13th January 2024

Central Control of Respiration

Central control of respiration is via the brain-stem respiratory network in the medulla and pons. There are three components to this complex series of neurons and nuclei:

1. Respiratory Neurons: that generate the underlying respiratory rhythm and act as the primary driver of respiratory activity. There are two groups of respiratory neurons: the Dorsal Respiratory Group (DRG) and the Ventral Respiratory Group (VRG).
2. Chemosensors: detect changes in blood gases and pH and trigger a physiological response to maintain each parameter within the normal range.
3. Respiratory Motor Groups: innervate the respiratory muscles.

The DRG is composed of inspiratory neurons and is closely associated with nucleus of the solitary tract. This area receives important vagal sensory input critical for reflex control of breathing: peripheral chemoreceptors (for pO2 and pCO2 from aorta and carotids), central chemoreceptors (pH in the ventral medulla) and lung vagal afferents (stretch, irritant and pain receptors). The VRG is composed of both inspiratory and expiratory neurons. The Pre-Botzinger Complex (a grouping of inspiratory neurons) within the VRG has some intrinsic pacemaker activity that generates an underlying respiratory rhythm. This complex contains mu-opioid receptors, which slow respiratory pacemaker activity when activated. Thus, we can see how opiates will trigger the mu receptors and slow the pacemaker activity, causing respiratory depression when given at sufficient doses.

The various chemosensors will respond to changes in the pCO2 and pO2 to trigger respiration. One of the primary aims of ventilation is to maintain the pCO2 within a range of 4.5- 6.0 kPa, and respiration is thus very sensitive to even slight changes in pCO2. Hypercarbia will trigger an increase in respiratory drive. In sleep, this can lead to an arousal, pulling patients from deeper sleep and thus disrupting sleep. Hypocapnia, in turn, can lead to a decrease in respiratory drive when, indeed, can lead to periodic central apnoeas (if it crosses the apnoeic threshold). The hypoxic drive alone is relatively insensitive, but when coupled with the hypercarbic drive, it has synergistic effects on increasing arousal and wakefulness and the initiation of some of the conscious waking respiratory drive.