Respiratory Flashcards
(184 cards)
1
Q
What lung function tests can be done at home, at a GP surgery or in a specialist lab?
A
Home: peak flow (asthma) and oximetry GP: spirometry and oximetry Specialist lab: spirometry, transfer factor, lung volumes, bronchial provocation testing (asthma), respiratory muscle function, exercise testing
2
Q
Define spirometry
A
Forced expiratory manoeuvre from total lung capacity until it’s empty followed by a full inspiration
3
Q
What are the pitfalls to spirometry?
A
- Need an appropriately trained technician
- Effort and technique dependent: need good patient understanding and needs to have ability to complete it
- Patient frailty
- Pain/Patient too unwell e.g. if patient has a chest wall injury
4
Q
Draw normal tidal breathing and label the different measurements that can be taken
What is the volume of normal tidal breathing?
A
Normal Tidal Breathing: 500ml
- Vital Capacity (VC): relaxed manouevre, the difference between total lung capacity and residual volume (the volume that cannot be blown out)
- Forced Vital Capacity (FVC): forced manouevre, patient breathes out as hard as possible
5
Q
What graphs can be determined using spirometry?
A
Time/Volume Plot
- X-axis = time; Y-axis = volume
Flow/Volume Loop
- X-axis = volume; Y-axis = flow
6
Q
Draw a time/volume graph and describe what it shows
A
- Most of the lung is emptied in the first second and then tails off as flow tails off until FVC
- FEV1 = Forced Expiratory Volume in 1 second i.e. the volume expelled from the lungs in one second
Can measure
- PEFR = Peak Expiratory Flow Rate
- FEV1
- FVC
- FEV1/FVC ratio: normal is >70% i.e. >70% of the VC should be expelled from the lungs in the first second. If <70%: airflow obstruction
7
Q
Draw and describe the shape of a flow/volume loop
A
2 parts to the graph
- Negative: inspiration and positive: expiration
Flow is rapid to begin then gradually tails off in a linear fashion
- Rapid flow: effort dependent
- Tailing off: effort independent
Tailing off
- Due to airway resistance, the pressure inside the airway gradually decreases toward the mouth
- When you breathe out hard, there is extrinsic compression of the aiway forming a choke point (where pressure outside airway > pressure inside) therefore causing dynamic airway collapse and air will not be able to pass that point of collapse
8
Q
What physiological process causes a gradual decline in flow in a linear fashion on a flow/volume loop?
A
- Due to airway resistance, pressure inside the airway decreases toward the mouth
- There is extrinsic compression of the airway when a person takes a hard breathe out
- This forms a choke point as the pressure outside the airway > pressure inside the airway, causing dynamic airway collapse
- Air cannot be forced past this point of collapse
9
Q
How does COPD alter the flow/volume loop?
A
- With COPD, there’s a loss of support holding the airway open therefore there is more airway obstruction and the dyanmic airway collapse will occur at lower extrinsic pressures
- Loop: maintain the rapid expulsion (effort dependent) but there’s much quicker tailing off
i. e. church and steeple pattern
10
Q
What are the normal reference ranges for FEV1?
A
FEV1 of 85% predicted may be considered normal
FEV1 of 100% predicted may represent significant decline if values were supra-normal at the beginning
- I.e. need to compare FEV1 values to previously recorded values
- Correlated for age, gender, race, height
11
Q
Define obstructive lung disease and the general sub-groups
A
Definition - FEV1:FVC ratio <70%
- This can be determined using a time/volume plot
- FEV1 (<80% predicted) and FVC are both reduced, but FVC is reduced to a lesser extent
Generally - asthma or COPD
(Emphysema and CF are also obstructive lung diseases)
12
Q
How do you determine the severity of COPD (using spirometry)?
A
- Severity stratified by %predicted FEV1
- Mild airflow obstruction: >80%
- Moderate: 50-80%
- Severe: 30-50%
- Very severe: <30%
13
Q
How do you determine obstructive lung disease and how do you differentiate between asthma and COPD using spirometry?
A
- Reduced % predicted FEV1
- Reduced FVC, but to a lesser extent
- FEV1:FVC ratio <0.7 defines obstructive lung disease
- Flow/Volume loop: church and steeple pattern is also suggestive of obstructive lung disease
To differentiate COPD and asthma: salbutamol reversibility testing
- 400mg salbutamol (nebulished/inhaled)
- Spirometry before and 15mins after salbutamol
- 15% increase in FEV1 and 400ml reversibility in FEV1 - suggestive of asthma
14
Q
What investigations can suggest asthma over COPD, other than reversibility salbutamol testing?
A
PEFR testing
- Look for diurnal variation (i.e. changes throughout the day)
- Response to inhaled corticosteroid with peak flow
Bronchial Provocation
- Tests sensitivity of airways with inhaled mist followed by spirometry
- Positive result = reduced breathing ability and suggests asthma
Spirometry before and after trial of inhaled/oral corticosteroid
Allergy testing
15
Q
Give three examples of causes of a restrictive pattern on spirometry
A
- Interstitial lung disease
- Chest wall abnormality
- Previous pneumonectomy
- Neuromuscular disease e.g. MND, Guillain-Barre syndrome
- Obesity
- Poor effort/technique
16
Q
How do you identify a restrictive pattern on spirometry?
A
Time/Volume loop
- FEV1 reduced <80% predicted
- FVC reduced to <80% predicted
- However, FEV1:FVC remains >70%
17
Q
How do you interpret spirometry to determine if obstructive or restrictive patterns?
A
- Look at FEV1:FVC ratio
- If <70%: obstructive - If obstructed, look at %predicted FEV1 (COPD severity) and any reversibility (COPD v asthma)
- If FEV1:FVC is >70%, look at % predicted FVC
- If low, it suggests restrictive abnormality
NB can get a mixed picture e.g. COPD and obesity
18
Q
What does transfer factor (TF) measure, how is it measured and what affects it?
A
TF: Measures the diffusion of respiratory gases at the lungs
How
- Single breath of a small concentration of carbon monoxide
- CO has a very high affinity to Hb
- Measure the conc. of CO in expired gas to derive uptake in the lung
Affected by
- Alveolar surface area
- Pulmonary capillary blood volume
- Hb concentration
- Ventilation and perfusion mismatch
19
Q
What conditions cause a reduction in Transfer Factor (TF)?
A
- Emphysema (loss of alveolar surface area)
- Interstitial lung disease (ventilation-perfusion mismatch)
- Pulmonary vascular disease
- Anaemia (lower Hb concentrations for oxygen uptake)
20
Q
How are lung volumes measured?
What affects lung volumes and how?
A
- Residual volume (RV) cannot be measured
2 methods of measuring total lung capacity:
- Helium dilution: inspire known quantitiy of inert gas
- Body plethysmography: respiratory manouevres in a sealed box and measuring air pressure changes
Restrictive lung disease: reduced lung volumes
Obstructive lung disease: RV increased in obstructive lung disease
21
Q
What is oximetry, what does it encorporate what are the pitfalls?
A
- Oximetry: non-invasive measurement of Hb saturation by oxygen
- Depends on oxyhaemoglobin and deoxyhaemoglobin absorbing infrared differently
- Result depends on oxygenation and adequate perfusion (shock/cardiac failure could cause poor tissue perfusion and affect oximetry)
Pitfall
- Doesn’t measure CO2 therefore cannot measure ventilation: this can cause false reassurance with patients on high-flow oxygen with normal saturations (e.g. acute asthma, COPD)
22
Q
What does the oxygen dissociation cuvre tell us and how does this affect COPD management?
A
There’s a plateau toward 100% Hb saturation
- If you increase dissolved blood O2 beyond this, there’s no increase in Hb saturations
Steep part of the dissociation curve
- At lower O2 pressures, small increases/decreases of inspired O2 cause much larger inc/decreases in O2 saturations
Affect on COPD management
- Can just give low-flow oxygen because a small inc. in inspired O2 greatly increases saturations
23
Q
Define hypoxaemia and describe it’s aetiology
A
Definition: an abnormally low concentration of oxygen in the blood
Aetiology:
Ventilation-Perfusion Mismatch e.g. COPD, pneumonia
- Perfusion areas of lung that aren’t well ventilated
Hypoventilation e.g. NMD, drugs
- Causes T2 respiratory failure as there is failure to clear CO2 as well not taking up O2
Shunt e.g. congenital heart disease
- Blood is bybassing the ventilated lung
Low inspired oxygen e.g. altitude, flight
24
Q
What is ventilation-perfusion mismatch and give two examples that cause V/Q mismatch?
A
Ventilation (V): the volume of gas inhaled and exhaled in a given time
Perfusion (Q): the volume of blood reaching the pulmonary capillaries in a given time
V/Q mismatch occurs to a degree in normal lungs:
- Apex: ventilation exceeds perfusion
- Base: perfusion exceeds ventilation (better perfusion in the bases due to gravity)
Examples of V/Q mismatch
- Pneumonic consolidation: areas of lung are perfused but not well ventilated. Blood from the well ventilated and poorly ventilated areas of lung mix causing hypoxaemia. Doesn’t fully correct with oxygen management.
- Shunt: extreme form of V/Q mismatch where the blood bypasses the lungs entirely, therefore there is no perfusion of lungs. No gas transfer at alveoli. Does not correct with oxygen adminisatration
25
How does reduced ventilation affect oxygen and CO2 levels?
The initial effect of reduced ventilation: T1 resp failure
i. e. reduced pO2 and normal/low CO2
- Oxygen levels are primarily affected because CO2 is more soluble and will still diffuse across the membrane
- All T1 resp failure can develop into T2 resp failure with low pO2 and pCO2
26
How do pneumonia, asthma and COPD cause reduced ventilation?
Pneumonia: alveoli are filled with exudate, impairing the delivery of air to the alveoli and lengthening the diffusion pathway for respiratory gases
Asthma: smooth muscle contraction, increasing resistance to airflow to the alveoli
COPD: structural airway damage caused by inflammatory changes lead to impaired gas exchange, which can worsen in an acute exacerbation
27
How is arterial pCO2 measured?
How is arterial pO2 measured?
pCO2 - arterial blood gas (ABG)
pO2 - oximetry
28
How do alveolar and arterial pO2 values differ?
What is the normal difference between these values?
What would an abnormal difference indicate?
- Alveolar pO2 will be higher than arterial
- The difference between alveolar and arterial oxygen partial pressures should be \< 2-4kPa
- More than this suggests V/Q mismatch
29
Describe the systematic approach to blood gas analysis
1. Always start with pO2
- Normal = 13kPa
- **Respiratory failure is defined as a pO2 \<8kPa** and will need additional oxygen
2. Look at pCO2: T1 v T2 resp failure
- If pCO2 \>6: T2 respiratory failure
- \<6: T1 respiratory failure
3. Consider acid-base balance
- High H+ (\>44) = acidotic
- If high H and T2 respiratory failure: acute respiratory acidosis
- Acute resp acidosis / decompensated T2 resp failure: elevated CO2, normal bicarb, acidotic
- If normal H and T2 resp failure: body has had time to compensate (days-weeks) by kidneys
- Compensated resp acidosis: elevated CO2, elevated bicard, not acidotic
- Acute on chronic resp acidosis: elevated CO2, elevated bicard, acidotic
30
Define COPD and list 3 aetiologies
Chornic Obstructive Pulmonary Disease
= characterised by progressive airflow obstruction, not fully reversible and do not change markedly over several months
Aetiology
- Smoking
- Environmental pollution
- Burning biomass fuel
- Occupational dust
- Alpha 1 anti-trypsin deficiency (genetic cause): alpha-1-antitrypsin is a serine proteinase inhibitor i.e. anti-protease
31
What are the effects of cigarette smoking on the lungs?
- Reduced cilia motility: cilia are damaged/destroyed by smoking therefore don't clear secretions as effectively and so there's an increased risk of infection
- Mucus hypertrophy and hypertrophy of Goblet cells (produce mucus)
- Airway inflammation: damaged lung proteases released from inflammatory cells and aren't very responsive to inflammatory treatment
- Increased protease activity and anti-proteases are inhibited (smoking activates proteases which digest lung tissue and not enough anti-protease activity)
- Oxidative stress: increased free radicals e.g. hydrogen peroxide
- Squamous metaplasia: high risk of developing lung cancer
- Smoking increases permeability of airways and therefore carcinogens from smoke are absorbed into the body, increasing the risk of other cancers
32
What is a-1-antirypsin deficiency and when would you screen for a-1-antitrypsin deficiency?
A-1-antitrypsin deficiency: genetic cause of COPD
- this enzyme is a serine proteinase inhibitor i.e. protease inhibitor
- Therefore the body cannot combat against destructive protease activity
When to Screen
- Will develop emphysema much earlier on: if there is a young person with severe COPD or emphysema, screen for alpha-1-antitrypsin
33
What would COPD look like in someone with a-1-antitrypsin deficiency who developed COPD?
COPD in a-1-antitrypsin
- Pan-acinar emphysema
- Bullae around the edges of the lungs
- Characterised by swelling and tissue damage in the alveoli
34
# Define the clinical syndromes of COPD
i.e. causing the pathogenesis
Chronic Bronchitis
- **A chronic cough with sputum production on most days for at least 3 months in at least 2 years**
- Narrowing of airways due to inflammation
- Other causes of a chronic cough need excluded
- A type of small airways disease
Emphysema
- **Abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles**
- Causes loss of elasticity and alveolar attachments leading to airway collapse on expiration
35
What is the pathogenesis of chronic bronchitis in COPD?
- Caused by inflammation of the airways \>4mm in diameter
- Smoking induces inflammatory infiltrate around the airways
- Inflammatory infiltrate: principally neutrophilic with CD8 lymphocytes and macrophages
- Neutrophilic infiltrates aren't very responsive to steroids
- Free oxygen radicals are released from neutrophils that destroy the support around the airways therefore loss of interstitial support
- Airways become distorted as inflammation leads to scarring and thickening
- Goblet cell hyperplasia therefore increased mucus production
- Airways become clogged leading to further inflammation
36
What happens as a result of small airway disease?
- Small airways = bronchioles
- Narrowing of bronchioles due to inflammation, mucus plugging and fibrosis
- Narrowed airways → insufficient breathing → air gets trapped in the peripheral lung
This leads to dynamic hyperinflation
- When you exercise, the respiratory cycle time shortens, less time to breath out so lungs don't empty properly causing hyperinflated lungs causing less comfortable breathing
37
What are the cell types involved in inflammation in COPD?
- Neutrophils
- CD8 lymphocytes
- Macrophages
38
What are the inflammatory mediators seen in COPD?
- TNF, IL-8 and other chemokines
- Neutrophil elastase, cathepsin G (from activated neutrophils): these breakdown airway supports
- Elastase and MMP (from macrophages)
- ROS
39
What are the different types of emphysema seen in COPD?
Centri-Acinar
- Damage around respiratory bronchioles
- Damage to one segment of lung supplied by one respiratory bronchiole
- Seen more in upper lobes (with **inhaled damage**)
Pan-Acinar
- The whole acinus is destroyed
- Uniform enlargement from the level of the terminal bronchiole distally
- Get large bullae
- Associated with a-1-antitrypsin deficiency
- Loss of surface area and papillary bed for gas exchange: leads to hypoxaemia
40
What is the mechanism of airway obstruction in COPD?
- Loss of elasticity and alveolar attachments due to emphysema causes airway collapse on expiration
- This causes air trapping and hyperinflation, leads to increased work of breathing and breathlessness
- Goblet cell metaplasia with mucus plugging of the lumen
- Thickening and inflammaiton of the bronchiolar wall: smooth muscle hypertrophy and peri-bronchial fibrosis
41
How do you diagnose COPD and what investigations would be carried out
Consider diagnosis of COPD for those \>35yrs, and smokers or ex-smokers with any of
- exertional breathlessness; chronic cough; regular sputum production; freq. winter bronchitis; wheeze
Spirometry
- obstructive pattern i.e. FEV1 \<80%, reduced FVC and FEV1/FVC ration \<70%
- church and steeple pattern on flow/volume loop
- can use FEV1 to determine severity of COPD
CXR
- Hyperinflated lungs: defined as 6 anterior or 9 posterior ribs above the diaphragm
- Dark lungs: loss blood vessels
- Flattened heart
- Flattened hemidiaphragms
- Ribs become flattened and more horizontal
42
How do you determine the treatment for a COPD patient?
What are the different treatment options?
Need risk assessment
- Look at exacerbations in last year and severity of airway limitation
- Look at symptoms and breathlessness
- Less exacerbations: treat symptoms
- More exacerbations: treat exacerbations
Treatment options
Inhaled bronchodilators: short acting (salbutamol (SABA)) and long acting (salmeterol (LABA) and tiotropium (LAMA))
Inhaled corticosteroids: beclomethasone, nudesonide (combination inhaler)
Mucolytics: carbocysteine (thins mucus and used symptomatically)
43
What is the class, indication, action and potential side effects of salbutamol?
Class: beta-adrenergic bronchodilator
Indications: COPD and asthma
Action:
- Short-acting beta-2 adrenoceptor agonist (SABA)
- Induces bronchodilating by relaxing bronchial smooth muscle
- Reduces airway inflammation: Inhibits pro-inflammatory cytokine release from mast cells and TNF-a from monocytes
- Increases mucus clearance from airways by stimulating cilia activity
Side effects:
- Tremour
- Tachycardia
- Sleep disturbances
- Headache
44
What is the class, indication, action and potential side effects of salmeterol?
Class: beta-adrenergic bronchodilators
Indication: asthma and COPD
Action:
- Long-acting beta-2 adrenoceptor agonist (LABA)
- Induces bronchodilation by relaxing smooth muscle
- Reduces airway inflammation: inhibits pro-inflammatory cytokine release from mast cells and TNF-a release from monocytes
- Increases mucus clearance by stimulating cilia activity
Side Effects:
- Tremour; tachycardia; sleep disturbances; headache
45
What is the class, indication, action and side effects of tiotropium?
Class: anti-muscarinic bronchodilator
Indication: asthma, COPD, rhinitis
Action:
- Long-acting M3 muscarinic receptor antagonist by producing bronchodilatory effects
- Reduces mucus secretion
- May increase bronchial mucus clearance by stimulating cilia activity
Side Effects:
- Dry mouth
- Constipation
- Cough
46
What is the class, indication, action and potential side effects of Beclamethasone?
Class: inhaled corticosteroid
Indication: COPD and asthma
Action:
- Anti-inflammatory effect on the airways
- Decrease the formation of pro-inflammatory cytokines
- Up-regulates beta-2-adrenoreceptors in the airways
Side effects:
- Osteoporosis
- Renal suppression
- Oral candidiasis
47
What is the basis for COPD personalised treatment?
Endotype ie. what's driving the COPD?
- Persistent systemic inflammation
- Eosinophilic or T-helper cell: more steroid responsive
- Persistent pathogenic bacterial colonisation: may need long-term antibiotics
- a-1-antitrypsin deficiency
Phenotype i.e. how clinically bad is the disease
- Frequent exacerbations
- Persistent breathlessness
- Chronic bronchitis
48
What is the significance of blue bloaters and pink puffers?
Blue bloaters: Chronic bronchitis
- Low respiratory drive
- Type 2 respiratory failure: low pO2, high pCO2
- Chronic cough with sputum production
- Cyanosis (hypoxaemia) and warm peripheries
- Peripheral oedema
- Crackles, wheeze
- Obese
- Fluid retention: bounding pulse, flapping tremor, peripheral oedema, elevated JVP
- Confusion, drowsiness
Pink Puffer: Emphysema
- High respiratory drive
- Type 1 resp failure: low pO2 and pCO2
- Desaturates on exercise
- Dyspnoea and tachypnoea
- Use accessory muscle to stabilise breathing
- Decreased breath sounds
- Hyperinflation (barrel chest)
- Cachexia (wasting of the body due to severe chronic illness)
49
Compare and contrast the cause, inflammation and reversibility airflow limitation in asthma and COPD
Cause
Asthma: sensitising agent
COPD: noxious agent
Inflammation
Asthma: **eosinophils,** CD4, T lymphocytes, steroid responsive
COPD: **neutrophils,** CD8, T lymphocytes, macrophages, less steroid responsive
Reversibility and airflow limitation
Asthma: completely reversible
COPD: irreversible
50
Compare the clinical features of asthma and COPD
Smoker/Ex-smoker
COPD: nearly all. Asthma: possibly
Symptoms \<35yrs
COPD: rare. Asthma: often
Chronic productive cough
COPD: common. Asthma: rare
Breathlessness
COPD: persistent and progressive. Asthma: variable
Night time waking with breathlessness and/or wheeze
COPD: uncommon. Asthma: common
Significant diurnal variability of symptoms
COPD: uncommon. Asthma: common
51
Define pneumothorax, comparing to normal, and list the causes
Definition: air within the pleural cavity (the potential, fluid-filled space between the parietal and visceral pulmonary pleura)
- Normally, there is negative intrapleural pressure formed by two opposing, balanced forces: outward with the chest wall and natural elastic recoil of the lung inward
- Any breach of the pleural space leads to **collapse** of the elastic lung
Causes:
- Traumatic: stabbing, fractured rib
- Iatrogenic: CT guided lung biopsy, pleural aspiration (if tip of needle touches lining of the lung, it may introduce air into pleural space)
- Spontaneous: primary (no underlying disease, patient tends to be younger) and secondary (underlying lung disease e.g. COPD, CF, emphysema)
52
What is a tension pneumothorax and describe the pathophysiology?
- Formation of a 'one-way valve' leading to increased intrapleural pressure
- Valve allows air to leak into the pleual space which then can't escape
- Eventually the pressure builds up within the chest wall which compresses the heart and lung
- The pressure can impair venous return to the heart and prevent proper filling of the heart, reducing cardiac output
- Venous return impaired then cardiac output and BP falls
- Will result in cardiac arrest of there is no intervention
- Tracheal deviation away from t. pneumothorax
53
What is the treatment for a tension pneumothorax?
Immediate: insert venflox 2nd intercostal space mid-clavicular line to relieve pressure
54
What are the risk factors for a spontaneous pneumothoax?
- Male
- Smoking
- Tall
- Underlying lung disease (secondary)
55
What is the pathophysiology of a primary pneumothorax?
- Development of subpleural blebs (bubble packaging underneath the pleural surface)/ bullae at the lung apex
- If one of these blebs/bullae pop, air will leak into the pleural space
- Possible additional diffuse, microscopic emphysema (air trapping) below the surface of the visceral pleura
- Spontaneous rupture leads to a tear in the visercal pleura
- Air flows from airways into pleural space
- Pressure gradiant: -ve in pleural space, +ve in airways
Elastic lung then collapses
56
How many lobes do the right and left lungs have?
What are the fissures of the right and left lungs and what do they separate?
What are the layers of the pleura surrounding the lungs?
Right lung
- 3 lobes: superior, middle and inferior
- 2 fissures: horizontal (between superior and middle lobes) and oblique (between superior and inferior lobes)
Left lung
- 2 lobes: superior and inferior lobes
- 1 fissure: oblique fissure
Pleural layers
- Outer: parietal layer (lines inside of the ribcage and diaphragm)
Inner: visceral layer (lines the lungs)
57
What is the pathophysiology of a secondary pneumothorax?
There is an underlying lung condition
- Inherent weakness and destroyed lung tissue (e.g. emphysema)
- Increased airway pressure (e.g. asthma, ventilated patient) which could lead to rupture of air spaces in the lung
- Increased lung elasticity (e.g. pulmonary fibrosis)
- Patient is more symptomatic (poor underlying lung function)
- Management is more complex and prognosis is worse (chest drain often required)
More likely to require intervention
58
What are the signs and symptoms of a pneumothorax?
What would be some differential diagnoses for some of these signs and symptoms?
Symptoms
- Pleuritic chest pain: sudden and intensive stabbing pain in the chest when inhaling and exhaling
- Breathlessness (can be minimal if primary)
- Respiratory distress syndrome (esp if secondary): a type of respiratory failure due to widespread inflammation in the lung. Develop confusion/drowsiness, severe SOB, feeling faint and rapid, shallow breathing
Signs
- Reduced air entry to affected side
- Hyper-resonant to percussion
- Reduced vocal resonance
- Tracheal deviation in tension pneumothorax (+/- circulatory collapse): late sign
Differential diagnosis:
- Musculoskeletal pain, pneumonia, pleurisy (would head a pleural rub that isn't heard with a pneumothorax)
59
What is the basis for management for a pneumothorax?
Determined by symptoms more than size
- A small pneumothorax could be very symptomatic in a severe COPD patient
- Complete lung collapse can be very well tolerated in a healthy patient
Size (2cm rim of air at axilla equates to 50% volume:
- \<2cm: small - \>2cm: large
60
What is the mainstay management for a pneumothorax
Management options:
Observation if small/asymptomatic
- Serial CXRs: repeat in 2 weeks
Aspiration
- 2nd intercostal space midclavicular line to aspirate air with a syringe
Intercostal chest drain with underwater seal
*NB a tension pneumothorax **always** requires a chest drain*
61
What are the management options for a pneumothorax if a chest drain doesn't work?
- Video Assisted Thoracic Surgery (VATS): considered if pneumothorax isn't resolved with a drain within 5 days
- Blebs can be stapled
- Talc pleurodesis: talc sprayed on the lining of the lung, causing an inflammatory reaction causing the lung to stick to the chest wall (very effective)
- Pleural abrasion/stripping: strip out the pleura and it will stick
- Surgical pleurodesis if a secondary pneumothorax occurs: high chance of recurrance
62
What professions need further advice following a pneumothorax, and what is that advice?
Flying: after a spontaneous pneumothorax has resolved on CXR, **wait 7+ days before flying**
- After a spontaneous pneumothorax has resolved on CXR, a patient **should not scuba dive again**
63
Define a pleural effusion and types
Definition: An abnormal buildup of fluid in the pleural space i.e. \>15mls
Types: transudate or exudate
64
Describe the presentation, history and examination for a pleural effusion
Common presentations: SOB, weight loss (red flag), cough, chest pain
Could also present with: haemoptysis, legarthy, fever
History
- Onset: fall, change in medication? (Warfarin/Anticoagulants with a fall could cause a pleural effusion)
- PMH: previous malignancy, TB
- Smoking history
- Occupational history: asbestos exposure
Examination
- Systemic: clubbing, ascites, lymphadenopathy, other cardiac signs (commonest cause of pleural effusion is HF)
65
How do you classify effusions as transudate or exudate?
Light's criteria
- Fluid protein : serum protein ratio \>0.5
- Fluid LDH : Serum LDH ratio \>0.6
Fluid LDH \>2/3 maximum normal serum value
Any one of these = exudate
- Always send paired samples (borderline/subtle results)
66
Compare transudate and exudate general pathology
T: occurs due to increased hydrostatic pressure or low plasma oncotic pressure ie. inc. pressure pushing fluid into the pleural space
E: occurs due to inflammation and increased capillary permeability ie. underlying pathology altering/damaging the tissue and disrupting normal drainage of pleural fluid
T: usually bilateral
E: usually unilateral
67
List 3 causes of a transudate and exudate pleural effusion
Transudate:
- Heart failure, cirrhosis, renal failure
Exudate:
- Malignancy, infection, empysema (collection of pus), haemothorax (collection of blood, due to trauma)
Commonest cause of a pleural effusion: Heart failure
68
Outline a basic approach for investigating pleural effusions
Imaging
- CXR: \>500ml to detect fluid
* If unilateral and not responsive to gravity: think empyema (infective)*
- CT: helps determine underlying pathology e..g. malignancy, heart
- US: allows visuals for interventions
Bloods
- To detect signs of infection
Sampling
- Local anaesthetic thoracoscopy
- Direct visuals of the pleural surface and can take biopsies of abnormal areas
- Indicated in undiagnosed cytology negative pleural effusions
- Diagnosis determined in 90%
- Well tolerated
- Only if necessary; want fewest number of interventions
- Never drain an undiagnosed effusion
69
What is one thing you should never do with a pleural effusion?
What are the main points about intervention?
- Never drain an undiagnosed pleural effusion
- Even if a patient is breathless with a large effusion, don't treat until a diagnosis/cause has been identified as it's safer to do more samples
- If very large, can drain some off but not dry
Note
- Minimal number of interventions
- Asymptomatic - hold off on drain
70
What is the treatment for a pleural effusion?
Guided by history, examinations and investigations
- Dependent on cause
- Take patient wellness into account: esp in the case of malignancy, how hard do you push for a diagnosis?
- **Drainage often required**
- If asymptomatic: hold off on drain
- Don't drain until diagnosis is confirmed
71
What is a malignant pleural effusion?
What is the diagnosis?
- The build-up of fluid and cancer cells that collect in the pleural space (between the chest wall and the lung)
Primary pleural malignancy = mesothelioma
- Linked to asbestos, poor prognosis, supportive treatment
Metastatic Spread
- Most common malignant pleural effusion is secondary to lung cancer
- Breast and ovarian can also spread here as well
Diagnosis
- Aspiration to determine present cells
- Want as much information as possible before drying effusion to determine what chemo/drug to use
- Genetic testing of tissue
72
What is the treatment and prognosis for a malignant pleural effusion?
Treatment: symptom driven and patient centred
- Chest drain +/- talc pleurodesis (no space for effusion to reoccur): 80% effective, longer stay in hospital but don't go home with a drain
- Indwelling pleural catherter: day patient but goes home with catheter, used if the lung doesn't re-expand to reach the chest wall
- Patient choice unless talc failed/lung trapping
Prognosis: poor
73
What pleural infection is closely associated with causing pleural effusions?
What type of effusions can result and how would they be treated?
- Pneumonia (50% have an associated effusion)
- Parapneumonic effusion: accumulation of exudative pleural fluid associated with ipsilateral lung infection, mainly pnuemonia ie. any pleural effusion secondary to pneumonia (simple, complicated or empyema)
- Simple effusion: minimal SOB, treat the infection
- Complex parapneumonic effusion: signs an effusion is becoming an empyema: *pH \<7.2, LDH \>1000, glucose \<2.2, loculated on ultrasound*
- Empyema: presence of pus or bacteria from culture, test pH and glucose if empyema is suspected
74
How would you confirm and treat an empyema?
Empyema: collection of pus in the pleural space
Confirm diagnosis: test pH and glucose levels
- pH \<7.2 and glucose \<2.2 would confirm empysema
- Also have loculated CXR, LDH \>1000
Treatment
- Drainage
- IV antibiotics
- Fibrinolytics: if drain and IV abx aren't working, these enzymes breakdown proteins in the space and start break down the fluid
- Surgery: if fibrinolytics also don't work
75
# Define obstructive sleep apnoea
Define obstructive sleep apnoea syndrome (OSAS)
obstructive sleep apnoea: recurrent episodes of partial or complete upper (pharyngeal) airway obstruction during sleep, intermittent hypoxia and sleep fragmentation
OSAS: manifests as excessive daytime sleepiness ie. apnoea with daytime somnolence (excessive daytime sleepiness)
76
What is the pathology of obstructive sleep apnoea?
- Pharyngeal narrowing causes negative thoracic pressure and decrease in pulmonary stretch receptors and increase in chemoreceptor stimuli ie. physiological arousal
Arousal will lead to sleep disturbance → sleepiness, reduced QoL, road traffic accidents
Arousal also reduces number of BP dips that normally occur overnight, therefore BP surges every time you awaken slightly → inc. risk of heart attacks and strokes
77
What factors predispose an individual to obstructive sleep apnoea?
- Overweight
- Male
- Older (40-50yrs)
- Neck circumference (thicker neck may have narrowed airway)
- A narrowed airway
78
How does someone with OSA present?
What would the clinical examination include?
- Snorer
- Witnessed apnoeas (from partner): witnessed times they're just stopped breathing
- Disruptive sleep: nocturia/choking/dry mouth/excessive sweating
- Unrefreshed sleep
- Daytime somnolence (sleeping during the day/excessive sleepiness)
- General fatigue, low mood, poor concentration
Clinical examination
- **weight,** BMI, neck circumference, BP, craniofacial appearance, nasal patency, prominant tonsils
79
What score is used to determine excessive daytime sleepiness and what is included within it?
Epworth Sleepiness Score
- How likely would it be to dose/fall asleep in certain situations:
* e.g. sitting reading, sitting in a public place, passenger in a car, sleeping while talking to someone, lying down in the afternoon, sleeping while stopped at lights when driving*
80
How would you investigate for OSA?
Limited Polysomnography (Limited sleep study)
- Home study
- Measurements: oxygen sats, HR, flow through the nose, thoracic and abdominal effect, position
Full Polysomnography (PSG)
- Stay in hospital overnight
- Measurements: sleep cycles (EEG), video, audio, thoracic and abdominal bands, position, flow, oxygen sats, limb leads, snore
- Advantages: accurate assessment, sleep staging (EEG), parasomnic activity
81
Define apnoea, hypoapnoea and respiratory effort related arousals
Apnoea: the cessation, or near cessation, of airflow
- 4% oxygen desaturation lasting \>10 seconds i.e. stopped breathing
Hypoapnoea: a reduction of airflow to a degree insufficient to meet criteria for an apnoea ie. apnoea to a lesser degree
Respiratory Effort Related Arousals: arousals associated with a change in airwflow that doesn't meet the criteria for apnoea or hypoapnoea
82
What is the apnoea-hypoapnoea index (AHI) and what does it tell you?
Calculated by adding the number of apnoeas and hypoapnoeas and dividing by the total sleep time (hrs)
\>15: diagnostic of OSA
5-15: OSA with convincing symptoms
\<5: normal
16-30: moderate
\>30: severe OSA
83
How would apnoeas and hypoapnoeas be differentiated with thermistor and canula results, and what are the different types of patterns?
- Flow is measured using a canula and thermistor
- Thermistor is more sensitive for detecting low levels of flow
Patterns: obstructive or central
Obstructive apnoea: no flow is detected but patient is still trying to breathe (presence of thoracic and abdo effort) ie. patient is trying to breathe through closed airway
Central apnoea: brain isn't telling the patient to breathe, so no flow is detected and no abdominal/thoracic effort is detected
e.g. opiates can cause central apnoea
Hypoapnoea: no flow across canulas but thermistor detects low levels of flow
Apnoea: no flow across either canula or thermistor
84
What is the aim of treatment for a patient with OSAS?
How would a patient with OSAS be managed?
Aim: treat the symptomatic and improve daytime somnolence and quality of life
Education: explain OSAS, weight loss, avoid triggering factors e.g. alcohol, sedation medication
Treat underlying conditions: big tonsils, hypothyroidism causing weight gain, nasal obstruction etc.
- Mainstay of treatment: **CPAP (Continuous Positive Airway Pressure)**
- Mandibular advancement device if CPAP in untolerated
- Maxillary-mandibular surgery for problematic patients e.g. severe retrognathia/micrognathia
- Sleep position trainers if patient has supine OSA (keeps patient from lying on back by causing vibrations)
85
Explain CPAP
Continuous Positive Airway Pressure
- Air gently directed through nose into throat to keep airway open
- Stops snoring and sleep fragmentation
- Improves daytime somnolence and quality of life
- Effective within 2 weeks but need good compliance (\>4hrs for \>70% days)
- Fixed (constant pressure all night) v auto (resistance detected and pressure adjusted accordingly, which will ensure no dip in CO2)
- Annual follow-up to ensure mask is right size and fitted correctly all night
86
What are the complications of untreated OSA?
- HTN
- Right heart strain
- CV disease
- Increased risk of MI and strokes
- Increased accidents at work/poor concentration
- Increased road traffic accidents
87
What are the driving restrictions for someone with OSA?
- OSA without daytime somnolence: don't need to stop but need to inform DVLA
- OSA with DTS: impairment on driving, need to inform DVLA
- OSA can keep licence if compliant to treatment and reduced DTS
88
What is the relationship between smoking prevalence and lung cancer
Male smoking prevalence is decreasing: correlates to a decrease in male lung cancer incidence rates
Female smoking prevalence is decreasing also but peak of women smoking was later than men: correlates to an increase in prevlance of lung cancer
89
what are the three most common cancers in the UK
1. breast
2. prostate
3. lung
lung is the 2nd most common cancer is both men and women
90
Give three risk factors for developing lung cancer
- tonacco smoking
- ionising radiation
- air pollution
- asbestos
91
What two types of lung cancer have the strongest link to smoking?
- small cell carcinoma
- squamous cell carcinoma
92
Compare central and peripheral lung tumours, including symptoms for each
Central:
- Tumour at the main bronchi/near hilum
- Involvement of a main airway could cause ulceration and obstruction of that airway
- mainly squamous or small cell
- Ulceration: cough and haemoptysis
- Obstruction: SOB, wheeze, pnuemonia
Peripheral
- Tumour out toward the chest wall
- May have few symptoms as most people have extra lung capacity
- mainly adenocarcinomas
- Symptoms: pain and effusion
Both: systemic features of cancer eg. weight loss, general malaise
93
Give three areas of local spread of lung cancer and their corresponding symptoms/signs
Pleura: cancerous cells would act as irritant, causing inflammation and damaged blood vessels; haemorrhagic effusion
Hilar lymph nodes: then to neck lymph nodes (mass)
Adjacent lung tissue: with involvement of large blood vessles, which may lead to haemoptysis if they rupture
Pericardium: pericardial effusion
Mediastinum:
- SVC obstruction: oedema of face and arms, raised JVP, dilated veins on chest wall, plethora, headache worse on stooping
- Recurrent laryngeal nerve compression: hoareness
- phrenic nerve paralysis: hemidiaphragn peralysis (bludge up)
94
What is a pancoast tumour and what signs/symptoms would it elicit?
- A tumour of the pulmonary apex which can involve brachiocephalic vein and artery, brachial plexus, subclavian vein, and the stellate ganglion
Signs/Symptoms:
- horner's syndrome (compressed stellate): ptosis, enophthalmos, miosis on unaffected side and anhidrosis on affected side
- severe pain in shoulder and scapula
- pain and weakness in arm and hand of affected side
95
How does lung cancer spread and list 3 common sites of lung cancer metastases?
Haematogenous:
- liver, bone, brain, adrenals
Lymphatic:
- cervical lymph nodes
96
Give 3 non-metastatic effects of lung cancer and what the result would be
inappropriate ACTH secretion
- adrenal hyperplasia, raised blood cortisol and Cushing's syndrome
inappropriate ADH secretion
- continual ADH secretion from tumour (no neg. feedback) causes continual stimulation of kidneys to retain water: dilutional hyponatraemia (SIADH)
Parathyroid Hormone Related Peptide (PTHrP) secretion
- squamous/small cell carcinomas
- PTH activates osteoclastic activity to raise blood calcium; hypercalcaemia with continual PTHrP secretion
other
- encephalopathy, neuropathy, myopathy
97
What is the main histological classification of lung cancer types?
Small cell carcinoma
- usually advanced at diagnosis and responds to chemo
Non-small cell carcinoma
- may be localised at diagnosis and treated with surgery/radiotherapy
- subdivisions: adenocarcinoma, squamous cell carcinoma, large cell carcinoma, carcinoid tumour
98
How would small cell carcinoma be identified on histology?
- oval/spindle shaped **small** cells
- inconspicuous nucleoli (not clearly visible)
- scant cytoplasm
nuclear moulding (cells hug together)
- high rates of cell division
99
What is the prognosis for small cell carcinoma?
What is the treatment?
- most aggressive form of lung cancer
- metastasises early and widely
- often initiall good response to chemo but most patients relapse
100
# Define a squamous cell carcinoma
- how does it arise
- effects
- how agressive is the tumour and how is it usually treated
Def: a malignant epithelial tumour showing keratinisation and/or intracellular bridges
Arise:
- arises centrally from major bronchi (central)
- often from dysplasic epithelium following squamous metaplasia
Effects:
- can undergo cavitation: thick-walled gas-filled spaces within the lung
- can block bronchi leadint ot retention pneumonia or lung collapse
Agressive:
- slow growing and metastasises late therefore good candidate for surgery
101
What are the main risk factors for adenocarcinoma
- where do they arise
- what is their appearance
RFs: female and smoking
Arise: peripherally, sometimes in relation to scarring
Appearance: variable
- glandular, solid, papillary patttern or lepidic (tumour grows along the walls of the airway **- looks like butterflies sitting on a fence)**
- mucin production
102
# Define a large cell carcinoma
- where do they normally arise
Def: an undifferentiated malignant epithelial tumour that lacks the cytological features of SCLC (small cell lung cancer) and glandular or squamous differentiation
- usually arise centrally
103
What is a carcinoid tumour?
Where does it arise
What is the prognosis
- a tumour of neuroendocrine cells
- classified as typical (those that do well) or atypical (bigger chance of metastasising)
Arise centrally or peripherally
Prognosis: can metastasise but much better progrosis than other conventional lung cancers
104
What is the pathogenesis of lung cancer?
Multi-step process
- chronic irritation/stimulation of cells by carcinogens
- leads to damage and inc. cell turnover: metaplasia (change from normal pseudostratified columnar ciliated epithelium to squamous epithelium)
- metaplasia develops into dysplasia then invasion
- progressive accumulation of genetic abnormalities in molecules involved in the cell cycle
105
What is a mesothelioma and what effect does it have on the lung
- what appearance does it take
- what is the main cause
= a primary pleural tumour
- encase the lung and compress it therefore reducing lung capacity
- appearance: epithelial or sarcomatoid appearance
Main cause: **asbestos exposure**
- ship-building, pottery type ocupations, engineering
- very long lag period between time of exposure and development of disease
106
Define sarcoidosis
A multisystem inflammatory disease of unknown aetiology that predominantly affects the lungs and intrathoracic lymph nodes, characterised by 'non-necrosing granulomatous inflammation'
- A disease involving abnormal collections of inflammatory cells that form granulomas
107
Describe the presentation of sarcoidosis
5% cases: asymptomatic
Presentation depends on extent and severity of the organs involved
- multisystem: therefore signs/symptoms relate to the affected organs
Systemic symptoms (45% cases):
- fever, anorexia/weight loss, faigue
- night sweats
Other symptoms: pulmonary (50% cases):
- dyspnoea on exertion, wheeze
- cough, chest pain, haemoptysis (rare)
108
Give 3 clinical signs can be seen with sarcoidosis
- pulmonary findings on CXR
- dermatological findings (nodules)
- ocular manifestations
- cardiac manifestations (heart rub)
- neurological manifestations (rare)
109
What are the stages of classification for lung findings on CXR for sarcoidosis?
Stage 1: biltaeral hilar lymphadenopathy without infiltration
Stage 2: biltaeral hilar lymphadenopathy with infiltration
Stage 3: infiltration alone
Stage 4: fibrotic bands, bullae, hilar retraction, bronchiectasis (widening of airways), diaphragmatic tenting (scarring, fibrosis)
These represent radiological patterns and don't indicate severity and patient's do not progress through stages 1-3.
Stages 1-3: can be resolved
Stage 4: cannot be resolved
110
How is sarcoidosis diagnosed?
Needle biopsy or cytology of a lymph node
Lymph node biopsy:
- a LN should be all blue/purple
- presence of large pink areas: abnormal infiltrate containing large bundles of nuceli of macrophages (ie. seeing non-necrotising granulomatous inflammation)
It's a diagnosis of exclusion:
- biltaeral hilar lymphadenopathy without signs/symptoms: sarcoidosis 99% of time and don't need to biopsy
- biopsy only if there's a discrepancy
111
Define pulmonary fibrosis
Scarring of the lungs
112
List 3 causes of pulmonary fibrosis
- occupational and environment: asbestos, hypersensitivity, pneumonitis
- drug induced: amiodarone, methotrexate
- CT disease: RA, lupus
- primary diseases: sarcoidosis
- genetics
113
What is idiopathic pulmonary fibrosis
- the clinical manifestation or equivalent of the pathological diagnosis of usual interstitial pneumonia (UIP)
114
What pattern does pulmonary fibrosis affect the lungs?
- loss of tissue
- cystic spaces
- middle and bottom of lungs are equally affected but the apex are less affected (diff. to emphysema which is an upper lobe feature)
115
What are the risk factors for developing idiopathic pulmonary fibrosis?
Age \>50
M:F - 2:1 (being female)
116
List 3 symptoms of idiopathic pulmonary fibrosis
List one sign of idiopathic pulmonary fibrosis
- Progressive breathlessness (worse with exercise)
- Hacking dry cough (fibrosis causes iritation but not creating more mucus)
- Clubbing: capillary proliferation
- fatigue, weakness and appetite/weight loss
Sign: bibasilar crackles (base of lungs, usually brief, caused by excess fluid in lungs)
117
Describe the histology of idiopathic pulmonary fibrosis
1. Spatial Heterogeneity
- diagnostic for IPF/UIP
- areas of normality and areas of abnormality
2. Temporal Heterogeneity
- different areas of established and ongoing fibrosis
3. Fibroblastic focus
- microscopic zones of acute lung injury (spec. to UIP) and ongoing fibrosis
Also see subpleural honeycombing
- clustered cystic air spaces surrounded by thick fibrous septa
- pink: CT (collagen) ie. scar tissue / fibrosis
- lined by blue
118
How is idiopathic pulmonary fibrosis diagnosed?
HRCT (High Resolution CT)
- Shows subpleural honeycombing: looks black on CT
If difficult to diagnose: video-assisted thoracoscopic surgery (VATS)
- need 3 samples for competent sample: biopsy an area that's affected on HRCT
119
what is extrinsic allergic alveolitis (EAA)
Immunological mediated inflammatory reaction in the alveoli and respiratory broncioles
- T-cell mediated
- granulomatous disease (production of granulomas)
- can be acute or chronic
120
What is the aetiology of extrinsic allergic alveolitis?
Give 3 examples of an EEA and their aetiology
**All causes are organic ducts and must be \<5um**
Eg.
- Farmer's lung: moudly hay
- Sawmill worker's lung: mouldy dust wood
- Bird fancier's lung: proteins in bird droppings
- Humidifier lung: contaminated humidifier water
HEAVY EXPOSURE
121
List 3 symptoms of acute and chronic extrinsic allergic alveolitis
Acute: Occur 4-8 hours post exposure
- flu-like illness
- cough
- high fever / chills
- dyspnoea, chest tightness
- malaise, myalgia
Chronic: occurs with repeated exposure
- dyspnoea in strain
- sputum production
- fatigue, anorexia, weight loss
122
What is the major consequence of chronic extrinsic allergic alveolitis?
Pulmonary fibrosis
123
Describe the pathology of extrinsic allergic alveolitis
Bronchiolocentric pattern
- Long and thin gaps which are also seen in sarcoidosis
- location of inflammation is the determining factor between EAA and sarcoidosis: inflammation in the alveolar spaces in EAA
Non-necrotising granulomatous inflammation
Foamy macrophages in alveolar spaces
- lung produces lots of surfactant and macrophages digest the surfactant
Chronic interstitial inflammation
Organising pneumonia
124
Define pulmonary embolism (PE)
Blockage of one of the pulmonary arteries by a blood clot that forms elsewhere in the body and travels to the lung
125
List 3 causes of pulmonary embolism
Major cause: DVT (Virchow's Triad)
1. Stasis - pregnancy, long flights, bedrest
2. Hypercoagulability: surgery, medication eg. OCP, HRT (ie. oestrogen replacement)
3. Damage to endothelial lining: smoking, cancer
126
List 3 clinical features of a pulmonary embolism:
Common
- sudden SOB and **dyspnoea**
- **pleuritic chest pain**
- cough +/- blood or sputum
Other:
- tachycardia, anxiety
- lightheaded/dizzy or syncope
- excessive sweating
- fever
- leg pain/swelling (DVT)
- discolouration and clammy (cyanosis)
127
What are the complications of a pulmonary embolism?
- Life-threatening (death)
- Pulmonary hypertension: when the BP in the lungs and RHS of the heart is too high. Obstruction of the arteries in the lungs causes RHS of heart to work harder to pump blood - right ventricular hypertrophy
128
What investigations are required for a patient with suspected pulmonary embolism?
Bloods:
- D-dimer: high levels suggestive of blood clot
(CXR to rule out other differentials)
CT pulmonary angiogram (CTPA)
- Can detect abnormalities wihtin the arteries of your lungs
Ventilation-Perfusion Scan (V/Q scan):
- ventilation without perfusion: PE
Pulmonary angiogram
- catheter and inject dye
- gives a clear picture of the blood flow in the arteries
129
How is pulmonary hypertension identified?
On CTPA
- measure the diameter of the main pulmonary artery and the aorta
- if ratio PA:aorta \>0.9 it's suggestive of an enlarged pulmonary artery and therefore pulmonary HTN
130
What is a saddle pulmonary embolism?
- a large PE that straddles the main pulmonary arterial trunk at it's bifurcation point
131
How would an ECG look in a patient with a pulmonary embolism?
Can be normal
Can have sinus tachycardia (the main abnormality seen)
S1Q3T3: pathopneumonic
132
What is the immediate treatment for a patient with a pulmonary embolism?
- IV Heparin
133
What is the class, indication and action of heparin?
Class: heparin
Indication:
- treatment and prophylaxis of thromboembolic diseases, including induction of Vit K antagonists
- renal dialysis (haemodialysis)
- Acute Coronary Syndrome treatment
Action:
- enhances activity of antithrombin III
- antithrombin III inhibits thrombin
- other inhibits multiple other factors of the coag cascade
- produces an anticoagulant effect
134
List 2 side effects of heparin
- haemorrhage
- heparin-induced thrombocytopenia
- osteoporosis
135
List three differences between low molecular weight herpain and unfractioned heparin
UH: continuous IV infusion or subcut injection
LMWH: subcut injection
UH: non-linear relationship between dose and effect therefore needs therapeutic dose monitoring (with activated partial thromboplastin time)
LMWH: more predictable dose-response relationship so regular monitoring not required
LMWH has a longer T 1/2 than UH
UH: easily reversed with protamine
LMWH: less readily reversed with protamine
136
What is the general pathway of treatment for a pulmonary embolism
1. parenteral therapy: short, sharp treatment when in hospital
- ie. IV heparin (LMWH)
2. Oral medication: long term (3-6 months)
- Warfarin, NOAC/DOAC (novel/direct oral anticoagulant)
137
Describe the clinical risk stratification for a pulmonary embolism
What is the clinical relevance of risk stratification
Shock or hypotension
PESI (Pulmonary Embolism Severity Index) class III-V
Signs of RV dysfunction on echo or CTPA
Cardiac lab biomarkers ie. troponin
High Risk:
- cateogoried by hypotension (sys. BP \<90 for \>15 minutes)
- positive for all categories
Intermediate risk:
- positive for PESI score or RV dys.
- +ve troponin: intermediate-high risk
- -ve troponin: intermediate-low risk
low risk:
- all negative
Risk stratification determines treatment
138
What are the options for primary reperfusion therapy for a pulmonary embolism
1. IV heparin
- if this doesn't work: use catheter directed thrombolysis
139
What is the class, indication and action of warfarin?
Class: Vitamin K antagonist
Indication:
- treatment of venous thromboembolism
- prophylaxis for AF / metallic heart valves / cardiomyopathy
Action:
- Inhibits Vit K epoxide reductase
- prevents recycling of Vit K therefore there are less vit K reserves
- Vitamin K needed for the synthesis of coag factors II, VII, IX and X
- this prevents thrombus formation
140
List 2 sides effects and 2 important pharmokinetics of warfarin
Side effects
- bleeding, warfarin necrosis, osteonecrosis
Pharmacokinetics
- numerous drug interactions
- reversal with vitamin K
- needs regular therapeutic dose monitoring with INR (international normalised ratio)
141
Give three examples of available NOAC/DOACs in the UK
- Dabigatran
- Rivaroxaban
- Apixaban
142
What is the class, indication and action of Dabigatran?
Class: direct thrombin inhibitor
Indication:
- prophylaxis of venous thromboembolism
- thrombopropylaxis in non-valvular AF
Action:
- direct thrombin inhibitor ie. inhibits coag factor IIa (thrombin)
- this prevents the conversion of fibrinogen to fibrin
- preventing thrombus formation
143
List 2 side effects and two pharmacokinetics of dabigatran
Side effects:
- bleeding and dyspepsia (indigestion)
Pharmacokinetics
- rapid onset of action
- no food/few drug interactions
- no need for therapeutic monitoring
- fixed dose
144
What is the class, action and indication of rivaroxaban
Class: factor Xa antagonist
Indication:
- prophylaxis and treatment of venous thromboembolism
- thromboprophylaxis of non-valvular AF
Action:
- inhibit coagulation factor Xa which converts prothrombin (II) to thrombin (IIa)
- inhibiting conversion of prothrombin to thrombin, reducing concentrations of thrombin in the blood
- inhibits formation of fibrin clots
145
List 2 side effects and two pharmacokinetics of factor Xa antagonists
Side effects:
- bleeding and nausea
Pharmacokinetics
- predictable drug interactions
- no need for therapeutic monitoring
- fixed dose
146
What is the class, indication and action of apixaban?
Class: factor Xa antagonist
Indication:
- prophylaxis and treatment of venous thromboembolism
- thromboprophylaxis of non-valvular AF
Action:
- inhibit coagulation factor Xa which converts prothrombin (II) to thrombin (IIa)
- inhibiting conversion of prothrombin to thrombin, reducing concentrations of thrombin in the blood
- inhibits formation of fibrin clots
147
What is an allergy?
- an immune system mediated intolerance (inability to cope with an exposure/condition that is normally acceptable)
the trigger is external
- if internal: would be autoimmunity
148
Define asthma
a chronic inflammatory disease of the bronchial tubes characterised by bronchial hyperresponsiveness and reversible airflow obstruction. This results in recurrent episodes of breathless, cough, chest tightness and wheeze that is often made worse by specific triggers and at least partially reversible (spontaneously or with treatment)
- It's also diurnal (worse in the morning, better in evening)
149
Give 3 causes of asthma
A interaction of genetics and environmental factors
Genetic: strong family link
Environmental:
- smoking during pregnancy / secondary exposure
- air pollution
- infection eg. rhinovirus, influenza virus, mycoplasma pneumoniae
- allergen exposure
150
Give 3 RFs for developing asthma
- +ve family history
- triad of atophy: eczema, atopic dermatitis, allergic rhinitis (hayfever)
- exposure to allergens: animal fur, pollen, dust mites, dusts, chemicals
151
List 3 signs and symptoms of asthma
Symptoms:
- chest tightness
- cough (often noctural)
- intermittent dyspnoea / shortness of breath
- wheeze
- exercise intolerance
- yellow sputum productions
- diurnal variation (symptoms worse at night/early morning)
- worsens in presence of percipitants
Signs:
- tachypnoea, widespread wheeze, hyper-resonant percussion
152
List 3 precipitators of asthma
- cold
- exercise
- stress
- allergens
- respiratory tract infections
- drugs eg. NSAIDS, beta-blockers
- smoking / passive smoking
153
Describe the pathophysiology of asthma
1. Airway inflammation
- exposure to allergen triggers IgE-mediated Type I hypersensitivity reaction within the lungs
- mast cells degranulate and production of inflammatory mediators (eg. histamine) and cytokines (IL-4/5)
- inflam cells inc. **eosinophils** migrate to area and propagate immune response
2. Airway obstruction
- inflammation causes bronchospasm, mucosal oedema and increased mucus secretion within airways
- chronic inflam may cause smooth muscle bronchial hypertrophy and airway remodelling which may cause airflow limitations which are only partially reversible
3. Bronchial hyperresponsiveness
- eosinophil products increase the resting tone of bronchial smooth muscle
- bronchi become hyperresponsive and produce a larger, more rapid response to the allergen on the next exposure
154
How do you investigate for asthma?
Spirometry
- Gold standard
- obstructive pattern: FEV1:FVC \<0.7
- and must show reversibility (\>15% improvement) after bronchodilators
Peak Expiratory Flow (PEF)
- typically lower than expected for that pt's age, gender and height
- monitoring allows to establish variability, triggers and efficacy of medication
CXR: may show hyper-inflation with chronic asthm
155
What are the treatment options for asthma?
- Inhaled corticosteroid: bethclomethasone
- Can add Long acting beta agonist (LABA): salmeterol (beta-adrenergic bronchodilator)
- Give salbutamol as required: SABA, beta-adrenergic bronchodilator
- can use tiotropium (LAMA): anti-muscarinic bronchodilator
156
What is the systemic approach to a CXR
DR ABCDE
**D**etails (pt. name, DOB, right image)
**R**IPE (image quality): **R**otation, **I**nspiration, **P**icture area, **E**xposure
**A**irways
**B**reathing
**C**irculation
**D**iaphragm
**E**xtras
157
Give 3 details you need to check with a CXR
- Name, DOB
- Ensure right image
- PA (routine) or AP (supine): with AP it's difficult to determine cardiothoracic ratio
- date and time
- previous CXR for comparison
158
How is image quality of a CXR assessed
Rotation: are vertebral bodies in the centre of the clavicles
Inspiration: are there adequate lung fields to assess?
- there should be 5-7 anterior ribs and 8-10 posterior ribs (more clearly seen in PA film and are more straight)
Picture area
- lung apices to coscodiaphragmatic recesses
- ensure scapula is pulled out of area
Exposure
- over-exposed: darker, under-exposed: lighter
- to assess: presence of fine lung markings extending to the edges of lung fields
159
How are airways assessed on CXR?
Want to determine if the trachea is central
- first assess rotation
- assess if trachea is central at the level of the clavicles (trachea branches after this)
- if no rotation but trachea is not central: tracheal deviation
160
How do you determine cause of tracheal deviation?
Trachea is **pushed** away from **volume expansion**
- volume expansion in one hemithorax will push trachea away
eg. pneumothorax, pleural effusion
Trachea is **pulled** toward area of **volume loss**
- volume loss in one hemithorax will pull trachea toward it
eg. lobectomy/pnuemonectomy, lobar collapse
161
How do you describe changes in opacification?
Morphology: LHS/RHS, uniform v patchy, which zone of the lung
Causative: consolidation, collapse, effusion, oedema, lesions, pneumothorax
162
List 3 causes of increased opacification in the lung
- consolidation
- collapse
- effusions
- pulmonary oedema
- lesions
- pneumothorax
163
How would pneumonia look on CXR
- non-uniform
- perihilar air bronchograms: visible bronchiole within consolidated areas, as they're surrounded by more dense material. Helps to differentiate consolidation and collapse (not inflated)
- focal or widespread
- lobar pneumonias exhibit a particular characteristic pattern on CXR to help determine the affected lobe
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How do you determine the affected lobe with consolidation in a CXR?
Look at the diaphragm and heart borders
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Describe how consolidation would look in the lobes in the right lung on CXR
Lower lobe:
- inc. opacity in the right lower zone
- r. hemidiaphragm isn't well defined
- r. heart border remains clear
Middle lobe:
- inc. opacification in right middle zone
- unclear right heart border
- well defined hemidiaphragm
Upper lobe:
- opacification in the right upper zone
- fluid in horizontal fissure
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Describe how consolidation would look in the lobes in the left lung on CXR
Upper lobe:
- opacification in LUZ-LMZ
- left hemidiaphragm clear
- unclear left heart border
Lower lobe:
- inc. opacification in LLZ
- unclear left hemidiaphragm due to inc. opacification
- clear left heart border
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differentiate lung collapse and lobar collapse
Individual lobes may collapse due to obstruction of the supplying bronchus (ie. not inflating that lobe)
- Lung tissue collapse is due to a pneumothorax (air in pleural space compressing the lung)
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Give 3 categories of causes of a lobar collapse and an example for each
ie. bronchus obstruction
- Intraluminal: mucus plugging, inhaled foreign body
- Luminal (within wall): bronchogenic carcinoma
- Extraluminal: compression from adjacent mass
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What three general patterns are seen with lobar collapses?
1. Inc. opacity: due to compacted and more dense lung tissue
Loss of volume:
2. can shift trachea toward affected side
3. pull hemidiaphragm of affected side up (raised)
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How would a right upper lobe collapse present on CXR?
- triangular, dense inc. opacification in right upper zone
- collapses superiorly and medially
- can generate **reverse S sign** (shifted minor fissure): if there's obstruction from a hilar mass eg. tumour in right main bronchus
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How would a left upper lobe collapse present on CXR?
- difficult to identify due to anatomy
- upper lobe collapses toward ant. chest wall
- **'veil like' opacification**: throughout entire left hemithorax which can obscure the aortic notch and left upper cardiac margin
- left hemidiaphragm still visible
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How would a middle right lobe collapse present on CXR?
- subtle uniform right middle zone opacification
- if suspecting a middle right lobe collapse: **need to order a lateral view** as it's difficult to identify on PA film
- right heart border obscured in PA film
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How would a right lower lobe collapse present on CXR?
- triangular dense opacification in RLZ, with apex toward hilar
- obscured medial portion, right hemidiaphragm is very obscured
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How would a left lower lobe collapse present on CXR?
- triangular dense opacity in LLZ, apex toward hila
- sits behind the heart, looks like a double left heart border = **sail sign**
- check for tracheal deviation (toward hemithorax where there's a collapse
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Differentiate interstitial and alveolar oedema
Interstitial:
- interstitial space: ocuppies the space between the interface of the capillaries and alveoli
- as this progresses, fluid leaks from interstitial space into alveoli
- affects gas exchange therefore get hypoxia
Alveolar oedema:
- fluid in the alevoli
- type of consolidation (alveoli are filled with more dense material
- also causes hypoxia
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How can interstitial oedema be recognised on CXR?
Peribronchial cuffing: walls of bronchi become thickened
- can see 'halo' of head-on bronchi as they're surrounded by fluid in the interstitium
Septal lines / Kerly B lines
- More specific to heart failure
- short parallel lines at the periphery
- represent fluid accumulation / thickening at the interlobular septa
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How can alveolar oedema be recognised on CXR?
- Air space opacification in batwing distribution
- Symmetrical perihilar opacification (sparing peripheries due to better lymphatic drainage)
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Compare and contrast how consolidation, collapse and effusion present on a CXR
Collapse:
- uniform opacification and affected lobe is smaller
- loss of volume therefore **pulls** - trachea deviation toward hemithorax and hemidiaphragm pulled up
Consolidation:
- non-uniform opacification
- Peri-hilar air bronchograms: visible bronchioles penetrating consolidated areas
Effusion:
- uniform opacification
- **meniscus sign** and fluid at lung bases subject to gravity
- inc. in volume therefore **pushes** - trachea deviated away and hemidiaphragm is flattened
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What needs assessed in relation to the heart (cardiac)
Cardiothoracic ratio
- cardiac and thoracic width
- normal \<50%/0.5
- \>0.5 = abnormal, indicated cardiomegaly or pericardial effusion
- if \>0.5 and querying cardiomegaly - look for other signs of HF
Heart shape and borders
Great vessels and aortic knuckle
Mediastinal width normally \<0.8cm on PA film (if larger - could suggest aortic dissection)
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What are the signs of heart failure on a CXR?
upper lobe venous divertion
- caused by inc. pulmonary venous pressure
- 'antler distribution'
Kerly B lines
- represents intersitital oedema
perihilar consolidation
- 'batwing distribution' and represents alveolar oedema
blurred coscophrenic angles
- represents fluid in pleural space ie. pleural effusion
cardiomegaly
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what can cause a 'white out' of one whole hemithorax?
large pleural effusion
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What aspects of the diaphragm need assessed in a CXR interpretation?
Position/Shape
- hemidiaphragm should be visible
- if not, query lower lobe collapse/consolidation
- raised (loss of vol) or flattened (inc. in vol)
Air under the diaphragm
- if present: pneumoperitoneum and query bowel perforation
- visualised on erect CXR
- NB gastric bubble seen under LHS and is normal
Costophrenic angles and cardiophrenic angles
- blunted costophrenic angles: pleural effusion
blunted cardiophrenic angles: lower lobe consolidation
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What extras need assessed on a CXR interpretation
Bones
- fractures, bone metastases
Soft tissue
- grey haze outside the ribcage
- check for swelling or masses
Equipment
- eg. confirming NG tube placement
- if equipment is in it's functional position and present
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