Lecture 22: Respiratory 4, Regulation And Acid-base Balance Flashcards
What are the respiratory control centres in the brainstem?
Motor neuron firing is triggered by synaptic input from brainstem control centres:
- DRG (medulla)- mostly inspiratory neurons
- VRG (medulla)-mostly expiratory neurons for active expiration
- PRGs (pons)- transition from inspiration to expiration, fine tuning of control
Regular respiratory rhythm generated by the respiratory central pattern generator
-sets the rhythm, receives sensory input and changes rhythm
Motor neuron activity and the respiratory cycle
- respiratory motor neurons have cyclical periods of activity and inactivity (AP bursts)
- the pattern of AP firing depends on the type of breathing (forced of unforced)
Sensory input to the central pattern generator
-central pattern generator receives a wide array of inputs
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Especially peripheral chemoreceptors and central chemoreceptors that pick up on conc of CO2, H+, O2 etc
What happens with the chemoreceptor reflex control of ventilation
Regulated variable: change in arterial blood gases ⬇ Sensors: chemoreceptors ⬇ Sensory receptors Integration centre: central pattern generator (brain stem) ⬇Somatic motor neurons Effectors: respiratory muscles ⬇ Change in alveolar ventilation ⬇ Restoration of blood gases
Tell me about the chemoreceptor responses
- chemoreceptors are cells that responds to a chemical change and send signals to other cells
- monitor PCO2, H+ (pH) and PO2 in major arteries and brain
- small changes in PCO2 and pH produce major changes in ventilation
- PO2 has little effect on ventilation unless it drops very low (hypoxemia)
Tell me about the peripheral chemoreceptors
- there located in carotid bodies, located near carotid sinus (and aortic bodies in arch of aorta)
- send signal via sensory neurons to central pattern generator
- direct contact with arterial blood
So
Increased (H+ and increased PCO2 and very low PO2) will = increased peripheral chemoreceptor activity therefore increased ventilation
Note: decreased (H+) or PCo2 will have the opposite effect, but increased PO2 won’t,
Tell me about the central chemoreceptors
- Neurons in the medulla that respond directly to changes in H+
- central chemoreceptors are indirectly activated by changes in arterial PO2
- central chemoreceptors are not sensitive to changes in O2
Activation of central chemoreceptors
Central chemoreceptors in the brain respond to changes in H+
- but, central chemoreceptors are protected by the blood brain barrier
- H+ can’t cross this barrier
CO2 can diffuse across the BBB into the CsF
- build up of Co2 in the CSF/medulla leads to H+ production
- H+ produced in the CsF/medulla activates central chemoreceptors
Central vs. peripheral chemoreceptors
Peripheral: (carotid and aortic bodies)
- responds quickly
- respond to small changes in arterial PCO2, pH (H+ concentration)
- respond to very low PO2
Central: (medulla of brain)
- response is slower than peripheral chemoreceptors but stronger
- respond directly t H+ changes in brain
- will respond when there are changes in arterial PCO2, brain blood flow or brain metabolism
- don’t respond to changes in Po2
Changes in arterial PCO are the main stimuli changes in ventilation
Ventilation- perfusion matching
For adequate gas exchange:
- airflow to alveoli (ventilation) = blood flow to alveoli (perfusion)
- total blood flow to lungs is controlled by the CVS
- cardiovascular disorders can cause inadequate gas exchange
- local mechanisms (via alveolar PO2 and PCO2) control blood vessels and bronchioles to ensure max gas exchange
Blood acid-base balance
PH is a measure of the concentration of H+ ions
-inverse relationship ie ⬆ in H+ causes decrease in pH.
Normal pH = 7.4
Blood pH is very tightly regulated
-a few seconds outside the pH range 6.8-8 leads to death.
-Acidosis (pH 7.42) leads to seizures, convulsions
H+ affect shape and function of proteins
What are the contributers to acid-base balance?
-blood pH can be altered by direct changes to the H+
(Adding extra H+ eg diet, keto acids, lactic acid)
-blood H+ and therefore pH is also influenced by the interaction of Co2 and H2O
-so changes in blood PCo2 or HCO3- will also alter blood pH
-⬆ PCO2 will shift the equation to Right and lead to ⬆ H+
-⬆ HcO3 will shift shift equation to left and leaf to decreased H+
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Disruptions to acid-base balance.
What causes changes to H+, HCO3 and PCO2?
Changes to H+:
- production of them by metabolism eg lactic acid, keto acids
- excretion of H+ by kidneys
- loss of stomach H+ by vomiting
Changes to HCO3:
- changes to HCO3 added back to the blood by the kidneys
- loss of HCO3 due to diarrhoea
Changes to PCO2
- hypoventilation of
- hyperventilation will in erase or decrease PCO2 respectively
How does the body compensate for acid-base disruptions
The body has 3 methods to limit blood pH disruptions
Buffering of H+
-by HCO3- and Hb
Respiratory compensation:
-changing blood PCO2 by changing ventilation
Renal compensation:
-change the amount of H+ excreted and HcO3- added to the blood
Tell me how buffering of H+ in the blood occurs?
Buffet = compound that binds to or releases, H+, altering pH
- first and fastest line of defence against pH change
- in plasma/ ECF, HCL3- is the most important buffer
- intracellular buffers are phosphates and proteins including Hb
