Resp. 5 - Control of Ventilation Flashcards

1
Q

Respiratory Control System

A
  1. Automatic Rhythm
  2. Rhythm Adjustment to Changing Demands

– E.g. – metabolic demands ( PO2 , PCO2 and pH)

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2
Q

Automatic rhythm used when were not consciously controlling breathing, in tune with

A

metabolic demands (partial pressure of O2 and CO2 and pH) that will increase or decrease ventilation or the depth of breathing or the rate.

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3
Q

Change in partial pressures are monitored by:

A
  • Peripheral Chemoreceptors (PCR)
  • Central Chemoreceptors (CCR)

-Drive the CPG (central pattern generator)

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4
Q

What does the CPG do?

A

Increase or decrease ventilation

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5
Q

Respiratory and Metabolic Acidosis/Alkalosis:

A
  • Respiratory acidosis →
  • Respiratory alkalosis →
  • Metabolic Acidosis →
  • Metabolic Alkalosis →
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6
Q

• Respiratory acidosis →

A

hypoventilation (CO2 production > CO2 elimination): not only PCO2 ↑ but also H+ concentration ↑

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7
Q

• Respiratory alkalosis →

A

hyperventilation (CO2 production < CO2 elimination): not only PCO2 ↓ but also H+ concentration ↓

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8
Q

• Metabolic Acidosis →

A

↑ in blood H+ concentration independent from changes in PCO2

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9
Q

• Metabolic Alkalosis →

A

↓ in blood H+ concentration independent from changes in PCO2

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10
Q

Where are peripheral chemoreceptors located

A

Carotid and aortic bodies

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11
Q

Peripheral Chemoreceptor Sense mostly changes in

A

arterial PO2 and will also be activated by changes in pH (H+ conc.).

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12
Q

• The carotid and aortic bodies sense primarily

A

hypoxia, which is a low arterial PO2 level

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13
Q

Which cells are coupled with blood vessels to monster the levels of O2 levels

A

The Glomus Cell Is the Chemosensor in the Carotid and Aortic Bodies

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14
Q

_______ that are responsible for evoking an increase in ventilation to a decrease in PaO2.

A

Glomus cells

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15
Q

Type I glomus cells -

A

chemosensitive; drive the response, or the change in ventilation, if there are changes in the arterial PO2.

  • Triggered when O2 falls below 60 mmHg.
  • sensitive to high conc. of H+ (low pH)
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16
Q

Chemical Control of Ventilation- CCR

A
  • Sensitivity to increase in PaCO2(H+)

* Indirectly does sensitive to PaCO2, and directly sensitive to H+ levels.

17
Q

Respiratory Acidosis vs Metabolic Acidosis

A

Both result in significant responses when viewed by CCR

Respiratory Acidosis: increase in PaCO2 and decrease in pH

Metabolic Acidosis: no change in PaCO2 but decrease in pH

18
Q

Metabolic acidosis Occurs with the production of

A

acids which are carried in the blood and are not associated with changes in PCO2

19
Q

Metabolic acidosis process

A

concentration of H+ → activation of PCR (glomus cells in carotid bodies) → increase ventilation → decrease alveolar PCO2 → decrease arterial PCO2 → return of arterial hydrogen ions towards normal levels

20
Q

• H+ stimulates mostly peripheral chemoreceptors because

A

H+ does not cross easily blood brain barrier (As CO2 does)

21
Q

Respiratory acidosis process

A

As CO2 crosses the BBB, producing more bicarbonate and H+, the pH will drop making it more acidic, the CCR then respond by increasing ventilation.

22
Q

Dependence of CSF pH on blood pH

A
  • the response for repository acid-base changes is far greater then metabolic acid-base changes because of the H+ easily detected by CCR.
  • the reps once for Metabolic acid-base changes is a lot smaller since H+ aren’t diffusible, and wont be detected (small relative change)
23
Q

Dependance of ventilation on CSF pH

A

Heavily relies on the CCR to monitor pH and increase ventilation when its to acidic.

24
Q

Very importantly for control of metabolism, or acidity of blood. Chngaes in CO2 and H+ on a regulatory pathways are

A

more important then any changes in O2.

25
Q

A decrease in PO2 < 60 mmHg in the arterial blood will be detected by

A

PCR, increase ventilation via the respiratory control centres.

26
Q

An increase in PCO2 in the arterial blood will be cause

A

An increase in H+ (decrease in pH) in both the arterial blood AND the cerebral spinal fluids.

  • H+ ions detected by PCR (PCR more sensitive to O2 changes) and will cause an increase in ventilation at the CPG.
  • H+ ions detected by CCR and will increase ventilation via CPG.
27
Q

Response to Hypercapnia Mediated by

A

Response to breathing a gas mixture containing carbon dioxide: acts through central or peripheral chemoreceptors

28
Q

Response to Hypercapnia Mediated by Central chemoreceptors

A

Increase in inspired CO2 → increase alveolar PCO2 → increase in arterial PCO2 → increase in brain extracellular fluid PCO2 → increase in brain extracellular fluid H+ ion conc. → H+ ions activate central chemoreceptors → CCR increase rate of firing → provide an excitatory drive to the ventral respiratory group → increase ventilation.

29
Q

Response to Hypercapnia Mediated by peripheral chemoreceptors

A

Increase in inspired CO2e → increase alveolar PCO2 → increase in arterial PCO2 → increase arterial concentration of H+ ions (reduction in pH) → glomus cells (carotid bodies) increase rate of firing and excite the glossopharyngeal nerve→ drive activity in the dorsal and ventral respiratory group, where the Pre- Bötzinger complex and pFRG are located → increase ventilation

30
Q

Activation of the peripheral and central chemoreceptors will activate

A

respiratory neurons in the medulla which will increase ventilation so the H+ conc. at the level of the periphery (arterial blood pH) and at the level of the brain will return to normal levels

31
Q

A direct increase of ventilation due to high levels of CO2 is always done by the

A

CCR as they are indirectly sensitive to CO2 and directly sensitive to H+.

32
Q

Integrated Responses to Hypoxia, Hypercapnia and Acidosis

A

CCR:
– 80 – 90% response to respiratory acidosis

PCR:
– slow
– fast

33
Q

Dependance on PO2

A

Change in O2 is VERY fast rxn form the glomus cells, increases ventilation

  • no response until O2 drops to 50 mmHg
  • even though O2 drops to 50, CO2 remains constant at 36 mmHg