Control of Ventilation and Responses to Stress
Key concepts on brainstem respiratory centers, chemoreceptors, and ventilatory responses to CO₂, hypoxia, and stress.
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Questions Covered in This Set
12 cards to master
What are the three components of the ventilatory negative-feedback loop?
Controller (brainstem centers), sensors (chemoreceptors and mechanoreceptors), and effectors (diaphragm, intercostals, accessory muscles). This holds arterial PCO₂ within ~±3 mmHg of 40.
What is the pre-Bötzinger complex?
A cluster within the ventral respiratory group that is the leading candidate for the respiratory pacemaker — isolated slices continue rhythmic bursting in vitro.
Compare the dorsal (DRG) and ventral (VRG) respiratory groups.
DRG: near nucleus tractus solitarius, primarily inspiratory, receives visceral afferents via CN IX and X. VRG: contains inspiratory and expiratory neurons, drives active expiration during exercise and coughing.
What does the pontine pneumotaxic center do, and what happens if it is damaged?
It acts as an inspiratory off-switch, tuning respiratory rate and tidal volume. Damage plus vagotomy causes apneusis — prolonged gasping inspirations.
What do central chemoreceptors actually sense?
[H⁺] in the CSF, not CO₂ directly. CO₂ crosses the blood–brain barrier freely (H⁺ and HCO₃⁻ do not), hydrates to carbonic acid, and lowers CSF pH.
Why is the CSF an amplified sensor for PCO₂ changes?
CSF has very little protein buffering, so a given ΔPCO₂ produces a larger pH change in CSF than in blood.
Why is the CO₂ drive blunted in chronic hypercapnia (COPD)?
Choroid plexus pumps HCO₃⁻ into the CSF, normalizing CSF pH despite high PCO₂; these patients rely relatively more on hypoxic drive.
How do peripheral chemoreceptors detect hypoxia?
Glomus (type I) cells have O₂-sensitive K⁺ channels; hypoxia closes them → depolarization → Ca²⁺ entry → dopamine release → increased afferent firing (CN IX from carotid bodies, CN X from aortic bodies).
Why don't anemia and CO poisoning stimulate ventilation?
Peripheral chemoreceptors respond to PaO₂, not O₂ content. Both conditions have a normal PaO₂ — a classic clinical trap.
What are the relative contributions of central vs. peripheral chemoreceptors to the CO₂ response?
Central ~70–80% (slower, seconds to a minute); peripheral ~20–30% (fast, ~1–3 s, providing breath-to-breath adjustments).
At what PaO₂ does peripheral chemoreceptor firing rise steeply, and how do hypoxia and hypercapnia interact?
Firing increases steeply below PaO₂ ≈ 60 mmHg (mirroring the oxyhemoglobin curve shoulder). Hypoxia and hypercapnia interact multiplicatively — the ventilation vs. PCO₂ slope steepens at low PaO₂.
What limits voluntary breath-holding?
Rising PCO₂ overwhelming voluntary cortical suppression — not falling PO₂.
