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Block 2 > Respiratory Anatomy and Physiology > Flashcards

Respiratory Anatomy and Physiology Flashcards

1
Q

Describe the anterior and middle scalene

A

Attached to the first rib from the cervical vertebra

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2
Q

Describe the posterior scalene

A

Attached to the second rib from the cervical vertebrae.

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3
Q

Describe the sternocleidomastoid muscle

A

Attached to the first rib from the mastoid process

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4
Q

What is compliance work?

A

The energy required to expand the lungs against the lung and chest elastic forces

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5
Q

What is tissue resistance work?

A

The energy required to overcome the viscosity of the lung and chest wall structures

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6
Q

What is airway resistance work?

A

The energy required to overcome airway resistance to movement of air into the lungs.

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7
Q

What is work of breathing?

A

The energy expended during respiration

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8
Q

Is there a positive or negative pressure within the pleural space?

A

Negative

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9
Q

Define compliance

A

A measure of the disposition of the lungs to expand under traction or pressure

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10
Q

Define elastance

A

A measure of the disposition of the lungs to return to resting position due to intrinsic elasticity

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11
Q

Define Hooke’s law

A

The force needed to extend or compress a string is proportional to that distance.

Not quite relevant to the lung - the lung is stiffer at high and low volumes

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12
Q

Does emphysema increase or decrease compliance?

A

Increase

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13
Q

Does fibrosis increase or decrease compliance?

A

Decrease

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14
Q

What cells secrete surfactant?

A

Type II epithelial cells (pneumocytes)

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15
Q

What is the major ingredient in surfactant?

A

Phospholipids (dipalmitoyl phosphatidylcholine)

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16
Q

As well as phospholipids, what other important substances are in surfactant?

A

Surfactant proteins A B C D

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17
Q

Which surfactant proteins activate macrophages and bind to pathogens?

A

A and D

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18
Q

Which nerve stimulates contraction of bronchial smooth muscle?

A

Vagus nerve CN X

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19
Q

Which type of drugs are used in the treatment of asthma? Which receptors do they act on?

A

Beta - agonists

B2 receptors.

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20
Q

What three things determine airway resistance?

A

Autonomic nervous system

Lung volume

Turbulent/laminar flow

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21
Q

What is vital capacity?

A

The difference in volume between maximum inhalation and maximum exhalation

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22
Q

What drug type is usually in a reliever inhaler?

A

Beta agonist

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23
Q

What drug type is usually in a preventer inhaler?

A

Steroid

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24
Q

What is residual volume?

A

The amount of air that remains in the lungs after full exhalation.

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25
Q

What is tidal volume?

A

The normal volume of air displaced between normal inhalation and exhalation, usually around 500mL

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26
Q

What is functional residual capacity?

A

The volume of air remaining in the lungs after expiration of a normal breath

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27
Q

What is the best indication of lung restriction on spirometry?

A

A reduction in vital capacity

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28
Q

What is the best indication of airways obstruction on spirometry?

A

An increase in residual volume

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29
Q

What would you expect to see on a restrictive spirometry?

A

Decreased inspiratory reserve volume

Decreased expiratory reserve volume

Decreased reserve volume

Decreased total lung capacity

Decreased forced vital capacity.

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30
Q

What would you expect to see on an obstructive spirometry?

A 
Increased total lung capacity
Decreased inspiratory reserve volume
Increased expiratory reserve volume
Increased reserve volume
Same or decreased forced vital capacity
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31
Q

Define metabolic acidosis

A

pH <7.35

Low HCO3-

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32
Q

Define respiratory acidosis

A

pH <7.35

High PaCO2

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33
Q

Define metabolic alkalosis

A

pH >7.45

High HCO3-

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34
Q

Define respiratory alkalosis

A

pH >7.45

Low PaCO2

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35
Q

What is the area of the thorax called where the heart and great vessels sit?

A

Mediastinum

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36
Q

What vertebral level is the suprasternal notch?

A

T2

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37
Q

What vertebral level is the sternal angle?

A

T4/5

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38
Q

What vertebral level is the xiphoid process?

A

T9/10

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39
Q

Name the three portions of the sternum

A

Manubrium

Body

Xiphoid process

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40
Q

Which rib sits at the sternal angle?

A

Rib 2

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41
Q

Why is the posterior angle of the rib an important anatomical landmark?

A

Used to perform intercostal nerve blocks.

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42
Q

Where is the neurovascular bundle?

A

In the costal groove

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43
Q

What is in the neurovascular bundle?

A

Posterior/anterior intercostal artery

Vein

Nerve

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44
Q

What joints sit between the ribs and vertebrae?

A

Synovial joints

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45
Q

Which ribs are vertebrosternal?

A

Ribs 1-7

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46
Q

Which ribs are vertebrocostal?

A

Ribs 8-10

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47
Q

Which ribs are floating ribs?

A

11 & 12

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48
Q

From outside in, name the 3 layers of intercostal muscle

A

External intercostal muscle

Internal intercostal muscle

Innermost intercostal muscle

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49
Q

Between what muscle layers does the neurovascular bundle run?

A

Internal and innermost intercostal muscles

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50
Q

Where does the internal thoracic artery arise from?

A

Subclavian artery

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51
Q

What comes off the internal thoracic artery?

A

Anterior intercostal artery

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52
Q

Name the right sided vein of the thoracic wall

A

Azygous vein

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53
Q

Name the left sided veins of the thoracic wall

Where do they drain into?

A

Accessory azygous vein

Hemiazygous vein

Both drain into the azygous vein on the right hand side which drains straight into the SVC

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54
Q

Where does the majority of the body’s lymph fluid drain into?

Where does the thoracic duct start?

A

Most of the lymph drains into the left subclavian vein (produces Virchow’s node in GI cancers)

Cisterna chyli

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55
Q

At what level does the IVC pierce the diaphragm?

A

T8

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56
Q

At what level does the oesophagus pierce the diaphragm?

A

T10

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57
Q

At what level does the aorta pierce the diaphragm?

A

T12

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58
Q

In what 3 ways is CO2 transported?

A

Dissolved CO2 (10%)

Cabamino compounds (21%)

HCO3- (69%)

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59
Q

What determines the concentration of H+ ions in the plasma?

A

Concentration of CO2

Concentration of HCO3-

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60
Q

Does arterial or venous blood carry more H+?

A

Venous blood

Deoxygenation results in uptake of H+

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61
Q

What is the Bohr effect?

A

Uptake of CO2 reduces the affinity of haemoglobin for O2

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62
Q

What is the Haldane effect?

A

Giving up O2 increase the carriage of CO2

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63
Q

What decreases haemoglobin’s affinity for O2?

A

Increased H+ ions
Increased CO2
Increased temperature
Increased 2,3-biphosphoglyceric acid.

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64
Q

How are carbamino compounds formed?

A

When CO2 reacts with protein amino groups

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65
Q

How is H+ linked to Ca2+?

A

Low H+ is linked with increase binding of Ca2+ to albumin

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66
Q

What 3 mechanisms minimise the changes in pH?

A

Buffer systems

Lungs - adjusting CO2

Kidneys - adjust the excretion of H+ into the urine

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67
Q

What is a buffer?

A

Any substance that can reversibly bind H+

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68
Q

What are the factors affecting diffusion in the respiratory system?

A

Surface area

Permeability of membrane

Pressure gradient (osmotic gradient)

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69
Q

What is the pO2 in the alveoli and circulatory system?

A

Alveoli - 13.3 kPA

Circulation - 6.0 kPa

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70
Q

What is the pCO2 in the alveoli and circulatory system?

A

Alveoli - 5.3 kPa

Circulation - 6.5 kPa

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71
Q

What limits O2 transfer?

A

O2 transfer is perfusion limited- limited by how much blood we can push through the lungs

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72
Q

When is O2 diffusion limited?

A

If the diffusion barrier is thickened e.g. fibrosis

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73
Q

What are the four lung volumes of spirometry?

A

Tidal volume

Inspiratory reserve volume

Expiratory reserve volume

Residual volume

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74
Q

How do you calculate total lung capacity?

A

IRV+TV+ERV+RV

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75
Q

How do you calculate Inspiratory capacity?

A

IRV+TV

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76
Q

How do you calculate vital capacity?

A

IRV+TV+ERV

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77
Q

How do you calculate functional residual capacity?

A

ERV+RV

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78
Q

What is minute ventilation (MV)?

A

The amount of air moved into and out of the lungs per minute

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79
Q

How do you calculate minute ventilation?

A 
Volume moved per breath (tidal volume, Vt)
Respiratory rate (RR)

MV = Vt x RR

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80
Q

What is alveolar ventilation rate (AVR)?

A

The amount of air that actually reaches the alveoli per minute

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81
Q

What are the two types of dead space?

A

Serial and distributive

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82
Q

Define serial dead space

A

The volume of the conducting airways (a.k.a. ‘anatomical dead space’)

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83
Q

Define distributive dead space

A

Some parts of the lung are not airways, but do not support gas exchange
e.g. damaged alveoli or alveoli with poor perfusion

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84
Q

How do you calculate alveolar ventilation rate?

A

(Vt - Vds) x RR

Vt = tidal volume
Vds = dead space volume
RR = resp rate
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85
Q

What alters the partial pressure gradient in the alveoli?

A

Alveolar ventilation rate

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86
Q

What is the ventilation perfusion ratio?

A

Ideally a ratio of 1, when the ventilation and perfusion are in equilibrium.
Mismatches cause a change in the V/Q ratio.

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87
Q

Does the V/Q ratio increase or decrease as you move towards the base of the lungs?

A

V/Q ratio decreases to less than 1 at the base of the lungs.

Perfusion increases, ventilation decreases

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88
Q

Why is ventilation greater at the bases of the lungs?

A

Because the basal lung is relatively compressed compared to the apex - more potential for expansion

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89
Q

Why does TB tend to consolidate at the apex of the lung?

A

Because the bacteria likes a well perfused area to grow in

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90
Q

What pathophysiology results in a reduction of ventilation?

A

Pneumonia

Therefore blood is less oxygenated
Decreases V/Q ratio

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91
Q

What pathophysiology results in reduced perfusion?

A

PE

Increases V/Q ratio

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92
Q

Where is the respiratory centre located?

A

Pons and medulla

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93
Q

What are the two respiratory centres called?

A

Dorsal and ventral respiratory centres

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94
Q

What are the two respiratory centres responsible for?

A

Rhythm of breathing

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95
Q

Which respiratory centre is found in the pons?

A

Pneumotaxic centre

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96
Q

What does the pneumotaxic centre do?

A

Regulates respiratory rate

Decreases tidal volume

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97
Q

How do central chemoreceptors monitor pH?

A

They are found in the brainstem and monitor arterial pCO2 through the pH of CSF.

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98
Q

Which chemoreceptors monitor pO2?

A

Peripheral chemoreceptors

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99
Q

Where are peripheral chemoreceptors found?

A

Aortic and carotid bodies

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100
Q

Which 2 nerves does the respiratory centre control?

A

Phrenic motor nerves (C3, 4, 5)

Vagus nerve (CNX)

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101
Q

What is the hypoxic drive?

A

The need to provide tissues with oxygen

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102
Q

Define hypercapnia

A

Rise in PaCO2

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103
Q

Define hypocapnia

A

Fall in PaCO2

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104
Q

Define hypoxia

A

Fall in PaO2

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105
Q

What are normal pAO2 and pACO2 values?

A = alveolar

A

pAO2 = 13.6 kPa

pACO2 = 5.3 kPa

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106
Q

What causes a rise in pAO2?

A

Increased ventilation

Decreased perfusion

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107
Q

What causes a rise in pACO2?

A

Decreased ventilation

Increased perfusion

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108
Q

At what pO2 does ventilation begin to increase and Hb start to desaturate?

A

8 kPa

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109
Q

Between which arteries does the carotid body sit?

A

Internal and external carotid artery

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110
Q

Via which nerve are impulses sent to the medulla from the carotid bodies?

A

CN IX

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111
Q

What is the principle function of the carotid bodies?

What other functions can it perform?

A

Stimulating the response to hypoxia

Detecting changes in pCO2, hypotension, temperature, some chemicals, pH

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112
Q

Which chemoreceptors detect hypoxia?

Which nerve detects this?

Where does it send messages to?

A

The carotid bodies between the internal and external carotid.

CN IX

Respiratory centres in the medulla

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113
Q

What actions are taken as a result of hypoxia detected?

A

Increased rate and depth of respiration

Increased BP, adrenal secretion

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114
Q

Where are the principle sensors of pCO2?

A

The ventral surface of the medulla.

Detect the composition of CSF

Information is then sent to the medullary centre which controls ventilation rate

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115
Q

Where is CSF secreted from?

A

The chyroid plexus

CSF is protein free

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116
Q

What is the blood brain barrier permeable to?

What is it impermeable to?

Why does this allow central chemoreceptors to respond to CO2?

A

Permeable to CO2

Impermeable to HCO3- and
H+

pCO2 is the same in arterial blood and CSF

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117
Q

What is base excess?

A

The amount of strong acid that must be added (or removed) for each litre of fully oxygenated blood to return the pH to 7.40 at a temperature of 37°C and a pCO2of 5.3kPa

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118
Q

What does a positive base excess mean?

A 
Metabolic alkalosis 
(more acid needs to be added to maintain pH)
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119
Q

What does a negative base excess mean?

A 
Metabolic acidosis
(less acid needs to be added to maintain pH)
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120
Q

What are the 5 causes of metabolic acidosis?

A

Lactic acidosis

Ketoacidosis

Acute renal failure

Excessive loss of HCO3- (raised plasma chloride)

All other causes e.g. poisons (aspirin, methanol)

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121
Q

What is a cute respiratory failure?

A

When the pulmonary system is no longer able to meet the metabolic demands of the body

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122
Q

Describe type 1 respiratory failure

A

Hypoxaemic respiratory failure

PaO2 <8 kPa when breathing room air

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123
Q

Describe type 2 respiratory failure

A

Hypercapnic respiratory failure
PaCO2 >6.7 kPa
(May also be hypoxaemic depending on FiO2)

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124
Q

What causes type 1 (hypoxic) respiratory failure?

A

Reduced diffusion or diffusion capacity

  • low pO2 (altitude)
  • reduced surface area
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125
Q

What causes type 2 (hypercapnic) respiratory failure?

A

Reduced alveolar ventilation

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126
Q

What determines arteriole pO2?

A

Alveolar pO2

Diffusion capacity of alveolar membrane

Ventilation

Perfusion

V/Q

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127
Q

What would cause the V/Q ratio to be 0?

A

If ventilation stops.

shunting

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128
Q

What can cause shunting?

A

Pneumonia

Pulmonary oedema

Atelectasis

Lung collapse

Pulmonary haemorrhage or contusion

Congenital heart disease (patent foramen ovale - right to left shunt - hypoxix vasoconstriction).

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129
Q

What are the clinical features of respiratory failure?

A

Respiratory compensation

Sympathetic stimulation

Tissue hypoxia

Hb desaturation

Hypercapnia

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130
Q

What are the signs of respiratory compensation?

A

Tachypnoea

Use of accessory muscles

Intercostal recession

Nasal flaring

Splinting of accessory muscles

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131
Q

What are some of the signs of tissue hypoxia?

A

Altered mental state
Lactic acidosis (anaerobic metabolism)
Low HR and BP

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132
Q

What are the signs of hypercapnia?

A

Flapping tremor
Confusion –> coma
Sympathetic stimulation
Respiratory acidosis

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133
Q

What are the two types of asthma?

A

Extrinsic (atopic) eosinophilic

Intrinsic (non-atopic) neutrophilic

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134
Q

What are the triad of features in asthma?

A

Airway obstruction
Airway hyper-responsiveness
Airway inflammation

135
Q

What are the signs of an asthma attack?

A 
Incomplete sentences
Wheeze 
Tachypnoea
Tachycardia
Use of accessory muscles
Reduced breath sounds
136
Q

What is the principle muscle of respiration?

What is its innervation?

A

The diaphragm

Phrenic nerve C3, 4, 5

137
Q

What muscles stabilise the position of the 1st rib?

A

Anterior and middle scalene

Sternocleido-mastoid

138
Q

What is work of breathing?

What are its 3 components?

A

The energy expended during respiration

  1. Energy required to expand lungs against elastic forces (compliance)
  2. Energy required to overcome viscosity of lung (tissue resistance work)
  3. Energy required to overcome airway resistance to movement of air into lungs (airway resistance work)
139
Q

Inhalation and exhalation in quiet breathing are…..

A

Inhalation is active - lungs need to be pulled open against elastic tissues promoting recoil and resistance of airways

Exhalation is passive - lungs return to functional residual capacity where opposing forces of lung and chest wall are in balance

140
Q

Which muscles are at work in forced exhalation?

A

Extracartilaginous portion of internal intercostals - move ribs downwards

Abdominal muscles - push diaphragm upwards

Muscles of abdominal wall

Pectoral girdle muscles

141
Q

What are the accessory muscles of respiration?

A

Scalene muscles - elevating the first 2 ribs

SCM muscles - raising the sternum

142
Q

Which 5 muscles are used in inhalation?

A

Scalenes - elevate 1st and 2nd rib

SCM - raising sternum

External intercostals

Intercartilaginous internal intercostals

Diaphragm

143
Q

Define functional residual capacity

A

The lung volume at which the opposing forces of the expansile skeletal structure of the chest wall (with muscles at rest) and the contractile lung are in balance with each other

144
Q

Why do movements of the diaphragm and chest wall permit expansion of the lung?

A

Parietal pleura = chest wall
Pleural fluid
Visceral pleura = lung surface

This provides a pleural seal

During inhalation, the chest wall is expanded. Pleural space is stretched which decreases intrapleural pressure

Because of pleural seal, the lung is expanded because of the movement of the chest wall as the force of the lung’s elastic recoil is exceeded

145
Q

What lung volume is represented when the forces inflating and deflating the lungs are equal?

At what phase of the respiratory cycle does this occur?

A

Functional residual capacity

End of exhalation of quiet breathing

146
Q

The lungs are not adherent to the inside of the thoracic cavity. What stops them from collapsing away from the chest wall?

A

Negative pressure within the pleural space

147
Q

What will a pneumothorax do to the intrapleural pressure?

What effect will this have?

A

It will raise the intrapleural pressure

The lung will collapse because of the unopposed force of it’s elastic recoil (no longer attached to the chest wall)

148
Q

Which way does the trachae deviate in a pneumothorax?

A

To the contralateral side

149
Q

What signs can be seen on an Xray in a tension pneumothorax?

A

Lung completely compressed

Tracheal deviation to contralateral side

Heart shifted to contralateral side

Ipsilateral hemidiaphragm compression

150
Q

What is compliance?

A

A measure of the disposition of the lungs to expand under traction or pressure

A measure of the stiffness of the respiratory system

151
Q

What is elastance?

A

A measure of the disposition of the lungs to return to resting position due to their intrinsic elasticity

152
Q

Describe the effect of emphysema on compliance

A

Compliance is increased in emphysema as there is less tissue to stretch due to tissue destruction

153
Q

Describe the effect of fibrosis on compliance

A

Compliance is reduced in fibrosis

154
Q

What effect does emphysema have on functional residual capacity?

A

Emphysema increases FRC because there is less elastic recoil to ‘close’ the lungs

155
Q

What effect does fibrosis have on functional residual capacity?

A

Fibrosis decreases FRC

156
Q

Describe why surface tension is an important factor in compliance

Which law is relevant to this idea?

A

Attractive forces between molecules of a liquid are stronger than those between liquid and gas

Surface tension of water is high and lungs would be difficult to expand in the absence of an agent to lower the surface tension

Lungs have surfactant to lower the surface tension and reduce the work of respiration

LAPLACE’S LAW

157
Q

Name the cells that secrete surfactant

Where are they found?

What is the major component of surfactant?

A

Type II epithelial cells (pneumocytes)

Lining the alveoli

Phospholipid and surfactant proteins

158
Q

List the 5 functions of surfactant

A

Reduce surface tension, increase compliance at low lung volumes

Reduce the liklihood of tissue fluid transudation

Lipids have antioxidant activity

Surface proteins A and D can bind to pathogens

Surface proteins A and D can activate macrophages and neutrophils

159
Q

Describe the interdependence of the lungs and why this is

A

The packing of alveoli supports each other

This is an additional factor limiting any tendency of the lungs to collapse

160
Q

Describe Poiseuille’s Law

A

For individual tubes (airways) with laminar flow, the resistance rises with the fourth power of the radius

161
Q

Where does the main part of airways resistance lie?

A

Smallest airways are many in number and collectively have the lowest resistance

Greatest resistance is in medium sized bronchi

162
Q

In health, what are the limiting factors to max inspiratory and expiratory flow?

A

Muscle strength

Resistance is negligible in health

163
Q

In disease, what is airway flow limited by?

A

Resistance

164
Q

What does peak expiratory flow rate measure?

A

Airways resistance

165
Q

List 3 factors that determine airways resistance

A

Autonomic NS

  • contraction of smooth muscle narrows airways
  • relaxation of muscle is generated by adrenaline acting on B2 receptors.

Lung volume
- increased lung volume increases airway radius

Turbulent vs laminar flow
- larger airways are more prone to turbulent flow than smaller airways

166
Q

Discuss Hooke’s Law

A

The force needed to extend/compress a spring by a distance is proportional to that distance

The lung is not an ideal spring

The lung is stiffer at low and high lung volumes

167
Q

What does the dorsal respiratory group contain?

Where is it found?

A

Inspiratory neurons

Medulla

168
Q

What does the ventral respiratory group contain?

Where is it found?

A

Inspiratory and expiratory neurons

Medulla

169
Q

What inputs do the respiratory centres receive?

A

Stretch receptors in lung

Higher centres

Central chemoreceptors
- pH of CSF

Peripheral chemoreceptors
- arterial pO2

170
Q

What will happen if ventilation increases without a change in the use of O2?

A

PaO2 will rise

PaCO2 will fall

171
Q

What will happen if ventilation decreases without a change in the use of O2?

A

PaO2 will fall

PaCO2 will rise

172
Q

Suppose that pO2 has fallen and pCO2 has risen (hypoventilation): how can this be corrected?

A

Increase the ventilation rate

173
Q

What happen if pO2 falls but pCO2 stays the same?

A

When you try and increase ventilation to increase pO2, this will cause a fall in pCO2 (hypocapnia)

This can happen in ventilation-perfusion mismatch

174
Q

At what level of pO2 does ventilation substantially rise?

A

If pO2 falls below 8kPa, ventilation will rapidly increase

175
Q

Which nerve carries impulses to the respiratory centre in the medulla?

A

CN IX (glossopharangeal)

176
Q

Describe the process of metabolic acidosis and the respiratory response to acidosis

A

When acids dissociate, they produce H+

In metabolic acidosis, production of acids overwhelms the buffering capacity of HCO3-

This limits the removal of H+ leading to metabolic acidosis

Excess CO2 will be excreted more rapidly than it is produced due to the effects of acidosis

Less CO2 is being made because there is less HCO3- relative to H+ to go to the other side of the equation

CO2 levels will drop

To compensate for acidosis, resp increases to excrete CO2 to reduce PaCO2

The ratio of HCO3- and CO2 is restored to a near normal value but both values are low: this is acidosis with compensation

Only way to restore normal ratios and values is to remove excess H+ e.g. sort out DKA

177
Q

Describe the process of metabolic alkalosis and the respiratory response to alkalosis

A

E.g. prolonged vomitting causes loss of H+

Loss of H+ means there is an increase in HCO3- and a metabolic alkalosis

CO2 will fall and less will be excreted from the lung

Compensation by decreasing respiratory rate

Decreasing respiratory rate and restoring CO2 levels above normal will restore pH.

But this is not normal because HCO3- and CO2 are above normal limits

This is compensated metabolic alkalosis

178
Q

What is normal FiO2 on room air?

A

0.21

21 kPa

179
Q

Define acute respiratory failure

A

When the pulmonary system is no longer able to meet the metabolic demands of the body

180
Q

What is hypoxaemic respiratory failure?

What is it?

A

Reduced diffusion or diffusion capacity

  • low pressure of inspired O2 (altitude)
  • surface area
  • diffusion coefficient (alveolar membrane)

PaO2 <8kPa on room air

181
Q

What is hypercapnic respiratory failure?

What is it?

A

Reduced alveolar ventilation

PaCO2 >6.7 kPa

182
Q

What is the oxygen cascade?

What is Pb?

A

kPa of O2 in different parts of the body

Pb is the barometric pressure = 101kPa at sea level

183
Q

What is RQ?

A

The respiratory quotient

The ratio of CO2 eliminated to O2 consumed

Usually 0.8
(10 litres of O2 inspired, 8 litres of CO2 produced)

184
Q

What 3 things can influence the arterial partial pressure of oxygen?

PaO2

A

Diffusing capacity

Lung perfusion

Ventilation-perfusion matching

185
Q

How do you calculate alveolar partial pressure of oxygen?

PAO2

A

Using the alveolar gas equation

186
Q

Describe the A-aO2 gradient

A

The different between the alveolar and arterial concentration of oxygen

Used to diagnose the extent of hypoxaemia

  1. Calculate PAO2
  2. Then calculate A-a O2

Normal values

16yo: 1.1kPa
80yo: 3.1 kPa

187
Q

How do you calculate PAO2?

A

PiO2 - PaCO2
OVER
R

188
Q

How do you calculate A-a O2?

A

PAO2 - PaO2

189
Q

The alveolar pressure is equal to…..

A

the sum of the partial pressures of the gases within the alveolus

190
Q

What is a shunt in regards to V/Q ratio?

What would the V/Q ratio be in this situation?

A

Non-ventilated alveoli remain perfused, but blood is poorly oxygenated. Blood leaving the lungs is not fully saturated.

Lungs are still perfused but not ventilated

V/Q = 0

191
Q

Outline the difference in V/Q ratios between the top and bottom of the lungs

A

Apex of lung – higher

Base of lung – lower

When someone is standing, the apex of the lung shows higher V/Q ratio, while at the base of the lung the ratio is lower but nearer to the optimal value for reaching adequate blood oxygen concentrations.

While both ventilation and perfusion increase going from the apex to the base, perfusion increases to a greater degree than ventilation, lowering the V/Q ratio at the base of the lungs.

The principal factor involved in the creation of this V/Q gradient between the apex and the base of the lung is gravity (this is why V/Q ratios change in positions).

192
Q

What is dead space ventilation?

What would the V/Q ratio be?

A

Ventilation is optimal, but there is no perfusion

V/Q can reach infinity

193
Q

For a constant metabolic rate, PaCO2 is largely dependent on alveolar ventilation.

What is the equation for alveolar ventilation?

What affects this equation?

A

Resp rate X (Vt - Vd)

Vt = tidal volume
Vd = dead space

Vd is made up of anatomical dead space, and physiological dead space as a result of V/Q mismatching

194
Q

What 3 things can cause hypoxaemia?

A

Low PiO2

Hypoventilation

V/Q mismatch

  • shunting, dead space
  • diffusion abnormality
195
Q

Where in the body can disease cause hypoventilation?

A

Airway

Lung

Pleura

Chest wall

Brainstem

Spinal cord

Nerve root

Nerve

NMJ

Respiratory muscle

196
Q

Describe the effect of hypoxic pulmonary vasoconstriction

A

Alveolar hypoxia causes local vasoconstriction

Reduction of perfusion to abnormal area means the proportion of shunted blood is reduced in that area

197
Q

What can cause shunting?

A

Pneumonia

Pulmonary oedema (HF)

Atelectasis

Lung collapse

Pulmonary haemorrhage/contusion

Any cause of right to left cardiac shunt

198
Q

Describe diffusion abnormalities

A

Abnormalities in the alveolar membrane or a reduction in capillaries can result in a reduction in the alveolar surface

Hallmark of disease is desaturation on exercise

Caused by ARDS and alveolitis

199
Q

List the 5 causes of hypoxaemia

A

Low PiO2

Hypoventilation

V/Q mismatching or shunting

Diffusion abnormality

Low cardiac output

200
Q

Give some signs of respiratory compensation and sympathetic stimulation in respiratory failure

A

Tachypnoea

Accessory muscle use

Intercostal recession

Nasal flaring

Splinting of accessory muscles

High HR
High BP
Sweating

201
Q

Give some sources of error in pulse oximetry

A

Poor perfusion

Poor probe position

False nails/nail varnish

Lipaemia

Excessive motion

SpO2 <85% less accurate

202
Q

What happens to O2 and CO2 if ventilation increases?

A

PP of O2 increases

PP of CO2 decreases

203
Q

What happens to O2 and CO2 if perfusion increases?

A

PP of O2 decreases

PP of CO2 increases

204
Q

What layers does oxygen have to travel through to reach a haemoglobin molecule?

A

Through gas to alveolar wall

Epithelial cell of alveolus

Epithelial basement membrane

Tissue fluid and connective tissue

Capillary basement membrane

Endothelial cell of capillary

Plasma

Red cell membrane and cytoplasm

205
Q

What factors can affect the diffusion rate of a gas?

Think of the equation

A

Diffusion rate

Area X diffusion constant X partial pressure difference
OVER
Thickness

206
Q

Oxygen has fully saturated haemoglobin by….

What does this mean in regards to oxygen transfer?

Why is this helpful?

A

….the time it is 25% along the capillary

This implies that oxygen transfer is perfusion limited

Perfusion limitation is seen for O2 and CO2 under normal conditions

This is helpful because it means there is a reserve if perfusion were to increase e.g. exercise

207
Q

What pathophysiology would lead to diffusion limited oxygen saturation?

Explain

A

Fibrosis would lead to diffusion limited oxygen transfer

Thickening of the alveolar membrane means it takes longer for the Hb to pick up oxygen, sometimes not fully saturated 100% of the way along the capillary

There is no reserve to cope with exercise and other demands in diffusion limitation

208
Q

What is total or minute ventilation?

How is it calculated?

A

The amount of air moved into and out of the lungs per minute

MV = tidal volume X RR

Tidal volume is the volume moved per breath

209
Q

What is the alveolar ventilation rate?

A

The amount of air that reaches the alveoli per minute

Calculation must allow for dead space

210
Q

What are the 2 types of dead space?

Describe them

A

Serial dead space = the volume of the conducting airways, anatomical dead space

Distributive dead space - some parts of the lungs that are not airways but do not support gas exchange, damaged alveoli or poorly perfused areas

The total of both is the physiological dead space

211
Q

Describe the difference in ventilation and perfusion between the apex and bottom of the lungs

What will this do to O2 and CO2 concentrations?

A

Increased ventilation at bases - because there is more potential for expansion

Increased perfusion at the bases - because of gravity

V/Q ratio decreases moving down the lung

Apical alveolar pO2 is relatively high to to the lower blood flow, and oxygen is perfusion limited

During exercise, apical capillaries can open further to meet oxygen demands

212
Q

What would pneumonia and a PE do to the V/Q ratio?

A

Pneumonia would reduce ventilation to an area. This would decrease V/Q ratio

PE would reduce perfusion. This would increase V/Q ratio

213
Q

What could atrophy in the 1st dorsal webspace indicate?

A

A rib that starts at C7 not T1

Compresses the brachial plexus

214
Q

Where would you find the neurovascular bundle?

A

In the costal groove on the inferior margin of the ribs

215
Q

What do the ribs articulate with?

A

The bodies of their own vertebrae and the one above it

The transverse process of their own vertebrae

216
Q

What type of joints are found between the ribs and the vertebrae?

A

Synovial joints

217
Q

Which ribs are vertebrosternal?

A

Ribs 1-7

218
Q

Which ribs are vertebrocostal?

A

Ribs 1-8

219
Q

Which ribs are floating ribs?

A

Ribs 11 & 12

220
Q

Where do the intercostal nerves arise from?

What do they provide?

A

The ventral rami of the spinal nerves

Provide motor and sensory innervation to intercostal space and surrounding tissue in a DERMATOMAL PATTERN

221
Q

Which artery is used for a CABG?

A

Internal thoracic artery

222
Q

Where do some of the posterior intercostal veins at the top of the chest drain into?

A

Some drain straight into R and L brachiocephalic instead of draining into azygous vein

223
Q

Which ribs does the diaphragm attach to?

Where does the diaphragmatic crura attach?

A

Costal margin of ribs 10-12

The lumbar vertebrae

224
Q

The lungs fill most of the space around the….

A

Mediastinum

225
Q

Describe the embryological development of the respiratory system

A

Develops as an outgrowth of the gut tube

The respiratory diverticulum appears at week 4

Diverticulum forms lung/bronchial buds

Buds grow into splanch0-pleuric mesoderm

Mesoderm of the embryo forms blood vessels, lymph, cartilage, smooth muscle and visceral pleura

Endoderm forms lining and glands

Septum between the oesophagus and trachea is formed between weeks 4 + 5

226
Q

Why is it difficult for babies to survivie before 26 weeks?

A

Simple squamous epithelium has not formed - hard to exchange gases

227
Q

Are the pulmonary arteries superior or inferior to the pulmonary veins?

A

Pulmonary artery is superior to the pulmonary veins

228
Q

Where do the phrenic and vagus nerve pass in relation to the hilum of the lungs?

A

Phrenic nerve passes anterior to hilum

Vagus nerve passes posterior to hilum

229
Q

Where are the parietal and visceral pleura?

A

Visceral pleura - covers lung surface and into the fissures then reflected as:

Parietal pleura - lines the pleural cavity walls

Only a potential space between the parietal layers

230
Q

What 6 things would be seen on an X-ray in a tension pneumothorax?

A

Mediastinal shift

Tracheal deviation

Diaphragmatic depression

Unilateral hyperinflation

Increased intercostal space size

Hyper-resonant

231
Q

What surface marking tells you where the middle lobe becomes the inferior lobe of the right lung?

A

6th rib mid-clavicular line

232
Q

What is the surface marking for the horizontal fissure of the right lung?

A

4th costal cartilage

233
Q

Where is the triangle of safety for safe chest drain insertion?

A

Apex – base of the axilla (3rd rib)

Anterior – lateral border of pectoralis major

Posterior – mid-clavicular line

Inferior – 5th intercostal space

Needle should go in either the 3rd or 4th intercostal space

234
Q

Which nerve is at risk if you insert a chest drain too far posteriorly?

A

The long thoracic nerve runs just behind the mid-axillary line

235
Q

Describe the lymphatic drainage from the lungs

A

All goes to the right lymphatic duct/right subclavian vein

EXCEPT

Left upper lobe to left thoracic duct/subclavian vein

236
Q

List some causes/triggers of asthma

A

Occupational exposure

Exercise

Atmospheric pollution

Drugs

Genetic factors

Viral infections

Cold air

Emotion

Irritant vapours and fumes

237
Q

Name the 2 types of asthma

A

Intrinsic

Extrinsic

238
Q

Describe extrinsic asthma

A

‘Atopic’

The result of an inappropriate adaptive immune response to an inhaled antigen

Typical onset in childhood
Associated with atopy e.g. eczema
Sensitisation and effector phases

239
Q

Describe intrinsic asthma

A

‘Non-atopic’

No personal/family history

Typical onset in middle age
Often onset following URTI

240
Q

Describe some of the macroscopic changes seen in asthma

A

Increased mucus

Increased goblet cells

Thickening of basement membrane and smooth muscle

Increased glands

Increased macrophages, eosinophils, lymphocytes and neutrophils

241
Q

Describe the pathophysiology of extrinsic asthma (type I hypersensitivity reaction)

A

First contact:
Allergen is picked up by dendritic cell (antigen presenting cell) that presents it via MHCII to T helper 2 cells

Th2 stimulates B cells via IL-4 and IL - 13 to differentiate into plasma cell and bind IgE to mast cells

Mast cells release histamine, leukotrines, prostaglandins, and cytokines - these promote vascular permeability, smooth muscle contraction and mucus production

Mast cells release chemokines - direct the recruitment of eosinophils via IL-5

Eosinophils release pro-inflammatory mediators

Contact again:
Allergen directly stimulates mast cell to release histamine, cytokines and leukotrines

242
Q

What are the 3 phases of asthma pathogenesis?

A

Early

Late

Remodelling (chronic)

243
Q

What changes are seen in chronic asthma (re-modelling)?

A

Smooth muscle hypertrophy

Smooth muscle and epithelial cell hyperplasia

Epithelial damage

Basement membrane thickening

244
Q

What primary pathogensis is seen in early asthma?

A

Constriction of smooth muscle cells

IgE release promoting release of histamine and PGs from mast cells

245
Q

What primary pathogensis is seen in late asthma?

A

Vascular leak

Eosinophil and neutrophil recruitment

Mucus secretion

246
Q

Asthma - history and symptoms

A

Chronic condition with acute exacerbations

Cough, wheeze, chest tightness, SOB, worse at night

Closely associated with atopy/allergy

247
Q

Signs of asthma exacerbation

A

Difficulty completing sentences

Wheeze

Tachypnoea

Tachycardia

Use of accessory muscles

Reduced breath sounds

248
Q

Asthma - diagnosis

A

Trial of treatment and assess response

Reversibility on spirometry before/after salbutamol

Diurnal variation on peak flow

Fractional exhaled nitric oxide - measures eosinophilic inflammation in airways

249
Q

Acute asthma management

A

O2 - sats 94-98%

B2-agonist bronchodilators
- salbutamol nebs repeated 15-30 minute intervals

Corticosteroids

  • prednisolone 40-50mg
  • hydrocortisone 100mgs QDS IV
  • continue for minimum 5 days

Ipratropium nebuliser

Magnesium sulphate - bronchodilator. Only severe asthma

Antibiotics - if signs of infection

250
Q

What do B2 agonists, anticholinergics and leukotrine antagonists do in asthma?

A

Reverse smooth muscle dysfunction

- reverse bronchoconstriction and airway hyper-reactivity

251
Q

What do glucocorticoids do in asthma?

A

Reverse airway inflammation

252
Q

Describe chronic bronchitis (COPD)

A

Seen in larger airways

Mucus gland hypertrophy and hyperplasia

Hypersecretion of mucus

253
Q

Describe emphysema

A

Lobules/acini

Air space enlargement - destruction of alveolar walls, decreases surface area for gas diffusion to take place

Alveolar wall destruction

Less alveoli means ‘old air’ is not forced out and sits in the lungs

254
Q

What 3 things can lead to alveolar wall destruction in emphysema?

A

Oxidative stress, increased apoptosis and senescence

Inflammatory cells and inflammatory mediators

Protease anti-protease imbalace

255
Q

Why can emphysema cause a pneumothorax?

A

Air escapes into the interpleural cavity via broken/damaged alveoli that cause ‘plebs’ and build cause secondary spontaneous pneumothorax

256
Q

List 3 reversible causes of airflow obstruction in COPD

A

Accumulation of inflammatory cells, mucus and plasma in bronchi

Smooth muscle contraction

Dynamic hyperinflamtion during exercise

257
Q

List 3 irreversible causes of airflow obstruction in COPD

A

Fibrosis and airway narrowing

Loss of elastic recoil due to alveolar destruction

Destruction of alveolar support that mains patency of small airways

258
Q

List some clinical features seen in COPD

A

Productive cough

Wheeze

Dyspnoea

Frequent infective exacerbations with purulent sputum

Signs of respiratory failure

259
Q

How is COPD diagnosed?

A

Spirometry
- reduced FEV1 : FVC ratio

CXR - may show hyperinflation

Haemoglobin - may be raised in chronic hypoxia

260
Q

COPD - management

A

Smoking cessation

Bronchodilators

  • salbutamol (B2 agonist)
  • ipratropium (anticholinergic)

Combination therapy

  • long-acting B2 agonist and inhaled steroid
  • long-acting anticholinergic

Home O2

Pulmonary rehab and MDT management

Vaccinations

  • pneumococcal
  • flu
261
Q

Acute exacerbation of COPD - management

A

Inhalers

Nebs

Corticosteroids
- PO prednisolone 7/7

Abx?
- ECOPD is bronchitis

NIV

262
Q

What are the ‘main’ cells in asthma and COPD?

A

Asthma - mast cells

COPD - macrophage

263
Q

BAM Lu-Glu

A

BAM (bronchodilation)

  • B2-agonist
  • Anticholinergics
  • Mthylxanthines

Lu-Glu (anti-inflammatory)

  • Leukotrine receptor antagonists
  • Glucocorticoids
264
Q

Sever acute asthma treatment

A

Oxygen

Salbutamol (beta2 agonist)
Hydrocortisone (glucocorticoid)
Ipratropium (anticholingergic)
Theophylline (methylxanthine)

265
Q

What type of nervous system response drives bronchodilation?

A

Sympathetic responses drive bronchodilation

266
Q

What type of nervous system response drives bronchoconstriction?

A

Parasympathetic response drives bronchoconstriction

267
Q

Give the MoA of B2-adrenoreceptor agonists

A

Stimulates B2 adrenergic receptors on bronchiolar smooth muscle cells

Increases action of adenylate cyclase which increases cAMP

cAMP activates protein kinase A which moves Ca2+ into storage vesicles

Protein kinase A inactivates MLCK and drives dephosphorylation of myosin light chain

Reduced cytoplasmic Ca2+ reduces smooth muscle constriction

Inactivation of MLCK and dephosphorylation of myosin light chain reduces smooth muscle contraction

268
Q

Give some examples of B2-adrenoreceptor agonists

A

Salbutamol & Terbutaline (short-acting)

Salmeterol & Formoterol (long-acting)

269
Q

Give some side effects of B2 adrenoreceptor agonists

A

Tremor

Tachycardia

Cardiac arrhythmia

270
Q

Which enzyme inactivates cAMP?

A

Phosphodiesterase enzyme

271
Q

What 3 actions does PKA have on bronchiole smooth muscle cells?

A

Reduces intracellular calcium

Reduces activity of MLCK

Dephosphorylation of myosin light chain

272
Q

Give the MoA of anticholinergics

A

Blocks M3 muscarinic acetylcholine receptors on bronchiolar smooth muscle cells

Reduces the action of phospholipase C enzyme, reducing Ca2+ release into the cytoplasm

Reducing cytoplasmic Ca2+ reduces smooth muscle contraction, resulting in bronchodilation

273
Q

Give some examples of anti-cholinergics

A

Ipratropium (short-acting)

Tiotropium (long-acting)

274
Q

What are the side effects of anti-cholinergics?

A

Dry mouth

Constipation

Urinary retention

275
Q

Give the MoA of methylxanthines

A

Blockade of phosphodiasterase enzymes in bronchiolar smooth muscle cells

Sustains cAMP levels by inhibiting its breakdown

Promotes activity of cAMP –> PKA

Reduces intracellular Ca2+ which reduces smooth muscle contraction

276
Q

Give some examples of methylxanthines

A

Theophylline

Aminophylline

277
Q

What are the side effects of methylxanthines?

A

Very toxic cardiac and neurological side effects

Cardiac arrhythmias

Seizures

278
Q

Give the MoA of leukotrine receptor antagonists

A

Mast cells secrete leukotrines which act on leukotrine receptors on bronchiole smooth muscle cells causing contraction

Leukotrine receptors of eosinophils guide eosinophil chemotaxis to site of inflammation

Leukotrine receptor antagonists target CysLT1 receptors on eosinophils in the lungs and bronchiole smooth muscle cells

This reduces inflammation (eosinophils) and bronchospasm (smooth muscle)

279
Q

Give some examples of leukotrine receptor antagonists

A

Montelukast

Zafirlukast

280
Q

Give some side effects of leukotrine receptor antagonists

A

Abdominal pain

Headaches

281
Q

Give the MoA of glucocorticoids

A

Targets the intracellular glucocorticoid receptor in immune cells of the lung (macrophages, T-cells, eosinophils)

Activated GR interacts with nuclear DNA and influences gene expression:

  • suppresses pro-inflammatory mediators
  • expresses anti-inflammatory products

Up-regulates B2-adrenoreceptors

282
Q

What genetic deficiency is though to have an effect in COPD?

A

a1 antitrypsin deficiency

Decrease in a1 antitrypsin causes a protease/antiprotease imbalance which leads to alveolar wall destruction

283
Q

Give the names of some glucocorticoids

A

Beclomethasone (inhaled)

Fluticasone (inhaled)

Prednisolone (PO)

Hydrocortisone (IV)

284
Q

Give some side effects of glucocorticoids

A

Moon face

Weight gain

Osteoporosis

Hyperglycaemia

285
Q

Why do test lung function?

A

Useful in symptomatic patients and those at risk of pulmonary disease

The evaluation of lung function patterns provides an aid to diagnosis

Drs can follow changes in lung function over time and in response to treatment

Can assess changes in response to specific stimuli in lab or environment

286
Q

What is vital capacity?

A

The volume of air moved from max inhalation to max exhalation

287
Q

What is residual volume?

A

The amount of air left in the lungs after full expiration

288
Q

What is expiratory peak flow?

Why is it useful?

What variability is diagnostic of asthma?

A

Easy to perform

Cheap equipment

Maximum achievable flow is determined by diameter of bronchiole tree and muscle power available

Blow down peak flow meter at maximum inhalation

> 20% variability in maximum peak flow is diagnostic of asthma

289
Q

Give some pros and cons to spirometry

A

Most readily available and useful test

10-15 minutes, cheap instrument, little risk

Achieving expertise takes training

Internationally accepted criteria ensures optimal and repeatable results

Normal values have been defined to differ between populations

290
Q

What is FEV1?

A

Forced expiratory b=volume in 1 second

291
Q

Describe some characteristics of a restrictive spirometry

A

A reduction in vital capacity

Decreased total lung volume

FEV1:FVC ration increased to over 70% because the FVC is the reduced factor

292
Q

Describe some characteristics of an obstructive spirometry

A

Reduced FEV1

Reduced FEV1 :FVC ratio below 70% because FEV1 is the most reduced factor

293
Q

List some contraindications to performing lung function tests

A

Haemoptysis

Closed/recent pneumothorax

Pre-eclampsia

HTN

Aneurysms

Acute illness that may alter results

Recent thoracic, ear, ocular, abdo surgery

294
Q

How many ATPs are made from one glucose molecule?

A

38 in presence of O2

2 in anaerobic conditions

295
Q

What does blood oxygen reversibly combine with?

A

Haem

Porphyrin compound coordinated to a single iron atom in its ferrous form Fe2+

296
Q

Describe haemoglobin

A

2 alpha and 2 beta globulin chains

Variable quaternary structure

Has ‘relaxed’ and ‘tense’ forms

Relaxed has higher O2 affinity - allows O2 access to haem groups

Tense quaternary structure inhibits O2 binding, 500x less available to O2

297
Q

Describe the concept of the minimum threshold for O2 and haem binding

A

When environmental O2 is low, no O2 is bound to haem and quarterny structure is tense

Hard to bind first O2 in this state

Initial binding requires threshold minimum O2

As O2 binds to one chain, others become more easily available

298
Q

At total saturation, the amount of O2 binding is dependent on…..

A

The amount of Hb available (anaemia)

Saturation is independent of Hb concentration

299
Q

At what kPa is Hb half saturated with O2?

A

3.5kPa

300
Q

Where on the dissociation curve is Hb on a plateau?

A

Above 8kPa

Hb is 90% saturated at this point

301
Q

Alveolar pO2 is 13.3kPa. What does this mean in relation to Hb saturation of O2?

A

Hb will be almost fully saturated at 95%

For typical Hb levels, O2 content in fully saturated blood is 200ml/L plus dissolved O2

302
Q

How much of its O2 does Hb give up at the tissues?

What is the saturation of Hb at the tissues?

A

Hb is 65% saturated at the tissues

Hb gives up 30% of its O2 at the tissues

60ml of O2 delivered per litre

303
Q

Why is it useful that Hb only gives off half of its O2 at the tissues?

A

Leaves room for reserve if demand increases e.g. exercise

Hb can give off more O2 if needed

304
Q

How does O2 diffuse from Hb to the tissues?

A

Down a concentration gradient

If the tissue pO2 is low, more O2 will be given up

Hb has less affinity for O2 as number of molecules bound decreases

There is a limit to how low tissue O2 concentration can drop before diffusion to cells is compromised

305
Q

Why can heart muscle tolerate a greater fall in tissue pO2 than other tissue?

A

Because it has high capillary density

With high capillary density, diffusion occurs across shorter distance and higher surface area

This allows maintenance of gradient between capillaries and cells

306
Q

What environmental factors can shift the Hb dissociation curve?

A

Acidic environments make Hb more tense - less affinity for O2

Increasing temperature makes Hb more tense - less affinity for O2

307
Q

What 4 factors will cause a ‘shift to the right’ in the O2 dissociation curve?

A

Acidity

Pyrexia

Increased CO2

Increased 2,3-DPG

Major shift favouring O2 offloading occurs at tissues where it is needed

308
Q

When is 2,3-DPG released?

What does it do?

A

Levels of 2,3-DPG in RBCs increases in response to hypoxia

This stabilises a tense state - less affinity for O2

309
Q

Describe the Bohr effect/shift

A

Acidic conditions O2 dissociation curve shifts right

Due to H+ ion and CO2 binding which stabilise Hb in the tense state

Result is at any give pO2 Hb binds less O2

O2 is released more easily in tissues with low pH and high CO2

310
Q

Describe the Haldane effect

A

Increasing O2 binding to Hb in lungs reduces the affinity for CO2 and H+ by modifying the quaternary

Effective in pulmonary capillaries as more CO2 is offloaded in the lungs

311
Q

How does an increase in metabolism affect O2 dissociation?

A

pH decreases with metabolism

Low pH through lactic acid and increased CO2 means tissues are metabolically active and need O2

Hb has increasingly less O2 affinity and releases 70% of its O2

312
Q

Outline the long-term physiological adaptations to chronic hypoxia

A

Chronic hypoxia triggers responses to try and increase O2 delivery to cells

Increased erythropoietin

Increased tissue capillary density

Increase 2,3-DPG levels

Increased ventilation

313
Q

What does dissolved CO2 react with?

A

Water in plasma

Water in RBCs

314
Q

Define acid

A

Any chemical that can donate H+ proton

HCl

315
Q

Define base

A

Any chemical that can accept H+

NaOH

316
Q

What is a strong acid?

A

One that completely dissociates in water releasing large amounts of H+

HCl –> H+ + Cl-

317
Q

What is a weak acid?

A

Incompletely dissociate in water. Reaches equilibrium with its conjugate base forming a buffer pair that can reversibly bind H+

H2CO3 H+ + HCO3-

318
Q

How is acidity measured?

A

pH scale

Measures the concentration of H+ ions in a solution

pH = negative logarithm to base10 [H+]

319
Q

What is the average pH of blood?

What is the range?

A

pH 7.4

7.36 - 7. 44

320
Q

A 1 unit change in pH is equivalent to…

A

A 10-fold change in H+

321
Q

What are the 2 sources of H+ in the body?

A

Volatile acids (easily vapourised)

Non-volatile acids (fixed/non-respiratory)

322
Q

Discuss volatile acids as a source of H+ in the body

A

Large amounts generated ach day from aerobic metabolism and CO2 production (H2CO3)

Can leave solution & enter atmosphere

Excreted by lungs

323
Q

Discuss non-volatile acids as a source of H+ in the body

A

Small amount generated each day from other metabolic process e.g. sulphuric acid, lactic acid, keto acid

Excreted by kidneys

324
Q

When does a buffer system work best?

Why is the HH equation different?

A

Buffer systems usually work best at a pH close to their pK

HH is a physiological buffer where physiological mechanisms control HCO3- and pCO2. Not just affected by the equation itself

This means pH can vary from pK and still be alright because there are other buffers

325
Q

Outline the respiratory portion of physiological buffering

A

If acid is produced, H+ reacts with HCO3- to give CO2.

C)2 is breathed out, restores pH

326
Q

Outline the renal portion of physiological buffering

A

If pCO2 is too high, kidneys excrete less HCO3-

Plasma HCO3- is raised, restoring pH

327
Q

Where in the blood is carbonic anhydrase found?

What does this mean?

A

RBCs, NOT in plasma

Reaction occurs more rapidly in RBCs

H+ is buffered Hb and HCO3- is transferred to plasma

328
Q

List some common places where carbonic anhydrase is found

A

In tissues whree HCO3- or proton production is coupled to transport

Salivary gland
Stomach
Pancreas
Renal tubular epithelium
Choroid plexus
Ciliary body
329
Q

What can H+ be buffered by?

Outline this process

A

Can be buffered by Hb to give HHb

Buffering ability of Hb is enhanced by deoxygenation

Venous blood can carry more H+

330
Q

What makes HCO3- leave a cell?

How does it leave the cell?

A

An increase in intracellular HCO3-

Cl-/HCO3- exchanger

331
Q

What happens if Hb gives off O2 without taking up CO2?

A

Cellular pH will rise (alkalosis)

Because Hb is deoxygenated, it will pick up excess H+, removing it from the environment

332
Q

Which effect allows O2 to be moved to tissues?

A

Bohr effect:

Taking up of CO2 reduces O2 affinity of Hb

333
Q

Which effect allows CO2 to be removed from tissues?

A

Haldane effect:

Releasing O2 increase CO2 carriage by blood

334
Q

How is CO2 transported as carbamino compounds?

A

Formed when CO2 reaction with protein amino groups (especially in Hb)

CO2 + protein-NH2

Protein-NHCOOH

Reaction with Hb results in carbaminohaemoglobin

Conformation change in Hb reduces affinity for O2 contributing to Bohr effect

Block 2 (10 decks)

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