🫁 Control of Breathing
The brainstem command centres, chemoreceptor physiology, the BBB acid trap, and the clinical scenarios that follow — all in one place.
The Brainstem Command Centre
Breathing is unique among the vital functions — it can be both automatic (you breathe during sleep without thinking) and voluntary (you can choose to hold your breath or deliberately pant). This duality reflects the anatomy: an automatic brainstem generator that can be overridden by cortical input from the motor cortex, but only temporarily — the brainstem will always win eventually.
The Primary Respiratory Centre
The medullary respiratory neurones are the true pacemakers of breathing. They possess intrinsic, spontaneous, rhythmical electrical activity — they fire without any external input, like a metronome that never stops ticking. Two key neurone groups live here:
Dorsal Respiratory Group (DRG)
Located in the nucleus tractus solitarius. Predominantly inspiratory neurones — they fire in a ramping pattern to drive the diaphragm and external intercostal muscles (the primary muscles of inspiration) via the phrenic nerve (C3, C4, C5) and intercostal motor nerves. This group is the primary driver of the basic respiratory rhythm.
Ventral Respiratory Group (VRG)
Located in the nucleus ambiguus and retrofacial nucleus. Contains both inspiratory and expiratory neurones. Normally largely silent during quiet breathing (which requires no active expiration). Recruited during forced breathing — exercise, coughing, straining — to actively drive the accessory muscles of inspiration and the muscles of active expiration (internal intercostals, abdominal muscles).
Why Quiet Expiration Is Passive
At rest, expiration is entirely passive — it requires no muscle activity. When the inspiratory neurones stop firing, the stretched elastic recoil of the lungs and chest wall passively returns the thorax to its resting volume, pushing air out. This is why a pneumothorax (loss of chest wall integrity) causes immediate respiratory failure — the passive elastic recoil mechanism breaks down. It is only during exercise or when there is airways obstruction that expiration becomes active.
Pontine Respiratory Centres
The pons contains two key centres that modify and smooth the raw rhythmical output of the medullary centres, preventing breath-holding and creating the smooth sinusoidal pattern of normal breathing:
Pneumotaxic Centre (Pontine Respiratory Group)
Located in the upper pons (nucleus parabrachialis). Acts as an “off switch” for inspiration — it continuously sends inhibitory signals to the DRG, terminating each inspiratory burst and preventing the lungs from over-inflating. By adjusting the strength of this off-switch signal, it regulates the depth and rate of breathing. Damage to the pneumotaxic centre causes apneustic breathing (prolonged, gasping inspirations).
Apneustic Centre
Located in the lower pons. Sends sustained excitatory signals to the inspiratory neurones, encouraging prolonged inspiration. In normal breathing, it is held in check by the pneumotaxic centre above it. If the pneumotaxic centre is damaged and the apneustic centre runs unchecked, the result is apneustic breathing — seen in severe pontine strokes.
The Pulmonary Stretch Receptors
Beyond the brainstem, the lungs themselves have a self-protective mechanism. Pulmonary stretch receptors (slowly adapting receptors in the airway smooth muscle) detect lung inflation. As the lung inflates during inspiration, these receptors fire increasingly. Their signals travel via the Vagus nerve (CN X) to the medulla, where they inhibit further inspiration and promote expiration.
The Hering-Breuer Reflex
This is the lung’s own brake — a negative feedback loop that prevents over-inflation. In adults it is only clinically significant at large tidal volumes (e.g., during forced breathing or mechanical ventilation). In neonates, it is the primary mechanism controlling respiratory rhythm. This is why newborns breathe so much faster — their Hering-Breuer reflex triggers at lower lung volumes. It also explains why high tidal volumes on a ventilator (“volutrauma”) can paradoxically cause apnoea — the reflex is overwhelmingly activated.
Summary — The Hierarchy
| Level | Structure | Role | Damage → Effect |
|---|---|---|---|
| Cortex | Motor cortex | Voluntary override — talking, singing, breath-holding | Loss of voluntary control; automatic breathing preserved |
| Upper Pons | Pneumotaxic Centre | Off-switch — terminates inspiration, sets rate/depth | Apneustic breathing — prolonged gasping inspiratory holds |
| Lower Pons | Apneustic Centre | Pro-inspiratory drive — sustains inspiration | Only dangerous if pneumotaxic is also lost |
| Medulla | DRG + VRG | The pacemaker — automatic rhythmical breathing | Apnoea — cessation of all breathing (fatal) |
| Lung | Stretch receptors (CN X) | Hering-Breuer reflex — prevents over-inflation | Loss → risk of volutrauma at high tidal volumes |