Station 1: Resp Flashcards
Approach to respiratory examination?
Inspection
Portable oxygen, sputum pot
Ask to breathe in - any obvious asymmetry in chest expansion
Cough - productive or non-productive
Hands
RA - symmetrical deforming polyarthropathy
Systemic sclerosis - sclerodactyly, thickened skin
DM - Gottron’s papules
Pancoast tumour - wasting in small muscles
Clubbing
CO2 retention - asterixis, erythema
Pulse
Face Horner's - meiosis, ptosis, anhidrosis Anaemia Cyanosis SLE - malar flush Systemic sclerosis - microstomia DM - heliotrope rash
Neck
Pulmonary HTN - raised JVP, large c-v waves
Tracheal deviation
Hyperinflation - reduced cricosternal distance
Cervical LN
Chest Scars - clamshell (transplant), thoracotomy (pneumonectomy/lobectomy), chest drain or pleural biopsy RV heave, palpable P2 Chest expansion Percussion TVF Auscultation + loud P2 Vocal resonance
At the end
Sacral or peripheral oedema
End exam by asking history, checking O2, possibly bedside spirometry
Respiratory causes of clubbing?
- Abscess or empyema
- Asbestosis
- Bronchiectasis
- Cystic fibrosis
- Interstitial pulmonary fibrosis
- Tumours (bronchogenic carcinoma, mesothelioma)
- Extra question: causes of clubbing and crackles?
- Asbestosis
- Bronchiectasis
- Bronchogenic carcinoma
- Interstitial pulmonary fibrosis
What is cor pulmonale?
- Right heart failure caused pulmonary hypertension as a result of disease affecting the lung and vasculature
- Permanent remodelling of pulmonary vasculature leading to pulmonary hypertension, which then alters the RV structure and function
Cor pulmonale - symptoms?
Dyspnoea Fatigue and lethargy Exertional chest pain Orthopnoea Hoarseness of voice (compression of left recurrent laryngeal nerve by dilated main pulmonary artery)
Cor pulmonale - clinical signs?
- Ruddy facial appearance (polycythaemia)
- Central cyanosis
- Bounding pulse, flapping tremor (C02 retention)
- Raised JVP - prominent a wave (right atrial hypertrophy), large v wave (TR)
- Left parasternal heave (RV hypertrophy) - may not be palpable in hyper inflated lungs
- Palpable P2
- Wide splitting of S2 (in inspiration), loud P2
- PSM loudest at lower LSE in inspiration (TR)
- EDM loudest in pulmonary area (Graham-Steele PR)
- 4th heart sound (RV hypertrophy)
- Hepatomegaly
- Sacral and ankle oedema
Cor pulmonale - investigations?
- Pulse oximetry
- ABG: type 1/2 resp failure + assess for requirement for LTOT
- CXR: cardiomegaly, prominent pulmonary arteries
- ECG: right axis deviation, prominent P waves (p pulmonale), RBBB
- ECHO: RV hypertrophy, TR, paradoxical inter ventricular septum movement
- Right heart catheterisation: gold standard to diagnose pulmonary HTN
Cor pulmonale - management?
- Manage underlying conditions
- Consider LTOT
- Diuretics (judicious use as excessive diuresis can reduce filling pressure and RV output)
Cor pulmonale - causes?
- COPD
- Interstitial lung disease
- OSA
- Hypoventilation disorders: OHS, neuromuscular disorders, kyphoscoliosis
Indications for LTOT?
PaO2 < 55mmHg (<7.2kPa) or SO2 < 88%
PaO2 < 60mmHg (<8kPa) with cor pulmonale or erythrocytosis
Definition of pulmonary hypertension?
Mean pulmonary artery pressure > 25mmHg
Left atrial pressure < 15mmHg
Caused by increase in pulmonary blood flow and increase in pulmonary vascular resistance
Causes of pulmonary hypertension?
WHO has classified pulmonary hypertension as follows:
- Pulmonary arterial hypertension - idiopathic, familial, disease related to collagen vascular disease, HIV and drugs
- Pulmonary venous hypertension - due to left-sided disease
- Chronic lung disease or hypoxaemia - COPD, ILD, OSA
- Chronic thromboembolic disease - PE, sickle cell disease
- Miscellaneous disorders - sarcoidosis, Langerhan cell histiocytosis, myeloproliferative disease, thyroid disease
Bronchiectasis - features and clinical signs?
Features:
- Dyspnoea
- Cough with daily copious purulent sputum
- Haemoptysis
- Pleuritic chest pain
- Weight loss, failure to thrive
- Recurrent infections
- Hx of sinusitis, childhood infection, TB, sub fertility
Clinical signs:
- Copious purulent sputum in sputum pot at bedside
- Cachexia
- Tachypnoea
- Central cyanosis
- Finger clubbing
- Hyperexpanded chest
- Coarse, late, inspiratory crepitations
- Wheeze
Bronchiectasis - investigations?
Labs
- Sputum C&S, AFB, MTB C&S, fungal, cytology
- Bloods: FBC (anaemia of chronic disease, polycythaemia less commonly, neutrophilia)
Lung function test - obstructive pattern (FEV1 low, FVC low or normal, FEV1/FVC < 0.7)
Imaging
- CXR: hyper inflated, finger-in-glove appearance (mucus plugging), tram lines and ring shadows (dilated and thickened airways), honeycomb patterns in severe cases
- HRCT (definitive test): tram tracking and ring shadows (thickened dilated bronchi), signet ring sign (thickened dilated bronchi > 1.5x larger than adjacent pulmonary vessels), pus/fluid levels in dilated bronchi, mucus plugging or bronchoceles
Bronchoscopy - rarely needed, required to obtain microbiological samples or exclude other conditions
Specific tests
- Serum Ig (hypogammaglobulinaemia)
- Alpha 1 antitrypsin level (deficiency)
- Aspergillum precipitins and IgE (ABPA)
- Autoantibodies (if CTD suspected)
- Sweat test (Cl > 60mmol/L) and genotyping (CF)
- Nasal brushings and electron microscopy to visualise ciliary structure (Kartagener’s) -> refer sp centre!
- AFB, MTB C&S, Tuberculin test (TB)
Bronchiectasis - treatment?
- General measures
- Education of patient and family
- Optimise nutrition e.g. calorie supplementation
- Smoking cessation
- Vaccination: pneumococcal and influenzae
- Physiotherapy: chest percussions, postural drainage, breathing exercises, nebulised saline - Medical
- Antibiotics for infective exacerbation, which often will need pseudomonas coverage
- Bronchodilators if evidence of reversibility
- Corticosteroids either inhaled or oral, during exacerbation
- Mucolytics
- Nebulised hypertonic saline for mucus plugging - Surgical - lobectomy or pneumonectomy (specific indications based on localised disease and good lung function), transplantation in CF
- Treatment of underlying disease
Bronchiectasis - causes?
Abrnomal, permanent dilatation of bronchi due to combination of infections, impaired drainage, obstruction and defective immune host response.
- Congenital
- CF: caucasian, short stature, clubbing, diabetes, sinusitis, infertility
- Young’s syndrome: similar clinical features to CF but no CF mutation, abnormal sweat or pancreatic insufficiency
- Kartagener’s syndrome: sinusitis, situs inversus, dextrocardia, subfertility, otitis media
- Yellow nail syndrome: yellow nail, pleural effusion, lymphoedema - Bronchial obstruction
- Foreign body
- Carcinoma
- Sarcoidosis/TB - Infection
- Whooping cough, TB, measles - Overactive immune response
- ABPA
- CTD: RA
- IBD - Underactive immune response - hypogammaglobulinaemia, HIV, leukaemia
- Chemical injury - recurrent aspiration in stroke, bulbar neurological disease, chronic alcoholism
- Other resp disease - COPD, fibrosis
Bronchiectasis - how to determine severity?
- Symptoms: Medical Research Council (MRC) Dyspnoea scale
- Lung function assessment: FVC/FEV1
- Imaging: number of bronchopulmonary segments involved
Bronchiectasis - complications and major pathogens?
Complications
- Pulmonary: recurrent infections, haemoptysis, empyema/abscess, cor pulmonale
- Extrapulmonary: anaemia, metastatic infections e.g. cerebral abscess, secondary amyloidosis
Major pathogens
- Pseudomonas aeruginosa
- Haemophilus influenza
- Streptococcus (less commonly)
- Burkholderia cepacia complex (in CF associated with accelerated decline in pulmonary function and decreased survival)
COPD - definition and types?
- Progressive airflow obstruction with limited reversibility
- Characterised by abnormal inflammatory lung response to cigarette smoke or other inhaled noxious particle
Types:
- Chronic bronchitis - clinical diagnosis of chronic productive cough for > 3 months in 2 consecutive years
- Emphysema - histological and radiological diagnosis of abnormal and permanent enlargement of airways distal to terminal bronchioles, and destruction of alveolar wall
COPD - clinical features?
Symptoms
- Chronic productive cough
- Exertional dyspnoea
- Recurrent infections
- Wheeze
Signs
- Bedside: inhalers, sputum pot, oxygen
- Inspection: cachexia, tachypnoea, pursed-lip breathing, barrel chest, use of accessory muscles, peripheral/central cyanosis, tar-stained fingers
- Asterixis and bounding pulse (CO2 retention)
- Hyperinflated chest
- Hyper-resonance to percussion + reduced hepatic and cardiac dullness
- Reduced breath sounds esp over bull
- Expiratory wheeze, prolonged expiratory phase
- Inspiratory coarse crackles
- Possible signs of prolonged steroid use: Cushingoid features, bruising, thin skin
- Signs of cor pulmonale: right parasternal heave, palpable and loud P2, raised JVP with prominent v waves, PSM of TR, peripheral oedema
COPD - investigations?
Labs
- Sputum culture
- Bloods: FBC (anaemia, polycthaemia, neutrophilia), raised CRP, low albumin (chronicity of disease)
- ABG: resp failure hypoxaemia and hypercapnia with chronic disease
- Alpha 1 antitrypsin: indicated in early-onset disease with minimal smoking history, or family history
Lung function test
- Airflow obstruction FEV1/FVC < 0.7
- Severity assessment based on FEV1
- Minimal reversibility with bronchodilator
- Increased TLC, residual volume and functional residual capacity
Imaging
- CXR
- Hyperinflated lungs with flattened diaphragm
- Bullae
- Cardiac enlargement: cor pulmonale
- Prominent pulmonary vasculature: pulmonary hypertension - HRCT
- Grade and classify emphysema: centrilobular in upper lobes, pan lobular in lower lobes, paraseptal anywhere/adjacent to septa and pleura - ECHO
- Evaluate pulmonary hypertension/cor pulmonale
COPD - role of spirometry?
- Diagnosis: FEV1/FVC < 0.7
- Assessment of severity of airflow obstruction: GOLD grade 1-4
- Follow-up assessment:
a) Therapeutic decision
- Surgical interventions e.g lung volume reduction surgery, bullectomy, transplantation
- Discrepancy between initial FEV1 severity and symptoms
b) Identification of rapid decline
COPD - treatment?
Aim: reduce symptoms, reduce frequency/severity of exacerbations, improve QoL and exercise capacity
Non-pharmacological
- Patient education
- Smoking cessation - slow rate of lung function decline
- Optimize nutrition
- Vaccination with influenza and pneumococcal vaccines
- Physiotherapy and behavioural therapy
Medical
- Short-acting bronchodilators
- SABA (salbutamol, terbutaline): improve symptoms and FEV1
- SAMA (ipratropium): improve symptoms - Long-acting bronchodilators
- Persistent symptoms or > 2 exacerbations per year
- Improve symptoms, lung function, QoL and reduce exacerbations
- LABA (formoterol, salmeterol, indacaterol, vilanterol)
- LAMA (tiotropium, glycopyrronium bromide, umeclidinium) - ICS -> in moderate to severe COPD
- LABA/ICS more effective than individual components: improve lung function, QoL and reduce exacerbations
- LABA/LAMA/ICS is better than LABA/ICS, LABA/LAMA or LAMA
- Regular ICS increases risk of pneumonia esp in severe COPD
- Greater benefit in preventing exacerbations with ICS treatment in serum Eos > 300cells/uL - Methylxanthines
- Theophylline, aminophylline -> unclear mechanism of action, suggested to relax airway smooth muscles
- Small bronchodilator effect in stable COPD
- Potential toxicity, not recommended as initial treatment - Long-term oxygen therapy
- PaO2 < 55mmHg (< 7.2kPa) or < 60mmHg (< 8kPa) in cor pulmonale or secondary polycythaemia
Surgical
- Lung volume reduction surgery
- Symptomatic despite maximal medical therapy, FEV1 > 20%, predominantly upper lobe emphysema
- Remove area of poorly functioning lung, so that physiologically useful lungs can expand
- Improve exercise capacity, QoL and mortality - Bullectomy
- Symptomatic despite maximal medical therapy, FEV1 < 50% and bullae > 1/3 hemithorax
- Reduce airway resistance and improve elastic recoil
- Improve symptoms and lung function - Lung transplant
- BODE > 5, FEV1 < 25%, accelerated decline in FEV1, resting hypoxaemia and hypercapnia, secondary pulmonary hypertension
- Improve functional capacity
COPD - how to define severity?
- Medical Research Council (MRC) Dyspnoea scale, grade 0-4
- Grade 0: breathless with strenuous exercise
- Grade 1: breathless hurrying on the level or walking uphill
- Grade 2: breathless walking at my pace on the level, slower than people my age
- Grade 3: breathless walking 100m on the level
- Grade 4: breathless at home or with dressing - Lung function assessment for airflow obstruction using GOLD staging:
- FEV1 > 80% predicted: mild
- FEV1 50-80% predicted: moderate
- FEV1 30-50% predicted: severe
- FEV1 < 30% or < 50% with chronic resp failure: very severe - BODE index (assess mortality and hospitalisation risk)
- Pulmonary and extra pulmonary manifestations
- FEV1, 6-min walking distance, MRC scale, BMI
COPD - difference between GOLD 1-4 grading and GOLD A-D groups?
GOLD 1-4 grading is to determine severity of airflow obstruction (FEV1) -> for prognosis
GOLD A-D groups is for information regarding:
- Symptoms burden
- Risk of exacerbation
- Guiding therapy for individualised patient care
-> GOLD grade (based on FEV1), group (based on symptoms and exacerbation)
COPD - how to differentiate with asthma?
- Clinical features:
- COPD: associated with smoking, persistent and progressive cough and breathlessness
- Asthma: variable symptoms, nocturnal awakening with breathlessness and wheeze, hx of atopy - Lung function
- COPD: minimal reversibility with bronchodilators
- Asthma: FEV1 improvement > 200-400ml with bronchodilators, serial peak flow shows diurnal or day-to-day variability
Treatments available to stop smoking?
- Nicotine replacement therapy - gum, patch, inhalers, sprays
- Bupropion - antidepressant which enhances CNS noradrenergic and dopaminergic activity
- Varenicline - nicotinic Ach receptor agonist
Some evidence of increased efficacy with combination therapy
Pleural effusion - clinical findings and important negatives?
Important negative: Clubbing (malignancy) Cachexia and nutritional status (malignancy, hypoalbuminaemia) Rheumatoid hands/nodules Butterfly rash Lymphoedema (malignancy, sarcoidosis) Raised JVP (RHF, pulmonary HTN)
Findings:
- Scars from chest tube
- Tracheal deviation away from effusion if large > 1000ml (if central in the context of large effusion, then suggests collapse)
- Reduced chest expansion
- Reduced vocal fremitus
- Stony dullness
- Diminished breath sounds with bronchial breathing at area above effusion
Pleural effusion - investigations?
Labs
- Pleural fluid analysis: LDH, protein, albumin, glucose, pH, AFB stain, culture, cytology
- Serum LFT, LDH, FBC, RP, ESR, CRP, blood culture
- Specific tests: TFT, ANA/RF (if CTD suspected), amylase (if pancreatitis suspected)
- Sputum culture, AFB
CXR
- Blunted CPA, meniscus sign
USG thorax
- Differentiate pleural effusion from pleural thickening
- Guide thoracocentesis
- Identify loculated effusions
If suspect malignancy/infection/TB:
- CT thorax
- Bronchosopy/CT-guided biopsy
- Pleural biopsy