Session 4 Flashcards

1
Q

What does carbon react with?

What other reactions take place?

A
  1. water & Hb (but at different site from O2)
  2. CO2 dissolves in plasma, and may form hydrogen ions and hydrogen carbonate (bicarbonate) ions -> slow because there is little carbonic anhydrase in the plasma

In the red cells carbon dioxide also reacts with water -> rapid as carbonic anhydrase is present in the RBC, to form H+ and HCO3-

Hydrogen ions are bound to Hb which has a large buffering capacity, enhanced further when it is de-oxygenated

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2
Q
  1. Why so much CO2 in blood going to the tissues? State the values for CO2 and O2 content?
  2. What is the equatin to figure out how much CO2 is dissolved in blood?
  3. solubility for CO2 at 37 degrees = ?
  4. What pCO2 value do we use and why?
A
  1. • Total content of gases (dissolved and reacted)
  • Total content CO2 in arterial blood ≈ 21 mmol.l-1
  • Total content O2 in arterial blood ≈ 8.9 mmol.l-1
  • Controlling CO2 has a major role in controlling blood pH (It is more important for pH than for transporting it from tissues to the lungs)
  1. [CO2] dissolved = solubility x pCO2
  2. 0.23

(0.01 for O2)

  1. 5.3 kPa because the amount of CO2 in the blood equilibriates with the amount in the alveoli
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3
Q
A
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4
Q
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5
Q
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6
Q
  1. Plasma contains 25mmol.l-1 HCO3- (the cation associated with this is mostly Na+ rather than H+). The high HCO3- concentration cannot come from the [CO2] dissolved why?
  2. pH = pK + Log ([HCO3-]/[pCO2 X 0.23])
    Given this information: pK is a constant; pK = 6.1 at 37oC
    Work out the pH
  3. What causes changes to plasma HCO3-?
  4. What controls plasma HCO3-
A
  1. Reaction to the right is favoured because [CO2] is 1.2mmol.l-1 and the [HCO3-] is 25mmol.l-1

​2. image

  1. H+ binding to Hb etc
  2. Secretion in the kidneys
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7
Q
  1. How does hydrogen carbonate buffers extra acid?
  2. How does the pCO2 differ in the venous system compared to the arteriole? Why?
  3. Buffering of H+ by Hb depends on level of oxygenation explain this statement
A
  1. Body produces acids e.g. Lactic acid, keto acids, sulphuric acid

Acids react with HCO3- to produce CO2

[HCO3-] decreases

  1. pCO2 higher in venous – metabolically active tissues - dissolves
  2. • If more O2 binds Hb -> R-state and less H+ ions bind – As at lungs

• If less O2 binds Hb -> T-state and more H+ ions bind – As at tissues - more HCO3- produced -> more CO2 in the dissolved & reacted form -> Dissolved CO2 increases a little
Much more converted to HCO3- due to the increased capacity of Hb for H+
There is only a very small change in plasma pH because both [HCO3-] and pCO2 have increased

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8
Q
  1. What happens to venous blood at the lungs?
  2. How are carbamino compounds formed?
  3. Function of carbamino

4.

A
  1. Image
  2. CO2 can bind directly to proteins. Binds directly to amine groups on globin of Hb.
  3. Binding of molecular CO2 onto Hb does not part of the acid base balance but contributes to CO2 transport. More carbamino compouds are formed at tissues because pCO2 is higher and unloading of O2 facilitates binding of CO2 to Hb this is co2 given up to the lungs
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9
Q

State the proportion of CO2 travelling in various forms LO

A

Plasma always higher than dissolved

HCO3- the highest

carbimino the middle

CO2 the least

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10
Q
A
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11
Q

Q. Total carbon dioxide in whole arterial blood = 21.5mmol.l-1
Total carbon dioxide in whole venous blood = 23.3 mmol.l-1
Using these values calculate the amount of CO2 transported

A

A. • = Total in venous blood – total in arterial blood
• = 23.3 – 21.5 mmol.l-1
• = 1.8 mmol.l-1
• Therefore only ~ 8% of the total is transported.
• The rest of the carbon dioxide is there as part of the pH buffering system

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12
Q

1. Of the 1.8 mmol.l-1 that is transported at rest
• Approximately –
• 60% travels as ?
• 30% travels as ?
• 10% travels as ?

  1. Complete the values for
    PaCO2
    PaO2
    Bicarbonate
    pH
A

1. hydrogen carbonate
carbamino compounds
dissolved CO2

A. 4.7 – 6.0 kPa
9.3 – 13.3 kPa
22 – 26 mmol/L
7.35 – 7.45

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13
Q
  1. Hypercapnia
  2. Hypoventilation
  3. At which level of pO2 can hypocapnia start to occur? (I.e. hyperventilation)
  4. What is the major buffer system in the blood?
  5. what effect does a RISE IN PH/ ALKALOSIS have?
A
  1. Abnormally increased arterial carbon dioxide tension
  2. Ventilation decrease without change in metabolism
  3. • Oxygen - Haemoglobin dissociation curve
    • Sigmoid curve
    • Flat from approx. 8kPa (below)
    • pO2 can fall considerably before saturation is markedly effected
    • Control system needs to avoid marked hypoxia
  4. Carbonic acid-bicarbonate buffer system
  5. TETANY - hypocalceamia
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14
Q
  1. Metabolic acidosis
  2. Metabolic alkalosis
  3. Control of which p? Is more important in breathing?
A
  1. body has accumulated too much acid and does not have enough bicarbonate to effectively neutralize the effects of the acid pH< 7.35
  2. pH of tissue is elevated beyond the normal range (7.35–7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations.
  3. pCO2 (pO2 just needs to be above 8kPa)
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15
Q

Peripheral chemoreceptors

  1. Where are they located?
  2. What stimulates the receptors? And what effects does this result in? (3)
  3. State a difference between the central & peripheral chemoreceptors besides their location?
  4. What do they detect?
  5. What effect does the central chemoreceptors exert when there is small changes in co2?
A
  1. Carotid & aortic bodies
  2. • Large falls in pO2 stimulate
    – increased breathing
    – changes in heart rate
    – Changes in blood flow distribution

• i.e. increasing flow to brain & kidneys

  1. • peripheral chemoreceptors -> pO2
    • central chemoreceptors in the medulla -> pCO2
  2. Arterial pCO2 (respond to changes in the pH of cerebro-spinal fluid (CSF))
  3. • small rises in pCO2 increase ventilation
    • small falls in pCO2 decrease ventilation
    • the basis of negative feedback control of breathing
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16
Q

Draw a diagram showing how CO2 effects the central chemoreceptors

A
17
Q

Describe how a rise in pCO2 can be detected by central chemoreceptors

A
  • Elevated pCO2 drives CO2 into CSF across blood brain barrier
  • CSF [HCO3-] initially constant
  • So CSF pH falls
  • Fall in CSF pH detected by central chemoreceptors
  • Drives increased ventilation
  • Increased ventilation
  • Lowers pCO2
  • and restores CSF pH
18
Q

What happens in persisting hypoxia and persisting hypercapnia?

A

1.– pO2 = 8.6 kPa
– pCO2 = 3.9 kPa
– pH = 7.47
• Hypoxia detected by peripheral chemoreceptors
– Increase ventilation
• BUT pCO2 will fall further
– Decrease ventilation
• SO: CSF composition compensates for the altered pCO2
• Choroid plexus cells selectively add H+ or HCO3- into CSF
• Central chemoreceptors ͞accept͟ the pCO2 as normal

  1. • Hypoxia and hypercapnia
    • Respiratory acidosis
    • Decreased pH of CSF
    • Peripheral and central chemoreceptors stimulates breathing
    • But acidic pH undesirable for neurons
    • Therefore choroid plexus needs to adjust pH of CSF
    • Addition of HCO3-
    • Central chemoreceptors ͞accept͟ the high pCO2 as normal