Respiratory Flashcards
Chronic obstructive pulmonary disease
- Combination of chronic bronchitis (excessive mucus secondary to cillary dysfunction) and emphysema (loss of alveolar intgrity due to proteases and protease inhibitor imbalance)
- Progressive, irreversible
- Mostly caused by smoking
Clinical features of COPD
Typically long-term smoker:
- Shortness of breath
- Cough
- Sputum production
- Wheeze
- Recurrent respiratory infections, particularly in winter
Signs on examination of COPD
- Tachypnoea
- Barrel chest (bulging of the chest)
- Hyperresonance on percussion
- Tar staining of fingers with peripheral cyanosis
Risk factors for COPD
- Age: usually diagnosed > 45
- Tobacco smoking: greatest risk factor
- Occupational exposure: dust, coal, cotton
- Alpha-1 antitrypsin deficiency: younger patients that present with COPD features
MRC dyspnoea scale for assessing breathlessness
- Grade 1: Breathless on strenuous exercise
- Grade 2: Breathless on walking uphill
- Grade 3: Breathlessness that slows walking on the flat
- Grade 4: Breathlessness stops them from walking more than 100 meters on the flat
- Grade 5: Unable to leave the house due to breathlessness
Diagnosis of COPD
- Clinical diagnosis and spirometry results
Spirometry:
- FEV1:FVC < 70%
- No response to bronchodilator testing with beta-2 agonists (e.g., salbutamol).
Severity
- Stage 1 (mild): FEV1 > 80% of predicted
- Stage 2 (moderate): FEV1 50-79% of predicted
- Stage 3 (severe): FEV1 30-49% of predicted
- Stage 4 (very severe): FEV1< 30% of predicted
FEV1 = forced expiratory volume, FVC = forced vital capacity, volume exhaled after max exhalation
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Medications for COPD
1) SABA: short-acting beta-adrenoceptor agonist (e.g. salbutamol) - leads to bronchodilation
2) SAMA: short-acting muscarinic antagonist (ipratropium) - inhibits smooth muscle contractions
3) LABA: long-acting beta-adrenoceptor
agonist (e.g. salmeterol) - leads to bronchodilation
4) LAMA: long-acting muscarinic antagonist (e.g. tiotropium) - inhibits smooth muscle contraction
5) ICS: inhaled corticosteroid (e.g. beclomethasone
Long-term management of COPD
- Smoking cessation
Annual flu and pneumococcal vaccine
Step 1: SABA or SAMA (e.g. ipratropium bromide) - Step 2: if no asthmatic or steroid-responsive features = combination inhalers containing LABA and LAMA
- If asthmatic or steroid-responsive features = LABA and ICS combination inhalers
- Step 3: LABA, LAMA and ICS combination inhalers
- Step 4: other meds under specialist
- Long-term oxygen for severe COPD with O2 sats < 92%
For acute excerbation of COPD, see A+E deck
Pneumonia
Infection of lung tissue > inflammation in alveolar space
CXR: consolidation
- Community-acquired pneumonia (CAP)
- Hospital-acquired pneumonia (HAP): > 48hrs in hospital
- Ventilator-acquired pneumonia (VAP): intubated pts on ICU
- Aspiration pneumonia
Clinical features of pneumonia
- Cough
- Sputum
- SOB
- Fever
- Generally unwell
- Haemoptysis
- Pleuritic chest pain (sharp, worse on inspiration)
- Delirium
Signs on examination in pneumonia
- Bronchial breath sound (harsh due to consolidation)
- Focal coarse crackles - air passing sputum
- Dull percussion - sputum or collapse
If tachycardia/pnoea, hypoxia, hypotension, fever, confusion = secondary sepsis
Severity assessment in pneumonia
- C – Confusion (new disorientation in person, place or time)
- U – Urea > 7 mmol/L
- R – Respiratory rate ≥ 30
- B – Blood pressure < 90 systolic or ≤ 60 diastolic
- 65 – Age ≥ 65
CRB-65 in primary care
Mortality: low risk: 0/1 (<3%), intermediate = 2 (3-15%), high = 3 (>15%)
Main bacterial causes of pneumonia
- Streptococcus pneumoniae (most common)
- Haemophilus influenzae
- Methicillin-resistant Staphylococcus aureus (MRSA) in hospital
Causes of atypical pneumonia
“Legions of psittaci MCQs”:
- Legions – Legionella pneumophila
- Psittaci – Chlamydia psittaci
- M – Mycoplasma pneumoniae
- C – Chlamydophila pneumoniae
- Qs – Q fever (coxiella burnetii)
Investigations for pneumonia
- Point of care CRP test in primary care to guide dx and abx use
- Hospital: CXR, FBC (raised WCC), renal profile (urea levels and AKI), CRP
- If severe: + sputum culture, blood culture, pneumonococcal andLegioella urinary antigen tests
WCC + CRP proportional to severity, used to measure tx response
Management of pneumonia
- Follow local guidelines as follows abx resistance in local area
- Mild: usually 5 days of oral amoxicillin/doycycline/clarithromycin
- Moderate/severe: IV abx, oral abx as condition improves
Pneumothorax
Air in pleural space, seprating
Investigations for pneumothorax
Erect CXR:
- Shows area between lung tissue and chest wall with no lung markings.
- Demarcation of lung edge and start of pneumothorax
- Measure = horizontal line from lung edge to chest wall at hilum level
Management of pneumothorax (British Thoracic Society)
- Consult seniors
- High risk (e.g. haem unstable, bilateral, hypoxia, underlying lung disease) = chest drain
- Low risk and <2cm = conservative + outpt review
- Low risk and >2cm, depends on pt preference:
- Conservative + outpt review
- Symptom relief with pleural vent ambulatory device
- Short-term drainage e.g. needle aspiration or chest drain
Where is a chest drain inserted?
Triangle of safety:
- 5th intercostal space (or the inferior nipple line)
- Midaxillary line (or the lateral edge of the latissimus dorsi)
- Anterior axillary line (or the lateral edge of the pectoralis major)
Surgical options for pneumothorax if chest drain ineffective
Pleurodesis - creating inflammatory response in pleural lining so it sticks together. sealing pleural space.
- Abrasive
- Chemical
- Pleurectomy
Tension pneumothorax
Trauma > one way valve letting air in but not out of pleural space > each breath traps more air > increased pressure pushes mediastinum + tangles big vessels > cardiorespiratory arrest
Clinical features of tension pneuthorax
Affected side:
- Tracheal deviation away
- Reduced air entry
- Increased resonance to percussion
- Tachycardia
- Hypotension
Management of tension pneumothorax
Chest drain, do not wait for Ix
Learn for exam: “insert a large bore cannua into 2nd intercostal space in midclavicular line”
However, advanced traumatic life support recommends ““4/5th intercostal space, anterior to the midaxillary line” for adults.+
+ Chest wall thinner there
Pulmonary embolism (PE)
Thrombus in pulmonary arteries.
Venous thromboembolism = PE + DVT collectively
Risk factors for PE
Virchow’s triad
- Venous stasis (e.g. long-haul flight, immobility)
- Hypercoagulability (malignancy, pregnancy, polycythaemia etc.)
- Vessel injury (e.g. recent surgery)
In exam, if pt presents with PE or DVT symptoms, ask about risk factors = extra points
Clinical features of a PE
Asymptomatic or subtle = sudden death so low threshold for suspicion
- SOB
- Cough
- Haemotysis
- Pleuritic chest pain (sharp, worse on inspiration)
- Hypoxia
- Tachycardia/ponea
- Low-grade fever
- Haem unstable (hypotension)
Watch out for DVT e.g. unilateral leg swelling/tenderness
Scores for assessing PE
Pulmonay embolism rule-out criteria (PERC) - use if clinician estimates <15% probability of PE, if all criteria met = no PE Ix needed
Wells score: predicts probability of PE, used when PE is suspected
Diagnosis of PE
Based on Wells score:
- Likely - CT pulmonary angiogram (1st line for PE)
- Unlikely - D-dimer, if +ve then CTPA
ABG = respiratory alkalosis with low pO2 as hypoxia = raised RR
CXR usually normal but used to exclude other pathology
D-dimer sensitive (95%) not specific, excludes VTE if low but can be raised in many other conditons (pregnancy, HF, malignancy)
Managment of PE
Depends on severity
- Admission
- O2 therapy
- Analgesia
- Monitoring
- Anticoagulation - 1st line is tx dose apoxaban/rivaroxaban, LMWH as alternative
Management of massive PE with haemodynamic compromise
Continuous infusion of unfractionated heparin and thromolysis (IV fibrinolytic agent) e.g. alteplase/tenecteplase
Long-term anticoagulation for PE
- DOAC (avoid if severe renal impairment - creatinine clearance < 15ml/min)
- Wafarin -1st line in pts with APLS, INR 2 - 3
- LMWH - 1st line in pregnancy
- 3 months if reversible cause then review
- > 3 months if unprovoked PE, recurrent VTE or an irreversible underlying cause (e.g., thrombophilia)
- 3-6 months in active cancer (then review)
Respiratory failure
Occurs when gas exchange is inadequate > hypoxia
Type 1: low PaO2 <8kPa, low/normal PaCO2, caused by ventilation/perfusion (V/Q) mismatch
Type 2: low PaO2< 8kPa, high PaCO2 > 6.0kPa, caused by alveolar hypoventilation +/- V/Q mismatch
V/Q mismatch
Causes of respiratory failure
Type 1: V/Q mismatch = PE, pneumonia, pulmonary oedema, asthma etc.
Type 2:
- Pulmonary disease: COPD, end-stage fibrosis, pneumonia
- Reuced resp drive: e.g. opiates
- Neuromuscular disease: e.g. masthenia gravis, GBS
Clinical features of respiratory failure
- Features of the underlying disease + features of hypoxia/hypercarnia (if present)
Hypoxia: dyspnoea, restlessness, agitation, confuion, central cyanosis. If long-term: polycythaemia, pulmonart HTN
Hypercarnia: headache, tachycardia, bounding pulse, tremor/flap, papilloedema, confusion, coma
Investigations for respiratory failure
Identify cause
- Bloods: FBC, U+E. CRP, ABG
Normal pH 7.35 - 7.45
Management of type 1 respiratory failure
- Senior support
- Treat underlying cause
- O2 therapy (nasal cannuala, face mask, ventri mask, non-rebreathing mask)
- Consider ICU support and high-flow nasal oxygen or CPAP if O2 req. > 40%)
+Oxford handbook of clinical medicine
Management of type 2 respiratory failure
- Senior support
- Treat underlying cause
- Controlled O2 therapy - SpO2 target 88 - 92% if COPD and CO2 retention
- Start at 24% O2
- Recheck ABG after 20 mins, if PaCO2 steady or lower, increase to 28% O2, if PaCO2 rising, consider NV-PPV
NVPPV - non-invasive positive pressure ventilation
Be careful with O2, as respiration may be driven by hypoxia
Asthma
Chronic inflammatory disease of the airway, with variable and reversible airway obstruction
Smooth muscles of the airway are hypersensitivite and react to stimuli by constricting = airway obstruction.
Presentation of asthma
Typically:
- SOB
- Chest tightness
- Dry cough
- Wheeze
- Episodic and diurnal variability
- Bronchdilator reversible - if not, alternative dx likely
Widespread “polyphonic” expiratory wheeze during exacebation
Triggers for asthma
- Infection
- Nighttime or early morning
- Exercise
- Animals
- Cold, damp or dusty air
- Strong emotions
- Non-selective beta blockers e.g. propanolol
- NSAIDs
Investigations for asthma
Initial Ix recommended by NICE:
- Fractional exhaled nitric oxide (FeNO) > 40ppb
-Spirometry (FEV1:FVC < 0.7) with bronchodilator reversibility (> 12% increase in FEV1)
If doubt
- Peak flow variaibiltiy (x2 a day, diary for 2 - 4wks) > 20%
- Direct bronchial challenge test (inhale histamine, measure FEV1), PC20 =< 8mg/ml
Long-term treatment for asthma
- SABA e.g. salbutamol
- low-dose ICS e.g. beclometasone
- Leukotriene receptor antagonist e.g. montelukast
- LABA e.g. salmeterol
- Consider MART (LABA and ICS combo)
- Moderate-dose ICS
- High-dose ICS
- Specialist mangement e.g. oral corticosteroids
MART is preventer and reliever and replaces all inhales
Acute exacerbation of asthma (acute asthma)
Rapid deterioration in symptoms:
- Progressively SOB
- Use of accessory muscles
- Tachypnoea
- Symmetrical ex. wheeze
- Tight chest on ascultation and reduced air entry
ABG in asthma
- Initially, respiratory alkalosis as PCO2 low
- Normal pCO2 or low pO2 = concerning
- Respiratory acidosis (high PaCO2) = very bad
Grades in asthma exacerbation
Moderate
- Peak flow 50 - 75% of best/predicted
Severe:
- Peak flow 33 - 50%
- RR > 25
- HR > 110
- Unable to complete sentences
Life-threatening
- Peak flow < 33%
- O2 sats < 92%
- PaO2 < 8kPa
- Exhaustion
- Confusion/agitation
- No wheeze/silent chest (no air entry)
- Shock
Management of mild asthma exacebation
- Escalate to seniors and ICU early, as can deteriorate quickly
Mild:
- Inhaled SABA via spacer
- 4x ICS for up to 2 weeks
- Oral steriods (prednisolone) if ICS ineffective
- Abx if infection
- Follow-up within 48 hrs
Monitor serum K if salbutamol as causes hypokalaemia
Management of moderate asdthma exacerbation
- Escalate to seniors and ICU early, as can deteriorate quickly
Same as mild AND:
- Consider admission
- Nebulised beta-2 agonists (e.g., salbutamol)
- Steroids (e.g., oral prednisolone or IV hydrocortisone)
Monitor serum K if salbutamol as causes hypokalaemia
Management of severe + life-threatening asthma exacerbation
- Escalate to seniors and ICU early, as can deteriorate quickly
- Same as mild and moderate AND
- Admission
- O2 to maintain 94 - 98%
- Neubulised ipratropium bromide
- IV Mg suplhate
- IV salbutamol
- IV aminophylline
Life-threatebing:
- Admission to HDU/ICU
- Intubation and ventilation
Monitor serum K if salbutamol as causes hypokalaemia
