Respiratory Flashcards
What are the adverse effects of bosentan?
Hepatotoxicity 10%
Which drugs may be associated with a prognostic / survival benefit in group 1 PAH?
Macitentan - may be associated with improved morbidity / mortality
Bosentan - favourable survival outcomes
Mortality benefit of PDE5 inhibitors and soluble guanylate cyclase stimulators unknown in PAH
What are the echocardiographic features of pulmonary hypertension?
- Use tricuspid regurgitant velocity (TRV) to estimate RVSP. RVSP is a surrogate for PASP, provided there is pulmonary stenosis or RVOT obstruction
Uses modified Bernoulli equation
Estimated PASP = RVSP = 4 x [TRV]^is 2 + RAP - RV hypertrophy / dilatation / systolic function
- RA enlargement
- Mid-systolic notch on pulmonary artery doppler
- Septal blowing (intraventricular septum shifts towards the LV cavity resulting in flattening, during systole)
- Can estimate the PCWP using the E/e’ ratio. PCWP is an indirect measurement of LA pressure.
Work up of suspected pulmonary hypertension
Overview of pulmonary hypertension management
Management of suspected VTE in pregnancy
Risk factors for developing CTEPH after PE
Management of haemodynamically stable PE
What are the mutation classes in cystic fibrosis?
- > 2000 mutations in CFTR (cystic fibrosis transmembrane conductance regulator) gene on chromosome 7
- autosomal recessive inheritance
- 5 classes of mutations - class I - III have more severe phenotype, class IV-V have milder phenotypes
Class I - no functional CFTR produced (22%), 2nd most common type, due to nonsense mutations, splice mutations and deletions
Class II - MOST common (88%), TRAFFICKING detect, CFTR is produced but misfolds and therefore does not move appropriately to cell surface membrane. MOST COMMON IS F508 deletion (“processing” mutation)
Class III - CFTR protein is produced and moves to cell surface but channel gate does not open correctly (6%). G551D (“gating” mutation)
Class IV - CFTR protein produced, moves to cell surface, but function of channel is faulty
Class V - normal CFTR protein is produced and moves to the cell surface, but in insufficient quantities
What is the Well’s score?
- Low (<2) –> do a PERC score and if low can rule out clinically
- Moderate (2-4) –> do a D-dimer
*High (>4) –> do a CTPA
What is the PERC criteria?
- If NONE of the 8 PERC criteria are present, PE can be ruled out clinically
Lung volumes
- Tidal volume - volume of air breathed in and out at rest (500mL)
- Inspiratory reserve volume - volume of air that can be inspired on deep inspiration in addition to TV (1900mL)
- Expiratory reserve volume - volume of air that can be expired in addition to TV on deep expiration (700mL)
- Residual volume - the volume of air that remains in the lungs in order to maintain airway patency, after a deep & forceful expiration (1100mL)
- Inspiratory capacity - the maximum volume of air that can be inspired after quiet expiration (2400mL)
TV + IRV - Functional residual capacity - the volume of air that remains in the lungs after quiet expiration during tidal breathing (1800mL)
RV + ERV - Vital capacity - the volume of air that can be expired after deep inspiration
TV + IRV + ERV - Total lung capacity - total volume of air that can be contained within the respiratory system, volume of air in the lungs after maximal voluntary inspiration
TV + IRV + ERV + RV
rarely also pulmonary sarcoidosis
What does an elevated residual volume to total lung capacity ratio indicate?
High RV: TLC, normal TLC - gas trapping
High RV: TLC, high TLC - gas trapping & hyperinflation
Normal RV: TLC, high TLC - large lung capacity (athletes etc.)
High RV: TLC ratio, low TLC but normal RV - chest wall deformity / neuromuscular weakness, obesity
Normal RV: TLC ratio, TLC reduced, RV reduced - restriction
What indicates gas trapping on RFTs?
Elevated residual volume to total lung capacity ratio with normal total lung capacity (ratio > 0.4 OR > 2 standard deviations from normal)
Spirometry will likely show a mixed obstructive / restrictive ventilatory deficit - where FVC is reduced due to gas trapping rather than due to a second restrictive pathology
What is a positive bronchodilator response?
What changes on respiratory function testing would be seen in obesity?
- Spirometry : restrictive ventilatory deficit
- RV: TLC ratio increased, due to reduced TLC but preserved RV (total lung capacity and forced vital capacity may be normal)
- most significant change in obesity is reduced expiratory reserve volume (ERV)
- therefore, there is a reduction in functional residual capacity proportional to the severity of obesity
- DLCO increases due to increase pulmonary blood volume
- KCO also increased due to reduction in alveolar volume
What do the RFTs / lung volumes show in COPD?
- Spirometry: post-bronchodilator FEV1/FVC ratio <0.7, FEV1 < 0.8
*there may be an element of bronchodilator reversibility - if bronchodilator response > 400mL - consider asthma or asthma-COPD overlap; if >200mL and 12% (but <400mL) - consider asthma / COPD overlap or asthma component - DLCO reduced in emphysema / pulm HTN, may be normal in chronic bronchitis
- RV increases due to gas trapping / airway closure (RV: TLC ratio increases)
- FRC increases due to increase in RV
- eventually TLC also increases reflecting hyperinflation
- expiratory reserve volume (ERV) decreases => therefore forced vital capacity decreases
- inspiratory capacity decreases
What is the benefit of pulmonary rehabilitation / regular physical activity in COPD?
- Improves symptoms, QoL, exercise capacity, anxiety & depression
- Reduces hospitalisation for exacerbations
- Improves peripheral muscle function and sense of control
- does NOT improve survival
Who should be started on triple agent inhaler therapy in COPD? What is the benefit of triple inhaler therapy?
Indications for inhaled corticosteroid therapy:
- FEV1 < 50%
- recurrent exacerbations and significant symptoms
- eosinophilia
Indications for triple inhaler therapy (ICS + LAMA + LABA)
- at least one severe exacerbation per year requiring hospitalisation, or 2 or more moderate exacerbations in last 12 months AND significant symptoms despite LAMA / LABA or ICS/LABA therapy
- OR in patients stabilised on a combination of LABA + ICS, plus LAMA
Triple therapy (ICS / LAMA / LABA) has a mortality benefit, reduces exacerbations and hospitalisations compared to dual therapy (LAMA/LABA)
- increased pneumonia rates compared to LAMA/LABA but similar to ICS/LABA
- especially in patients with frequent exacerbations, blood eosinophil count > 200, when low-medium ICS used
Who is eligible for home O2 therapy in COPD?
Long term O2 therapy has a survival benefit for hypoxaemic COPD patients
- must use for at least 16-18 hours per day to have a benefit
- PaO2 <55mHg (severe hypoxia)
- PaO2 55-59mmHg with evidence of R heart failure, pulm HTN, polycythaemia
- No cigarettes for 3 months
- No evidence of improvement for moderate hypoxia - PaO2 60-79mmHg
Exertional (portable) oxygen
**improves exercise tolerance
- SaO2 <88% after 6 minutes walking
- SaO2 improves with O2 therapy
- No cigarettes for 3 months
Refer patients with possible persisting hypoxaemia (SaO2 <92%) for consideration of home o2
What factors determine prognosis in COPD?
BODE index- predicts 4 year survival in COPD patients
1. FEV1
2. Distance walked in 6 minutes
3. mMRC dyspnoea scale
4. BMI
Who should be referred for lung transplantation in COPD?
- progressive symptoms (despite maximal treatment including medications, pulm rehab and O2 therapy)
- NOT a canddiate for endoscopic or surgical lung volume reduction
- BODE index 5-6
- PaCO2 > 50 and/or PaO2 <60mmHg
- FEV1 <25% predicted
What determines poor prognosis in COPD exacerbations?
DECAF
- dyspnoea
- eosinopenia
- consolidation
- acidaemia
- atrial fibrillation
What are the indications for NIV in COPD exacerbations?
What are the contraindications for NIV in COPD exacerbations?
Why is NIV effective in COPD exacerbations?
Indications for use of BiPAP in COPD exacerbations (CPAP not helpful as does not improve ventilation)
- PaCO2 > 45mmHg, pH <7.35 (i.e. hypercapnic respiratory acidosis)
- Increased WOB
- Severe dyspnoea with clinical signs of respiratory muscle fatigue
Large body of evidence to support use of NIV in COPD patients that are hypercapnic
- nearly 50% reduction in mortality
- reduced rate of intubation by 65%
- reduced hospital stay
NIV improves alveolar ventilation - decreases RR, increases tidal volume, increased minute ventilation
Contraindications for NIV (scenarios where invasive ventilation is first-line)
- cardiac or respiratory arrest
- inability to cooperate, protect own airway or clear secretions
- upper airway obstruction
- high aspiration risk
- non-respiratory organ failure that is acutely life-threatening or evidence of multi-organ failure
- pneumothorax
- haemodynamic instability
- reduced GCS or coma - relative C/I, can trial NIV if hypercapnic encephalopathy
- facial trauma, deformity, surgery
- recent oesophageal anastomoses or other upper GI surgery / bleed
What is the stepwise inhaler therapy for COPD?
What is the advantage of using dual long-acting bronchodilators for COPD?
Dual therapy with LAMA & LABA reduces mod-severe exacerbations when compared to LAMA therapy alone
LAMA + LABA vs ICS + LABA leads to similar exacerbations and quality of life
What are the predictors of mortality in asthma?
- history of near fatal asthma / requiring ICU or mechanical ventilation
- history of asthma hospitalisation in last 12 months or repeated ED attendance
- history of brittle asthma (sudden, severe exacerbations)
- poor adherence with treatment
- signficant comorbidities - pneumonia, genitourinary disease, septicaemia, diabetes, arrhythmia
- escalated SABA use (more than 12 cannisters per year OR more than 1 cannister per month)
- requirement of 3 or more classes of asthma maintanence treatment
- poor lung function
- oral corticosteroid use > 75mg during previous admission and dose of oral steroids > 110mg per month
- comorbid food allergy - especially anaphylaxis
- rural or remote location
- psychosocial issues (depression or other psychiatric illness, substance misuse, smoking, social isolation, financial or domestic problems etc.)
**protective factor - ICS > 4 cannisters / year
What factors determine prognosis after discharge from admission with acute exacerbation of COPD?
CODEX - predicts mortality and/or hospital readmission from 3 months to 1 year after discharge
C = comorbidity
O = obstruction
D = dyspnoea
EX = previous severe exacerbations
NIV for specific conditions
What is the mechanism of dupilumab?
Anti IL-4 and IL-13
Targets eosinophilic asthma
Especially in patients with chronic rhinosinusitis and nasal polyposis
Risk factors for fixed airflow obstruction in asthma
- No ICS treatment
- Smoking
- Occupational exposure
- Mucus hypersecretion
- Blood eosinophilia
Who is eligible for home o2 therapy?
PaO2 <55mmHg or SaO2 <88% at rest OR
PaO2 55-59mmHg or SaO2 < 89% WITH polycythaemia (HCT > 0.55), pulm HTN or RV dysfunction / cor pulmonale
No cigarettes for 3 months
What are the features of allergic bronchopulmonary aspergillosis? (ABPA)
Characterised by:
(1) Chronic asthma
(2) Central bronchiectasis with lots of sputum production & mucus plugging
(3) Recurrent pulmonary infiltrates
- Very high total IgE (>1000)
- Evidence of aspergillus sensitivity (IgE or aspergillus precipitins testing)
- Aspergillus in sputum
What is the management of insomnia?
Address contributing factors
1st line therapy is CBT
Pharmacotherapy
-> Sleep initiation
Melatonin receptor agonist (Ramelteon), melatonin, sedating anti-depressants (mirtazepine, amitriptyline)
-> Sleep maintenance
Orexin receptor antagonists ‘orexant’ -> block orexin A and B that promote wakefulness (Suvorexant and Lemborexant), low dose doxepin, sedating antidepressants (amitriptyline, mirtazepine), gabapentin
What is the benefit of home O2 therapy for COPD?
Can improve survival if used > 16 hours per day
Improves dyspnoea, QoL, exercise capacity, cognitive function, depression
Does not reduce hospitalisations, pulmonary dynamics, polycythaemia
What are the causes of metabolic alkalosis?