Respiratory Flashcards

1
Q

How much air do you normally inhale per breath?

A

500mL

12-15 breaths/minute= 6-8L/min total ventilation

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2
Q

How much O2 enters the body per minute?

A

250mL

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3
Q

How much CO2 is expired per minute?

A

200mL

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4
Q

How many times does the airway divide between the trachea and alveolar sacs?

A

23 times

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5
Q

What are the first 16 divisions of the airways?

A

The conducting zones- dead space = 150mL per breath

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6
Q

What are the last 7 divisions of the airways?

A

Transitional and respiratory zones- for gas exchange = 350mL per breath= alveolar ventilation

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7
Q

Is anatomical dead space = physiological dead space?

A

In a normal person, yes

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8
Q

How is gas moved in the alveolar region?

A

Chiefly by diffusion

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9
Q

Where do you find type I and type II pneumocytes?

A

They line the alveoli

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10
Q

What are type I pneumocytes?

A

They are flat, large cytoplasmic extensions and are the primary lining of the cells. Simple squamous epithelial cells

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11
Q

What are type II pneumocytes?

A

They are granular pneumocytes, thicker and have numerous lamellar inclusion bodies. They secrete surfactant

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12
Q

What are the other cells present in the lungs?

A

Macrophages, lymphocytes, plasma cells, APUD cells, mast cells

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13
Q

What is the volume of the conducting zone?

A

About 150mL

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14
Q

What is the volume of the lung excluding the conducting zone during resting conditions?

A

About 2.5-3L

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15
Q

How do you distinguish a respiratory from a terminal bronchiole?

A

Respiratory bronchioles have alveoli lining the walls

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16
Q

What is the predominant mode of gas flow in the respiratory bronchioles?

A

Diffusion rather than convection

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17
Q

How many alveoli are there and how big are they?

A

300million, 0.3mm

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18
Q

What makes the alveolar structure stable?

A

Surfactant- lowers the surface tension

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19
Q

How are large particles filtered out of the airways?

A

By the nose

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20
Q

How are particles that reach the airway removed?

A

By the mucus escalator which is propelled by millions of tiny cilia

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21
Q

Where does the mucus in the airway come from?

A

From mucous glands and goblet cells in the bronchial walls?

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22
Q

How are particles that reach the alveoli removed?

A

They are engulfed by macrophages and then material from the alveoli is removed from the lung via lymphatics

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23
Q

What is the blood supply to the lungs?

A

Mainly from RV- 5L/min

Additionally from bronchial circulation from aorta- this supplies conducting airways down to terminal bronchioles

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24
Q

What is the mean pressure in the pulmonary artery at rest

A

~15mmHg

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25
Q

What is the average diameter of the capillaries that cover the alveoli?

A

10 micrometers- just big enough for an RBC

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26
Q

What is the thickness of the blood-gas barrier?

A

<0.3 micrometer

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27
Q

How much time does blood spend in the capillaries?

A

3/4 of a sec

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28
Q

What is the total area of the B-G barrier?

A

50 square meters

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29
Q

What happens if the pressure in the capillaries rises to unphysiologically high levels?

A

The blood gas barrier can be damaged

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30
Q

What happens to venous return during inspiration?

A

It increases

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31
Q

What changes about the time that an RBC spends exposed to alveolar gas during exercise?

A

Spends less time

750ms at rest, 250ms during exercise

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32
Q

What are the 3 volumes that can’t be measured with simple spirometry

A
  1. Residual volume
  2. Functional residual capacity because it involves residual volume ERV+RV
  3. TLC for same reason
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33
Q

What is the pulmonary blood flow per minute?

A

5L/min

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34
Q

What decreases the functional residual capacity of the lung? (4)

A
  1. Supine position
  2. Term pregnancy
  3. Post-operative atelectasis
  4. Chronic bronchitis with sputum retention
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35
Q

How should you initially treat an acute fall in FRC?

A

With high flow mask oxygen

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36
Q

What can cause a restrictive defect in ventilatory function? (4)

A
  1. Fractured ribs
  2. Upper abdominal surgery
  3. Lobar pneumonia
  4. Old T6 spinal cord injury
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37
Q

What is the closing volume of the lung?

A

The lung volume when small airway closure begins to occur

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38
Q

What is the approx value of the closing volume of the lung?

A

Between the residual volume and the functional reserve capacity

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39
Q

What can increase the closing volume of the lung?

A

Age

Small airways disease

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40
Q

What is alveolar ventilation?

A

The volume of fresh gas entering the alveoli per minute (or volume of gas leaving)

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41
Q

What is the formula for alveolar ventilation?

A

Tidal volume-dead space = 500-150=350mL per breath

Thus can be increased by increasing tidal volume

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42
Q

What is the relationship between alveolar ventilation and respiratory rate?

A

Directly related to RR but when RR increases, TV gets compromised

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43
Q

What is the relationship between alveolar ventilation and alveolar PCO2?

A

Inverse

If alveolar ventilation increases (hyperventilation)x3 PACO2 decreases by 1/3

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44
Q

What are 3 factors contributing to alveolar PO2?

A
  1. Inspired oxygen concentration
  2. Alveolar ventilation
  3. Oxygen consumption of the body
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45
Q

What are the factors that contribute significantly to the oxygen tension difference between alveolar gas & systemic arterial blood (A-a PO2 diff)?

A
  1. Anatomical R) to L) shunt

2. Low ventilation/ perfusion ratio in regions of the lung

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46
Q

What is the difference of the effect of oxygen on the microcirculation of the pulmonary circulation vs the systemic circulation?

A

In pulmonary circulation, decreased O2 causes constriction of capillaries, in systemic, causes dilatation.

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47
Q

What happens when a healthy person hyperventilates before renal compensation kicks in? (4 things)

A
  1. PACO2 of about 20mmHg
  2. A decrease in plasma bicarb
  3. A decrease in ICP
  4. A PaO2 of about 120mmHg
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48
Q

When can the amount of anatomical dead space increase?

A

With a big inspiration because of traction or pull exerted on the bronchi by surrounding lung parenchyma

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49
Q

What is physiological dead space?

A

The volume of gas that does not eliminate CO2

May be the same as anatomical dead space in normal individuals

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50
Q

What can increase physiological dead space?

A

Lung disease due to inequality of blood flow and ventilation within the lung

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51
Q

How can you measure physiological dead space?

A

Using Bohr’s equation (PACO2-PECO2)/PACO2

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52
Q

What is physiological dead space the sum of?

A

Anatomical + alveolar dead space (alveolar dead space is negligible in health)

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53
Q

What is the ratio of physiological dead space to tidal volume?

A

0.3 I.e. 150/500mL

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54
Q

What is the role of pulmonary acini?

A

All oxygen uptake occurs in the acini

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55
Q

What changes in the acini during inspiration?

A

The percentage change in volume of the acini during inspiration exceeds that of the whole lung

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56
Q

What is the relationship of the volume of the acini to total volume of the lung at FRC?

A

It is greater than 90% of the total volume of the lung at FRC

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57
Q

What is Fick’s Law?

A

Law of diffusion of a gas through tissue slice

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58
Q

What is the diffusion rate of a gas through tissue slice proportional to? (Fick’s law of diffusion, 3 things)

A
  1. The surface area
  2. The partial pressure difference btw the 2 sides
  3. The solubility of the gas in the tissue
59
Q

What is the diffusion rate of gas inversely proportional to?

A

The thickness of the tissue and to the square root of the molecular weight

60
Q

Which diffuses more rapidly, CO2 or O2?

A

CO2, about 20 times more rapidly

61
Q

How does the example of carbon monoxide exemplify diffusion limitation of Fick’s law?

A
  1. CO diffuses freely through B-G barrier
  2. Binds intimately with Hb therefore exerts no effect on pCO in blood
  3. More can diffuse through but only 3/4/ of a second to do so, there fore is diffusion limited
  4. Amount absorbed is entirely dependent on the surface area available
62
Q

How does NO exemplify the perfusion limitation of Fick’s law?

A
  1. It does not bind with Hb after diffusing across the B-G barrier, partial pressure rises rapidly
  2. 3/4 second to diffuse, but no NO can be transferred after a while
  3. Thus the amount of gas taken up by blood depends entirely on amount of blood flow
63
Q

What is oxygen uptake like compared to CO and NO?

A

The rate of uptake sits somewhere between CO and NO

64
Q

How quickly does pO2 of blood equal that of the alveolar gas?

A

After 1/3 of its time in the capillary

65
Q

How much time does the blood spend in the alveolar capillary at rest?

A

3/4 of a second

66
Q

How much time does blood spend in an alveolar capillary during exercise?

A

Approx 1/4 of a second

67
Q

What challenges the diffusion process of oxygen going across the blood gas barrier?

A

Exercise, alveolar hypoxia and thickening of the blood gas barrier

68
Q

What’s the relationship between oxygen uptake by Hb in the lung capillaries and pH?

A

Directly related I.e. if blood more alkaline, oxygen is more easily taken up by Hb, more acidotic, harder to take up

69
Q

What is the relationship between oxygen uptake by Hb in the lung capillaries and PACO2?

A

Varies inversely with PACO2, if too much CO2 in blood, less is taken up by Hb

70
Q

Which direction does the dissociation curve move in after birth?

A

To the left

71
Q

How does oxygen uptake by Hb in lung capillaries relate to 2,3DPG?

A

It varies inversely, so the more 2,3DPG, the harder it is to take up oxygen

72
Q

Which gas is used to measure diffusion capacity?

A

CO (carbon monoxide)

73
Q

What is the value of normal diffusion capacity?

A

25mL/min/mmHg

74
Q

What happens to diffusion capacity during exercise?

A

Increases 2-3x

75
Q

What is the definition of the diffusion capacity?

A

The volume of gas that will diffuse through the membrane each minute for a partial pressure difference of 1mmHg.
I.e. the ease with which gases can find themselves transported into alveolar capillary blood

76
Q

What is the equation for measuring DC?

A

Net rate of gas transfer/ partial pressure gradient

I.e. for CO V(CO)/ PCO

77
Q

In a normal person, what would happen if you doubled the DC?

A

Increase maximal oxygen uptake at high altitude

78
Q

What can limit the diffusion of oxygen during exercise?

A

High altitude

79
Q

How is DC affected when one lung is removed?

A

It is decreased

80
Q

Is DC decreased or increased in pulmonary fibrosis?

A

Decreased as pulmonary fibrosis leads to thickening of the blood gas barrier

81
Q

What are 4 things that reduce the DC of the lung for CO?

A
  1. Emphysema due to loss of the pulmonary capillaries
  2. Asbestosis- causes thickening of the blood gas barrier
  3. Pulmonary embolism as blood supply cut off to part of the lung
  4. Severe anaemia
82
Q

What is the pressure within the right atrium?

A

~2mmHg

83
Q

What is the pressure within the right ventricle?

A

25/0mmHg

84
Q

What is the pressure in the pulmonary artery?

A

25/8mmHg- mean pulmonary pressure is 15mmHg

85
Q

What is the pressure in the pulmonary capillary bed?

A

~8-12mmHg

86
Q

What is the pressure returning to the Left Atrium?

A

~5mmHg

87
Q

What can happen to the alveolar vessels if the alveolar pressure increases?

A

They can get compressed

88
Q

What is the pressure in the extra-alveolar vessels?

A
89
Q

How are the extra-alveolar vessels opened?

A

Pulled open by the radial traction of the surrounding parenchyma

90
Q

What causes constriction of the alveolar arteries?

A

Alveolar hypoxia

91
Q

What increases the caliber of the alveolar and extra-alveolar vessels?

A

Lung inflation

92
Q

What is the equation for determining pulmonary vascular resistance?

A

Vascular resistance= (input pressure-output pressure)/blood flow (6L/min)
=15-5/6=1.7mmHg/Lmin

93
Q

What is the relationship of pulmonary vascular resistance to systemic resistance?

A

PVR is normally v small, about 10% of the systemic vascular resistance

94
Q

What controls pulmonary vascular resistance locally?

A

Oxygen tension in the adjacent alveoli

95
Q

Name 3 things that increased PVR is associated with

A
  1. High and low lung volumes
  2. Alveolar hypoxia because of constriction of small pulmonary arteries
  3. Drugs that cause contraction of muscle e.g. serotonin, histamine, Noradrenaline
96
Q

Name 2 things that are associated with decreased PVR?

A
  1. Exercise because of recruitment and distension of capillaries
  2. (Acutely) increasing venous pressure
97
Q

What causes a fall in PVR during exercise? (4 things)

A
  1. Increased pulmonary arterial pressure
  2. Increased pulmonary venous pressure
  3. Recruitment of pulmonary capillaries
  4. Distension of pulmonary capillaries
98
Q

What does the body’s blood vessels normally do in response to hypoxia?

A

Vasodilate

99
Q

What happens to the vessels in the lungs when there is hypoxia and what does this do?

A

Constriction, this shunts blood to better ventilated regions

100
Q

What does alveolar hypoxia do to small pulmonary arteries?

A

Causes constriction

101
Q

Why does alveolar hypoxia cause constriction of the alveolar blood vessels?

A

Probably a direct effect of the low PO2 on the vascular smooth muscle
The mechanism involves K+ channels in the vascular smooth muscle

102
Q

What is the role of hypoxia pulmonary vasoconstriction at birth?

A

It’s critical in the transition from placental to air breathing

103
Q

How does hypoxic pulmonary vasoconstriction help in those with lung disease?

A

It directs blood flow away from poorly ventilated areas, thus it is going to areas where it is more likely to pick up lots of oxygen

104
Q

What can reduce hypoxic pulmonary vasoconstriction?

A

Inhaling low concentrations of nitrous oxide

105
Q

What are the 3 vascular functions of the lung?

A
  1. Gas exchange
  2. Storehouse for blood
  3. Filter for blood- clots get trapped in the lungs and don’t go to the brain
106
Q

What are 5 metabolic functions of the lung?

A
  1. Converting angiotensin I-II by ACE
  2. Inactivating bradykinin
  3. Removing serotonin
  4. Removing leukotrienes
  5. Removes 30% of NA
107
Q

What are biologically active substances metabolised by the lungs?

A
  1. Synthesised and used in the lungs- surfactant
  2. synthesised and stored or released into blood- PG’s, histamine, kallikrenin
  3. Partially removed from the blood- PG’s, bradykinins, adenine nucleotides, serotonin, NA, ACH
  4. Activated in the lungs- Angi-AngII
108
Q

How is the accumulation of water in pulmonary alveoli prevented?

A
  1. Surfactant which maintains a low surface tension in alveoli
  2. A low hydrostatic pressure in the alveolar capillaries
109
Q

What is the pO2 in air?

A

150mmHg

110
Q

What is the pO2 by the time it reaches the alveoli?

A

100mmHg

111
Q

What are the 3 factors that determine alveolar pO2?

A
  1. Alveolar ventilation (most important)
  2. FiO2
  3. How much O2 is taken up by the Hb
112
Q

What are the 6 layers that O2 has to move through the B-G barrier to get from alveoli to RBC?

A
  1. Surfactant
  2. Epithelial cell
  3. Interstitium
  4. Endothelial cell
  5. Plasma
  6. RBC membrane
113
Q

What are the systemic effects of arterial hypoxia? (List 4)

A
  1. An increased RR
  2. Dilatation of coronary arterioles
  3. Respiratory alkalosis
  4. Constriction of renal arterioles
114
Q

Name four causes of hypoxaemia

A
  1. Hypoventilation
  2. Diffusion limitation
  3. Shunt
  4. Ventilation- perfusion inequality
115
Q

What effect does hypoventilation have on alveolar and arterial PCO2 vs PO2?

A
  1. Always increases alveolar and arterial PCO2
  2. Always decreases alveolar and arterial PO2 unless additional O2 is inspired
    Therefore hypoxaemia is easy to reverse by increasing FiO2
116
Q

What are 4 causes of hypoventilation?

A
  1. Drugs that reduce respiratory drive e.g. morphine, barbiturates
  2. Damage to chest wall
  3. Paralysis of respiratory muscles
  4. High resistance to breathing e.g. diving in deep water
117
Q

What is a shunt when talking about the lungs?

A

It refers to blood that enters the arterial system without going through ventilated areas of lung

118
Q

What happens when you try to treat hypoxaemia from shunting with added inspired O2?

A

Not much, it responds poorly

When 100% O2 is inspired, the arterial PO2 does not rise to the expected level- a useful diagnostic test

119
Q

What do regional difference of V/Q cause in the upright human lung?

A

A pattern of regional gas exchange

120
Q

What is the V/Q pattern in the upright lung?

A

They decline in a linear fashion from bases to apices

121
Q

What are the V/Q ratios like in the upper part of the lung?

A

They are high in the upper portion, high PO2 because perfusion is lower at apices

122
Q

What does V/Q mismatch result in?

A

It impairs the uptake or elimination of all cases by the lung

123
Q

Is the elimination of CO2 impaired by V/Q mismatch?

A

Yes, but it can be corrected by increasing the ventilation to the alveoli, by contrast, the hypoxaemia resulting from V/Q inequality cannot be eliminated by increases in ventilation.
The different behaviour of the 2 gases is due to the different shapes of their dissociation curves

124
Q

How is O2 carried in the blood?

A

Combined with Hb- presence of Hb in blood increases O2 concentration by 70x
Dissolved

125
Q

Why would dissolved O2 alone not be enough to meet tissue demands?

A

Because it obeys Henry’s law- amount dissolved is proportional to the partial pressure- this in itself is not enough to meet tissue demand

126
Q

What is directly responsible for how much O2 tissues will get?

A

HbO2= saturation of O2 on Hb

The drive for HbO2 is the pO2 and relationship via sigmoid curve

127
Q

What is the oxygen saturation of Hb for a pO2 of 100mmHg?

A

97.5%

128
Q

What is the Hb saturation at a pO2 of 40mmHg (like in venous blood)?

A

75%

129
Q

What is the p50?

A

The pO2 for 50% of O2 saturation

Normally about 27mmHg

130
Q

What is the significance of the flat part of the O2 dissociation curve?

A

Even if the pO2 in alveolar gas falls somewhat, loading of O2 will be little affected

131
Q

What is the significance of the steep part of the curve?

A

Means that even a small drop in pO2 affects significantly how much O2 will get on the Hb

132
Q

What do you do if you want to get more O2 to the peripheries?

A

Pump up the pO2 with high flow O2, this ensures more O2 gets on the Hb and therefore gives more O2 for the tissue

133
Q

What shifts the curve to the left (increased O2 affinity)?

A
CO
HbF
Hypothermia
Decreased PCO2
Decreased 2,3-DPG
134
Q

What shifts the curve to the right (decreased O2 affinity)?

A

Hyperthermia
Increased PCO2
Low pH
Increase 2,3-DPG

135
Q

What happens to O2 offloading in exercise?

A

Exercising muscle is acid, hypercarbic and hot and thus benefits from increased unloading of O2 from its capillaries

136
Q

What is associated with elevated levels of 2,3-DPG?

A

Associated with chronic hypoxia- high altitude, chronic lung disease

137
Q

Does oxygen uptake by Hb in the lung capillaries vary directly or indirectly with blood pH?

A

Directly

138
Q

How does oxygen uptake by Hb in the lung capillaries vary with increased PACO2?

A

It varies inversely

139
Q

How does carbon monoxide interfere with O2 transport?

A

It binds closely with Hb
Has 240 times the affinity of O2 for Hb I.e. for the same partial pressure, CO will bind 240x more strongly than O2
Therefore Hb concentration in blood may be normal, but O2 conc greatly reduced

140
Q

Does COHb shift the curve to the left of the right?

A

The left and thus interferes with the unloading of O2

141
Q

What are 5 features of CO poisoning?

A
  1. Reduced O2 concentration of arterial blood
  2. Reduced O2 concentration of mixed venous blood
  3. O2 dissociation curve shifted to the left
  4. CO is colourless and odourless
  5. Normal arterial pO2
142
Q

What are the physiological changes that occur at high altitude?

A

At high altitude, sympathetic activity, heart rate, and cardiac output, increase. Plasma volume is reduced leading to haemoconcentration. Hyperventilation leads to respiratory alkalosis and increases pulmonary arteriolar resistance that may lead to pulmonary hypertension.

143
Q

What are the physiological changes that occur at high altitude?

A

At high altitude, sympathetic activity, heart rate, and cardiac output, increase. Plasma volume is reduced leading to haemoconcentration. Hyperventilation leads to respiratory alkalosis and increases pulmonary arteriolar resistance that may lead to pulmonary hypertension.