CHEMICAL

CONTROL OF
BREATHING
 Introduction
Respiration
• Systemic function
• Needs to be controlled
Control
1. Automatic – Rhythmic discharge of motor neurons supplying the respiratory muscles
2. Voluntary
Brain stem
Medulla
Chemical control

pO2
CPG Respiratory pCO2
centers pH

Chemoreceptors
Two types
• Peripheral – Aortic bodies and carotid bodies
• Central

1. Carotid bodies
Small chemosensitive organs
2mm, 2 mg , 40x blood flow, 3x metabolism wrt brain
Bifurcation common carotid artery
Afferent nerves carotid bodies Glossopharyngeal nerve brain stem

Type 1 – Glomus cells

Rich blood supply -sinusoidal capillaries

Voltage gated channels and granules (catecholamines)
Hypoxia – low pO2
Release of substances
Dopamine –D2 receptors

Type 2- sustentacular cells

2. Aortic bodies
Less effective as compared to carotid bodies
Same glomus cells
Vagal nerve
 Problem Hypoxia
Nerve • pO2 – oxyHb binding less (oxyHb>Hb) – pH ^
discharge • Dominant factor 60mm of Hg 104 <100<80<60
RC stimulates • Inhibits the K+channels
Mechanism Ventilation ^ Directly Gutathione
Mitochondrial NADH
Heme bound
Directly - cAMP oxidase
protein
Reduced:oxidised
oxygen sensor
Inhibition of K
+ channels
Neurotransmitters
released
Depolarisation of
Glomus cell

Influx of Ca
VG Ca2+
2+
channels
open
Hypercapnia
Simpler- CO2^
- CO2 in blood increase Acidosis
- Taken up by Glomus cells pH falls due to pathologically high levels of
- H2CO3^ metabolism
Na-H+ exchanger blocked
- H+^
- pH falls H+ intracellular increase
- The H+ block K + channels K+ channel inhibited
• 40% ventilation
• Hypoxia increases sensitivity to Cyanide poison
pCO2 increases 60mm Hg blood pressure 104 pO2
Central chemoreceptors
Ventrolateral surface of pCO2 is the same in
medulla CSF and arterial
Closer to the junction blood
between pond and medulla Metabolic vs
Parts respiratory acid base
• Rostral disturbance
• Intermediate
• Caudal
Normal cases
Mechanism Combined effect of
Changes in H+ in hypoxia acidosis and
interstitial fluid and CSF hypercapnia
(pCO2)
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YOU