1
Q
How is airway resistance (Raw) measured, and what does it reflect?
A
- Measured by body plethysmography
- Mainly reflects resistance in central (rather than peripheral) airways
2
Q
What is the normal value for airway resistance (Raw)?
A
<2cm H20/L per second
3
Q
Why is airway resistance (Raw) different in asthma and emphysema?
A
Asthma involves increased resistance in the central and peripheral airways and therefore Raw is increased in acute asthma.
Emphysema involves early closure of the peripheral airways only.
Airway resistance measurement tends to be insensitive to peripheral airway obstruction.
4
Q
DLCO (diffusing capacity of the lung for CO) with single breath holding technique is typically DECREASED in…?
A
Diseases that:
- thicken or destroy alveolar membranes (eg. PULMONARY FIBROSIS, EMPHYSEMA)
- affect pulmonary vasculature (eg. PULMONARY HYPERTENSION)
- reduce alveolar capillary Hb (eg. ANAEMIA)
5
Q
DLCO (diffusing capacity of the lung for CO) with single breath holding technique may be INCREASED in…?
A
- pulmonary haemorrhage
- acute CCF
- asthma
- polycythaemia
6
Q
Explain the difference between FRC and RV
A
FRC is the volume trapped in the lung at the end of passive expiration (ie. during tidal breathing).
It is determined by the balance between inward elastic recoil of the lung and the outward recoil of the chest wall.
The airways also contribute due to dynamic airflow limitation.
- DECREASED in IPF - increased recoil, decreased TLC
- DECREASED in mod. obesity - decreased outward recoil
- NORMAL in MG as passive expiration not affected by respiratory muscle weakness
- INCREASED in obstructive airways disease due to early dynamic airway closure and gas trapping (and in emphysema - decreased recoil).
High FRC in dynamic hyperinflation: breathing at a higher resting lung volume to decrease airway resistance (like autoPEEP).
RV is the volume trapped in the lung at the end of active expiration (ie. vital capacity).
It is determined by the balance between inward lung recoil + activity of expiratory muscles vs. outward recoil of the chest wall. The airways also contribute due to dynamic airflow limitation.
- DECREASED in IPF - increased recoil, decreased TLC
- NORMAL in mod. obesity - respiratory muscles normal
- INCREASED in MG - respiratory muscle weakness
- INCREASED in obstructive airways disease due to increased gas trapping from early airway closure
7
Q
How is obstructive airways disease diagnosed?
A
FEV1/FVC < LLN for age (ie. <70% of predicted)
8
Q
How is response to bronchodilator therapy diagnosed?
A
An increase in FEV1 OR FVC of 12% or more
PLUS
An increase of 200mLs or more.
9
Q
How is restrictive defect diagnosed?
A
Defined as TLC < LLN (TLC <80% predicted) and FEV1/FVC normal (ie. no obstructive defect).
(If spirometry only: decreased FVC and normal or increased FEV1/FVC. Can say that appears to be restrictive defect, but spirometry is lowsy for diagnosing restrictive defect and will only be correct ~50% of the time).
10
Q
Methods for measuring lung volumes?
A
- Inert gas dilution: known amount of non-absorbable inert gas (helium or neon) is inhaled. Concentration then measured on expiration. Gas in lung at time of inhalation dilutes the inert gas and allows calculation of lung volumes. Single breath or rebreathing from closed circuit until equilibration.
* Often UNDERESTIMATES true lung volumes (poorly ventilated areas due to airway obstruction do not contribute to dilution). - Body plethysmography - measures compressibility of gas within the chest. Patient sits in closed box and pants against closed shutter. Changes in pressure (at the mouth) and volume (in the box) measured and then FRC calculated (because Boyle’s law implies that P1V1 = P2V2).
TLC and RV are then derived (TLC - add inspiratory capacity; RV - subtract expiratory reserve volume).
Difficulty is in determining normal values for different populations. Major determinants of healthy lung volumes are: height, age, gender, race.
eg. TLC values:
12% lower in African Americans
6% lower in Asian Americans
11
Q
Most important determinants of normal lung volumes in healthy subjects?
A
Height, age, gender, race.
eg. TLC values:
12% lower in African Americans
6% lower in Asian Americans
12
Q
Mechanisms of following lung volume results:
- TLC normal
- RV/TLC ratio increased
- RV increased
- FRC normal
A
- Gas trapping secondary to airflow limitation
- Neuromuscular disease (though often TLC will be decreased also)
13
Q
Mechanisms of following lung volume results:
- TLC normal
- RV/TLC ratio increased
- RV increased
- FRC increased
A
Hyperinflation secondary to airflow limitation
Patient is breathing at a higher resting lung volume to decrease airways resistance
14
Q
Mechanisms of following lung volume results:
- TLC increased
- RV/TLC ratio increased
- RV increased
- FRC increased
A
Hyperinflation AND Over-distension
- loss of elastic recoil
- airflow limitation
eg. emphysema
15
Q
Mechanisms of following lung volume results:
- TLC decreased
- RV/TLC ratio normal
A
Restrictive defect
- ILD eg. IPF
- Chest wall abnormality eg. kyphoscoliosis
- External constraints that limit ability to maximally inspire and expire eg. obesity, poor volition, chest pain, tight clothing.
16
Q
Mechanisms of following lung volume results:
- TLC decreased
- RV/TLC ratio increased
A
- Mixed obstructive and restrictive defect
- Neuromuscular disease
17
Q
What is the alveolar gas equation? Explain the components.
A
PAO2 = FIO2 (Pbar - PH2O) - PACO2/R
PAO2 = Alveolar partial pressure of oxygen FIO2 = Fraction of inspired oxygen (0.21 room air at sea level) Pbar = Barometric pressure = 760mmHg at sea level PH2O = Saturated vapour pressure of H2O = 47mmHg at sea level PACO2 = Alveolar partial pressure of CO2 which is assumed to = PaCO2 R = Respiratory quotient = VCO2/VO2 which is assumed to = 0.85 (average American diet). R = rate of oxygen uptake (determined by body's metabolic oxygen consumption and related to average CO2 production rate - depends on fuel metabolised). Rate of 0.85 means that more oxygen is absorbed than CO2 is excreted.
18
Q
Radiological signs that suggest airspace opacity is due to collapse:
A
Collapse = Volume loss. Secondary signs are:
- mediastinal shift - eg. tracheal deviation
- elevation of hemidiphragm
- hyperlucency (implies hyperinflation) of lobe that remains inflated
19
Q
Radiological signs that suggest that airspace opacity is due to consolidation:
A
Consolidation = Filling of Airspaces with mucous or pus
- Maintenance of lung / lobar volume
- Air bronchograms
20
Q
Tracheal deviation occurs TOWARDS:
A
Atelectasis
Pleural fibrosis
Pneumonectomy / Agenesis of lung
Volume loss PULLS the trachea to the ipsilateral side
(Other causes: medistinal masses, tracheal masses, kyphoscoliosis)
21
Q
Tracheal deviation occurs AWAY from:
A
Pneumothorax
Pleural effusion
Large intrathoracic mass
PUSHED away by increased pressure
(Other causes: medistinal masses, tracheal masses, kyphoscoliosis)
22
Q
Radiological signs of RUL collapse:
A
- Wedge shaped opacity in RUZ on PA and lateral films
(Minor fissure moves upwards) - Tracheal deviation to R
23
Q
Radiological signs of RLL collapse:
A
- RHB preserved
- Additional inferomedial wedge-shaped density (collapses down and towards mediastinum)
- Elevated hemidiaphragm
- Paucity of vascular markings in R lung field suggesting hyperinflation
- Loss of lower zone lucency on lateral
24
Q
Radiological signs of LUL collapse:
A
- Hazy opacification - “veil like” (because aerated lung posterior)
- Obscures heart border but with obvious aortic knuckle and descending aorta (as lower lobe abuts)
- Hilum looks abnormal
- Whole major fissure moved anteriorly on lateral film
- Lower lobe may be hyperinflated (esp. if gradual process such as lung cancer)
25
Radiological signs of LLL collapse:
- Wedge-shaped density behind heart, obscuring medial diaphragm
- Elevated L diaphram
- Loss of lower zone lucency on lateral
26
HRCT signs of Usual Interstitial Pneumonia (UIP) - pattern seen in IPF:
1. Reticulation (>ground glass)
2. Lower zone predominance (apico-basal gradient)
3. Honeycombing (subpleural; and differentiated from traction bronchiectasis)
4. Absence of findings NOT consistent with IPF (ground glass, nodules, consolidation)
Need all 4 for confidant diagnosis.
Note: IPF is a multi-disciplinary Dx and clinical information very important.
Impression may be altered by lung biopsy also, but CT findings trump biopsy results in Dx of IPF!
27
Flow Volume Loop in Upper Airway Obstruction: Fixed Upper Airway Obstruction
Truncation of inspiratory and expiratory flow.
FEF50% ~ FIF50% (Mid-exp flow approximates Mid-insp flow)
Causes: Firm tracheal lesions -
- Tracheal stenosis
- Extrinsic compression eg. goitre
28
Flow Volume Loop in Upper Airway Obstruction: Variable Extrathoracic
Truncation of INSPIRATORY flow
FEF50% / FIF50% >1
Causes:
- Laryngomalacia
- Tracheomalacia (extrathoracic)
- Vocal cord abnormalities eg. paradoxical vocal cord motion, focal cord paralysis
- Glottic strictures
29
Flow Volume Loop in Upper Airway Obstruction: Variable Intrathoracic
Truncation of EXPIRATORY flow
FEF50%/FIF50% <1
Causes:
- Tracheomalacia (intrathoracic)
- Bronchogenic cysts
- Tracheal lesions (often malignant)
30
Flow volume loop with FEF50% > FIF50%. Where is the obstruction?
Variable EXTRATHORACIC upper airway obstruction
31
Flow volume loop with FEF50% = FIF50% but markedly curtailed flow in expiration and inspiration. Where is the obstruction?
Fixed Upper Airway Obstruction - firm tracheal lesions
32
Flow volume loop with FEF50%/FIF50% <1. Where is the obstruction?
Variable INTRATHORACIC upper airway obstruction
33
Define TLCO (or DLCO)
```
TLCO = Transfer factor of the lung for CO.
DLCO = Diffusion capacity of the lung for CO.
```
The amount of CO that can access available Hb
(mL CO/min/mmHg at STPD = 760mmHg, dry, O degrees celsius)
34
Define Alveolar Ventilation
Volume of the lung that is exposed to test gas
(calculated using dilution of inert gas)
Units – (L BTPS)
In healthy lung it approximates TLC, but in obstructive airways disease it may underestimate TLC.
35
Define KCO (Transfer Coefficient)
KCO = TLCO/VA
Gas exchange per unit of lung volume.
ie. corrected for lung volume.
ie. not influenced by processes that reduce lung volume (pneumonectomy, neuromuscular disease), which lower DLCO.
KCO will be normal if the remaining lung is normal with normal function of the alveolar blood membrane.
It is increased in pulmonary haemorrhage.
36
Which factors will affect TLCO measurement?
1. Hb level (low Hb - decrease TLCO; high Hb - increase TLCO)
2. HbCO - will decrease gradient and decrease TLCO (eg. recent cigarette)
3. PACO2 - if high will decrease TLCO (as decreases PAO2 and thus less competition with CO for access to Hb)
4. Pulmonary capillary blood volume - decrease with decrease TLCO
5. Posture - supine position increases TLCO
37
Mechanisms of decreased TLCO?
1. Blood – gas barrier (Diffusion Properties)
- Thickening of the membrane
- Reduction in surface area of the
membrane
2. Capillary Blood (Rate of Combination)
- Reduction in capillary blood volume
- Anaemia
38
Restrictive pathophysiology of respiratory disease: break into 3 categories and give examples of each
1. Parenchymal disease:
- IPF
- asbestosis
- DIP (desquamative interstitial pneumonitis)
- sarcoidosis
2. Neuromuscular weakness
- ALS (amyotrophic lateral sclerosis) - motor neuron disease
- Guillain-Barre syndrome
3. Chest wall / Pleural disease
- kyphoscoliosis
- ankylosing spondylitis
- chronic pleural effusions
39
Explain the cough reflex - 1. stimuli, 2. sensory pathway, 3. motor response.
1. Chemical or mechanical stimulation of sensory nerve endings in pharynx, larynx, airways (to terminal bronchioles), oesophagus, external auditory meatus.
2. Vagus and superior laryngeal nerve convey sensory signals to the brainstem (nucleus tractus solitarius).
Note: may be vaguely labelled the "cough centre" but no true cough centre.
3. Involuntary muscular actions (may be mediated by cortical pathways):
- vocal cords adduct (transient UAW occlusion)
- expiratory muscles contract (generates high positive intrathoracic pressure)
- sudden release of laryngeal contraction --> rapid expiratory flows
- narrowing of airways (smooth muscle contraction, dynamic compression) --> high velocity of expiration
- dislodges foreign material - eg. mucous from airways or foreign body from cords.
Deep breath prior to cough optimises function of expiratory muscles.
Repetitive coughing at successively lower lung volumes sweeps the point of maximal expiratory velocity progressively further into the lung periphery.
40
What is the mechanism of ACEi-induced cough?
Inhibition of metabolism by ACE of bradykinin, substance P and other tachykinins --> accumulation of bradykinin ---> sensitisation of sensory nerve endings --> increased cough reflex.
41
DDx of cough by chronicity (acute, subacute, chronic) and definitions of timecourse
Acute (8 weeks):
- post-nasal drip syndrome (non-allergic rhinitis, allergic rhinitis, vasomotor rhinitis, chronic bacterial rhinitis)
- asthma (eg. cough-variant)
- GORD
- Rx ASE - eg. ACEi
- chronic bronchitis
- eosinophilic bronchitis
- bronchogenic carcinoma
- sarcoidosis
- Tb
- bronchiectasis
- CCF
42
Drug classes for symptomatic management of cough
- Demulcents (eg. sucrose, glycerol - protective later over sensory receptors --> suppress cough)
- Opioid cough suppressants (use only in non-productive cough): codeine, dihydrocodeine, pholcodine, dextromethorphine.
- Expectorants
- Mucolytics (decrease viscosity of secretions and promote expectoration - may decrease frequency and duration of exacerbations in some COPD patients)
BEWARE combination products (eg. suppressant and expectorant), paracetamol-containing preparations and sympathomimetic decongestants.
43
Clinical features suggestive of post-nasal drip syndrome (as possible cause of cough):
- frequent throat clearing
- sneezing
- rhinorrhoea
- O/E nose: excess secretions, inflamed nasal mucosa, polyps
- O/E oropharynx: cobblestoning, secretions
Causes: infections, allergy, vasomotorhinitis --> secretions
--> stimulate receptors in hypopharynx / trachea
* Note: while a common cause of cough, many people with post-nasal drip do not have a cough (need to consider other causes)
44
Clinical features suggestive of GOR as cause of cough:
- retrosternal burning (after meals, during recumbency)
- frequent eructation (belching)
- hoarseness
- throat pain
Although can have silent GOR without Sx
1. stimulation of receptors in lower oesophagus --> cough
2. reflux to level of pharynx --> aspiration of gastric contents --> chemical bronchitis +/- pneumonitis --> cough for days after an aspiration event
* Note: while a common cause of cough, many people with GOR do not have a cough (need to consider other causes)
45
Chronic eosinophilic bronchitis as cause of cough - Dx and Tx
Sputum eosinophilia >3%
Normal CXR
No airflow obstruction or airway hyperresponsiveness (ie. not due to asthma)
Tx = ICS
46
Mechanisms of haemoptysis and causes of each:
1. Diffuse alveolar haemorrhage - bleeding is from low pressure pulmonary circulation (alveolar capillaries).
(a) Inflammatory (small vessel vasculitis / capillaritis): GPA, microscopic polyangitis, SLE, Goodpasture's disease, Post-BMT
(b) Non-inflammatory: direct inhalational injury (fires, elicit Rx like cocaine, toxic chemicals) - increased risk if bleeding diathesis
2. Small-to-medium-sized airways: bleeding from bronchial arteries under systemic pressure.
(a) Infection
- Acute bronchitis (likely viral)
- Chronic bronchitis with bacterial superinfection (eg. S.pneumoniae, H.influenzae, M.cattarhalis)
- Bronchiectasis (eg. in advanced CF)
- Pneumonias: Tb (cavitation); S.aureus, K.pneumoniae (necrotising); pre-disposed if scarring from previous infection
- Paragonimiasis (lung fluke - SEA, China - crayfish / crabs)
(b) Airway irritation: toxic chemical inhalation, thermal injury, direct trauma (eg. suctioning), foreign body
(c) Malignancy
- Primary - bronchogenic cancer esp. SCC, SCLC, carcinoid
- Secondary -
3. Pulmonary vascular disease:
(a) CCF --> pink, frothy (rupture of small alveolar capillaries due to raised LAP)
(b) MR with focal jet (raises PCWP)
(c) pulmonary AVM
(d) PE
(e) PAH - rarely
47
Mucocutaneous telangiectasias - how are they relevant in haemoptysis?
A feature of Hereditary Haemorrhagic Telangiectasia (Osler-Weber-Rendu disease).
Patients can have silent cerebral and pulmonary AVMs (can become life-threatening).
48
Investigations in haemoptysis
Will depend on amount / acuity of bleeding and other Hx / RFs.
*Rule out other sources of bleeding first (haematemesis, epistaxis)
CXR
FBC, Coags, Renal function and urinalysis (RBCs, RC casts), +/- ANA, ANCA, Anti-GBM Abs
CT chest
Bronchoscopy
Other management: Airway management in massive haemoptysis (200-600cc in 24 hours)
Embolisation, resection in continued heavy bleeding
49
Clinical phases of Bordatella pertussis infection in patient without previous immunity
Incubation period - usually 1 week but up to 3+
1. Catarrhal phase: First 1-2 weeks. General malaise, rhinorrhoea, mild cough. Mild fever, not high. Excessive lacrimation and conjunctival injection.
2. Paroxysmal phase: Begins in second week.
Paroxysmal cough = series of severe, vigorous coughs during a single expiration.
Rapid inspiration afterwards may produce "whoop" in young infants.
Post-tussive vomiting or syncope may occur.
Day and night, but may be worse at night.
May be triggered by minor irritants or activity.
Usually well between paroxysms.
Without treatment this lasts 2-3 months.
3. Convalescent phase: Usually lasts 1-2 weeks but may be prolonged. Symptoms gradually decrease / resolve.
Total duration all 3 phases approx. 3 months.
In adolescent / adult with previous exposure or vaccination the symptoms may be attenuated (but neither gives life-long immunity. May simply present as chronic cough.
50
Investigations for pertussis
...
51
Treatment of pertussis (case and contacts)
...
52
Radiographic subtypes of bronchiectasis and associated signs:
1. Cylindrical:
- bronchus visualised within 1cm of pleural surface
- lack of tapering
- increased broncho-arterial ratio (ratio of diameter usually 0.6-1.0; up to 1.5 can be normal; >1.5 bronchiectasis) --> "signet ring sign"
- centrilobular nodules ("tree in bud" sign) due to mucous plugging
("Tram tracks" sign seen on CXR)
2. Varicose - uncommon, beaded appearance
3. Cystic - Severe; cyst-like bronchi that extend to pleural surface; air-fluid levels.
4. Traction bronchiectasis - surrounding fibrosis
53
Radiographic signs of constrictive bronchiolitis (bronchiolitis obliterans) on HRCT:
- mosaic attenuation with alternating oligemia and pseudo-ground glass, apparent on comparison of inspiratory and expiratory films
- normal parts of the lung are over-perfused and have increased attenuation, while abnormal lung regions are underperfused due to hypoxic vasoconstriction, due to unequal ventilation with air trapping.
54
Types (stages) of pleural effusion associated with infection:
1. uncomplicated parapneumonic effusion
2. complicated parapneumonic effusion
3. empyema
55
Features of uncomplicated parapneumonic effusion:
A and B and C
(no need for B or C if minimal though):
A: - free flowing, minimal (10mm but <1/2 hemithorax)
B: sterile (gram stain and culture negative)
- regardless of prior AB use
C: pH ≥7.20
Typically:
- exudative
- resolve with treatment of pneumonia
- low risk of poor outcome
- do not require drainage
56
Pathophysiology of (1) uncomplicated vs (2) complicated parapneumonic effusion vs (3) empyema
(1) increased interstitial fluid with neutrophils moves into pleural space during pneumonia (effusion if exceeds resorptive capacity)
(2) bacterial invasion of pleural space --> acidosis, increased LDH and increased neutrophilia. However, bacteria are rapidly cleared so gram stain and culture are negative. Fibrin deposition and loculation
(3) increasing bacterial replication --> frank pus on aspiration or positive gram stain, but usually not positive culture (anaerobes tricky to culture, usually have received ABs, loculated areas of infection).
57
Features of complicated parapneumonic effusion or empyema (likely to require drainage):
Any of A, B or C:
A: - large (≥1/2 hemithorax) free flowing
- loculated
- thickened parietal pleura on con-CT (suggests empyema)
B: - positive gram stain
- pus
C: pH <7.20
58
Light's criteria for pleural exudates:
LDH: pleural / serum >0.6 or >0.67 of the ULN for serum LDH
Protein: pleural / serum >0.5
59
Criticisms of light's criteria:
Highly sensitive, at expense of specificity --> will over-classify as exudates.
However, this is accepted as it is important that exudates are not missed.
2-rule (pleural cholesterol and LDH) and 3-rule tests (pleural chol, LDH and protein) exist that do not require concurrent serum results. Their accuracy is similar to Light's criteria.
60
Pathophysiology of tuberculous pleuritis (pleural effusion):
- develops contiguous to parenchymal focus of Tb (50% tuberculous effusions)
OR
- infection of parenchymal space via haematogenous spread, without underlying parenchymal disease
Delayed hypersensitivy reaction to mycobateria and mycobacterial antigens leads to pleuritis.
61
Diagnostic evaluation for suspected tuberculous pleural effusion:
1. Pleurocentesis - exudate, lymphocytosis, signs of empyema (low pH, low glucose), culture (<30% positive)
2. Pleural biopsy - most sensitive test
3. Additional assays on pleural fluid, including adenosine deaminase level (others - lysozyme and IFN gamma concentrations).
4. Sputum culture
- obviously more likely to be positive in those with parenchymal changes (89% positive in one series) than if no parenchymal changes (11% positive sputum culture).
5. Routine lab investigations for Tb (mantoux, etc). HIV testing.
62
Findings in pleural fluid in tuberculous effusion:
- exudate (protein, LDH)
- predominantly lymphocytes
- may have low glucose and low pH but then more likely Tb empyema
- <30% positive culture
- additional: adenosine deaminase level raised
63
Findings on pleural biopsy that are indicative of tuberculous pleuritis:
pleural caseating granulomas (in 50-97% of cases)
positive culture from pleural tissue (40-80% of cases)
Sensitivity increases with number of pleural biopsies taken.
64
Changes in PFTs typical of obesity?
Reduced: FVC, FEV1, TLC.
Normal or raised: KCO (reduced DLCO)
These changes are usually only small unless BMI>40 (Class III Obesity).
65
Which features on clinical assessment would raise suspicion for cause of large airway obstruction rather than asthma?
What are some causes of large airway obstruction?
"Asthma" which never improves / doesn't fluctuate.
History of choking on food.
Monophonic wheeze.
Stridor.
```
Causes:
FB
Stricture
Polyp / adenoma
Carcinoma
```
66
How can you easily remember flow-volume loops for large airway obstruction?
INTRAthoracic (variable) obstruction will cause a plateau in EXPiration.
EXTRAthoracic (variable) obstruction will cause a plateau in INSPiration.
(ie. I-E and E-I).
Fixed upper airway obstruction causes truncation of both insp and exp curves.
67
What are the possible adverse effects of low tidal volume (TV=6mL/kg), low airway pressure (which may result in permissive hypercapnia) in ARDS?
ASEs of permissive hypercapnia:
- pulmonary vasoconstriction and pulmonary hypertension
- cerebral vasodilatation --> increase ICP (ie. concerning in closed head injury / cerebral oedema)
- inceased SNS activity - may be proarrhythmic
permissive hypercapnia should probably be used with caution in patients with heart disease and is relatively contraindicated in those with elevated intracranial pressure
RACP Written Exam
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