Resp Flashcards
Describe how the structure of the nose is conducive to warming, humidifying and filtering/trapping particles in inspired air
Warming:
- Good blood supply close to the mucosal membrane
- Conchae cause turbulence and slow down airflow.
Humidifying:
- Mucous and blood keeps the area warm
- Conchae cause turbulence and slow down airflow.
Filtering/ trapping particles:
- Hairs
- Mucous
Describe how the structure of the paranasal sinuses are conducive to warming, humidifying and filtering/trapping particles in inspired air
Warming:
-Good blood supply
Humidifying:
-Goblet cells produce mucous
Filtering/trapping particles:
-Mucous traps particles
Name the paranasal sinuses?
Maxillary
Ethmoidal
Frontal
Sphenoidal
What is the name of the muscle that connects the two cartilaginous rings together of the trachea and what is the function?
Trachealis muscle
Pull the rings together to constrict the trachea to increase the air pressure in the lungs for example during a cough
The airways are separated into two areas, what are they called?
Conducting airway and respiratory airways
What is included in the conducting airways?
Trachea Primary Bronchi Secondary Bronchi - lobar bronchi Tertiary bronchi - segmental bronchi Bronchioles Terminal bronchioles
What is included in the respiratory airways?
Respiratory bronchioles
Alveolar ducts
Alveoli
What part of the respiratory system is extrapulmonary and intrapulmonary?
Extrapulmonary: Nasal Cavity Pharynx Larynx Trachea Primary bronchi
Intrapulmonary: Secondary bronchi - lobar bronchi Tertiary bronchi - segmental bronchi Bronchioles Terminal bronchioles Respiratory bronchioles Alveolar ducts Alveoli
Explain why hoarseness of voice/ voice change may be a sign of intra-thoracic disease?
Left recurrent laryngeal nerve innervates the intrinsic laryngeal muscles except cricothyroid.
The route of the recurrent laryngeal nerve is:
Originates from the left vagus nerve as it passes over the arch of the aorta inferior to the left superior intercostal vein. It passes medially and posteriorly deep to the ligamentum arteriosum before curving inferior to the arch of the aorta. It then passes superiorly over the left main bronchus to ascend in the groove between the left side of the trachea and the anterior of the oesophagus.
Branches: mucosa of upper oesophagus, inferior thyroid artery, inferior thyroid veins. Paratracheal lymph nodes, parathyroid glands, lateral lobe of thyroid gland, cardiac and tracheal branches.
At the level of the thyroid gland it passes beneath the inf border of cricopharyngeus to run deep to it and sup towards the pharynx and larynx.
If there is pathology in any of the areas of the route of travel then there could be effects seen in the terminal branches of the larynx.
Describe the structure of the bony thorax?
12 Thoracic vertebrae 12 ribs:1-7 attached ribs 8-12 false ribs 11-12 floating ribs 1 sternum
Superior thoracic aperture is where the lungs stick out of the top of the ribs.
Inf thoracic aperture is the location of the diaphragm
Sternum:
Manubrium
Body
Xiphoid process
Costal cartilage connect the rib bones to the sternum.
Parts of the rib post to ant:
Head -> Neck
Costal groove on the inside separate the sup and inf part of the rib.
Crest separates the facet joints of the head of the rib.
Joints: Thoracic vertebrae: Demifacets on each. Sup demifacet of T2 and Inf demifacet of T1 will articulate with Rib 1 etc. Articular facet of rib articulates with transverse costal facet of the vertebrae.
Thoracic vertebrae is connected with a rib by superior costotransverse ligament and lateral costotransverse ligament.
Describe rib movements during respiration?
Bucket handle movement.
During inspiration:
Ribs move up and out to increase thoracic volume and decrease pressure. Lateral and anterior dimensions increase.
During expiration:
Ribs move down and in to decrease thoracic volume
Describe the intercostal muscles, their nerve supply and actions in respiration?
3 layers of intercostal muscles:
External intercostal membrane above the muscles.
External m. - direction of fibres: obliquely, inferiorly, post to ant
Action: inspiration - contraction brings ribs up and out. Expiration - relaxed.
Internal m. - direction of fibres: Obliquely, inferior, ant to post
Action: forced expiration they will contract bringing ribs down and in
Innermost m. - direction of fibres: Obliquely, inferiority, ant to post
Action: forced expiration they will contract bringing ribs down and in
Nerve supply: Major bundle below costal groove -intercostal nerve between each rib bundled with intercostal artery and vein. Minor bundle (collateral branches) run slightly above the rib.
Describe the diaphragm, their nerve supply and actions in respiration?
Nerve supply: Phrenic nerve
Action is contraction to increase thoracic volume during inspiration.
Expiration relaxation
Musculophrenic artery, inferior phrenic artery, pericardiacophrenic arteries - supplies the diaphragm muscle.
Central tendon of diaphragm - is the middle portion of the diaphragm.
Describe the course of the intercostal nerves, arteries and veins
Intercostal nerve is a branch off the spinal column from the ventral ramus- sympathetic nerve.
Major branch - run beneath costal groove
Minor branch - runs above costal groove
Major and minor branches both have intercostal arteries and veins in them.
Dual blood supply to intercostal muscles therefore increasing risk of blood loss if there is damage.
Anterior perforating branches of intercostal vessels and ant. cutaneous branch of intercostal nerve cover the anterior portion of the muscle and come over to the skin.
Lateral branches of the intercostal nerve and vessels come out the sides to cover the lateral portion of the area.
Blood goes up and down the thoracic cavity in the anterior part next to the body of the sternum called internal thoracic artery and vein.
Blood goes up and down the thoracic cavity in the posterior part ant to the vertebrae called posterior intercostal artery and vein.
They vessels run between the internal and innermost intercostal muscles.
How would you insert a chest drain/ pleural tap and avoid damaging any neurovascular supply to the surrounding tissues?
Insert slightly above the rib as this is where there is a less risk of damaging important neurovascular supplies.
At what vertebral level do the following pass through the diaphragm:
Vena cava
Oesophagus
Aortic hiatus
Vena cava - T8
Oesophagus - T10
Aortic hiatus - T12
What is the venous drainage of the ribs?
Left T1 - T3 = goes into superior vena cava at T2
Left T4 - T8 = Accessory hemiazygous vein L side which then crosses over to R side into the azygous vein
Left T9-T12 = hemiazygous vein on L side then crosses at T9-T10 into the azygous vein
Right T1 - superior vena cava at T1-T2
Right T2-T4 = Into opening of the azygous vein into the SVC at T4
Right T5-T12 = Azygous vein
What nerves roots innervate the diaphragm?
C3/4/5
Keeps the diaphragm alive
What is the part of the lung called where the trachea bifurcates?
Carina
What separates the lobes of the lung?
Fissures
Right lung - Transverse fissure and oblique fissure
Left lung - oblique fissure only as there are only 2 lobes.
Describe the pleural cavity and pleura incl nerve supply and role of pleural fluid and seal in lung expansion?
2 layers of pleura: visceral pleura and Parietal pleura. It is a potential space.
Between there is 10ml of serous fluid that acts as lubricant to allow easy chest expansion. Surface tension creates a seal which ensures that when the thorax expands on inspiration the lungs expand too.
Visceral pleura is on the surface of the lung and the parietal is on the surface of the thorax. Visceral pleura has somatic innervation and so is painful to pierce or irritation occurs.
Describe the blood supply to and from the lungs
Pulmonary trunk - right and left pulmonary arteries.
Left (2) pulmonary veins
Right (3) pulmonary veins
Blood supply to the lungs for its own blood supply = Superior left bronchial artery + inferior left bronchial artery
Right bronchial artery - branch from right third posterior intercostal artery
On surface markings what is the height of the diaphragm at rest?
Right side up to 5th rib (higher) and left side up to 5th intercostal space (lower) in the mid-clavicular line
Describe in simple terms in relation to the trachea what happens in a tension pneumothorax as seen in an x-ray?
Tracheal deviation
Black areas where the lung should be - due to air entrapment
Lung would be scrunched up in the middle where the air has been removed
What is the gap between the diaphragm and the ribs at the base of the thorax called?
costo-diaphragmatic recess
Peripheral gutter around the outer edges of the diaphragm into which only the parietal pleura extends.
How does the epithelium change in the respiratory system?
Nasal cavity - Bronchioles= pseudostratified ciliated epithelium with goblet cells
Terminal bronchioles = simple columnar epithelium with cilia and club (clara) cells but no goblet cells
Respiratory bronchioles - alveolar ducts = simple cuboidal epithelium with a few sparsley scattered cilia and club (clara) cells.
Alveoli - simple squamous/ type 1 (+septal/type 2) cells.
How does the cartilage change in the respiratory system?
Trachea - cartilage rings encircle the lumen anteriorly - semi-circle rings.
Sec and tertiary bronchi - cartilages arranged as irregular crescent plates or islands rather than rings
Bronchus-bronchioles - small diameter bronchis with cartilage reduced to small islands
Bronchiole - no subepithelial cartilage
What is contained in the secretions of the epithelium and submucosal glands of the trachea and bronchi?
Mucins, water
Serum proteins
Lysozyme (destroys bacteria)
Antiproteases (inactivated bacterial enzymes)
Lymphocytes contribute immunoglobulins (esp IgA)
Why is the absence of cartilage in walls of bronchioles problematic and in which condition specifically?
Air passages constrict and almost close down when smooth muscle contraction becomes excessive. Such bronchoconstriction can become excessive in asthma and cause more difficulty with expiration than inspiration (during expiration the bronchial walls are no longer held open by the surrounding alveoli - by traction.
When do clara cells become apparent in the respiratory tract?
Bronchioles get smaller and goblet cells give way to club cells interspersed between ciliated cuboidal cells.
Club cells secrete a surfactant lipoprotein, which prevents the walls sticking together during expiration.
What are the connections of an alveolus?
Respiratory bronchiole
Alveolar duct
Alveolar sac
Another alveolus (via an alveolar pore)
Why are alveoli good at their function?
Abundant capillaries
Supported by a basketwork of elastic and reticular fibres
Have a covering composed chiefly of type 1 pneumocytes
Have a scattering of intervening type 2 pneumocytes
What cells of the respiratory tract produce the surfactant?
Type 2 pneumocytes
What is the shape of the type 1 and 2 pneumocytes?
Type 1 - squamous - 90%
Type 2 - cuboidal - 10%
Describe what happens in emphysema?
Destruction of alveolar walls and permanent enlargement of air spaces which can result from smoking or alpha-1antitrypsin deficiency.
Alveolar walls normally hold bronchioles open, allowing air to leave the lungs on exhalation.
When these walls are damaged, bronchioles collapse making it difficult for the lungs to empty. Air becomes trapped in the alveoli.
What is chronic bronchitis?
Productive cough that lasts for 3 months of the year and for at least 2 years in a row. Infection of the bronchi.
(Acute bronchitis is inflammation that is temporary and lasts up to 3 weeks)
What is pneumonia and what are the common bacteria causing is?
Inflammation of the lung caused by bacteria. The lung consolidates as the alveoli fill with inflammatory cells.
Most common organism is strep pneumoniae
Others: Haemophilus influenzae, Staph. aureus, Legionella pneumophila and Mycoplasma pneumoniae.
How could you tell the difference between bronchi and bronchioles histologically?
Bronchus - small islands of cartilage and glands in submucosa with cilia.
Bronchiole - no cartilage or glands and very few if any cilia.
Bronchus is much larger in diameter compared to the bronchiole
What structures are included in the upper respiratory tract?
Nostrils to the lower border of the cricoid cartilage of the larynx and comprises of the nose and paranasal sinuses, pharynx and larynx.
What cells line the paranasal sinuses?
Respiratory epithelium - pseudostratified ciliated columnar epithelium.
What is the name of the junction between the manubrium and the body of the sternum?
Sternal angle
What costal cartilage articulates with the sternum at the level of the sternal angle?
2nd costal cartilage
What is the area above the manubrium called?
Jugular notch/ suprasternal notch
How much of chest expansion in quiet respiration is due to diaphragm contraction?
> 70%
What defines the beginning and end of the trachea?
Beginning - lower border of the cricoid cartilage (of the larynx) in the neck and terminates by dividing into the right and left main bronchi at the level of the sternal angle
What is a bronchopulmonary segment?
Area of lung supplied by a segmental bronchus and the accompanying segemental branch of the pulmonary artery. It is drained by a segmental pulmonary vein. These segments are pyramid shaped with the apex facing towards the segmental bronchus and the base toward the lung surface
How many lobes are there in each lung?
Right lung 3 lobes and left lung 2 lobes
Where does the blood in the bronchial artery end up?
Pulmonary vein via a shunt. A small amount of blood returns via the bronchial veins which drain via the azygous vein into the SVC atrium.
What does a bronchial artery supply?
Bronchial tree (but not the alveoli) and visceral pleura with oxygenated blood.
Why in PE’s is not all the distal portion of the lung affected?
In PE’s if a clot occurs then due to the dual blood supply of the bronchial arteries some parts of the lung can be saved. The blood comes from bronchial arteries and the pulmonary arteries which anastamose at the precapillary level and capillary level (these maintain some blood supply to lung parenchyma in patients with PE’s)
What is the lymphatic drainage from the lungs?
Drain into the hilar nodes, also known as the bronchopulmonary nodes. Effects from these nodes run to tracheobronchial nodes. Enlared tracheobronchial nodes can cause widening of the carina.
What is the nerve supply to the lung?
Fibres from right and left vagus nerves and the sympathetic trunk. Parasympathetic efferent fibres from the vagus are motor to the bronchial smooth muscle (bronchoconstrictor), and secretomotor to mucous glands. The vagal afferent fibres are those for the cough reflex and some subserving pain.
The sympathetic efferent fibres are bronchodilator and vasoconstrictor.
How far does the oblique fissure on either side extend using surface markings?
Spinous process of T2 vertebra posteriorly to the 6th costal cartilage anteriorly. The surface marking of the oblique fissure approximately follows the medial border of the scapula when the arm is abducted.
What are the surface markings for the horizontal fissure?
Horizontal fissure only on Right side. Extends from the mid axillary line anteriorly along the 4th rib, to the anterior edge of the lung, separating the right upper and middle lobes.
What can cause blunting of the costophrenic angle?
Pleural effusion - fluid in pleural cavity that collects in the costo-diaphragmatic space in the upright position.
COPD when the diaphragm maybe pushed down and the lungs fail to expand - air trapping
Define and give an approximate Tidal volume
The volume of air which enters and leaves the lungs with each breath
Volume: 500ml
Define and give an approximate Inspiratory reserve volume
During normal respiration the increase in lung volume is not maximal. It is increased to the extend of the inspiratory reserve volume.
Volume: 3000ml
Define and give an approximate expiratory reserve volume
During normal respiration the decrease in lung volume is maximal and extends to the expiratory reserve volume
Volume: 1000ml
Define and give an approximate residual volume
We cannot however empty our lungs completely, so even after normal expiration a residual volume will remain.
Volume: 1200ml
Define and give an approximate inspiratory capacity
End of quiet expiration to maximum inspiration.
Tidal volume + Inspiratory reserve volume
500ml+3000ml=3500ml
Define and give an approximate functional residual capacity
Expiratory reserve volume + Residual volume
1000ml+1200ml=2200ml
The resting volume at which the elastic recoil pressure of the lung inward equals the elastic recoil pressure of the chest outwards
Define and give an approximate vital capacity
Tidal volume + Expiratory reserve volume + Inspiratory reserve volume =
Inspiratory capacity + expiratory reserve volume
500+3000+1000=3500+1000 = 4500ml
Define and give an approximate total lung volume/ capacity
Tidal volume + Expiratory reserve volume + Inspiratory reserve volume + Residual volume
500+1000+3000+1200=5700ml
What are the fixed points in the breathing cycle?
Maximum inspiration
Maximum expiration
End of quiet expiration
Define anatomical dead space
The volume in the conducting airways
Define alveolar dead space
Air in alveoli which are not perfused or are damaged also do not take part in gas exchange and ventilation of these alveoli, are wasted
Define physiological dead space
Anatomical dead space + alveolar dead space
Define and calculate pulmonary ventilation rate
Total pulmonary ventilation (aka minute volume) = tidal volume x respiratory rate
Define and calculate alveolar ventilation rate
(Tidal volume - dead space) x resp rate
Explain what is resting expiratory level
At rest, (i.e. end of quiet respiration, when the respiratory muscles are relaxed) the lung is subject to two equal and opposing forces. One is directed inwards and the other outwards.
Inward: lungs elasticity and surface tension generate inwardly directed force that favours small lung volumes
Outward: muscles and various connective tissues associated with the rib cage also have elasticity. At rest these elastic elements favour outward movement of the chest wall.
Net effect: at rest two forces balance each other and also creates a negative pressure within the intra-pleural space relative to atmospheric pressure.
Describe the mechanism of normal quiet inspiration
Contraction of muscles and the pleural seal ensure that the lungs expand along with the thorax. As the lung volume increases, the air pressure within the lungs fall below atmospheric pressure and air flows into the lungs.
Describe the role of inspiratory muscles of normal quiet inspiration
Contraction of diaphragm
External intercostal muscles expand the thoracic cavity outwards
Describe the mechanism of quiet expiration and the role of elastic recoil
Muscle contraction eases. Elastic recoil of the lung results in thoracic cavity and lung returning to the original equilibrium position. Thus quiet expiration is a passive process. The pleural fluid between the two layers has surface tension- which holds the outer surface of the lungs to the inner surface of the chest wall. It is this seal which ensure that the chest wall and lungs move together.
Explain the changes in alveolar pressure during respiratory cycle
Alveolar pressure changes but only relatively small amounts compared to the pleural pressure.
The pressure during inspiration becomes more negative compared to atmospheric pressure which then forces air into the alveoli for the first part but as the time goes along the pressure equilibriates with the pleural pressure till it reaches the end of inspiration. Then at expiration the pressure of the alveoli become positive compared to the atmosphere which forces air out of the lungs. But this goes on for half of the duration of expiration after which the pressure starts to fall as the pressure equilibrates with the atmosphere.
Explain the changes in pleural pressure during respiratory cycle
The intrapleural pressure which is negative at rest becomes more negative during the inspiratory phase due to expansion of the thorax and returns to the resting (negative) pressure at the end of quiet expiration. The resting intrapleural pressure is -4 mmHg compared to the atmosphere and reaches -8 at the end of quiet inspiration.
During quiet inspiration what is the percentage of the muscles of respiration used and what is the split?
Diaphragm - 70%
External intercostal muscles - 30%
During quiet expiration what is the percentage of the muscles of respiration used?
None passive due to the elastic recoil
Describe the mechanism of forced inspiration and the accessory muscles of inspiration
Forced inspiration - when ventilation is increased during exercise or resistance to respiration is present - accessory muscles of inspiration are used. These are Sternocleidomastoid muscle and scalene muscles of the neck, serratus anterior and pectoralis major muscles of the chest wall
Describe the mechanism of forced expiration and the accessory muscles of and expiration
Muscles - internal intercostal muscles and abdominal wall muscles (external and internal oblique and rectus abdominus muscles).
Define the term ‘compliance of the lungs’
Stretchiness of the lungs is known as compliance.
Compliance is defined as the volume change per unit pressure change.
To stretch the lungs the elastic recoil of the lung must be overcome by: elastic tissue in the lungs and surface tension forces of the fluid lining the alveoli (surfactant).
Describe the factor which affect the compliance of the lungs?
Surfactant production by type 2 pneumocytes and the surface tension they create.
What is the lung surfactant made of in simple terms?
phospholipids and proteins with detergent properties
How does the surfactant work in the lungs?
Hydrophilic heads - inside the alveolar fluid and hydrophobic tails project into the alveolar gas. The surfactant molecules disrupt the interaction between fluid molecules on the surface thereby reducing the surface tension.
How does the surface tension of the alveolar fluid vary with the surface area of the alveolus?
Alveolus expands - surfactant molecules spread further apart making them less efficient - surface tension then increases - causing alveoli to shrink down to previous size.
Alveolus shrinks - surfactant molecules come closer together increasing their conc on the surface - more efficient to reduce surface tension - easier to expand the alveolus.
Therefore the force required to expand smaller alveoli is less than that required to expand large ones - because of the amount of surfactant.
How does the law of Laplace on bubbles affect alveoli?
Pressure = 2 x surface tension / radius
The larger the radius the lower the pressure.
Smaller radius the higher the pressure.
Surface tension increases then the pressure increases.
Pressure increases then either radius decreases or sufactant increases - in the body the surfactant amount would be constant but the effect on pressures would be different and the radius would be changing.
What would happen if there were two unequal sized alveoli connected by an airway using the law of Laplace?
Pressure = 2 x surface tension / radius.
One smaller sized alveolus would have much higher pressure and the larger sized alveolus would have much lower pressure. The smaller alveolus air would then enter the larger alveolus due to the change in pressure and then as a result collapse into the larger alveolus creating a huge air-filled space called a bullae.
What happens when we breathe in, in terms of pressure within 2 different sized alveoli?
Higher the surface tension and higher the radius the pressure would be greater.
Pressure = 2x10/5 = 4
Pressure 2x30/10=6 - higher radius higher pressure = pushes air into the smaller alveolus keeping it patent.
The amount of pressure is the same even though there was less
Describe the factors which influence airway resistance in the normal lung. Resistance = pressure/rate of flow = [8 x viscosity of air x length of tube] / Pi x (radius)^4
Resistance of a single tube increases sharply with a reducing radius.
However, the combined resistance of the small airways is normally low because they are connected in parallel over a branching structure where the total resistance to flow in the downstream branches is less than the resistance of the upstream branch. Most of the resistance to breathing is in the anatomical dead space, except when the small airways are compressed during forced expiration.
What is airway resistance?
Resistance of an airway to flow air through it
Describe how airway resistance changes over the breathing cycle
Inspiration - alveoli increase in size and so radius increases. This then causes resistance to decrease by a factor of 4 in a small margin.
Describe the `interstitial space’
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
Explain why fibrous tissue deposition in the interstitial space causes a restrictive type of lung disease (ILD)
Fibrous tissue has the following effects in the interstitium:
- Lungs stiffer - harder to expand since collagen is less stretchy than elastin fibres - lung compliance is reduced
- Elastic recoil of the lungs is increased (of elastin and collagen fibres)
- Lungs become smaller than normal
- Causes a restrictive type of ventilatory defect
- On examination chest expansion is reduced
- Thickening of alveolar walls increases distance oxygen has to diffuse. The effect on diffusion of oxygen is much greater than CO2 which is more soluble than oxygen.
What happens to inspiratory capacity, functional residual capacity and vital capacity in ILD?
Inspiratory capacity = TV + IRV = 500+3000mls. TV decreases as reduced lung compliance and IRV also decreases as smaller lungs due to the inc elastic recoil.
FRC = ERV + RV. ERV and RV dec as less compliance and expansion of the lung.
VC = ERV + TV + IRV.
The lung elastic recoil > chest wall elastic recoil. Therefore FRC will be reduced
What is respiratory distress in the newborn?
Disorder resulting in stiffer lungs - reduced compliance
RDS in the new born is caused by a deficiency of surfactant in premature babies particularly in <30 weeks old
From what age is surfactant produced?
From 32 weeks of gestation
What effect does the surfactant levels in RDS in new the born cause?
Reduced surfactant production
Higher surface tension of the fluid in the lungs
Harder to open up the alveoli when breathing in and so there are fewer alveoli open therefore no gas exchange occurring in these.
Increased effort to then breath and overcome the surface tension
Impaired ventilation
Typically babies have signs of respiratory distress (cyanosis, grunting, intercostal and subcostal recession)
What are the signs of respiratory distress?
Cyanosis, grunting, intercostal and subcostal recession
How do you treat RDS in the new born?
Surfactant replacement via an endotracheal tube
Supportive treatment with oxygen and assisted ventilation
How do you treat ILD?
Steroids to reduce inflammation and removal of cause e.g. drugs
How do you treat Emphysema?
Stop causative agent e.g smoking + steroids to reduce inflammation
LAMA+LABA would just increase airways even further which is the problem
What long acting inhalers can you use in asthma treatment?
LABA as want smooth muscle relaxation and NAC to increase secretion viscosity +/- steroids to reduce the causative agent
How do you treat RDS in the new born?
Give surfactant via endotracheal tube + Oxygen + assisted ventilation
What is the pathophysiology of emphysema?
Opposite to those of lung fibrosis
Loss of elastin and breakdown of alveolar walls causing increased lung compliance (stretchiness) and narrowing of small airways due to the loss of elastic fibres exerting an outward pull (radial traction) on the small bronchioles
Lungs are easier to expand - inc lung compliance
Elastic recoil is reduced
Lungs - hyperinflated
Airway narrowing causing an obstructive type of ventilatory defect on spirometry.
What are the symptoms of emphysema?
SOB
Reduced exercise tolerance
What is a pneumothorax?
Disorder where air enters the pleural space, with loss of pleural seal and lung collapse.
Air in the pleural space
What causes a pneumothorax?
An opening is created which allows the pleural cavity to communicate with the outside (e.g. trauma to the chest) or with the lung (spontaneous rupture of a weak area of the lung), air flows into the pleural cavity down the pressure gradient until the pressure in the pleural cavity reaches atmospheric pressure.
What is atelectasis?
Either incomplete expansion of the lungs (neonatal atelectasis) or the collapse of previously inflated lung, producing areas of relatively airless pulmonary parenchyma.
What are the main types of acquired atelectasis?
Compression atelectasis results whenever significant volumes of air (pneumothorax) or fluid (pleural effusion) accumulate within the pleural cavity
Resorption atelectasis - stems from complete obstruction of an airway. Over time air is resorbed from the alveoli which collapse.
What is the main cause of resorption atelectasis?
Bronchial carcinoma
Mucous plug
How does asthma cause airway obstruction?
Broncho constriction prevents air coming in and out of the alveoli. The bronci/oles are narrowed partly due to the excessive secretions, local oedema/ smooth muscle hypertrophy. Narrowed lumen due to the above causing an obstruction to the airways hence an obstructive picture on spirometry
How does COPD (emphysema) cause airway obstruction?
Lung compliance is increased - less elasticity to bring lungs back to normal shape. Hyperinflated lungs. Small airways elastin are destroyed - therefore less radial traction on the terminal bronchioles. Airway narrowing is the result causing obstruction.
Explain the relevance of Boyles law in ventilation of the lung
The pressure of a fixed quantity of gas at a constant temperature is inversely proportional to its volume. Pressure is measured in kPa. The higher the pressure the lower the volume.
Ventilation - inspiration and expiration.
As we inspire the volume of the lungs increases. The higher the volume the lower the pressure. Therefore gas moves from an area of high pressure to low pressure i.e. the lungs hence we inspire
Explain the concept of the ‘partial pressure’ of an individual gas in a gas mixture
Dalton’s law
In a mixture of a gases, each component gas exerts a partial pressure in proportion to its volume percentage in the mixture. Since atmospheric pressure is 101.1kPa and air contains 20.9% oxygen, the partial pressure of O2 in atmospheric air is 101.1x0.209=21.1kPa.
Calculate the partial pressures of constituent gases in atmospheric air and explain the effects of altitude upon them
pOxygen - 21.1kPa pNitrogen - 79.6 kPa pCO2 as 0.04 kPa pH2O as 0.5kPa As altitude increases there is less pressure and although the partial pressures are the same.
Explain the effect of saturated vapour pressure on partial pressure of inhaled gases such as oxygen
Evaporated water <=> dissolved H2O in liquid phase.
At equilibrium the gas mixture is saturated with water vapour, and the pressure it exerts is called the saturated vapour pressure (SVP). SVP depends only on temperature. At body temp 37 degrees the SVP of water is 6.28kPa.
In humidified air, water vapour contributes 6.28kPa which means that the rest of the gases account for 94.28kPa (101-6.28kPa). Since the other gases remain in the same proportions as in dry air the pO2 of humidified air = (100-6.28)*20.9% = 19.8kPa.
Inhaled air becomes more saturated with water vapour as it passes along the resp tract so that in a given volume of air, the percentage of O2 drops to about 20% with a drop in pO2 to about 19.8kPa.
What is meant by “partial pressure of oxygen” in blood and what are the values of it in the arteries, veins and mixed blood from the lung?
Mixed venous blood reaching the pulmonary capillaries has a pO2 of 6kPa and a pCO2 of 6kPa. After gas exchange the blood leaving the alveoli has pO2 of 13.3kPa and pCO2 of 5.3kPa which is the same as that of alveolar air. Partial pressure of oxygen in blood is the pressure exerted in the blood by oxygen
Explain why “partial pressure of oxygen” in blood is different from the “content” of oxygen in the blood.
Partial pressure in blood = alveolar partial pressure.
Henry’s law - the amount of gas that dissolves in a specific volume of liquid is proportional to the partial pressure of that gas in a gas phase and its solubility coefficient. O2 is not water soluble; Solubility coefficient is 0.01mmol/L/kPa.
Plasma = alveolar air pO2 is 13.3kPa but the content will be 0.01x13.3 = 0.13mmol/L.
Blood = amount of gas chemically bound + amount of gas in free solution.
Amount bound to Hb= 8.8mmol/L, O2 content therefore= 8.8+0.13=8.93mmol/L.
How is alveolar pO2 and pCO2 related to inspired air and mixed venous blood related to arterial blood.
Alveolar pO2/ pCO2= equilibrium between rate of uptake by blood and rate of replenishment by alveolar ventilation.
Blood at alveolar capillaries equilibrates to alveolar air therefore having the same partial pressure.
State the normal PO2 and PCO2 in alveolar air, arterial blood and mixed Venus blood
Inspired air= pO2= 21.2kPa
Alveolar air = pO2 = 13.3kPa, pCO2 = 5.3kPa
Mixed venous blood = pO2= 6kPa, pCO2 = 6kPa
Arterial blood = pO2 = 13.3kPa, pCO2 = 5.3kPa.
Inspired air is dry, alveolar air is saturated with H20.
Describe the layers making up the diffusion barrier at the air-blood interphase
Gas in alveoli Alveolar epithelial cell Interstitial fluid Capillary endothelial cell Plasma Red cell membrane 5 cell membranes, 3 layers of intracellular fluid and 2 layers of extracellular fluid.
Describe factors affecting the rate of diffusion across the air blood interphase
Diffusion solubility Distance Blood flow Oxygen concentration gradient Time RBC spend in the alveolar capillary
Name 3 diseases that cause diffusion defects in the alveoli/ blood interphase
ILD
Emphysema
Pulmonary oedema
How does ILD cause diffusion defects in the alveoli/ blood interphase?
Characterised by excessive deposition of collagen in the interstitial space. Thickening of alveolar walls. Increased diffusion distance.
How does pulmonary oedema cause diffusion defects in the alveoli/ blood interphase?
Fluid in interstitium - increased diffusion distance
How does emphysema cause diffusion defects in the alveoli/ blood interphase?
Destruction of alveolar walls - reduced elastin. Small alveoli fall into large airspaces and so reducing the total gas exchange surface area.
Explain why gas exchange depends on the partial pressure gradient across the diffusion barrier
Gases go from an area of high concentration to an area of low concentration therefore having a pressure gradient would be similar where gases would go from an area of high pressure to an area of low pressure. Solubility also has an effect on this.
Describe the role of diffusion resistance in gas exchange
Carbon monoxide is used to calculate diffusion resistance. Single maximal breath of CO and Helium. CO is used because its extreme affinity to Hb. Almost all CO in blood binds to Hb. Conc gradient for PaCO (alveoli to blood) remains the same the entire time blood remains in contact with alveolar gas. Amount of CO transferred is an estimate of the diffusion resistance of the barrier.
State and explain the difference in the diffusion rates of O2 and CO2
CO2 is 21 times faster at diffusing than O2. O2 has a much lower solubility and diffusion time compared to CO2 and so by having less being able to dissolve in the water a carrier is required whereas CO2 doesn’t require a carrier because it is so soluble in liquid.
Define Oxygen saturation (SaO2, ‘Sats’)
How much of the haemoglobin is saturated with O2. Measured as a % comparing oxy-Hb and deoxy-Hb.
Pulse oximetry only detects pulsatile arterial blood NOT venous blood.
DOESN’T say how much Hb in blood
Define Arterial PaO2 (partial pressure of oxygen)
The force exerted by O2 in blood in the arterial system after it has been oxygenated by the lungs. PaO2 = 8.93 mmol/Litre.
Define Oxygen content of blood
O2 bound + O2 dissolved. Usually 8.93mmol/Litre if the blood is exposed to 13.3kPa of O2 in the alveoli.
Draw an oxygen-haemoglobin dissociation curve, label the axes correctly and indicate the normal values of (i) alveolar pO2 (ii) capillary pO2 in a typical tissue
x-axis= PO2 (kPa)
y-axis= % saturation
Alveolar pO2 = 99% at the peak and sigmoid curve.
pO2 = 13.3kPa
Capillary pO2 in tissues= 75% sats. pO2=5.3kPa.
p50= 50% oxygen saturation the curve is at 3.6kPa.
What factors affect the oxygen carrying capacity of Hb in the alveoli and at tissues.
Hb which holds the oxygen molecule. Each Hb has 4 iron atoms and can hold 8 atoms of O2.
2,3-DPG accumulates in RBC when O2 tension is low. Binds to Hb and shifts dissociation curve to the right in both tissues and the lungs - causing low O2 sats in higher O2 kPa therefore more O2 is unloaded in the respiring tissues.
pH- higher respiring tissues have a low pH. More acidic environment. This would shift the curve to the right therefore more O2 released in these respiring tissue areas.
Temperature- higher temperature shifts oxygen sats curve to the right- more O2 released in higher pO2 therefore more released in respiring tissues.
CO2- higher levels of CO2 would also shift the curve to the right as there is more respiring tissues and so more O2 is needed at higher pO2 therefore more is released in the respiring tissues.
Does hyperventilation increase the oxygen content of the blood significantly?
No - it does not significantly effect O2 sats
Define cyanosis and explain its significance
Bluish coloration due to unsaturated Hb
Deoxy-Hb less red than oxy-Hb
Can peripheral due to poor circulation
Central (mouth, tongue, mucous membranes) due to poorly saturated blood in systemic circulation.
Problem oxygenating the blood. Centrally is worse than peripherally
What are the 2 ‘moods’ of Hb?
Relaxed and Tensed states
Low affinity - Tensed - difficult for O2 to bind
High affinity - Relaxed - easy for O2 to bind
At low PO2 what state is Hb in?
Tensed - hard for first O2 molecule to bind
As each O2 binds the molecule becomes more relaxed and binding of the next O2 molecule is easier.
Understand why anaemia causes tissue hypoxia despite normal arterial PaO2 and normal Oxygen saturation (SaO2, ‘Sats’)
Anaemia - low Hb levels in the blood.
Less Hb= less O2 carried around the body
Hypoxia - low [O2] at the tissues or body
Even at normal O2 saturation - all the Hb is oxygenated but that doesn’t mean there is enough O2 being carried around to meet the demands hence hypoxia occurs.
What disease cause local hypoxia due to reduced blood flow?
Shock = reduce blood flow - peripheral vasoconstriction can cause peripheral hypoxia
Name the diseases that cause local hypoxia due to O2 use> O2 delivery to the tissue
Peripheral arterial disease/ Raynaud’s = tissues using O2 faster than it is delivered
Up to how much of the Hb can be saturated with CO before it can cause fatality?
> 50% HbCO
Why is there a need for Hb to react to changes in temperature or pH?
Exercise increases metabolism up to 10x but CO can only go 5x. Therefore needs to be a more efficient method of O2 transfer - improved extraction at the tissues. This occurs by physical changes in Hx due to temp and pH to offload more O2.
Up to how much HbO2 can dissociate in extremely low pO2.
70% HbO2 can be given up due to temp and acidity
What is the Bohr shift?
pH effects the affinity of Hb.
Lower pH more O2 given up at higher pO2.
The shift in the sigmoid O2 sat/PO2 curve to the right is the Bohr shift.
pH promotes a tensed state so more O2 is given up as it is harder to bind O2.
How low can tissue pO2 get and explain why so low.
Tissue pO2 must be high enough to drive diffusion of O2 to cells (down conc gradient)
Can’t fall below 3kPa in most tissues.
What does the body do in tissue where the pO2 needs to get very low to supply the highly metabolically active tissues?
Higher capillary density - the lower the pO2 can fall (doesnt have to diffuse as fa)
Very metabolically active tissues have a higher capillary density
What is a typical pO2 in tissues?
5kPa depending on how metabolically active though.
How could you calculate the amount of O2 given up at tissues?
% O2 sat in Arterial blood - % O2 sat in tissues
100%-65% = 35% given up.
Arterial pO2 = 8.8mmol/L
8.8mmol/L x 0.35= 3mmol/L
What happens to oxygen content in the blood, O2 saturation and pO2 in anaemia where the lungs are functioning normally?
pO2 would be the same as it is the amount of O2 dissolved in the blood
O2 saturation would be normal
Oxygen content would be lower as there is less Hb and this accounts for 8.8mmol/L.
List the reactions of CO2 in blood
H20 + CO2 H2CO3 H+ + HCO3-
H+ + Hb HbH
Describe the buffering action of haemoglobin in red cells
Hb takes H+ and so increases the pH of the surrounding blood/ RBC.
Deoxy-Hb is a better buffer than oxy-Hb which would be the case in the tissues.
Because H+ + Hb HbH it draws more H+ from H20 + CO2 H2CO3 H+ + HCO3-. This then brings the [HCO3-] 20x greater than CO2 (25mmol/L : 1.2mmol/L)
Describe the process of transport of CO2 from tissues to lungs
CO2 enter the RBC. Carbonic anhydrase converts that with H20 to H2CO3. This then produces H+ and HCO3-. H+ reacts with Hb to make HbH. This is a reversible reaction.
CO2 is also dissolved in plasma.
CO2 also reacts with protein part of Hb forming carbamino compounds (carbamino Hb).
State the proportion of CO2 traveling in various forms from tissues to lungs
1L of plasma has 600ml plasma and 400ml of RBC. 600ml plasma = 1.33mmol/L dissolved CO2 600ml plasma = 27mmol/L HCO3 400ml RBC = 0.98mmol/L dissolved CO2 400ml RBC = 2.9mmol/L carbamino 400ml RBC = 11.69 mmol/L HCO3. Then as proportions of each in blood 600ml blood = 0.8mmol/L dissolved CO2 600ml blood = 16.19mmol/L HCO3 400ml RBC blood = 0.39mmol/L dissolved CO2 400ml RBC blood = 1.17mmol/L carbamino 400ml RBC blood = 4.66 mmol/L HCO3. Total 23.21mmol/L blood.
Most is HCO3- in plasma.
Describe the function of carbamino compounds
Carry CO2 that is bound to the protein part of the Hb
State the factors influencing the hydrogen carbonate concentration of plasma
Amount of carbonic anhydrase enzyme in the plasma (little amount anyway)
Buffering capacity of Hb (more so than pCO2)
Define hypoxia
Low amount of O2 in the blood reaching the tissues
Define hypercapnia
Rise in alveolar and hence arterial pCO2
Define hypocapnia
Reduction in alveolar and hence arterial pCO2
Define hyperventilation In terms of CO2 and metabolism
Removal of CO2 from alveoli is more rapid than its production. Ventilation increase without change in metabolism
Define hypoventilation In terms of CO2 and metabolism
Removal of CO2 from lungs is less rapid than its production. Ventilation decrease without change in metabolism
Describe the effects on plasma pH of hyper ventilation
More CO2 removed than produced
Dec alveolar pCO2
Less [CO2] in the blood
Less H+ available and therefore respiratory alkalosis/ increase in pH.
Describe the effects on plasma pH of hypo ventilation
Less CO2 removed than produced
Inc alveolar pCO2
More [CO2] in the blood
More H+ in the blood and therefore respiratory acidosis / decrease in pH
Describe the general effects of acute hypo ventilation
Respiratory acidosis occurs
CO2 is retained in the blood and so becomes more acidic
Decreased O2
Increased CO2
Describe the general effects of acute Hyper ventilation
Respiratory alkalosis occurs (Less CO2 and therefore less H+)
Decreased CO2
Increased O2
Define Respiratory Acidosis
Less CO2 removed than produced
Inc alveolar pCO2
More [CO2] in the blood
More H+ in the blood and therefore respiratory acidosis / decrease in pH
Define Respiratory Alkalosis
More CO2 removed than produced
Dec alveolar pCO2
Less [CO2] in the blood
Less H+ available and therefore respiratory alkalosis/ increase in pH.
Define Compensated Respiratory Acidosis
Respiratory acidosis occurs (more pCO2 more H+)
Kidneys reduce the excretion of HCO3 to mop up the H+ - thus restoring the ratio of [HCO3]/[Dissolved CO2] and pH to near to normal - compensated respiratory acidosis
Define Compensated Respiratory Alkalosis
Respiratory alkalosis occurs (Less CO2 and therefore less H+)
Kidneys inc excretion of HCO3 so the ratio of [HCO3]/[Dissolved CO2] returns to near normal, therefore pH is restored but buffer base concentration is reduced
Compensated respiratory alkalosis
What happens if there is a decrease in O2 but no change in CO2 on RR and then what would be the result on CO2?
Decrease O2
RR increases to bring O2 up
Inadvertently CO2 is blown off
Decrease in CO2 and Increase in O2
Define the term Metabolic Acidosis
If tissues produce acid this reacts with HCO3
Fall in [HCO3] leads to a fall in pH
Metabolic acidosis occurs
Define the term Metabolic Alkalosis
If plasma [HCO3] rises (e.g. after vomiting)
Plasma pH rises
Metabolic alkalosis occurs
Define the term Compensated Metabolic Acidosis
If tissues produce acid this reacts with HCO3
Fall in [HCO3] leads to a fall in pH
Metabolic acidosis occurs
Compensation occurs by changing ventilation
Increased ventilation lowers pCO2
Restores pH towards normal
Define the term Compensated Metabolic Alkalosis
If plasma [HCO3] rises (e.g. after vomiting)
Plasma pH rises
Metabolic alkalosis occurs
Compensation occurs by changing ventilation
Decreased ventilation raises pCO2
Restores pH towards normal
However there is a risk of hypoxia therefore a limit of compensation
Describe the acute effects upon ventilation of falling inspired pO2
Increased ventilation to bring up the pO2
Decreased pCO2 occurs as more is blown off
pH will then increase and become more alkalotic. The kidneys will try and compensate by removing HCO3 to allow more H+ to have an effect and bring the pH back to normal
Describe the acute effects upon ventilation of increases in inspired pCO2
Increased inspired CO2 would then increase pCO2 in the alveoli and therefore the blood
The body would compensate by increasing the HCO3 kept in the blood to neutralise the H+ production.
This would then change respiratory acidosis to a compensated resp acidosis.
RR should increase to try and blow off the rise in pCO2.
Describe the acute effects upon ventilation of falls in arterial plasma pH
Fall in pH = more H+
In order to remove the H+ need to remove the CO2 to then push the equation towards removing the H+ and producing more CO2. As a result RR/ Ventilation will increase
Describe the location of peripheral chemoreceptors and their nerve supply
- Carotid bodies at the bifurcation of the carotid arteries to the brain. Sinus nerve branch of the glossopharyngeal nerve (CN IX)
- Aortic bodies - Found in the arch of the aorta. Aortic nerve a branch of the vagus nerve (CN X).
Describe the response of peripheral chemoreceptors to changes in arterial pO2 and its role in the regulation of respiration
Large falls in pO2 stimulate the carotid and aortic bodies
Increased RR and HR
Change in blood flow distribution - inc flow to brain and kidney
Describe the response of peripheral chemoreceptors to changes in arterial pH and its role in the regulation of respiration
Directly activated by change in the pH of the blood. A low pH results in increased respiratory rate and tidal volume.
Describe the response of peripheral chemoreceptors to changes in arterial pCO2 and its role in the regulation of respiration
Peripheral chemoreceptors are not particularly sensitive to pCO2, needing a large change in pCO2 to stimulate them. They are not crucial for the precise regulation of respiration, due do respond quickly to large changes in pCO2.
What receptors are sensitive for changes in pCO2, pO2 and pH the most?
pCO2 and pH - central chemoreceptors
pO2 and pH - Carotid and aortic chemoreceptors
Describe the location of central chemoreceptors
Located on the ventral surface of the medulla and are exposed to CSF. They respond to a drop in pH which occurs when the arterial pCO2 rises.
Describe the central chemoreceptors response to changes in arterial pCO2 in the regulation of respiration
Arterial pCO2 changes -> CSF pCO2 changes -> pH changes. Which are sensed by central chemoreceptors. Impulses from chemoreceptors travel to the brain stem -> breathing rate changes to feedback on the loop.
Describe the roles of the CSF in the response of central chemoreceptors to changes in arterial pCO2
CSF therefore is sensitive to pH changes as it is maintained by its own [HCO3-]/[Dissolved CO2] buffer system. It contains no Hb.
CSF Dissolved CO2 is determined by arterial dissolved CO2.
Describe the roles of the blood-brain barrier in the response of central chemoreceptors to changes in arterial pCO2
BBB has free passage of CO2 but not HCO3- through it.
Describe the roles of the choroid plexus in the response of central chemoreceptors to changes in arterial pCO2
CSF HCO3- is determined by the activity of choroid plexus cells which pump HCO3- into and out of the CSF and is largely independent of plasma HCO3-.
Thus ratio of [HCO3-] and [dissolved CO2] determines the pH.
Explain the effect of prolonged elevation of pCO2 on the central chemoreceptors.
Persisting changes in CSF pH stimulate the choroid plexus to pump more HCO3- into the CSF and change [HCO3-] to bring the [HCO3-]/[dissolved CO2] ratio back towards normal
CSF pH is corrected much more quickly than blood pH because of small volume. As CSF pH is corrected, changes in ventilation driven by alteration of pCO2 disappear, and the control system is reset to operate around a different pCO2.
2 capillaries exit an alveolus but one of those capillaries is from a poorly ventilated alveolus (due to a mucous plug) how would you work out the combined blood oxygen saturation and pO2? Would it just be average of the two pO2?
Using the oxygen saturation curve you would look at the two pO2’s of each capillary leaving the alveolus. Then you would cross reference that on the curve with the oxygen saturations. The average of the two oxygen saturations should be taken. Then cross reference that on the oxygen sat curve and find the pO2 value of the two. This would give you the combined pO2 of the mixed venous blood returning to the heart.
State the normal range plasma pH
7.35-7.45
Describe the CO2/ Bicarbonate buffer system and the factors influencing pCO2 and [HCO3-]
pCO2 = RR controls this, dissolved CO2, Carbamino Hb
Renal function controls [HCO3-] more so than changes in pCO2
What effect does pH have on serum calcium salts?
Alkalaemia reduces the solubility of calcium salts, which means that free Ca2+ leaves the ECF, binding to bone and proteins
What effect does pH have on enzyme function in general (E.g. in the blood)?
Acidaemia denatures enzymes
What effect does pH have on serum potassium?
Acidaemia = inc H+. H+ moves K+ out of cells, producing hyperkalaemia which can be fatal.
Potassium is replaced by H+ in transporters on the cell membranes (K-ATPase) and so cells become acidotic and blood becomes hyperkalaemic.
What about the relationship of HCO3 and pCO2 causes a change in pH?
It is the ratio of the two that controls pH and not absolute values.
What happens if acid is produced metabolically to HCO3?
Recovery of all filtered HCO3 is insufficient to restore plasma [HCO3] so HCO3 will have to be created within the kidney. This will create H+ ions which are then excreted directly or indirectly into the urine and to avoid damaging the urinary acidity, it must be buffered by either other filtered substances or buffers created by the kidney.
What area of the kidney handles HCO3 reabsorption?
Proximal tubule - 80-90%
Thick ascending limb of the loop if Henle - 15%
Distal nephron
What transporter controls H+ excretion on the apical membrane of the kidney?
H+/ Na+ channel. H+ is excreted for N+, Na moves down its concentration gradient.
What is the reaction that produces HCO3- which then leaves the cell into the blood?
H+ reacts with HCO3- in the lumen. This produces CO2 which diffuses across into the cell (through the cell membrane). The CO2 reacts with water and the reverse reaction occurs to produce HCO3 and H again. The HCO3- is pumped out of the cell into the blood. H+ again moves through the Na+/H+ transporter causing Na to be reabsorbed and the cycle goes again.
What is the reaction in the distal nephron that is the final site for HCO3- absorption?
Through intercalated cells
H+ pumped across apical membrane by H+-ATPase pump as the Na+ ion gradient is insufficient.
What is the reaction in the distal nephron that is the final site for HCO3- absorption?
Through intercalated cells.
H+ pumped across apical membrane by H+-ATPase pump as the Na+ ion gradient is insufficient.
By this point there is little HCO3 remaining - so little CO2 enters the cell.
The CO2 used is produced by the cells own metabolism - so generating new HCO3- to enter the plasma
What buffers the excreted H+ from the urine?
Monobasic phosphate (HPO2 -4) buffers the H+ and becomes more effective as the pH of the urine falls.
How is an amino acid used to remove H+ and produce useful HCO3-?
H+ is held by ammonium ions. (NH4+).
Ammonium ions are produced from the amino acid Glutamine.
Each alpha-ketoglutorate produces 2x HCO3- which enters the blood stream and H+ is excreted.
What is the yield in the reaction with ammonium ions and glutamate producing?
Glutamine –> NH4+ + Glutamate –> NH4+ + alpha-ketoglutorate
What pH disturbance can be caused by hypokalaemia?
Metabolic alklosis
What pH disturbance can be caused by hyperkalaemia?
Metabolic acidosis . Capacity of the kidney to reabsorb and create HCO3- is reduced
Why does ECF pH fall as acid secretion increases?
Large changes in renal tubular pH consequent upon changes in the rate of export of HCO3- to plasma. HCO3- is more controlled rather than pH - which leads to changes to HCO3-.
Explain how the kidneys respond to respiratory acidaemia?
pCO2 rises in the blood. Decreased ratio of HCO3-/pCO2 (less HCO3) therefore decreased pH.
Fall in renal tubular pH induced by diffusion of extra CO2 leads to extra H+ being excreted. With consequent production and export into the plasma of HCO3-, restoring the ratio of HCO3- to PCO2 nearer to normal
Explain how the kidneys respond to respiratory alkalaemia?
Rises in tubular pH induces less HCO3- resorption by reducing H+ export and suppressing H+ secretion - so HCO3- is excreted and [HCO3-] falls, again restoring the ratio of HCO3- to pCO2 nearer to normal
Explain how the kidneys respond to metabolic acidaemia?
If excess acid produced - associated anion (e.g. lactate) will replace HCO3- in plasma which will influence the anion gap.
Broadly name causes of metabolic acidaemia
Excess metabolic production of acids, acids are ingested, HCO3- is lost or there is a problem with renal excretion of acid.
What is an anion-gap?
Difference between the sum of [Na] and [K] and the sum of [Cl-] and [HCO3-]. If HCO3- is replaced by another anion which is not included in the calculation the gap will increase.
([Na+] + [K+]) / ([Cl-] + [HCO3-] = anion gap.
What is the usual reference ranges for the anion gap?
8-14mmol/L
What is the anion gap representative of?
Unmeasured anions in the ECF (anions that aren’t routinely measured)
What does an increase in the anion gap indicate?
Inc in the percentage of one or more unmeasured anions. This occurs with acidic conditions characterised by higher organic acids present in the blood i.e. lactic acid.
If there are problems in renal excretion of H+ ions what is the result on the anion gap?
[HCO3-] will change directly without replacement by an unmeasured ion, so the anion-gap is less likely to change
Identify ‘Tidal volume’, Inspiratory reserve volume’, Expiratory reserve volume’, Residual volume’ on a spirometry tracing
^Tidal volume
——————————————
^Residual volume
——————————————
Identify ‘Inspiratory Capacity’, ‘Functional Residual Capacity’, ‘Vital Capacity’ and Total lung volume on a spirometry tracing
IRV + TV = IC
ERV + RV = FRC
TV + IRV + ERV = VC
TV + IRV + ERV + RV = TLC
Describe the measurement of forced vital capacity (FVC)
VC = TV + IRV + ERV FVC = the total amount of air exhaled during the FEV test
Describe the measurement of forced expiratory volume in the first second (FEV1.0)
Forced expiratory volume (FEV) measures how much air a person can exhale during a forced breath. The amount of air exhaled during the first second (FEV1)
Describe the measurement of the FEV1/FVC ratio
Obstructive and restrictive deficits are distinguished by measuring the ratio.
In normal individuals FEV1 >70% of FVC.
<70% indicates an obstructive deficit
≥70% indicates an restrictive deficit as it is a ratio
What is FEV?
Forced expiratory volume (FEV) measures how much air a person can exhale during a forced breath
How do you do a spirometry test?
Spirometry is a test that measures the amount of air a person’s lungs can move in and out and at what rate.
1 - The person places his or her mouth on the mouthpiece that is attached to a recording device (spirometer).
2 - The person breathes in (inhales) as deeply as possible.
3 - The person then blows out (exhales) as hard, fast, and completely as possible.
What FEV1/FVC ratio is described as an obstructive deficit on spirometry and what part of the equation would indicate a problem?
<70% = obstructive deficit
FVC = nearly normal
FEV1 = reduced markedly
e.g. if normally FEV1 = 3.3litres and FVC = 4litres
Therefore 3.3/4= 82.5%
But in obstructive FEV1 ≤2.8litres and FVC would remain the same/ nearly the same.
Obstruction prevents air leaving the airways quickly and so FEV1 would be reduced.
What FEV1/FVC ratio is described as an restrictive deficit on spirometry and what part of the equation would indicate a problem?
Restriction - due to fibrosis - less lung compliance and smaller lungs as can’t expand as much due to collagen deposition.
If reduced physical lung space = FVC would be reduced
But as you can contract the airways normally due to the increased recoil the FEV1 might be normal - therefore it is reduced proportionately.
FEV1/FVC ratio would then be normal or slightly higher than normal.
What would a typical tracing pattern of a time-volume graph look like in obstructive deficit?
x-axis - time; y-axis - volume
Technically the FVC is 4litres but it would technically never reach there.
There is a much slower increase as the FEV1 would go up to e.g. 2.8litres - then a much slower incline to reach FVC.
What would a typical tracing pattern of a time-volume graph look like in a restrictive deficit?
x-axis - time; y-axis - volume
FEV1/FVC ratio is technically the same as normal therefore the shape is the same as a normal persons.
However as there is restriction the actual FVC would be much lower and so therefore the FEV1 would also have to match proportionately.
What would a typical tracing pattern of a time-volume graph look like in a normal patient?
x-axis - time; y-axis - volume
FVC=4litres FEV1=3.3litres. Therefore rapid increase initially then a slower decline till reaches approx - 3 seconds where it hits the maximum level of 4litres of FVC.
Explain expiratory and inspiratory flow volume loops
Obstructive deficits in particular are more sensitively revealed by deriving an expiratory flow volume loop. Here expiratory flow rate is plotted against lung volume
Explain expiratory and inspiratory flow volume loops
X-axis - volume (litres) Y-axis - flow (positive and negative values in litres/ second)
Obstructive deficits in particular are more sensitively revealed by deriving an expiratory flow volume loop. Expiratory flow rate is plotted against lung volume.
VC is measured by maximal exhalation at the starting position to a maximal inhalation. This will then give a point by which the patient can then exhale which would be done as forcefully as possible up to a point of maximal exhalation or the VC is reached as it would have done.
Explain expiratory and inspiratory flow volume loops in the changes seen in obstructive
In obstructive disease the volume flow loops will show a normal FVC but FEV1 will be reduced. The graph is showing flow on the Y-axis will show a scalloping indicating that the there is a slowing down of the flow of the expiratory process. Mild obstruction - shows scalloping but severe obstruction will show a reduced peak expiratory flow rate.
On a flow volume loop what is the peak of the loop called?
Peak expiratory flow rate (PEFR)
What causes a maximal peak on the flow volume loop?
Start of expiration, when the lungs are expanded and the airways are stretched open, the expiratory flow is at its maximum
In a flow volume loop what explains the early fall in expiratory flow rate?
As expiration occurs the small airways are narrowed by compression of the lungs, and where there is small airway obstruction this narrowing produces a characteristic early fall in expiratory flow rate
Explain expiratory and inspiratory flow volume loops in the changes seen in restrictive disease
Reduced FVC but FEV1 will be normal.
The graph is showing flow on the Y-axis.
Graph will show much less air entering the lungs during the inspiration part of the loop and the graph will be normal on the expiration part of the loop.
The graph will look narrower but proportions will be the same.
PEFR will be the same
Narrow and tall flow volume loop
How would you measure residual volume?
Volumes of air remaining in the lungs after expiration may be measured by the helium dilution test
How do you measure dead space?
Nitrogen washout method
How do you measure diffusion capacity?
Diffusion conductance is the resistance to diffusion across the alveolar membrane and is estimated by the carbon monoxide transfer factor (TLCO)
What would happen to the flow volume loop in an asthmatic patient after bronchodilators?
PEFR would be normalised
FEV1 would be more than normal
FVC would be normalised
No scalloping
What would happen to the flow volume loop in a COPD patient after bronchodilators?
PEFR would be unchanged
FEV1 would be unchanged
FVC would be marginally better
What results would you expect in spirometry in an ILD patient?
FVC would be reduced and so would the FEV1 but not massively. Might even be better.
Describe, in outline, the pathophysiology, of cystic fibrosis
Autosomal recessive disease.
CFTR gene leads to reduced chloride release into the mucous membranes which become thicker.
Commonly affect respiratory system.
Describe, in outline, the diagnosis of cystic fibrosis
Sweat test - >60mmol/L of chloride in sweat
Identification of two CF mutations - genotyping
Demonstration of abnormal nasal epithelial ion transport (nasal potential difference)
Describe, in outline the clinical features of cystic fibrosis
- Meconium ileus - bowel is blocked by sticky secretions. Signs of intestinal obstruction soon after birth with bilious vomiting, abdominal distension and delay in passing meconium
- Intestinal malabsorption - most evident in infancy - severe deficiency of pancreatic enzymes
- Recurrent chest infections
- Newborn screening
Describe, in outline principles of treatment of cystic fibrosis
1 - resp infections - physio and antibiotics (Tx and prophylactic)
2 - High calorie intake meals + pancreatic enzyme replacements
3 - Laxatives
4 - CF related diabetes
5 - Avoid other CF patients
6 - Avoid people with current infections
7- Avoid jacuzzies (pseudomonas)
8 - Annual influenza immunisations
9 - sodium chloride tablets in hot weather/ vigorous exercise
Describe, in outline, the pathophysiology of bronchiectasis
Chronic dilation of the one or more bronchi
Bronchi exhibit poor mucous clearance
A predisposition to recurrent or chronic bacterial infection
Describe, in outline, the clinical features/ causes of bronchiectasis
> Post infective - whooping cough, TB
Immune deficiency - hypogammaglobulinaemia
Genetic/ mucociliary defects- CF, primary ciliary dyskinesia, Youngs syndrome (bronchiectasis, sinusitis, reduced fertility), Kartagener syndrome (bronchiectasis, sinusitis, situs inversus)
Obstruction - foreign body, tumour, extrinsic lymph node
Describe, in outline, the principles of treatment of bronchiectasis
Treat underlying cause
Physio - mucous clearance
Antibiotics - sensitivities, chronic suppressive therapy
Supportive - flu vaccine, bronchodilators PRN
Pulmonary rehab - MRC dyspnoea score ≥3
Name the organisms most commonly affecting bronchiectasis
Haemophilus influenza Pseudomonas aeruginosa Moraxella catarrhalis Fungi - aspergillus, candida Non-tuberculous mycobacteria Less common - Staph aureus (think CF)
What is the MRC dyspnoea scoring system?
Graded on breathlessness depending on the activity performed.
Scored 1-5. 1 -not troubled by breathless except on strenuous exercise
5 - too breathless to leave the house or breathless when dressing/undressing
In basic terms what is the concept of ventilation perfusion
Ventilation (V) = 4900ml/min
Pulmonary blood flow (Q) = 4900ml/min
V/Q = 1
At an alveolar level, gas exchange is optimal when alveolar ventilation and perfusion are matched.
V/Q mismatch is the most common cause of hypoxaemia
What happens if V is reduced in V/Q mismatch?
Ventilation is reduced to part of the lung
Disorders include Pneumonia, asthma, COPD, respiratory distress syndrome in the new born
Poorly ventilated alveoli have a V/Q ratio of <1 as ventilation is low compared to perfusion
What happens to V/Q mismatch due to pulmonary embolism in an example form?
Assume PE obstructed Left upper lobar (L/UL) branch of the pulmonary artery. Blood is redirected to rest of the pulmonary circulation. Alveoli of L/UL are ventilated as normal because the L/UL bronchus is patent, but no gas exchange.
Diversion creates an increased perfusion of normal parts of the lung (i.e. R lung and L/LL). These areas need extra ventilation to match V/Q back to maintain a ratio of 1.
If hyperventilation does not sufficiently increase alveolar ventilation to match the extra perfusion the V/Q will be <1 = hypoxia.
Therefore although the PE is in the L/UL artery the hypoxia arises due to V/Q mismatch in the R lung and L/LL
Is it possible to be hypoxic without being hypoxaemic?
Yes, for example in severe anaemia which reduces the oxygen carrying capacity of the blood can result in tissue hypoxia despite a normal pO2. Similarly, poor perfusion can cause hypoxia of the affected tissue (e.g. MI), despite normal gas exchange in the lungs and a normal arterial pO2.
pO2 of the blood depends on normal gas exchange in the lung
Define type 1 respiratory failure
Characterised by a low ARTERIAL pO2 (<8kPa) with a normal or low pCO2
Define type 2 respiratory failure
Characterised by a low ARTERIAL pO2 (<8kPa) with a high pCO2 of >6.2kPA (Normal pCO2 4.5-6kPa) (Normal pO2 >10.6)
Outline the important causes of ventilation/perfusion mismatch
Low inspired pO2
Hypoventilation (low pO2 high pCO2 - T2 resp failure)
Diffusion impairment
Right to left shunts
Standing up causes V/Q in apex of lungs to be 3.3 but base of lungs 0.63
Outline the important causes of ventilation/perfusion mismatch
Low inspired pO2
Hypoventilation (low pO2 high pCO2 - T2 resp failure)
Diffusion impairment
Right to left shunts
Standing up causes V/Q in apex of lungs to be 3.3 but base of lungs 0.63
Asthma (variable airway narrowing)
Pneumonia (exudate in affected alveoli)
RDS in new born (some alveoli not expanding)
Pulmonary oedema
Pulmonary embolism
Explain why ventilation/perfusion mismatch causes Type 1 respiratory failure
<8kPa pO2. Normal slightly lower pCO2.
Gas exchange is impaired at the alveolo-capillary membrane.
If there is an obstruction of the alveoli, they get perfused but do not get enough ventilation they will have a V/Q mismatch. Therefore the CO2 will be released but the O2 will not be able to diffuse across as quickly, so there will be a low pO2 and a higher pCO2. The normally ventilated alveoli will still undergo normal gas exchange.
Hyperventilation then sets in to try and inc pO2 but that alveolus is still poorly ventilated.
Unaffected segments will then have a V>Q there V/Q >1.
pO2 rises and pCO2 falls. Rise in pO2 increase dissolved O2 (small amount), Hb is fully saturated when pO2 is above 10kPa. Further inc in pO2 has not effect on Hb. O2 content not significantly inc. Insufficient to compensate for low pO2 from segments with V/Q >1.
Drop in pCO2 accompanied by reduction in total CO2 in blood. Sufficient to compensate for CO2 retention from segments with V/Q <1
What are 4 signs of hypoxia?
Impaired CNS function - fluctuating GCS
Central cyanosis - blueish discolouration due to >50gm/litre of unsaturated Hb
Cardiac arrhythmias
Hypoxic vasoconstriction of pulmonary vessels
What are 4 effects of hypercapnia?
Respiratory acidosis
Impaired CNS function - drowsiness, confusion, coma, flapping tremors
Peripheral vasodilation - warm hands, bounding pulse
Cerebral vasodilation - headache
What are 4 acute effects of hypoxia?
Impaired CNS function - fluctuating GCS
Central cyanosis - blueish discolouration due to >50gm/litre of unsaturated Hb
Cardiac arrhythmias
Hypoxic vasoconstriction of pulmonary vessels
What are 4 acute effects of hypercapnia?
Respiratory acidosis
Impaired CNS function - drowsiness, confusion, coma, flapping tremors
Peripheral vasodilation - warm hands, bounding pulse
Cerebral vasodilation - headache
What occurs in asthmatic V/Q mismatch and what is the response?
Asthma - variable airway narrowing - V/Q <1 in these alveoli
alveolar pO2 falls / pCO2 rises
hypoxic vasoconstriction occurs -> diverts some blood to better ventilated areas.
If V/Q <1 alveolar pO2 will be low and pCO2 high - mixed blood will be the same
Central and peripheral chemoreceptors stimulated -> hyperventilation
Why does a PE cause V/Q mismatch?
Embolus redistributes the blood to areas that have unaffected circulation
Leads to V/Q ratio <1 if hyperventilation cannot match the increased perfusion
Causes hypoxaemia
Hyperventilation sufficient to remove CO2
Other alveoli get more blood than ventilated hence V/Q <1 even more so
Describe how hypoventilation results in type 2 respiratory failure
When the entire lung is poorly ventilated alveolar ventilation (minute volume) is reduced
Alveolar pO2 falls -> arterial pO2 falls - hypoxaemia
Alveolar pCO2 rises -> arterial pCO2 rises - hypercapnia
Hypoventilation always causes T2 respiratory failure
Hypoxaemia secondary to hypoventilation will correct with added oxygen (does not solve hypercapnia problem though)
Outline important causes of hypoventilation that results in type 2 respiratory failure
Acute hypoventilation - Opiate overdose Head injury Very severe acute asthma Chronic hypoventilation - Severe COPD Lower respiratory tract infection End stage pulmonary fibrosis Obesity Polio Guillian-Barre Syndrome
Outline important causes of hypoventilation that results in type 2 respiratory failure
Acute hypoventilation -
Opiate overdose, Head injury, Very severe acute asthma, Guillian-Barre Syndrome, Pneumothorax, large pleural effusion,
Chronic hypoventilation -
Severe COPD, Lower respiratory tract infection, End stage pulmonary fibrosis, Obesity, Polio, Laryngeal oedema/ foreign body, Myasthenia gravis, Myopathy, Muscular dystrophy
Explain the chronic effects of hypercapnia
Chronic - Respiratory acidosis compensated by rentention of HCO3- by kidney
Acclimation to CNS effects
Vasodilation mild but may still be present - pink puffers
CO2 diffuses into CSF -> CSF pH drops -> stimulates central chemoreceptors to increase ventilation. Choroid plexus - secretes more HCO3- into CSF. CSF returns to normal pH. pCO2 in blood is still high but in CSF is now unresponsive to this pCO2.
Therefore persistent hypoxia stimulates peripheral chemoreceptors - respiratory drive is now driven by hypoxia (via peripheral chemoreceptors)
What are chronic effects of hypoxia?
- Polycytheamia (inc Hb) due to increase EPO secretion to inc O2 carrying capacity of blood
- Increase in RBC 2,3,DPG levels which allows better unloading of O2
- Hypoxia induced vasoconstriction of pulmonary arteries which eventually leads to pulmonary hypertension
- Right heart failure (cor pulmonale) due to pulmonary hypertension
What is the problem when treating hypoxia in patients with chronic type 2 respiratory failure?
Uncontrolled O2 therapy to correct hypoxia may worsen existing hypercapnia by two mechanisms:
1 - Persistent hypercapnia - choroid plexus imports extra HCO3- into CSF to restore the CSF pH to normal therefore resetting the chemoreceptors to higher CO2 levels. The hypoxic stimulus persists and respiration is now driven by hypoxia. O2 therapy corrects the hypoxia, removing the stimulus for respiration. Leading to respiratory depression, resulting in a rise in pCO2 to dangerous levels.
2 - Oxygen therapy worsens V/Q mismatch in poorly ventilated alveoli by removing the hypoxia induced vasoconstriction. This leads to increasing perfusion of poorly ventilated alveoli, diverting blood away from better ventilated alveoli.
Define asthma
Chronic inflammatory disorder of the airways. In susceptible individuals, inflammatory symptoms are usually associated with widespread but variable airflow obstruction and an increase in airway responsiveness to a variety of stimuli. Obstruction is often reversible, either spontaneously or with treatment. 5 defining characteristics: Chronic inflammatory process Susceptibility Variable airflow obstruction Airway hyper-responsiveness Reversibility
Describe the nature of the air flow obstruction in asthma
Obstruction is often reversible, either spontaneously or with treatment.
What is the difference between asthma and COPD in the responsiveness to treatment?
FEV1 in asthma will improve after bronchodilators but in COPD there is no improvement (or very little improvement)
Describe, in outline, the pathophysiology of asthma
Chronic inflammatory process driven by Th2 cells
Macrophages process and present antigens to T-lymphocytes activating T cells with TH2 cells being preferentially activated.
TH2 cells release cytokines, which attract and activate inflammatory cells, including mast cells and eosinophils. TH2 cells also activate B cells, which produce IgE.
Typically, in sensitising atopic asthma, exposure to antigen results in a 2-phase response consisting of an immediate response (reaching a max in ~20mins) followed by a late phase response (3-12hours later).
What is the ‘immediate response’ in asthma?
Example of a type 1 hypersensitivity.
It is caused by interaction of the allergen and specific IgE antibodies, leading to mast cells degranulation and release of mediators (histamine, tryptase, prostaglandin D2 and leukotrienes) which cause bronchial smooth muscle contraction leading to bronchoconstriction
What is the ‘late phase response’ in asthma?
Example of a type 4 hypersensitivity
It involves inflammatory cells, incl eosinophils, mast cells, lymphocytes and neutrophils
Release mediators and cytokines which cause airway inflammation
What is the ‘late phase response’ in asthma?
Example of a type 4 hypersensitivity
It involves inflammatory cells, incl eosinophils, mast cells, lymphocytes and neutrophils
Release mediators and cytokines which cause airway inflammation
Eosinophils release leukotriene C4 which is very toxic to epithelial cells, causing them to shed. This can be very easily controlled by steroid therapy
Describe the changes in the airways that cause air flow obstruction in asthma
Airway inflammation causes reduced airway calibre:
- Mucosal swelling (due to vascular leak)
- Thickening of bronchial walls due to infiltration by inflammatory cells
- Mucous over production that is abnormally thick and slow moving - dry cough
- Smooth muscle contraction
- Epithelium is shed and is incorporated into the thick mucous
- Hyper-responsiveness of airways to triggers.
What can happen if asthma is poorly controlled in the long term?
Airway remodelling (some of which is not reversible)
- Hypertrophy and hyperplasia of smooth muscle
- Hypertrophy of mucous glands
- Thickening of basement membrane
What is the effect of airway narrowing in asthma?
Causes an audible wheeze and other clinical features of asthma
Results in a obstructive pattern on spirometry (FEV1/FVC ratio will be <70%) and typical flow volume loops will show reversibility with bronchodilators.
Air trapping increases residual volume
Describe the types of allergens and other triggers that may precipitate episodes of asthma
Allergens - pollen, animals, house dust mite faeces
Cold air, exercise, fumes, cigarette smokes, perfumes, chemicals, drugs (NSAIDs and beta blockers), emotional distress
What 4 symptoms are indicative of asthma?
SOB Cough - dry, nocturnal - parasympathetic action on smooth muscle @ night Wheeze Chest tightness History of atopy Typically younger people/ children
How is asthma diagnosed?
Volume flow loop/ Peak flow meter/ Spirometry
What are the symptoms indicative of COPD?
Productive cough (dry cough in asthma)
Wheeze
History of smoking
Typically older adults
What is the treatment algorithm when treat a patient with a high probability of asthma
Initiate the treatment -> Assess response objectively (lung function test) -> good response -> Asthma -> Adjust maintenance dose and provide self management + ongoing review
What is the treatment algorithm when treat a patient with an intermediate probability of asthma
Test for airway obstruction -> Spirometry +bronchodilator reversibility
-> Test for eosinophilic inflammation/ atopy -> Blood eosinophils, Skin-prick test, IgE, FeNO (nitric oxide exhalation test)
AND/OR
-> Test for variability -> Reversibility, PEF chart, Challenge tests
-> Watchful waiting if asymptomatic or commence treatment and assess response objectively.
What are common signs and symptoms of acute severe asthma?
Can't speak in full sentences RR ≥25 O2 sats >92% ideally >96% PEF 33-50% reduction from best/ average HR ≥115 BPM Still hear a wheeze due to small amount of air movement
What are common signs and symptoms of life threatening asthma?
RR is reduced/ lower than normal O2 sats <92% PEF (struggling) <33% of best/ average Reduced HR Altered consciousness Silent chest on auscultation
What ABG results would you see in acute severe asthma?
pH - alkalosis
pO2 - Low/close to normal
pCO2 - Low (hyperventilation)
HCO3 - Normal (not yet had time for renal compensation)
Uncompensated Respiratory Alkalosis
Type 1 Respiratory failure as pO2 is low but pCO2 is normal/ low
How do you manage acute severe asthma?
1 - Oxygen 2 - SABA (salbutamol nebs) 3 - IV Steroids (asthma IgE mediated which respond to steroids) IV-> PO switch when stable 4 - Admit 5 - CXR to rule out pneumothorax 6- Aminophylline/ Magnesium sulphate
Describe the causes of Chronic Obstructive Pulmonary disease (COPD)
Abnormal inflammatory response of the lungs to noxious particles or gases.
2 main aetiology- Tobacco smoking - 90% of COPD, air pollution occupational exposure are other causes.
Alpha-1 anti-trypsin deficiency which is an inherited condition is less common. Alpha-1 anti-trypsin is an antiproteinase. This leads to destruction of alveolar walls and to emphysema that usually presents at an early age.
Describe the pathophysiology of COPD including the nature of air flow obstruction
Inhaled noxious substances -> Chronic inflammatory process and oxidative injury affecting central and peripheral airways, lung parenchyma, alveoli and pulmonary vasculature.
Pathology- Enlargement of mucous-secreting glands of the central airways, increased number of goblet cells (which replace ciliated respiratory epithelium), ciliary dysfunction, Breakdown of elastin leading to destruction of alveolar walls and loss of elastic recoil, formation of larger air spaces with reduction in total surface area, vascular bed changes leading to pulmonary hypertension
What 2 features describe COPD?
Emphysema and chronic bronchitis
Co-exist and are progressive and usually not reversible
What is chronic bronchitis?
Final outcome is excessive mucous secretion and impaired removal of the secretions (due to ciliary dysfunction)
What 3 ways does COPD lead to an obstructive airway problem?
1 - Luminal obstruction of airways by excess secretions
2 - Narrowing of small bronchioles which are usually kept patent by radial traction exerted on their walls by elastin in the surrounding alveoli
3 - Decreased elastic recoil leads to reduced expiratory force, hence air trapping. Expiratory flow limitation promotes hyperinflation
What is the problem with progressive hypoxia and what are the main consequences of this?
Pulmonary vasoconstriction + vascular smooth muscle hypertrophy (thickening) -> pulmonary hypertension -> right heart failure (cor pulmonale)
What are the clinical features in a COPD patients history?
Gradual onset +/- long history of smoking
Cough - usually initial symptom, frequently morning cough but becomes constant as disease progresses, usually productive cough and sputum quality may change with exacerbations or superimposed infection
SOB - occurs initially on exertion but may progress to SOB even at rest
Recurrent Lower Respiratory Tract Infections
Prolonged respiratory phase
Purse lip breathing
GORD
Pulmonary hypertension
Respiratory failure
Previous exacerbations
What are the clinical features in a COPD patients Physical Examination and why?
Tachypnoea - Compensation for hypoxia and hypoventilation.
Use of accessory muscles - due to difficulty in moving air in and out of lungs
Barrel Chest - increase AP diameter of chest due to hyperinflation and air trapping secondary to incomplete expiration
Hyper-resonance on percussion due to hyperinflation and air trapping
Reduced intensity breath sounds - caused by barrel chest, hyperinflation and air trapping
Reduced air entry -secondary to loss of lung elasticity and lung tissue breakdown
Wheezing may be present
Late features -
Central cyanosis hypoxia due to respiratory failure
Flapping tremors due to CO2 retention
Signs of right sided heart failure - distended neck veins, hepatomegaly, ankle oedema secondary to pulmonary hypertension
Describe the tests used to diagnose and assess a patient with COPD
Spirometry shows an obstructive pattern with a FEV1/FVC ratio <70% and limited reversibility following bronchodilator therapy. Time volume plots and flow volume loops show the obstructive pattern (scalloping)
Decreased diffusing capacity of the lung for carbon monoxide is a feature of emphysema.
High-resolution CT/ CXR - hyper-inflated lungs a) flattened diaphragm b) hyper-lucent lungs c) increase AP diameter. d) complications= pneumothorax, pneumonia, lung Ca
Pulse oximetry/ ABG - hypoxia, hypercapnia
Alpha-1 antitrypsin level- if positive family Hx, atypical COPD (young patient and non-smoker)
Clinically how would you differentiate between COPD and asthma?
COPD - older age, smoking Hx, no reversibility, no trigger factors, no FHx of atopy
Asthma - younger age, triggers, FHx/ Hx of atopy, daily variability in symptoms, overt wheezing rapidly responds to bronchodilators. Sputum/ blood esosinophilia is suggestive of asthma
Outline the treatment of COPD
Smoking cessation
Pneumococcal vaccination
Bronchodilators
Inhaled corticosteroids
Pulmonary rehab - Exercise, disease education and nutritional advice
LTOT- extended periods of hypoxia can cause pulmonary hypertension therefore continuous low dose oxygen for at least 16 hours a day has been shown to improve survival
Surgical intervention - Removal of large bullae, lung volume reduction, lung transplant.
Outline the treatment of acute exacerbations of COPD
Monitor for hypoxia and hypercapnia using pulse oximetry and ABG analysis
Appropriate antibiotics is CRP/ WCC - raisedparticularly to cover haemophilus influenzae and Streptococcus pneumoniae
Nebulised bronchodilators
Oral steroids (short high dose course) - is raised eosinophil count
24% or 28% oxygen therapy while keeping CO2 under review
Consider non-invasive ventilation for worsening type 2 respiratory failure
Define an acute exacerbation of COPD
An acute worsening of respiratory symptoms that result in additional therapy
Define acute infectious exacerbation of COPD
Acute, severe shortness of breath, fever and chest pain
Why do patients get polycythaemia as a complication in long standing COPD?
Increase oxygen carrying capacity due to hypoxaemia
What are the 4 main complications of COPD?
Right sided heart failure (cor pulmonale)
Recurrent pneumonia
Pneumothorax - occurs because of lung parenchyma damage with sub-pleural
What is the pitfall with measuring FEV1?
Some people have not developed lungs fully which spirometry doesn’t take into account
In which age population is COPD more prevalent?
Older population, Generally >51 years old with the most being 71-80 years old getting the diagnosis
Using the Gold scoring system how would you measure the severity of airflow obstruction?
Gold 1 = Mild - FEV1 ≥80% predicted
Gold 2 = Moderate - ≤50% FEV1 ≤80% predicted
Gold 3 = Severe - 30% ≤FEV1 ≤50% predicated
Gold 4 = Very severe - FEV1 <30% predicted
What role does low dose opiates have in COPD?
Helps with dyspnoea
Where are muscarinic receptors mainly found in the lungs?
Proximal airways
Where are noradrenergic/ adrenergic receptors mainly found in the lungs?
Distal airways - bronchioles
What are the commonly found microbes of the respiratory tract?
Viridans streptococci,
Neisseria spp
Anaerobes
Candida sp
Do Streptococcus pneumoniae, Streptococcus pyogenes, Haemophilus influenzae make up the normal resident microbiota?
No
outline the natural defences of the respiratory tract against infection
Muco-ciliary clearance
Nasal hairs
Ciliated columnar epithelium of the resp tract
Cough & sneeze reflex
Respiratory mucosal immune system - lymphoid follicles of the pharynx and tonsils, alveolar macrophages, secretory IgA and IgG
Alveolar microbiota
What is the most common cause of URTI?
Viral - rhinovirus, coronavirus, influenza, parainfluenza, respiratory syncytial virus
What does pneumonitis mean?
Inflammation due to non-infective causes such as physical or chemical damage
What is the common feature of pneumonias in terms of the alveoar space?
Cellular exudate is released into the alveolar spaces
What are the subcategories/ descriptions for pneumonia?
Lobar pneumonia and bronchopneumonia
What is lobar pneumonia?
Localisation of the infection to a particular lobe only
What is bronchoneumonia?
Infection/ inflammation in a more diffuse and patchy way
What are the ways we can classify pneumonias apart from the areas they affect?
Source of infection and other aetiological features. This is because there are different organisms and factors involved in each case.
What are the 4 main classifications of pneumonia?
CAP
HAP
Aspiration pneumonia
Pneumonia in the immuno-compromised patient
What is the most common causative organism in CAP?
Streptococcus pneumoniae
What are less common causative organisms in CAP?
Haemophilus influenzae, Moraxella catarrhalis, Klebsiella pneumoniae and Staphylococcus aureus
What are the atypical organisms that cause pneumonia?
Mycoplasma pneumoniae
Chlamydia pneumoniae
Legionella pneumophilia
What defines a nosocomial infection?
Infection of the lower respiratory tract in hospitalised patients, occuring >48hours after admission and was not incubating at the time of admission
In a nosocomial infection what is the main reason of the infection?
Impaired host defences
What are the important causative organisms in a nosocomial pneumonia?
Gram negative bacteria and Staphylococcus aureus including MRSA
What is aspiration pneumonia?
Aspiration of food, drink, saliva, vomitus can lead to pneumonia. The above can enter the respiratory tract where they can cause infection.
Broadly what are the causative organisms in aspiration pneumonia?
Oral flora and anaerobes from GIT
What 3 main causative organisms cause pneumonia in the immunocompromised patient?
Pneumocystis jiroveci
Aspergillus spp
Cytomegalovirus
What are the 5 main symptoms of pneumonia?
Malaise Fever Cough productive of sputum Pleuritic chest pain Breathless (dyspnoea)
What descriptors could be used for the sputum produced in pneumonia?
Purulent
Rusty coloured (due to blood)
Frank blood stained
How do you assess the severity of a pneumonia?
CURB-65 scoring system
What are the constituents of the CURB-65 scoring system?
Confusion - new Urea - above 7mmol/L Respiratory rate - >30/min Blood pressure - SBP <90 or DBP <60mmHg Age >65 years
What is different in the prodromal period in atypical pneumonias compared to typical pneumonias?
The prodromal period is more prolonged with symptoms lasting for several weeks
What clinical features are important in determining prognosis in pneumonia?
High CURB-65 score Very high or very low white cell count Absence of fever Extensive x-ray shadowing Significant hypoxia Rise in blood urea
What is the difference in the antibiotic used in atypical pneumonia vs typical pneumonia?
Less susceptible to cell-wall inhibitors and so should use drugs working on protein synthesis such as macrolides or tetracyclines
What are the complications of pneumonia?
Pleural effusion
Empyema
Lung abscess formation
How would you manage a pneumonia?
Oxygen IV fluids IV antibiotics Analgesics for the pleuritic pain Antipyretics for the fever
What does communicable disease mean?
A disease that is spread from person to person
Describe mycobacterium tuberculosis microbiologically
Bacilli
Aerobic
Acid and alcohol fast bacilli
Demonstrated on smears stained by Ziehl-Nielsen method
Grow slowly on culture (media such as Lowenstein-Jensen Medium taking 2-6 weeks to form colonies
How is TB transmitted from person to person?
Through infected droplets from coughing or sneezing including talking and natural breathing
Close contact with someone is required for at least 8 hours a day for up to 6 months
After how long with treatment does the infectivity of sputum become minimal?
2 weeks of commencing treatment with effective anti-TB chemotherapy
How long is TB treatment for?
6 months typically for pulmonary TB
What is the pathogenesis and pathology of TB?
Alveolar macrophages phagocytose MTB deposited in alveoli but are unable to kill them (possibly due to cell wall lipids of MTB blocking the fusion of the phagosomes and lysosomes). These macrophages initiate the development of cell mediates immunity which eventually leads to the emergence of activated macrophages with enhances ability to kill MTB. This takes about 6 week to develop.
How do tubercles develop in a TB infection?
Ingestion of MTB by macrophages causes a granulomatous reaction. The characteristic lesion of TB is a spherical granuloma with central caseation (aka tubercles)
Explain the process of the primary infection in TB?
The primary infeciton occurs on first exposure to MTB. The deposition of TB bacilli in the alveoli is followed usually by development of a sub-pleural focus of tubercles called the primary focus of Ghon's focus. This may be in any lung zone. TB bacilli drain from the primary focus into the hilar lymph nodes. The primary (Ghon's) focus + the draining lymph nodes together are called the primary complex.
In the primary infection in TB what is included in the primary complex?
The primary (Ghon’s) focus and the draining lymph (hilar) nodes together
What is the problem with TB infection before full healing occurs?
Calcification of the primary complex can occur
Most patients there is some haematogenous spread of some TB bacilli into the blood stream (probably via lymph drainage to the venous system). This can cause seeding of tubercle bacilli to other parts of the lung as well as other organs (extra pulmonary sites)
What is imperfect about the way the body deals with TB?
Development of cell mediated immunity the infection is contained. The primary complex heals, but a small number of organisms remain viable in the lungs/ other organs
What is the state where TB bacilli persist within the human without causing disease called?
Latent tuberculosis
How long can latent TB persist for?
Years, or until death occurs due to other causes
In latent TB what risk factors lead to the reactivation?
Old age, Malnutrition, HIV, Immunocompromised, Organ transplant, Haematological malignancy, Severe Kidney Disease/ Haemodialysis, DM, Silicosis, TNF-alpha antagonists, prolonged therapy with corticosteroids
How would you test for latent TB?
Positive QuantiFERON test or a positive tuberculin skin test
Describe the QuantiFERON test?
Interferon Gamma release assay
Test based on the ability of some Mycobacterium tuberculosis antigens to stimulate host production of interferon gamma.
Lymphocytes from the patients blood are cultured with these antigens if the patient has been exposed to TB before, T lymphocytes produce interferon gamma in response.
Because the antigens used in the test are not present in non-TB mycobacterium (atypical mycobacterium) or in the bacilli used in the BCG vaccine, the test can distinguish Latent TB from previous BCG or exposure to atypical mycobacteria.
How can the Quantiferon test distinguish between latent TB and previous BCG vaccine/ exposure to atypical mycobacterium?
Because the antigens used in the test are not present in non-TB mycobacterium (atypical mycobacterium) or in the bacilli used in the BCG vaccine, the test can distinguish Latent TB from previous BCG or exposure to atypical mycobacteria.
What is the tuberculin skin test for and how is the test performed?
Tuberculin is a protein derived from mycobacteria that is injected intradermally
Presence of a skin reaction after 48-72 hours later indicates previous exposure to TB and is due to a type IV hypersensitivity reaction
What is post primary TB?
The vast majority of clinical cases of TB are due to reactivation of latent TB and occurs most often in the lungs
What is post primary pulmonary TB?
Most often seen in the upper lung zones
Higher alveolar pO2 in the upper zones of the lungs relative to the rest of the lung is believed to predispose to reactivation of TB bacilli at these sites
What are the sequelae to post primary pulmonary TB?
Cavity formation Haemorrhage Spread to involve rest of the lung Pleural effusion Miliary TB
Why does a cavity form in post primary pulmonary TB?
Softening and liquefaction of the caseous material which is discharged into a bronchus results in cavity formation
Fibrous tissue forms around the periphery of such lesions but is usually unable to limit extension of the tuberculous process
Why does haemorrhage occur in post primary pulmonary TB?
Extension of the caseous process into vessels in the cavity walls -> causes haemoptysis
Why does spread to other parts of the lung occur in post primary pulmonary TB?
Caseous and liquified material spread the infection through the bronchial tree to other lung zones
Why does a pleural effusion occur in post primary pulmonary TB?
Seeding of the TB bacilli in the pleura or hypersensitivity can result in a pleural effusion
Why does miliary TB occur in post primary pulmonary TB?
Rupture of a caseous pulmonary focus into the blood vessel may result in widespread dissemination of bacilli throughout the body, resulting in miliary tuberculosis with the formation of multiple ‘miliary’ (millet see like) 0.5mm-2mm tuberculous foci in the lung in and in other organs
What are sites of extrapulmonary TB?
Lymph nodes Bones Joints CNS GIT Urinary tract
What are the clinical features of pulmonary TB?
Gradual onset over weeks or months with tiredness, malaise, weight loss, fever, sweats and cough.
Cough may be dry of productive of mucoid sputum and haemoptysis may occur.
No clinical signs OE even when the CXR is abnormal. Crackles may be present.
If there is cavitation/ fibrosis or a pleural effusion then signs of these may be present
What would a CXR of TB look like?
Pulmonary shadowing
Patchy or solid lesions
Cavitated solid lesions, streaky fibrosis and flecks of calcification
How would you diagnose active TB?
Identification of the tubercle bacillus in the appropriate body fluid by direct smear, culture and other tests when indicated
What is the treatment of TB?
4 drugs in combo over several months
Rifampicin, Isoniazid, Pyrazinamide, Ethambutol - for 2 months then just Rifampicin and Isoniazid for a further 4 months.
Why is pyridoxine given in TB treatment?
Prevents peripheral nerve damage given with Isoniazid
How would you test for legionella/ pneumococcus if the patient isn’t producing sputum?
Urine antigen test
How long is the treatment of a mild CAP and a severe CAP?
5-7 days for mild
7-10 days for severe
What is first line for mild-moderate CAP?
Amoxicillin/ Doxycycline/ Clarithromycin
What is the first line treatment for a moderate-severe CAP?
Co-amox + Clari/Doxy
Hospital admission
What antibiotics are indicated for a pneumonia with pseudomonas risk?
Anti-pseudomonal beta lactam (Tazocin, Meropenem, Ceftazidine)
Or
Anti-pseudomonal fluoroquinolone - Ciprofloxacin
What immunosuppressed type of patient is at risk of getting Pneumocystis jirovecci, TB, atypical mycobacteria?
HIV
What immunosuppressed type of patient is at risk of getting a fungal infection: Aspergillus spp?
Neutropenia
What immunosuppressed type of patient is at risk of getting cytomegalovirus?
Bone marrow transplant patient
What does a pneumococcal vaccine prevent against?
Strep pneumoniae
How often does a pneumococcal vaccine have to be given?
5 yearly
What patient groups would be given chemoprophylaxis?
Asplenia
Dysfunctional spleen
Immunodeficiency
What chemoprophylaxis medication is given to asplenic patients?
Oral penicilin or erythromycin
What patient groups are at risk of getting a TB infection?
Non-UK born = South Asia, Sub-Saharan Africa HIV Other immunocompromised patients Homeless Drug users Prison Close contact with someone who has an active TB infection Young adults/ Elderly Males > Females
What is the generation time of MTB as opposed to e.g. Staph aureus?
MTB - 15-20hours
Staph aureus - 10-20mins
Why is MTB so infectious even though it grows so slowly?
The infectious dose is 1-10 bacilli which makes it super contagious but it isn’t easy to acquire the infection
What is the difference in sputum smears and cultures in a latent TB infection and acute TB disease?
In latent TB infection the sputum smears and cultures will come back negative as there are inactive bacilli but in acute TB disease they will come back positive
What is a rare allergic reaction to primary TB?
Erythema nodosum
What is the risk per lifetime of getting post-primary TB?
5-10% lifetime risk
What is the treatment duration of CNS TB?
18-24 months
What is the BCG vaccine?
Bacille Calmette-Guerin live attenuated M. bovis strain
Given to babies in high prevalence communities only since 2005
Protection wanes though
Little evidence in adults
70-80% effectiveness in preventing severe childhood TB
What test needs to be done before giving a BCG vaccine?
HIV test as it is a live attenuated vaccine - can lead to a full blown infection
What is the most common cause of death from cancer in the UK?
Lung cancer
What ages have the highest incidence of lung cancer diagnosis?
65-80years
What are the risk factors for lung cancer?
Smoking Radon gas Asbestos Occupation Genetics
How is lung cancer staged?
TNM staging IA1-IA3 IIA-B IIIA-C IVA-B
What lung cancer staging is inoperable?
3a onwards
What lung cancer stage is M1?
IVA
At what lung cancer stage is the patient considered to be palliative?
IIIB onwards
What are the differences between the nodal lung cancer staging criteria?
N1- mets in ipsilateral peribronchial and/or hilar lymph nodes
N2 - Mets in ipsilateral mediastinal and/or subcarinal lymph nodes
N3 - Mets on contralateral mediastinal/ hilar or ipsilatera/ contralateral scalene or supraclavicular node(s)
What are the differences in the metastasis stages?
M1 - distant met
M1a-c = distant met would include a contralateral lobe too. Single extrathoracic met in single organ -> Multiple extrathoracic met in one or several organs
What imaging tests would be done to stage a lung cancer?
CXR, CT scan, PET scan, MRI, USS, Bone scan, ECHO
What tissue sampling tests would be done to stage a lung cancer?
Bronchoscopy - endobronchial wash, endobronchial US, USS - neck node, lung/ chest wall mass, pleural fluid, liver
CT biopsy - lung, pleura
Thorocoscopy - medical
Surgical - mediastinoscopy, VATS, pleural biopsy, rigid bronchoscopy, neck and axillary nodal excision, VATS excision biopsy, adrenal biopsy, brain biopsy, bone biopsy
Glandular biopsy as opposed to the tumour because if it has a tumour then confirmed cancer and done staging test. It could be reactive too like infection/ non-cancerous.
What are the symptoms of a primary lung tumour?
Cough, dyspnoea, wheezing, haemoptysis, lung infection, chest/ shoulder pain, weight loss, lethargy/ malaise
What is the pathophysiology of a bloated face in lung cancer?
SVC obstruction
What is the pathophysiology of hoarseness in lung cancer?
left recurrent laryngeal nerve palsy
What is the pathophysiology of dyspnoea in lung cancer?
anaemia, pleural or pericardial effusion
What is the pathophysiology of dysphagia in lung cancer?
oesophageal compression
What is the pathophysiology of chest pain in lung cancer?
parietal pleural involvement
What areas are commonly associated with regional mets in lung cancer?
Bone pain/ fractures
CNS
What is the pathophysiology of bone pain/ fractures in lung cancer?
Distant mets in the bones causing weakness
What is the pathophysiology of CNS symptoms in lung cancer?
distant mets in the brain causing headache, double vision, confusion etc
What is the pathophysiology of thirst in lung cancer?
Hypercalcaemia
What is the pathophysiology of constipation in lung cancer?
Hypercalcaemia
What is the pathophysiology of seizures in lung cancer?
Hyponatraemia - SIADH/ Small cell
Name the signs of lung cancer
Cachexia - severe chronic illness - loss of muscle and fat mass Pale conjunctiva- anaemia / dec O2 sats Cervical lymphadenopathy - mets Horners syndrome - Miosis, ptsosis, anhydrosis Consolidation SVC obstruction Signs of pleural effusion Muffled heart sounds Liver enlargement Skin metastases Neurological long tract signs Finger clubbing
What are 5 paraneoplastic syndromes found in lung cancer?
Endocrine Haematological Cutaneous Neurological Skeletal
What endocrine disorders can be seen in a paraneoplastic lung cancer?
Hypercalcaemia
Cushings syndrome
Inappropriate ADH secretion (SIADH) - most commonly in small cell lung cancer
What haematological disorders can be seen in a paraneoplastic lung cancer?
Anaemia
Thrombocytosis
What cutaneous disorders can be seen in a paraneoplastic lung cancer?
Dermatomyositis
What skeletal disorders can be seen in a paraneoplastic lung cancer?
Finger clubbing
What Neurological disorders can be seen in a paraneoplastic lung cancer?
Encephalopathy
Peripheral neuropathy
Eaton-Lambert syndrome
Pancoast tumour
What are the different types of lung cancer and what is their percentage of the overall number?
Non-small cell lung cancer=
-Squamous cell carcinoma - 40%
-Adenocarcinoma - 35%
Large cell carcinoma - 5%
Small cell lung cancer= 12%
Aggressive tumours that are sensitive to chemotherapy and radiation
Rare tumours= 5%
-carcinoid
What are molecular markers/ mutations for lung cancer?
EGFR, ALK, KRAS, PD1, PDL1 MUTATIONS
What are performance status levels?
0 - 5
0- no symptoms, normal activity
1 - Symptomatic, but able to cary our normal daily activities
2 - symptomatic, in bed or chair less than half the day, meeds some assistance
3 - symptomatic in bed or chair more than half the day
4 - bedridden
5 - dead
What are the treatment options for lung cancer?
Surgery - mainly for non-small cell
Radiotherapy - radical - curative intent or palliative
Combination chemo - small cell - potentially curative, non-small cell- modest survival, neoadjuvant, adjuvant
Combination therapy - chemo and radiotherapy
Biologics - based on mutation analysis
Palliative and symptom control
Describe the features of a pleural effusion on a chest x-ray
If there is blunting of the costophrenic recess
On a chest X-ray what needs to be included?
1st rib
Lateral margins of ribs
Costophrenic angle
How do you check for rotation on the chest x-ray?
Spinous process and clavicles
How do you check for lung volumes in a chest x-ray?
Inspiratory phase
Normal - 5th (R) to 7th (L) anterior ribs at the mid clavicular line
How do you see if there is adequate penetration on a chest x-ray?
Vertebrae just visible through the heart
Complete left hemidiaphragm is visible
How do you tell where the hilum of the lung is?
Right hilar point is lower than the left hilar point
It is where the white opacity looks like a V shape pointing outwards
How do you split up the lung to easily identify locations?
Zones=
Upper zone
Middle zone
Lower zone
What is the gap seen between the base of the lung and the attachment point of the diaphragm to the ribs?
Costophrenic recess
What is the mnemonic to help with the systematic approach to looking at x-rays?
Airway Breathing Circulation Diaphragm/ Dem bones Review areas
How do you describe adequacy of a chest x-ray?
RIP mnemonic
Rotation
Inspiration
Penetration
What are you looking for in a chest x-ray with the airway?
Trachea is visible and aligned centrally
Bronchi - Hila point can be seen
What are you looking for in a chest x-ray with the breathing aspect?
Lungs - compare R + L and the zones in each
Pleural spaces - lung markings and costophrenic angle
Lung interfaces - silhouette of lung
What are you looking for in a chest x-ray with the circulation?
Mediastinum-
Aortic arch
Pulmonary vessels - Hila
Right heart border - Right atrium, middle interface
Left heart border - Left ventricle, Lingula interface
What are you looking for in a chest x-ray with the diaphragm/ dem bones?
Free gas - looking for perforation
Nodules
Fracture/ dislocation
Mass
What are you looking for in a chest x-ray with the review areas?
Apices = pneumothorax Thoracic inlet = mass. Clear - could miss a thyroid mass Paratracheal stripe = mass/ lymph nodes AP window = Lymph nodes. If aortopulmonary notch obliterated then may have mass. Hila = mass/ collapse Behind heart = mass Below diaphragm= pneumoperitoneum/ mass Bones = Fracture, mass, missing bones Edge of films
What is the silhouette sign?
Adjacent structures of differing density form a crisp silhouette of the heart next to the lung.
White next to black.
If this is lost then it is called the silhouette sign which is usually due to pathology.
What can the silhouette sign at the right heart border indicate?
Right middle lobe pathology
What can the silhouette sign at the left heart border indicate?
Pathology at the lingula
What can the silhouette sign at the paratracheal stripe indicate?
Mediastinal disease
What can the silhouette sign at the chest wall indicate
Lung/ pleural/ rib pathology
What can the silhouette sign at the aortic knucle indicate?
Ant mediastinum/ upper lobe pathology
What can the silhouette sign at the diaphragm indicate?
Lower lobe pathology
What can the silhouette sign at the horizontal fissure indicate?
Ant segment upper lobe pathology
What does a mediastinal shift indicate?
Pushed = increase volume or pressure
Pulled = decrease volume or pressure
Each direction has a particular pathology
How can you tell there is mediastinal shift?
Trachea displacement
Cardiac shadow
What can cause a mediastinal shift - push?
Large pleural effusion
Tension pneumothorax
What can cause a mediastinal shift - pull?
Lung collapse
What is a descriptive terms for size in a chest x-ray?
Large
Small
Varied
What is a descriptive terms for side in a chest x-ray?
Right/ left
Unilateral/ bilateral
What is a descriptive terms for number in a chest x-ray?
Single
Multiple
What is a descriptive terms for distribution in a chest x-ray?
Focal
Widespread
What is a descriptive terms for position in a chest x-ray?
Anterior
Posterior
Lung zone
What is a descriptive terms for shape in a chest x-ray?
Round
Crescentic
What is a descriptive terms for edge in a chest x-ray?
Smooth
Irregular
Spiculated
What is a descriptive terms for pattern in a chest x-ray?
Nodular
Reticular
What is a descriptive terms for density in a chest x-ray?
Air Fat Soft tissue Calcium Metal
What are the different chest x-ray findings?
Pneumothorax Pleural effusion Consolidation Space occupying lesion Lobar collapse Estimate the cardiac index
What is a pneumothorax and how does it occur?
Air trapped in the pleural space between visceral and parietal pleura
Spontaneous (primary) or secondary - result of underlying lung disease/ trauma
Iatrogenic - high pressure ventilation, central line placement
What is the most common cause of a pneumothorax?
Trauma with laceration of the visceral pleura by a fractured rib
What lung measure would indicate a large pneumothorax?
lung edge measures 2cm from inner chest wall at the level of the hilum
What features on a chest x-ray would mean the patient has a tension pneumothorax?
Tracheal or mediastinal shift away from the pneumothorax and depressed hemidiaphragm
Visible pleural edge
Lung markings not visible beyond this edge
What x-ray findings would be seen in a pleural effusion/ fluid?
Collection of fluid in the pleural space Uniform white area Loss of costophrenic angle Hemidiaphragm obscured Meniscus at upper border
What can cause a lobar lung collapse?
Luminal - aspirated foreign object, mucous plugging, iatrogenic
Mural - Bronchogenic carcinoma
Extrinsic - Compression by adjacent mass
On chest x-ray what is found in lobar lung collapse?
Elevation of the ipsilateral hemidiaphragm
Crowding of the ipsilateral ribs
Shift of the mediastinum towards the side of atelectasis
Crowding of the pulmonary vessels
What could be included in consolidation of the lung?
Pus - pneumonia
Blood - haemorrhage
Fluid - oedema
Cells - cancer
What size of a SOL is classed as a nodule?
<3cm
What size of a SOL is classed as a mass?
> 3cm
What could a SOL be confused with?
Bone lesion
Cutaneous lesion
Nipple shadow
Of a SOL what is a diffuse spotted appearance most indicative of?
TB until proven otherwise
How do you work out cardiac index and what is the normal?
Cardiac length/Thoracic length on a PA image
<50% is normal
What is the term used to describe the heart location being on the right side?
Situs invertus
What pathology is present in a spontaneous pneumothorax commonly?
Small sub-pleural bleb or bulla (air filled sac) that bursts, allowing air into the pleural cavity
What patient characteristics increase the chance of getting a spontaneous pneumothorax?
Young, tall and thin males
What underlying diseases increase the risk of getting a secondary pneumothorax?
COPD/ Asthma
Bronchiectasis including CF
Lung cancer
Pulmonary infections including pneumonia and TB
What are the signs and symptoms of a simple pneumothorax?
Sudden onset
Pleuritic chest pain and breathlessness
+/- history of lung disease/ trauma (if secondary)
Reduced chest movement on affected side
Hyperresonant on percussion on affected side
Vesicular/ reduced/ absent breath sounds on affected side
Reduced vocal resonance (saying 99)
What x-ray findings would indicate a pneumothorax?
Ipsilateral side is hyperlucent - darker than normal side - no blood vessels to create a shadowing on the image
Absent lung markings on affected side
Edge of collapsed lung is seen
How do you treat a symptomatic simple pneumothorax?
Insertion of a chest drain
In the safe triangle - 5th intercostal space, mid-axillary line just above the 6th rib to avoid the neurovascular bundle below the rib
Why is an underwater seal used for treatment of a pneumothorax?
Chest drain underwater seal prevents back flow of air into the pneumothorax area
What is the biggest problem with a tension pneumothorax?
Cardiovascular collapse as there is less venous return to the heart and there is a high amount of pressure on the heart from the air above it
What is the aetiology of a tension pneumothorax?
Occurs when there is a communication between the outside atmosphere and the pleural space without the air leaving on expiration. This is due to a flap that closes on expiration acting like a one-way valve. Air can enter from either the chest wall or the visceral pleura
What are the signs and symptoms of a tension pneumothorax?
Severe distress and dyspnoea Pleuritic chest pain Fatigue Tachycardia and hypotension Raised JVP Deviated trachea Displaces apex beat Hyper-resonant percussion note Absent breath sounds
What is the treatment of a tension pneumothorax?
Emergency needle decompression of the chest
Insert a plastic cannula into the second intercostal space in the mid-clavicular line
Cannula left in place till chest drain inserted in the 5th ICS mid axillary line when the patient is stable
What is the aetiology of a pleural effusion?
Excess of fluid in the pleural cavity
Imbalance in the normal rate of fluid production and absorption
Pleural fluid is a transudate or exudate from blood
What is a chylothorax?
Fluid in the thoracic cavity is lymph e.g. leak from the lymphatic duct due to trauma
What is an empyema?
Fluid is puss in the thoracic cavity
How much pleural fluid is normal produced per day?
2400ml
What causes pleural fluid to be produced?
Starling forces in the systemic capillaries in the parietal pleura.
Hydrostatic pressure and colloid osmotic pressure
What are the most common causes of a pleural effusion that is transudate in nature?
Congestive heart failure - increased pressure in the venous end of capillary
Hypoproteinaemia - nephrotic syndrome or liver failure
What are the most common causes of a pleural effusion that is exudative in nature?
Infection - pneumonia/ TB Cancer - primary or secondary - cancer blocking the lymphatic drainage site Pulmonary infarction due to PE Pancreatitis Oesophageal rupture Collagen vascular disease Chylothorax/ haemothorax
What would the parameters show in a transudate vs exudate in terms of pleural:serum protein?
Transudate < 0.5
Exudate ≥0.5
What would the parameters show in a transudate vs exudate in terms of pleural:serum LDH?
Transudate <0.6
Exudate ≥0.6
What would the parameters show in a transudate vs exudate in terms of pleural fluid LDH?
Transudate <2/3 upper limit of normal
Exudate >2/3 upper limit of normal
What are the signs and symptoms of a pleural effusion?
Breathlessness (gradual onset - days)
Chest pain (pleuritic)
+/- features of causative disease (CHF or malignancy)
Reduced chest movement on affected side
Stony dull on percussion on affected side
Vesicular/ Reduced/ Absent breath sounds on affected side
Reduced voice resonance
What is the treatment for a pleural effusion?
Treatment of the underlying condition
Indwelling pleural catheter if recurrent effusions due to malignancy for example
Pleurodesis - obliteration of the pleural space - usually by introducing Talc into the pleural space after draining effusion causes the visceral and parietal pleura to become adherent
What does dyspnoea mean?
Subjective awareness of increased effort of breathing
Symptom rather than a sign
But maybe objectively measured - inc RR, accessory muscle use
Where is pleuritic chest pain usually felt?
Thoracic wall or shoulder tip - referred - intercostal nerve or phrenic nerve
Sharp
Well localised
Worse with coughing and breathing in
What happens to the vocal cords during a cough reflex?
Adduction of VCs to allow increased air pressure in the lungs
followed by sharp VC abduction to release the increased pressure
What causes a barking cough?
Croup
What colour of sputum can be present and what does it mean?
Chronic bronchitis and COPD - clear sputum
Infection - yellow/ green sputum (live/dead neutrophils)
Bronchiectasis - Large volumes of yellow/ green sputum
Haemoptysis - blood in sputum
Describe the causes of a wheeze and what the sound is like?
High pitched, musical note
Mostly on expiration (but also on inspiration)
Narrowing in intra-thoracic airways e.g. from bronchial smooth muscle contraction, oedema, mucous
Narrowing exacerbated during expiration
Lower respiratory tract cause
Describe the cause of a stridor and what the sound is like?
High pitch, constant, loud
Mostly on inspiration
Indicated narrowing in extra-thoracic airway - supraglottis, glottis, infraglottis or trachea
Narrowing exacerbated during inspiration
What is the cause of pursed lip breathing and why does it happen?
Commonly seen in COPD
Increases airway resistance during expiration
Keeps small airways open for longer - prolonged period for gas exchange and allows more air to empty
What is a barrel shaped chest indicative of and how would you measure it?
AP diameter > Lateral diameter
Associated with hyperinflation of the lungs seen in severe COPD (especially in emphysema)
What does vesicular breathing mean on auscultation?
Rustling leaves
Inspiration and first part of expiration
No gap between inspiratory and expiratory components
What does bronchial breathing sound like on auscultation?
Blowing harsh sound
Inspiration and expiration
Gap between
What does pleural rub sound like on auscultation?
Scratching, coarse sound
Inflammation of the pleura
What is a PE?
Obstruction of the pulmonary vessels by a foreign object/ substance or a blood clot that travels through the blood stream causing a plug of that vessel. Pulmonary - material passes through the right side of the heart and enters the pulmonary circulation/ artery
What can embolise?
Thrombus Tumour Air Fat Amniotic fluid
What does a doughnut sign indicate on a chest x-ray?
PE due to a fat thrombus
What imaging technique can diagnose a PE?
CTPA - dye sent through pulmonary vasculature and if there is a gap in the blood flow then you would be highly suspicious of a PE
What is usually the cause of a PE?
DVT - 90%
Popliteal vein and more proximal veins including pelvic veins
What are the 5 biggest risk factors of a thromboembolism?
Pregnancy - 6x Prolonged immobilisation - 3x Previous VTE - 3x Contraceptive pill - 3x Long haul travel >4hrs - 3x
What are the hyper-coagulable conditions that needs to be found out in a potential PE?
Anti-thrombin 3 deficiency Protein C or protein S deficiency/ resistance - factor V leiden mutation Lupus anticoagulant Homocysteinuria Occult neoplasm Connective tissue disorders such as RA
What are the 3 main pathophysiological clinical outcomes in a PE?
Acute right ventricular overload
Respiratory failure
Pulmonary infarction
What causes acute right ventricular overload after PE?
Pulmonary artery pressure increases if more than 30% of the total cross section of the pulmonary arterial bed is occluded
This leads to acute right ventricular dilation and strain
Also ionotropes are released by the body in an attempt to maintain systemic BP - causing pulmonary artery vasoconstriction that further exacerbates the problem
What causes respiratory failure in PE?
Due to areas of V/Q mismatch
Low right ventricle output
Shunt with patent foramen ovale
What causes pulmonary infarction in PE?
Small distal emboli may create areas of alveolar haemorrhage
Resulting in haemoptysis, pleuritis and small pleural effusion.
Maybe seen on a CXR as a wedge shape
What are symptoms of PE?
Dyspnoea Pleuritic chest pain Substernal chest pain Cough Haemoptysis Syncope Unilateral leg pain Fever Chest wall tenderness
What are signs of a PE?
Tachypnoea Rales/ decreased breath sounds Accentuated second heart sound Tachycardia Fever Diaphoresis Clinical signs suggesting thrombophlebitis Lower extremity oedema Cardiac murmur Cyanosis
What are the differential diagnosis of a PE?
Pneumothorax Pneumonia MI Pericarditis Pleurisy MSK chest pain
What investigations should be done when considering a PE diagnosis?
Blood gas - hypoxaemia, hypocapnia - resp alkalosis
CXR
ECG - right ventricular heart strain. T wave inversion in the right precordial leads V1 - V4 and the inferior leads 2, 3 and aVF
Blood test - D-dimer
Imaging - pulmonary angiogram, Ventilation perfusion Lung scintigraphy
What is the classical ECG findings in the leads?
S1Q3T3 = Deep S wave in lead 1 Q wave in lead 3 Inverted T wave in 3 T wave inversion in right precordial leads
What is D-dimer
A fibrin degradation product, a small protein fragment released into the blood when a thrombus is degraded by fibrinolysis
A normal D-dimer effectively rules out a PE in those at low likelihood of having a PE
What is the treatment for a PE?
- Oxygen
- Immediate heparinisation - 1 - Stops thrombus propagation in the pulmonary arteries and allows the body’s fibrinolytic system to lyse the thrombus 2 - Stops thrombus propagation at the embolic source and reduces the frequency of further PE
- Haemodynamic support
- Respiratory support
- Exogenous fibrinolytics (streptokinase/ tPA)
- Percutaneous catheter directed thrombectomy
- Surgical pulmonary embolectomy
- IVC filter
After stopping smoking how long do ACh receptors take to desensitise after the last cigarette?
6-12 weeks
How does nicotine in smoking affect the brain?
Nicotine acts on Nicotinic ACh receptors stimulating dopamine release
Why when PE’s occur can some of the lung be saved and at what level does this occur at?
In PE’s if a clot occurs then due to the dual blood supply of the bronchial arteries some parts of the lung can be saved. The blood comes from bronchial arteries and the pulmonary arteries which anastamose at the precapillary level and capillary level (these maintain some blood supply to lung parenchyma in patients with PE’s)
What type of respiratory disease (On flow volume loops) is caused by ILD?
Restrictive
