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HOM > Lungs > Flashcards

Lungs Flashcards

1
Q

How many zones can the trachea > alveoli be divided into?

A

24 (0-23)

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2
Q

Which are the conducting zones?

A

First 17

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3
Q

Which zones are highly cartilaginous and have their own blood supply?

A

First 4

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4
Q

Which are the respiratory zones?

A

Last 6

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5
Q

Why do particulates settle before the alveoli?

A

Velocity falls as flow is distributed

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6
Q

What is the expiratory/inspiratory reserve volume?

A

Everything you can breathe out/in after normal breathing

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7
Q

Which values can’t be measured by spirometry?

A

Residual volume and functional residual capacity

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8
Q

What is functional residual capacity?

A

Residual volume + expiratory reserve volume

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9
Q

What is distending pressure?

A

Positive transpulmonary pressure to keep lungs inflated

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10
Q

Volume of one mole of dry ideal gas?

A

22.4 litres

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11
Q

How is the conducting zone kept open?

A

Kept open by elastic connections between airways and lung parenchyma

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12
Q

What is the most important variable determining alveolar ventilation?

A

Frequency

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13
Q

Why is water vapour not an ideal gas?

A

pV =/= nRT because n changes with temperature

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14
Q

WHat is anatomic dead space?

A

Conducting portion

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15
Q

What is alveolar dead space?

A

Little or no blood flow

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16
Q

What is expired minute volume?

A

Air in and out of lungs per unit time

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17
Q

Why is expired minute volume not quite right?

A

V in =/= V out because more O2 in than CO2 out

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18
Q

What % of expired CO2 has come from alveoli?

A

All of it

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19
Q

What happens to alveolar PCO2 as alveolar ventilation increases?

A

Decreases

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20
Q

Why does alveolar PN2 increase?

A

Because RER

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21
Q

Why is total pressure in venous blood below atmospheric?

A

Because PO2 decreases more than PCO2 increases

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22
Q

What happens to arterial PCO2 if you double VA?

A

Halves

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23
Q

What will rectify a doubling of PACO2?

A

Doubling ventilation

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24
Q

Why must alveolar PO2 decrease if arterial PCO2 rises?

A

Pressure can’t exceed atmospheric

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25
Q

Why must alveolar ventilation increase after exercise?

A

Alters CO2 production and therefore VECO2

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26
Q

WHat is static compliance?

A

Measured when no air flow

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27
Q

What is normalised static compliance called?

A

Specific

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28
Q

What is FRC?

A

Equal and opposite compliance recoil forces of chest wall and lung

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29
Q

What happens to FRC is a less compliant lung?

A

Lung pulls in more so lower FRC

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30
Q

What can causes a less compliant lung?

A

Elevated diaphragm, muscle rigidity

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31
Q

What does DPPC stand for?

A

Dipalmitoyl phosphadityl choline

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32
Q

Which parts of DPPC are in gas and which are in air?

A

Palmitate in gas, glycerol, choline and phosphate in liquid

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33
Q

Three roles of surfactant?

A

Reduce surface tension, allow different-sized alveoli to coexist, keep alveoli dry

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34
Q

How does surfactant allow different-sized alveoli to coexist?

A

Pressure = 2T/r so smaller alveoli have more pressure so gas would flow small>big. Surfactant lowers T in small alveoli.

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35
Q

How does surfactant keep alveoli dry?

A

Force collapsing alveoli would also pull water from capillaries, surfactant reduces ability to do this

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36
Q

What is the flow in between laminar and turbulent called?

A

Transitional

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37
Q

When do you get peak flow rate? Why?

A

Large lung volume because elastic recoil pressure highest

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38
Q

Where is airway resistance highest?

A

Very high because there are lots of branches in parallel at lower areas

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39
Q

Where is equal pressure point at high and low lung volume?

A

Further down at low lung volume (less elastic recoil), low compliance tissues at high lung volumes

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40
Q

Factors affecting airway resistance?

A

Lung volume, bronchial smooth muscle, gas viscosity and density

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41
Q

What happens to forced expiratory flow in obstructive diseases?

A

Lower - same lung capacity but can’t expire at high rate

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42
Q

What happens to forced expiratory flow in restrictive diseases?

A

The same - same expiration rate but lower lung capacity

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43
Q

Why can PO2 sometimes not be reached fast enough if diffusion reserve increases?

A

CO2 solubility is greater so it diffuses faster

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44
Q

Which chains does haemoglobin have?

A

2 alpha, 2 beta

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45
Q

Which chain is wrong in HbS?

A

AA substitution in beta chain

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46
Q

Whihc type of Hb is less sensitive to DPG?

A

HbF

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47
Q

What does DPG do to curve?

A

Keeps it right-shifted

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48
Q

What shifts Hb saturation curve to the right?

A

Decreased pH, increased PCO2, increased DPG

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49
Q

What is PO2 of maternal blood to fetus? Why is this significant?

A

30 - large Hb saturation difference here

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50
Q

What is hypercapnia?

A

Excess CO2 from hypoventilation

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51
Q

What is hypocapnia?

A

Below normal PCO2 from hyperventilation

52
Q

What is hypoxic hypoxia?

A

Low arterial PO2 and inadequate Hb

53
Q

What is anaemic hypoxia?

A

Reduced ability to carry O2, low RBC count

54
Q

What is circulatory hypoxia?

A

Too little blood

55
Q

What is histotoxic hypoxia?

A

Normal O2 delivery but can’t use it eg) cyanide

56
Q

What happens in capillary blood takes too long to reach equilibrium?

A

Out of breath

57
Q

WHy is Hb not affected by barometric pressure variations?

A

Virtually saturated above 60mmHg

58
Q

Three ways to transport CO2?

A

Dissolved, carbamino compunds, bicarbonate

59
Q

How does CO2 bind to protein?

A

Reversibly binds to amine group

60
Q

How does the Haldane effect graph work?

A

Plot a line for PO2 = 40 (veins) and then see how much CO2 is lost between different PCO2s BUT PO2 also changes so must compare between different curves

61
Q

What must happen if one HCO3- is moved?

A

Must be replaced with Cl- to prevent electrochemical gradient forming

62
Q

What ratio must stay the same for pH to stay at 7.4?

A

[CO2] : [HCO3-]

63
Q

What should be the pKa of a good buffer?

A

7.4, so kidney can release or withold HCO3- into urine

64
Q

What do Davenport diagrams show?

A

Relationship between pH, pCO2 and HCO3-

65
Q

What happens to pulmonary resistance as arterial pressure increases? Why?

A

Decreases - more pulmonary vessels are recruited and then they distend

66
Q

What are the two circulatory systems in the lungs?

A

Bronchial (to serve conducting airways) and pulmonary for gas exchange

67
Q

How does pulmonary circulation protect organs against emboli?

A

Endothelial cells release fibrinolytic enzymes and absorb air emboli

68
Q

Why is pulmonary circulation a passive system?

A

Autonomic nerves don’t control diameter

69
Q

What happens to blood vessel diameter at high lung volumes?

A

Reduced because alveoli stretch vessels, the others increase their diameter because of -ve pleural pressure

70
Q

Where is pulmonary vascular resistance lowest?

A

Very close to FRC (optimum balance)

71
Q

What is regional hypoxia?

A

Reduced blood to hypoxic areas, localised vasoconstriction and compensatory dialtion somewhere else

72
Q

What is general hypoxia?

A

Reduced blood flow to all areas, eg) CF or oedema from high blood pressure

73
Q

What can cause pulmonary oedema?

A

Left heart failure causing increased capillary pressure, oxidant damage and endotoxins cause increase in capillary permeability, loss of plasma proteins decreases colloid osmotic pressure, lymphatic blockage

74
Q

How does lack of surfactant increase intersitial pressure?

A

Increases surface tension

75
Q

Why does drowning in fresh water cause cardiac arrest?

A

RBCs burst, K+ released from inside and Na+ is diluted

76
Q

What is usual value of Va/Q ratio?

A

0.8

77
Q

What are units of Va/Q ratio?

A

No units

78
Q

Which area of the lungs is Va/Q ratio lower in?

A

The bottom

79
Q

Does ventilation or perfusion have a larger difference top to bottom?

A

Perfusion

80
Q

How do high Va/Q ratios affect blood O2 content?

A

Minimal effect because ventilation wasted, PCO2 falls so pH increases so localised increases in airway resistance so ventilation shifted to other alveoli.

81
Q

How do low Va/Q ratios afect blood O2 content?

A

Large effect - Increase in overall ventilation to compensate, acute response, regional vasoconstriction from localised hypoxia shunts blood from poorly ventilated alveoli

82
Q

Two causes of venous admixtures?

A

Shunting or low Va/Q ratio

83
Q

What are the types of shunting?

A

R>L anatomic or alveolar (passes alveolus but doesn’t contact air from pneumonia/collapsed alveoli)

84
Q

What does the apneustic centre do?

A

Prolongs inspiration

85
Q

What does the pneumotaxic centre do?

A

Inhibits inspiration

86
Q

What does vagal afferent input do?

A

Terminates inspirations

87
Q

What does cutting below medulla do?

A

Stops breathing

88
Q

What does cutting above central medulla do?

A

Rhythmic but irregular breathing

89
Q

What does cutting at upper pons do?

A

Slows respiration but increases tidal volume

90
Q

What happens if saline and CO2 is added to chemosensitive areas?

A

Add CO2 and ventilation increases, add saline and it decreases

91
Q

What produces cerebrospinal fluid?

A

Choroid plexus

92
Q

What is the composition of cerebrospinal fluid?

A

Low protein, HCO3-, K+ and Ca2+. High Na+, Cl-

93
Q

Are carotid or aortic bodies dominant in breathing control?

A

Carotid

94
Q

Which cells in the carotid bodies are responsible?

A

Glomus

95
Q

What can carotid bodies sense?

A

PCO2, pH, PO2

96
Q

What do the pulmonary stretch receptors in the airway do?

A

Discharge in response to distension via the vagus nerve

97
Q

What is the Hering-Breuer inflation reflex?

A

Discharge of pulmonary stretch receptors slows breathing frequency by inhibiting inspiration and prolonging expiration

98
Q

What is the deflation reflex?

A

Lung deflation induces inspiration

99
Q

What must tidal volume be greater than for CPG?

A

1 litre

100
Q

What happens to tidal volume and breathing frequency if vagal afferent input to higher brain is blocked?

A

Nothing

101
Q

What does the intrinsic ramp pattern of the pontine respiratory group do?

A

Stimulation terminates inspiration, still get breathing pattern if afferent input is cut

102
Q

What does the apneustic centre innervate?

A

Respiratory muscles

103
Q

Why is blood flow bad at the top of the lung?

A

Alveolar pressure is greater than artery and vein pressure, so blood vessels closed

104
Q

Why is blood flow good a the bottom of the lung?

A

Artery and vein pressure greater than alveolar pressure so vessels stay open

105
Q

What are the ventilation/perfusion zones of the lung called?

A

West Zones

106
Q

Are the base and apex over-perfused or over-ventilated?

A

Base is overperfused, apex is over-ventilated

107
Q

How do the medullary central chemoreceptors monitor PCO2?

A

Use H+ (CO2 crosses blood-brain barrier into CSF and forms H+)

108
Q

Why can’t protons in blood just cross the blood brain barrier to the chemoreceptors?

A

They could have come from lots of places

109
Q

What does cutting pneumotaxic centre cause?

A

Goes to full tidal volume because pneumotaxic centre aids inspiration termination

110
Q

What does cutting apneustic centre do?

A

Get small variable inhalations because it contains motor nerves which drive inspiration

111
Q

What do stretch receptors carried by the vagus stimulate?

A

Pneumotaxic which inhibits apneustic so exhalation

112
Q

What is rate limiting at altitude?

A

O2 diffusion

113
Q

What do hyperventilation at altitude do?

A

Decreases PCO2 so alveolar PO2 increases again - BUT falling PCO2 opposes low PO2 which triggers ventilation increase

114
Q

Hyperventilation at altitude causes alkaline CSF - what does this do?

A

Choroid plexus stops producing HCO3- which removes the “braking effect” - a good thing here.

115
Q

What is Caisson disease?

A

The bends

116
Q

Why is He used instead of N2?

A

Reduces bends risk because it’s half as soluble

117
Q

What is the neurogenic response?

A

Increases Ve at the start of exercise

118
Q

What does the humeral response do?

A

Maintains increased Ve during exercise

119
Q

Why don’t PCO2, PO2 and pH not change during exercise?

A

NOBODY KNOWS

120
Q

What do peripheral chemoreceptors control?

A

Adding/removing CO2

121
Q

What can blood supply vasoconstriction during low O2 cause?

A

High pressure so fluid pools in alveoli

122
Q

What is the vicious circle from chemoreceptors signalling opposite things at altitude?

A

Normal CO2 and decreased O2 > increased ventilation > increased O2 and decreased CO2 > decreased ventilation > back to where we started

123
Q

What is “central adaptation”?

A

To stop decreased ventilation, [HCO3-] is removed from CSF so more H+ produced (so goes back to normal) which is detected by chemoreceptors so ventilation increases again - NOT TO MAKE VENTILATION INCREASE, JUST TO STOP IT GOING DOWN

124
Q

What is the Haldane effect?

A

The CO2 content of blood is modulated by PO2/saturation - more CO2 is carried in deoxygenated that oxygenated blood

125
Q

Why is more CO2 carried in deoxygenated than oxygenated blood?

A

Deoxy Hb is a weaker acid so will bind more protons at physiological pH which maintains gradient for bicarb production AND deoxy Hb forms more carbamino compounds

126
Q

Why is the slope of “adding carbonic acid” line steeper on a Davenport diagram than titrating plasma?

A

Because of Hb buffering properties

HOM (7 decks)

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