Respiratory Flashcards
Describe FEV1 and FVC in terms of restriction and obstruction
FEV1 / forced expiratory volume - maximum inspiration exhaled as fast as possible. Healthy should be 80% of vital capacity, assessment of lung health
FVC / forced vital capacity - total amount of air expired. Compared to predicted values should be at least 80%
Low forced vital capacity = airway restriction (FEV1 / FVC normal) (entire lungs less)
Parenchyma / chest walls - interstitial lung disease (fibrosing alveolitis, sarcoid)
FEV1 / FVC < 0.7 = airway obstruction (can’t breath out fast), FVC normal
Airways - asthma, COPD obstructive
Describe type 1 and 2 respiratory failure
Type 1 respiratory failure: partial CO2 is low or normal, gas exchange is impaired at level of alveolar-capillary membrane
Pulmonary oedema, pneumonia, asthma, acute respiratory distress syndrome
Type 2 respiratory failure: partial CO2 is high, is due to respiratory pump failure
COPD, Guillain-Barre, opioid overdose
(Type 1 has 1 change (low pO2) type 2 has 2)
Pathophysiology of COPD and common associations
Cigarette smoking major cause (m gland hypertrophy), also chronic exposure to pollutants (working in building, chemicals, cooking), alpha1 antitrypsin causes early onset (proteolytic lung damage)
Increased number of mucus secreting goblet cells especially in larger bronchi, in advanced cases bronchi become inflamed with pus in the lumen
V/Q mismatch leads to fall in PaO2, CO2 excretion less effected, long term insensitivity to CO2 and start relying on hypoxaemia to breathe. Due to risk of hypercapnia have to be careful giving oxygen (target of 88-92%, 94-98 if pCO2 normal)
Associated with chronic bronchitis: hypertrophy and hyperplasia of mucus glands, wall inflammation (infiltration) and mucosal oedema. Inflammation causes scarring and thickening of walls
Also emphysema: dilation and destruction of lung tissue distal to terminal bronchioles, causes loss of elastic recoil, expiratory limitation and airway trapping (premature closing of airways)
Presentation of COPD
Productive cough with white or clear sputum, wheeze, breathlessness, frequent cold and infections, symptoms worsened by cold weather
Usually following many years of smokers cough
Signs: tachypnoea, accessory muscles, hyperinflation, reduced chest expansion, resonant percussion, quiet breath sounds, wheeze, cyanosis, cor pulmonale
Systemic: hypertension, osteoporosis, depression, weight loss, general weakness
Investigations for COPD
Lung function: airway obstruction - FEV1/FVC < 0.7, FEV less than 80% of predicted
FEV1 shows GOLD stages: 1 80%, 2 - 50-79%, 3 - 30-49%, 4 - <30%
Will have little response to salbutamol
Chest x ray (hyperinflation, flat hemidiaphragms, large pulmonary arteries, bullae), CT - emphysema, ABG, alpha1 antitrypsin test, FBC (chronic hypoxia - polycythaemia)
Cor pulmonale - pathophysiology, causes, signs and symptoms
Right sided heart failure caused by respiratory disease, increased pressure + resistance in pulmonary arteries limits RV → back pressure into RA, vena cava and venous system
Causes: COPD, PE, interstitial lung disease, CF, primary pulmonary hypertension
Sx: SOB, peripheral oedema, breathless on exertion, syncope, chest pain
Signs: hypoxia, cyanosis, raised JVP, peripheral oedema, parasternal heave, loud S2 heart sound, murmur (pan systolic tricuspid regurgitation), hepatomegaly
What is the pathogenesis of asthma
Narrowing airways (obstruction) due to smooth muscle contraction (bronchoconstriction), thickening of airway walls (inflammation, cellular infiltration), increased mucus secretions in lumen
Atopic: hypersensitive IgE response to environmental triggers, mast cells become sensitised when IgE bind and respond when allergens present. Histamine released (bronchoconstriction), cytokines - more mast cells and attract eosinophils
Chronic asthma - airway smooth muscle hypertrophy and hyperplasia, further thickening due to deposition of collagens and matrix proteins, epithelium is damaged - loss of ciliated columnar cells
Presentation of asthma
Episodic wheeze + dyspnoea, cough (especially nocturnal), provoking factors, classically diurnal (often worse at 3-4am). 50% have reflux - treating can improve lung function
Signs: tachypnoea, (widespread, polyphonic, expiratory) wheeze, hyperinflation, hyperresonant percussion, reduce air entry, prolonged expiration
During attacks: progressive dyspnoea, use of accessory muscles, tachypnoea, symmetrical expiratory wheeze, reduced air entry. Severe unable to speak, tachycardia, confused
Investigations for asthma
Lung function test: > 12% improvement in PEFR or FEV1 with bronchodilator, reduced FEV1, FEV:FVC <0.7. Fractional exhaled nitric oxide > 40 ppb (airway inflammation)
Peak flow diary: twice daily over 4w, more than 20% is positive
Direct bronchial challenge testing (opposite of reversibility): inhaled histamine / methacholine, reduction in FEV1 by 20%
Severity: RCP3 - recent nocturnal waking? Usual daily asthma symptoms? Interferences with activities of daily living
How is severity of an asthma attack worked out
Moderate PEFR 50-75%, RR < 25, pulse < 100
Severe attack: PEFR 33-50%, inability to complete sentence, pulse > 110, RR > 25
Life threatening attack ACHEST: altered conscious, PaCO2 normal (cyanosis), hypoxia (<92%), exhaustion, silent chest, threatening PEFR < 33%
Management of asthma and asthma attacks
Maintenance: SABA reliever, low dose ICS preventer (beclomethasone); + LTRA (montelukast) (if not enough consider stopping); + LABA fixed dose with ICS (beclometasone/formoterol) or MART (also includes salbutamol) regime; moderate dose ICS; specialist therapies (high dose ICS< LAMA, theophylline, biologicals)
Children 5+ treated the same, stop LTRA if not helping
<5: SABA, + trial of moderate ICS, SABA + low ICS + LTRA, stop LTRA and refer
Intermittent reliever SABA - salbutamol, regular maintenance ICS - beclomethasone (cleanil), initial add on LTRA - montelukast, LABA - salmeterol instead of montelukast
Life threatening: oxygen 15L non breathe, nebulised salbutamol, oral prednisolone (5d following), no response - nebulised ipratropium bromide, IV magnesium sulphate / salbutamol / aminophylline
Pathogenesis of lung cancers
Cigarette smoking accounts for 80%, also occupational (asbestos, coal, chemicals)
Asbestos causes mesothelioma: pleura, latent period, very aggressive
Small cell carcinoma (20%): from endocrine (Kulchitsky) cells, secretes polypeptide hormones - paraneoplastic syndrome (PTH, ADH, ACTH), high grade and aggressive.
Lambert eaton myasthenic syndrome caused by antibodies against small cell
Non-small cell: adenocarcinoma (mucus gland, 40%) usually single lesion, metastases common; squamous (keratin producing epithelium, 20%), frequently caviate with central necrosis; large cell carcinoma
Lungs are a common site for metastases (more common than primary)
Presentation of lung cancer
Local disease: cough (3 weeks merits CXR), SOB, breathlessness, haemoptysis, chest pain, recurrent infections, weight loss
Signs: finger clubbing, lymphadenopathy (subclavicular), cachexia, consolidation, pleural effusion
Metastatic disease: weight loss, bone pain, headache, seizures, neurological deficit, hepatic pain, abdominal pain
Extrapulmonary: recurrent laryngeal / phrenic nerve palsy, superior VC obstruction, paraneoplastic
Investigations + referral and management of lung cancer
X ray (hilar enlargement, peripheral opacity - round / fluffy, lung collapse, pleural effusion), contrast CT (or PET) to stage, bronchoscopy (assessment and biopsy), cytology, bloods - polycythaemia
Molecular testing used to find appropriate adjuvant chemotherapy
Referral criteria - 2w Xray: 40+ clubbing, lymphadenopathy, recurrent chest infections, thrombocytosis, chest signs
Recommend Xray if 2+ unexplained symptoms and never smoked, 1+ unexplained if smoke / asbestos exposure
Small cell: limited disease - combined chemo and radio, extensive - chemo (may respond but often relapses), palliative - endobronchial, pleural drainage, SVC stent if required
Non small cell: if no metastatic spread and peripheral - surgical excision, curative radio if respiratory reserve is poor, chemo +/- radio if advanced disease also monoclonal antibodies (cetuximab)
Pathophysiology of pulmonary embolism
Majority from lower DVT, also pelvic and abdominal veins; run to inferior vena cava, enter the right atrium and pulmonary circulation before lodging
Other causes: RV thrombus (post MI), septic emboli, fat (bone fracture), air, neoplastic, parasites, foreign material from IV drugs
Lung tissue is ventilated not perfused - intrapulmonary dead space, stops producing surfactant and alveoli collapse - hypoxaemia. Reduction in pulmonary area, increased resistance (and pulmonary pressure) so a reduction in cardiac output
Presentation of PE
Depends on number and size, small will often be asymptomatic. Sudden onset dyspnoea is often the only symptom
Dyspnoea, cough, haemoptysis, pleuritic chest pain, dizziness + syncope
Signs: hypoxia + cyanosis, tachycardia, raised respiratory rate, low grade fever, hypotension + haemodynamic instability, raised JVP, pleural rub, DVT
Investigations and scoring of PE
CT pulmonary angiogram + D-dimer (95% sensitive not specific), ventilation perfusion scan
X ray and ECG more to rule out others. Echocardiogram (RVHF) if CTPA not available
Blood gases - may be normal, significant will have arterial hypoxaemia/ type 1 respiratory failure - low PaO2 and CO2, respiratory alkalosis due to hyperventilation
Pulmonary embolism rule out criteria, Well’s score
Management of PE
Haemodynamically stable: apixaban / rivaroxaban FL, enoxaparin / dalteparin SL; continue for 3m
Haemodynamically unstable (hypotension): IV fluids, high flow oxygen, continuous infusion unfractionated heparin (start before thrombolysis), thrombolysis with IV alteplase, morphine
Surgical embolectomy, catheter thrombectomy, vena cava filter, ted stockings
Following: DOAC in most (apixaban), warfarin (INR 2-3) in antiphospholipid / severe CKD, LMWH in pregnancy
Prophylaxis: high risk give enoxaparin / dalteparin (LMWH), compression stockings
Pathogenesis of upper respitatory infections
Overcomes defence: commensal flora (sinuses should be sterile), swallowing, mucus and ciliated epithelium in lungs, cough + sneeze, immune cells + humoral
Viral most common, usually transient: rhinovirus, influenza A, coronavirus, adenovirus
Emergency: SARS, MERS, avian influenza
Most bacterial infections from commensals. Common: group A strep (throat), strep pneumoniae (sinusitis)
Whooping cough is caused by bordetella pertussis, multiple virulence factors (several toxins), lymphoid hyperplasia causes chronic inflammation
Catarrhal phase (1-2w): malaise, anorexia, rhinorrhoea, highly infectious. Paroxysmal (1-6w): coughing spasms terminating in vomiting, inspiratory whoop (only in younger)
