Control of Breathing

Master answer

Central control of ventilation

1. Brainstem
   • Medulla (DRG, VRG)
   • Pons (Pneumotaxic, Apneustic)
2. External inputs
   • Sensors from lungs/airways/chemoreceptors
3. Cortex
   • Can override brainstem function and alter breathing patterns
4. Limbic/Hypothalamic Systems
   • Alters breathing patters depending on affective states (fear/anxiety/pain)

Peripheral Receptor Inputs alter respiratory rate/depth (ventilation)

1. URT receptors (in nose, NP, larynx, trachea)
   • mechanical/chemical stimuli
   • bronchoconstriction, sneezing/coughing reflexes, and laryngeal spasms
2. Joint/Muscle receptors
   • limb movement (Eg. exercise) can stimulate ventilation
3. Gamma-system (in muscle spindles)
   • muscle spindles sense muscle elongation,
   • can cause sensation of dyspnoea
4. Arterial baroreceptors (in AB and CB)
   • ↓ BP causes ↑ ventilation
   • ↑ BP can cause ↓ ventilation (and even apnoea)
5. Nociceptors
   • pain causes apnoea initially, then stimulates ventilation
6. Thermoreceptors
   • ↑ temperature stimulates ventilation
   • ↓ short deep inspiration

Hypocaponea/Hypoxia sensed by Chemoreceptors

• Central CR response
  • ↓’d perfusion → ↑[H]/↓PaO2 → CR stimulation
    • Afferent signal → Sinus nerve (of herring) / Vagus Nerve → Chemosensitive area of medulla
  • Vasomotor area → ↑ peripheral vasoconstriction
  • Respiratroy center → ↑rate and depth of respiration → ↑ venous return
• Peripheral CR response
  • PCRs found in “Glomus cells”
    • ↓ PaO2 – via inhibition of O2 sensitive K-channels
    • ↑ PaCO2 and/or ↓pH – via effect on pH sensitive K-channels
  • Type I cells (rich in NAd, DA, ACh)
    • Hypoxia causes release of NTs
    • NAd/ACh – ↑ AP firing rate of AB or CB afferent fibres
    • DA – Damping of type 2 cell responses
  • Type II cells (rich in capillary supply)
    • ↓ PaO2, ↑ PaCO2 and/or ↓pH
    • ↓ IC [ATP] which leads to ↑ NT production and release
    • ↑ AP firing rate of AB or CB afferent fibres

Response to:

• ↓ PaO2
  • Gradual ↑ MV PaO2 < 500mmHg,
  • Rapin ↑MV PaO2 < 50 mmHg
• ↑ PaCO2
  • Central CRs (CCRs)
    • Most (80%) of response to ↑ PaCO2 by CCRs
  • Peripheral CRs
    • Response to ↑ PaCO2 is < 20% of total response
    • Much FASTER cf. CCR response
    • Role is to match ventilation to sudden ∆ in PaCO2
    • ↓ blood pH
    • Sensed by PCRs in CB only

CO₂ most important factor

• Minute ventilation is directly proportional to PaCO2 MV ↑ by 2-3 L/min per mmHg PaCO2
• Hypoxaemia has a synergistic effect on hypercapnoeic-ventilatory drive↓ PaO2 causes↑ MV for a given PaCO2, 
• ↑ ∆ MV per ∆ PaCO2

O₂ Less important in normal ranges

• PaO2 plays a SMALL role in ventilatory control
• Effect of PaO2 on ventilation:At normal PaCO2PaO2 < 500 mmHg MV ↑ slowly as ↓ PaO2 decrease
• PaO2 < 50 mmHg MV ↑ drastically
• There is synergistic ↑ in ventilatory response in the presence of hypercapnoea and/or acidosis
• MV ↑ drastically when PaO2 is < 100 mmHg

Gladwin 2016

Answer by Gladwin