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BMS 242 - CVS respiratory > Acid base balance II > Flashcards

Acid base balance II Flashcards

1
Q

Where are the CENTRAL chemoreceptors found?

A

In the central nervous system

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2
Q

What is the primary tonic driving force for normal breathing when the blood gas parameters are normal?

A

The central chemoreceptors

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3
Q

What is the main activator of the central chemoreceptors?

How is this different to peripheral chemoreceptors?

A

Hypercapnia (high CO2)

Peripheral chemoR - Hypoxia (low O2)

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4
Q

What actually activates the chemoR?

A

H+

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5
Q

If increase PCO2 from 40 to 45mmHg, what happens to the ventilation?

A

Doubles

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6
Q

Who discovered chemoreceptors?

A

Isidore Leusen

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7
Q

Where are the central chemoreceptors found?

A
  • Within the BRAIN PARENCHYMA, bathed in brain extracellular fluid (BECF)
  • Separated from the ARTERIAL blood supply BBB
  • In the VENTROLATERAL MEDULLA and other BRAINSTEM NUCLEI
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8
Q

What is an important property of the BBB?

A

Poor ion solubility

BUT

CO2 can cross

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9
Q

What happens to the BECF when there is an increase ARTERIAL PCO2?

A
  • This is reflected in the BECF (As CO2 can cross the BBB)
  • Changing the pH of the BECF
  • Stimulating the central chemoreceptors to signal to the brain
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10
Q

What is the buffering power of BECF?

Why?

What does this mean?

A

Lower than the plasma
But has a HCO3- buffering system

Due to LESS PROTEINS

Means:
- When there is a change in CO2 in the arterial blood supply, there is a larger change in pH the BECF than in the plasma

  • System in the brain is MORE SENSITIVE
  • Central chemoR are stimulated more strongly than peripheral chemoR
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11
Q

What can be used as a LONG-TERM compensation to minimise prolonged changes in pH in the BECF?

A

Upregulation of transportation of HCO3- from the blood into the BECF

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12
Q

How does metabolic acidosis effect the central chemoreceptors?

A

WEAK activation of the chemoreceptors:
- Metabolic means change in [H+]

  • H+ cannot cross the BBB
  • Smaller change in pH compared to the plasma
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13
Q

How does respiratory acidosis effect the central chemoreceptors, compared to metabolic acidosis?

A

10-35% increase in the pH compared to metabolic:
- CO2 passes the BBB

  • pH in the BECF similar to that in the plasma
  • Stronger stimulation for the same pH change in metabolic (H+ cannot cross)
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14
Q

What are the 2 types of central chemoreceptors?

What neurotransmitters do they release?

A

1) Acid ACTIVATED
- Release serotonin

2) Acid INHIBITED
- Release GABA

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15
Q

What chemoR are activated in respiratory acidosis?

A

BOTH central and peripheral

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16
Q

If O2 is normal, what % do central chemoreceptors play in acid base response in respiratory acidosis?

A

65-80%

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17
Q

In respiratory acidosis, which chemoR act first?

A

Peripheral

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18
Q

Why does severe metabolic acidosis lead to hyperventilation?

A

Rapidly decreases PCO2

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19
Q

In ACUTE metabolic acidosis, which chemoR are more important?

A

Peripheral

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20
Q

In CHRONIC metabolic acidosis, which chemoR are more important?

A

Central - long-term role

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21
Q

What happens when you breath FASTER?

A

1) Decrease in PCO2
2) Decrease in [H+]
3) Increase in pH (alkalosis)
4) INHIBIT chemoR
5) Decrease rate of breathing to reduce loss of CO2

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22
Q

What happens when you breath SLOWER?

A

1) Increase in PO2
2) Increase in [H+]
3) Decrease in pH (acidosis)
4) Activate ChemoR
5) Increase rate of breathing to increase loss of CO2

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23
Q

What is the ONLY system for the long-term regulation of acid base status of the body?

A

Kidney (Renal system)

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24
Q

What are the 3 mechanisms used by the kidney the excrete acid from the body?

A

1) HCO3- handling
2) Urine acidification
3) Ammonia synthesis

25
Q

What is the proximal cell model for the reabsorption of HCO3-?

A

1) Na+ into the cell at the APICAL MEMBRANE from tubular fluid
- Through Na+/H+ EXCHANGER
2) H+ combines with HCO3- in the filtrate –> form CARBONIC ACID(H2CO3)
3) H2CO3 dissociates into H2O and CO2 - both move into the cell
4) H2O + CO2 –> H2CO3
5) H2CO3 –> H+ + HCO3-
6) HCO3- reabsorbed through the BASOLATERAL membrane through the Na+/HCO3- COTRANSPORTER
7) H+ recycles across the apical membrane

26
Q

What enzyme is responsible for H+ + HCO3- –> H2CO3?

What enzyme is responsible for H2CO3 –> H+ + HCO3?

A

Carbonic anhydrase on the extracellular apical membrane

Carbonic anhydrase on the inside of the cell

27
Q

How does CO2 move into the proximal cell?

A

Diffusion

28
Q

How does H2O move into the proximal cell?

A

Through aquaporins

29
Q

What is the distal tubule model for reabsorption of HCO3-?

A

Same as the proximal tubule model, but H+ efflux is through the PROTON PUMP

30
Q

How does HCO3- reabsorption allow the regulation of acid in the body?

A

H+ not reabsorbed - secreted

HCO3- reabsorbed - combine with H+ to produce H2CO3 and then H2O and CO2

31
Q

Where does HCO3- handling happen?

A

90% in the PROXIMAL TUBULE

10% in the DISTAL TUBULE

32
Q

How much does acidification of the urine contribute to excretion of H+ in the urine?

A

25%

33
Q

How much does ammonia synthesis contribute to excretion of H+ in the urine?

A

75%

34
Q

What does base conservation allow?

What are the methods of base conservation?

A

Excretion of acid in the urine whilst retaining HCO3- produced by the cell as a consequence of metabolism

Methods:

  • Acidification of urine
  • Ammonia synthesis
35
Q

What is alkaline phosphate?

What is it used for?

A

Alkaline salt in the tubular fluid

Used to bind H+ and turn into the acidic form (acid phosphate) - for acid excretion

Na2HPO4 + H+ –> NaH2PO4

36
Q

What is the model of urine acidification?

A

1) Filtered Na2HPO4 (alkaline phosphatase) loses Na+ –> NaHPO4-
2) NA+ into the cell at the APICAL membrane through the Na+/H+ exchanger
3) H+ combines with NaHPO4- —> NaH2PO4 (acid phosphatase) which is EXCRETED into the urine
4) HCO3- produced from the metabolism when CO2 combines with H2O (under influence of CA)
5) HCO3- reabsorbed through the BASOLATERAL membrane

37
Q

What is ammonia production used for?

A

To excrete H+ ions into the tubular fluid so that the H+ are no free in the substance

38
Q

Is ammonia/ammonium permeable?

Why?

A

Ammonia is permeable (NH3)

Ammonium is NOT (NH4+) - ions can’t diffuse through membrane

39
Q

How does ammonia production take place inside the cel?

A

1) Glutamine broken down into ALPHA-KETO GLUTARATE
2) Forms NH3 and H+ - excreted into the tubular fluid, where they combine to form NH4+
3) NH4+ cannot pass back through the membrane - DIFFUSION TRAPPED

40
Q

Where is glutamine broken down into ALPHA-KETO GLUTARATE?

A

In the KIDNEY

41
Q

What is the renal response to acidosis?

A
  • INCREASE H+ excretion
  • Normal HCO3- excretion of 0 (FULL reabsorption)
  • DECREASE pH of URINE
  • INCREASE pH of PLASMA
42
Q

What is the renal response to alkalosis?

A
  • DECREASE H+ excretion
  • INCREASE HCO3- excretion
  • INCREASE pH of urine
  • DECREASE pH of plasma
43
Q

When is respiratory acidosis seen?

A

When CO2 level INCREASES (reduced elimination in the lungs)

44
Q

What are the causes of respiratory acidosis?

A

Lung disease:

  • Emphysema
  • Chronic bronchitis
45
Q

What is the renal compensation for respiratory acidosis?

A
  • Increase H+ secretion

- Increase absorption of new HCO3- by UPREGULATING the formation of HCO3- from the metabolism

46
Q

In respiratory acidosis, why can the reabsorption of filtered HCO3- not be seen?

A

Already at 100%

47
Q

Does increase in HCO3- fix the problem of increased CO2?

A

No, CO2 is STILL HIGH - just a compensation mechanism, to minimise the effect

48
Q

When is respiratory alkalosis seen?

A

When CO2 levels decrease (increase elimination)

49
Q

What are the causes of respiratory alkalosis?

A
  • Hyperventilation
  • Fear
  • Stress
  • Pain
50
Q

What is the renal compensation for respiratory alkalosis?

A
  • REDUCED secretion of H+

- REDUCED generation and reabsorption of HCO3-

51
Q

What is the fall in pH in the renal compensation for respiratory alkalosis at the expense of?

A

A further drop in HCO3-

52
Q

What is metabolic acidosis causes by?

A
  • Ingestion of acid

- Loss of alkaline fluid (diarrhoea, cholera, diabetic ketoacidosis)

53
Q

What is the respiratory compensation for metabolic acidosis?

A
  • Increase respiratory rate
  • Decrease arterial PCO2
  • Increase in pH BUT causes the PCO2 to drop LOWER than normal
54
Q

What is the renal correction for metabolic acidosis?

A
  • Increase secretion of H+

- Decrease secretion of HCO3-

55
Q

What is metabolic alkalosis caused by?

A
  • Ingestion of alkaline

- Loss of acid (vommiting)

56
Q

What is the respiratory compensation for metabolic alkalosis?

A
  • Reduce breathing rate
  • Increase arterial PCO2
  • Decrease pH BUT causes PCO2 to INCREASE
57
Q

What is a ‘mixed disorder’?

A

When the person has MORE than 1 acid-base disorder eg:

  • Resp acidosis (High PCO2)
  • Met acidosis (High H+/low HCO3-)
58
Q

What are the consequences of a mixed disorder?

A

If both the same type (eg. acidosis) effects are ADDITIVE (pH change add together)

If both DIFFERENT effects in pH are SUBTRACTIVE

59
Q

What are examples of mixed disorders?

A

1) Alcoholic patient - subtractive
2) Asthma - additive
3) COPD - subtractive
4) Aspirin poisoning - subtractive

BMS 242 - CVS respiratory (15 decks)

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