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FINALS > Respiratory > Flashcards

Respiratory Flashcards

1
Q

ASTHMA

What is the pathophysiology of asthma?

A
  • Airway narrowing + obstruction due to bronchial muscle contraction as well as inflammation caused by mast cell degranulation + increased mucus production
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2
Q

ASTHMA

What are the three main characteristics of asthma?

A
  • Airflow limitation (reversible)
  • Airway hyperresponsiveness to various stimuli
  • Bronchial inflammation
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3
Q

ASTHMA

What three histopathological changes are seen in asthma?

A
  • Basement membrane thickening
  • Epithelium metaplasia (increased goblet cells)
  • Increase in inflammatory gene expression on many cell types
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4
Q

ASTHMA

What 2 broad aetiological categories can asthma be split into?

A
  • Allergic (extrinsic, eosinophilic) = T1 IgE mast cell mediated hypersensitivity reaction caused by allergens, atopy (eczema, hayfever)
  • Non-allergic (intrinsic, non-eosinophilic) = idiopathic but triggers
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5
Q

ASTHMA

What are some triggers and risk factors for asthma?

A
  • Smoking, allergens, exercise, damp, NSAIDs, B-blockers

- LBW, child exposure to smoke, PMH/FHx atopy, air pollution

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6
Q

ASTHMA

What is the clinical presentation of asthma?

A
  • Episodic Sx with diurnal variability (worse night/early morning)
  • Dry cough with wheeze, dyspnoea + chest tightness
  • Widespread polyphonic wheeze on auscultation
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7
Q

ASTHMA

What first-line lung function tests can be used to help diagnose asthma?

A
  • Fractional exhaled nitric oxide (FeNO)
  • Spirometry
    (- Peak expiratory flow rate variability)
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8
Q

ASTHMA

What results show inflamed airways for FeNO testing?

A
  • > 40ppb adults

- >35ppb paeds

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9
Q

ASTHMA

What would spirometry show in asthma?

A
  • Obstructive pattern = FEV1 <80%, FEV1/FVC <0.7

- Beta-2-agonist reversibility with FEV1 ≥12% improvement

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10
Q

ASTHMA

What would PEFR show in asthma?

A
  • Diurnal variation >20% on ≥3d/w
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11
Q

ASTHMA

What other investigations may you consider in asthma?

A
  • Skin prick tests for atopy
  • Serial PEFR at work/away if occupational (usually due to isocyanates = paints + flour)
  • CXR = ?hyperinflation
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12
Q

ASTHMA

What lifestyle advice would you give to someone with asthma?

A
  • Correct inhaler technique
  • Avoid triggers + smoking
  • Monitor peak flow
  • Yearly flu jab + asthma r/v
  • Asthma self-management programme
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13
Q

ASTHMA

What are the 5 main drugs used in the treatment of asthma?

A
  • Short-acting beta-2-adrenergic receptor agonists (SABA, salbutamol)
  • Inhaled corticosteroids (ICS, beclometasone, bumetanide)
  • Long-acting beta-2-adrenergic receptor agonists (LABA, salmeterol)
  • Leukotriene receptor antagonists (LTRA, montelukast)
  • Theophylline
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14
Q

ASTHMA
What is the mechanism of action of…

i) SABA/LABA?
ii) ICS?
iii) LTRA?
iv) theophylline?

A

i) Adrenaline acts on airway smooth muscle to dilate bronchioles (short/long acting)
ii) Reduced inflammation + reactivity of airways
iii) Blocks leukotrienes which are produced by immune system + cause inflammation, bronchoconstriction + mucous secretion
iv) Relaxes bronchial smooth muscle and reduces inflammation

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15
Q

ASTHMA

What is an important drug safety aspect of theophylline?

A
  • Narrow therapeutic window + toxic in excess so monitor plasma theophylline levels 5d after starting and 3d after dose changes
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16
Q

ASTHMA

Adult and 5–16y/o asthma management: what are the first 4 steps?

A
  • Step 1 = SABA (if newly-diagnosed but Sx ≥3/w or night-waking STEP 2)
  • Step 2 = add low-dose ICS
  • Step 3 = add LTRA
  • Step 4 = add LABA (continue LTRA depending on patient’s response)
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17
Q

ASTHMA

Adult and 5–16y/o asthma management: what are steps 5–7?

A
  • Step 5 = SABA ± LTRA plus switch ICS + LABA for low-dose ICS MART (Fostair = beclo/form, Symbicort = buden/form)
  • Step 5 = SABA ± LTRA plus medium-dose ICS MART (or fixed dose moderate-dose ICS + separate LABA)
  • Step 7 = SABA ±LTRA plus high-dose ICS (if not on MART), trial PO theophylline, specialist input
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18
Q

ASTHMA

Paediatric <5y/o management: what are steps 1 and 2?

A
  • Step 1 = SABA

- Step 2 = add 8w trial of moderate-dose inhaled ICS

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19
Q

ASTHMA

After the 8w trial how would you manage their response?

A
  • No response = stop + consider alternative Dx
  • Sx resolved but reoccurred <4w = restart ICS at low-dose
  • Sx resolved but reoccurred >4w = repeat 8w trial
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20
Q

ASTHMA

Paediatric <5y/o management: what are steps 3 and 4?

A
  • Step 3 = SABA + low-dose ICS plus LTRA

- Step 4 = stop LTRA and refer to paeds asthma specialist

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21
Q

ASTHMA

How does an acute asthma attack present?

A
  • Worsening dyspnoea, wheeze + cough not responding to SABA

- Use of accessory muscles

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22
Q

ASTHMA

What constitutes a moderate asthma exacerbation?

A
  • PEFR 50–75% predicted
  • RR <25/min
  • HR <110bpm
  • Speech normal
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23
Q

ASTHMA

What constitutes a severe asthma exacerbation?

A
  • PEFR 33–50% predicted
  • RR ≥25/min (>30 if >5y/o, >40 if <5y/o)
  • HR ≥110 (>125 if >5y/o, >140 if <5y/o)
  • Unable to complete full sentences
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24
Q

ASTHMA

What constitutes a life-threatening asthma exacerbation?

A
  • PEFR <33% predicted
  • SpO2 <92%
  • Silent chest (airways tight so no air entry) + cyanosis
  • HD unstable
  • Exhaustion/altered GCS
  • ABG = normal CO2
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25
Q

ASTHMA

What investigations would you do in an acute asthma exacerbation?

A
  • Bloods = FBC, U&E, CRP
  • ABG if SpO2 <92%
  • CXR to exclude differentials
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26
Q

ASTHMA

How might an ABG change during an acute asthma exacerbation?

A
  • Initially respiratory alkalosis due to tachypnoea dropping CO2
  • Normal pCO2 or hypoxia is concerning sign as indicates exhaustion
  • Respiratory acidosis due to high CO2 is very bad sign = near-fatal asthma
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27
Q

ASTHMA

What is the management of an acute asthma exacerbation?

A

O SHIT ME –

  • Oxygen (SpO2 94–98%), 15L NRB and titrate down
  • Salbutamol 5mg spacer or neb (oxygen driven, IV if no response)
  • Hydrocortisone 100mg IV or PO pred 40–50mg for 5d
  • Ipratropium bromide 0.5mg neb (severe/life-threatening or not responding to SABA/steroid)
  • Theophylline IV (senior)
  • Mag sulf 2g IV (senior) this before theophylline
  • Escalate early > ICU
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28
Q

ASTHMA

What are the discharge criteria following an asthma exacerbation?

A
  • Stable on d/c meds (no nebs or oxygen) for 12–24h
  • Inhaler technique checked + recorded
  • PEFR >75% predicted
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29
Q

COPD
What is COPD?
What is it made up of?

A
  • Non-reversible, progressive deterioration in airflow through the lungs caused by damage to lung tissue causing airway obstruction making it more difficult to ventilate the lungs making them prone to developing infections
  • Chronic bronchitis (blue bloaters) and emphysema (pink puffers)
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30
Q

COPD
What is…

i) chronic bronchitis?
ii) emphysema?

A

i) Hypertrophy + hyperplasia of mucus glands in bronchi = V/Q mismatch due to bronchoconstriction so cyanosis but no hyperventilation, rely on hypoxic drive
ii) Enlargement of air spaces + destruction of alveolar walls so air trapping post exhalation = inability to oxygenate so hyperventilation but no cyanosis

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31
Q

COPD

What are the causes of COPD?

A
  • Smoking = major contributor

- Early-onset emphysema in alpha-1-antitrypsin deficiency due to increase in proteases which damage lung tissue

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32
Q

COPD

What are the symptoms and signs of COPD?

A
  • Chronic cough, sputum (often white), dyspnoea
  • Tachypnoea, pursed-lip breathing, cachexia, expiratory wheeze, accessory muscle use, hyperinflated barrel chest (reduced cricosternal distance)
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33
Q

COPD

What initial investigations might you do in COPD?

A
  • ECG = P pulmonale (RA hypertrophy) + RVH if cor pulmonale
  • FBC (polycythaemia if chronic hypoxia)
  • A1AT levels
  • ABG (high bicarb indicates chronic CO2 retainer)
  • CXR = hyperinflated chest (>6 ant. ribs), flat hemidiaphragm, bullae
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34
Q

COPD
What diagnostic investigation would you do in COPD?
How is it classified?

A
  • Spirometry = obstructive with no reversibility (FEV1 <80%, FEV1/FVC <70%)
    All have FEV1/FVC <70% –
  • Stage 1 mild = Sx for diagnosis as FEV1≥80%
  • Stage 2 moderate = FEV1 50–79%
  • Stage 3 severe = FEV1 30–49
  • Stage 4 very severe = FEV1 <30%
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35
Q

COPD
What are bullae?
How may they present?

A
  • Air spaces in lung due to alveolar damage

- If large can mimic pneumothorax presenting as lucency without a visible wall

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36
Q

COPD

What is the lifestyle management of COPD?

A
  • Smoking cessation #1
  • Yearly flu + one off PCV
  • Pulmonary rehab (exercise, nutrition, breathing exercises, education)
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37
Q

COPD

What is the mechanism of action of short/long-acting muscarinic antagonists and give examples?

A
  • Block ACh receptors which are usually stimulated by PSNS causing bronchial smooth muscle contraction + bronchoconstriction
  • Short = ipratropium bromide
  • Long = tiotropium bromide (Spiriva)
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38
Q

COPD
What is the first step in COPD management?
What is considered in step 2?

A
  • SABA or SAMA PRN
  • Features suggestive of steroid responsiveness = previous atopy Dx, eosinophilia, reduced FEV1 or diurnal FEV1 variation
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39
Q

COPD

What is the further management of COPD in someone with no steroid responsive features?

A
  • LABA + LAMA (Ultibro) (if on SAMA swap to SABA PRN)

- If still breathless or exacerbations then triple therapy with LABA + LAMA + ICS (Trimbow)

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40
Q

COPD

What is the further management of COPD in someone with steroid responsive features?

A
  • LABA + ICS (Fostair)
  • If still breathless or exacerbations then triple therapy with LABA + LAMA + ICS (Trimbow) (if on SAMA swap to SABA PRN)
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41
Q

COPD
If triple therapy fails, what else might be considered?
What other interventions may be considered?

A
  • PO theophylline, mucolytics like carbocisteine, specialist input
  • Long-term oxygen therapy (LTOT)
  • Lung volume reduction surgery or transplant if severe in select
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42
Q

COPD

What is the criteria for LTOT?

A
  • 2x ABGs 3w apart showing PaO2 <7.3 or 7.3–8 with 1 of: nocturnal hypoxia, polycythaemia, peripheral oedema or pulmonary HTN
  • Non-smokers only due to fire hazard
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43
Q

COPD
How does an acute exacerbation of COPD present?
What are the common causes?

A
  • Increased dyspnoea, cough + wheeze ± purulent sputum

- Haemophilus influenzae #1, strep. pneumoniae, Moraxella catarrhalis, viral

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44
Q

COPD

What investigations would you do in someone with an acute COPD exacerbation?

A
  • FBC, U&E, CRP, ABG, blood cultures if septic

- Sputum MC&S, ECG, CXR

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45
Q

COPD

What is the initial management of an acute COPD exacerbation?

A

ABCDE

  • Oxygen (15L NRB then titrate using venturi 28–40) aim for 88–92%
  • Increase bronchodilator use ± nebs (salbutamol 5mg 4h, ipratropium 0.5mg 6h)
  • PO pred 30mg OD 5d or IV hydrocort 200mg if severe
  • PO amox/doxy/clari if sputum purulent or clinical signs of pneumonia
  • Chest physio to aid sputum clearance
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46
Q

COPD

If the initial acute COPD management fails, what can be done?

A
  • Escalate to NIV ± intubation with ICU support
  • CPAP = T1RF and pulmonary oedema
  • BiPAP = T2RF
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47
Q

LUNG CANCER
What are the 2 main types of lung cancer? Which is more common?
What are some risk factors?

A
  • Non-small cell lung carcinoma (majority)
  • Small cell lung carcinoma
  • Smoking, occupational (asbestos, silica), HIV, radiation
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48
Q

LUNG CANCER

What are the three subtypes of NSCLC? What are some features of each?

A
  • Adenocarcinoma (#1) = most common type in non-smokers but most pts smokers, peripheral
  • Squamous = smokers, central, cavitates, poor prognosis
  • Large cell = peripheral, large, poorly differentiated
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49
Q

LUNG CANCER

What specific sequelae can adenocarcinomas and squamous cell carcinomas lead to?

A
  • Adeno = gynaecomastia

- Squamous = high Ca2+ from ectopic PTH-rP = primary hyperparathyroidism and hypertrophic pulmonary osteoarthropathy

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50
Q

LUNG CANCER

What are some features of SCLC?

A
  • Almost always smokers, central, early mets, causes paraneoplastic syndromes and SVC obstruction, worst prognosis
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51
Q

LUNG CANCER

What are some SCLC paraneoplastic syndromes?

A
  • ADH > SIADH
  • ACTH = Cushing’s + also ?bilateral adrenal hyperplasia with high cortisol leading to hypokalaemic alkalosis
  • Lambert-Eaton myasthenic syndrome
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52
Q

LUNG CANCER

What is the referral criteria for lung cancer?

A

≥40y and ≥2 unexplained Sx in a non-smoker or ≥1 smoker = urgent 2w CXR
- SOB, cough, chest pain
- Fatigue, weight loss, appetite loss
CXR ?lung cancer or haemoptysis in ≥40y = urgent 2ww appt

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53
Q

LUNG CANCER
What signs are concerning for lung cancer?
What is the referral criteria?

A

Consider 2w urgent CXR if ≥40y with any of:

  • Persistent or recurrent chest infection
  • Finger clubbing
  • Supraclavicular or persistent cervical lymphadenopathy
  • Fixed monophonic wheeze
  • Thrombocytosis on FBC
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54
Q

LUNG CANCER
What is the first-line investigation used in lung cancer?
What might it show?

A
  • CXR
  • Peripheral/hilar opacity indicating nodule
  • Pleural effusion due to inflammatory reaction
  • Pneumothorax or atelectasis (collapse of lung or lobe)
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55
Q

LUNG CANCER

What further investigations are required to diagnose lung cancer?

A
  • CT CAP (staging)
  • Biopsy for cytology either via bronchoscopy (EBUS) if central or CT guided biopsy with fine needle aspiration if peripheral
  • PET scan
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56
Q

LUNG CANCER

What are some potential complications due to lung cancer?

A
  • L recurrent laryngeal nerve palsy = hoarse voice
  • Phrenic nerve palsy = diaphragm weakness with SOB
  • Brachial plexus = shoulder pain
  • Sympathetic ganglion = Horner’s syndrome (anhidrosis, miosis, ptosis in apical Pancoast tumours)
  • Mets to bone, brain, liver
  • SVCO
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57
Q

LUNG CANCER

How does SVCO present?

A
  • Oncological emergency = SOB, swelling of face, neck + arms, visual disturbance and dilated veins
  • Pemberton’s test = lift arms = facial plethora and cyanosis
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58
Q

LUNG CANCER

What is the management of SVCO?

A
  • STAT PO dexamethasone

- ?stenting or chemo/radiotherapy

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59
Q

LUNG CANCER

What is the management of NSCLC?

A
  • Lobectomy first-line if isolated
  • Curative radiotherapy if stage I–II
  • Chemotherapy if stage III–IV to control disease + improve QOL
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60
Q

LUNG CANCER

What is the management of SCLC?

A
  • Often just palliative chemotherapy
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61
Q

PNEUMONIA

What are the three main types of pneumonia?

A
  • CAP = outside hospital
  • HAP = >48h after admission
  • Aspiration = acute aspiration of gastric contents into lungs, seen in neuro deficit (CVA, MS, MND), LOC, intoxication + tracheostomy
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62
Q

PNEUMONIA

What are the common causes of CAP?

A
  • Strep pneumoniae #1
  • Haemophilus influenzae (COPD)
  • Staph aureus (commonly after influenza)
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63
Q

PNEUMONIA

What are the common causes of HAP?

A
  • Pseudomonas aeruginosa
  • Staph aureus
  • Gram -ve enterobacteria
  • Klebsiella pneumoniae
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64
Q

PNEUMONIA

What are some unique features of klebsiella pneumonia?

A
  • Seen in alcoholics
  • Red-currant sputum
  • Upper lobes affected giving cavitating pneumonia
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65
Q

PNEUMONIA

What are the atypical pneumonias?

A

Legions of psittaci MCQs –

  • Legions = legionella pneumophila
  • Psittaci = chlamydia psittaci
  • M = mycoplasma pneumoniae
  • C = chlamydophila pneumoniae
  • Q = Q fever (Coxiella burnetti)
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66
Q

PNEUMONIA

What are the features of legionella pneumophila?

A
  • From infected water supplies + aircon

- Dry cough, relative bradycardia, confusion, lymphopaenia, hyponatraemia + deranged LFTs

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67
Q

PNEUMONIA
What are the features of…

i) chlamydia psittaci?
ii) Q fever?

A

i) Infected birds, flu-like Sx, splenomegaly

ii) animal + their bodily fluids exposure

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68
Q

PNEUMONIA
What are the features of mycoplasma pneumoniae?
What are some complications?

A
  • Erythema multiforme, dry cough, flu-like Sx, neuro Sx in young
  • Complications = cold agglutins IgM haemolytic anaemia, neuro (GBS, encephalitis), peri/myocarditis, bullous myringitis
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69
Q

PNEUMONIA

What fungal cause of pneumonia is there?

A
  • Pneumocystis jiroveci seen in immunocompromised
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70
Q

PNEUMONIA

What are the symptoms and signs of pneumonia?

A
  • Fever, SOB, cough with purulent sputum (dry in atypicals), haemoptysis + pleuritic CP
  • Pyrexia, tachypnoea, tachycardia, focal coarse creps, dull to percuss, bronchial breathing
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71
Q

PNEUMONIA

What initial risk tool would you calculate in someone with suspected pneumonia?

A

CURB-65 –

  • Confusion
  • Urea >7mmol/L
  • RR >30
  • BP <90/60
  • ≥65 years old
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72
Q

PNEUMONIA

What investigations would you do in pneumonia?

A
  • Bloods = FBC (neutrophilia, raised WCC), U&E, LFT, CRP, cultures
  • Sputum MC&S, mycoplasma and COVID-19 PCRs
  • Pneumococcal + legionella urinary antigen tests
  • CXR
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73
Q

PNEUMONIA
What might a CXR show in pneumonia?
What would you expect in aspiration pneumonia?

A
  • Lobar, multilobar, cavitation or pleural effusions

- R middle/lower lobe consolidation due to R bronchus being more vertical

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74
Q

PNEUMONIA

What are some complications of pneumonia?

A
  • Pleural effusion + empyema
  • Lung abscess
  • Pneumothorax
  • Sepsis
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75
Q

PNEUMONIA
How would empyema present?
How do you manage it?

A
  • WCC/CRP/temp won’t settle after Abx, foul smelling sputum

- Chest drain

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76
Q

PNEUMONIA
What is the initial management of pneumonia?
What follow-up is required?

A
  • Oxygen to maintain SpO2 >94%
  • Abx
  • Follow-up appt + CXR in 6w
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77
Q

PNEUMONIA
What Abx are given for…

i) CURB 0-1?
ii) CURB 2?
iii) CURB ≥3?
iv) HAP?
v) aspiration?
vi) atypicals?

A

i) PO amox in community
ii) PO amox + clari in hospital
iii) IV co-amox + clari ?ICU
iv) Not severe = PO co-amox, severe = IV piperacillin with tazobactam
v) IV metro + cephalosporin
vi) Macrolides, fluoroquines (levofloxacin) or doxy

78
Q

PNEUMOTHORAX
What is a pneumothorax?
What are the three main types of pneumothorax?

A
  • Air within the pleural space

- Spontaneous, traumatic and tension

79
Q

PNEUMOTHORAX

How is spontaneous pneumothorax subdivided?

A
  • Primary (no underlying pathology) = tall, thin, young male, smoker
  • Secondary = COPD, asthma, Marfan’s, TB, pneumonia, CF, cancer
80
Q

PNEUMOTHORAX

How is traumatic pneumothorax subdivided?

A
  • Iatrogenic = insertion of central line, pericardiocentesis or positive pressure ventilation
  • Non-iatrogenic = penetrating trauma or blunt trauma with rib #
81
Q

PNEUMOTHORAX

What is a tension pneumothorax?

A
  • Trauma creates a one-way valve which allows pressure in the thorax to rise
82
Q

PNEUMOTHORAX

What is the clinical presentation of pneumothorax?

A
  • Sudden onset SOB + pleuritic chest pain
  • Reduced chest expansion
  • Hyperresonance to percuss
  • Reduced breath sounds
83
Q

PNEUMOTHORAX

How does a tension pneumothorax present?

A

The same plus

  • Contralateral tracheal deviation
  • Systemic features = shock, distended neck veins
84
Q

PNEUMOTHORAX

What investigation would you do in pneumothorax and what would you expect to see?

A
  • CXR

- Lung markings don’t extend all the way to the periphery and pleural line

85
Q

PNEUMOTHORAX

What is the management of a tension pneumothorax?

A
  • ABCDE, 15L oxygen via NRB
  • Urgent 14G cannula needle decompression in 2nd intercostal space mid-clavicular line prior to Ix (aim for above 3rd rib)
  • Chest drain insertion
86
Q

PNEUMOTHORAX

What forms the safe triangle for chest drain insertion?

A
  • 5th intercostal space
  • Base of axilla
  • Lateral edge of pectoralis major
  • Lateral edge of latissimus dorsi
87
Q

PNEUMOTHORAX

What is the management of primary pneumothorax?

A
  • Rim of air <2cm + not SOB = ?d/c, OP review in 2–4w

- Rim of air >2cm or SOB = needle aspiration > chest drain if fails

88
Q

PNEUMOTHORAX

What is the management of secondary pneumothorax?

A
  • Rim of air <1cm + not SOB = supplemental oxygen + admit for 24h
  • Rim of air 1–2cm + not SOB = needle aspiration > chest drain if fails
  • Rim of air >2cm OR SOB = chest drain
89
Q

PNEUMOTHORAX

How do you manage an iatrogenic pneumothorax?

A
  • Observation, majority resolve and are less likely to recur

- Aspiration if no resolution

90
Q

PNEUMOTHORAX

What discharge and post-pneumothorax advice should be given to patients?

A
  • Stop smoking to reduce recurrence
  • Fit to fly = 2w after successful drainage if no residual air post CXR
  • Scuba diving = permanently avoid unless bilateral surgical pleurectomy + normal lung function + CT chest post-op
91
Q

PLEURAL EFFUSION
What is a pleural effusion?
What are the 2 main categories, how is it quantified and how are they commonly distributed?

A
  • Abnormal buildup of fluid in the pleural cavity
  • Transudative, <30g/L protein, often bilateral
  • Exudative, >30g/L protein, often unilateral
92
Q

PLEURAL EFFUSION

What are some transudative causes of pleural effusions?

A
  • # 1 = heart failure (increased capillary hydrostatic pressure)
  • Reduced capillary oncotic pressure (hypoalbuminaemia) = cirrhosis, nephrotic syndrome, GI malabsorption
  • Other = hypothyroidism, Meig’s syndrome
93
Q

PLEURAL EFFUSION

What are some exudative causes of pleural effusions?

A
  • # 1 = pneumonia, other infections like TB
  • Neoplasia = lung cancer, mesothelioma, mets
  • Inflammatory = RA, SLE, acute pancreatitis
  • PE
94
Q

PLEURAL EFFUSION

What are the symptoms and signs of a pleural effusion?

A
  • SOB, reduced exercise tolerance + chest pain
  • Stony dull to percuss, reduced/absent breath sounds over effusion ±bronchial breathing at upper border, ipsilateral reduced chest expansion
95
Q

PLEURAL EFFUSION

What first-line and diagnostic investigations would you do in pleural effusions?

A
  • PA CXR in all patients
  • Diagnostic ultrasound-guided pleural aspiration with fluid sent for pH, protein, LDH, glucose, amylase, cytology + microbiology
96
Q

PLEURAL EFFUSION

What might you see on a CXR in pleural effusion?

A
  • Blunting of costophrenic angles ± meniscus
  • Fluid in lung fissures
  • White out of one hemifield ± contralateral tracheal deviation if large
97
Q

PLEURAL EFFUSION

What would you expect in the pleural aspirate in empyema?

A
  • pH <7.2
  • Low glucose
  • High LDH
98
Q

PLEURAL EFFUSION
In the pleural aspirate, what would you consider if there was…

i) low glucose?
ii) high amylase?
iii) heavy blood staining?

A

i) RA, TB, malignancy
ii) Pancreatitis
iii) Mesothelioma, PE, TB

99
Q

PLEURAL EFFUSION

If the protein is equivocal (25–35g/L), what can you do to determine if the effusion is transudative or exudative?

A

Light’s criteria showing exudates likely if ≥1 of:

  • Pleural fluid protein ÷ serum protein >0.5
  • Pleural fluid LDH ÷ serum LDH >0.6
  • Pleural fluid LDH >2/3rd upper limits of normal serum LDH
100
Q

PLEURAL EFFUSION

How do you manage a pleural effusion?

A
  • ABCDE ± supplemental oxygen and treat underlying cause as may resolve if small
  • If aspirate purulent/cloudy, or clear but pH <7.2 with suspected pleural infection = chest tube for drainage
101
Q

PLEURAL EFFUSION

What is the management of recurrent pleural effusions?

A
  • Pleurodesis = obliteration of pleural space

- Chemically = tetracycline or bleomycin or surgical = thoracotomy or thoracoscopy

102
Q

TUBERCULOSIS

What is the pathophysiology of TB?

A
  • Mycobacterium tuberculosis is engulfed by macrophages leading to a caseating granuloma (Ghon focus) which then migrates to the hilar lymph nodes (Ghon complex)
103
Q

TUBERCULOSIS

What can happen after primary TB?

A
  • Secondary = reactivation of latent TB secondary to immunosuppression
  • Miliary = bloodstream disseminated TB > millet-seeds on CXR
104
Q

TUBERCULOSIS

What are some risk factors for developing TB?

A
  • Ethnic minority groups e.g., sub-Saharan Africa + South Asia
  • Homeless + drug + alcohol abuse
  • Close contact with infected patient
  • Immunosuppression (HIV, cancer, organ transplant)
105
Q

TUBERCULOSIS
What is the general presentation of TB?
Where does it affect most commonly?
Where else can it affect?

A
  • Subacute/chronic night sweats, fever, weight loss + erythema nodosum
  • Pulmonary
  • CNS, GU, MSK, cardio
106
Q

TUBERCULOSIS
What is the presentation of TB affecting…

i) lungs?
ii) CNS?
iii) GU tract?
iv) MSK system?
v) heart?

A

i) Chronic cough ±haemoptysis
ii) Headache, meningism + focal neurology
iii) Sterile pyuria, abscesses, epididymo-orchitis
iv) Arthritis, osteomyelitis, Pott’s disease of spine
v) Pericardial effusions + constrictive pericarditis

107
Q

TUBERCULOSIS
What investigations can…

i) aid acute diagnosis?
ii) screen for latent TB?

A

i) CXR and 3x samples of sputum MC&S

ii) Mantoux ‘tuberculin’ test and interferon gamma release assays

108
Q

TUBERCULOSIS
What might a CXR show in…

i) primary TB?
ii) post-primary TB?

A

i) Consolidation, pleural effusion + bilateral hilar lymphadenopathy
ii) Upper lobe cavitation, healing > fibrosis, pleural effusions

109
Q

TUBERCULOSIS

What would sputum MC&S show in TB?

A
  • Acid fast bacilli

- Stains red with Ziehl-Neelsen stain on Lowenstein-Jenson culture medium

110
Q

TUBERCULOSIS
What does the Mantoux test show?
Why would you do the interferon gamma release assay?

A
  • > 15mm = active TB, 6–15mm = previous exposure (?BCG vs. latent)
  • Can confirm latent TB as differentiates from BCG
111
Q

TUBERCULOSIS
How can TB be prevented?
What are the logistical aspects to a TB diagnosis?

A
  • BCG vaccine in high risk neonates (FHx, relatives from countries with high TB rate) + healthcare workers
  • Contact tracing and notification of PHE
112
Q

TUBERCULOSIS
What is the medical treatment of…

i) active TB?
ii) latent TB?
iii) directly observed therapy?

A

i) RIPE = rifampicin 6m, isoniazid 6m (co-prescribe vitamin B6 pyridoxine after puberty as prophylaxis for peripheral neuropathy), pyrazinamide 2m, ethambutol 2m
ii) Isoniazid + vitamin B6 for 6m or 3m isoniazid + vitamin B6 + rifampicin
iii) 3x/w for prisoners, homeless or poorly adherent patients

113
Q

TUBERCULOSIS

What are some side effects from the medications used in TB?

A
  • Rifampicin = red urine, CYP450 inducer, hepatitis
  • Isoniazid ‘I’m-so-numb-azid’ = peripheral neuropathy, hepatitis
  • Pyrazinamide = gout due to hyperuricaemia, rash, arthralgia
  • Ethambutol ‘eye-thambutol’ = optic neuritis, reduced acuity + colour > CHECK VISUAL ACUITY BEFORE
114
Q

BRONCHIECTASIS

What is bronchiectasis?

A
  • Permanent dilatation of the airways (bronchi + bronchioles) leading to impaired clearance of bronchial secretions, secondary bacterial infection and progressive lung damage due to bronchial inflammation
115
Q

BRONCHIECTASIS

What is the aetiology of bronchiectasis?

A
  • Post-infective = TB, measles, pertussis, pneumonia
  • Congenital = CF, Kartagener’s + Young’s syndromes
  • Bronchial obstruction = cancer, foreign body
  • Immune deficiency = hypogammaglobulinaemia
  • Allergic bronchopulmonary aspergillosis
116
Q

BRONCHIECTASIS

What is the clinical presentation of bronchiectasis?

A
  • Chronic cough with purulent sputum (thick, foul-smelling + green)
  • Haemoptysis
  • Signs = finger clubbing, coarse inspiratory creps + wheeze
117
Q

BRONCHIECTASIS

What investigations would you do in bronchiectasis?

A
  • Sputum culture
  • Spirometry = obstructive (FEV1<80%, FEV1/FVC<70%)
  • CXR
  • High resolution CT chest = diagnostic
118
Q

BRONCHIECTASIS
What organisms are most commonly isolated in bronchiectasis?
What does the CXR show in bronchiectasis?
What does the HR CT chest show in bronchiectasis?

A
  • H. influenzae #1, also p. aeruginosa + klebsiella spp.
  • Thickened bronchial walls + cystic appearance (tramlines + ring shadows)
  • Widespread tram-track + signet ring signs
119
Q

BRONCHIECTASIS

What is the conservative management of bronchiectasis?

A
  • Support groups + patient education
  • Smoking cessation
  • Chest physio for sputum clearance
  • Annual flu + one-off pneumococcal vaccine
120
Q

BRONCHIECTASIS
What is the medical management of bronchiectasis?
What is the surgical management of bronchiectasis?

A
  • Abx for exacerbations + long-term rotating Abx in severe cases
  • Bronchodilators (salbutamol) if SOB + wheeze
  • Mucolytic carbocisteine to reduce sputum viscosity
  • Surgical excision if localised disease or severe haemoptysis control
121
Q

INTERSTITIAL LUNG DISEASE

What causes fibrosis predominately affecting the upper zones?

A

CHARTS –

  • Coal worker’s pneumoconiosis
  • Hypersensitivity pneumonitis
  • Ankylosing spondylitis
  • Radiation
  • TB
  • Silicosis/sarcoidosis
122
Q

INTERSTITIAL LUNG DISEASE

What causes fibrosis predominately affecting the lower zones?

A
  • Idiopathic pulmonary fibrosis
  • Connective tissue disorders like SLE
  • Drug-induced like amiodarone, methotrexate, nitrofurantoin
  • Asbestosis
123
Q

INTERSTITIAL LUNG DISEASE
What is the clinical presentation of interstitial lung disease?
What is a long-term complication of this?

A
  • Progressive, exertional dyspnoea + dry cough
  • Bibasal fine end-inspiratory creps, finger clubbing, cyanosis
  • Cor pulmonale as fibrosis causes gradual pulmonary HTN
124
Q

INTERSTITIAL LUNG DISEASE
What investigations would you consider in interstitial lung disease?
What is the diagnostic investigation?

A
  • Spirometry, gas transfer test, CXR

- High-resolution CT chest

125
Q

INTERSTITIAL LUNG DISEASE
In ILD, what would the following show…

i) spirometry?
ii) gas transfer test?
iii) CXR?
iv) HR CT chest?

A

i) Restrictive = FEV1 normal/low, FVC low, FEV1/FVC increased
ii) Impaired gas exchange as reduced transfer factor (TLCO)
iii) Bilateral lower zone reticular opacities
iv) Bilateral interstitial shadowing = small, irregular, peripheral (ground glass) opacities which leads to honeycombing

126
Q

INTERSTITIAL LUNG DISEASE

What is the management of ILD?

A
  • Conservative = stop smoking, pulmonary rehab
  • Medical = LTOT, ?pirfenidone antifibrotic in select few
  • Surgical = lung transplant curative in select few
127
Q

ANAPHYLAXIS
What is anaphylaxis?
What are some potential causes?

A
  • Severe, life-threatening IgE hypersensitivity reaction with sudden ABC issues
  • Foods (commonest in paeds) like nuts, meds (Abx, IV contrast) + venom (stings)
128
Q

ANAPHYLAXIS

What is the clinical presentation of anaphylaxis?

A
  • A = swelling of throat + tongue > hoarse voice + stridor
  • B = wheeze, SOB, cyanosis
  • C = hypotension + tachycardia
  • D = skin/mucosal changes > widespread pruritus, urticaria, angioedema
129
Q

ANAPHYLAXIS

What is the acute management of anaphylaxis?

A
  • ABCDE with 15L oxygen via NRB, IV fluid boluses required

- IM adrenaline 1:1000 every 5 minutes to the anterolateral aspect of middle third of thigh

130
Q

ANAPHYLAXIS

What are the doses of adrenaline for the various age ranges?

A
  • <6m = 100–150 micrograms
  • 6m–6y = 150 micrograms
  • 6–12y = 300 micrograms
  • > 12y = 500 micrograms
131
Q

ANAPHYLAXIS
What is refractory anaphylaxis?
What is the management?

A
  • ABC problems persisting despite 2 doses of IM adrenaline

- IV fluids, expert help for ?IV adrenaline infusion

132
Q

ANAPHYLAXIS

What is the post-acute management of anaphylaxis once you’ve stabilised the patient?

A
  • Non-sedating PO antihistamine e.g., chlorphenamine
  • Serum mast cell tryptase 1–6h after event to confirm
  • Specialist allergy clinic referral
  • 2x adrenaline auto-injectors (300mcg) if may be exposed to trigger again
133
Q

ANAPHYLAXIS

What must you be cautious of after managing anaphylaxis?

A
  • Biphasic reactions may occur

- Risk-stratified approach to discharge crucial

134
Q

SARCOIDOSIS
What is sarcoidosis?
Who does it normally affect?

A
  • Multisystem disorder characterised by non-caseating granulomas
  • Young, Afro-Caribbean women
135
Q

SARCOIDOSIS
What is the acute presentation of sarcoidosis?
What systems can sarcoidosis affect?

A
  • Erythema nodosum, swinging fever, polyarthralgia, bilateral hilar lymphadenopathy = Lofgren’s syndrome
  • Pulmonary, systemic, neuro, cardiac, ocular, abdo, derm
136
Q

SARCOIDOSIS
How does sarcoidosis present in the following systems…

i) pulmonary?
ii) systemic?
iii) neuro?
iv) cardiac?
v) ocular?
vi) abdo?
vii) derm?

A

i) Dry cough, SOB
ii) Fatigue, weight loss, arthralgia, fever
iii) Meningitis, peripheral neuropathy, bilateral Bell’s palsy
iv) Arrhythmias, restrictive cardiomyopathy
v) uveitis, conjunctivitis
vi) Hepatosplenomegaly
vii) Lupus pernio (raised, purple skin lesion on nose)

137
Q

SARCOIDOSIS

What investigations would you do in sarcoidosis?

A
  • Bloods = raised ESR, ACE + calcium, reduced lymphocytes
  • CXR/CT-chest
  • Spirometry (restrictive)
  • Tissue biopsy = diagnostic for non-caseating granulomas
138
Q

SARCOIDOSIS

How can sarcoidosis be staged on CXR/CT-chest?

A
  • 1 = BHL
  • 2 = BHL + interstitial infiltrates
  • 3 = diffuse interstitial infiltrates only
  • 4 = diffuse fibrosis
139
Q

SARCOIDOSIS

What is the management of sarcoidosis?

A
  • Usually self-limiting with bed rest and NSAIDs

- PO steroids if symptomatic stage 2/3, hypercalcaemia or eye, heart or neuro involvement

140
Q

PULMONARY HTN
What is the normal pulmonary arterial pressure?
What is pulmonary HTN?

A
  • 18–25mmHg
  • > 25mmHg which causes strain on the right heart which is pumping blood to the lungs with more resistance as well as systemic back pressure
141
Q

PULMONARY HTN

What is the aetiology of pulmonary HTN?

A
  • Left heart disease = mitral stenosis/regurg, LVF
  • Lung disease = COPD, interstitial lung disease, CF
  • Pulmonary vasculitis = SLE, granulomatosis with polyangiitis
142
Q

PULMONARY HTN

What is the clinical presentation of pulmonary HTN?

A
  • SOB #1

- May have HF Sx (raised JVP, peripheral oedema, hepatomegaly) + can have functional TR (pansystolic murmur)

143
Q

PULMONARY HTN
What are some investigations for pulmonary HTN?
What is gold standard?

A
  • ECG = RVH, RAD + P pulmonale
  • CXR = enlarged proximal pulmonary arteries, RVH
  • ECHO = RV dilatation + hypertrophy
  • Gold = right heart catheterisation showing pressure >25mmHg
144
Q

PULMONARY HTN

What is the management of pulmonary HTN?

A
  • IV prostacycline analogues like epoprostenol
  • Endothelin receptor antagonists like bosentan
  • Phosphodiesterase-5 inhibitors like sildenafil
  • CCB like nifedipine
145
Q

OSA
What is obstructive sleep apnoea (OSA)?
What are some predisposing factors?

A
  • Intermittent closure + collapse of upper airway > apnoeic episodes in sleep
  • Obesity #1, macroglossia (acromegaly, hypothyroidism), large tonsils, Marfan’s
146
Q

OSA

What is the clinical presentation of OSA?

A
  • Partner often reports excessive snoring ± apnoea
  • Daytime sleepiness + poor sleep quality
  • HTN due to drop in blood O2 and rise in CO2 levels during apnoea
  • Compensated resp acidosis
147
Q

OSA

What investigations would you do in OSA?

A
  • Epworth sleepiness scale = completed by pt + partner
  • Multiple sleep latency test = measures time to fall asleep in dark room
  • Diagnostic = polysomnography measuring parameters such as overnight pulse ox
148
Q

OSA

What is the management of OSA?

A
  • Weight loss
  • CPAP first-line in mod–sev to maintain airway
  • Intraoral devices like mandibular advancement if CPAP not tolerated
  • DVLA informed if excessive daytime sleeping
149
Q

MESOTHELIOMA

What is a mesothelioma?

A
  • Malignant tumour of mesothelial cells which line the pleura often due to asbestos
150
Q

MESOTHELIOMA

What is the clinical presentation of mesothelioma?

A
  • Long latency period of 30–40y from exposure-tumour
  • SOB, weight loss, chest wall pain
  • Signs = finger clubbing, pleural effusion
151
Q

MESOTHELIOMA

What are the investigations of mesothelioma?

A
  • Suspicion raised by CXR showing pleural effusion or pleural thickening
  • Next = pleural CT + aspiration if effusion present
  • Diagnostic = thoracoscopy for histology
152
Q

MESOTHELIOMA

What is the management of mesothelioma?

A
  • Industrial compensation

- Poor prognosis so symptomatic, ?chemo, ?surgery

153
Q

GPA

What is granulomatosis with polyangiitis (GPA)?

A
  • Autoimmune condition associated with necrotising granulomatous small vessel vasculitis, affecting both upper/lower resp tract + kidneys
154
Q

GPA

What is the clinical presentation of GPA?

A
  • URT = epistaxis, sinusitis, nasal crusting, saddle-shape nose deformity
  • LRT = SOB, haemoptysis
  • Renal = rapidly progressive pauci-immune glomerulonephritis (protein & haematuria on urine dipstick)
155
Q

GPA

What investigations might you do in GPA?

A
  • cANCA +ve in >90%
  • CXR = bilateral nodular + cavity infiltrates
  • Renal biopsy may show epithelial crescents in Bowman’s capsule
156
Q

GPA

What are the other ANCA vasculitides and how do they present?

A

Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
- Similar = sinusitis + SOB
- Differences = asthma, pANCA + eosinophilia
Microscopic polyangiitis
- pANCA, rapid glomerulonephritis, pulmonary haemorrhage > haemoptysis

157
Q

GPA

What is the management of GPA?

A
  • Steroids e.g., pred
  • Cyclophosphamide
  • Plasma exchange
158
Q

ANTI-GBM DISEASE
What is anti-GBM disease/Goodpasture’s syndrome?
What is the epidemiology?

A
  • Small vessel vasculitis caused by anti-glomerular basement membrane (anti-GBM) antibodies against type IV collagen
  • More common in men, bimodal age distribution + HLA-DR2 associated
159
Q

ANTI-GBM DISEASE

What is the clinical presentation of anti-GBM disease?

A
  • Pulmonary haemorrhage = haemoptysis

- Rapidly progressive glomerulonephritis = rapid onset AKI + protein/haematuria

160
Q

ANTI-GBM DISEASE
How do you diagnose anti-GBM disease?
What is the management of anti-GBM disease?

A
  • Renal biopsy = linear IgG deposits along the basement membrane
  • Plasma exchange, steroids + cyclophosphamide
161
Q

EAA

What is hypersensitivity pneumonitis/extrinsic allergic alveolitis (EAA)?

A
  • Hypersensitivity induced lung damage due to inhaled organic particles leading to a type 3 hypersensitivity reaction (immune-complex mediated tissue damage)
162
Q

EAA

What are some causes of EAA?

A
  • Bird fanciers’ lung = avian proteins from bird droppings
  • Farmer’s lung = spores from wet hay
  • Malt + mushroom worker’s lung
163
Q

EAA

What is the clinical presentation of EAA?

A
  • Acute (4–8h post-exposure) = SOB, dry cough + fever

- Chronic (weeks–months) = SOB, lethargy, productive cough, anorexia + weight loss

164
Q

EAA

What are the investigations for EAA?

A
  • FBC = NO eosinophilia
  • CXR/CT chest = upper zone fibrosis
  • Bronchoalveolar lavage = lymphocytosis
  • Serologic assays for specific IgG Ab
165
Q

EAA

What is the management of EAA?

A
  • Avoid precipitants = #1

- PO pred

166
Q

ACUTE BRONCHITIS

What is acute bronchitis?

A
  • Inflammation of the trachea + major bronchi + so is associated with oedematous large airways + sputum production
167
Q

ACUTE BRONCHITIS

What is the clinical presentation of acute bronchitis?

A
  • Cough ± productive
  • Sore throat, rhinorrhoea but not really SOB
  • Normal chest exam but may have low-grade fever + wheeze, no focal creps
168
Q

ACUTE BRONCHITIS

What is the management of acute bronchitis?

A
  • First line Abx = PO doxy, if not PO amox
  • CRP 20–100mg/L = delayed Abx, >100 = Abx
  • Systemically very unwell or pre-existing comorbidities = Abx
169
Q

INFLUENZA

What is the pathophysiology of influenza?

A
  • RNA virus which exists in three serotypes: A, B (most common) and C which is determined by surface antigens haemagglutinin + neuraminidase which are rearranged in host organisms such as animals to produce different strains
170
Q

INFLUENZA

What is the clinical presentation of influenza?

A
  • Fever ≥37.8
  • Coryzal Sx
  • Fatigue
  • Myalgia
  • Headache
  • Dry cough
  • Sore throat
171
Q

INFLUENZA

How do you investigate influenza?

A
  • Viral nasal/throat swabs for PCR

- COVID-19 PCR

172
Q

INFLUENZA

What are some complications of influenza?

A
  • Pulmonary = viral or secondary bacterial pneumonia, worsening of chronic disease
  • Neuro = encephalitis
  • Cardio = myocarditis
173
Q

INFLUENZA

What influenza prophylaxis is available and who is able to receive it?

A
  • Free influenza vaccination

- ≥65, young children, pregnant women, those with chronic health conditions (COPD, asthma, DM) + healthcare workers

174
Q

INFLUENZA

What is the management of influenza?

A
  • Mostly supportive with analgesia, antipyretics, fluids + oxygen
  • Infection control/isolation measures
  • If risk of complications = PO oseltamivir (Tamiflu)
175
Q

ATELECTASIS

What is the pathophysiology of atelectasis?

A
  • Collapse of either basal alveolar or even most/entire lobes caused by resorptive atelectasis as residual air in affected lung resorbed by circulating blood at greater rate than it’s replaced by ventilated air causing volume loss + opacification on CXR
176
Q

ATELECTASIS

What are the causes of atelectasis?

A

Bronchial obstruction

  • Luminal = foreign object, mucus plugging, misplaced endotracheal tube
  • Mural = lung cancer
177
Q

ATELECTASIS

What is the clinical presentation of atelectasis and how would you investigate it?

A
  • SOB + hypoxia, especially 72h post-op

- CXR = air space opacification, tracheal deviation towards atelectasis

178
Q

ATELECTASIS

What is the management of atelectasis?

A
  • Position pt upright, treat cause

- Chest physiotherapy with deep breathing exercises

179
Q

ABPA

What is allergic bronchopulmonary aspergillosis (ABPA)?

A
  • Allergy to Aspergillus spores often with background of bronchiectasis + eosinophilia
180
Q

ABPA

What is the clinical presentation of ABPA?

A
  • Bronchoconstriction = wheeze, cough, dyspnoea

- Proximal bronchiectasis

181
Q

ABPA

What investigations and management would you do in ABPA?

A
  • FBC = eosinophilia
  • Immediate positive radioallergosorbent (RAST) test to Aspergillus
  • Positive IgG precipitins + raised IgE
  • PO pred 1st line, ?itraconazole 2nd line
182
Q

OCCUPATIONAL LUNG DISEASES

What is the pathophysiology of coal worker’s pneumoconiosis?

A
  • Inhaled coal dust is engulfed by macrophages which becomes overwhelmed + accumulate in alveoli triggering an immune response damaging lung tissue
183
Q

OCCUPATIONAL LUNG DISEASES

What are the two types of coal workers’ pneumoconiosis?

A
  • Simple pneumoconiosis = commonest, no Sx, increased risk of lung diseases (COPD)
  • Progressive massive fibrosis = upper zone fibrosis, SOBOE + cough
184
Q

OCCUPATIONAL LUNG DISEASES

What various pathologies can result due to asbestos exposure?

A
  • Pleural plaques
  • Pleural thickening
  • Asbestosis
  • Mesothelioma + lung cancer
185
Q

OCCUPATIONAL LUNG DISEASES
What are pleural plaques?
What is the management?

A
  • Benign and do not undergo malignant change

- No follow up

186
Q

OCCUPATIONAL LUNG DISEASES

How does asbestosis present?

A
  • Lower lobe fibrosis presenting with SOB + reduced exercise tolerance
  • Severity related to length of exposure (unlike mesothelioma)
187
Q

OCCUPATIONAL LUNG DISEASES

What are the investigations and management for occupational lung diseases?

A
  • CXR = fibrosis (zone depends on condition)
  • Spirometry = restrictive pattern
  • Avoid exposure if possible + industrial compensation via Industrial Injuries Act
188
Q

ARDS

What is acute respiratory distress syndrome (ARDS)?

A
  • Increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli (non-cardiogenic pulmonary oedema)
189
Q

ARDS

What are the causes of ARDS?

A
  • Pulmonary = chest sepsis, inhalation injury, transfusion-related lung injury, aspiration
  • Non-pulmonary = other sepsis, DIC, acute pancreatitis
190
Q

ARDS
What is the clinical presentation of ARDS?
How is ARDS diagnosed?

A
  • Acute onset + severe SOB, tachypnoea, bilateral lung crackles + hypoxia
  • American-European Consensus Conference
191
Q

ARDS

What are the aspects of the American-European Consensus Conference for ARDS diagnosis?

A
  • Acute onset (<1w of known risk factor)
  • Pulmonary oedema = bilateral infiltrates on CXR
  • Non-cardiogenic (pulmonary artery wedge pressure if doubt)
  • PF ratio (pO2/FiO2) <40kPa implies acute lung injury, <28kPa severe on ABG
192
Q

ARDS

What is the management of ARDS?

A
  • ITU setting as high mortality, prone positioning
  • Oxygenation/ventilation for hypoxaemia with low tidal volume
  • General organ support e.g., vasopressors to maintain MAP >60mmHg

FINALS (20 decks)

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