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Flashcards in Respiratory Deck (160):

LO 1.1 Explain the broad functions of the respiratory system in health

The respiratory system works to ensure that all tissues receive the oxygen that they need and can dispose of the CO2 they produce.

Blood carries gases to and from tissues, where the lungs exchange them with the atmosphere.


LO 1.9 State Boyle’s law

If a given amount of gas is compressed into a smaller volume, the molecules will hit the wall more often. Therefore pressure will rise.
If temperature is constant, Pressure is Inversely Proportional to Volume


LO 1.9 State The Kinetic Theory of Gases

Kinetic Theory of Gases
Gases are a collection of molecules moving around a space, generating pressure by colliding with the walls of the space.
As collisions become more frequent, and harder, pressure goes up.


LO 1.9 State Charles’ Law

The kinetic energy of molecules Increases with Temperature.
As temperature increases, the molecules hit the walls more often, so pressure increases.
Pressure is Proportional to Absolute Temperature (scale starts at absolute zero)


LO 1.9 State the Universal Gas Law

The universal gas law allows the calculation of how volume will change as pressure and temperature changes.
Pressure x Volume = Gas Constant x Temperature (0K)


Describe partial pressure, vapour pressure, saturated vapour pressure and tension

Partial Pressure
In a mixture of gases molecules of each type behave independently. So each gas exerts its own pressure, which is a portion of the total pressure (a partial pressure).
It is calculated as the same fraction of the total pressure as the volume fraction of the gas in the mixture.

Vapour Pressure
In biological systems gas mixtures are always in contact with water.
So gas molecules dissolve, and water molecules evaporate, and then exert their own partial pressure. This partial pressure is known as vapour pressure.

Saturated Vapour Pressure
When the rate of molecules entering and leaving water at the same time is equal, this is the Saturated Vapour Pressure.
When gases enter our body, they are completely saturated with water vapour, so they don’t dry out our lungs.

Gas tension in liquids indicates how readily gas will leave the liquid, not (at least directly) how much gas is in the liquid.
At equilibrium (achieved very quickly in the body), Tension = Partial Pressure.


How to work out the Content of Gas in a Liquid

The amount of Gas that enters a liquid to establish a particular tension is determined by Solubility.

Content = Solubility x Tension
(How easily gas will dissolve x How readily it will leave)

If the gas reacts with a component of the liquid however, this reaction must be complete before tension, and therefore content can be established.

Total Content = Reacted Gas + Dissolved Gas

Plasma just dissolves O2
A pO2 of 13.3kPa (ppO2 in the lungs), gives a blood content of 0.13 mmol/L of O2

Whole blood contains Haemoglobin, which reacts chemically with Oxygen.
At pO2 of 13.3kPa, Haemoglobin binds 8.8mmol/L of O2

Total Content = O2 Bound to Haemoglobin + O2 dissolved in Plasma
= 8.8 + 0.13
= 8.93 mmol/L


LO 1.10 Define the terms Tidal Volume, Respiratory Rate and Pulmonary Ventilation Rate

Tidal Volume
The lung volume that represents the amount of air that is displaced between normal inspiration and expiration, when extra effort is not applied

Respiratory Rate/Pulmonary Ventilation Rate
The number of breaths taken in a set time, usually 60 seconds


Describe the Pulmonary Circulation and the pressure in the arteries, capillaries and veins of the pulmonary system.

The lungs have two circulations – pulmonary and bronchial.
The bronchial circulation is part of the systemic circulation, and meets the metabolic requirements of the lungs. The pulmonary circulation is the blood supply to the alveoli, required for gas exchange.

The pulmonary circulation must accept the entire cardiac output, and works with low resistance due to short, wide vessels, lots of capillaries connected in parallel (lower resistance) and arterioles with relatively little smooth muscle. This low resistance leads to the circulation operating under low pressure.

Pulmonary Artery - 15mmHG
Pulmonary Capillaries - 10mmHG
Pulmonary Vein - 5mmHG


Explain Ventilation/Perfusion Matching

For efficient oxygenation, ventilation of the alveoli needs to be matched with perfusion. The optimal Ventilation/Perfusion ratio is 0.8. Maintaining this means diverting blood from alveoli that are not well ventilated.
This is achieved by hypoxic pulmonary vasoconstriction. Alveolar hypoxia results in vasoconstriction of pulmonary vessels, and the increased resistance means less flow to the poorly ventilated areas and greater flow to well ventilated areas.

Chronic hypoxic vasoconstriction can lead to right ventricular failure. The chronic increase in vascular resistance puts a high afterload on the right ventricle, leading to its failure.


LO 1.2 Define the terms upper and lower respiratory tracts
LO 1.3 Describe the component parts of the upper and lower respiratory tract

Upper Respiratory Tract
The parts of the respiratory system lying outside the thorax
o Nasal Cavity
o Pharynx
o Larynx

Lower Respiratory Tract
The parts of the respiratory system lying inside the thorax
o Trachea
o Main/Primary bronchi
o Lobar Bronchi
- Three on right
- Two on left
- Bronchi have cartilage in their walls
o Segmental Bronchi
o Sub-segmental Bronchi
o Bronchioles
- No Cartilage in the walls
- More smooth muscle than Bronchi
o Terminal Bronchioles
- ~200,000
o Respiratory Bronchioles
o Alveolar Ducts
o Alveoli
- ~300,000,000


LO 1.4 Outline the broad function of the different parts of the respiratory tract

The lungs are a means of getting air to one side, and blood to the other of a very thin membrane, with a large surface area.

The trachea and bronchi have cartilaginous rings in order to hold them open and provide a path for air to travel to the alveoli.
Bronchioles draw air into the lungs by increasing their volume, using the smooth muscle in their walls.
Alveoli provide the single cell thickness membrane for diffusion (Type I cells, Simple Squamous epithelia). They also produce surfactant (Type II cells) to reduce the surface tension of the alveoli.


LO 1.5 Describe the structure and function of the nose

The nose is part of the respiratory tract, superior to the hard palate. It is comprised of the external nose and nasal cavity, which is divided into the right and left cavities by the nasal septum.
The functions of the nose include smelling, respiration, filtration of dust, humidification of inspired air, and reception and elimination of secretions from the paranasal sinuses and nasolacrimal ducts.

Air passing over the respiratory area of the nose is warmed and moistened before it passes through the rest of the upper respiratory tract to the lungs.
The olfactory area contains the peripheral organ of smell


LO 1.5 Describe the structure and function of the Conchae (Terbinates)

The superior, middle and inferior Nasal Conchae (or terbinates) curve inferiormedially, hanging like short curtains from the lateral wall of the nasal cavity.
The conchae are scroll-like structures that offer a vast surface area for heat exchange.

The inferior concha is the longest and broadest and is formed by an independent bone (the Inferior Concha).
The middle and superior conchae are the medial processes of the Ethmoid Bone.

A recess or nasal meatus underlies each of the terbinates, diving the nasal cavity into five passages.
The Sphenoethmoidal Recess, lying superoposterior to the superior conca, receives the opening of the sphenoidal sinus


LO 1.5 Describe the structure and function of the Pharynx

The Pharynx is the superior, expanded part of the Alimentary System, posterior to the nasal and oral cavities and extending inferiorly past the larynx.

The Pharynx extends from the Cranial Base to the Inferior Border of the Cricoid Cartilage Anteriorly and the Inferior Border of C6 Vertebra Posteriorly.
It is widest (Approximately 5cm) opposite the hyoid and narrowest (approximately 1.5cm) at its inferior end, where it is continuous with the oesophagus.

The Pharynx is divided into Three Parts:
o Nasopharynx
 Posterior to the nose and superior to the soft palate
 Respiratory Function as it is the posterior extension of the nasal cavities
 Lymphoid tissue forms a tonsillar ring around the superior part of the pharynx, which aggregates to form Tonsils
o Oropharynx
 Posterior to the mouth
 Extends from the soft plate to the superior border of the epiglottis
 Digestive Function
 Involved in swallowing (GI LO 2.7)
o Laryngopharynx
 Posterior to the Larynx
 Ends from the superior border of the epiglottis to the inferior border of the cricoid cartilage, where it becomes continuous with the oesophagus.


LO 1.5 Describe the structure and function of the Larynx

The Larynx connects the inferior Oropharynx to the Trachea. It also contains the complex organ of voice production (The ‘voice box’).
It extends from the Laryngeal Inlet, through which it communicates with the Laryngopharynx to the level of the inferior border of the cricoid cartilage. Here the laryngeal cavity is continuous with the Trachea.

The Larynx’s most vital function is to guard the air passages, especially during swallowing when it serves as the sphincter/valve of the lower respiratory tract, thus maintaining the airway.

The voice box controls sound production. It is composed of nine cartilages, connected by membranes and ligaments containing the vocal folds.


LO 1.5 Describe the structure and function of the Middle Ear

The cavity of the middle ear, or tympanic cavity is the narrow air-filled chamber in the petrous part of the temporal bone.
The Tympanic cavity is connected with:
o Nasopharynx
- Anteromedially
- Pharyngotympanic (Eustachian)Tube
o Mastoid cells
- Posterosuperiorly
- Mastoid Antrum


LO 1.6 Describe the Histology of the Respiratory Tract and relate it to the functions and defence of the lungs

The respiratory system contains Mucous Membranes, which line the conducting portion of the respiratory tract, bearing mucus-secreting cells to varying degrees
Serious Membranes, which line the pleural sacs that envelop each lung

Pseudostratified Cilia with Goblet Cells
Nasal Cavity
Primary / Secondary Bronchi

Simple Columnar Cilia with Clara Cells but NO Goblet cells
Terminal Bronchioles

Simple Cuboidal with Clara Cells and Sparsely scattered Cilia
Respiratory Bronchioles
Alveolar Ducts
Simple Squamous Alveoli


LO 1.7 Describe the structure of the airways in the lung, distinguish bronchi from bronchioles and define what is meant by terminal bronchiole, alveolar duct and alveolus

The presence of lack of cartilage, glands and differing diameters distinguishes Bronchi from Bronchioles.

Terminal Bronchiole
o No alveolar openings

Respiratory bronchiole
o Bronchiole wall opens onto some alveoli

Alveolar Duct
o Duct wall has openings everywhere onto alveoli

o A single alveoli

Alveolar Sac
o Composite air space onto which many alveoli open


LO 1.8 Describe the structure of the Alveoli

o Abundant capillaries
o Supported by a basketwork of elastic and reticular fibres
o Covering composted chiefly of Type I pneumocytes
o Simple Squamous
o Cover 90% of surface area
o Permit gas exchange with capillaries
o Scattering of intervening Type II pneumocytes
o Simple Cuboidal
o Cover 10% of surface area
o Produce surfactant
o Macrophages line alveolar surface to phagocytose particles.

New alveoli continue to develop up to the age of 8 years, when there are approximately 300,000,000.
Alveoli can open into a respiratory bronchiole, an alveolar duct or sac or another alveolus (via an alveolar pore).


LO 2.10 Describe the properties of the mechanical system comprising the lungs, chest wall and diaphragm

o Bronchioles dilate, increasing their volume and lowering the pressure inside the lungs, moving air in

Chest Wall
o Parietal pleura secretes fluid, the surface tension of which adheres the two pleural layers together
o So when the chest wall expands, the Parietal Pleura (attached to chest wall) moves with it, as does the Visceral Pleura, which is attached to the lung, causing it to expand
o External intercostals elevate the ribs in a ‘bucket handle’ type movement
o Accounts for 30% of chest expansion during quiet respiration

o Contracts and descends
o Accounts for 70% of chest expansion during quiet respiration


LO 2.11 Describe the roles of the muscles involved in inspiration and expiration from the resting expiratory level

Quiet Breathing

o Inhalation
External Intercostals

o Exhalation


LO 2.12 Describe the roles of the diaphragm and accessory respiratory muscles in different types of breathing

Forced Breathing

o Inhalation
External Intercostals
Pectoralis Minor
Serratus Anterior

o Exhalation
Internal Intercostals
Innermost Intercostals
Abdominal Muscles


What are the lung volumes, define them

Measurement of Respiration
The movement of air during breathing can be measured with Spirometry.

Lung Volumes

Tidal Volume
The lung volume that represents the amount of air that is displaced between normal inspiration and expiration, when extra effort is not applied

Inspiratory Reserve Volume
The extra volume that can be breathed in when extra effort is applied

Expiratory Reserve Volume
The extra volume that can be breathed out when extra effort is applied

Residual Volume
The volume left in the lungs at maximal expiration. This cannot be measured with a spirometer; it must be measured by helium dilution


What are the Lung Capacities, define them

Lung Capacities
Lung volumes change with breathing pattern. Capacities do not, as they are measured from fixed points in the breathing cycle.

Vital Capacity
The biggest breath that can be taken in, measured from the max inspiration to max expiration. It often changes in disease, and is about 5L in a typical adult.

Functional Residual Capacity
The volume of air in the lungs at resting expiratory level (Expiratory reserve volume + residual volume). It is typically about 2L.

Inspiratory Capacity
The biggest breath that can be taken from resting expiratory level (lung volume at the end of quiet expiration). It is typically about 3L.


What are the factors affecting diffusion in the lung

Blood flowing through alveolar capillaries picks up oxygen and loses carbon dioxide by diffusion of those gases across the alveolar wall. The rate at which gases exchange is determined by three factors:

The area of the alveolar surface is large because there are a huge number of alveoli, generating in a normal lung an exchange area of around 80m2. In normal lungs, the area available is not a limiting factor on gas exchange.

Resistance to diffusion
The diffusion pathway from alveolar gas to alveolar capillary blood is short, but there are several structures between the two. First gas must diffuse through the gas in the alveoli, then through:
o The alveolar epithelial cell
o Interstitial fluid
o Capillary endothelial cell
o Plasma
o RBC membrane
This means gases have to diffuse through 5 cell membranes, 3 layers of intra cellular fluid and 2 layers of extra cellular fluid. Despite this the overall barrier is less than 1 micron.

Two gases have to diffuse, oxygen into the blood and carbon dioxide out of it. The resistance is not the same for the two gases. For most of the barrier (the cells, membranes and fluid) the rate of diffusion is affected by the solubility of the gas in water, and carbon dioxide diffuses much faster, because it is more soluble.

Overall, Carbon Dioxide diffuses 21 times as fast as oxygen for a given gradient. This means that anything affecting diffusion will only change oxygen transport, as that is limiting (If there is a problem affecting the exchange of gases, O2 will be affected first)

Partial Pressure
The partial pressure of oxygen and carbon dioxide in the alveolar gas must therefore be kept very close to their normal values (O2 – 13.3kPa/CO2 – 5.3kPa) if the tissues of the body are to be properly supplied with oxygen and lose their carbon dioxide. This is achieved by exchange of gas between alveolar gas and atmospheric air brought close to it through the airways of the lung by the process of ventilation.

Air is driven through the airways of the lungs by the pressure changes produced by increases and decreases in the volume of the air spaces next to the alveoli. The movement of breathing lowers pressure in the terminal and respiratory bronchioles during inspiration, so air flows down the airways to them and then increased pressure during expiration so air flows back out again.

Fresh atmospheric air does not enter the alveoli, and exchange of oxygen and carbon dioxide occurs by diffusion between alveolar gas and atmospheric air in the terminal and respiratory bronchioles.


LO 2.14 Define the terms Serial Dead Space and Physiological Dead Space

Serial (Anatomical) Dead Space
Air enters and leaves the lungs by the same airways. So the last air in is the first air out, does not reach the alveoli and is therefore unavailable for gas exchange. The volume of the conducting airways is known as the Anatomical or Serial Dead Space and is normally about 150ml.

Physiological Dead Space
The air contained in the conducting airways is not the only air that fails to equilibrate with alveolar capillary blood. Some alveoli receive an insufficient blood supply; others are damaged by accident or disease, so that even in the air that reaches the alveolar boundary, there is a proportion that fails to exchange.
The volume of air in alveoli not taking part in gas exchange is known as the Alveolar (or Distributive) Dead Space.

Anatomical Dead Space + Alveolar Dead Space = Physiological Dead Space


How do you measure Serial Dead Space

Nitrogen Washout Test

o The patient takes a maximum inspiration of 100% oxygen.
o The oxygen that reaches the alveoli will mix with alveolar air, and the resulting mix will contain Nitrogen (there is 79% Nitrogen in air)
o However, the air in the conducting airways (dead space) will still be filed with pure oxygen.
o The person exhales through a one way vale that measures the percentage of Nitrogen in and volume of air expired
o Nitrogen concentration is initially zero as the patient exhales the dead space oxygen.
o As alveolar air begins to move out and mix with dead space air, nitrogen concentration gradually climbs, until it reaches a plateau where only alveolar gas is being expired
o A graph can be drawn to determine the dead space, plotting Nitrogen % against Expired Volume.


How do you measure Physiological Dead Space

Physiological Dead space is determined by measuring pCO2 (or pO2) of expired alveolar air. The alveolar air is diluted by dead space air to form the expired air, and the degree of dilution is a measurement of a physiological dead space.


LO 2.15 Calculate alveolar ventilation rate given pulmonary ventilation rate, dead space volume and respiratory rate

Alveolar Ventilation Rate
The amount of air that actually reaches the alveoli

Alveolar Ventilation Rate
= Pulmonary Ventilation Rate – Dead Space Ventilation Rate
= (Tidal Volume x RR) – (Dead Space Volume x RR)


LO 3.1 Describe the mechanical system of the lungs and thorax and what is a pneumothorax

Air is drawn into the lungs by expanding the volume of the thoracic cavity. Work is done during breathing to move the structures of the lungs and thorax and to overcome the resistance to flow of air through the airways.

The space between the lungs and thoracic wall, the pleural space, is normally filled with a few millilitres of fluid, the surface tension of which forms a pleural seal holding the outer surface of the lungs to the inner surface of the thoracic wall. Therefore the volume of the lungs changes with the volume of the thoracic cage.

If the integrity of the pleural seal is broken, the lungs will tend to collapse.
E.g. If air gets in between the two layers of the pleura, fluid surface tension is lost and the lungs collapse.


LO 3.2 Define the term ‘Compliance’ of the lungs and state how, in principle, it is measured

Lung Compliance
The ‘stretchiness’ of the lungs is known as compliance.
It is defined as volume change per unit pressure change.

High Compliance means that the Lungs are Easy to Stretch.

Compliance is measured by measuring the change in lung volume for a given pressure. The greater the lung volume the greater the compliance and vice versa. However, even with the constant elasticity of lung structures, compliance will also depend on the starting volume from which it is measured, so it is more usual to calculate Specific Compliance, which is:

Volume Change Per Unit Pressure Change / Starting Volume of Lungs


LO 3.3 Describe the factors which affect the compliance of the lungs, including the role of surfactant

The elastic properties of the lungs arise from two sources, Elastic Tissues in the lungs and Surface Tension forces of the fluid lining the alveoli.

Surface Tension
Surface tension is interactions between molecules at the surface of a liquid, making the surface resist stretching. The higher the surface tension, the harder the lungs are to stretch (lowers compliance).

At low lung volumes, the surface tension of the lungs is much lower than expected. This is due to the disruption of interactions between surface molecules by Surfactant, produced by Type 2 Alveolar Cells.

Surfactant is a complex mixture of phospholipids and proteins, with detergent properties. The hydrophilic ends of these molecules lies in the alveolar fluid and the hydrophobic end projects into the alveolar gas. As a result they float on the surface of the lining fluid, disrupting interaction between surface molecules.

Surfactant reduces surface tension when the lungs are deflated, but not when fully inflated. So little breaths are easy, and big breaths are hard, and it takes less force to expand small alveoli than it does large ones.

Bubbles in the Lung
Alveoli form an interconnecting set of bubbles. If Laplace’s law is applied (Pressure is inversely related to the radius of a bubble), large alveoli would ‘eat’ small ones.
As alveoli get bigger, the surface tension in their walls increases, as surfactant is less effective. So pressure stays high and stops them from ‘eating’ the smaller alveoli.


LO 3.4 Describe the factors which influence airway resistance in the normal lung and how airway resistance changes over the breathing cycle

Overall, work is done against:
o The elastic recoil of the lungs and thorax
o Elastic properties of the lungs
o Surface tension forces in the alveoli
o Resistance to flow through airways
o Of little significance in health, but often affected by disease


LO 3.5 Explain simple Spirometry

The patient fills their lungs from the atmosphere, and breathes out as far and fast as possible through a Spirometer.

Simple Spirometry allows measurement of many lung volumes and capacities. Vital capacity is particularly significant. Tables can be used to predict the vital capacity of an individual of known age, sex and height.

Vital Capacity may be less than normal because the lungs are not:
1. Filled normally in inspiration
2. Emptied normally in expiration
3. Or Both


LO 3.6 Describe the measurement of forced vital capacity (FVC) and forced expiratory volume in one second (FEV1)

Forced Vital Capacity (FVC)
FVC is the maximum volume that can be expired from full lungs.

Forced Expiratory Volume in One Second (FEV1)
FEV1 is the volume expired in the first second of expiration from full lungs.
It is affected by how quickly air flow slows down, so is low if the airwards are narrowed (Obstructive deficit, see below).


LO 3.7 Explain obstructive and restrictive patterns of Spirometry

Restrictive and obstructive deficits can be separated by asking patients to breathe out rapidly from maximal inspiration through a single breath spirometer, which plots volume expired against time.

Maximal filling of the lungs is determined by the balance between the maximum inspiratory effort and the force of recoil of the lungs. If the lungs are unusually stiff, or inspiratory effort is compromised by muscle weakness, injury or deformity, then a Restrictive Deficit is produced.
FVC Reduced
FEV1 >70% FVC

During expiration, particularly when forced, the small airways are compressed. This increases flow resistance, eventually to the point where no more air can be driven out of the alveoli.
If the airways are narrowed, then expiratory flow is compromised much earlier in expiration, producing an Obstructive Deficit.
FEV1 Reduced
FVC Relatively Normal


LO 3.8 Explain expiratory and inspiratory flow volume loops and how they are affected by upper and lower airway obstruction

Flow Volume Curves
Flow volume curves are a graph of Volume Expired against Flow Rate, derived from a Vitalograph trace.

A – When the lungs are full, the airways are stretched so resistance is at a minimum. Flow is therefore at maximum (Peak Expiratory Flow Rate PEFR)

B-D – As the lungs are compressed, more air is expired and the airways begin to narrow, so resistance increases and flow rate decreases.

In normal individuals, peak flow is affected most by the resistance of the large airways, but will also be affected by severe obstruction of the smaller airways (e.g. Asthma).

Mild obstruction of the airways produces a ‘scooped out’ expiratory curve. More severe obstruction will also reduce PEFR.


LO 3.9 Describe in principle the measurement of residual volume

Helium Dilution Test
The Helium Dilution Test is used to measure Functional Residual Capacity (FRC), which is used to calculate the residual volume. Helium is an inert, colourless, odourless, tasteless gas that is not toxic. It cannot transfer across the alveolar-capillary membrane and is therefore contained within the lungs.
o At the end of a normal tidal expiration the patient is connected to a circuit, which is connected to a contained containing a gas mixture with a known Helium Concentration (C1) and Volume (V1)
- End of Tidal Expiration:
- Lung Volume = FRC = ERV +RV
o The patient continues to rebreathe into the container until equilibrium occurs
- Usually takes 4 – 7 minutes
o The new concentration of Helium = C2

o C1 x V1 = C2 x V2
- V2 = V1 + FRC

o Since C1, V1 and C2 are all known, FRC can be calculated.
o Residual Volume = FRC – ERV
- ERV measured by Spirometry


LO 3.9 Describe in principle the measurement of transfer factor

Transfer Factor
The Carbon Monoxide Transfer Factor measures the rate of transfer of CO from the alveoli to the blood in ml per minute per kPa (ml/min/kPa). It is a way of measuring the diffusion capacity of the lung, because the amount transferred will depend on how well gas diffusion takes place.
Inhaled CO is used because of its very high affinity for Hb. Since almost all the CO entering the blood binds to Hb, very little remains in plasma so we can assume plasma ppCO is zero.
Therefore, the concentration gradient between alveolar ppCO and capillary ppCO is maintained. As a result the amount of CO transferred from alveoli to the blood is limited only by the diffusion capacity of the lung.

o The patient performs a full expiration, followed by a rapid maximum inspiration of a gas mixture composed of air, a tiny fraction of CO and a fraction of an inert gas such as helium.
 Tiny fraction of CO as it is toxic
 Fraction of inert gas to make an estimate of total lung volume
o The breath is held for 10 seconds.
o The patient exhales, and gas is collected mid-expiration, to gain an alveolar sample
o Concentration of CO and inert gas
o From these measurements, the Carbon Monoxide Transfer Factor is calculated


LO 3.10 Explain the nitrogen washout curve

Nitrogen Washout Test
Serial (Anatomical) Dead Space is measured by the Nitrogen Washout Test.
o The patient takes a maximum inspiration of 100% oxygen.
o The oxygen that reaches the alveoli will mix with alveolar air, and the resulting mix will contain Nitrogen (there is 79% Nitrogen in air)
o However, the air in the conducting airways (dead space) will still be filled with pure oxygen.
o The person exhales through a one way vale that measures the percentage of Nitrogen in and volume of air expired
o Nitrogen concentration is initially zero as the patient exhales the dead space oxygen.
o As alveolar air begins to move out and mix with dead space air, nitrogen concentration gradually climbs, until it reaches a plateau where only alveolar gas is being expired
o A graph can be drawn to determine the dead space, plotting Nitrogen % against Expired Volume.


LO 4.1 State the solubility of Oxygen in body fluids

Oxygen is not very soluble in water. At a partial pressure of 13.3kPa and a temperature of 370C, plasma contains 0.13mmol/L of dissolved oxygen.

At rest we need 12mmol of Oxygen per minute. The volume that would contain this amount is 92 Litres.


What is the typical pp02 in the tissues and lungs

Typical ppO2 in the lungs is 13.3kPa

Typical ppO2 in tissues is ~5kPa


LO 4.3 List the properties of the haemoglobin molecule that facilitate the transport of oxygen in the blood

Haemoglobin (Hb) reversibly binds to oxygen over a very narrow range of ppO2. It is a tetrameric protein (2xA, 2xB subunits) containing four Haem groups, allowing it to bind four molecules of oxygen.
Hb can exist in two states - a low affinity T-state (tense) and a high affinity R-state (relaxed). Transition between these two states gives Hb its sigmoidal binding curve, so Hb’s affinity to O2 increases as more O2 binds.


LO 4.4 Draw the effects on the haemoglobin oxygen dissociation curve of a fall in pH and a rise in temperature

H+, Increasing Temperature and CO2 and decrease the affinity of Hb for O2. At sites of low pH (high [H+]), and increased CO2, for example muscle tissue during exercise, more oxygen is required and will be released. This is called the Bohr effect.

The oxygen dissociation curve shifts to the RIGHT.


LO 4.5 Estimate the rate of delivery of oxygen to the tissues at different capillary pO2’s and pH’s

If the pO2 in the capillaries of tissues falls, pH falls and temperature rises so that Hb will give up more oxygen. Therefore the saturation of Hb leaving the capillaries will be greatly reduced.

If venous pO2 is known, a dissociation curve can be used to calculate the percentage of oxygen that has been given up to that tissue.


LO 4.6 State the factors influencing the diffusion of gases across the alveolar membrane

Blood flowing through alveolar capillaries picks up oxygen and loses carbon dioxide by diffusion of those gases across the alveolar wall. The rate at which gases exchange is determined by three factors:
o Area available for the exchange
o Resistance to diffusion
o Gradient of partial pressure


LO 4.8 List the Reactions of CO2 in the blood

o Dissolves in water
More soluble than O2

o Reacts with water
Forms H+ and HCO3-
Reversible reaction depending on concentrations of reactants

o Binds directly to proteins
Forms Carbamino compounds


LO 4.9 Write the Henderson-Hasselbach equation and be able to calculate the plasma pH, given the pCO2 and [HCO3-]

pHG = 6.1 + log (HCO3/[pCO2*0.23])


LO 4.10 State the factors influencing the Hydrogen Carbonate concentration of plasma

o In Plasma
CO2 dissolves in plasma and undergoes a slow reaction (little carbonic anhydrase) with water, creating HCO3-

o In RBCs
CO2 also reacts with water, rapidly (carbonic anhydrase is present) to form H+ and HCO3-.
H+ ions bind to Hb, drawing the reaction towards HCO3- production
The amount produced depends primarily upon the buffering effects of Hb


LO 4.11 Describe the buffering actions of Hb in RBCs

H+ ions bind to Haemoglobin, so it acts as a buffer by ‘mopping up’ H+ ions. This drives the reaction of CO2 with Water, producing more H+ ions and HCO3-.


LO 4.12 Describe the function of carbamino compounds

Carbamino Compounds
Carbamino compounds bind directly to proteins, contributing to CO2 transport, but not acid base balance.
There is slightly more formed in venous blood, as pCO2 is higher.


LO 4.13 State the normal content of CO2 in arterial and venous blood

Arterial Blood CO2 – 21.5 mmol/Litre
Venous Blood CO2 – 23.5 mmol/Litre


LO 4.14 Describe the process of transport of CO2 from tissues to lungs, and state the proportion of CO2 traveling in various forms

Venous Blood CO2 – Arterial Blood CO2 = Amount transported from tissues  lungs
= 23.5 – 21.5
= 2mmol/Lire

o 80% travels as HCO3-
Depending on how much O2 Hb has lost, allowing it to bind H+
o 11% travels as carbamino compounds
o 8% travels as dissolved CO2


LO 5.1 Define the terms hypoxia, hypercapnia, hypocapnia, hyperventilation, hypoventilation

Hypoxia – A fall in alveolar, thus arterial pO2

Hypercapnia – A rise in alveolar, thus arterial, CO2

Hypocapnia – A fall in alveolar, thus arterial CO2

Hyperventilation – Ventilation increases with no change in metabolism
(Breathing more than you actually have to)

Hypoventilation – Ventilation decreases with no change in metabolism
(Breathing less than you actually have to)


LO 5.2 Describe the effects on plasma pH of hyper- and hypo-ventilation

pCO2 affects plasma pH (Henderson-Hasselbach)

o Hyperventilation
pCO2 down
pH up

o Hypoventilation
pCO2 up
pH down


LO 5.3 Describe the general effects of acute hypo- and hyper-ventilation

o Hypercapnia and Respiratory Acidosis
o pH falls bellows 7.0
o Enzymes become lethally denatured

o Hypocapnia and Respiratory Alkalosis
o pH rises above 7.6
o Free calcium concentration falls enough to produce fatal tetany
Ca2+ is only soluble in acid, so when pH rises, Ca2+ cannot stay in the blood. Nerves become hyper-excitable.


LO 5.4 Define the terms Respiratory Acidosis, Respiratory Alkalosis, Compensated Respiratory Acidosis and Compensated Metabolic Alkalosis

Respiratory Acidosis
CO2 is produced more rapidly than it is removed by the lungs (hypoventilation). Alveolar pCO2 rises, so [Dissolved CO2] rises more than [HCO3-], producing a fall in plasma pH.

Compensated Respiratory Acidosis
Respiratory Acidosis persists, and the kidneys respond to low pH by reducing the excretion of HCO3-, thus restoring to ratio of [Dissolved CO2] to [HCO3-], and therefore the pH.

Respiratory Alkalosis
CO2 is removed from alveoli more rapidly than it is produced (hyperventilation). Alveolar pCO2 falls, disturbing the ratio of [Dissolved CO2] to [HCO3-], producing a rise in plasma pH.

Compensated Respiratory Alkalosis
Respiratory Alkalosis persists, and the kidneys respond to the high pH by excreting HCO3-, thus restoring the ratio of [Dissolved CO2] to [HCO3-], and therefore the pH.


LO 5.5 Define the terms Metabolic Acidosis, Metabolic Alkalosis, Compensated Metabolic Acidosis, Compensated Metabolic Alkalosis

Metabolic Acidosis
Metabolic production of acid displaces HCO3- from plasma as the acid is buffered; therefore the pH of blood falls.

Compensated Metabolic Acidosis
The ratio of [Dissolved CO2] to [HCO3-] may be restored to near normal by lowering pCO2. The lungs increase ventilation to correct pH.

Metabolic Alkalosis
Plasma [HCO3-] rises, causing the pH of blood to rise (e.g. after vomiting).

Compensated Metabolic Alkalosis
The ratio of [Dissolved CO2] to [HCO3-] may be restored to near normal by raising pCO2. The lungs decrease ventilation to correct pH.


LO 5.6 Describe the acute effects upon ventilation of: falling inspired pO2, increase in inspired pCO2 and falls in arterial plasma pH

Falling Inspired pO2
The falling arterial pO2 is detected by Peripheral Chemoreceptors located in the Carotid and Aortic bodies.
The carotid and aortic bodies are stimulated by a decrease in oxygen supply relative to their own oxygen usage, which is small. They only respond to large drops in O2.
Stimulation of the receptors:
o Increases the tidal volume and rate of respiration
o Changes in circulation directing more blood to the brain and kidneys
o Increased pumping of blood by the heart

Increase in Inspired pCO2
The Peripheral Chemoreceptors in the Carotid and Aortic bodies also detect changes in pCO2, but are insensitive.
Central Chemoreceptors in the Medulla of the brain are much more sensitive, altering breathing on a second to second basis.

Central chemoreceptors detect changes in Arterial pCO2.
o Small rise in pCO2 -> Increase Ventilation
o Small falls in pCO2 -> Decrease Ventilation
o Are the basis of negative feedback control of breathing


LO 5.7 Describe the location and function of the Peripheral Chemoreceptors and their role in ventilator and other responses to Hypoxia

The arterial pO2 is detected by Peripheral Chemoreceptors located in the Carotid and Aortic bodies.
The carotid and aortic bodies are stimulated by a decrease in oxygen supply relative to their own oxygen usage, which is small. They only respond to large drops in O2.
Stimulation of the receptors:
o Increases the tidal volume and rate of respiration
o Changes in circulation directing more blood to the brain and kidneys
o Increased pumping of blood by the heart


LO 5.8 Describe the location and function of the central chemoreceptors, their role in the vetilatory respiratory to changes in arterial pCO2 and the roles of the cerebro-spinal fluid, blood brain barrier and choroid plexus in that response

Central Chemoreceptors in the Medulla of the brain are much more sensitive, altering breathing on a second to second basis.

Central chemoreceptors detect changes in Arterial pCO2.
o Small rise in pCO2  Increase Ventilation
o Small falls in pCO2  Decrease Ventilation
o Are the basis of negative feedback control of breathing
- If pCO2 rises, central chemoreceptors stimulate ventilation
- Which blows off CO2, returning pCO2 to normal
- Vice-versa
The central chemoreceptors actually respond to changes in the pH of cerebro-spinal fluid (CSF).

The CSF is separated from the blood by the blood-brain barrier. The pCO2 of the CSF is determined by arterial pCO2, but HCO3- and H+ cannot cross.

CSF [HCO3-] is controlled by Choroid Plexus Cells.

The pH of CSF is determined by the ratio of [HCO3-] to pCO2. In the short term, [HCO3-] is fixed (cannot cross BBB), so falls in pCO2 -> Inc. pH and rises in pCO2 -> Lower pH. Persisting changes compensated for via the Choroid Plexus Cells altering CSF [HCO3-].


LO 5.9 Define Hypoxia

Hypoxia – A fall in alveolar, thus arterial pO2


LO 5.10 What are the five factors necessary to maintain arterial pO2 in the normal range

There are five factors necessary to maintain arterial pO2 in the normal range, and problems with any of them may result in hypoxia

1. Low pO2 in inspired air
Everything is normal, the air breathed in just has low pO2
People living at high altitudes

2. Hypoventilation
o Always associated with increased pCO2 (Type 2 Respiratory Failure)
o Neuromuscular Problems
Respiratory depression due to opiate overdose
Head injury
Muscle weakness (NMJ/Nerve/Muscle diseases)
o Chest wall problems (Mechanical)
Morbid obesity
o Hard to Ventilate lungs
Airway obstruction
COPD & Asthma when the airway narrowing is severe and widespread
Severe fibrosis

3. Diffusion Impairment
o O2 diffuses much less readily than CO2, so is always affected first
o pCO2 is therefore low/normal – Always Type 1 Respiratory Failure
o Structural Changes
Lung fibrosis causing thickening of alveolar capillary membrane
o Increased Path Length
Pulmonary Oedema
o Total area for diffusion reduced

4. Ventilation Perfusion Mismatch
o O2 diffuses much less readily than CO2, so is always affected first
o pCO2 is therefore low/normal – Always Type 1 Respiratory Failure
o Reduced Ventilation of some Alveoli
Lobar Pneumonia
o Reduced Perfusion of Some Alveoli
Pulmonary Embolism

5. Abnormal Right to Left Cardiac Shunts
o E.g. Cyanotic Heart Disease such as Tetralogy of Fallot (See CVS)


LO 5.11 Interpret uncomplicated blood gas abnormalities, type 1 vs type 2 resp failure

Type 1 Respiratory Failure
o Respiratory Rate increased
o pO2 down
o CO2 nomral or down

Type 2 Respiratory Failure
o Respiratory Rate increased
o pO2 decreased
o CO2 increased


LO 5.12 Describe the nature of the air flow obstruction in asthma

Asthma is a chronic disorder characterised by Airway Wall Inflammation and Re-modelling.
It is a Reversible Airflow Obstruction.

Airways in asthma have thickened smooth muscle and basement membranes.

Triggers cause the airway smooth muscle to contract, reducing airway radius, increasing resistance and reducing airflow


LO 5.13 Describe the epidemiology of Asthma

Asthma is:
o Increasing in prevalence
o More common in the developed world
o Increasing in populations who move from developing -> developed countries

o 5.4 million people in the UK current receive treatment
o 1.1 million children
o 4.3 million adults

o Genetic risk
o Sensitisation to airborne allergens
- House Dust Mite
- Pollens
- Air pollution
- Tobacco smoke (Pre-/post natal exposure, active)
o Hygiene hypothesis


LO 5.14 Describe the typical clinical presentations of asthma including the symptoms commonly reported by asthmatic patients and the signs detected on physical examination

The diagnosis of asthma is a clinical one. There is no standard definition of the type, severity or frequency of symptoms, nor of the findings on investigation.

Asthma is defined as more than one of the following recurring symptoms:

o Wheeze
High pitched, expiratory sound
Wheeze originates in airways which have been narrowed by compression or obstruction
In asthma the wheeze is of variable intensity and tone (Polyphonic)
o Cough
Often worse at night (Lack of sleep, poor performance at school)
Exercise induced (Decreased participation in activities)
Dry cough
o Breathlessness
With exercise
o Chest Tightness
o Variable Airflow Obstruction

o Chest
Scars, deformities
Hyper-expansion (Barrel Chest)
o General health
Eczema, hay-fever
Can they speak?
o Room
o Hyper-resonant
o Polyphonic wheeze


LO 5.15 Describe the tests used to assess the condition of a patient suspected of asthma, and how they are interpreted

Spirometry – Flow Volume Loop
o Low PEFR
o Low FEV1/FVC Ratio
o >12% increase in FEV1 following salbutamol

Allergy Testing
o Skin prick to aero-allergens, e.g. cat, dog, HDM
o Blood IgE levels to specific aero-allergens

Chest X-Rays
o Performed to exclude other diseases/inhalation of foreign body/pneumothorax


LO 5.16 Describe, in outline, the pathophysiological changes underlying the asthmatic condition

o Mast Cells
Increased in asthma
Release prostaglandins, histamine etc
o Eosinophils
Large numbers in the bronchial wall and secretions of asthmatics
o Dendritc Cells and Lymphocytes
Dedritic cells have a role in the initial uptake and presentation of allergens to lymphocytes
T-Helper lymphocytes (CD4) release cytokines that play a key part in the activation of mast cells
Th2 phenotype favour the production of antibody production by B lymphocytes to IgE.

o Epithelium
Stressed and damaged with a loss of ciliated columnar cells
o Basement membrane
Deposition of collagens, causing it to thicken
o Smooth Muscle
Hyperplasia causing thickening of the muscle


LO 5.17 Describe the major precipitating factors for asthmatic attacks

Although they may occur spontaneously, asthma exacerbations are most commonly caused by:
o Lack of treatment adherence
o Respiratory Virus Infections associated with the common cold
o Exposure to allergen or triggering drug (e.g. NSAID)


LO 5.18 Describe, in outline, the principles of treatment of asthma

Educate patients to correctly recognise their symptoms, to use their medication timely, use services appropriately and to develop their own Personal Asthma Action Plan.

Primary Prevention
o Stop smoking
o Fresh air
o Reduce exposure to allergens/triggers
o Weight Loss

Pharmacological Management
o B2-adrenoagonists
o Muscarinic antagonists
o Short term relief
o E.g. Salbutamol
o Anti-inflammatory agents
o Corticosteroids
o Preventer therapies


LO 6.1 Describe the nature of COPD

Chronic Obstructive Pulmonary Disease (COPD) is a chronic, slowly progressive disorder characterised by airflow obstruction, which does not changed markedly over several months.

Airflow Obstruction
o Reduced FEV1
o Reduced FEV1/FVC Ratio


LO 6.2 Describe the epidemiology and main causes of COPD

o 89% of the population is unaware
o 3.7 million affected in the UK
o 1 million symptomatic
o 30,000 deaths
o 1 million hospital inpatient days/year

Causes of COPD
COPD is caused by the abnormal inflammatory response of the lung to noxious particles or gases, such as cigarette smoking and atmospheric pollutants.
A much less common cause of emphysema is the inherited deficiency of A1-antitrypsin.


LO 6.3 Describe the symptoms and signs of COPD

o Productive Cough
White or clear sputum
o Wheeze
o Breathlessness
o Usually following many years of a smoker’s cough

o May be no signs, or just quiet wheezes
o Hyperventilation with prolonged expiration (prolonged disease)
Expiratory airflow limitation
o Accessory muscles of respiration are used
o Hyperinflation of the lungs


LO 6.4 Outline the assessment of COPD in terms of impairment, disability and handicap

o History
Including MRC Dyspnoea scale

o Chest X-Ray
Not really to diagnose COPD, mainly to make sure they don’t have something else (e.g. cancer)

o FEV1
Reduced FEV1
Reduced FEV1/FVC ratio

o Other lung function tests
Lung volumes, loop

o High resolution CT scan
Detect emphysema


LO 6.8 Outline the principle of oxygen therapy

Oxygen is given to patients to increase oxygen saturation and alleviate symptoms. It is a treatment for hypoxaemia, NOT breathlessness.

o Long term
Patient uses a much during the day as possible
o Portable
o Intermittent
When required


LO 6.9 Outline the management of COPD

Smoking Cessation
The single most useful measure in the management of COPD is persuading the patient to stop smoking (if they do). Even in advanced disease this may slow down the rate of deterioration.

Drug Therapy
Used for both the short-term management of exacerbations and for the long-term relief of symptoms. Many of the drugs used are similar to those used in asthma.
o Bronchodilators
o Corticosteroids
o Antibiotics
Shortens exacerbations
Given as soon as sputum turns yellow or green

Oxygen Therapy
Increase blood oxygen saturation by administering oxygen (see above).

Pulmonary rehabilitation
Exercise training can modestly increase exercise capacity. Regular training periods can be used as home, e.g. walking fixed distances or climbing stairs.

A1-antitrypsin Replacement
If deficient

Treat co-morbid condition
o Cardiac
o Metabolic
o Nutritional
o Osteoporosis
o Anxiety/depression


LO 6.10 Outline the distribution and composition of the normal flora of the respiratory tract, common, less common and other

o Viridans streptococci
o Neisseria spp
o Anaerobes
o Candida spp

Less Common
o Streptococcus pneumonia
o Streptococcus pyogenes
o Haemophillus influenza

o Pseudomonas
o E. coli


LO 6.11 Outline the natural defences of the respiratory tract against infection

o Cough and sneezing reflex

o Muco-ciliary clearance mechanisms
Ciliated columnar epithelium
Nasal hairs

o Respiratory mucosal immune system
Lymphoid follicles of the pharynx and tonsils
Alveolar macrophages
Secretary IgA and IgG


LO 6.12 List the main infection diseases of the upper respiratory tract and state the organism commonly causes these infections

Upper Respiratory Tract Infections
o Rhinitis (common cold)
o Pharyngitis
o Epiglottitis
o Laryngitis
o Tracheitis
o Sinusitis
o Otitis media (Inflammation of middle/inner ear)

URT Infections are most commonly caused by Viruses:
o Rhinovirus
o Coronavirus
o Influenza/parainfluenza
o Respiratory Syncytial Virus (RSV)

May also be caused by Bacterial Super-Infection:
o Common with sinusitis and otitis media
o Can lead to
Brain abscess


LO 6.13 Define the terms ‘pneumonia’; distinguish the terms acute ‘lobar’, ‘broncho’, ‘interstitial’, ‘aspiration’ and chronic pneumonias

Pneumonia is a general term denoting inflammation of the gas-exchanging region of the lung, usually due to infection (bacterial or viral). Pneumonia is therefore an infection of the lung parenchyma.
Inflammation due to other causes, such as physical or chemical damage is often called pneumonitis.

Lobar Pneumonia
Pneumonia localised to a particular lobe/s of the lung.
Most often due to Streptococcus pneumoniae

Broncho Pneumonia
Pneumonia that is diffuse and patchy. Infection starts in the airways and spreads to adjacent alveoli and lung tissue.
Streptococcus pneumoniae, Haemophilus influenza, Staphylococcus aureus, anaerobes, coliforms

Aspiration Pneumonia
Aspiration of food, drink, saliva or vomit can lead to pneumonia. This is more likely in individuals with an altered level of consciousness, e.g. due to anaesthesia, alcohol or drug abuse, or if there are problems swallowing due to nerve or oesophageal damage.
Organisms include oral flora and anaerobes.

Interstitial Pneumonia
Inflammation of the Intersticium of the lung
(Alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues)

Chronic Pneumonia
Inflammation of the lungs that persists for an extended period of time


LO 6.14 Describe the infection aetiology of acute community acquired and acute hospital acquired pneumonias

Community Acquired

Common Bacteria
o Streptococcus pneumoniae – 30%
o Haemophilus influenza – 13%
o Klebsiella pneumoniae

Atypical Bacteria
o Chlamydia pneumophilia - 10%
o Mycoplasma pneumoniae
o Legionella pneumophila

Hospital Acquired Bacteria
o Gram –‘ve enteric bacteria - 10%
o Pseudomonas
o Staphylococcus aureus

Aspiration Pneumonia
o Anaerobes
o Oral flora


What are the associated features of S. pneumoniae infection in pneumonia

Elderly, co-morbidities, acute onset, high fever, Pleuritic chest pain


What are the associated features of H. influenza infection in pneumonia



What are the associated features of Legionella infection in pneumonia

Recent travel, younger patient, smokers, illness, multi-system involvement


What are the associated features of Mycoplasma infection in pneumonia

Young, prior antibiotics, extra-pulmonary involvement (haemolysis, skin and joint)


What are the associated features of S. aureus infection in pneumonia

Post-viral, Intra-Venous Drug User


What are the associated features of Chlamydia in pneumonia infection

Contact with birds


What are the associated features of Coxiella infection in pneumonia

Animal contact (sheep)


What are the associated features of Klebsiella infection in pneumonia

Thrombocytopenia, leucopenia


What are the associated features of S. milleri infection in pneumonia

Dental infections, abdominal source, aspiration


LO 6.16 Understand the spectrum of clinical features of acute community acquired and acute hospital acquired pneumonias

The presentation of pneumonia can be variable. There is almost always malaise, fever and a productive cough. The sputum may be purulent, or rusty coloured (little blood) or stained with lots of blood. There is commonly plueritic chest pain. Patients often feel breathless.
Pneumonias may be of very rapid onset, particularly if pneumococcal or staphylococcal, with a fatal outcome in a short period of time.

Symptoms of Pneumonia
o Fever, chills, sweats, rigors
o Cough
o Sputum
Clear / purulent / ‘rust coloured / haemoptysis
o Dyspnoea
o Pleuritic chest pain
o Malaise
o Anorexia and vomiting
o Headache
o Myalgia
o Diarrhoea

o Chest Signs
Bronchial breath sounds
Dullness to percussion
Reduced vocal resonance

Hospital Acquired Pneumonia
o Pneumonia occurring 48hrs after hospital admission
o Makes up ~15% of all hospital acquired infections
o Common in ventilated/post surgical patients


What is the main deciding factor on whether pneumonia treatment

CURB 65 Score
The severity of pneumonia can be assessed using the CURB 65 score, where the presence of two or more of the following features is an indication for hospital treatment, and patients with high scores may required ICU treatment.

C – New mental Confusion
U – Urea > 7mmol/L
R – Respiratory rate > 30 per minute
B – Blood pressure (Systolic < 90 or Diastolic < 60 mmHg)


LO 6.16 Understand the principles of collection of specimens for laboratory diagnosis of pneumonias

Samples Collected to Investigate Pneumonia
o Sputum
o Nose and Throat swabs
o Endotracheal aspirates
o Broncho Alveolar Lavage fluid (BAL)
o Open Lung Biopsy
o Blood culture -Preferably before antibiotics
o Urine -Detect the antigens of legionella/pneumococcus
o Serum -= Antibody detection

Microbiological Investigations of Pneumonia
o Macroscopic - Sputum, purulent, blood stained
o Microscopy - Gram staining, Acid fast
o Culture - Bacteria and viruses
o PCR - Respiratory viruses
o Antigen detection - Legionella
o Antibody detection - Serology


LO 6.17 List the common opportunistic pathogens causing pneumonias in immunosuppressed hosts

Pathogens infecting immunosuppressed hosts may be:

o Virulent infection with common organism
o Infection with opportunistic pathogen
Viruses – Cytomegalovirus (CMV)
Bacteria – Mycobacterium avium intracellulare
Fungi – Aspergillus, candida, pneumocystis jiroveci
Protozoa – Cryptosporidia, toxoplasma


LO 6.18 Describe the principles of anti-microbial therapy in pneumonia and understand the rationale for selecting different antibiotics for different pneumonias

Management of Pneumonias
o Oral fluid/IV fluids if severe - Avoid dehydration
o Anti-pyretic drugs - Reduce fever and malaise
E.g. Paracetamol
o Stronger analgesics - Deal with the pain (Pleuritic)
o Oxygen - If there is cyanosis

The infection is treated with antibiotics, which vary with the type of pneumonia.

Community Acquired Pneumonia
The target organism is normally Pneumococcus, which is usually sensitive to Penicillin or related antibiotics.

Hospital Acquired pneumonia
The target organism is more likely to be Gram –‘ve, making it necessary to use antibiotics that cover these organisms, e.g. IV Co-Amoxiclav.


What are the possible Outcomes of Pneumonia

o Resolution
Organisation (Fibrous scarring)

o Complications
Lung abscess
Empyema (pus in pleural cavity)


What are the methods of Prevention of Pneumonia

Flu vaccine – Given annually to high risk patients
Pneumococcal vaccine – Two vaccines

Oral penicillin / erythromycin to patients with higher risk of lower respiratory tract infections
E.g. asplenia, dysfunctional spleen, immunodeficiency


LO 7.1 Describe the microbiology of mycobacterium tuberculosis

Mycobacteria possess a lipid-rich cell wall that retains some dyes, even resisting decolourisation with acid (acid-fast).


LO 7.2 Describe the pathology of TB infections

Tuberculosis is spread from person to person by the aerosol route, making the lung the first site of infection.

The Primary Complex
Most infections resolve with local scarring (Primary Tuberculosis)

Post-Primary Infection
Post-Primary Infection refers to the development of tuberculosis beyond the first few weeks.

The infection may progress throughout the body (Miliary Spread). This may resolve spontaneously, or develop into localised infection (E.g. meningitis).

Mycobacterium Tuberculosis is ingested by macrophages, but escapes from the phagolysosome to multiply in the cytoplasm.

The intense immune response causes local tissue destruction (Cavitation in the lung) and cytokine-mediated systemic effects (Fever and Weight loss).

TB may affect every organ of the body, mimicking both inflammatory and malignant diseases. Pulmonary tuberculosis may present with a chronic cough, haemoptysis, fever and weight loss or as recurrent bacterial pneumonia.
Untreated the infection follows a chronic, deteriorating course.
Tuberculous meningitis presents with fever and slowly deteriorating level of consciousness.
Kidney infection may lead to signs of local infection, fever and weight loss, complicated by ureteric fibrosis and hydronephropathy.
The lumbosacral spine is a common site of bone infection – progression may cause vertebral collapse and nerve compression.
Inflammation of large joints may lead to destructive arthritis.


LO 7.3 Describe the host response to TB infection

Mycobacterium Tuberculosis is ingested by macrophages, but escapes from the phagolysosome to multiply in the cytoplasm.

At the same time it provokes an immune response, stimulating the release of IL-12.

IL-12 in turn drives the release of IFN-Y and TNF-A from NK and CD4 cells. These cytokines activate and recruit more macrophages to the site of infection, resulting in the formation of Granulomas.


LO 7.4 Describe the primary and post-primary changes in TB

Primary Changes
o Few Symptoms
o Lymph nodes may become enlarged in young people

Post-Primary Changes
The Classical Presentation:
o Cough (Not always productive)
o Fevers towards the end of the day or at night
o Weight loss and general debility

Chest X-Ray reveals pulmonary shadowing, which may be patchy solid lesions, cavitated solid lesions, streaky fibrosis or flecks of calcification.


LO 7.5 Describe the signs, sympyoms and radiological changes in Respiratory TB

Weight Loss
Palpable lymph nodes

Primary usually asymptomatic
Tiredness and malaise
Weight loss and anorexia
Haemoptysis occasionally

X-Ray Changes
Miliary seeds


Describe pleural Tb

Pleural Tuberculosis
More common in males, there are two mechanisms of pleural involvement. There is almost always some pulmonary disease present:
o Hypersensitivity response in primary infection
o Tuberculous empyema with ruptured cavity.
Tuberculosis empyema has a tendency to burrow through the chest wall.


LO 7.7 Describe the diagnosis of TB

TB is diagnosed by:

o Clinical Features
Cough, night fever, weight loss

o Radiological Features
Shadowing, cavities, consolidation, cardiomegaly, miliary seeds

o Microbiology
Identification of bacillus
Direct smear and subsequent culture of the appropriate body fluid
Important to isolate organism and determine its susceptibility to drugs


LO 7.8 Describe the principles of management of TB (including drugs, toxicity, schedules, problems with compliance)

Initially patients are treated with four drugs for two months, after which two of them are dropped and the others are continued for another four months.
Multiple drugs are used in an attempt to combat resistance (e.g. in 5-10% of patients TB is resistance to Isoniazid).

As this is quite a long drug regime, with several different pills to take there can be problems with compliance. As such 15% of patients in the US receive Directly Observed Therapy (DOT), giving benefits including improved cure rates, reduction in rate, drug resistance and relapses.

Initial Phase
(2 months)
Rifampicin - Hepatitis, rash, flu-like symptoms, shock, ARF, thrombocytopenic purpura
Isoniazid - Rash, peripheral neuropathy, hepatitis
Pyrazinamide - Rash, hepatitis, arthralgia
Ethambutol - Optic neuritis

Continuation Phase
(4 months)


LO 7.9 Describe the mechanisms of drug resistance in TB (Molecular mechanisms and causes)

There is a rising trend of Multidrug-Resistant TB (MDRTB). About one in a million bacilli are spontaneously resistant.
A case of MDRTB is suggested by a history of previous incomplete treatment, residence in a country with high incidence of MDRTB or failure to respond clinically to an adequate regimen.
A regimen of several drugs at once (see above) is used in an attempt to combat resistance.


LO 7.10 Describe the role of BCG vaccination (UK regulations and issues over vaccination)

BCG Vaccine
The BCG vaccine is a vaccination against tuberculosis that is prepared from a strain of the Attenuated Live Bovine Tuberculosis Bacillus.
The bacteria retain a strong enough antigenicity to act as a vaccine for human tuberculosis.

The vaccine has a variable efficacy, depending on genetic variation of populations and BCG strains.
Efficacy only lasts 15 years at most.

UK Regulations
In the UK up until 2005 all children ages 13 were immunised along with all neonates born into high-risk groups.
Post 2005 the vaccination was only given to high-risk groups, as falling incidence of TB had reduced the vaccine’s cost effectiveness.


LO 7.11 List groups at high risk of TB in the UK

Overcrowding - Prison’s, homeless shelters
IV Drug abusers
Chronic Lung Disease (Smokers)
Ethnicity - Asians more likely
Corticosteroids / anti A-TNF antibody (Infliximab)


LO 7.12 Describe the relationship between TB and HIV infections

HIV is a major risk factor for tuberculosis.
The risk of developing TB is estimated to be between 20-37 times greater in HIV infected people than uninfected people.
TB is a leading cause of morbidity and mortality among HIV patients.


LO 7.13 Describe in broad terms the public health issues surrounding a case of TB (Including details of notification)

If TB is suspected, contact is immediately made with TB radiology. The patient goes straight into a TB clinic, with no waiting times, and is given a questionnaire and sputum samples taken.
Treatment begins within 7 days.


LO 7.14 Describe the incidence of lung cancer in different groups

o Males
Commonest male cancer
Mortality rate is around 100 per 100,000
Incidence slowly falling due to reduction in smoking

o Females
Exceeds breast cancer as a cause of death in women
Mortality rate is around 40 per 100,000
Incidence is steadily rising

o Socio-economic groups
Wide variation
Rate three times higher in lowest compared with highest


LO 7.15 Give an account of the aetiological factors involved in lung cancer

Lung cancer is overwhelmingly related to smoking, with the risk being proportional to the duration of the habit and the number of cigarettes smoked. Around 90% of lung cancer in men and 80% in women are caused by smoking.

Other Aetiological Factors include:
o Asbestos exposure
o Radon exposure
o Genetic factors
o Dietary factors


LO 7.16 Describe the typical pattern of symptoms reported by patients with lung cancer

Primary Tumour
Chest pain
Post-obstructive pneumonia
Weight loss
Lethargy / Malaise

Regional Metastases
Superior vena cava obstruction
Hoarseness (Left recurrent Laryngeal nerve palsy)
Dyspnoea (Phrenic nerve palsy)

Distant Metastases
Bone pain / Fractures
CNS symptoms (Headache, double vision, confusion etc.)


LO 7.17 Describe the common clinical signs associated with the disease and understand the structural abnormalities underlying them

Paraneoplastic Syndrome
Paraneoplastic syndrome is the presence of a symptom or disease due to the presence of cancer in the body, but not due to the local presence of cancer cells.
They are mediated by humoral factors (cytokines and hormones) secreted by tumour cells, or the immune response against tumour cells.

o Endocrine
Cushing’s syndrome
o Neurological
Peripheral neuropathy
o Skeletal
Finger clubbing
Disseminated Intravascular Coagulation (DIC)
o Other
Nephrotic syndrome
Anorexia or cachexia


LO 7.18 Understand the imaging techniques used in the diagnosis and staging of the disease

Imaging investigations of various types are central to both the diagnosis and assessment of the disease (staging). Staging is one of the most important determinants of treatment and prognosis.
o First clinical suspicion
Plain Chest X-Ray
o Diagnosis and staging
CT scan
PET scan
Isotope bone scan

There are two staging systems for Lung Cancer: Number and TMN


Describe the TNM staging system for Lung Cancer

TNM Staging System

T – Size and position of tumour
o T1 – Cancer contained within lung (<3cm diameter)
o T2 – Cancer has grown (3-7cm diameter)
Into main bronchus <2cm from the carina
Into the visceral pleura
Made part of the lung collapse
o T3 – Cancer has grown (> 7cm diameter)
Invading chest wall, mediastinal pleura, diaphragm, pericardium
Complete lung collapse
> 1 cancer nodule in the same lobe of lung
o T4
Cancer invading mediastinum, heart, major blood vessel, trachea, carina, oesophagus, spine, recurrent laryngeal nerve
Cancer nodules in more than one lobe of the same lung

N – Lymph node involvement
o N0 – No cancer in lymph nodes
o N1 – Cancer in lymph nodes nearest the affected lung
o N2 – Cancer in lymph nodes in mediastinum, on the same side
o N3 – Cancer in lymph nodes on the opposite side of the mediastinum / supraclavicular lymph nodes

M – Metastases
o M0 – No evidence of distal cancer spread
o M1 – Lung cancer cells in distant parts of the body, such as pleura, opposite lung, liver or bones etc


Describe the Number Staging System fro lung cancer

Stage 1 – Small cancer, localised to one area of the lung
Stage 2 and 3 – Larger Cancer, may have grown into surrounding tissues (lymph nodes)
Stage 4 – Cancer has metastasised


LO 7.19 Describe the common methods used to obtain material for histological diagnosis

Tissue for diagnostic purposes is usually obtained either by bronchoscopy, needle biopsy of the lung or Surgical biopsy.
Making a histological diagnosis is important not only to confirm that the patient has lung cancer, but also to decided the cell type, which important both in terms of the prognosis and treatment.


LO 7.20 Give an account of the histology and classification of common lung tumours

Lung tumours are divided into two groups depending on the presence or absence of cells:
o Non-Small Cell Lung Cancer
o Small Cell Lung Cancer


LO 7.21 Describe the behaviour of different histological types and their relationship to prognosis and treatment

Non-Small Cell
o More than 2/3rds have inoperable disease at presentation

Small Cell
o ¾ have metastatic disease at presentation

Prognosis Depends On:
o Cell type
Small Cell worse than Non-Small Cell
o Stage of disease
o Performance status
o Biochemical markers
o Co-morbidities
E.g. Cardiac or chronic respiratory disease


LO 7.22 Describe in outline the different treatments available and how they may affect survival

o Surgery
Mostly Non-Small Cell (<20% operable)
o Radiotherapy
Radical – Curative
Palliative – Symptom control
o Chemotherapy
Small cell – Potentially curative (Minority)
Non small cell – Modest survival increase, symptom control
o Combination therapy
Combination of chemo and radiotherapy
o Biological targeted therapies
E.g. EGFR and VEGF
o Palliative care

Management of Non-Small Cell Lung Cancer
Usually involves multiple modality therapy:
o Palliative Radiotherapy for local symptoms
o Chemotherapy – 50 – 60% response rates.
o Combination Therapy – Important in locally advanced disease
o Targeted Agents – EGFR and VEGF

Management of Small Cell Cancer
o Rarely operable
o Combination Therapy – Responds well, adding ~1 year
o Palliative Chemotherapy for symptoms
o Death from cerebral metastases common


LO 8.3 Estimate the Cardiac Index (Cardiothoracic ratio)

The widest part of the heart and ribcage are measured laterally. If the heart is over 50% of the width of the thorax, it is enlarged.


What is Pneumoperitoneum

Lungs are normal on XRAY, but air is seen under the diaphragm. This is a sign of bowel perforation.


What does Lung Hyper-expansion look like on XRAY and what can cause it

COPD can lead to hyperinflation of the lungs. This leads to blunting of both costophrenic angles, and flattened hemidiaphragms.


Asbestos Plaques on XRAY

Calcified asbestos related pleural plaques have a characteristic appearance, and are generally considered to be benign.

They are irregular, well defined and classically said to look like holly leaves.


What does Tracheal Displacement look like on an XRAY and what causes it?

If the trachea is genuinely displaced to one side (the patient is not rotated) try to establish if it has been pushed or pulled by a disease process.

Anything that increases pressure or volume in one hemithorax will push the trachea and mediastinum away from that side.
(E.g. Tension pneumothorax, pleural effusion, tumour)

Any disease that causes volume loss in one hemithorax will pull the trachea over towards that side.
(E.g. collapsed lung, fibrosis)


Tension Pneumothorax on XRAY

If there is tracheal or mediastinal shift away from the pneumothorax, the pneumothorax is said to be under tension. This is a medical emergency.

Trachea is pushed away by air in the pleural cavity.


Pneumothorax causes

A pneumothorax forms when there is air trapped in the pleural space. This may occur spontaneously, or as a result of underlying lung disease. The most common cause is trauma, with laceration of the visceral pleura by a fractured rib.


Pleural effusion XRAY

A Pleural effusion is a collection of fluid in the pleural space. Fluid gathers in the lowest part of the chest, according to the patient’s position.

If the patient is upright when the X-ray is taken, a pleural effusion will obscure the Costophrenic angle/Hemidiaphragm.

If a patient is supine, a pleural effusion layers along the posterior aspect of the chest cavity, and is difficult to see on a chest X-Ray.

Pleural effusions appear on X-rays as uniformly white, with a concave area at the top. This is called the Meniscus sign.


Lobar Collapse XRAY

Displacement of the horizontal fissure is an indicator of lobar collapse.

If there is volume loss of the right upper lobe (e.g. collapse), the horizontal fissure is displaced upwards.

If there is volume loss of the right lower lobe (e.g. collapse), the horizontal fissure is displaced downwards.


What is Interstitial Lung Disease

The Interstitial space is a potential space between alveolar cells and the capillary basement membrane, which is only apparent in disease states, when it may contain fibrous tissue, cells or fluid.


Interstitial Lung Disease pathophysiology

o The development of fibrous tissue in the Intersticium, making lungs less compliant, producing a restrictive ventilatory defect.

o Airway resistance is NOT increased. In fact, the FEV1/FVC ratio can be > 70%, due to the increased radial traction on the airway, which keeps the airway open.

o Lengthening of the diffusion path between alveolar air and blood impairs gas exchange, with oxygen uptake being affected selectively, as CO2 diffuses much more readily.


Interstitial Lung Disease Clinical Features

o Shortness of breath, reduced exercise tolerance, dry cough

o Tachypnoea, tachycardia, reduced chest movement (bilaterally) and coarse crackles. Cyanosis and signs of right heart failure may be present. Clubbing is seen in cryptogenic fibrosing alveolitis.


Fibrosing Alveolitis

o Progressive inflammatory condition, unknown cause
o Relatively rare, 3-5 cases per 100,000. Two times more common in males
o Histologically there are increased activated Alveolar Macrophages
Attract Neutrophils and Eosinophils
Local lung damage due to ROS and proteases
Tissue destruction and fibrosis
o Patients report progressive shortness of breath on exercise, often with non-productive cough.
o Most patients have finger clubbing
o Chest X-Ray shows small lungs with micro-nodular shadowing predominating in the lower loves, with ragged heart borders
o Can be restrained by treatment with high dose oral steroids in the early stages, less effective once fibrosis has developed
Effectiveness of treatment is monitored by repeated lung function tests


Extrinsic Allergic Alveolitis

o Inhalation of organic material triggers an allergic reaction in alveoli and bronchioles.
o Condition may be Acute or Chronic:

o Sudden onset, rapidly progressing
o Farmer’s Lung
Antigen = Thermophillic actinomycetes found in mouldy hay
Influenza like illness 4-9 hours later with a dry cough and breathlessness on exertion
Fine mid and late inspiratory crackles
May be a wheeze

o Bird Fancier’s Lung
Long Term Antigen Exposure = Pigeons / budgerigars
Insidious malaise (feeling particularly unwell)
Dry cough and breathlessness over months and years
Inspiratory crackles
o Finger clubbing does not occur in either Acute or Chronic.
o Acute disease chest x-ray shows diffuse micro-nodular infiltrate denser towards the hila.
o Chronic disease chest x-ray may be almost normal, progressing to fibrosis in late disease.
o Lung function tests will show reduced compliance and reduced gas transfer.



o Inhalation of asbestos fibres, disease often develops long after the exposure.
o Asbestosis inhalation is associated with three forms of disease (along with a marked increase in lung cancer):
Benign pleural plaques
Asbestosis (pulmonary fibrosis)
o Asbestos fibres that penetrate to the alveoli produce alveolitis
Influx of macrophages produces characteristic asbestosis bodies
Alveolitis progresses to fibrosis
o History of asbestos exposure
o Patient breathless on exertion and a dry cough.
o Inspiratory crackles at the lung bases, which rise as the disease advances.
o No treatment
o Lung function tests show small lungs, reduced compliance and impaired gas transfer



o Disease of unknown cause, characterise by Non-Caseating Granulomas (Non-necrotising) in multiple organs and body sites
o Most commonly in the lungs
o Fluid is collected by lavage of the airways, and alveoli contain lots of cells, including macrophages and lymphocytes
o Commoner in Afro-Caribbean and Asians than in Caucasians - Genetic predisposition
o Highest incidence in 30’s and 40’s with more female cases
o Often asymptomatic, but may have Cough, breathlessness
o Grading system 0 – 4
o X-ray shows miliary and nodular shadowing and diffuse fibrosis
o Stages 1 – 3 steroids are usually effective in suppressing the disease
o Lung function tests show small lungs, reduced compliance and impaired gas transfer. May be evidence of air flow obstruction.


LO 8.11 List a number of occupational lung diseases and the environmental factors associated with each

Lab Worker - Rat urine

Diffuse fibrosis
Boiler/Pipe Laggers - Asbestos
Railway/Construction - Asbestos

Nodular Fibrosis (E.g. pneumoconiosis)
Coal Miner - Coal Dust
Miner - Silican
Demolition - Asbestos

Farmer - Fungal spores from hay
Pigeon Fancier - Avian antigens


LO 8.12 Describe the typical X-Ray picture of patients presenting with Fibrosing Alveolitis

Small lungs
Micro-nodular shadowing (Lower lobes)
Ragged heart borders


LO 8.12 Describe the typical X-Ray picture of patients presenting with Extrinsic Allergic Alveolitis

Micro-nodular infiltrate, denser towards the hila.


LO 8.12 Describe the typical X-Ray picture of patients presenting with Extrinsic Allergic Alveolitis

Almost normal, progressing to fibrosis in late disease


LO 8.12 Describe the typical X-Ray picture of patients presenting with Sarcoidosis

Miliary and Nodular shadowing
Diffuse fibrosis


LO 8.12 Describe the typical X-Ray picture of patients presenting with Asbestosis

Plaques – See above (Holly leaf)


LO 8.13 Describe the structure of the visceral and parietal pleura, and the functions of pleural fluid

The pleura is a serous membrane consisting of a single layer of mesothelial cells with a thin layer of underlying connective tissue.
The Parietal Pleura lines the inside of each hemi thorax (the bony thoracic cage, diaphragm and mediastinal surface) and becomes continuous at the hilum of the lung with the Visceral Pleura, which lines the outside of the lung. The visceral pleura extend between lobes of the lung into the depths of the oblique and horizontal fissures.

Pleural Cavity
The pleural cavity, or space, is a potential space between the two layers of pleura that are continuous at the hilum.
Both layers of pleura are covered with a common film of fluid produced from the parietal surface and absorbed by the parietal lymphatic vessels.
The pleural fluid allows the two layers to slide on one another, thus in health the pleura allows movement of the lung against the chest wall while breathing.

The surface tension of the pleural fluid provides the cohesion that keeps the lung surface in contact with the thoracic wall. As a result, when the thorax expands in inspiration, the lung expands along with it and fills with air.

The lungs do not occupy all the available space in the pleural cavity, even in deep inspiration.


LO 8.14 Describe the factors influencing the formation and reabsorption of pleural fluid

Pleural Fluid

o 15ml turnover per day (Can increase to 300ml)

o Produced by Capillary Filtration at the Parietal Pleura (Starling Forces)
Increased Lung interstitial fluid increase
Increased Hydrostatic Pressure (E.g. heart failure)
Increased Permeability (E.g. inflammation, spesis or malignancy)
Decreased Oncotic Pressure (E.g. liver failure)

o Absorbed via lymphatic drainage
Decreased Lymphatic blockage
Increased Systemic venous pressure


LO 8.15 Define the term ‘Pleural Effusion’ and distinguish the terms haemothorax, chylothorax, empyema and simple effusion

Pleural Effusion

Any collection of extra fluid in the pleural space is known as a ‘Pleural Effusion’.

Blood – Haemothorax

Chyle (Lymph with fats in it) – Chylothorax

Pus – Empyema

Serous Fluid – Simple Effusion


LO 8.16 State the difference between an exudate and transudate, and the main conditions leading to each in the case of pleural effusion

Simple pleural effusions (Serous Fluid) is further characterised by protein content:
Transudates have low protein content – < 30g/Litre
Exudates have high protein content – > 30g/Litre

o Increased Hydrostatic Pressure
Cardiac Failure
o Decreased capillary Oncotic Pressure
Nephrotic Syndrome
o Increased capillary Permeability

o Neoplasms
Cancer involving pleural surface
Secondary’s from breast, lung, ovarian, GI, lymphoma
Primary tumour of pleura
o Infection
Pneumonia, TB
o Immune Disease
Connective tissue diseases (RA, SLE)
o Abdominal Disease
Pancreatitis (Diaphragmatic inflammation)
Ascites (Transverse the diaphragm)
Subphrenic abscess


LO 8.17 Describe the characteristics of pleurisy and its major causes

Pleurisy, or pleuritis, is an inflammation of the pleura.
o Sharp Pain on inspiration
o Pain worse with coughing, sneezing, laughing etc.
o Patients take small breaths, and hold affected side of chest
o Involvement of diaphragmatic pleura causes pain in the shoulder on the same side (Referred pain)
o Characteristic physical sign is Pleural Rub, a creaking noise heard through a stethoscope with respiratory movements

Causes of Pleurisy:
o Infection is the most common cause
o Autoimmune
o Lung Cancer
o Pneumothorax
o Pulmonary Embolism

Pleural Fibrosis
Unabsorbed pleural effusion may lead to fibrosis of the pleura.
A small degree of thickening has no effects, but wide spread fibrosis restricts expansion, with a measurable reduction in lung volumes and compliance.

Pleural Tumours
o Secondary deposits of tumours are not uncommon in the pleura.
o The commonest primary tumour is a malignant mesothelioma.
o Almost all victims exposed to asbestos 20 – 40 years before
o Early symptoms are lose of pleural effusion, but with a duller pain
o Signs are that or a large pleural effusion


LO 8.18 Describe how, in principle, congenital abnormalities, injury, motor and neurological diseases may affect breathing

Chest Wall Abnormalities

Deformation of the ribs, sternum and thoracic spine
o Sternal abnormalities (E.g. Pectus Carcinatum/excavatum) rarely produce functional impairment, just cosmetic
o Scoliosis and kyphosis may produce significant function impairment of the thoracic cage
Acquired abnormalities:
o Trauma producing broken ribs, possible pneumothorax
o Some old patients may have had surgery for TB, designed to collapse their lung

Muscle and Neurological Disease
The muscles involved in breathing may be affected by generalised muscular diseases, such as muscular dystrophy or by neurological disease such as motor neurone disease or polio.
Muscle weakness produces respiratory failure with lower resistance to respiratory tract infections because of poor clearance of secretions.


Chronic Effects of Respiratory Failure

CO2 retention
o CSF acidic corrected by choroid plexus
o Initial acidosis corrected by the kidney
o Reduction of respiratory drive
o Persisting hypoxia

Right Heart Failure (Cor pulmonare)
o Effect of hypoxia on pulmonary arteries -> Pulmonary hypertension

o Chronic respiratory failure is severely disabling


Management of Respiratory Failure

o Oxygen therapy
o Removal of secretions
o Assisted ventilation
o Treat acute exacerbations


What are the Paranasal Sinuses

The paranasal sinuses are air-filled extensions of the respiratory part of the nasal cavity into cranial bones (Frontal, Ethmoid, Sphenoid and Maxilla).
The sinuses are named according to the bones in which they are located.


Describe the Frontal Sinuses and where they drain

The Right and Left Frontal Sinuses are between the outer and inner tables of the frontal bone, posterior to the superciliary arches and the root of the nose. They are usually detectable in children by 7 years of age. They each drain through a Frontonasal Duct into the ethmoidal infundibulum, which opens into the semilunar hiatus of the Middle Nasal Recess.


Describe the Ethmoidal Cells (Sinuses) and where they drain

The Ethmoidal cells (Sinuses) are small invaginations of the mucous membrane of the middle and superior nasal recesses into the Ethmoid bone.
The Ethmoidal cells usually are not visible in plain radiographs before 2 years of age.

The Anterior Ethmoidal Cells drain directly or indirectly into the middle nasal recess through the ethmoidal infundibulum.
The Middle Ethmoidal Cells open directly into the middle nasal recess.
The Posterior Ethmoidal Cells open directly into the superior nasal recess.


Describe the Sphenoidal Sinuses and where they drain

The Sphenoidal Sinuses are located in the body of the sphenoid and may extend into the wings of the bone.
The body of the sphenoid is fragile, and only thin plates of bone separate the sinuses from several important structures (Optic nerves and chiasm, the pituitary gland, internal carotid arteries). They drain directly into the Sphenoethmoidal Recess.


Describe the Maxillary Sinuses and where they drain

The Maxillary Sinuses are the largest of the paranasal sinuses. They occupy the bodies of the Maxillae. They drain by one or more openings, the Maxillary Ostium (ostia), into the middle nasal recess by way of the semilunar hiatus.


Describe Lymph Node Tuberculosis

More common in children, women and Asians. It is often painless, and occurs most commonly in the neck.
Osteo-articular TB
TB burrows into bone.
o Tuberculous Spondylitis
Most common form of oesteoarticular TB
Starts in sub-chondral bone and spread to vertebral bodies and joint space, before following the longitudinal ligaments, anterior and posterior to the spine.
Mainly occurs in the lower thoracic and lumbar spine, but can be very high (Cervical tuberculosis)
Parapledia and quadriplegia occurs in 25% of cases
o Poncet’s Disease
Aseptic polyarthritis
Knees, ankles and elbows


Describe miliary Tb

Miliary Tuberculosis
o Bacilli spreading through the blood stream
o Either during primary infection or as reactivation
o Lungs are always involved
Even spread throughout both lungs, as it is in the blood
Many visible through the lungs on an X-Ray
o Headaches suggest meningeal involvement
o Few respiratory symptoms
o Ascites may be present
o Retinal involvement in children