Respiration

Ventilation is driven by complex neural circuits located in the brainstem, including a central pattern generator and chemosensor along with feedback from peripheral sensory nerves located in the carotid bodies, aortic arch, muscles, and lungs.

Hypoxia caused by either high altitude or disease can engage the carotid chemoreceptors which are powerful drivers of increased minute ventilation.

Failure of any of the components can lead to respiratory failure.

Spontaneous respiration produced by rhythmic motor neuron discharge that innervate the respiratory muscles and such impulses originate in the brain.

Dependence of brain impulses is evident by the lack of breathing that occurs transection of the spinal cord above the origin of the phrenic nerves.

Separate voluntary and automatic neural mechanisms exist to regulate respiration.

The voluntary system is located in the cerebral cortex and sends impulses to the respiratory motor neurons via the corticospinal tracts.

The automatic neural control of respiration is driven by pacemaker cells in the medulla.

In normal respiratory control, negative feedback allows a steady level of alveolar gas concentrations to be maintained, and therefore stable tissue levels of oxygen and carbon dioxide (CO2)

Alveolar ventilation = body CO2 production/end-tidal CO2 fraction.

Through respiratory control reflexes, any small transient fall in ventilation leads to a corresponding small rise in alveolar CO2 concentration which is sensed by the respiratory control system so that there is a subsequent small compensatory rise in ventilation above its steady state level that helps restore CO2 back to its steady state value. 

In general, transient or persistent disturbances in ventilation, CO2 or oxygen levels can be counteracted by the respiratory control system in this way.

In some pathological states, the feedback is more powerful than is necessary to simply return the system towards its steady state. 

Instead, ventilation overshoots and can generate an opposite disturbance to the original disturbance. 

If this secondary disturbance is larger than the original, the next response will be even larger, and so on, until very large oscillations have developed.

Medulla impulses activate motor neurons in the cervical and thoracic spinal cord that innervate inspiratory muscles.

Impulses from the cervical spinal cord activate the diaphragm via the phrenic nerve and the thoracic spinal cord activatesthe external intercostal muscles.

Motor neurons to expiratory muscles are inhibited when the inspiratory muscles are activated, and vice versa.