotid bodies use Glossopharyngeal nerve (CN IX)

The PO₂ on peripheral chemoreceptors

Their main aveolar ventilation drive would have adapted to be Peripheral Chemoreceptors.

If PO₂ increased they would lose their main drive.

• Mechanoreceptors located in the smooth muscle of airways
• Distention(stretching) of lungs and airways leads decreased inspiration and ventilation.
• (Hering-Breuer reflex= prolong expiratory period)

• Mechanoreceptors located in joints and muscles.
• When limb movement is detected breathing rate is increased

• Located between epithlial lining of the airways.
• Respond to noxious chemicals and particles.
• Increase breathing rate and constirct bronchial smooth muscle.

• Located in aveolar wall(near pulmonary capillaries)
• Sense when capillaries are filled with blood and increases breathing rate.
• (e.g. left-side heart failure→ rapid shallow breathing and dysnea(shortness of breath)

Periods or hyperventilation (10-20 sec) altering with similiar periods of apnea(not breathing)

Causes:

-Severe Hypoxemia (high altitude especially at night)

-Lesions in the CNS

-Cardiovascular diseases (e.g. heart failure)

Mechanism:

During apnea→↑brain PCO₂→ stimulate ventilation maximally→ ↓alveolar PCO₂ below the set point→ inhibiting respiration.

Thus, chemoreceptors recieve the information too late to regulate it properly

A group of disorders in which breathing during sleep stops for more than 10 seconds and usually more than 20 times an hour. Causes measurable blood deoxygenation.

1. Central sleep apnea: due to decreased respiratory center output; longer intervals between breathing. Usually do to damage in the brain.

2. Obstructive sleep apnea: upper airway blockage despite normal airflow drive (most common).

3. Mixed central and obstructive sleep apnea.