6. Pulmonary blood flow and gas exchange 2+3: Haemoglobin +gas transport Flashcards

1
Q

Why does the blood transport O2 from the lungs to the tissues?

A

to use O2 in energy production (and Co2 travels from tissues to lungs for removal)

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2
Q

How much O2 dissolves per litre plasma in ml?

A

3ml (solubility= 3/0.03ml/L/mm

Hg)

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3
Q

By how much does haemoglobin in RBCs increase O2 carrying capacity? (ml/L)

A

increases it to 200ml/L

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4
Q

How is a bulk of CO2 transported in the blood?

A

in solution in plasma (in various forms)

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5
Q

What is pulmonary circulation in terms of flow and pressure?

A

-high flow
-low pressure
system

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6
Q

What is the partial pressure gradient between alveoli and pulmonary arteries in mmHG for O2?

A

100mmHg (alveoli) to 40mmHg

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7
Q

What is the partial pressure of O2 in the air? (mmHg)

A

160mmHg

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8
Q

What is the partial pressure of O2 in tissues and veins? (mmHg)

A

40mmHg

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9
Q

Why isn’t the partial pressure of O2 in alveoli 160mmHg, and instead it’s 100mmHg?

A

when air enters the airways, it’s diluted down to 100mG by the time it travels down and reaches alveoli

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10
Q

What is the partial pressure gradient between pulmonary artery to alveoli in mmHG for CO2 (during removal)?

A

46mmHg to 40mmHg

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11
Q

Partial pressure gradient for O2 is 10 x greater than that for CO2, yet their rate of diffusion is quite similar- why?

A

because CO2 is much more soluble in water (which makes up for it)

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12
Q

What happens to pulmonary vessels if ventilation to an area of lung is compromised?(when O2 decreases and CO2 increases)

A

-local vasoconstriction in compromised region (pulmonary circulation only)

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13
Q

What does shunt refer to?

A

blood flowing through a poorly ventilated region without being oxygenated (it’s then redirected to better ventilated areas)

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14
Q

What does alveolar dead space refer to?

A

alveoli which are ventilated but not perfused

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15
Q

When can an alveolar dead space arise? (physiological)

A

when blood clot present blocking blood supply

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16
Q

Can ventilation in alveoli still occur when there is no blood perfusion?

A

yes

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17
Q

Why isn’t the partial pressure of O2 not the same as arterial content of O2?

A

because partial pressure only refers to O2 IN SOLUTION (the 3ml of O2 in plasma)

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18
Q

O2 in solution (how much O2 is dissolved in the plasma) is determined by what 2 factors?

A
  1. O2 solubility (which is fixed)
  2. partial pressure of O2 in gaseous phase (in alveoli)

both are driving O2 into solution

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19
Q

What is the general rule which drives the gas into solution?

A

value assigned to partial pressure of the gas in solution = partial pressure of gas in gaseous phase that is driving the gas into the solution

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20
Q

Describe the calculation that proves that partial pressure of O2 is 100mmHg (PP in alveoli)

A
  • solubility of O2 in water is low; 0.03ml/L/mmHg

- we have 3ml/L of O2 in plasma so PP that is driving O2 into the liquid phase in plasma must be 100mmHg (3/0.03=100)

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21
Q

What is the general conclusion regarding PO2 in solution and gaseous phase.

A

the PO2 in solution= the PO2 in gaseous phase which results in that oxygen concentration in the liquid phase

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22
Q

What is another word for the PO2 (in arteries) which is at 100mmHg?- ie O2 arterial partial pressure

A

oxygen tension

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23
Q

Why do gases not travel in their gaseous phase in the plasma?

A

It would cause bubbles in the blood which could lead to fatal air embolisms

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24
Q

Why doesn’t the arterial PP of arteries not tell us anything about the oxygen levels?

A

because most of the oxygen is attached to haemoglobin in the plasma and not dissolved in the plasma (only 3ml)

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25
Q

Is O2 conc. higher in gaseous or liquid phase?

A

gaseous (because O2 isn’t dissolved in plasma (water))

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26
Q

Is this statement true?

Alveolar O2= Arterial O2

A

Yes

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27
Q

Describe the equation for O2 delivery

A

arterial O2 content x cardiac output = o2 delivery to tissues

3ml/L x 5L/min = 15ml/min (without haemoglobin, just pure O2 in solution)

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28
Q

What is the O2 demand of RESTING tissues?(how much O2 needed for tissues to function)

A

250ml/min

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29
Q

How much haemoglobin is there per litre in blood?

A

150g/L (there is 1.34ml O2 per g)

so 150x1.43=200ml/L

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30
Q

How much O2 WITH haemoglobin is found in the body?

A

1000ml/min

200ml/L x 5L/min

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31
Q

How much of arterial O2 is extracted by peripheral tissues at rest?

A

Only 25% ( 250ml/min is the O2 demand of resting tissues yet 1000ml/min of O2 is circulating in our blood)

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32
Q

Why do we have so much excess oxygen supply (with haemoglobin) in our blood and only 25% is used by resting tissues?

A

so body has excess O2 in reserve for actions such as exercise or increase in movement or body processes which need more energy

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33
Q

Each litre of systemic arterial blood contains approx. how much oxygen?

A

~200ml of oxygen

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34
Q

How much of the 200ml of oxygen in systemic arterial blood is bound to haemoglobin?

A

more than 98% (rest is dissolved in plasma)

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35
Q

How many haem groups and binding sites are associated with each

A
  • 1 haem group

- 4 binding sites

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36
Q

How many molecules of oxygen bind to each haemoglobin?

A

4 molecules of oxygen

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37
Q

How much O2 in ml binds to each gram of haemoglobin?

A

1.34ml of O2

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38
Q

Is oxygenation and oxidation the same thing?

A

NO:

-oxidation is more lasting and permanent whereas oxygenation describes quick changes with O2 switching places

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39
Q

What is the most common type of haemoglobin that makes up 92% of our whole haemoglobin?

A

HbA

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40
Q

What 3 other forms of haemoglobin is the rest of haemoglobin made up of? (the remaining 8%)

A
  • HbA2
  • HbF
  • glycosylated Hb (e.g. HbA1a)
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41
Q

What is the major determinant of the degree of haemoglobin saturation with O2 in arterial blood?

A

partial pressure of O2 in arterial blood

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42
Q

What binding process describes O2 binding to haem groups which make their sites more available for binding other O2 molecules?

A

cooperative binding

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43
Q

What is the life span of an RBC?

A

120 days

44
Q

Why is glycosylated haemoglobin measured in diabetic patients?

A

to watch patient’s longterm glucose control (better indicator of glucose levels and intake than glucose and blood which can fluctuate more easily)

45
Q

Partial pressure gradient that sucks O2 out of alveoli is maintained until what happens?

A

until the Hb becomes saturated with O2 (up to 98% of its maximum O2 carrying capacity)

46
Q

Saturation of Hb is complete after how many seconds after contact with alveoli?

A

0.25 seconds (total contact time is ~0.75%)

47
Q

What is fundamental in determining how much O2 binds to Hb?

A

partial pressure of O2 in plasma (as PO2 is increased in blood, the more O2 is pushed onto haemoglobin)

48
Q

If PO2 decreased from 100mmHg to 60mmHg, would the haemoglobin remain highly saturated?

A
  • Yes, it would still be ~90% saturated with O2 at 60mmHg (even 75% saturated at 40mmHg in veins ).
  • this permits a relatively normal uptake of oxygen by the blood even when alveolar PO2 is moderately reduced
49
Q

PP of oxygen has to roughly fall below which PP value before big losses of O2 occur?

A

below 60mmHg which emphasises the high affinity for O2 the Hb has

50
Q

Why is the term “deoxygenated blood” slightly misleading?

A

the blood isn’t completely deoxygenated as even though it has a lower PO2 of 40mmHg, the Hb still has a relatively high saturation of approx. 75% in case the body requires a reserve of oxygen

51
Q

What is the PO2 in arterial blood?

A

100mmHg

52
Q

What is the PCO2 in venous blood?

A

40mmHg

53
Q

What 2 molecules have a higher affinity for O2 than HbA ( which is the most common type of haemoglobin)?

A
  1. HbF (foetal haemoglobin)

2. myoglobin

54
Q

Why do HbF and myoglobin have a higher O2 affinity?

A

so O2 can be easier extracted from maternal/ arterial blood

55
Q

Which fibres in the body contain larger stores of myoglobin?

A

Oxidative fibres ( muscles) as they are more hungry for oxygen for efficient muscle function

56
Q

Which fibres are not as hungry for O2 as oxidative fibres?

A

glycosidic fibres

57
Q

If a patient’s PO2 falls to a drastically low level of 28mmHg for example (fallen by 72%), what would happen to the total O2 carrying capacity?

A

It would decrease by only 50%; which isn’t too big compared with the big drop in PO2 due to oxygen’s high O2 affinity.

58
Q

What PO2 of O2 is regarded as the “death zone” in mmHg?

A

around 40mmHg and less (makes uptake of oxygen very difficult)

59
Q

What is anaemia?

A

condition where the oxygen carrying capacity of the blood is compromised

60
Q

What can cause anaemia? (3)

A
  1. iron deficiency (inadequate supply of iron)
  2. haemorrhage (e.g. trauma or burst ulcer)
  3. vitamin B12 deficiency
61
Q

Why would PO2 be still normal in anaemic patients?

A

because PO2 refers to only O2 dissolved in solution which anaemic patients have no problem with- instead anaemics have problems with binding O2 to haemoglobin on RBCs which makes up VAST MAJORITY of the blood

62
Q

Is it possible for an anaemic to have a normal PaO2 while total O2 content of blood is low?

A

Yes; as most O2 is on RBCs and not in solution so it’s possible to have a normal PaO2

63
Q

Is it possible for anaemics to have a low PaO2 and a normal TOTAL O2 content?

A

No; as anaemics have a problem with the total O2 content in the blood (which is on RBCs)

64
Q

What is the primary determinant of saturation of haemoglobin?

A

partial pressure of O2

65
Q

In anaemics, is it possible for RBCs to be fully saturated with O2?

A

YES; in anaemia there is just less haemoglobin which means less O2 is carried in the body. But the haemoglobin that is in the body, is still nearly 100% saturated

66
Q

What chemical factors change the affinity of haemoglobin for O2? (4)

A
  1. pH
  2. pPCO2
  3. Temperature
  4. DPG (2,3-diphosphoglycerate)
67
Q

In venous blood at 40mmHg, what is the approx. saturation of haemoglobin?

A

around 75% (still very high)

68
Q

What produces DPG? When is it produced

A

-RBCs (erythrocytes); produced in hypoxic conditions when PO2 falls

69
Q

Who might have increased levels of DPG in their blood?

A

people living in high altitudes (also people with anaemia, hyperthyroidism, chronic alkalosis and chronic hypoxia)

70
Q

What pH conditions decrease Hb affinity for O2?

A

pH decrease

71
Q

What CO2 and temperature conditions decrease Hb affinity for O2?

A

increase in CO2 and increase in temperature

72
Q

What is Bohr effect?

A

more oxygen is released in tissues that have higher CO2 absolute/relative values and a smaller pH (decreasing Hb affinity for O2)

73
Q

Why does an increase in Co2 result in a decrease in pH?

A

because CO2 reacts with water to form carbonic acid reducing blood pH

74
Q

Can Hb give up its O2 in extreme conditions to surrounding tissues?

A

Yes; in extreme circumstances where O2 is desperately needed to keep tissues alive

75
Q

Conditions involving changes to pH, temperature and PCO2 exist locally or more widespread in the body?

A

exist locally in actively metabolising tissues

76
Q
What effect does: 
-increase in temperature 
-increase in PCO2 
-decrease in pH 
-DPG increase
have on Hb affinity for O2?
A

facilitates the dissociation of O2 from Hb (causes Hb to lose its affinity for O2)

77
Q
What effect does: 
-decrease in temperature 
-decrease in PCO2
-increase in pH
have on Hb affinity for O2?
A

increase affinity of Hb for O2 (in pulmonary circulation)

78
Q

DPG can be synthesised in situations that have inadequate O2 supplies, such as?

A

-high altitudes
-heart or lung disease
-hyperthyroidism
-anaemia
-chronic hypoxia
-chronic alkalosis
(helps maintain O2 release in the tissues)

79
Q

What effect does DPG have on Hb affinity for O2?

A

affinity of Hb for O2 is decreased

80
Q

CO binding to Hb forms what molecule?

A

carboxyhaemoglobin

81
Q

How many times greater is the affinity of CO to Hb than O2 to Hb?

A

250 times greater

82
Q

Why is CO very problematic once it dissolves in circulation?

A

because it binds very readily and dissociates very slowly

83
Q

PCO of what pressure can cause progressive carboxyhaemoglobin formation?

A

PCO of only 0.4mmHg (not much needed to cause progressive damage)

84
Q

What are some common symptoms of CO poisoning?

A
  • hypoxia
  • anaemia
  • nausea
  • headaches
  • cherry red skin and mucous membranes
  • potential brain damage and death
85
Q

Why is respiration rate unaffected during CO poisoning?

A

due to normal arterial PCO2 (breathlessness doesn’t happen)

86
Q

Define hypoxia

A

Inadequate supply of O2 to tissues.

87
Q

What are 5 main types of hypoxia?

A
  1. hypoxic hypoxia
  2. anaemic hypoxia
  3. ischaemic (stagnant) hypoxia
  4. histotoxic hypoxia
  5. metabolic hypoxia
88
Q

What is hypoxic hypoxia?

A
  • most common
  • reduction in O2 diffusion at lungs either due to decreased PO2(atmos) or tissue pathology
  • affects often people at high altitudes due to low PaO2
89
Q

What is anaemic hypoxia?

A

-reduction in O2 carrying capacity of blood due to anaemia (RBC loss/ iron deficiency/haemorrhage)

90
Q

What is ischaemic (stagnant) hypoxia?

A
  • heart disease results in inefficient pumping of blood to lungs/around the body
91
Q

What is histotoxic hypoxia?

A

-poisoning prevents cells utilising oxygen delivered to them e.g. CO or cyanide

92
Q

What is metabolic hypoxia?

A
  • O2 delivery to the tissues does not meet increased O2 demand by cells
  • system not adapted
  • more likely to be transient (not permanent)
93
Q

CO2 moves out of cells along or against its partial pressure (PP) gradient?

A

Along (down its PP gradient)

94
Q

When CO2 diffuses from tissues into blood, how much remains dissolved in the plasma and eythrocytes?

A

only 7% of CO2

95
Q

When CO2 diffuses from tissues into blood, how much combines in erythrocytes with deoxyhaemoglobin to form carbamino compounds?

A

23% of CO2

96
Q

When CO2 diffuses from tissues into blood, how much combines in the erythrocytes with water to form carbonic acids?

A

70% of CO2

97
Q

What does the carbonic acid produced from CO2 and water, then dissociates to yield?

A

bicarbonate and H+ ions

98
Q

What happens to bicarbonate ions released from carbonic acid?

A
  • moves out of erythrocytes and into the plasma in exchange for Cl ions (chloride shift)
99
Q

What happens to excess H+ ions released from carbonic acid?

A

they bind to deoxyhaemoglobin in erythrocyte

100
Q

How does the bicarbonate ion end up in the alveoli?

A
  • it’s transported to lungs through various circulation
  • reverse process occurs in pulmonary capillary (reverse to systemic capillary process)
  • dissolved CO2 moves into alveoli down its conc. gradient
101
Q

Is arterial or venous blood is better at buffering H+ ions?

A

venous(better at carrying Co2 than arterial blood)

102
Q

When is Hb most likely to attach to CO2?

A

Once O2 levels fall and O2 is lost

103
Q

What equation allow Co2 to change ECF pH?

A

CO2+H2O->H2CO3->HCO3 +H

CO2 into carbonic acid into bicarbonate and H

104
Q

How does constant CO2 expiration affects the pH?

A

it maintains a stable and constant pH in the body

105
Q

Can hypoventilation and hyperventilation alter plasma PCO2 and cause plasma H variation?

A

Yes; it can alter plasma PCO2

106
Q

How does hypoventilation affect the pH? (on a molecular level)

A
  • causes CO2 retention (nervous person)
  • leads to increase in H (shift equation to the right)
  • brings about respiratory acidosis
107
Q

How does hyperventilation affect the pH? (on a molecular level)

A
  • blowing off more CO2 (relaxed person)
  • leads to decrease in H (shift to the left)
  • brings about respiratory alkalosis