Respiratory Flashcards
Type 1 Respiratory Failure
Low O2, low CO2
Emphysema, astham, pneumonia, pulmonary oedema, PE
Type 2 Respiratory Failure
Low O2, high CO2
Chronic bronchitis, COPD, life-threatening asthma, Guillain-Barre with respiratory failure
Asthma
Chronic inflammatory disorder of the airways. Often with family history of atopy (asthma, allergic rhinitis, eczema). Occupational asthma also present.
Triggers
- URTI, allergens, irritants, drugs (NSAIDs, B-blockers)
Signs
- Dyspnea, wheezing, chest tightness, nocturnal cough, sputum
Partly controlled asthma:
- Daytime: >2/wk
- Night-time: any
- Limitations of activity: any
- Reliever treatment: >2/wk
- Exacerbation: >1/yr
Investigations
- O2 sats
- ABGs
- Pulmonary function test
Treatment:
- Education, avoid triggers
- Pharmacological: SABA, inhaled corticosteroids, LABA, anti-IgE
Hospital admission:
- Require bronchodilator more than 3 hourly
- Persisting oxygen desat at <92%
Emergency management
1) inhaled SABA
2) systemic steroids
3) anticholinergic therapy + Mg
4) intubation in life threatening cases
5) SC adrenaline
6) corticosteroid therapy at discharge
Chronic obstructive pulmonary disease
Progressive and irreversible condition of the lung. 2 types: chronic bronchitis and emphysema
Bronchitis:
- chronic productive cough, purulent sputum, hemoptysis, mild dyspnea
- cyanosis, peripheral edema from cor pulmonale, crackles, wheeze, prolonged expiration
Emphysema:
- dyspnea, minimal cough, tachypnea, decreased exercise tolerance
- pink skin, pursed lip breathing, accessory muscle use, hyperinflation, decreased breath sounds
Treatment
Prolong survival: smoking cessation, vaccination, home oxygen
Symptomatic relief: bronchodilators (SA: ipratropium/salbutamol, LA: tiotropium/salmeterol), corticosteroids, lung transplant.
Acute exacerbations of COPD
- Causes: viral URTI, bacteria, air pollution, CHF, PE, MI
- Management: O2 (88-92% for CO2 retainers), bronchodilators, systemic corticosteroids, antibiotics (amoxicillin, cefaclor, erythromycin)
- ICU admission for life threatening exacerbations
Complications:
- Polycythemia secondary to hypoxemia
- Pulmonary HTN due to vasoconstriction
- Cor pulmonale
- Pneumothorax
Bronchiectasis
Irreversible dilatation of airways due to inflammatory destruction of airway walls by persistently infected mucous.
P. aeruginosa, S. aureus, H. influenza are common pathogens.
Features: chronic cough, purulent sputum, hemoptysis, recurrent pneumonia, local crackles, wheezes, clubbing.
Treatment:
- Vaccination, influenza, pneumonia
- Abx and inhaled corticosteroids for acute exacerbations
- Chest physiotherapy, breathing exercises, physical exercise
Cystic fibrosis
Chloride transport dysfunction, thick secretions from exocrine glands (lung, pancreas, skin, reproductive organs) and blockage of ducts.
Features: chronic bronchitis, pancreatic insufficiency, diabetes, azoospermia.
Infections: S.aureus, P. aeruginnosa, B. cepacia, Aspergillus fumigatus
Investigations:
- Sweat chloride test >60 mmol/L in children
- PFTs, ABGs, CXR
Treatment
- Chest physiotherapy and postural drainage
- Bronchdilators
- Inhaled mucolytic, hypertonic saline DNase
- Inhaled tobramycin
- Abx: ciprofloxacin
- Pancreatic enzyme replacement
Interstitial lung disease
Inflammatory and/or fibrosing process in the alveolar walls, distortion and destruction of normal alveoli. Associated with lung restriction, decreased lung compliance, impaired diffusion, hypoxemia (V/Q mismatch), pulmonary HTN or cor pulmonale
Features: SOB, nonproductive cough, fine crackles, clubbing, cor pulmonale features
Unknown etiology:
- Idiopathic interstitial pneumonias
- Sarcoidosis
- Langerhans-cell histocytosis
- Pulmonary infiltrates with eosinophilia
Known etiology:
- Systemic rheumatic disorders: scleroderma, RA, SLE, polymyositis, mixed connective disease
- Environmental: hypersensitivity pneumonitis, pneumoconioses
- Drugs/treatment
- Pulmonary vasculitis: Wegener’s granulomatosis, Goodpasture’s syndrome, idiopathic pulmonary hemosiderosis
- Inherited disorders: familial IPF, neurofibromatosis, tuberous sclerosis, Gaucher’s disease
- Alveolar filling disorders: chronic eosinophilic pneumonia, pulmonary alveolar proteinosis
Idiopathic pulmonary fibrosis
Progressive, irriversible fibrosis of the lung parenchyma with no known cause.
Features: commonly presents >50 yrs with SOB and dry cough
Causative agents of interstitial lung disease
Hypersensitivity pneumonitis
- extrinsic allergic alveolitis, due to sensitisation to inhaled agents.
- Farmer’s lungs, Bird Fancier’s lung, Humidifier lung
- Presents 4-6h after exposure in acute, insidious onset in chronic presentation.
Pneumoconioses
- Reaction to inhaled organic dust
- Asbestosis: lower lobes, calcified pleural plaques, round atelectasis, mesothelioma
- Silicosis: upper lobes, nodular disease
- Coal worker’s pneumoconiosis: upper lobe, coal macule
Drug induced ILD
- Antineoplastic: methotrexate, cyclophosphamide, chlorambucil
- Antibiotics: nitrofurantoin, penicillin, sulfonamide
- Cardiovascular: amiodarone
- Illicit: heroin, methadone
Radiation-induced
- early pneumonitis ~wks
- late fibrosis 6-12 months
Sarcoidosis
Idiopathic non-infectious granulomatous multisystem with lung involvement.
Features: cough, dyspnea, fever, arthralgia, malaise, erythema nodosum, chest pain.
Investigations:
- FBC
- Serum U&E, Ca (vit D activation by granulomas)
- Elevated ACE
- CXR predominantly nodular opacities in upper lung zones + bilar adenopathy
- PFT
Diagnosis:
- Biopsy
Treatment:
- Earlier stages may resolve spontaneously
- Steroids, methotrexate and other immunosuppressives may be used
Pulmonary hypertension
MAP of pulmonary artery >25 mmHg or systolic >40 mmHg.
Mechanisms:
Hypoxic vasoconstriction - down regulation of NO synthase and alteration of endothelium leading to vasoconstriction
Decreased area of pulmonary vascular bed - rise in resting pulmonary arterial pressure
Volume and pressure overload - excessive volume overload.
Classifications
I) Pulmonary arterial HTN - idiopathic, collagen vascular disease, Eisenmenger syndrome, portopulmonary HTN, HIV infection, sickle cell disease
II) Pulmonary HTN due to left heart disease - LV dysfunction, aortic stenosis, mitral stenosis
III) Pulmonary HTN due to lung disease/hypoxia - parenchymal lung disease, chronic alveolar hypoxia
IV) Chronic thromboembolic pulmonary HTN - thromboembolic obstruction of pulmonary arteries
V) Pulmonary HTN with unclear mechanisms - hematologic disorders, systemic, metabolic disorders
Idiopathic pulmonary arterial hypertension
Features: young women 20-40yrs, sporadic, present with dyspnea, fatigue, syncope, exertional chest pain , Raynaud’s pheonmenon.
Investigations:
- CXR: enlarged central pulmonary arteries
- ECG: RVH/strain
- Cardiac catheterization
Treatment:
- Trial of CCB
Prognosis:
- 2-3yr mean survival
Pulmonary embolism
Risk factors:
- Stasis: immobilisation, obesity, CHF, chronic venous insufficiency
- Endothelial damage: post-operative, trauma
- Hypercoagulable states: malignancy, cancer treatment, estrogen, pregnancy, prior DVT/PE, nephrotic syndrome, coagulopathies, increasing age
Investigations:
- Pulmonary angiogram
- D-dimer
- CT angiogram
- Venous duplex US or Doppler
- ECG (S1Q3T3)
- CXR (atelectasis, pleural effusion
Treatment
- Oxygen
- Analgesia
- Acute anticoagulation: IV heparin, enoxapain
- Long term anticoagulation: warfarin, enoxaparin (pregnancy, active cancer)
- IV thrombolytic therapy/interventional thrombolytic therapy,
- IVC filter for absolute CI to anticoagulants
Thromboprophylaxis
- LMWH
- Fonaparinux
- Warfarin
- Dabigatran
- Heparin
- TED stockings
Pulmonary vasulitis
Wegner’s Granulomatosis
- systemic vasculitis of med/small arteries
- necrotising granulomatous lesions of upper and lower resp tract
- GN, focal necrotising lesions
- C-ANCA positive
Churg-Strauss Syndrome
- multisystem disorder characterised by allergic rhinitis, asthma, prominent peripherla eosinophilia
- asthma, infiltrates
- life threatening systemic vasculitis
Goodpasture’s Disease
- disorder chrarcterised by diffuse alveolar hemorrhage and glomerulonephritis (anti-GBM antibodies)
- hemoptysis
- anemia, glomerulonephritis
SLE
RA
Scleroderma
Mediatinal masses
Anterior compartment
- Thymoma
- Thyroid enlargement
- Teratoma
- Thoracic aneurysm
- Tumours: lymphoma, parathyroid, esophageal angiomatous
Middle compartment
- Pericardial cyst
- Bronchogenic cyst/tumour
- Lymphoma
- Lymph node enlargment
- Aortic aneurysm
Posterior compartment
- Neurogenic tumours
- Meningocele
- Enteric cysts
- Lymphoma
- Diaphragmatic hernias
- Esophageal tumour
- Aortic aneurysm
Signs
- Asymptomatic 50%
- Chest pain, cough, dyspnea, recurrent respiratory infections
- Hoarseness, dysphagia, Horner’s syndrome, SVC compression
- Paraneoplastic syndromes (myarthenia gravis)
Mediatinitis
Most commonly caused by post-op complications of cardiovascular or thoracic surgery.
Signs
- Fever, substernal pain
- Pneumomediastinum, mediastinal compression
Pleural effusions
Light’s criteria
Transudate: p:s protein ratio <0.5, p:s LDH ratio <0.6, pleural LDH <2/3 ULN of serum LDH
Exudate: p:s protein ratio >0.5, p:s LDH ratio >0.6, pleural LDH >2/3 ULN of serum LDH
Transudative effusion
- Increased capillary hydrostatic pressure: CHF, PE
- Decreased plasma oncotic pressure: cirrhosis, nephrotic syndrome
Exudative effusion
- Infectious: bacterial pneumonia, empyema, TB pleuritis, viral infection
- Malignancy: lung carcinoma, lymphoma, metastases
- Inflammatory: RA, SLE, PE, post CABG, drug reaction
- Intra-abdominal: sub-phrenic abcess, pancreatic disease, Meig’s syndrome
- Intra-thoracic: esophageal perforation
- Trauma: chylothorax, hemothorax, pneumothorax
Investigations:
- PA CXR seen >200mL
- lateral CXR seen >50mL
Treatment:
- Thoracentesis
- Chest drain
Empyema
Pus in pleural space due to infection.
Treatment:
- Chest drain
- Antibiotics for 4-6wks
Pneumothorax
Air in pleural space
Etiology:
- Traumatic: chest injuries
- Iatrogenic: central venous catheter, thoracentesis, mechanical ventilation
- Spontaneous: primary in young healthy males, secondary due to underlying lung disease
CXR: separation of visceral and parietal pleura, increased density and decreased lung volume on affected side
Treatment:
- small, will resolve spontaneously
- large chest drain with underwater seal
- repeated requires pleurodesis or apical bullectomy
Hypoxemic respiratory failure
Types
1) Low FiO2: high altitude, PaCO2 normal, A-a gradient normal, give oxygen therapy
2) Hypoventilation: drug overdose, PaCO2 high, A-a gradient normal, give oxygen and ventilation
3a) Shunt: pneumonia, ARDs, PaCO2 normal, A-a gradient high, improve cardiac output
3b) Shunt (right to left): pulmonary hypertension, PaCO2 normal, A-a gradient high, ventilation and increase cardiac output worsens breathing
4) Low mixed venous O2 content: shock, PaCO2 low, A-a gradient high, give oxygen and improve cardiac output
5) V/Q mismatch: COPD, PaCO2 high, A-a gradient high, give oxygen and ventilation
6) Diffusion impairment: ILD, emphysema, PaCO2 normal, A-agradient high, give oxygen and CPAP
Hypercapnic respiratory failure
Types:
1) high inspired CO2
2) Low total ventilation: COPD, asthma, CF, brainstem stroke, Guillain-Barre
3) High deadspace ventilation: PE, shock
4) High CO2 production: fever, sepsis, acidosis
Treatment
- reverse underlying pathology
- suction of secretions, bronchodilators, treatment of infections
- oxygenation, careful with chronic CO2 retainers
Acute respiratory distress syndrome
Severe pulmonary distress, hypoxemia, non-cardiogrnic pulmonary edema.
Disruption of alveolar capillary membranes, leading to interstital pulmonary edema, reducing compliance, increase shunting, hypoxemia and pulmonary hypertension.
Clinical course
- Exudative phase: first 7 days
- Fibroproliferative phase: improves but may develop fibrotic lungs.
Causes:
- Direct lung injury: aspiration, pneumonia, inhalation injury
- Indirect lung injury: shock, sepsis, trauma, head trauma, intracranial hemorrhage, drug overdose
Lung cancer
Bronchogenic cancers:
Small cell lung cancer - smoking correlation, centrally located with dissemination, oat cells, neuroendocrine cells
Non-small cell lung cancer:
- Squamous - most common, smoking correlation, central location with local invations, keratin, intercellular bridges
- Adenocarcinoma - poor smoking correlation, peripheral location with early distant metastasis, glandular, mucin producing
- Large cell cancer
Benign
- Papillomas
- Adenomas
2/3 of primary lung cancer is found in the upper lobes, 2/3 of metastases occur in the lower lung.
Primary lesion
- cough, dynpnea, chest pain, hemoptysis, clubbing
Metastasis
- lung: pleural effusion, atelectasis, wheezing
- pericardium: pericarditis, pericardial tamponade
- esophageal compression: dysphagia
- phrenic nerve: paralyzed diaphragm
- recurrent laryngeal nerve: hoarsness
- SCV syndrome: facial swelling, dilated neck veins, Pemberton’s sign
- Pancoast tumour: Horner’s syndrome, brachial plexus palsy (C8 and T1)
- rib and vertebrae: erosion
- paraneoplastic syndromes
Paraneoplastic syndromes
Bronchogenic cancer: acanthosis nigricans, dermatomyositis
Squamous cell carcinoma: PTHrP
Small cell carcinoma: ectopic ACTH, SIADH, Lambert-Eaton syndrome, polymyositis
Solitary Pulmonary nodules
Benign
- Infectious granuloma: TB
- Other infections: abcess, aspergilloma
Benign neoplasms: hamartoma, lipoma, fibroma
- Vascular: AV malformation, pulmonary varix
- Developmental: bronchogenic cyst
- Inflammatory: Wegener’s, rheumatoid, sarcoidosis
Malignant
- Bronchogenic carcinoma
- Metastatic lesions
- Pulmonary carcinoid
Management:
- Compare with previous CXR
- CT thorax if appears malignant or changed
- Repeat CXR in 3-6m if appears benign
Sleep apnea
Obstructive
- transient episodic obstruction of upper airway
- weight loss, decreased alcohol/sedatives, nasal decongestion
- CPAP, postural therapy
Central
- transient episodic decrease in CNS drive to breathe
- nasal BiPAP/CPAP
