Respiratory Flashcards
Patient’s ABG shows high C02 but normal pH, do they have chronic or acute hypercapnia?
Chronic- as compensatory mechanisms are being utilised.
Indicates 02 sats should be aimed at 88-92%
What colour are Venturi masks delivering 24-28% O2?
Blue- 24%
White- 28%
Which type of O2 mask should not be used if patient is requiring less than 5L of 02?
Face mask, at low flow rates = more C02 rebreathing
A patient is known COPD, so 02 sats of 88-92% are aimed for with venturi mask. What would prompt you to start aiming treatment to 94-98%?
ABG shows low PaC02 (under 6)
Unless they have a PMH of needing NIV or IPPV.
If over 6, suggests hypercapnia- keep on lower sats.
If acidic pH <35 consider NIV.
Accessory muscle usage suggests what 3 things?
Small airway disease- asthma or COPD
Pneumothorax
Pleural effusion
3 respiratory causes of central cyanosis:
- Cor pulmonale
- Idiopathic fibrosis
- Bronchiectasis
Causes of lymphadenopathy in the respiratory exam:
Carcinoma
TB
Lymphoma
Sarcoidosis
Which muscles are the accessory muscules used in respiratory distress?
From front to back- sternocleidomastoid, scalene, trapezius
Causes of stridor:
Heard on inspiration, partial obstruction of upper aiways + larynx
Children- Pertussis, Croup, Epiglottitis
Adults- extubation, vocal cord paralysis, airway foreign body
What is the normal cricosternal angle height and cause of a shortened one?
3cm- shortened when chest is hyperexpanded in COPD
5 causes of reduced chest expansion:
External aspects restricting expansion:
- Effusion
- Consolidation
- Pneumothorax
Parenchymal aspects restricting:
- Fibrosis
- Collapse
Cause of dullness on percussion
Increased solid matter: Consolidation Effusion Pleural thickening Raised hemidiaphragm
Lack of air entry:
Pneumonectomy, lobectomy (fluid and great vessels move to fill the space)
How do you differentiate an exudate from a transudate?
Light’s criteria: helpful when fluid protein is 25-35g/L
Pleural:serum protein ratio >0.5 (exudate)
Pleural:serum LDH ratio >0.6 (exudate)
Or pleural LDH 2/3s upper limit of normal serum LDH
Causes of bronchiectasis:
Conned by the Postman, had a Measley Tustle, but I Pneu he was TB Obstructive Over this + Underhand:
Congenital (CF, Kartagener’s, primary ciliary dyskinesia)
Post-infection (Measles, Pertussis, Pneumonia, TB)
Bronchial obstruction (tumour, foreign body)
Overactive immune (RA, UC, APBA)
Underactive immune (hypogammaglobulinaemia)
Lung complications of rheumatoid arthritis:
Fibrosing alveolitis (due to RA or secondary to methotrexate)
Pleural effusion
Bronchiectasis
Obliterative bronchiolitis (inflamed small airways- terminal)
Causes of Apical fibrosis (BREASTS-X)
Berylliosis (beryllium metal allergic response)
Radiation
Extrinsic allergic alveolitis (organic allergens- dust, mushroom, sugar)
Ank spond (HLA B27)
Sarcoidosis
TB
Silicosis
Histiocytosis X (granulomas of dendritic cells
Causes of basal fibrosis of lung:
RAAID
Rheumatoid arthritis Autoimmune disease Asbestosis Idiopathic pulmonary fibrosis Drugs- amiodarone, nitrofurantoin, methoxtrexate, crystal meth)
Commonest cause of interstitial lung disease?
Idiopathic pulmonary fibrosis
What causes early inspiratory crackles?
Asthma + COPD
What causes mid/end expiratory crackles?
‘Fine’
Mid- bronchiectasis
End- pulmonary oedema, pneumonia, fibrosis
Causes of bronchial breathing:
Increased solids:
Consolidation
Fibrosis
Which connective tissue diseases are associated with interstitial lung disease (pulmonary fibrosis)?
RUTSSS:
Rheumatoid arthritis Ulcerative colitis Thyroid (autoimmune) SLE Systemic sclerosis Sjogrëns
Drug causes of fibrosis:
Methotrexate (rheum)
Amiodarone (anti-arrhythmic)
Nitrofurantoin (UTIs)
What are the 4 diagnostic criteria for a diagnosis of ARDS?
Acute injury or systemic condition = release of inflammatory mediators + ^ capillary permeability = non-cardiogenic pulmonary oedema
ARDS: Acute onset Refractory hypoxaemia Diffuse bilateral infiltrates on CXR Small pulmonary capillary wedge pressure <19mmHg (or no CCF clinically)- a high pressure would suggest cardiac failure and blood backing up was the cause instead
Causes of ARDs
BEAT ARDS
Lung injury > release of inflammatory mediators > capillary permeability
Blood transfusion/ burns
Embolism (fat/amniotic fluid)
Aspiration (gastric)
Trauma
Acute pancreatitis/liver failure
Radiation, rheum (vasculitis)
DIC/drugs/Drowning/Diffuse pneumonia
Sepsis/shock
Loss of lung volume, with bilateral lower reticulonodular shadowing on xray is due to:
Interstitial processes:
Idiopathic pulmonary fibrosis
Sarcoid
Fibrosis (connective tissue disease, radiotherapy, drugs etc)
Patient has tender bruises on shins, a dry cough with SOB and a raised ESR. What is the diagnosis?
Sarcoid- erythema nodosum + multisystem granulomatous disorder
Investigations suggestive of sarcoid:
High calcium + high 24h urine calcium
High ESR, low lymphocytes, high Ig
CXR- bilateral hilar lymphadenopathy
Diagnostic- tissue biopsy (non-caseating granuloma)
What is obstructive sleep apnoea?
Intermittent closure or collapse of pharyngeal airways causing apnoeic episodes during sleep, terminated by partial arousal.
Sx: loud snoring, poor sleep quality
Daytime somnolence, morning headache
Reduced libido and cognitive performance
How is significant sleep apnoea defined?
> 15 episodes of apnoea or hypoapnoea during 1 hour of sleep
Management of obstructive sleep apnoea?
Can cause pulmonary hypertension, type II respiratory failure
Conservative: weight reduction, avoid tobacco and alcohol
Medical: CPAP if moderate to severe disease
Surgical: relief of pharyngeal obstruction occasionally indicated
What is cor pulmonale and what causes it?
Right heart failure caused by chronic pulmonary arterial hypertension
Lung: COPD, severe asthma, bronchiectasis, pulmonary fibrosis, lung resection
Vascular: PE, pulmonary vasculitis, ARDS, sickle-cell, parasites
Thoracic cage: kyphosis, scoliosis
Neuromuscular: myaesthenia gravis, polio, MND
Hypoventilation: sleep apnoea, enlarged adenoids in kids
What is the difference between coal worker’s pneumoconiosis and progressive massive fibrosis?
Coal worker’s pneumoconiosis > macrophage ingestion of dust
PC: Asymptomatic
CXR: 0.1-1cm nodules in upper zones
Progressive massive fibrosis
PC: progressive dyspnoea, fibrosis, cor pulmonale eventually
CXR: 1-10cm masses in upper zone
What is Caplan’s syndrome?
Rheumatoid arthritis
+ rheumatoid pulmonary nodules
+ pneumoconiosis (occupational inhaled lung disease)
Those with RA are more likely to develop pneumoconiosis
What does asbestos cause?
Pleural plaques
Asbestosis- basal fibrosis
Mesothelioma
Bronchial adenocarcinoma
Management of malignant mesothelioma?
Pemetrexed: folate antimetabolite
Blood and imaging findings of idiopathic pulmonary fibrosis?
Raised CRP, immunoglobulins
30% ANA +ve
CXR:
Reticulo-nodular shadows in lower zones
Honeycomb lung
can resemble pulmonary oedema, but no cardiomegaly
Rx of idiopathic pulmonary fibrosis?
Conservative: pulmonary rehabilitation, palliative care input
Medical: opioids, oxygen
Surgical: lung transplant
Causes of interstitial lung disease:
A= apical, B= basal
- Idiopathic
- Occupational- asbestosis (b), silicosis (a), coal worker’s pneumoconiosis
- Connective tissue- RA (b), SLE, scleroderma, polymyositis, Srögrens
- Immunologic- sarcoid (a), allergic extrinsic alveolitis (a)
- Treatment related- radiation, methotrexate, bleomycin, amiodarone, nitrofurantoin (b)
What is extrinsic allergic alveolitis and how is it different from asbestosis or pneumoconiosis?
In sensitized individuals, inhalation of organic allergens (fungal spores, avian proteins) causes hypersensitivity reaction.
Acute: alveoli are infiltrated with inflammatory cells
Chronic: granuloma forms > obliterative bronchiolitis (bronchiole inflammation often without CXR findings)
What 4 types of extrinsic allergic alveolitis are there?
Apical fine inspiratory fbrosis
- Bird-fancier’s
- Farmer’s lung, mushroom worker’s lung
- Malt worker’s lung
- Sugar worker’s lung
Features of sarcoid:
PC: progressive dyspnoea, dry cough, chest pain
CXR: bilateral hilar lymphadenopathy ± pulmonary infiltrates
IHX: high ESR, LFTs, Ca, serum ACE, Ig
Diagnostic: tissue biopsy (of lung, liver, lymph gland)
Which sarcoid patients need steroids?
Parenchymal lung disease
Uveitis
Hypercalcaemia
Neuro or cardiac involvement
Causes of bilateral hilar lymphadenopathy?
STONE on the xray
Sarcoid
TB
Organic dust disease- silicosis, berylliosis
Neoplasm- lymphoma, carcinoma, mediastinal tumours
Extrinsic allergic alveolitis
Cause of transudates:
<25g/L
Increased venous pressure:
cardiac failure
constrictive pericarditis
fluid overload
Hypoproteinaemia:
Cirrhosis
Nephrotic syndrome
Malabsorption
Hypothyroidism
Meig’s syndrome- R pleural effusion + ovarian fibroma
What are the stages of sarcoid on CXR?
- Normal
- Bilateral hilar lymphadenopathy
- BHL + peripheral pulmonary infiltrates
- Pulmonary infiltrates alone
- Progressive fibrosis, bulla formation (honeycombing), pleural involvement
Non-pulmonary signs:
Subcutaneous nodules, erythema nodosum
Phalangeal bone cysts
Uveitis, conjunctivitis, keratoconjunctivitis sicca, glaucoma
Enlarged lacrimal/parotid glands, lupus pernio
Bell’s palsy
Cardiomyopathy, lymphadenopathy, hepatosplenomegaly
Neuropathy, meningitis, SOL
Causes of exudates in pleural effusions?
Increased leakiness of pleural capillaries:
Infection- pneumonia, TB
Inflammation- RA, SLE, pulmonary infarction
Malignancy- bronchial carcinoma, mets, lymphoma, mesothelioma, lymphangitis carcinomatosis (lymph gland obstruction)
Signs of pleural effusion:
Decreased expansion
Stony dull percussion note
Diminished breath sounds
Bronchial breathing above the effusion- where the lung is compressed (=turbulent air flow in large airways)
How should a diagnostic aspiration of pleural effusion fluid be performed?
Us guidance
Percuss borders of effusion
Lidocaine at the pleural edge
Insert needle with syringe attached just above the upper border of the rib (avoids neuromuscular bundle)
Clinical chemistry, microscopy, cytology, if indicated imunology (RF, ANA, complement)