4 Flashcards

(55 cards)

1
Q

Why is there a substantial amount of CO2 in arterial blood?

A
  • has a vital role in acid base balance
  • more soluble than O2
  • reacts chemically with water
  • also reacts with Hb (but at a different site from O2)
  • arterial blood contains 2.5x as much CO2 as O2
  • more dissolved and more reacted with water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the total content of CO2 and O2 in arterial blood?

A
  • total content of CO2 = 21 mmol/L

- total content of O2 = 8.9 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why is the there so much CO2 in blood going to the tissues?

A

-to help control blood pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does CO2 help control blood pH in arterial blood?

A
  • ph must be maintained at 7.35-7.45 (slightly alkaline)
  • amount of CO2 dissolved is directily proportional to pCO2
  • [CO2]dissolved = solubility factory (0.23) x pCO2
  • at pCO2 of 5.3 kPa, water dissolves 1.2 mmol/L of CO2
  • dissolved CO2 reacts with water in plasma and in RBC
  • CO2 in arterial blood is not there as a WASTE product
  • pCO2 in arterial blood is lower but more CO2 is dissolved than O2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How come dissociation of CO2 does not occur in the arterial blood?

A
  • it is resisted by the high concentration of HCO3 ions present in plasma (normal 25mmol/L)
  • HCO3 is NOT formed from dissolved CO2 in plasma
  • comes from a reaction of CO2 in RBC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the change in pH in the plasma from pCO2 and [HCO3]

A
  • ph FALLS if pCO2 RISES
  • pH RISES if [HCO3] RISES
  • pH depends on the RATIO of [HCO3] to pCO2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the reaction for CO2 in plasma ?

A

CO2 + H2O H+ + HCO3-

  • reaction is pushed to the left because conc. Of HCO3 is higher than conc. Of CO2 dissolved
  • reaction is reversible
  • depends on dissolved CO2 and conc. Of HCO3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is the pCO2 of alveoli (determining factor) controlled?

A

-controlled by altering the rate of breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain the Henderson-Hasselbalch equation

A

PH = pKa + Log ([HCO3-]/(pCO2 x 0.23))

  • provides a way of calculating pH from pCO2 and [HCO3-]
  • pKa is a constant at 6.1
  • 20 times as much HCO3- as dissolved CO2
  • so Log20 = 1.3
  • pH = 6.1 + 1.3 = 7.4
  • buffer is working far from its pKa, because of the excess hydrogen carbonate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

In plasma, what is the ratio of [HCO3] to dissolved CO2?

A

20:1

25mmol/L: 1.2mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where is all the HCO3 produced?

A

In the RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain HCO3 production in RBC

A
  • same reaction as in plasma but much faster since carbonic anhydrase is present
  • reaction is driven to the right since the H+ ions are taken by Hb
  • HCO3 is taken out of RBC by the chloride bicarbonate exchanger
  • creates the plasma conc. Of 25mmol/L
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What factor influences the amount of HCO3 produced in the RBC?

A
  • depends primarily upon the buffering effects of Hb

- only minor effects of changes in pCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How are H+ ions taken up by Hb?

A
  • Hb has a negative charge so H+ is attracted to it
  • Hb has a large capacity for binding H+ ions
  • amount of HCO3 the RBC produces depends on binding of H+ to Hb
  • erythrocytes produce HCO3 but they dont control conc. Of HCO3 in plasma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What controls the conc. Of HCO3 in plasma?

A

-kidney and lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When CO2 reacts directly with the protein part of Hb, what is formed? How?

A

Carbamino compounds (carbamino Hb)

  • binds directly to amine groups on globin of Hb
  • binding of molecular CO2 on Hb is not part of acid base balance but contributes to CO2 transport
  • more carbamino compounds are formed at the tissues because pCO2 is higher and unloading of o2 facilitates binding of CO2 to Hb
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does the kidney control [HCO3]?

A
  • kidney controls amount of HCO3 by varying excretion
  • therefore pH is dependent on how much CO2 is present (controlled by rate of breathing)
  • and how much bicarbonate is present (controlled by kidneys)
  • pH = pkA + Log ([HCO3]/(pCO2 x 0.23))
  • [HCO3]=kidneys
  • pCO2=lungs
  • only the ratio matters, not the absolute values
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How much CO2 is in arterial blood and venous blood respectively?

A

In arterial blood

  • pCO2 is normally 5.3 kPa
  • 60% of blood is plasma, 40% cells
  • for each litre of blood there is 21.31mmol of CO2

In venous blood

  • pCO2 is normally 6.0 kPa
  • Hb is less saturated with O2 so is a better buffer
  • for each litre of blood there is 23.21 mmol of CO2

Overall

  • 8% of transported CO2 travels as dissolved CO2 (rest is part of pH buffering system)
  • 80% as hydrogen carbonate
  • 12% as carbamino compounds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does HCO3 buffer extra acid?

A
  • body produces acids such as lactic acid, keto acid sulphuric acid
  • acid reacts with HCO3 to produce CO2
  • therefore [HCO3] goes down
  • CO2 produced is removed by breathing and pH changes are minimized (buffered)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does CO2 transports to lungs work in venous blood?

A
  • buffering of H+ by Hb depends on level of oxygenation
  • if MORE O2 binds to Hb then Hb is in R-state so LESS H+ ions bind (occurs at lungs)
  • if LESS O2 binds to Hb then Hb is in T-state and MORE H+ ions bind (occurs at tissues)
  • if Hb binds more H+ in RBCs then more HCO3 can be produced
  • therefore more CO2 is present in plasma in the venous blood (both in dissolved and reacted form)
  • thus more HCO3 is made due to increased capacity of Hb for H+
  • small change in plasma pH for venous blood since both pCO2 and [HCO3] have increased

When venous blood goes to lungs

  • Hb picks up O2 and goes into R-state
  • causes Hb to give up H+ ions
  • H+ reacts with HCO3 to form CO2
  • CO2 is breathed out
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What 3 forms can CO2 be transported as?

A
  • dissolved CO2
  • as HCO3
  • as carbamino compounds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Of the 8% (1.8mmol/L) of CO2 that is transported at rest, how much is in each form?

A
  • 60% travels as HCO3
  • 30% travels as carbamino compounds
  • 10% travels as dissolved CO2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What do i need to know about the amounts of CO2 in arterial and mixed venous blood

A

LOOK AT THE CHARTS

24
Q

How does hyperventilation affect CO2 in the blood?

A
  • significantly reduces the pCO2 and CO2 content in the blood
  • hence CO2 retention is rarely a problem, as long as ventilation is adequate
25
How does hyperventilation affect the O2 in the blood?
- dissociation curve is sigmoid shaped - increasing the alveolar pO2 above 13.3 kPa by heyperventilation doesn’t significantly increase O2 content since Hb is already 100% saturated
26
What will happen to the total content of oxygen in the blood if a normal individual breathes air at twice the normal atmospheric pressure?
- total content of O2 would increase | - but wouldn’t make a significant difference since we are already at max capacity
27
How do i calculate oxygen and CO2 content and pp in blood using graphs?
LOOK iN WORKBOOK
28
A 24-year-old man with aplastic anemia complains of extreme tiredness which is attributed to tissue hypoxia. Investigations: o Hb is 60 gm/L (normal range in adult male 130 -180 gm/L). o Oxygen saturation is 97% (normal range 94-98%) o PO2 is 13.3 kPa (9.3 – 13.3). 1 gm of Hb binds approximately 1.34 ml of oxygen when Hb is fully saturated. Explain why he has tissue hypoxia despite his oxygen saturation and pO2 being in the normal range.
- low number of Hb | - O2 binding is good but not enough Hb
29
What is the significance of central cyanosis?
- occurs in central structures such as lungs and heart - can see it on mouth - hard to fix
30
What is the significance of peripheral cyanosis?
- when extremities are blue such as fingers and toes - necrosis can occur - can potentially warm up extremities and get it back to normal - due to arteriole clots possibly from AF
31
A patient suddenly develops a respiratory illness which leads to a rise in arterial pCO2 from 5.3k to 6.5kPa (normal range 4.7 – 6.0). In what direction will the plasma pH change if we assume that the [HCO3-] of the blood remains 25 mmol.l-1 in the short term. You return to the same patient a week later, and find that although cyanosis from peripheral cyanosis? the pCO2 has not changed, her plasma pH is now 7.38. What has changed? Which organ do you think is responsible?
- more acidic because more CO2 converts to H+ ions - but since HCO3 remains the same, does not drive the reaction the other way - pH has risen - kidneys are responsible - HCO3 concentration rises
32
What is hyperkapnia?
Rise in pCO2
33
What is hypokapnia?
Fall in pCO2
34
What is hypoxia?
Fall in pO2
35
What is hypoxiaemia?
Fall in arterial pO2
36
What occurs to the pO2 and pCO2 levels in exercise?
PO2 drops and pCO2 rises | -breathing more will restore both
37
What is hyperventilation?
- ventilation increase without change in metabolism - pO2 will rise - pCO2 will fall - removal of CO2 from alevoli is more rapid than its production - pH rises resulting in respiratory alkalosis - if conditions persists, kidney responds by excreting HCO3 so pH is restored but buffer base concentration is reduced - results in Compensated respiratory alkalosis
38
What is hypoventilation?
- ventilation decreases without change in metabolism - pO2 will fall - pCO2 will rise - removal of CO2 from lungs is slower than its production - ph falls resulting in respiratory acidosis - if condition persists, kidneys respond to low pH by reducing excretion of HCO3 which will increase plasma HCO3 conc. And bring pH near to normal - results in Compensated respiratory acidosis
39
What happens if pO2 changes without a change in pCO2?
- correction of pO2 will cause pCO2 to drop | - leads to hypocapnia
40
How can hypoxia be displayed on a graph?
- O2-Hb dissociation curve - sigmoid curve - flat from approx. 8kPa - pO2 can fall considerably before saturation is markedly affected - control system needs to avoid marked hypoxia - drop in inspired pO2 has very little influence upon respiration until it has fallen markedly - however a small increase in inspired pCO2 produce large increases in minute volume - drop in pH (acidosis) also increases the minute volume
41
What is the major buffer system in blood?
Carbonic acid-bicarbonate buffer system
42
How does pCO2 affect plasma pH?
- if pCO2 increases then pH falls - if pCO2 decreases then pH rises - small changes in pCO2 leads to large changes in pH
43
How can major changes in plasma pH affect the body?
Normal plasma pH: 7.38-7.46 - if pH falls below 7.0 then enzymes are denatured - if pH rises above 7.6, then free calcium conc. Drops leading to tetany (muscles cant work)
44
Explain excess metabolic production of acid
- if excess acid is formed in body, it reacts with HCO3 in body and uses it up - fall in [HCO3] leads to fall in pH - results in reduction of buffer base: metabolic acidosis - can be restored to almost normal by increasing ventilation - increasing ventilation will lower pCO2 which will correct the ratio and pH but depletion of buffer base remains (Compensated Metabolic Acidosis) - until it is eventually corrected by kidney
45
Explain metabolic production of excess [HCO3]
- if there is excess [HCO3] in plasma (eg. After vomiting) - Plasma pH rises - results in metabolic alkalosis - pH can be corrected by elevating pCO2 which will correct ration - decrease ventilation but this will increase risk of hypoxia
46
Describe the respiratory control pathways
- sensors located in the CNS, periphery feed info back to the Respiratory control center for processing - ventilation is adjusted as necessary Sensors - central chemoreceptors (H+) - peripheral chemoreceptors (O2, CO2, H+) - pulmonary receptors (stretch) - joint and muscle receptors (stretch, tension) Effectors - diaphragm - inspiration (external intercostals, accessory muscles) - expiration (internal intercostals, abd muscles0
47
What are peripheral chemoreceptors?
- located in the carotid and aortic bodies - respond to changes in pO2, pCO2 and pH - large falls in pO2 stimulate increased breathing, changes in HR and changes in blood flow distribution (ie. increasing flow to brain and kidneys) - impulse from carotid bodies are carried via the glossopharyngeal nerve - impulses from aortic bodies are carried via vagus nerves to the brainstem respiratory centre which modulate rate and depth of ventilation
48
How do peripheral chemoreceptors respond to oxygen?
- carotid and aortic bodies are stimulated by decrease in O2 - only respond to large falls in pO2 (not slight changes) - do not adapt to chronic hypoxia; there is a respiratory drive as long as pO2 is low - stimulation results in an increase in tidal volume and rate of respiration - also causes changes in circulation, directing more blood to brain and kidneys and increased heart pumping
49
How do peripheral chemoreceptors respond to CO2?
- carotid and aortic bodies not very sensitive to pCO2, so need a large change in pCO2 to stimulate them - respond quickly to large changes
50
How do peripheral chemoreceptors respond to pH?
- carotid bodies can sense and respond to changes in blood pH - low pH results in an increased RR and tidal volume
51
What are central chemoreceptors?
- located on ventral surface of medulla and are exposed to CSF - very sensitive to changes in pCO2 - can detect changes in CSF pH - small rises in pCO2, increase ventilation - small falls in pCO2, decrease ventilation
52
How do central chemoreceptors detect changes in CSF pH?
- CSF separate from blood so allows free passage of CO2 but NOT HCO3 - CSF has no Hb - [Dissolved CO2] in CSF is determined by plasma pCO2 - [HCO3] in CSF is determined by the activity of choroid plexus cells which pump HCO2 in and out of CSF - CSF pH is determined by the ratio of [HCO3] to [dissolved CO2] - if arterial pCO2 changes, then CSF pCO2 will change - impulses from chemoreceptors travel to brain stem resp. Centre which will change breathing to restore CSF pH - negative feedback controls the ventilation - if ventilation doesn’t work (i.e in hypoxia since increased ventilation will occur, but drop in pCO2 will result in decreased ventilation) then the choroid plexus cells will pump more or less HCO3 into the CSF which will bring ratio back to normal
53
What controls CSF [HCO3]?
- choroid plexus cells - if pCO2 remains altered for any length of time the activity of the choroid plexus cells serve to “reset” the central chemoreceptors so they’re no longer sensitive to the existing pCO2 and only respond if pCO2 rises further
54
Why is CSF pH corrected much more quickly than blood pH?
-CSF has a smaller volume
55
What occurs in persisting hypercapnia?
- hypoxia and hypercapnia - respiratory acidosis occurs - results in drop in CSF pH - peripheral and central chemoreceptors stimulate breathing - but acidic pH is undesirable for neurons - therefore choroid plexus needs to adjust pH of CSF - addition of HCO3 - central chemoreceptors “accept” the high pCO2 as normal