Respiratory Flashcards
What is COPD?
Disease state which is characterised by persistent airflow limitation that is not fully reversible. Associated response in the airways and the lungs to noxious particles or gases.
NICE: “COPD is characterised by airflow obstruction… usually progressive, not fully reversible and does not change markedly over several months. The disease is predominantly caused by smoking.”
What is a COPD exacerbation?
An acute event characterised by a worsening of the respiratory system that is beyond normal day-to-day variations and leads to a change in medication.
What is emphysema?
Abnormal and permanent enlargement of air spaces distal to terminal bronchiole, accompanied by destruction of alveolar walls.
What is the FEV1 in COPD?
<80% predicted.
What is the FEV1/FVC in COPD?
<0.7.
What is the most common cause of COPD?
Smokers account for 90% but only 10-20% of smokers develop.
What is COPD associated with the development of?
Emphysema and chronic bronchitis.
What is chronic bronchitis?
Cough with sputum for 3 months per year for 2 or more consecutive years.
What are the types of emphysema?
- Centri-acinar emphysema: distension and damage more concentrated around the respiratory bronchioles whereas the more distal alveolar ducts and alveoli tend to be well preserved, most common
- Pan-acinar emphysema: associated with alpha1-antitrypsin deficiency. Distension and destruction affect the whole acinus so severe airflow limitation and mismatch
- Irregular emphysema: scarring and damage which affects the lung parenchyma patchily, independent of acinar structure.
What are the causes of COPD?
Cigarette smoking.
Chronic exposure to: pollutants at work, air pollution.
Alpha-1-antitrypsin deficiency: alpha-1-antitrypsin is a proteinase inhibitor produced in the liver which inhibits proteolytic enzymes which are capable of destroying alveolar wall connective tissue.
Respiratory infections are often the precipitating cause of acute exacerbations.
What is the pathophysiology of COPD?
Vascular changes: poor V/Q (ventilation/perfusion) match, low PaO2, poor ventilation may give high pCO2, obliteration and vasoconstriction causes pulmonary hypertension.
Mechanisms underlying airflow limitation in COPD:
• Small airways disease: airway inflammation with predominance of neutrophils, CD8 lymphocytes and macrophages which results in scarring and airway fibrosis and luminal plugs and increased airway resistance
• Parenchymal destruction: loss of alveolar attachments and decrease of elastic recoil.
Cigarette smoke causes mucosal gland hypertrophy in larger airways and leads to an increase in neutrophils, macrophages and lymphocytes in airways and walls of bronchi and bronchioles. These cells release inflammatory mediators that attract inflammatory cells (amplify the process), induce structural changes and break down connective tissue in lung (emphysema). This also inactivates alpha-1 antitrypsin.
What is the pathophysiology of chronic bronchitis?
- Airway narrowing (bronchoconstriction) and so airflow limitation as a result of hypertrophy and hyperplasia of mucous secreting glands (goblet cells) of bronchial tree, bronchial wall inflammation and mucosal oedema
- Epithelial layer may become ulcerated and eventually squamous epithelium replaces the columnar cells by squamous metaplasia whilst the ulcer heals
- Inflammation is followed by scarring and thickening of walls which narrows small airways
- The capillary bed remains intact and the body responds to increased obstruction by decreasing ventilation and increasing cardiac output
- Causes a poor ventilation to perfusion mismatch which causes hypoxia
- Obstruction causes increasing residual lung volume (bloating).
So overall, compensatory increase in cardiac output leads to hypoxia.
Acute bronchitis likely to have a viral cause and then a bacterial infection with Strep. Pneumoniae or H. influenzae.
What is the pathophysiology of emphysema?
- Destruction of lung tissue distal to terminal bronchioles
- Results in loss of elastic recoil (normally keeps airways open during expiration)
- Leads to expiratory airflow limitation and air trapping
- This causes premature airway closure which limits expiratory flow while loss of alveoli decreases capacity for gas transfer
- Also causes damage to capillary bed so inability to oxygenate and hyperventilation (puffing).
So overall, compensatory hyperventilation prevents hypoxia.
What is the MRC dyspnoea scoring?
1: SOB on marked exertion
2: SOB on hills
3: slow down or stop on flat
4: exercise tolerance
5: housebound/SOB on minor tasks.
What are the symptoms of COPD?
Shortness of breath.
Chest tightness.
Systemic effects: hypertension, osteoporosis, depression, weight loss, reduced muscle mass with general weakness and right heart failure.
What are the signs of COPD?
- Tachypnoea with prolonged expiration
- Poor chest expansion
- Pursed lips on expiration and intercostal indrawing on inspiration
- Hyper-expansion of lungs: gives barrel shaped chest
- Cyanosis if become insensitive to CO2
- Weight loss
- Cor pulmonale: HF, raised JVP, cardiac output maintained.
What is the phenotype for emphysema?
• Pink puffer: increased alveolar ventilation, weight loss, breathless, emphysematous, maintained paO2, normal or low paCO2, may progress to type 1 respiratory failure.
What is the phenotype for chronic bronchitis?
Blue bloated: cough, phlegm, cor pulmonale, type 2 respiratory failure, decreased alveolar ventilation, low paO2, high paCO2, respiratory centres relatively insensitive to CO2.
What are the FEV1% stages in COPD?
Stage 1: >=80% (mild)
Stage 2: 50-79% (moderate)
Stage 3: 30-49% (severe)
Stage 4: <30% (very severe).
What is the FEV1/FVC for airways obstruction?
<0.7.
What are the investigations for COPD?
• COPD Assessment Score
• Spirometry
• Lung function test: shows progressive airflow limitation with increasing severity and breathlessness. Check it pre and post bronchodilator inhalation.
FEV1% and FEV1/FVC.
Multiple peak flow measurements to exclude asthma.
• Chest X-ray: may be normal or show evidence of hyperinflated lungs (>6 ribs visible) indicated by low, flattened diaphragms and a long narrow heart shadow. There may be reduced peripheral lung marking and bullae (complete destruction of lung tissue producing an airspace > 1cm). Blood vessels may be ‘pruned’ with large proximal vessels. Will show barrel chest in emphysema, flat diaphragm.
• Pulse oximetry
• ABG: may be normal or show hypoxia +/- hypercapnia
• High resolution CT: show emphysematous bullae, particularly useful when X-ray is normal, bronchial wall thickening
• Carbon dioxide gas transfer factor is low when significant emphysema is present
• Haemoglobin level and packed cell volume: can be elevated as a result of persistent hypoxaemia (secondary polycythaemia)
• Sputum examination: may reveal Step.pneumoniae or H.influenzae and Moraxella catarrhalis which can cause infective exacerbations
• ECG: often normal, but may show tall P wave if the patient has pulmonary hypertension secondary to COPD and there might be a RBBB and evidence of right ventricle hypertrophy
• FBC: raised packed cell volume.
What is bronchiectasis?
Airways become abnormally widened resulting in build-up of excess mucus making lungs more susceptible to infection.
What is the difference between asthma and COPD?
Asthma: • Lots of inflammation • Smooth muscle hypertrophy • Basement membrane thickening • Little fibrosis and little alveolar disruption • Cells: mast cells, eosinophils, CD4 T cells, macrophages, • Affects all airways • Responds to steroids • Spirometry may be normal. COPD : • Lots of inflammation • Lots of fibrosis • Lots of alveolar disruption • Little smooth muscle hypertrophy and basement membrane thickening • Cells: neutrophils, CD8 T cells, macrophages • Affects peripheral airways • Does not respond to steroids • Spirometry always abnormal.
What is the management for COPD?
- SABA (short acting beta-2-agonist)/SAMA (short acting anti-cholinergics)
- LABA (long-acting beta-2-agonist)
- LAMA (long-acting anti-cholinergic)
- LAMA + inhaled corticosteroids.
- Smoking cessation: most useful, may slow rate of deterioration/ Pharmacotherapy and nicotine replacement increase long term abstinence rates. Encourage patients to exercise regularly.
- Beta-agonists: short acting beta-2-agonists e.g. salbutamol and terbutaline, long acting beta-2-agonists e.g. formoterol and salmeterol
- Anti-cholinergics/muscarinic: short acting: e.g. ipratropium, long acting cholinergics e.g. tiotropium bromide
- Combinations of short/long acting beta-2 agonists + anticholinergic in an inhaler
- Inhaled corticosteroids e.g. beclomethasone
- Phosphodiesterase-4-inhibitors e.g. Roflumilast which has anti-inflammatory properties (used in addition to bronchodilators in patients with FEV1 <50% and chronic bronchitis)
- Oral corticosteroids in acute exacerbations
- Antibiotics shortens exacerbations and azithromycin can improve quality of life long term
- Mucolytic agents reduce sputum viscosity and reduce the number of acute exacerbations
- Influenza and pneumococcal vaccines offered
- Alpha1-antitrypsin replacement given weekly or monthly.
What are the bronchodilators used in COPD?
- Beta-2 agonists
- Anticholinergics
- Theophylline
- Combination therapy.
What is the combined therapy in COPD?
Inhaled corticosteroid combined with long-acting beta-2-agonists are more effective in improving lung function, health status and reducing exacerbations in moderate to severe COPD.
What are the inhaled corticosteroids used in COPD?
e.g. beclomethasone. Regular treatments with inhaled corticosteroids improve symptoms, lung function, quality of life and reduces frequency of exacerbations and FEV1< 50% predicted. Associated with an increased risk of pneumonia and can lead to exacerbation in some patients. Avoid chronic treatment with systemic corticosteroids due to unfavourable benefit-to-risk ratio. More likely to be beneficial if eosinophilia.
How are COPD exacerbations treated?
ABC: airways, breathing, circulation
Oxygen: titrate to improve hypoxaemia. Target PaO2 saturation in COPD with a risk of hypercapnia is 88-92% and target saturation for normal patients is 94-98%.
Monitor ABG.
Bronchodilators: SABA (+/- SAMA) are preferred.
Systemic corticosteroids and antibiotics:
Antibiotics should be given to patients who have 3 cardinal symptoms: increased dyspnoea, increased sputum volume and increased sputum purulence, and also to those that require mechanical ventilation.
Non-invasive ventilation: CI in asthma, facial burns, vomiting.
Patients should be encouraged to cough up secretions and physiotherapy can help with chest clearance.
When might somebody need oxygen on flights?
FEV1<50%.
What score is used to monitor COPD?
BODE: B odd mass index. D egree of airflow obstruction. D yspnoea. E exercise capacity. A patient with a bode index of 0-2 has a 4 year mortality rate of 10% compared with 80% in someone with a BODE index of 7-10.
What are the indications for specialist referral in COPD?
- Onset of cor pulmonale
- Bullous lung disease
- <10 pack years smoking or <35
- Frequent infections: to exclude bronchiectasis.
What are the complications of COPD exacerbations?
- Accelerated lung function decline
- Polycythaemia
- Respiratory failure
- Cor pulmonale: oedema, raised jugular venous pressure
- Pneumothorax: ruptured bullae
- Lung carcinoma.
What is asthma?
Reversive obstruction of the airways. Airway hyper-responsiveness to a wide range of stimuli with histamine and methacoline. Bronchial inflammation with T lymphocytes, mast cells, eosinophils with associated plasma exudation, oedema, smooth muscle hypertrophy, matrix deposition, mucus plugging and epithelial damage.
What is atopy?
Tendency to develop IgE (produced by B cells) mediated reactions to common allergens.
What are the 2 types of asthma?
Eosinophilic (extrinsic):
• Atopic: associated with allergy (occupation, pets exposures, fungal allergy)
• Non-allergic variant: typically later onset
• T cells involved in allergy (Th2 cells) recruited to lung which trigger eosinophils that damage the epithelium and so excess production of mucous and narrowing/damage of the airways.
Non-eosinophilic (intrinsic): • Pathology poorly understood • Smoking • Obesity-related • Sensitisation to occupational agents • Intolerance to NSAIDs • Prescription of B adrenoceptor blocking agents that block the protective effect of endogenous catecholamines.
What are the environmental causes of asthma?
- Early childhood exposure and childhood infections
- Maternal smoking
- ‘Hygiene hypothesis’: growing up in a relatively clean environment
- Fungal spores in aspergillus fumigatus.
What triggers asthma?
NSAIDs, particularly aspirin and ibuprofen trigger asthma.
What type of hypersensitivity reaction is asthma?
Type 1.
Triggers cause an inflammatory cascade in the bronchial tree. Mast cells, eosinophils, T lymphocytes and dendritic cells increased in bronchial wall, membranes and secretions. Lymphocytes produce interleukins to start the cascade and so IgE is produced. There is increased contraction of smooth muscle in the bronchial wall and remodelling causes more muscle mass in wall and an increased number of goblet cells.
What are the 3 factors contributing to airway narrowing in asthma?
- Bronchial muscle contraction triggered by a variety of stimuli
- Mucosal swelling/inflammation caused by mast cell and basophil degranulation resulting in release of inflammatory mediators
- Increased mucus production.
Why does the diameter of the lumen narrow in asthma?
- Increased number of and hypertrophy of smooth muscle
- Constriction of smooth muscle cells (bronchoconstriction)
- Increased mucous production
- Swelling and inflammation of mucosa
- Thickened basement membrane
- Airway hyperactivity, cellular infiltration.
What are the precipitating factors for asthma,a?
- Occupational asthma: wood dust, bleaches and dyes, isocyanates (industrial coating and spray painting), latex
- Cold air and cold water
- Exercise
- Atmospheric pollution and irritant dust e.g. exhaust fumes and tobacco smoke
- Emotion: high risk asthma attacks in those who are anxious
- Drugs: such as NSAIDs and particularly asthma.
What are the symptoms of asthma?
- Dyspnoea
- Wheeze, exercise induced is driven by release of histamines, prostaglandins, leukotrienes from mast cells, as well as stimulation of neural reflexes
- Cough (often nocturnal)
- Sputum production
- Breathlessness
- Tight chest
- Associated symptoms: eczema and hayfever (rhinitis), nasal disease (Samter’s triad), other food and drug allergies, reflux disease.
What makes a diagnosis of asthma less likely?
- Dizziness/tingling
- No wheeze
- Change in voice
- Normal PEF when symptomatic
- Cardiac disease
- Significant smoking history
- Symptoms with colds only.
What are the signs of asthmma?
- Episodic wheeze: polyphonic, expiratory and widespread
- Tachypnoea
- Tripoding
- Hyperinflated chest
- Hyper-resonant percussion
- Diurnal variation: often worse in morning (nocturnal waking), good days and bad days
- 40-60% have acid reflux
- Provoking factors: allergens, infections, menstrual cycle, exercise, cold air, laughter/emotion, drugs
- Brittle disease: type 1 (severe) is all the time, type 2 (sudden dips where sometimes you’re fine and others you’re not.
What are the investigations in asthma?
Lung function tests: airway obstruction may be present so reduced FEV1 and reduced FEV1/FVC ratio <0.7.
Peak flow test:
• Peak expiratory flow rate reduction from percent predicted variability
• Increased responsiveness to challenge agents e.g. mannitol, methacholine
• Can often be lower in morning and then have a normal one the rest of the time.
Reversibility testing so give treatment (beclomethasone) and see if they get better or not. Increase in lung capacity with bronchodilators or anti-inflammatory treatment. Increase of greater than 15% in FEV1 or PEFR together with increase of 200ml in volume is positive, >=400ml increase makes asthma highly likely. 20% variability in PEFR also suggests asthma.
Bloods for eosinophils:
• Measure FeNO (fraction exhaled nitric oxide)
• Good to test whether there is eosinophilic inflammation in lung
• Marker of eosinophilic inflammation
• Sputum eosinophilia is a more specific diagnostic test.
Tests for atopy and allergy:
• Skin prick tests, IgE
• RAST.
Chest X-ray: to exclude pneumothorax, lung cancer, COPD, infection etc. Shows hyperinflation in chronic or an acute episode. May be useful in detecting the pulmonary infiltrates associated with allergic bronchopulmonary aspergillosis.
Oxygen saturations.
ABG: normal or slightly low PaO2 but low PaCO2 (hyperventilation). If PaCO2 is normal or high, refer to ITU for ventilation because this is a sign of failing respiratory effort.
Carbon monoxide transfer test.
Histamine or methacholine provocation test: suspected patients given increasingly higher doses of histamine or methacholine which induces transient airflow limitation in susceptible individuals. The severity of airway hyper-responsiveness can be graded according to the dose or concentration of the agonist that produces a 20% fall in FEV. Can also be assess by exercise testing or inhalation of cold, dry air, mannitol or hypertonic saline.
Exhaled nitric oxide is a measure of airway inflammation and an index of corticosteroid response. It is used to measure the efficacy of corticosteroids.
Allergen provocation tests is useful in patients with suspected occupational asthma but not ordinary asthma.
What is the management of asthma?
Occasional symptoms: SABA (salbutamol), if using more than once daily or night-time symptoms, go to step 2.
Mild: SABA (salbutamol) + ICS (beclomethasone)
Moderate: SABA (salbutamol) + LABA (salmeterol) + ICS (beclomethasone)
Severe: SABA (salbutamol) + LABA (salmeterol) + ICS (beclomethasone) + 4th drug e.g. omalizumab anti-IgE monoclonal antibody, oral leukotriene.
Very severe: add oral prednisolone. 30mg given daily for 2 weeks with lung function measure before and immediately after. Improvement of >15% in FEV1 confirms the presence of a reversible element.
Rescue courses of prednisolone can be used at any time.
Why are drugs inhaled in asthma?
To avoid first pass metabolism in the liver so lower doses are needed and fewer side effects.
What are the treatments for asthma?
Bronchodilators (SABA, LABA, SAMA, LAMA) treat symptoms not disease. Others include:
• Leukotriene receptor antagonists e.g. Motelukast
• Methylxanthines: theophylline and aminophylline
New biologics, monoclonal antibodies (for eosinophilic, not non-eosinophilic):
• Omalizumab: anti-IgE for atopic disease, chelates free IgE and downregulates the number and activity of mast cells and basophils.
• Mepolizumab, reslizumab, benralizumab: anti-IL-5
• Against Th2 cytokine targets such as thymic stromal lymphopoietin.
Anti-inflammatory drugs like sodium cromoglicate and nedocromil sodium prevent activation of many inflammatory cells, particularly mast cells, eosinophils and epithelial cells (but not lymphocytes) by blocking a specific chloride channel, which in turn prevents calcium influx.
Bronchial thermoplasty for non-eosinophilic asthma heat up bronchial wall from inside using a bronchoscope and kill smooth muscle (rarely used), decreasing bronchoconstriction.
Do not give beta blockers as they innervate PSNS which causes bronchoconstriction.
Mixed evidence for use of macrolide antibiotic azithromycin in long term treatment which has both anti-inflammatory and antibacterial actions.
What is the treatment for acute asthma attacks?
• High flow oxygen
• Emergency beta agonists and steroids: nebuliser salbutamol 5mg (+ipratropium nebuliser if life threatening), repeated IV infusion. Prednisolone orally 30-60mg +/- hydrocortisone 200mg IV. Consider magnesium sulphate or aminophylline IV (bolus/load) if not improved
• Monitor response to treatment: PEFR check within 15-30 minutes/regularly. Oximetry to maintain SaO2>92%. Repeated ABG within 2 hours of severe attack or patient is deteriorating. Watch K+ and glucose. Consider rehydration.
Discharge when patient is ready: need to be off nebuliser and on stable treatment for at least 24 hours. Give steroids for a minimum 7-14 days. Early clinical review (48 hours after at GP surgery).
What are the features of an acute severe asthma attack?
- An inability to complete a sentence in one breath
- A respiratory rate of >=25 breaths per minute
- A tachycardia of >=110 bpm
- A PEFR of 33-50%.
How do you recognise a life-threatening asthma attack?
- A silent chest, cyanosis or feeble respiratory effort
- Exhaustion or altered level of consciousness
- Bradycardia, hypotension or arrhythmia
- PEFR of <33% of predicted normal or best (approximately 150ml in adults) or SpO2 <92%.
- ABG: gases of acute severe or low saturations (<92% on air, or needing oxygen)
- Chest X ray if suspect pneumothorax, consolidation, life-threatening asthma, failure to respond
- Pulse oximetry is useful in monitoring oxygen saturation
- A high PaCO2 >6
- Severe hypoxaemia: PaO2<8 despite treatment with oxygen
- A low or falling arterial pH.
How are asthma attacks classified?
- Uncontrolled/moderate: PEFR >50%, respiratory rate <25, pulse <110, normal speech
- Severe: PEFR 33-50% predicted, respiratory rate >=25, heart rate >=110, inability to complete sentences.
- Life-threatening: PEFR: <33%, SaO2<92% or PaO2<8kPa, normal PaCO2 4.6-6 kPa, altered conscious level, exhaustion, arrhythmia, hypotension, silent chest, poor effort, cyanosis
- Near fatal: raised PaCO2 and/or requiring ventilation with raised airway pressures.
What is a pulmonary embolus?
Blood clot in the lungs. Thromboembolus blocks right ventricular outflow, pulmonary arteries and branches.
What causes a pulmonary embolus?
Blood clots breaking off and passing through veins into inferior vena cava then into right side of the heart before lodging in pulmonary circulation. Emboli usually arise from thrombi in the iliofemoral veins (DVT).
What are the risk factors for PE?
- Change in blood flow: immobility e.g. post-op or paralysis, obesity, pregnancy
- Change in blood vessels: smoking, hypertension
- Change in blood constituents: dehydration, malignancy, high oestrogen combined contraceptive pill, polycythaemia, nephrotic syndrome
- Recent surgery: especially abdominal/pelvic or hip/knee replacement, always suspect PE in sudden collapse 1-2 weeks after surgery
- Family history or past history of thromboembolism.
What is a risk for thrombosis in PE?
Thrombosis risk: • Active cancer or cancer treatment • >=60 years • Dehydration • Known thrombophilias • Obesity • Medical comorbidities • Use of HRT • Oestrogen containing contraceptive pill • Varicose veins with phlebitis • Pregnancy or <6 weeks postpartum.
What are the 3 main factors which predispose you to clots?
- Circulatory stasis
- Endothelial injury
- Hypercoagulable state.
What is the pathophysiology of a PE?
Blood clots (usually in pelvis or legs) break off and pass through veins, into IVC then through the right side of the heart into pulmonary circulation where it becomes lodged, most likely in the small capillaries suppling the alveoli.
A large embolus obstructs the right ventricle outflow tract and suddenly increases pulmonary vascular resistance which causes right heart failure.
A small embolus impacts in a terminal, peripheral pulmonary vessel and may be clinically silent until it causes pulmonary infarction.
Lung tissue is ventilated but not perfused so there is impaired gas exchange.
After some hours, non-perfused lung no longer produces surfactant and so alveolar collapse which exaggerates hypoxaemia.
Primary haemodynamic consequence of PE is a reduction in cross-sectional area of pulmonary atrial bed which causes an elevation of pulmonary atrial pressure due to the increased resistance and a reduction in cardiac output.
Right ventricle ischaemia can be detected by elevations of troponin and creatinine kinase.
What are heritable thrombophilias?
- Factor V Leiden: mutation in clotting factor V that causes activated clotting factor V to be resistant to inactivation by activated protein C and so leads to an increase in thrombin formation. Thrombin converts soluble circulating plasma fibrinogen into insoluble fibrin
- Mutation in the 3’ untranslated region of the prothrombin gene: causes levels of prothrombin to rise
- Antithrombin: a serine protease inhibitor (serpin) that inhibits predominantly thrombin and factor Xa reactions that are catalysed by heparin. Reduced antithrombin means more thrombin (can also be low in liver disease or acute illness). Because antithrombin is required for the action of heparin, those with antithrombin deficiency may be relatively resistant to heparin
- Protein C and protein S deficiency: vitamin K dependent, naturally occurring anticoagulants. Together they inhibit the activated forms of the clotting system co-factors Va. Deficiency leads to an increase in thrombin generation. Can be deficient with vitamin K deficiency, liver disease, warfarin of in the case of protein S, in pregnancy or oestrogen therapy.
What is the extrinsic system?
Inactive circulating clotting factors become locally activated and the binding of circulating factor VII to tissue factor (a receptor expressed on subendothelial and adventitial cells) and leads to the generation of activated factor X. This is the extrinsic system. This in turn results in initial thrombin generation and subsequent amplification of the process through the intrinsic system, leading to further factor X and thrombin generation.
What are the symptoms of PE?
- Sudden onset dyspnoea
- Pleuritic chest pain
- Haemoptysis.
What are the signs of a PE?
- Pyrexia
- Hypotension
- Tachypnoea
- Pleural rub
- Exudative pleural effusion
- Tachycardia
- Raised JVP (if massive)
- RV heave (if massive)
- Second heart sound and gallop (if massive).
What is the definitive investigation for a PE?
CT pulmonary angiograph, or if not available a transthoracic echocardiogram.
What are the investigations of a PE?
Definitive: CT pulmonary angiograph, or if not available a transthoracic echocardiogram.
Chest X-ray: • Often normal • Decreased vascular marking • Blunting of costophrenic angle • Wedge-shape areas of infarction • Pulmonary oligaemia (local reduction in blood perfusion) in massive embolism • Raised hemi diaphragm.
Bloods: raised troponin.
Ventilation-perfusion isotope lung scanning:
• Perfusion phase: technetium labelled aluminium aggregates are injected intravenously and blood flow to the lungs is assessed
• Ventilation phase: patients inhale radiolabelled xenon or technetium to assess air delivery to the lungs.
Diagnosis is made if perfusion is abnormal but ventilation is normal.
ECG: • May be normal • May show sinus tachycardia • Right atrial dilation with tall peaked P waves in lead II • Right bundle branch block • RV strain: inverted T wave in V1-V4 • May exclude differentials e.g. MI.
ABG:
• May be normal
• With significant PE, there will be arterial hypoxaemia i.e. low PaO2 and low PaCO2 (type 1 respiratory failure).
Plasma D-dimer: subset of fibrinogen degradation products released into circulation when clots begin to dissolve. Not diagnostic as it can be raised in other conditions e.g. cancer, pregnancy, post-op. Negative D-dimer excludes chance that it could be a PE.
Ultrasound: look at leg and pelvis for clots.
Echocardiography: diagnostic and can be performed at bedside, good for massive.
What is raised in a PE?
Troponin and plasma D-dimer.
What is the treatment for a PE?
- High flow oxygen
- LMWH e.g. enoxaparin or dalteparin initially then warfarin when PE is confirmed (warfarin not given originally as it needs at least 5 days to provide therapeutic anticoagulation. When INR is 2 or more on 2 consecutive days can stop heparin)
- DOACs or warfarin
- IV fluids and inotropic agents to improve pumping of right ventricle
- Thrombolysis for massive PE (severe hypotension): actually dissolve the blood clots, alteplase
- Analgesia
- Surgical embolectomy: when thrombolysis is CI
- If high risk of recurrence or CI to anticoagulation e.g. active bleeding, do vena cava filter. Prevents blood clot from the deep veins in the leg from entering the lungs.
What treatment in PE is CI in pregnancy?
Warfarin and DOACs cross the placenta and so should not be used in pregnancy. Warfarin causes embryopathy between the 6th and 12th weeks., later in the pregnancy it causes bleeding in the foetus. Women on warfarin at the time of becoming pregnant are safe until 6 weeks.
LMWH is safe in pregnancy.
Both warfarin and LMWH safe in breast-feeding but DOACs should be avoided. LMWH more effective than warfarin in patients with active cancer.
What are the monitoring scores for a PE?
Revised Geneva score to predict probability of PE.
Two level-Wells score for prediction.
What are the complications of a PE?
Acute right heart failure, syncope and death follow a massive PE rapidly.
Mortality rate by 1 month is around 5% (half are due to associated comorbidities). Most common cause of hospital-related death.
Where does the upper respiratory tract go from?
Upper respiratory tract goes from nose to larynx above vocal cords.
What are types of upper respiratory tract infections?
Viral illnesses: • Rhinoviruses (45-50%) • Influenza A virus (25-30%) • Coronaviruses (10-15%) • Parainfluenza viruses (5%) • Respiratory syncytial viruses (5%).
Emergency respiratory infections:
• Severe acute respiratory syndrome (SARS): associated with coronavirus, outbreak from China, severe respiratory illness with respiratory failure
• Middle East Respiratory Syndrome novel Coronavirus (MERS-nCV): from middle east, similar to SARS but low person-to-person spread (camels, bats etc)
• Avian flu: novel form of influenza A virus, occasional human cases with severe illness, seen in SE Asia, associated with poultry exposure, low person-to-person spread.
What are complications of upper respiratory tract infections?
Sinusitis, pharyngitis, otitis media, bronchitis. Influenza A in particular causes systemic symptoms.
What are the defences in upper respiratory tract infections?
Defences:
Mucosal defences:
• Cough reflex
• Mucus barrier and respiratory cilia (mucocilliary escalator which clears gunk)
• Swallowing
• Commensal flora: colonisation resistance.
Innate immune defences:
• Alveolar macrophages: orchestrate immune response, phagocytic
• Soluble factors: IgA, defensins, collectins, lysozyme
• Neutrophils: first cells recruited, phagocytic.
Adaptive immune defences:
• B cells: antibody formation
• T cells: cell mediated CD8 cytotoxicity, CD4 helper cell function, regulatory function.
What are the types of influenza?
Member of the Orthomyxoviridae family with three separate genera: serotype A, (worldwide pandemics) B (localised outbreaks) and C (akin to common cold). Further divided into 2 key surface antigens:
• Haemagglutinin (15 subtypes): virus binding and entry to cells e.g. “grappling hook” for getting in so facilitates entry into host respiratory cell
• Neuraminidase (9 subtypes): “bolt cutter” for getting out, cuts newly formed virus loose from infected cells and prevents it clumping together so facilitates release of virions from infected cells. Immunity to subtype reduces amount of virus released from cells resulting in a less severe disease.
How is influenza transmitted?
Mainly via aerosols generated by coughs and sneezes. Also possible via hand-to-hand contact, other personal contact or fomites.
It is seasonal.
What is the incubation period for influenza?
1-3 days.
What are the symptoms of influenza?
- Abrupt fever
- Aching in limbs
- Sore throat
- Dry cough
- Headache
- Myalgia and weakness
- Diarrhoea in H5N1 ‘bird flu’.
How is a diagnosis of influenza made?
Definitive diagnosis can be established by demonstrating a four-fold increase in complement-fixing antibody or haemagglutinin antibody measure at onset and after 1-2 weeks or taking nasopharyngeal swabs.
Viral PCR, rapid antigen testing, viral culture of clinical samples (swabs).
What medical treatment is given in influenza?
Antivirals e.g. Tamiflu (neuraminidase inhibitor):
• Reduce risk of transmission to others
• Reduce severity and duration of symptoms
• Only give if at increased risk.
Bed rest and paracetamol, with antibiotics to prevent secondary infection in those with chronic bronchitis or cardiac renal disease.
What precautions are taken in a patient with influenza?
Inpatients should be cared for in a side room.
What is a complicated influenza?
Includes lower respiratory tract infection, exacerbation of any underlying medical condition, all needing hospital admission.
What drugs are given in complicated influenza?
- Oseltamivir, first line
* Zanamivir e.g. in type AH1N1.
In how many people are the influenza vaccines effective?
About 70%.
Who is routine flu vaccine suggested for?
for >65 years or if younger and have chronic heart, lung (including asthma), kidney disease, diabetes mellitus or in the immunosuppressed. Should be careful in those with egg protein allergy.
What are the complications of influenza?
Bacterial pneumonia, staphylococcus aureus can be life-threatening. Particularly streptococcus pneumoniae and H influenzae.
- Post infectious encephalomyelitis
- Exacerbation of chronic lung disease
- Otitis media
- Diarrhoea and vomiting.
Who is the mortality risk in influenza high in?
- Chronic cardiac, pulmonary and liver diseases
- Old age
- Chronic metabolic diseases
- Chronic renal diseases
- Immunosuppressed
- Diabetes mellitus
- Pregnancy
- BMI
- > 65 years
- BMI> 40.
What is pharyngitis/tonsillitis?
Infections in the throat that cause inflammation. If tonsils primarily affected, tonsillitis. If throat primarily affected, pharyngitis.
What are the causes of pharyngitis/tonsillitis?
Viral (70-80%): • Adenovirus (most common) • Rhinovirus • EBV • Acute HIV.
Bacterial: • Lancefield Group A Beta-haemolytic strep e.g. S.pyogenes • Mycoplasma pneumoniae • Neisseria gonorrhoea • Fusobacterium necrophorum.
What are the symptoms of pharyngitis/tonsillitis?
- Sore throat for >24 hours
* Fever.
What can glandular fever present with?
Tonsillitis.
What are the signs of pharyngitis/tonsillitis?
- Tender glands in neck
- Red oropharynx and soft palate
- Inflamed and swollen tonsils
- Stable vitals
- Tender anterior cervical lymph nodes.
What is persistent/severe tonsillitis treated with?
Phenoxymethylpenicillin or cefaclor.
What is sinusitis?
Infection of the paranasal sinuses. Bacterial or occasionally fungal.
What are the causes of sinusitis?
- Virus is most common
- Bacterial: strep. Pneumoniae (40%), H. influenza (30-35%)
- Most commonly associated with upper respiratory tract infection and occasionally asthma and allergic rhinitis.
What are the symptoms of sinusitis?
- Frontal headache
- Facial pain
- Fever.
What are the signs of sinusitis?
- Purulent nasal discharge
* Tenderness.
What is the management of sinusitis?
- Nasal decongestants e.g. xylometazoline
* Broad spectrum antibiotics e.g. co-amoxiclav (H.influenzae can be resistant).
What is acute epiglottitis?
Inflammation of the epiglottis (flap of cartilage behind the root of the tongue which is depressed during swallowing to cover opening of the windpipe).
Why is acute epiglottitis now rare?
H. influenzae B vaccine.
What are the causes of acute epiglottitis?
- H. influenzae type B (Hib)
- Causes of pharyngitis and other bacterial infections of airway
- Caused by additional pathogens in immunocompromised e.g. AIDs.
What are the symptoms of acute epiglottitis?
- Sore throat and pain on swallowing (odynophagia)
- High pitched wheeze (inspiratory stridor)
- Diarrhoea
- Fatigue
- Weight loss
- High fever.
What are the signs of acute epiglottitis?
- Severe airflow obstruction
- Meningitis
- Septic arthritis
- Osteomyelitis.
What is the management for acute epiglottitis?
- Endotracheal intubation
* IV antibiotics: amoxicillin, co-amoxiclav, erythromycin, doxycycline.
Who does whooping cough affect?
Children <5.
What are the causes of whooping cough?
- Bordatella pertussis: gram negative coccobacillus (rod)
* Brodatella parapertussis and bordatella bronchiseptica produce milder infections.
What are the symptoms of whooping cough?
- Chronic cough
- Vomiting
- Malaise
- Anorexia
- Rhinorrhoea.
What are the signs of whooping cough?
- Classic inspiratory whoop: only seen in younger individuals in whom the lumen of the respiratory tract is compromised by mucous secretion and mucosal oedema
- May be associated with complications: pneumonia, encephalopathy, sub-conjunctival haemorrhage.
How is a diagnosis of whooping cough made?
- Chronic cough and one clinical feature indicated pertussis
- Culture of nasopharyngeal swab
- PCR
- ELISA for IgG against PT.
What is the management for whooping cough?
- Antimicrobials: eliminate carriage of bacteria e.g. clarithromycin
- Vaccination.
What is croup/acute laryngotracheobronchitis a complication of?
Acute laryngitis is an occasional complication of URT infections, particularly those caused by parainfluenza and measles.
When is croup/acute laryngotracheobronchitis most severe?
In children under 3.
What causes croup/acute laryngotracheobronchitis?
Parainfluenza viruses.
What is the pathophysiology of croup/acute laryngotracheobronchitis?
Inflammatory oedema extends to vocal cords and epiglottic, causing narrowing of airway (may be associated with tracheobronchitis). Progressive airway obstruction may occur, with recession of soft tissue of neck and abdomen during inspiration and in severe cases central cyanosis.
What is the main symptom of croup/acute laryngotracheobronchitis?
Prominent barking cough (croup).
What are the signs of croup/acute laryngotracheobronchitis?
- Febrile
- Respiratory rate of 40
- Cyanosis
- Inspiratory stridor
- Hoarse throat.
What is the management for croup/acute laryngotracheobronchitis?
- Nebulised adrenaline: short term relief
* Oral or IM corticosteroids e.g. dexamethasone + oxygen and fluids.
What is pneumonia?
Pneumonia is the general term attached to inflammation of the lung parenchyma.
What are the most common causes of pneumonia?
Usually due to infection that affects distal airways and alveoli with formation of an inflammatory exudate. Usually bacterial but can be viral or fungal. With intense infiltration of neutrophils in and around alveoli and terminal bronchioles.
How are the types of pneumonia categorised?
The setting which person has contracted the infection in.
What are types of pneumonia?
- Community-acquired pneumonia
- Hospital-acquired pneumonia: acquired at least 48 hours after hospital admission, usually most resistant. In the elderly, ventilator-associated, post-op, immunocompromised, aspiration pneumonia (inhaling something that shouldn’t be allowed e.g. food which isn’t sterile)
- Aspiration pneumonia: associated with the aspiration of food material or stomach contents into the lungs and caused by impaired swallowing. Most likely to end up in the right middle lobe or the right upper lobe.
- Pneumonia in immunocompromised patient: acquired through either a genetic defect, immunosuppressive medication or acquired immunodeficiency, as in HIV
- Ventilator-acquired pneumonia: acquired through mechanical ventilation on a critical care e.g. Acinetobacter baumanii).
What is the common cause of immunocompromised pneumonia?
Pneumocystis jirovecii.
Radiographic appearance is diffuse bilateral alveolar and interstitial shadowing, localised infiltration and first line treatment co-trimoxale.
What is the most common cause of community acquired pneumonia?
Strep pneumoniae.
What type of bacteria is strep pneumonia?
Gram positive cocci. Alpha haemolytic.
What are the causes of community acquired pneumonia?
Strep pneumoniae (40%). Chlamydophila pneumoniae (13%). Mycoplasma pneumoniae (11%). H. influenzae B (5%). Legionella pneumophilia (5%). Klebsiella pneumoniae (rare). S. aureus. No diagnosis (31%).
What type of bacteria is H. influenzae?
Gram negative coccobacilli.
What is atypical pneumonia?
Immunosuppressed, pre-existing lung disease and don’t respond to amoxicillin.
