The document summarizes the chemical control of respiration through respiratory chemoreceptors. There are three types of chemoreceptors: peripheral chemoreceptors located in the carotid bodies and aortic bodies that detect changes in arterial pCO2, pO2, and pH; central or medullary chemoreceptors located in the brainstem that are stimulated by increased hydrogen ion concentration in cerebrospinal fluid; and both peripheral and central chemoreceptors work together to maintain homeostasis and stimulate respiration in response to changes in oxygen, carbon dioxide, and hydrogen ion levels in order to regulate respiration.

1. Physiology Seminar
18/02/2013
CHEMICAL
CONTROL OF
RESPIRATION
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©Dr. Anwar Siddiqui

2. Need for chemical regulatory mechanism?
Maintenance of alveolar pCO2 at constant level
Combat the effect of excess H+ in the body
Raising pO2 if it falls to potentially lethal level
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3. Respiratory chemoreceptors
Three types of respiratory chemoreceptors
Peripheral chemoreceptor
Medullary or central chemoreceptors
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4. Peripheral chemoreceptors
Carotid and aortic bodies
 Discovered by Heymans C and Neil E in 1930.
 Carotid body near the carotid bifurcation on each
side, and usually two or more aortic bodies near the
arch of the aorta.
 These chemoreceptors increase their firing rate in
response to increased arterial pCO2, decreased
arterial PO2, or decreased arterial pH.
 Carotid and aortic body (glomus) contains islands of
two types of cells, type I and type II cells, surrounded
by fenestrated sinusoidal capillaries
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5. Figure 1 Figure 2
Fig 1-Position of aortic and carotid
bodies.
Fig 2 and fig 3-Organization of carotid
body
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6. Mechanism of neurotransmitter release by type 1 cells
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Image courtesy-http://www.colorado.edu/intphys/Class/IPHY3430-200/015breathing.htm

7. Stimulus for activation of peripheral receptors
 Hypoxia- decrease in arterial pO2
 Vascular stasis- amount of O2 delivered to receptors is
decreased
 Asphyxia- lack of O2 plus CO2 excess
 Drugs- cyanide, nicotine etc
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8. Why are these receptors
not activated in anaemia
and carbon monoxide
poisoning???
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9. Central chemoreceptor
• Also known as medullary chemoreceptor
• Located on the ventral surface of medulla near VRG.
• Stimulated by the H+ concentration of CSF and brain
interstitial fluid.
• Magnitude of stimulation is directly proportional to
H+ concentration ,which increases linearly with
arterial pCO2.
• Gets inhibited by anaesthesia, cyanide and sleep.
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10. • Rostral (R) and caudal (C) chemosensitive areas on the ventral surface of
the medulla.
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11. pH pCO2 HCO3-
7.33 44 22
7.4 40 24
HCO3-
Representation of the central chemoreceptor showing its relationship to carbon dioxide (CO2),
hydrogen (H+), and bicarbonate (HCO3–) ions in the arterial blood and cerebrospinal fluid (CSF).
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12. Chemical factors affecting respiration
• Effect of Hypoxia.
• Effect of CO2
• Effect of H+ concentration
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13. Effect of hypoxia on respiration
• Decrease in O2 content of inspired air increases
respiratory minute volume.
• The increase is slight when the IpO2 is above 60 mm
Hg and marked when the IpO2 falls below 60 mm Hg.
The red curve demonstrates the effect of
different levels of arterial PO2 on alveolar
ventilation, showing a sixfold increase in
ventilation as the PO2 decreases from the
normal level of 100 mm Hg
to 20 mm Hg.
Ref –Guyton and Hall physiology
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14. Effect of CO2 respiration
• The arterial PCO2 is normally maintained at 40 mm
Hg.
• If arterial PCO2 rises as a result of increased tissue
metabolism, ventilation is stimulated and the rate of
pulmonary excretion of CO2 increases until the
arterial PCO2 falls to normal.
• This feedback mechanism keeps CO2 excretion and
production in balance.
• There occurs an essentially linear relationship
between respiratory minute volume and pCO2
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15. Figure depicts responses of normal
subjects to inhaling O2 and
approximately 2, 4, and 6% CO2. The
increase in respiratory minute volume
is due to an increase in both the depth
and rate of respiration.
Ref-Ganong review of medical
physiology
• When the PCO2 of the inspired gas is close to the
alveolar PCO2, elimination of CO2 becomes difficult.
• When the CO2 content of the inspired gas is more
than 7%, the alveolar and arterial PCO2 begin to rise
abruptly in spite of hyperventilation.
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16. • The resultant accumulation of CO2 in the body
(hypercapnia) depresses the central nervous
system, including the respiratory center, and produces
headache, confusion, and eventually coma (CO2
narcosis).
• CO2 primarily acts on central chemoreceptors but
when central chemoreceptors are depressed by
anaesthesia stimulation of peripheral chemoreceptors
occur.
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17. Effect of H+ concentration on
respiration
• H+ normally cannot act through modification of
central chemoreceptors.
• Acidosis (increase H+ concentration in blood)
produces marked respiratory stimulation causing
hyperventilation
• Alkalosis (decrease H+ concentration in blood)
depresses respiratory centre and causes
hypoventilation.
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18. Interaction of chemical factors in
regulating respiration
Interaction of CO2 and O2.
Ventilation at various alveolar PO2 values when PCO2 is held constant at 49,44,
or 37 mm Hg. (Data from Loeschke HH and Gertz KH.) 18

19. Interaction of CO2 and H+.
• The stimulatory effects of H+ and CO2 on respiration
appear to be additive .
• In meatabolic acidosis the same amount of respiratory
stimulation is produced by lower arterial pCO2
levels.
• The CO2 response curve shifts 0.8 mm Hg to the left
for each nanomole rise in arterial H+.
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20. Thanks….
A presentation by Dr Anwar Hasan Siddiqui
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