Resp. 5 - Control of Ventilation Flashcards
Respiratory Control System
- Automatic Rhythm
- Rhythm Adjustment to Changing Demands
– E.g. – metabolic demands ( PO2 , PCO2 and pH)
Automatic rhythm used when were not consciously controlling breathing, in tune with
metabolic demands (partial pressure of O2 and CO2 and pH) that will increase or decrease ventilation or the depth of breathing or the rate.
Change in partial pressures are monitored by:
- Peripheral Chemoreceptors (PCR)
- Central Chemoreceptors (CCR)
-Drive the CPG (central pattern generator)
What does the CPG do?
Increase or decrease ventilation
Respiratory and Metabolic Acidosis/Alkalosis:
- Respiratory acidosis →
- Respiratory alkalosis →
- Metabolic Acidosis →
- Metabolic Alkalosis →
• Respiratory acidosis →
hypoventilation (CO2 production > CO2 elimination): not only PCO2 ↑ but also H+ concentration ↑
• Respiratory alkalosis →
hyperventilation (CO2 production < CO2 elimination): not only PCO2 ↓ but also H+ concentration ↓
• Metabolic Acidosis →
↑ in blood H+ concentration independent from changes in PCO2
• Metabolic Alkalosis →
↓ in blood H+ concentration independent from changes in PCO2
Where are peripheral chemoreceptors located
Carotid and aortic bodies
Peripheral Chemoreceptor Sense mostly changes in
arterial PO2 and will also be activated by changes in pH (H+ conc.).
• The carotid and aortic bodies sense primarily
hypoxia, which is a low arterial PO2 level
Which cells are coupled with blood vessels to monster the levels of O2 levels
The Glomus Cell Is the Chemosensor in the Carotid and Aortic Bodies
_______ that are responsible for evoking an increase in ventilation to a decrease in PaO2.
Glomus cells
Type I glomus cells -
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)
Chemical Control of Ventilation- CCR
- Sensitivity to increase in PaCO2(H+)
* Indirectly does sensitive to PaCO2, and directly sensitive to H+ levels.
Respiratory Acidosis vs Metabolic Acidosis
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
Metabolic acidosis Occurs with the production of
acids which are carried in the blood and are not associated with changes in PCO2
Metabolic acidosis process
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
• H+ stimulates mostly peripheral chemoreceptors because
H+ does not cross easily blood brain barrier (As CO2 does)
Respiratory acidosis process
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.
Dependence of CSF pH on blood pH
- 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)
Dependance of ventilation on CSF pH
Heavily relies on the CCR to monitor pH and increase ventilation when its to acidic.
Very importantly for control of metabolism, or acidity of blood. Chngaes in CO2 and H+ on a regulatory pathways are
more important then any changes in O2.
A decrease in PO2 < 60 mmHg in the arterial blood will be detected by
PCR, increase ventilation via the respiratory control centres.
An increase in PCO2 in the arterial blood will be cause
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.
Response to Hypercapnia Mediated by
Response to breathing a gas mixture containing carbon dioxide: acts through central or peripheral chemoreceptors
Response to Hypercapnia Mediated by Central chemoreceptors
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.
Response to Hypercapnia Mediated by peripheral chemoreceptors
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
Activation of the peripheral and central chemoreceptors will activate
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
A direct increase of ventilation due to high levels of CO2 is always done by the
CCR as they are indirectly sensitive to CO2 and directly sensitive to H+.
Integrated Responses to Hypoxia, Hypercapnia and Acidosis
CCR:
– 80 – 90% response to respiratory acidosis
PCR:
– slow
– fast
Dependance on PO2
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
