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Semester 3 > Respiratory system 1-6 > Flashcards

Respiratory system 1-6 Flashcards

1
Q

What is the purpose of the respiratory system?

A

Ensure all tissues receive the oxygen they need and disposes of the CO2 they produce.

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2
Q

How is pressure generated by gases?

A

By collision of molecules with the walls - more frequent and harder collisions, higher pressure

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3
Q

What is Boyles law?

A

the product of the pressure and volume for a gas is a constant for a fixed amount of gas at a fixed temperature.

PV = constant

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4
Q

What is Charles law?

A

if a given quantity of gas is held at a constant pressure, its volume is directly proportional to the absolute temperature. (Kelvin)

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5
Q

What is the universal gas law?

A

PV=RT

Allows calculation of how volume will change as pressure and temperature changes

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6
Q

How do gases behave when mixed with other gases?

A

Behave independently so each gas exerts a partial pressure

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7
Q

How do you calculate the partial pressure of each gas in a mixture?

A

The same fraction of the total pressure as the volume fraction of the gas in the mixture

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8
Q

What happens when gas comes in contact with water?

A

Water molecules evaporate and gas molecules dissolve.

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9
Q

What effect does evaporated water mixing with a gas have?

A

Exerts vapour pressure

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10
Q

How is the saturated vapour pressure achieved?

A

When molecules leave and enter water at the same rate.

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11
Q

What does the saturated vapour pressure depend on?

A

Temperature

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12
Q

What is the pressure of a gas in a liquid referred to as?

A

Tension - at equilibrium tension is the same as the partial pressure of gas in gas mixture

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13
Q

What does the tension of a gas in a liquid indicate?

A

How readily the gas will leave the liquid NOT how much gas is in the liquid

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14
Q

What does solubility determine?

A

The amount of gas which enters the liquid to establish a particular tension
content = solubility x tension

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15
Q

How does reactions of a gas with a component of liquid affect tension?

A

Reaction must complete before tension can be established

reacted gas + dissolved gas = content

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16
Q

How much oxygen must the blood pick up per minute at rest?

A

12 mmol

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17
Q

Explain how the lungs and blood are able to supply enough oxygen to the body.

A

300 million alveoli each surrounded by a capillary

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18
Q

Describe the differences between bronchi and bronchioles.

A

Bronchi have cartilage in walls and less smooth muscle

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19
Q

Describe the resistance and pressure of the pulmonary circulation

A

Low resistance and pressure.

Receives entire cardiac output

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20
Q

Why is it important that very little tissue fluid is formed by the pulmonary circulation?

A

Would fill space between alveoli and capillaries affecting gas exchange

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21
Q

How is air drawn into the lungs?

A

By increased volume of terminal and respiratory bronchioles as lungs expand in inspiration. Each breath draws a tidal volume into and out of the lungs

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22
Q

What effects ventilation?

A

Tidal volume and respiratory rate

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23
Q

Where does the nasal cavity lie?

A

Extends from the nostrils to posterior nares

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24
Q

What divides the nasal cavity?

A

septum - medial wall of each nasal cavity. Made of cartilage and bone

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25
Q

What makes up the lateral wall of the nasal cavity?

A

Bony projections lined by pseudo stratified columnar ciliated epithelium

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26
Q

How many tubinates and meatus do we have in the lateral wall of the nose?

A

3 - superior, middle and inferior

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27
Q

What are the functions of the nose?

A

Respiration - filters, humidifies and warms air
Smell
Receives local secretions from sinuses and nasolacrimal duct

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28
Q

How is the structure of the nose related to th function?

A

nostrils contain hairs which filter large particles
Epithelium moistened with mucus - traps particles
Cilia helps transport any trapped particels
Watery nasal secretions - water evaporates to humidify air
Vessels just below epithelium - warms air
Turbinates - slows airflow, helps mix air

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29
Q

How many paranasal sinuses are there and what are they called?

A 
4
Frontal
Ethmoid
Maxillary
Sphenoid
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30
Q

What epithelia line the sinuses?

A

pseudo stratified columnar ciliated containing goblet cells and glands

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31
Q

What are the potential paranasal sinuses function?

A

Extension of nasal cavity - humidification and warming of inspired air
Secretion of mucus to moisten nasal chamber
Lightening weight of skull
Buffer for trauma
Insulating sensitive structure from temp variations

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32
Q

What are the 3 parts of the pharynx?

A

Nasopharynx
Oropharynx
Laryngopharynx

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33
Q

Where is the soft pallete?

A

Between the nasopharynx and oropharynx

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34
Q

Where is the epiglottis?

A

Between the oropharynx and laryngopharynx

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35
Q

Where does the eustachian tube enter the pharynx?

A

Nasopharynx

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36
Q

What is the larynx?

A

Vocal cords act as a valve guarding the entrance to the trachea.

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37
Q

When is the larynx open/closed?

A

Open during respiration
Closed to protect LRT during swallowing
Initially closed then open during coughing reflex

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38
Q

What is the glottis?

A

2 vocal cords and the opening (aperture) between themm

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39
Q

What muscle moves the vocal cords?

A

The intrinsic muscle of the larynx

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40
Q

Does abduction or adduction open the glottis?

A

AB

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41
Q

What is the aperture of the glottis called?

A

rima glottidis

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42
Q

What nerve supplies the intrinsic laryngeal muscles?

A

Recurrent laryngeal nerve (branch of vagus)

Does not supply cricothyroid - superior laryngeal nerve

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43
Q

What symptoms may lesions of the recurrent laryngeal nerve cause?

A

Hoarseness of voice

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44
Q

Describe the course of the recurrent laryngeal nerve

A

Right - curves under sub clav. artery
Left - curves under aortic arch
Comes back up in the groove between the trachea and oesophagus

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45
Q

Where might URTIs spread?

A

sinuses via openings into nasal cavity and may result in sinusitis
Middle ear via eustachian tube

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46
Q

WHat disorders of the larynx may cause respiratory difficulty?

A

Oedema of the larynx
Tumours of the larynx
Aspiration of foreign body
Bilateral vocal cord paralysis

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47
Q

What disorders of the pharynx may cause respiratory difficulty?

A

Tongue falling back in unconscious patients

Sleep Apnoea

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48
Q

What disorders in the nose may cause respiratory difficulty?

A

Nasal polyps

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49
Q

What is the conducting portion of the respiratory tract?

A

nasal cavity to bronchioles

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50
Q

What is the respiratory portion of the resp tract?

A

Respiratory bronchioles and alveoli

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51
Q

What type of epithelia are in the terminal bronchioles?

A

Simple columnar with cilia but no goblets

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52
Q

What epithelia are in the resp bronchioles and alveolar ducts?

A

Simple cuboidal epithelium with Clara cells and a few sparsely scattered cilia

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53
Q

What type of epithelia are in the alveoli?

A

Simple squamous

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54
Q

What is olfactory?

A

Sense of smell
Axons run through the columnar epithelia pseudostratified and non-motile cilia.
No goblets
Contain bowmans glands - exocrine function

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55
Q

Which bronchus is more likely to be obstructed by a foreign body?

A

Right - more vertical

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56
Q

What happens to the cartilage surrounding the trachea with age?

A

Transforms to bone

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57
Q

Where is the trachealis muscle?

A

In the fibroelastic membrane

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58
Q

Why is the absence of cartilage in walls of bronchioles problematic?

A

It allows th air passages to constrict and almost close down when smooth muscle contraction becomes excessive eg in asthma and cause more difficulty with expiration than inspiration

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59
Q

What are Clara cells?

A

Interspersed between siliated cuboidal cells. secrete a surfactant lipoprotein which prevents the walls sticking together during expiration. Also secrete Clara cell protein

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60
Q

Where can Clara cell protein be measured?

A 
In bronchoalveolar lavage fluid (if lowered - lung damage)
in serum ( if raised - leakage across air-blood barrier
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61
Q

Why is it important there are no goblet cells in terminal bronchioles?

A

Narrow - prevent drowning in own mucus

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62
Q

Where can alveoli open into?

A

Resp. bronchiole
Alveolar duct
alveolar sac
alveolus

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63
Q

At what age do you stop developing alveoli?

A

8

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64
Q

What are alveolar walls like?

A

Have abundant capillaries
Supported by a basketwork of elastic and reticular fibres
Covering composed chiefly of type 1 pneumocytes
Have a scattering of intervening type II pneumocytes

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65
Q

What cell types are present in alveoli?

A

Type I (squamous) - 90% of surface area and permit gas exchange with capillaries
Type II cells (cuboidal) - cover 10% of surface area and produce surfactant
Numerous macrophages line alveolar surface (phagocytose particles)

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66
Q

What might cause obstruction of the pharynx to an unconscious patient?

A

Tongue falling back
A foreign body
Vomit

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67
Q

What are the 3 sections of the sternum?

A

Manubrium
Body
Xiphisternum

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68
Q

Describe the connection of the ribs to the sternum

A

1-7 conected via costal cartilage
8-10 connected via costal cartilage above them
11 and 12 floating ribs - end free in abdominal muscle

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69
Q

What are considered “typical ribs”?

A

3-9
Head, neck, tubercle, shaft, costal groove
2 articular facets separated by crest on head
Articular and non articular facets on tubercle

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70
Q

Describe the structure of the first rib

A

Shortest broadest and most curved. Head has single facet

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71
Q

How do the 11th and 12th rib differ to typical ribs?

A

Single facet on head and no tubercle and tapering anterior end

10th rib also has only a single facet on head

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72
Q

How many intercostal muscles are there in each space?

A

3- external, internal and innermost

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73
Q

What is the purpose of the costal groove?

A

Protection of the neurovascular bundle which runs along it

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74
Q

What are the intercostal nerves and where do they lie?

A

Anterior rami of thoracic spinal nerves T1-T12. Run between internal and innermost intercostal muscles. Supply the intercostal muscles in the corresponding space, the parietal plura and overlying skin

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75
Q

What is the intercostal arterial supply?

A

Thoracic artery -> posterior intercostal arteries
Internal thoracic artery -> anterior intercostal artery
anastomose to supply the muscles of each space, parietal pleura and overlying skin

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76
Q

What is the venous drainage of the thoracic wall?

A

Primarily into the Aqygos system -> SVC

Some into the internal thoracic vein

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77
Q

Which intercostal muscle is key in inspiration?

A

External - elevates ribs

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78
Q

Which ribs increase the thoracic lateral diameter in inspiration?

A

Lower

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79
Q

Which ribs increase the A-P diameter of the thorax?

A

Upper

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80
Q

What is the main muscle of inspiration?

A

Diaphragm - descends. Accounts for 70% of chest expansion in quiet respiration

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81
Q

What nerve supplies the diaphragm and what are its roots?

A

Phrenic nerve roots C3,4,5

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82
Q

What are the sensory functions of the phrenic nerve?

A

Both surfaces of diaphragm (margins of diaphragm receive innervation from intercostal nerves)
Mediastinal part of parietal pleura
Diaphragmatic part of parietal pleura

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83
Q

Explain how expiration is passive in quiet respiration

A

Elastic recoil of the chest wall and lungs

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84
Q

What is the function of the internal and innermost intercostal muscles?

A

forced expiration along with the abdominal muscles

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85
Q

What is the central compartment of the thoracic cavity called?

A

Mediastinum

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86
Q

What does the parietal pleura cover?

A

Bony thorax
Diaphragm
Mediastinum

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87
Q

What does the visceral pleura cover?

A

Lungs

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88
Q

Explain the sliding of pleural surfaces over each other

A

Film of fluid lubricates it but its surface tension resists the surfaces being pulled apart (forms a pleural seal)
Thus, when the thorax expands along with the parietal pleura -> the visceral pleura and lungs move with it -> the lungs expand

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89
Q

What are the contents of the pleural cavity?

A

Lungs

Costodiaphragmatic recess - pleural lined gutter surounds the upward convexity of the diaphragm

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90
Q

Where does the trachea start and end?

A

Starts at the border of the cricoid cartilage and ends by dividing into the right and left main bronchi at the carina (T4/5)

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91
Q

Describe the structure of the trachea.

A

Fibro-cartilaginous tube with 18-22 U shaped cartilages. Posteriorly, the trachealis muscle bridges the gap between the cartilage

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92
Q

What does the trachealis muscle do?

A

Construction and dilation of the trachea as air moves through it.
Stabilises the hyaline cartilage

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93
Q

Describe the main bronchi

A

Right - shorter, wider and more vertical. Splits into 3 lobar bronchi
Left - longer, more horizontal. Splits into 2 lobar bronchi

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94
Q

What do the lobar bronchi divide into?

A

Segmental bronchi - each of which supplies a bronchi-pulmonary segment

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95
Q

Describe the right lung.

A

3 lobes - upper, middle and lower.

2 fissures - horizontal and oblique

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96
Q

Describe the left lung

A

2 lobes - upper and lower

1 fissure - oblique

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97
Q

What is a bronchopulmonary segment?

A

An area of lung supplied by its own segmental bronchus and segmental branches of the pulmonary artery and vein

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98
Q

Describe the blood supply to the lungs

A

Bronchial arteries from the aorta supply the bronchial tree to the terminal bronchioles.
Pulmonary arteries carry deoxygenated blood from the right heart to the alveoli for oxygenation.

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99
Q

What is the hilum of the lungs?

A

The pulmonary vessels, main bronchus, nerves and lymphatics enter/exit via the hilum at the mediastinal surface of the lungs

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100
Q

Describe the borders of the areas of the mediastinum.

A

Between right and left pleural sacs
Anterior between body of sternum and fibrous pericardium
Middle between anterior and posterior
Superior bound superiorly by the thoracic inlet and inferiorly by plane passing though sternal angle and lover border of T4

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101
Q

Where are the oblique fissures in relation to the vertebra and costal cartilage?

A

Extend from spinous process of T2 to 6th costal cartilage

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102
Q

Where are the horizontal fissures in relation to the ribs and costal cartilage?

A

Extends from oblique fissure along border of 4th rib and costal cartilage

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103
Q

How does alveolar air differ to atmospheric air?

A

Less oxygen (13.3 kPa), more carbon dioxide (5.3 kPa)

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104
Q

What is the typical pO2 and CO2 in venous blood?

A

pO2 = 6.0 kPa
pCO2 = 6.5 kPa
this varies with metabolism

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105
Q

Why does oxygen diffuse into blood and carbon dioxide diffuse out?

A

pO2 is higher in alveolar gas than blood therefore moves out of the alveoli and into the blood. The opposite is true for CO2

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106
Q

What does diffusion in the lungs (and generally) depend on?

A

Area
gradients
Diffusion resistance (dependent on nature of the barrier and nature of the gas)

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107
Q

What are the diffusion barriers for O2 from the alveoli to the blood?

A 
Through gas to the alveolar wall
Epithelial cell of alveolus
Tissue fluid
Endothelial cell of capillary
Plasma
Red cell membrane
(Gas to alveolar wall, 5 cell membranes, 3 layers of cytoplasm and 2 layers of tissue fluid. 0.6 micrometers)
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108
Q

How is the rate of diffusion of a gas through a gas linked to molecular rate?

A

rate is inversely proportional to molecular weight - big molecules diffuse slower therefore carbon dioxide is slower than oxygen

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109
Q

How is the rate of diffusion of a gas through liquid determind?

A

Rate is proportional to solubility. CO2 is much more soluble than O2 so diffuses 21 times faster

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110
Q

Which gas limits diffusion in the lungs?

A

Oxygen as carbon dioxide diffuses much faster than oxygen overall

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111
Q

How long do blood cells stay in capillaries?

A

1s. Oxygen exchange is complete in 0.5 seconds so plenty of leeway and gas diffusion is not limiting on the lung

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112
Q

What determines gas composition of the arterial blood/

A

Composition of alveolar air - same pO2 and CO2

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113
Q

How does ventilation occur?

A

Expansion of lungs increases volume of the respiratory bronchioles and alveolar ducts so air flows down the airways to them

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114
Q

How do you measure ventilation?

A

Using a spirometer, the subject breathes from a closed chamber over water whose volume changes with ventilation

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115
Q

What are the types of lung volume?

A

Tidal - volume in and out with each breath
Inspiratory reserve volume- extra volume that can be breathed in over that at rest
Expiratory reserve volume - extra volume that can be breather out over that at rest
Residual volume - volume left in the lungs at maximal expiration (cannot be measured by spirometer - use helium dilution)

116
Q

Why do lung capacities not change with breathing pattern?

A

They are measured from fixed points in breathing cycle

117
Q

What is vital capacity?

A

Biggest breath that can be taken - measured from max inspiration to max expiration. Approx 5l in typical adult. Often changes with disease

118
Q

What is inspiratory capacity?

A

Biggest breath that can be taken from resting expiratory level. Approx 3l

119
Q

What is functional residual capacity?

A

Volume of air in lungs at resting expiratory level. Typically 2l. (expiratory reserve + residual volume)

120
Q

What is ventilation rate?

A

The amount of air moved in and out of a space per minute

Product of volume moved per breath and respiratory rate

121
Q

How do you measure pulmonary ventilation rate?

A

Tidal volume x respiratory rate. Typically 8l/min at rest and can exceed 80l/min in exercise

122
Q

What is dead space?

A

Space in airways where air is “wasted” as it does not reach the alveoli to exchange gas. Last air in and first out.

123
Q

What is the alveolar ventilation rate?

A

The amount of air that actually reaches the alveoli. To calculate, need to allow for ‘wasted’ ventilation in dead spaces.
Pulmonary ventilation - dead space ventilation

124
Q

What is physiological dead space?

A

Serial dead space (volume of airways measured by nitrogen washout, typically 0.15l) and distributive dead space (other parts of the lungs that do not support gas exchange - dead or damaged alveoli or alveoli with poor perfusion, typically 0.17 l)
Must be completely filled with air at each breath

125
Q

How do you calculate dead space ventilation?

A

dead space vol x resp rate

126
Q

Approx how much inspired air is “wasted”?

A

one third. Almost 2/3 in rapid shallow breathing. Less is wasted in slow deep breathing but is most work so at rest we adopt an intermediate rate and depth

127
Q

What work must be done during breathing?

A

Move the lungs and thorax and move air through the airways

128
Q

What would happen to the lungs if taken out of the thorax?

A

Collapse

129
Q

What holds the lungs at a larger volume in the thorax?

A

Pleural seal created by a thin layer of fluid between the visceral and parietal pleura. Changes volume as thorax does

130
Q

What is pneumothorax?

A

Collection of air in the pleural space. Forms if the integrity of the pleural seal is broken - lungs collapse

131
Q

Describe the equilibrium of forces in the thorax.

A

Lungs pull up and in
Thoracic cage pulls out
Passive stretch of diaphragm pulls down

132
Q

How does the resting expiratory level occur?

A

All forces in balance. Like a set of springs - if disturbed will spring back to the resting expiratory level.

133
Q

What way do the muscle fibres in the diaphragm run?

A

Medial to lateral - contraction flattens it

134
Q

What is forced expiration?

A

Breathing out beyond resting expiratory level. Requires force exerted by abdominal muscles. Inspiration to resting level is then passive

135
Q

What requires the most work in quiet breathing?

A

Stretching the lungs unless diaphragm cannot easily move into abdomen because of pregnancy, obesity or corsets

136
Q

What is lung compliance?

A

The stretchiness of the lungs
Volume change per unit pressure change
Higher compliance means easier to stretch

137
Q

What makes the lungs elastic/stiff?

A

Airways have elastic walls but compliance is reduced by surface tension of lining fluid - interactions between molecules at surface of a liquid. Makes the surface resist stretching.

138
Q

What chemicals decrease surface tension?

A

Detergents. Disrupt interactions between surface molecules. Lungs have a mixture of detergents called surfactant produced by type 2 alveolar cells

139
Q

How does the action of surfactant change as lung volume changes?

A

Reduces surface tension when lungs are deflated but not when fully inflated so little breaths are easy and big breaths are hard

140
Q

Why is hysteresis important in the lungs?

A

The energy put into stretching a film of surfactant is not all recovered when the film recoils. This loss is greatest when tidal volume is max. This is why little breaths are best

141
Q

How is a bubble created?

A

Film of fluid surrounds a gas and shrinks to compress gas until equilibrium between tension and pressure

142
Q

What is Laplace’s law?

A

Pressure = 2 x surface tension/radius

Therefore big bubbles have low pressure, little bubbles have high pressure

143
Q

What is the law of bubbles?

A

If a big bubble is connected to a small bubble air will flow from high pressure to low so small bubble collapses into big.
‘Big bubbles eat little bubbles’

144
Q

By the law of bubbles, larger alveoli should ‘eat’ little alveoli. How come this does not occur?

A

As alveoli get bigger, surface tension in their walls increases because surfactant is less effective so pressure stays high and stops them eating the little ones

145
Q

Describe Respiratory Distress Syndrome.

A

Babies born prematurely have too little surfactant so lungs are very stiff. They have few, large alveoli and breathing and gas exchange is compromised.
Give mum steroids if premature labour expected - promotes surfactant production

146
Q

Why do small tubes have high resistance?

A

Poiseulles law -

147
Q

How does the anatomy of the lungs reduce the high tension that should occur in the airways due to their small tubes?

A

At each branch the increase in the number of airways in parallel compensates for the increase in their resistance. The smaller the tubes get, the lower the resistance actually becomes in the airways - highest resistance in trachea and lowest in small airways so breathing is easy however the slightest change in small airways diameter has major effects on the effort required to push air through them

148
Q

What limits forced expiration?

A

Small airways are narrowed as the lungs are compressed, resistance dramatically increases and air is trapped in the alveoli as the resistance in the airways is too large. (airways are not totally obstructed)

149
Q

What is obstructive airway disease?

A

If the small airways are narrowed by disease eg asthma or chronic bronchitis, resistance increases much earlier in expiration. Breathing out can become very difficult

150
Q

What do lung function tests assess?

A

The mechanical condition of the lungs
Resistance of the airways
Diffusion across the alveolar membrane

151
Q

How might lung function be inferred non invasively?

A 
From the lungs:
Volumes
Pressures/flows
Composition
Measured from the mouth
152
Q

How is volume measured?

A

Spirometer - vital capacity by max inspiration and expiration

153
Q

What limits maximum inspiration?

A

Compliance of the lungs

Force of inspiratory muscles

154
Q

What might limit maximum expiration?

A

Increasing airway resistance

Lungs compressed

155
Q

How does a single breath spirometry work?

A

Subject fills lungs from atmosphere and breathes out as far and fast as possible through a rapid responding spirometer

156
Q

What is a vitalograph trace?

A

Plot of volume expired vs time

Initial rapi rise tails to a plateau

157
Q

What is FEV1.0?

A

Volume expired in the first second. Affected by how quickly air flow slows down so less if airways narrowed. Usually >70% FVC

158
Q

What is FVC?

A

the maximum volume that can be expired from full lungs. Typically 5l in adult

159
Q

Why might the lungs be difficult to fill?

A

Stiff (potentially due to fibrous tissue)
Weak
Problem with chest wall

160
Q

What effect will stiff lungs have on the FVC and FEV?

A

Start less full so FVC will be reduced but air will come out normally so FEV will be >70% FVC

161
Q

How does obstructive deficit affect ventilation?

A

If airways are narrowed lungs will still be easy to full but resistance will increase in expiration so air will come out more slowly and FEV will be reduced but FVC will be relatively normal

162
Q

What is a flow volume curve?

A

Plot of volume expired against flow rate derived from vitalograph

163
Q

Why is flow rate of expiration maximum when lungs are full?

A

Airways stretched so resistance minimum.

164
Q

What limits the PEFR? (Peak Expiratory Flow Rate)

A

The largest airways in the lungs

165
Q

How does an obstruction/narrowing in the airways effect the flow rate of expiration?

A

Same PEFR but more rapid fall in the flow rate falls

166
Q

How might PEFR be measured and why is it often used for screening test for airway narrowing?

A

Simple cheap device that can be easily used at home by blowing into it.

167
Q

Why are flow volume curves used to indicate airway narrowing?

A

Very sensitive

Can also discriminate between large and small airway narrowing

168
Q

How is residual volume in the lungs measured?

A

Helium dilution. Helium is not normally present in air and is insoluble in blood. If a known concentration is breathed in starting at FRC, you can measure how much the concentration is reduced by mixing with air already in the lungs. Need to know to measure airway disease

169
Q

What is nitrogen washout used for?

A

Measure serial dead space in the lungs

indirectly measure ventilation perfusion matching

170
Q

Describe the nitrogen washout test.

A

Subject takes one normal breath of pure oxygen, breathes out via meter measuring % nitrogen. Initially only oxygen is expired from the airways. Then mixture of oxygen and air (inc nitrogen) from alveoli. Volume expired at transition is serial dead space.

171
Q

How do you measure diffusion conductance?

A

Difficult to measure directly how easily oxygen diffuses into the blood so carbon monoxide is used because binding to Hb means no partial pressure in mixed venous blood.
Measure how easily CO crosses from alveolar air to blood. Measure pCO in the air sample, how much is exhaled and can then figure out how much perfuses.

172
Q

How much oxygen does a person need in 1 minute at rest?

A

12 mmol

173
Q

Why is haemoglobin necessary?

A

To transport oxygen which is not very soluble in water - at 13.3kPa it dissolves 0.13 mmol/l. Haem used because it reacts with oxygen reversibly - oxygenation not oxidation

174
Q

What does a dissociation curve show?

A

The reversibility of oxygen binding
amount of oxygen bound vs pO2.
Tells you how much oxygen will be bound or given up.
Generally expressed as a percentage of amount of O2 bound at saturation as amount bound is dependent on amount of pigment

175
Q

How is chemical binding saturated?

A

Above a given pO2

176
Q

What is the structure of haemoglobin?

A

Tetramer - 2 alpha and 2 beta subuniits each containing one haem + globin. Overall structure has variable quaternary structure. May be tense (T) - does not readily bind to O2 or relaxed (R) - readily binds

177
Q

When is haemoglobin in its T state?

A

Low pO2. Hard to bind first O2 but as it does, changes to R state so next is easier

178
Q

What shape is the oxygen dissociation curve?

A

Sigmoidal. Initially shallow but binding facilitates further binding so the curve steepens rapidly as pO2 rises until saturation

179
Q

At what pO2 is haemoglobin saturated?

A

above 8.5kPa (compare to alveolar 13.3kPa)
half at 3.5-4kPa
0 at 1kPa

180
Q

How much haemoglobin is in the blood?

A

2.2mmol/l and each caries 4 O2 therefore oxygen content is 8.8mmol/l

181
Q

What is the pO2 in the tissues?

A

Around 5kPa - haemoglobin 65% saturated so leaves around 3mmol/l.

182
Q

How can extra O2 be released from haemoglobin into cells?

A

Higher capillary density allows the pO2 to be lower (cannot generally fall below 3kPa)
The mood of haemoglobin depends on pH - more relaxed in alkaline, more tense in acidic conditions. Tissues have lower pH and higher temp (same effect).
Up to 70% of bound O2 can be given up, about 27% normally.

183
Q

What is the Bohr effect?

A

In more acidic conditions (lower pH) the dissociation curve shifts along the pO2 axis - shifts right. Hb binds less O2 at a given pO2

184
Q

Compare carbon dioxide and oxygen in the blood.

A

Carbon dioxide is more soluble and reacts chemically with water. More CO2 in the blood - almost 3 times as much. CO2 plays a major part in controlling blood pH

185
Q

How much CO2 dissolves in water at pCO2 5.3kPa and what effect does this dissolution of CO2 have on the blood?

A

1.2mmol/l. Forms H+ and HCO3- reversible reaction in equilibrium - dependent on concentration of reactants and products. If pCO2 rises, pH falls (more H ions) if pCO2 falls, pH rises.

186
Q

What else other than CO2, maintains the HCO3 equilibrium in the plasma?

A

Sodium hydrogen carbonate stops nearly all CO2 from reacting so pH is alkaline

187
Q

What is the standard ratio of hydrogen carbonate to dissolved CO2 in blood that maintains the pH?

A

20:1 maintains pH 7.4

188
Q

Other than oxygen, what does haemoglobin bind to that is usually in the blood?

A

hydrogen ions bind to the globin increasing the reaction of CO2 with H2O to produce more H+ and HCO3-

189
Q

When HCO3 leaves the red blood cell, what is exchanged for it?

A

Chloride

190
Q

Why is the HCO3 conc in plasma so high?

A

CO2 reacts with H2O in the RBC forming H+ and HCO3-. H+ binds to globin causing the reaction to continue in a forwards direction to try and reach equilibrium. HCO3 then leaves the RBC in exchange for Cl-. The reaction continues increasing the HCO3 conc. Dependent on how much H+ binds to Hb and excretion by kidneys.
Variation is dependent on kidneys as RBC is generally constant

191
Q

How does the body buffer pH change?

A

If acid is produced, this reacts with HCO3 to form CO2 which is breathed out
The less O2 Hb is bound to, the more H+ binds to it so more bound in venous blood therefore there is more HCO3 in plasma

192
Q

What controls arterial dissolved CO2?

A

Alveolar pCO2 - affects pH

193
Q

How is the increased amount of CO2 in venous blood buffered?

A

Less O2 bound to Hb so more H+ bound, so more CO2 converted to H+ + HCO3-.
As both pCO2 and [HCO3] increase, pH does not change much

194
Q

If CO2 picked up from the body reacts to form H+ + HCO3-, how is it removed by the lungs?

A

Hb picks up O2 so gives up H+ which reacts with HCO3 to form CO2 and it is breathed out

195
Q

What else does CO2 react/bind with in the blood (other than water)?

A

Proteins - carbamino compounds. This contributes to CO2 transport but not acid base balance (not that significant)

196
Q

How much CO2 in total is in the arterial blood (dissolved and reacted)?

A

21.5mmol/l

197
Q

How much CO2 in total is in the venous blood (dissolved and reacted)?

A

23.5mmol/l

198
Q

How much CO2 is created by the body?

A

10mmol

199
Q

What forms does CO2 travel as?

A

80% HCO3
11% carbamino compounds
8% dissolved

200
Q

What is a rise/fall in pCO2 called?

A

hyper/hypocapnia

201
Q

What is a fall in pO2 called?

A

Hypoxia

202
Q

What might cause a decrease in pCO2 and and an increase in O2?

A

Increase in ventilation with no change in metabolism (hyperventilation)

203
Q

At what pO2 is saturation of Hb significantly reduced?

A

8kPa

204
Q

Why is a change in pCO2 harmful?

A

Affects plasma pH - acidic

pH=pKa + log ([HCO3-]/(pCO2 x o.23))

205
Q

What effect does a fall in blood pH below 7 do?

A

Lethally denatures enzymes

206
Q

What effect does a rise in plasma pH above 7.6 do?

A

Free calcium concentration falls enough to produce fatal tetany - Loss of H+ ions bound to plasma proteins enables Ca2+ to bind instead…

207
Q

What is respiratory acidosis?

A

Fall in pH due to hypercapnia from hypoventilation - can cause fatal tetany
(respiratory alkalosis is the opposite)

208
Q

How is plasma pH maintained if pCO2 changes?

A

Compensated for by change in [HCO3] by the kidneys. This takes 2-3 days

209
Q

What is metabolic acidosis?

A

Tissues produce acid which reacts with HCO3 causing a fall in pH. Can be compensated for by increasing ventilation rate - Lower pCO2 maintains ratio

210
Q

What is metabolic alkalosis?

A

Rise in [HCO3] eg after vomiting, causes a rise in pH. Can be compensated to a degree by decreasing ventilation

211
Q

What monitors arterial pO2?

A

Peripheral chemoreceptors in the carotid bodies and aortic bodies

212
Q

What changes occur in the body due to a large fall in pO2?

A

Increased breathing
Changes in heart rate
Diversion of blood flow to the brain

213
Q

What detects changes in pCO2?

A

Peripheral chemoreceptors but they are rather insensitive.
Central chemoreceptors in the medulla of the brain are much more sensitive and cause negative feedback control of breathing - small rises in pCO2 increases ventilation…

214
Q

HOw do central chemoreceptors know of the changes in pCO2 in the arteries?

A

Respond to changes in the pH of CSF which is separated from the blood by the blood-brain barrier but it’s pCO2 is determined by arterial pCO2 - elevated pCO2 drives it across the barrier

215
Q

What controls the [HCO3] in the CSF?

A

Choroid plexus cells. Fixed in short term. but persisting changes in pH are corrected by the cells

216
Q

What is the equation for the ventilation perfusion ratio?

A

Alveolar ventilation/Blood flow

217
Q

What causes diffusion impairment between the alveoli and blood?

A

Problems with the alveolar capillary membrane:

  • Fibrotic lung disease: thickened alveolar membrane slows gas exchange
  • Pulmonary oedema: fluid in the interstitial space increases diffusion distance
  • Emphysema: destruction of alveoli reduces surface area for gas exchange
218
Q

What are the 2 types of respiratory failure?

A

1 - Not enough oxygen enters the blood but CO2 removal is not compromised

2 - Not enough oxygen enters the blood and not enough CO2 leaves it

219
Q

How is oxygen saturation of haemoglobin in arterial blood measured and what should it be?

A

Pulse oximeter

>95%

220
Q

How are blood gases analysed?

A

Arterial blood sample obtained by arterial stab (usually from radial artery) and the sample is put through a blood gas analyser

221
Q

What are the symptoms of type 1 respiratory failure?

A

Breathlessness
Exercise intolerance
Central cyanosis

222
Q

What is type 1 respiratory failure?

A

Ventilation perfusion mismatch. Some alveoli are poorly perfused so there is poor uptake in some alveoli that cannot by compensated by increase in others

223
Q

What might cause type 1 respiratory failure?

A 
Fibrosis - fibrosing alveolitis, extrinsic allergic alveolitis, pneumoconiosis, asbestosis
Pulmonary oedema
Pneumonia
Consolidation
Early stages of acute asthma
Pulmonary embolism
224
Q

What are the symptoms of type 2 respiratory failure?

A

Poor respiratory effort
Chest wall problems
Hard to ventilate lungs

225
Q

What might cause poor respiratory effort?

A

Respiratory depression - adverse drug reaction to narcotics

Muscle weakness due to upper/lower motor neurone problems

226
Q

What might cause chest wall problems?

A

Scoliosis/kyphosis
Trauma
Pneumothorax

227
Q

Why might it be difficult to ventilate the lungs?

A

High airway resistance
COPD
Asthma

228
Q

What is emphysema?

A 
Destruction of lung tissue (alpha 1 antitrypsin)
Changes in compliance
Ventilation perfusion mismatch
Affects oxygen supply
Type 1 resp failure initially
229
Q

What pO2 is diagnosed as acute hypoxia?

A

<8 kPa

230
Q

What are the acute effects of type 2 respiratory failure?

A

pCO2 rises, pO2 falls

Breathlessness - some compensation but poor ventilation due to disease may prevent full compensation

231
Q

What is COPD?

A

Chronic obstructive pulmonary disorder. Type 2 resp failure. Slowly progressive, does not change markedly over several months. Most of the lung function is fixed although some reversibility can be produced by bronchodilator or other therapies.

232
Q

What are the symptoms of COPD?

A

Dyspnoea and cough

233
Q

What are some component disorders of COPD?

A

Emphysema
Chronic bronchitis
Asthma

234
Q

What are the causes of COPD?

A

Cigarette smoking
Coal mining
Anti protease deficiency

235
Q

What is the basic problem of COPD?

A

Lung inflammation

236
Q

Where are the sites of pathology in COPD?

A

Changes in large airways, small airways, lung parenchyma, pulmonary arteries

237
Q

How is COPD diagnosed?

A

Reduced FEV1 and FEV1/FVC ratio which does not change markedly over several months

238
Q

What are some causes of COPD?

A

Smoking
Environmental factors
Genetic predisposition

239
Q

What is the mechanism of COPD?

A 
Airway and systematic inflammation
Alveolar destruction
Hyperinflation
Respiratory muscle inefficiency
Skeletal muscle dysfunction
240
Q

What are the consequences (symptoms) of COPD?

A 
Airway obstruction
Dyspnoea
Exercise limitation
Nutritional depletion
Respiratory failure
241
Q

What are the impacts of COPD on a persons life?

A 
Mobility
Health status
Mood
Exacerbation
Hospitalisation
Death
242
Q

How do you investigate COPD?

A 
History
Chest xray
FEV1
Other lung function tests (vol, loop, TLCO)
High resolution CT scan
243
Q

What is the treatment of COPD?

A

Stop smoking
Promote effective inhaled therapy - Bronchodilators/inhaled steroids
Provide pulmonary rehabilitation for all who need it
Use non-invasive ventilation
Exacerbation management
Oxygen therapy

244
Q

What is the pattern of decline in chronic lung disease?

A

Health status
Functional performance
Symptoms
Hospital admissions

245
Q

What is the MRC dyspnoea scale?

A

Shows degree of breathlessness related to activities by grade

246
Q

What are the physiological benefits of pulmonary rehabilitation?

A 
Muscle mass
Fibre CSA
Mitochondria density
Capillarisation
Mitochondria
Enhanced performance
Reduced dyspnoea
247
Q

What are the pulmonary causes of respiratory failure?

A

Hypoventilation
Ventilation/perfusion imbalance
Alveolar/capillatry diffusion block: Pulmonary oedema, fibrosing alveolitis
True shunt - VSD, av malformation

248
Q

What microbial flora is common in the upper respiratory tract?

A 
Viridans streptococci
Neisseria spp
Anaerobes
Candida sp
Less common: Streptococcus pneumonia, streptococcus progenies, haemophillus influenza, Peudomonas, escherichia coli
249
Q

What are the defences of the upper respiratory tract?

A

Muco-ciliary clearance mechanisms, nasal hairs, ciliated columnar epithelium
Cough and sneezing reflex
Resp mucosal immune system lymphoid follicles of the pharynx and tonsils, alveolar macrophages, secretory IgA and IgG

250
Q

How are acute and chronic bronchitis caused?

A

Acute: viruses and bacteria. May lead to pneumonia
Chronic: Not primarily infective. Exacerbations have been associated with many organisms but the role of infection remains controversial

251
Q

What is pneumonia?

A

Infection of pulmonary parenchyma with consolidation
Involves the distal airspaces and results in inflammaatory exudation
Fluid filled air spaces and consolidation (heavy and stiff lung)
Gas exchange is impaired resulting in local and systemic manifestations

252
Q

How is pneumonia classified?

A

Clinical setting
Presentation
Organism
Lung pathology

253
Q

What is the most common cause of pneumonia?

A

Streptococcus pneumoniae

254
Q

What is lobar pneumonia?

A

Confluent consolidation involving a complete lung lobe
Most often due to Streptococcus pneumonia
Usually community acquired with acute onset

255
Q

What is the pathology of lobar pneumonia?

A

A typical acute inflammatory response. Exudation of fibrin rich fluid
Neutrophil infiltration
Macrophage infiltration

256
Q

How is pneumonia resolved?

A

Antibodies lead to opsonisation, phagocytosis of bacteria

257
Q

What is bronchopneumonia?

A

Infection starting in airways and spreading to adjacent alveoli and lung tissue
Most often seen in the context of pre-existing disease. The consolidation is patchy and not confined by lobar architecture.

258
Q

How can bronchopneumonia be caused?

A

Complication of viral infection
Aspiration of gastric contents
Cardiac failure
COPD

259
Q

How is acute bacterial pneumonia treated?

A

Target the most common pathogens
Amoxicillin (mild to moderate)
Co-amoxiclav if severe

260
Q

What is the outcome of acute pneumonia?

A 
Resolution by organisation (fibrous scarring)
Complications :
- Lung abcess
- Bronchiectasis
Empyema (pus in the pleural cavity)
261
Q

What investigations diagnose pneumonia and determine the pathogen?

A

Sputum gram stain and culture of - oral flora
Chest x-ray
Look for antigens in urine and antibody in blood

262
Q

Describe viral pneumonia

A

Damage to cels lining the airways/alveoli by the virus and immune system
Fluid filled air spaces interferes with gas exchange
Mild to severe
Severe - necrosis/haemorrhage in the lung parenchyma
Patchy or diffuse ground glass opacity on chest x-ray

263
Q

What causes influenza?

A

RNA virus who’s genetic makeup changes constantly through mutations. Can also acquire large genetic elements - have lead to epidemics and pandemics

264
Q

When is infection of influenza severe?

A

Pregnancy and immunocompromised. Offer antiviral drugs

265
Q

What is hospital acquired pneumonia?

A

Pneumonia occurring 48 hrs after hospital admission approx 15% of all hospital acquired infections
Common in ITU and ventilated patients and post surgical.

266
Q

What organisms cause hospital acquired pneumonia?

A 
Enteric Gram negative bacteria (E. coli)
Pseudomonas
Anaerobes
S aureus
MRSA

Usually require treatment with broad spectrum antibiotics

267
Q

What is aspiration pneumonia?

A

Aspiration of exogenous material or endogenous secretions into the respiratory tract
Mixed infection - viridans streptococci and anaerobes

268
Q

Who commonly gets aspiration pneumonia?

A

Patients with neurological dysphagia, epilepsy, alcoholics, drowning
At risk groups - nursing home residents and drug overdose

269
Q

What are the symptoms of pneumonia?

A 
Fever/chills/sweats/rigors
Sough
Sputum- clear / prudence / rust coloured / haemoptysis
Dyspnoea
Pleuritic chest pain
Malaise
Anorexia and vomiting
Headache
Myalgia
Diarrhoea
270
Q

What are the specific chest signs of pneumonia?

A 
Bronchial breath sounds
Crackles
Wheeze
Dullness to percussion
Reduced vocal resonance
271
Q

What are the investigations of pneumonia?

A

CXR
O2 saturation and blood gases
FBC, WCC, platlets
Urea LFT and CRP

272
Q

What are useful markers of pneumonia?

A

WCC (>20 or <4) indicates severe disease
CRP useful in assessing response to treatment
Radiology - very reliable - rarely radiological signs can lag behind clinical characteristics

273
Q

What microbiological samples can be taken to investigate pneumonia?

A 
Sputum
Nose and throat swabs or NPAs 
Endo Tracheal aspirates
Broncho Alveolar Lavage fluid (BAL) 
Open lung biopsy
Blood culture
Urine (to detect antigens of legioella / pneumococcus)
Serum (acute and convalescent sera)
274
Q

What microbiological investigations of pneumonia can be done?

A 
Macroscopy
Microscopy - gram stain, acid fast
Culture - bacteria and viruse
PCR - resp viruses
Antigen detection (legionella)
Antibody detection (serology)
275
Q

What is the CURB 65 prognostic index?

A

Confusion (AMT 7)
RR (>30)
Blood pressure (65 yrs old

Add 1 point if yes for each criteria - if score >2, hospitalisation +/- ITU referral advised

276
Q

What is the management of a patient with pneumonia?

A

Depends on severity and co-morbidities
Supportive treatment
Antibiotics - cover most likely organisms
Review patient - change if microbiology results or poor responses

277
Q

What antibiotics are given for pneumonia?

A

Penicillin class (amoxycillin) are the first choice
Penicillin + Clavulanic acid for severe infections (co-amoxiclav)
Legionella pneumonia - treat with Levofloxacin
Other typical organisms treat with Tetracyclines or Macrolides
Poor response / atypical presentation - discuss with microbiology

278
Q

What preventative measures can be taken against pneumonia?

A

Immunization - flu vaccine (high risk), pneumococcal vaccine (x2). Given to patients with co-morbidities /increased risk of pneumococcal disease
Chemoprophylaxis - Oral penicillin / erythromycin to patients with higher risk of lower resp tract infections (asplenia, dysfunctional spleen, immunodeficiency)

279
Q

When would you inform ITU of a case of pneumonia?

A 
Respiratory failure
Rising pCO2
Worsening metabolic acidosis
Hypotension despite fluid resuscitation
Age and quality of life and co-morbidities determine decision
280
Q

How is a final diagnosis of pneumonia made?

A

High index of suspicion
Teamwork (physician, microbiologist, pathologist)
Broncho-alveolar lavage
Lung biopsy (with lots of special stains)

281
Q

How common is cystic fibrosis?

A

1 in 2500 live caucasian births

282
Q

What are the problems associated with cystic fibrosis?

A

Viscid bronchial secretions
Early infections - H influenza and S aureus
Later, Pseudomans auruginosa and Burkholderia cepecia
(more susceptible to disease)

283
Q

What is PneumoCystis Pneumonia?

A

Opportubistic Pneumonia affecting immunosuppressed patients
Pneumocystis jirovecii -> acute alveoli tis

Treat with cotrimoxazole

284
Q

How is PneumoCystis Pneumonia diagnosed?

A 
Specimens
Induced sputum
BAL
Lung Bx
PCR to detect P jiroveci
DNA
285
Q

What is whooping cough and what causes it?

A

Disease of the reps tract caused by Bordetella pertussis
Starts with cold like symptoms, develops into bouts of severe coughing followed by characteristic whoop or vomiting for 2-3 months

286
Q

How is whooping cough spread and who is most at risk?

A

Droplet spread
Most dangerous <1yr
Older children and adults have prolonged cough

287
Q

How is whooping cough diagnosed and treated/prevented?

A

Specimens for diagnosis - per nasal swabs, nasopharyngeal swabs or aspirates. Culture/PCR
Treat with erythromycin
Prevention with childhood vaccination
Vaccination of pregnant mothers (28-30 weeks)

Semester 3 (19 decks)

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