Chemical control of breathing + Long term changes

Question 1

What happens to pO2 and pCO2 in hyper and hypoventilation? Why?

Answer 1

Hyperventilation; breathing in more with NO change in metabolism means pO2 rises and pCO2 falls

Hypoventilation: Breathing less with NO change in metabolism means pO2 falls and pCO2 rises

Question 2

What happens if pH falls below 7?

What happens if pH rises above 7.6?

Answer 2

below 7: plasma K+ rises and enzymes lethally denatured

above 7.6: free calcium concentration falls enough to produce fatal tetany

Question 3

Explain why respiratory acidosis and alkalosis occur

What compensates for this, and how long does it typically take?

Answer 3

Resp. Acidosis: hypoventilation leads to accumulating CO2 (Hypercapnia), pH falls and acidosis occurs

Resp. Alkalosis: Hyperventilation diminishes CO2 levels, Hypocapnia occurs and pH rises

Kidneys compensate for this by increasing/decreasing production of HCO3, takes typically 2-3 days

Question 4

Explain the difference between a correction and a compensation

Answer 4

Correction: directly returning the disturbed variable to normal

Compensation: Indirect: adjust a different variable to change the disturbed variable

Question 5

How would you compensate for a metabolic acidosis?

Answer 5

Tissues produce lactic acid which reacts with HCO3-, and decreases the pH

Increase ventilation to lower pCO2

Question 6

Why is there limited compensation that can be done in a metabolic alkalosis?

Answer 6

Plasma [HCO3-] can rise, e.g after vomiting, making the pH rise as well

Can compensate to a degree with decreased ventilation (increasing plasma pCO2) but cannot ask someone to completely stop breathing

Question 7

What mechanism monitors pO2, how does it monitor pO2 and where is it?

Answer 7

Peripheral chemoreceptors in the carotid sinus and aortic body, sense a fall in pO2 and stimulate:

1. Increased breathing
2. Change in HR
3. Diversion of blood to kidneys, heart and brain

Question 8

What do central chemoreceptors do? Where are they?

Answer 8

Central chemoreceptors in the medulla oblongata detect changes in CSF pH and arterial pCO2:

Since CO2 can pass the BBB (and HCO3- cannot), an elevated arterial pCO2 drives CO2 across the BBB and CSF pH falls. Central chemoreceptors detect this and signal for an increase in ventilation

Question 9

What happens when CSF changes become long-term and persistent

Answer 9

Need choroid plexus cells: They control the [HCO3-], turn off/re-set the central chemoreceptors and import HCO3- into the CSF

Question 10

How can Type 1 resp failure occur?

Answer 10

When there’s a pulmonary elbolism or mismatched ventilation/perfustion rate

Question 11

When does hypoxia occur?

Answer 11

1. Type 1 Resp failure

2. High altitidues

Question 12

When does acute hypoxia occur? Why is this so dangerous?

Name 4 symptoms (Hint: one is fatal)

Answer 12

At very high altidudes: >20-29,000 ft

1. First, peripheral chemoreceptors attempt to increase ventilation: so pCO2 falls and CSF becomes alkaline
2. BUT the alkaline CSF inhibits central chemoreceptors as they’re only sensitive to decreases in pH, which tells the body to decrease ventilation

System is trapped:
If you breathe more: you’ll die of alkalosis
If you breathe less: you’ll die from hypoxia

Symptoms: nausea, lack of coordination, euphoria, death

Question 13

How can you overcome/prevent acute hypoxia from occuring both short and long term?

Answer 13

Short term Acclimatisation/Gradual exposure…

1. Mild hypoxia stimulates ventilation to raise CSF pH slightly (but not enough to inhibit central chemoreceptors)
2. Choroid plexus cells respond and export HCO3- into CSF and CSF pH is corrected
3. Hypoxic drive comes in: subject breathes more

Longer-term Acclimitasation:

1. O2 increased carrying capacity:
   - polycythaemia: increased RBCs
   - 2,3 DPG: Bohr shift: means Hb in T state and is binds to less O2, so more O2 is available
2. CO increases and is directed towards vital organs

Question 14

What happens to the ventilation rate during mild exercise?

Answer 14

Ventilation rate jumps suddenly before oxygen begins: neural anticipation for oxygen, joint and muscle receptors stimulate body to be ready to supply O2

During exercise: Ventilation rate increases until it plateaus by matching exercise

pCO2 and pO2 are normal due to central chemoreceptors control

Question 15

What happens to the ventilation rate during strenous exercise?

Answer 15

Subject may hyperventilate and possibly go into hypocapnia (despite abundant CO2 being produced metabolically).
At the end of exercise ventilation drops abruptly, and gently goes back to normal

Question 16

What does the Henderson Hasselback equation tell us?

Answer 16

pH is inversely proportional to pCO2

Question 17

After choroid plexus cells have imported HCO3- into the CSF, what happens next with the plasma HCO3 and O2?

Answer 17

The plasma is in a slight HCO3- deficit, so the kidney will resorb more HCO3- to compensate. Since pO2 levels are still low, so peripheral chemoreceptors will stimulate an increase in ventilation (and HR, and redirect bloodflow)

Question 18

What is the key difference between type 1 and 2 respiratory failure? Name one example of type 2 resp failure

Answer 18

Type 1: low pO2 and normal or low pCO2

Type 2: low pO2 and high pCO2, e.g; chronic bronchitis