chemical control of respiration

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Physiology Seminar 18/02/2013 POWERPOINT ® SEMINAR SLIDE PRESENTATION PREPARED BY DR. ANWAR HASAN SIDDIQUI, senior resident, dep't of physiology, jnmc, amu, aligarh ©Dr. Anwar Siddiqui CHEMICAL CONTROL OF RESPIRAT ION 1

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Page 1: Chemical control of respiration

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Physiology Seminar18/02/2013

POWERPOINT® SEMINAR SLIDE PRESENTATION PREPARED BY DR. ANWAR HASAN SIDDIQUI, senior resident, dep't of physiology, jnmc, amu, aligarh

©Dr. Anwar Siddiqui

CHEMICAL CONTROL OF RESPIRATION

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Need for chemical regulatory mechanism?

Maintenance of alveolar pCO2 at constant level

Combat the effect of excess H+ in the bodyRaising pO2 if it falls to potentially lethal level

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Respiratory chemoreceptors

Three types of respiratory chemoreceptors Peripheral chemoreceptorMedullary or central chemoreceptors

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Peripheral chemoreceptorsCarotid 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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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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Mechanism of neurotransmitter release by type 1 cells

Image courtesy-http://www.colorado.edu/intphys/Class/IPHY3430-200/015breathing.htm

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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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Why are these receptors not activated in anaemia and

carbon monoxide poisoning???

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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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• Rostral (R) and caudal (C) chemosensitive areas on the ventral surface of the medulla.

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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).

HCO3-

pH pCO2 HCO3-

7.33 44 22

7.4 40 24

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Chemical factors affecting respiration

• Effect of Hypoxia.

• Effect of CO2

• Effect of H+ concentration

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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 Hgto 20 mm Hg.Ref –Guyton and Hall physiology

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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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• 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.

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

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• 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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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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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.)

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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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A presentation by Dr Anwar Hasan Siddiqui

Thanks….