8 - Chemical Control of Breathing Flashcards
What is the difference between hypoxia and hypoxaemia?
Hypoxaemia is a low O2 in the blood, due to dissociation curve body can tolerate small changes
What are normal values for:
- PaCO2
- PaO2
- Bicarbonate
- pH
What is hypo and hyper capnia?
Hyper = increase pCO2
Hypo = decreased pCO2
Small changes in pCO2 can have big effects on pH
During exercise pCO2 increases and pO2 decreases, how is this overcome?
What happens to partial pressures during hyperventilation and what can this lead to?
- Can lead to rise in pH as alveolar pCO2 decreases leading ro respiratory alkalosis
- This is corrected by kidneys secreting more HCO3- returning the ratio of HCO3 to CO2 to normal but buffer base concentration is reduced –> compensated respiratory alkalosis (2-3 days)
What happens to partial pressures during hypoventilation and what can this lead to?
- Dissolved CO2 rises so plasma pH falls so respiratory acidosis
- Kidney reduces secretion of HCO3- so compensated respiratory acidosis. Takes 2-3 days
When does hypocapnia occur?
When does hypoxia start to occur?
- 100% saturation at 8kPa so pO2 can fall quite a lot before hypoxia
What happens if the pH of blood falls below 7 or rises above 7.6?
- Below 7 enzymes are denatured
- Above 7.6 free calcium concentration drops so tetany
How does metabolic acidosis occur and how does the body compensate for this?
- Tissues produce acid so HCO3- reacts with them lowering pH
- Can increase ventilation to lower pCO2 to restore pH
- Buffer base is deplete until corrected by the kidney
How does metabolic alkalosis occur and how does the body compensate for this?
- If plasma HCO3- rises, e.g after losing protons in vomiting or blood loss, the pH falls
- Can only be slighlty compensated by lowering breathing as don’t want to risk hypoxia so mainly corrected by kidneys
What is the difference between correcting respiratory acidosis/alkalosis to metabolic acidosis/alkalosis?
- Respiratory is mainly restored by the kidney altering HCO3- levels
- Metabolic is usually by changes in ventilation rate and therefore alveolar pCO2
What factors affect changes in ventilation rate the most?
These changes are detected by chemoreceptors and send impulses to the respiratory centre in the brain stem to alter rate and depth of respiration
What are the two types of chemoreceptors and what changes do they detect?
H+ means changes in pH
Where are peripheral chemoreceptors and what is their response when levels of CO2, O2 and H+ change?
- Carotid and aortic bodies
- O2: large falls in pO2 cause an increase in tidal volume and resp rate. Also direct more blood to brain and kidney and increase pumping of heart. Do not adapt to chronic hypoxia
- CO2: Not very sensitive, only when large changes. Not crucial for controlling resp but when they do respond they respond quickly to large changes in pCO2
- pH: carotid bodies detect low pH and increase tidal volume and resp rate
Where are central chemoreceptors and what is their response when levels in the blood change?
- Ventral surface of the medulla, exposed to CSF
- Respond to drop in pH, which occurs when high pCO2 as the blood brain barrier only allows CO2 across not HCO3 so pH is affected directly by pCO2
- Impulses to brain are negative feedback so if low pH in CSF means high pCO2 SO tidal volume and ventilation rate increase
How is bicarbonate concentration in the CSF controlled if bicarbonate cannot pass the blood brain barrier?
- Choroid Plexus pumps HCO3- in and out of CSF
- This plexus is long term solution if issues with hypoxia or lung disease
What is the difference in the response to falling pO2 and falling pCO2?
O2: increased ventilation only when fall is large. Respiratory drive lasts as long as the hypoxia so chemoreceptors do not reset
CO2: small changes in levels lead to rapid changes in ventilation. Central chemoreceptors reset central chemoreceptors so if have hypoxic episode in chronic hypercapnia this will be detected and driven by peripheral receptors
