Respiratory Flashcards
Learning objectives
Answer
Define acute respiratory distress syndrome
• A syndrome of acute and persistent lung inflammation with increased vascular permeability. Characterised by:
o Acute onset
o Bilateral infiltrates consistent with pulmonary oedema
o Hypoxaemia
o No clinical evidence of increased left arterial pressure (pulmonary capillary wedge pressure)
o ARDS is the severe end of the spectrum of acute lung injury
Explain the aetiology / risk factors of acute respiratory distress syndrome
Severe insults to the lungs and other organs leads to the release of inflammatory mediators. These lead to increased capillary permeability, pulmonary oedema, impaired gas exchange and reduced lung compliance . Causes o Sepsis o Aspiration o Pneumonia o Pancreatitis o Trauma/burns o Transfusion o Transplantation (bone marrow and lung) o Drug overdose/reaction There are THREE pathological stages of ARDS: o Exudative o Proliferative o Fibrotic
Summarise the epidemiology of acute respiratory distress syndrome
1 in 6000
Recognise the presenting symptoms of acute respiratory distress syndrome
- Rapid deterioration of respiratory function
- Dyspnoea
- Respiratory distress
- Cough
- Symptoms of CAUSE
Recognise the signs of acute respiratory distress syndrome on physical examination
- Cyanosis
- Tachypnoea
- Tachycardia
- Widespread inspiratory crepitations
- Hypoxia refractory to oxygen treatment
- Signs are usually bilateral but may be asymmetrical in early stages
Identify appropriate investigations for acute respiratory distress syndrome and interpret the results
• CXR - bilateral alveolar infiltrates and interstitial shadowing
• Bloods - to figure out the cause (FBC, U&Es, LFTs, ESR/CRP, Amylase, ABG, Blood Culture)
o NOTE: plasma BNP < 100 pg/mL could distinguish ARDS from heart failure
• Echocardiography
o Check for severe aortic or mitral valve dysfunction
o Low left ventricular ejection fractions = haemodynamic oedema rather than ARDS
• Pulmonary Artery Catheterisation
o Check pulmonary capillary wedge pressure (PCWP)
• Bronchoscopy
o If the cause cannot be determined from the history
Define Aspergillus Lung Disease
• Lung disease associated with Aspergillus fungal infection
NOTE: Aspergillus infection is usually caused by Aspergillus fumigatus
Explain the aetiology/risk factors for Aspergillus lung disease
Inhalation of Aspergillus spores can produce THREE different clinical pictures:
• Aspergilloma
o Growth of an A. fumigates mycetoma ball in a pre-existing lung cavity (e.g. post-TB, old infarct or abscess)
• Allergic Bronchopulmonary Aspergillosis (ABPA)
o Colonisation of the airways by Aspergillus leads to IgE and IgG-mediated immune responses
o Usually occurs in asthmatics
o The release of proteolytic enzymes, mycotoxins and antibodies leads to airway damage and central bronchiectasis
• Invasive Aspergillosis
o Invasion of Aspergillus into lung tissue and fungal dissemination
o This occurs in immunosuppressed patients (e.g. neutropenia, steroids, AIDS)
Summarise the epidemiology of Aspergillus lung disease
- UNCOMMON
* Mainly occurs in the ELDERLY and IMMUNOCOMPROMISED
Recognise the presenting symptoms of Aspergillus lung disease
• Aspergilloma o ASYMPTOMATIC o Haemoptysis (potentially massive) • ABPA o Difficult to control asthma o Recurrent episodes of pneumonia with wheeze, cough, fever and malaise • Invasive Aspergillosis o Dyspnoea o Rapid deterioration o Septic picture
Recognise the signs of Aspergillus lung disease on physical examination
- Tracheal deviation (only with very large aspergillomas)
- Dullness in affected lung
- Reduced breath sounds
- Wheeze (in ABPA)
- Cyanosis (possible in invasive aspergillosis)
Identify appropriate investigations for Aspergillus lung disease
• Aspergilloma o CXR • May show a round mass with a crescent of air around it • Usually found in the upper lobes o CT or MRI - may be used if CXR is unclear o NOTE: sputum cultures may be negative if there is no communication between the cavity colonised by Aspergillus and the bronchial tree • ABPA o Immediate skin test reactivity to Aspergillus antigens o Eosinophilia o Raised total serum IgE o Raised specific serum IgE and IgG to A. fumigatus o CXR • Transient patchy shadows • Collapse • Distended mucous-filled bronchi • Signs of complications: Fibrosis in upper lobes Bronchiectasis o CT • Lung infiltrates • Central bronchiectasis o Lung Function Tests • Reversible airflow limitation • Reduced lung volumes/gas transfer • Invasive Aspergillosis o Aspergillus is detected in cultures or by histological examination o Bronchoalveolar lavage fluid or sputum may be used diagnostically o Chest CT
- Nodules surrounded by a ground-glass appearance (halo sign)
- This is caused by haemorrhage into the tissue surrounding the fungal invasion
Define asthma
• Chronic inflammatory airway disease characterised by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation
Explain the aetiology / risk factors of asthma
Genetic Factors o Family history o Atopy (tendency for T lymphocytes to drive production of IgE on exposure to allergens) Environmental Factors o House dust mites o Pollen o Pets o Cigarette smoke o Viral respiratory tract infections o Aspergillus fumigatus spores o Occupational allergens
Summarise the epidemiology of asthma
- Affects 10% of children
- Affects 5% of adults
- Prevalence appears to be increasing
Recognise the presenting symptoms of asthma
• Episodic history • Wheeze • Breathlessness • Cough (worse in the morning and at night) IMPORTANT: ask about previous hospitalisation due to acute attacks - this gives an indication of the severity of the asthma Precipitating Factors o Cold o Viral infection o Drugs (e.g. beta-blockers, NSAIDs) o Exercise o Emotions Check for history of atopic disease (e.g. allergic rhinitis, urticaria, eczema)
Recognise the signs of asthma on physical examination
• Tachypnoea • Use of accessory muscles • Prolonged expiratory phase • Polyphonic wheeze • Hyperinflated chest Severe Attack o PEFR < 50% predicted o Pulse > 110/min o RR > 25/min o Inability to complete sentences Life-Threatening Attack o PEFR < 33% predicted o Silent chest o Cyanosis o Bradycardia o Hypotension o Confusion o Coma
Identify appropriate investigations for asthma and interpret the results
ACUTE o Peak flow o Pulse oximetry o ABG o CXR - to exclude other diagnoses (e.g. pneumonia, pneumothorax) o FBC - raised WCC if infective exacerbation o CRP o U&Es o Blood and sputum cultures CHRONIC o Peak flow monitoring - often shows diurnal variation with a dip in the morning o Pulmonary function test o Bloods - check: • Eosinophilia • IgE level • Aspergillus antibody titres o Skin prick tests - helps identify allergens
Generate a management plan for asthma
ACUTE
o ABCDE
o Resuscitate
o Monitor O2 sats, ABG and PEFR
o High-flow oxygen
o Salbutamol nebulizer (5 mg, initially continuously, then 2-4 hourly)
o Ipratropium bromide (0.5 mg QDS)
o Steroid therapy
• 100-200 mg IV hydrocortisone
• Followed by, 40 mg oral prednisolone for 5-7 days
o If no improvement –> IV magnesium sulphate
o Consider IV aminophylline infusion
o Consider IV salbutamol
o Anaesthetic help may be needed if the patient is getting exhausted
o IMPORANT: a normal PCO2 is a BAD SIGN in a patient having an asthma attack
• This is because during an asthma attack they should be hyperventilating and blowing off their CO2, so PCO2 should be low
• A normal PCO2 suggests that the patient is fatiguing
o Treat underlying cause (e.g. infection)
o Give antibiotics if it is an infective exacerbation
o Monitor electrolytes closely because bronchodilators and aminophylline causes a drop in K+
o Invasive ventilation may be needed in severe attacks
o DISCHARGE when:
• PEF > 75% predicted
• Diurnal variation < 25%
• Inhaler technique checked
• Stable on discharge medication for 24 hours
• Patient owns a PEF meter
• Patient has steroid and bronchodilator therapy
• Arrange follow-up
CHRONIC THERAPY
o Start on the step that matches the severity of the patient’s asthma
o STEP 1
• Inhaled short-acting beta-2 agonist used as needed
• If needed > 1/day then move onto step 2
o STEP 2
• Step 1 + regular inhaled low-dose steroids (400 mcg/day)
o STEP 3
• Step 2 + inhaled long-acting beta-2 agonist (LABA)
• If inadequate control with LABA, increase steroid dose (800 mcg/day)
• If no response to LABA, stop LABA and increase steroid dose (800 mcg/day)
o STEP 4
• Increase inhaled steroid dose (2000 mcg/day)
• Add 4th drug (e.g. leukotriene antagonist, slow-release theophylline or beta-2 agonist tablet)
o STEP 5
• Add regular oral steroids
• Maintain high-dose oral steroids
• Refer to specialist care
• Advice
o Teach proper inhaler technique
o Explain important of PEFR monitoring
o Avoid provoking factors
Identify the possible complications of asthma and its management
- Growth retardation
- Chest wall deformity (e.g. pigeon chest)
- Recurrent infections
- Pneumothorax
- Respiratory failure
- Death
Summarise the prognosis for patients with asthma
- Many children improve as they grow older
* Adult-onset asthma is usually chronic
Define bronchiectiasis
Lung airways disease characterised by chronic bronchial dilation, impaired mcuociliary clearance and frequent bacterial infections
Explain the aetiology/risk factors for bronchiectasis
Chronic lung inflammation leads to fibrosis and permanent dilation of the bronchi.
This leads to pooling of mucus, which predisposes to further cycles of infection, damage and fibrosis of bronchial walls
Causes of bronchiectasis:
Idiopathic (50%)
Post-infectious (e.g. pneumonia, whooping cough, TB)
Host-defence defects (e.g. Kartagener’s syndrome, cystic fibrosis)
Obstruction of bronchi (e.g. foreign body, enlarged lymph nodes)
GORD
Inflammatory disorders (e.g. rheumatoid arthritis)
Summarise the epidemiology of bronchiectasis
Most often arises initially in CHILDHOOD
Incidence has decreased with the use of antibiotics
1/1000 per year
Recognise the presenting symptoms of bronchiectasis
Productive cough with purulent sputum or haemoptysis
Breathlessness
Chest pain
Malaise
Fever
Weight loss
Symptoms usually begin after an acutre respiratory illness
Recognise the signs of bronchiectasis on physical examination
Clubbing
Coarse crepitations (usually at lung bases) - these shift with coughing
Wheeze
Identify appropriate investigations for bronchiectasis
Sputum Culture and sensitivity Common organisms: Pseudomonas aeruginosa Haemophilus influenzae Staphylococcus aureus Streptococcus pneumoniae Klebsiella Mycobacteria
CXR Dilated bronchi (may be seen as parallel lines going from the hilum to the diaphragm (tramline shadows)) Fibrosis Atelectasis Pneumonic consolidations May be normal
High resolution CT
Best diagnostic method for bronchiectasis
Shows dilated bronchi with thickened walls
Bronchography - rarely used
Others: swear electrolytes (for cystic fibrosis), serum Ig, mucociliary clearance study
Generate a management plan for bronchiectasis
Treat acute exacerbations with TWO IV ANTIBIOTICS, which cover Pseudomonas aeruginosa
Prophylactic antibiotics should be considered in patients with frequent exacerbations (>3/year)
Inhaled corticosteroids (e.g. fluticasone) - reduces inflammation and volume of sputum but does NOT affect the frequency of exacerbations or lung function
Bronchodilators - considered in patients with responsive disease
Maintain hydration
Flu vaccination
Physiotherapy - enables sputum and mucus clearance. This can reduce frequency of acute exacerbations and aid recovery.
Bronchial artery embolisation - if life-tthreatening haemoptysis due to bronchiectasis
Surgical - localised resection, lung or heart-lung transplantation
Identify the possible complications of bronchiectasis
Life-threatening haemoptysis Persistent infections Empyema Respiratory failure Cor pulmonale Multi-organ abscesses
Summarise the prognosis for patients with bronchiectasis
Most patients continue to have symptoms after 10 years
Define chronic obstructive pulmonary disease (COPD)
Chronic, progressive lung disorder characterised by airflow obstruction, with the following:
Chronic Bronchitis - Chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years.
Emphysema - Pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles.
Explain the aetiology / risk factors of chronic obstructive pulmonary disease (COPD)
Bronchial and alveolar damage is caused by environmental toxins (e.g. cigarette smoke)
RARE CAUSE: a1 antitrypsin deficiency
Though this is rare, consider it in young patients, who have never smoked, presenting with COPD type symptoms (and may have accomopanying symptoms of cirrhosis)
Chronic Bronchitis
Narrowing of the airways resulting in bronchiole inflammation (bronchiolitis)
Bronchial mucosal oedema
Mucous hypersecretion
Squamous metaplasia
Emphysema
Destruction and enlargement of alveoli
Leads to loss of elasticity that keeps small airways open in expiration
Progressively larger spaces develop called bullae (diameter > 1cm)
Summarise the epidemiology of chronic obstructive pulmonary disease (COPD)
Very Common (8% prevalence) Presents in middle age or later More common in males - this may change because there has been a rise in female smokers
Recognise the presenting symptoms of chronic obstructive pulmonary disease (COPD)
Chronic cough Sputum production Breathlessness Wheeze Reduced exercise tolerance
Recognise the signs of chronic obstructive pulmonary disease (COPD) on physical examination
Inspection Respiratory distress Use of accessory muscles Barrel-shaped over-inflated chest Decreased cricosternal distance Cyanosis Percussion Hyper-resonant chest Loss of liver and cardiac dullness Auscultation Quient breath sounds Prolonged expiration Wheeze Rhonchi - rattling, continuous and low-pitched breath sounds that sounds a bit like snoring. They are often caused by secretions in larger airways or obstructions. Sometimes crepitations Signs of CO2 retention Bounding pulse Warm peripheries Asterixis LATE STAGES: signs of right heart failure (cor pulmonale) Right ventricular heave Raised JVP Ankle oedema
Identify appropriate investigations for chronic obstructive pulmonary disease (COPD) and interpret the results
Spirometry and Pulmonary Function Tests
Shows obstructive picture
Reduced PEFR
Reduced FEV1/FVC
Increased lung volumes
Decreased carbon monoxide gas transfer coefficient
CXR
May appear NORMAL
Hyperinflation (> 6 anterior ribs, flattened diaphragm)
Reduced peripheral lung markings
Elongated cardiac silhouette
Bloods
FBC - increased Hb and haematocrit due to secondary polycythaemia
ABG - may show hypoxia, normal/raised PCO2
ECG and Echocardiogram
check for cor pulmonale
Sputum and Blood Cultures - useful in acute infective exacerbations
a1 antitrypsin levels - useful in young patients who have never smoked
Generate a management plan for chronic obstructive pulmonary disease (COPD)
STOP SMOKING
Bronchodilators
Short acting beta 2 agonists (e.g. salbutamol)
Anticholinergics (e.g. ipratropium bromide)
Long acting beta 2 agonists (if > 2 exacerbations per year)
Steroids
Inhaled beclamethasone considered in all patients with FEV1 < 50% of predicted
OR
> 2 exacerbations per year
Regular oral steroids should be avoided if possible
Pulmonary rehabilitation
Oxygen therapy
Only for those who stop smoking
Indicated if:
PaO2 < 7.3 kPa on air during a period of clinical stability
PaO2: 7.3 - 8 kPa and signs of secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulmonary hypertension
Treatment of Acute Exacerbations
24 % O2 via Venturi mask
Increase slowly if no hypercapnia and still hypoxic (do an ABG)
Corticosteroids
Start empirical antibiotic therapy if evidence of infection
Respiratory physiotherapy to clear sputum
Non-invasive ventilation may be necessary in severe cases
Prevention of infective exacerbations: pneumococcal and influenza vaccination
Identify the possible complications of chronic obstructive pulmonary disease (COPD) and its management
Acute respiratory failure Infections Pulmonary hypertension Right heart failure Pneumothorax (secondary to bullae rupture) Secondary polycythaemia
Summarise the prognosis for patients with chronic obstructive pulmonary disease (COPD)
High morbidity 3 year survival of 90% if < 60 yrs, FEV1 > 50% predicted 3 year survival of 75% if > 60 yrs, FEV1: 40 - 49% predicted
