L5 - Acid Base Balance Flashcards

1
Q

Why is acid-base balance important?

A

A small change in pH can have a large effect on body function
Log scale – 1 unit change = x10 change in [H+]

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2
Q

What can fluctuations in plasma H+ concentrations have an effect on?

A

Excitability of muscle and nerve
Enzyme activities
K+ levels

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3
Q

pH at venous end of tubule?

A

7.35

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4
Q

pH at arterial end of tubule?

A

7.45

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5
Q

What are the different pH value around the body?

A

Gastric secretion – 0.7
Cerebrospinal fluid – 7.3
Pancreatic secretions – 8.1
Urine – 5.4

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6
Q

What are the different sources of acid and alkali?

A

Metabolism – large amounts of acid produced
- 15 moles/ day CO¬¬2
- 40 mmol/day H+ (western diet has an excess of H+)
Diet – alkali and acid in food
- 20 mmol/day H+
- Lose 10 mmol/day OH-
Overall excess 70 mmol/day H+

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7
Q

What are the 3 different systems involved in acid-base balance?

A

Blood and tissue buffers (seconds)
Respiration (minutes)
Renal (hours) – only mechanism for the extrusion of acid/alkali

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8
Q

Where are buffers present throughout the body?

A

Blood – plasma and red blood cells
Extracellular and intracellular fluid
Urine
E.g. haemoglobin, inorganic phosphate, weak acids/bases, HCO¬¬-3

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9
Q

Carbonic acid/bicarbonate ECF buffer

A

CO2 + H2O H2CO3 H+ + HCO3

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10
Q

What is the Henderson-Hasselbach equarion

A

pH = pK + log [HCO3]/[H2CO3]
pK is a constant of 6.1 at 37oC
Ratio of [HCO3]/[CO2] = 20:1
6.1+log 20 = 6.1+1.3 = 7.4

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11
Q

What does chemical control of ventilation control?

A

Controls blood gas composition – PO2, PCO2, pH

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12
Q

How is ventilation chemically controlled?

A

Peripheral and central chemoreceptors - negative feedback system
Stimulated by hypoxia, hypercapnia, acidosis – all increase ventilation
- Increase in PO2
- Decrease in PCO2
- Increase in pH

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13
Q

What are peripheral chemoreceptors triggered by?

A

Mainly stimulated by decreased PO2 – hypoxia

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14
Q

What do peripheral chemoreceptors do once triggered?

A

When activated send signals through the sinus, gloss-pharyngeal and the vagus nerve to the medulla

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15
Q

What is the structure of carotid receptors?

A

Small – 2mg
High blood flow (40X higher than the brain per unit mass)
High metabolic rate
Glomus cells
Parasympathetic/sympathetic cells – regulate blood flow Aortic receptors smaller and less well studied

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16
Q

What do glomus cells do?

A

Fire action potentials when O2 drops
Neural phenotype
Type II – supporting

17
Q

What is the mechanism of glomus cells?

A
  1. Inhibition of BK K channels – decreased PO2, increased PCO2, decreased pH
  2. Depolarisation and action potential firing
  3. Ca channels open increasing intracellular Ca
  4. Ach, dopamine, 5-HT, substance P, noradrenaline released
    - Some SIDS babies have higher concentration of carotid body noradrenaline and dopamine
  5. Afferent nerve fibre stimulation
18
Q

Sensitivity to PO2 changes with?

A

Acid/base status

Higher pH = less action potentials

19
Q

Sensitivity to PCO2 changes with?

A

pH

Higher pH = less action potentials

20
Q

What are central chemoreceptors stimulated by?

A

Increased CO2 - hypercapnia
Change in PCO2 from 40 - 45 mmHg - doubles ventilation
Same increase in ventilation only seen with 50% fall in PO2

21
Q

What factor is actually measured that triggers central chemoreceptors?

A

pH

Perfused cerebral ventricles with acidic solution – observed hyperventilation

22
Q

Where are central chemoreceptors located?

A

Within the brain parenchyma and bathed in brain extracellular fluid
Separated from arterial blood by the blood brain barrier
- BBB has poor ion permeability
- H+ and bicarbonate can’t cross
- CO2 can cross
Increase in arterial PCO2 = increase in brain extracellular fluid PCO2

23
Q

Where are central chemoreceptor neurones located?

A

Ventrolateral medulla and other brainstem nuclei

24
Q

What are the two types of central chemoreceptor neurone?

A

Acid activated – serotonin

Acid inhibited – GABA

25
Q

What are the characteristics of central chemoreceptor neurones?

A

Less non-bicarbonate buffering power (fewer proteins) in the BECF, so larger fall in pH
- Some long term compensation via transport of HCO-3 from blood
Poor ion permeability
- Metabolic disorders change BECF pH by 35% of that observed with respiratory disorders for the same change in blood pH
- Respiratory disorders are better at stimulating the chemoreceptors

26
Q

Do peripheral and central chemoreceptors respond at the same time?

A

Yes - integrated responses

27
Q

How do peripheral and central chemoreceptors respond to respiratory acidosis?

A

Both central and peripheral chemoreceptors
Normoxic central 65-80%
Peripheral chemoreceptors respond faster
As PO2 falls response to PCO2 enhanced

28
Q

How do peripheral and central chemoreceptors respond to metabolic acidosis?

A

Severe cases lead to hyperventilation (Kussmaul breathing)
Decreased PCO2
Peripheral chemoreceptors - acute response role
Central chemoreceptors - longer term role

29
Q

What are the changes in acid-base balance when you breathe faster?

A

Decrease in CO2 = decrease in [H+] = increase in pH

Increased pH of body fluids = chemoreceptors = decreased breathing rate

30
Q

What are the changes in acid-base balance when you breathe slower?

A

Increase in CO2 = increase in [H+] = decrease in pH

Decreased pH of body fluids = chemoreceptors = increased breathing rate