Respiratory Flashcards
Control of airway smooth muscle?
NA on β2 receptors = bronchodilation
ACh on M3 receptors = bronchoconstriction
Muscles of passive inspiration vs forced inspiration vs expiration?
Passive inspiration = diaphragm, external intercostals
Forced inspiration = SCM, scalenes, pectoralis major
Expiration = internal intercostals, subcostals, transversus thoracis, anterior abdominal wall muscles
Location of central vs peripheral chemoreceptors?
Central = medulla oblongata
Peripheral = carotid and aortic bodies
Brain centres for inspiration, expiration, breath inhibition and prolongation?
Inspiration = dorsal (medullary) group
Expiration = ventral (medullary) group
Inhibition = pneumotaxic (pontine) centre
Prolongation = apneustic (pontine) centre
What does the oxygen dissociation curve demonstrate?
Relationship between pO2 and SpO2%
List causes of left shift on the oxygen dissociation curve (↑ O2 affinity,↓ O2 delivery).
HbF
Low pCO2
Low H
Raised pH
Low 2,3-DPG
Low temperature
List causes of right shift on the oxygen dissociation curve (↓ O2 affinity,↑ O2 delivery).
Raised pCO2
Raised H
Low pH
Raised 2,3-DPG
Raised temperature
List some gram +ve vs gram -ve cocci?
Gram +ve = staphylococcus, streptococcus
Gram -ve = neisseria meningitidis, neisseria gonnorhoeae, moraxella catarrhalis
Classification of streptococci?
α = viridans and pneumoniae
β = pyogenes (group A) and agalactiae (group b)
γ = enterococci
List some gram +ve vs gram -ve bacilli?
Gram +ve = bacillus, clostridium, corynebacterium, listeria, mycobacterium
Gram -ve = shigella, salmonella, legionella, klebsiella, E.coli, campylobacter, pseudomonas, haemophilus
Cause of obstructive vs restrictive lung disease and examples?
Obstructive = reduced airflow
→ asthma, COPD, bronchiectasis
Restrictive = reduced expansion
→ IPF, sarcoidosis, pneumoconiosis
FEV1, FVC and FEV1/FVC in obstructive lung disease?
FEV1 = significantly reduced
FVC = reduced or normal
FEV1/FVC = reduced (< 0.7)
FEV1, FVC and FEV1/FVC in restrictive lung disease?
FEV1 = reduced
FVC = significantly reduced
FEV1/FVC = normal or increased (> 0.7)
What is TV, IRV, ERV and RV?
TV = air breathed in/out during normal respiration
IRV/ERV = extra air breathed in/out after TV
RV = air left in lungs after maximum expiration
IC, VC, FRC and TLC calculations?
IC = TV + IRV
VC = IC + ERV
FRC = ERV + RV
TLC = VC + RV
ABG interpretation steps?
1st = PaO2 (hypoxic or not)
2nd = pH (acidosis, alkalosis)
3rd = PaCO2 (check if respiratory system causing acidosis/alkalosis or compensating)
4th = HCO3 (check if metabolic system causing acidosis/alkalosis or compensating)
5th = BE (> +2 = excess HCO3, < -2 = lack of HCO3)
Examples of added breath sounds and associated conditions?
Wheeze (e.g. asthma)
Stridor (e.g. epiglottitis)
Coarse crepitations (e.g. bronchiectasis)
Fine end-inspiratory crackles (e.g. pulmonary fibrosis)
Atopic triad and Ig mediator?
Asthma, allergic rhinitis, atopic eczema
→ IgE (type I hypersensitivity)
Features of asthma?
Wheeze
Breathlessness
Chest tightness
Cough (often worse at night)
Diurnal variation of symptoms
PMH or FH of atopy e.g. eczema
Investigations for asthma?
Peak expiratory flow rate (PEFR)
Spirometry (FEV1/FVC)
Bronchodilator reversibility test (BDR)
Fraction of expired nitric oxide (FeNO)
BDR, PEFR and FeNO results indicative of asthma?
BDR = ≥12% FEV1 improvement
PEFR = ≥20% variability
FeNO = > 40 ppb (adults) or > 35 ppb (kids)
Investigation if asthma diagnosis unclear?
Fraction of expired nitric oxide (FeNO)
Drugs which can worsen asthma?
Aspirin
Other NSAIDs (e.g. ibuprofen)
Beta blockers (e.g. bisoprolol)
Drug options for asthma (adult)?
1st line = SABA + ICS
2nd line = SABA + ICS + LABA
3rd line = ↑ ICS or SABA + ICS + LTRA
Drug options for asthma (kids)?
1st line = SABA
2nd line = SABA + very low dose ICS (≥ 5) or SABA + LTRA (< 5)
3rd line = SABA + very low dose ICS + LABA/LTRA (≥ 5) or SABA + very low dose ICS + LTRA (< 5)
4th line = ↑ ICS or specialist referral
Outline good inhaler technique?
- Remove cap and shake well
- Sit/stand straight with chin tilted up
- Exhale slowly until lungs empty
- Make a tight seal around mouthpiece
- Press inhaler whilst inhaling slowly until lungs full
- Remove inhaler and hold breath for 10 seconds
- Exhale and wait 30 seconds if 2nd dose needed
- Wash mouth out if inhaler contains steroid
Indication for step-up asthma treatment?
SABA used 3 or more times a week
ICS dosage in step-down asthma treatment?
Reduce by 25-50%
Key signs of a severe vs life-threatening asthma attack?
Severe = PEFR 33-50%, SaO2 < 92%, can’t talk
Life-threatening = PEFR < 33%, SaO2 < 92%, pCO2 normal, silent chest, confusion, poor resp effort
Hospital management of asthma attack?
15L/min O2 via non-rebreather then:
1st line = nebulised salbutamol/ipratropium
2nd line = oral prednisolone or IV hydrocortisone
3rd line = IV magnesium sulphate
4th line = IV aminophylline
N.B. give antibiotics if infective exacerbation
Main cells involved in asthma vs COPD?
Asthma = mast cells, eosinophils, T helper cells (CD4+)
COPD = neutrophils, cytotoxic T cells (CD8+)
Example of a SABA, LABA, SAMA, LAMA, ICS and LTRA.
SABA = salbutamol
LABA = salmeterol
SAMA = ipratropium
LAMA = tiotropium
ICS = beclamethasone
LTRA = montelukast
Pathology of chronic bronchitis and emphysema?
Chronic bronchitis = goblet cell proliferation and mucus hypersecretion
Emphysema = permanent alveoli hyperinflation and membrane loss
Types of emphysema, location and their associated cause?
Centriacinar (upper lobes) = tobacco smoking
Panacinar (lower lobes) = A1AT deficiency
Features of COPD?
Cough (often productive)
Breathlessness
Chest hyperinflation
Accessory muscle use
Smoking history
Complications of COPD?
Pneumothorax (ruptured bulla)
Cor pulmonale (PHTN)
Polycythaemia (chronic hypoxia)
Infection (reduced ciliary clearance)
CXR features of COPD?
Hyperinflation (> 6 ribs visible)
Pulmonary bullae
Loss of lung markings
Flattened hemidiaphragms
Type 1 vs type 2 respiratory failure and cause?
Type 1 = hypoxia without hypercapnia
→ V/Q mismatch (low oxygen but well perfused)
Type 2 = hypoxia with hypercapnia
→ alveolar hypoventilation
Pathogenesis of CO2 retention?
- Loss of elastic recoil means lungs can’t fully empty CO2
- Chronic hypercapnia makes respiratory centre less sensitive to PaCO2 so relies on PaO2
- Giving O2 will ↓ respiratory drive and ↑ PaCO2
Drug options for COPD?
1st line = SABA or SAMA
2nd line = SABA + LABA + LAMA (no asthmatic features) or SABA/SAMA + LABA + ICS (asthmatic features)
3rd line = SABA + LABA + LAMA + ICS
Most important management for survival in COPD?
Smoking cessation
Smoking cessation management options?
Normal = NRT or bupropion or varenicline
Pregnant = NRT
When to commence NRT, bupropion and varenicline?
NRT = on quit day
Bupropion/varenicline = 7-14 days before quit day
Indications for LTOT in COPD?
2 readings of PaO2 < 7.3 or PaO2 7.3-8 with COPD complications e.g. PHTN
Indication for NIV (BiPAP) in COPD?
Respiratory acidosis pH 7.25-7.35
COPD severity categories and associated FEV1?
Mild (FEV1≥ 80%)
Moderate (FEV1 50-79%)
Severe (FEV1 30-49%)
Very severe (FEV1 < 30%)
Management of a COPD exacerbation?
4L/min O2 via Venturi 24-28% then:
1st line = nebulised salbutamol/ipratropium
2nd line = oral prednisolone or IV hydrocortisone
3rd line = IV theophylline
N.B. give antibiotics if infective exacerbation
Target SpO2 for COPD exacerbation before vs after ABG results?
Before = 88-92%
After = 94-98% (if pCO2 normal)
N.B. if very hypoxic high-flow O2 given regardless
Vaccination advice for COPD patients?
One-off pneumococcal + annual influenza
Most common bacterial cause of COPD and bronchiectasis exacerbations and antibiotic options?
Haemophilus influenzae
1st line = amoxicillin
2nd line = doxycycline
Antibiotic prophylaxis for recurrent COPD and bronchiectasis exacerbations and screening test?
Azithromycin
ECG (can cause QT prolongation)
Features of bronchiectasis?
Productive cough (LOTS of sputum)
Recurrent infections
Breathlessness
Finger clubbing
Investigation for bronchiectasis and key feature?
High-resolution CT (HRCT)
Signet ring appearance
Outline α1-antitrypsin (A1AT) deficiency effect on the lungs?
- A1AT is an antiprotease which inhibits neutrophil elastase
- Deficiency allows neutrophil elastase to destroy alveolar walls (emphysema)
Malignancy associated with α1-antitrypsin deficiency?
Hepatocellular carcinoma
Features of PHTN?
Breathlessness
Tachycardia
Raised JVP
Peripheral oedema
Hepatomegaly