Wk8 - Respiratory Flashcards
How can we measure lung function?
At home- Peak flow, (oximetry)
At the GP surgery- Spirometry, oximetry
In a specialist lab- Spirometry, transfer factor, lung volumes, blood gases, bronchial provocation testing, respiratory muscle function, exercise testing etc.
Spirometry
- Definition
Definition: Forced expiratory manoeuvre from total lung capacity followed by a full inspiration
“take a big breath in as far as you can and blow out as hard as you can for as long as possible- then take a big breath all the way in”
Best of 3 acceptable attempts (within 5%) - best effort is taken as their spirometry
Spirometry pitfalls
Appropriately trained technician
Effort and technuque dependent
What is the normal FEV1/FVC ratio?
> 70% = N
If <70% = airflow obstruction
Reference ranges for lung function
FEV1 of 85% predicted may be considered “normal”
FEV1 of 100% percent predicted may represent significant decline if values supra-normal at the start
Corrected for age, gender, race, height and atmospheric values
Obstructive lung disease
Generally asthma or COPD
FEV1/ FVC ratio <70% (0.7 ratio).
Severity of COPD stratified by %predicted FEV1 mild >80% mod 50-80%, severe 30-50%, very severe <30%
Reversibility testing
Nebulised or inhaled salbutamol given
Spirometry before and 15 min after salbutamol
15% AND 400ml reversibility in FEV1 suggestive of asthma
Other investigations ofr asthma
PEFR testing
Look for diurnal variation and variation over time
Response to inhaled corticosteroid
Occupational asthma
Bronchial provocation
Spirometry before and after trial of inhaled/ oral corticosteroid
Restrictive lung disease
FEV1 AND FVC reduced
FEV1/ FVC ratio >70%
Causes of restrictive spirometry
Interstitial lung disease (stiff lungs) Kyphoscoliosis/ chest wall abnormality Previous pneumonectomy Neuromuscular disease Obesity Poor effort/ technique
Interpreting spirometry
First look at FEV1/ FVC ratio
If <70%, obstruction
If obstructed, look at % predicted FEV1 (severity) and any reversibility (COPD vs asthma)
If FEV1/ FEV ratio normal, look at % predicted FVC (if low, suggests restrictive abnormality)
Can also get mixed picture, eg obesity and COPD
Transfer factor
Is a measure of gas exchange
Single breath of a very small concentration of carbon monoxide
CO has very high affinity to Hb
Measure concentration in expired gas to derive uptake in the lungs
Affected by: Alveolar surface area Pulmonary capillary blood volume Haemoglobin concentration Ventilation perfusion mismatch
Reduced in: Emphysema Interstitial lung disease Pulmonary vascular disease Anaemia (increased in polychthaemia)
2 methods of measuring lung volume
(unable to measure residual volume by spirometry) Helium dilution (inspire known quantity of inert gas) Body plethysmography (respiratory manoevures in a sealed box lead to changes in air pressure- can derive lung volumes. Archimedes principle!)
Lung volumes reduced in
restrictive lung disease
Increased RV and RV/TLC in
obstructive lung disease
Oximetry
Non-invasive measurement of saturation of haemoglobin by oxygen
Depends on oxyhaemoglobin and deoxyhaemoglobin absorbing infrared light differently
Depends on adequate perfusion (shock, cardiac failure)
Does NOT measure carbon dioxide, so no measurement of ventilation
False reassurance in a patient on oxygen with normal saturations (acute asthma, COPD, hypoventilation)
Causes of hypoxaemia
Hypoventilation (eg drugs, neuromuscular disease)
Ventilation/ perfusion mismatch (eg COPD, pneumonia)
Shunt (eg congenital heart disease)
Low inspired oxygen (altitude, flight)
Ventilation perfusion mismatch
Happens to a degree in normal lungs
Main cause of hypoxaemia in medical patients (e.e.g pneumonia)
Areas of lung that are perfused but not well ventilated (eg pneumonic consolidation)
Mixing of blood from poorly ventilated and well ventilated parts of the lung causes hypoxaemia
Does not fully correct with oxygen administration
Shunt an “extreme” form of V/Q mismatch where blood bypasses the lungs entirely. Does not correct with oxygen administration
Blood gas analysis - what you are looking at
Always look at the pO2 first
Is the patient in respiratory failure requiring additional oxygen?
Then look at the PCO2 (type 1 vs type 2 respiratory failure)
Then consider acid base balance
Acute respiratory acidosis- elevated pCO2, normal bicarbonate, acidosis
Compensated respiratory acidosis- elevated pCO2, elevated bicarbonate (renal compensation), not acidotic
Acute on chronic respiratory acidosis- elevated pCO2, elevated bicarbonate, acidotic
COPD definition
COPD is characterised by airflow obstruction.
The airflow obstruction is usually progressive, not fully reversible and does not change markedly over several months.
The disease is commonly caused by smoking.
Effects of cigarette smoking on the lungs
Cilial motility is reduced (cilia are damaged/destroyed by smoking) - (so sputum is not cleared - increased infections)
Airway inflammation (neutrophilic inflammation)
Mucus hypertrophy and hypertrophy of Goblet cells
Increased protease activity, anti-proteases inhibited
Oxidative stress (increased free radicals e.g. hydrogen peroxide)
Squamous metaplasia → higher risk of lung cancer
Genetics for COPD
Alpha 1 antitrypsin deficiency: genetic present in 1 – 3 % of COPD patients serine proteinase inhibitor M alleles normal variant SS and ZZ homozygotes have clinical disease Unable to “counterbalance” destructive enzymes in lung Non-smokers get emphysema in 30s – 40s Smokers get emphysema much earlier
Smokers have increased risk of COPD if it is in the family
Clinical syndrome of COPD
Chronic Bronchitis:
the production of sputum on most days for at least 3 months in at least 2 years
Emphysema:
abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles
Features seen in airways in patient with cOPD
Infiltration with neutrophils and CD8+ lymphocytes Loss of interstitial support Increased epithelial mucous cells Mucus gland hyperplasia Squamous metaplasia
Features of chronic bronchitis
Chronic Bronchitis:
larger airways > 4mm in diameter
Inflammation leads to scarring and thickening of airways
Small airways disease:
“Bronchiolitis” in airways of 2 -3 mm
May be an early feature of COPD
narrowing of the bronchioles due to mucus plugging, inflammation and fibrosis
Cell type involvement in COPD inflammation
Cell types
Macrophages, CD8 and CD4 T lymphocytes, neutrophils
Inflammatory Mediators
TNF, IL-8 and other chemokines
Neutrophil elastase, proteinase 3, cathepsin G
(from activated neutrophils)
Elastase and MMPs (from macrophages)
Reactive oxygen species
Airway inflammation persists after smoking ceased
What are 2 most clinically signifiacnt types of emphysema
Types causing airflow obstruction:
Centri-acinar –
damage around respiratory bronchioles
more in upper lobes
Pan-acinar –
uniformly enlarged from the level of terminal bronchiole distally
can get large bullae
associated with α1 anti-trypsin deficiency
Consequent loss of surface area for gas exchange
Name the 3 types of emphysema
Centriacinar
Panacinar
Paraseptal
Mechanisms of airflow obstruction in COPD
Loss of elasticity and alveolar attachments due to emphysema - airways collapse on expiration
causes airtrapping and hyperinflaltion →increased work of breathing→breathlessness
Goblet cell metaplasia with mucus plugging of lumen
Inflammation of the airway wall
Thickening (and scarring) of the bronchiolar wall
- smooth muscle hypertrophy and peribronchial fibrosis
Clinical COPD on CxR
Hyperinflation with emphysema - also blacker as lost lung tissue and blood vessels
6 anterior ribs seen (?)
Diagnosing COPD
Consider the diagnosis of COPD for people who are over 35, and smokers or ex-smokers, with any of: exertional breathlessness chronic cough regular sputum production frequent winter ‘bronchitis’ wheeze
Spirometry - FEV1/FVC ratio <70%
Stage 1 (mild) - FEV1 % predicted - 80%
2 (moderate) - 50-79%
3 (severe) - 30-49%
4 (very severe) - <30%
Or FEV1 <50% with respiratory failure = very severe
Treatment of COPD
Inhaled bronchodilators
Short-acting beta-agonists: salbutamol
Long acting: salmeterol, tiotropium
Inhaled corticosteroids
Budesonide and fluticasone – combination inhalers
Oxygen therapy
Oral theophyllines
Mucolytics - carbocysteine
Nebulised therapy
The 2 phenotypes in respiratory failure with COPD
Blue bloater: Hypocapnic low respiratory drive Type 2 respiratory failure ↓PaO2, ↑PaCO2, cyanosis warm peripheries bounding pulse flapping tremor confusion, drowsiness, right heart failure Oedema, raised JVP
Pink puffer: Emphysemitis high respiratory drive Type 1 respiratory failure ↓PaO2, ↓PaCO2
desaturates on exercise pursed lip breathing use accessory muscles wheeze indrawing of intercostals tachypnoea
Recognition of different inflammatory processes in COPD and asthma
Asthmatic airway inflammation: CD4+ T lymphocytes Eosinophils - completely reversible
COPD airway inflammation: CD8+ T lymphocytes Macrophages Neutrophils - Irreversible
COPD vs asthma features
-
Causes of raised acnion gap (in metabolic acidosis)
renal failure Diabetic or other ketoacidosis lactic acidosis toxins e.g. salicylate, some IEM (Excess production of H+ or inability to excrete it
Causes of N anion gap in metabolic acidosis
renal tubular acidosis Diarrhoea carbonic anhydrase inhibitors ureteric diversion (Excess HCO3- loss)
What can be used to measure DKA
Serum Osmolal Gap
OG = measured osmolality - calculated osmolality
Normal OG <10mOsm/kg
N serum osmolality = 275-295mOsm/kg
Non-invasive ventilation in COPD
Provides positive pressure to the airways to support breathing
Recommended as the first line intervention in addition to usual medical care in COPD exacerbations with persistent hypercapniac respiratory failure
Considered if there is a respiratory acidosis (pH < 7.35, H+ > 45) present or if acidosis persists despite maximal medical therapy
Reduces respiratory rate
Improves dyspnoea and gas exchange
Lowers mortality
Reduces need for ventilation in ITU
Reduces length of hospital stay
Cor pulmonale is a syndrome of…
Right heart failure secondary to lung disease
Salt and water retention leading to peripheral oedema
Signs of cor pulmonale
Peripheral oedema
Raised jugular venous pressure
A systolic parasternal heave
Loud pulmonary second heart sound
Pulmonary hypertension and right ventricular hypertrophy may develop
Treatment - diuretics to control peripheral oedema
What is allergy?
Allergy is an immune system mediated intolerance
Clinical reaction
Acute - sudden or slow - progressive
Based on immune system intolerance
Requires exposure to a trigger
Memory,
characteristic clinical features
Dependent on which arm of the immune system
Chronic allergy leads to tissue remodelling
Acute inflammation - repair
Allergy in the airways
Affects airflow
Increases resistance
Causes wheeze/stridor - turbulence
Measured by spirometry
Imaging (CXR) not helpful
Gas transfer not helpful
Extra-thoracic disease
not susceptible to intra-thoracic pressure For example Laryngeal oedema (thyroid, scarring, epiglotitis) Stridor Flow-volume loops CXR not helpful Aspiration to Right middle/lower lobe
Bronchial disease - clinical consequences
Susceptible to intra-thoracic pressure
Clinical consequences: Medium - Small airways flaccid walls Not supported by cartilage Expiratory phase narrowing - wheeze Muco-ciliary clearance impairment – sputum Characteristic flow-volume loops CXR – unhelpful (hyperinflation)
Pathological, Physiological and clinical aspects of asthma
Pathological: Inflammation Scabby epithelium Thickened BM Thickened smooth muscle Mast cells in smooth muscle
Physiological: Yellow mucous Repair pathways Non elastic airways Increased responsiveness Increased sensitivity
Clinical: Cough Cough/wheeze Wheeze Hyper-reactivity
Hyper-sensitivity
Definition of asthma
Appropriate symptoms with signs:
- Wheeze, cough, yellow/clear sputum
- Breathlessness, exercise intolerance
Episodic, triggered, variable – paroxysmal
- Exercise,
- cats - Allergy
- Chemical/physical (salicylate/aspirin) - - Hyper-reactivity
- Diurnal – nocturnal awakening
Respond to asthma therapies
Asthmatic airways
Airway smooth muscle hypertrophy is seen (smooth muscle is is infiltrated by mast cells (contain histamine - whos main target is mooth muscle)
Diagnosis of asthma
Appropriate clinical story
Supportive physiological tests:
1. Patient is given a diary and a peak flow meter
2. Pharmacological hypersensitivity (more sensitive to histamine) - not done now (not diagnostic, is a supportive test)
What cytokines are increased in asthmatic ariways?
IL-5
TSLP
IL-13
TNFalpha
TGFbeta
VEGF
These drive inflammation as recruit –> mast cells, lymphocytes, macrophages, epithelial cells
Family of drugs used against asthms
Anti-IgE biological therapy
Corticosteroids
Anti-leukotriene receptor drugs
Bronchodilators
Triggers EAA
Bird dander – Pigeon fancier’s lung, budgie lung Mushroom worker’s lung Farmer’s lung (fungal spores) Aspergillus lung Cheese workers Wheat weevil Mollusc shell workers Malt worker’s lung Humidifier lung
Pneumothorax definition
‘Air within the pleural cavity’
Negative intrapleural pressure
Opposing forces of chest wall (outwards) and lung (inwards)
Any breach of the pleural space leads to collapse of the elastic lung
Can be traumatic, iatrogenic or spontaneous
Traumatic - stabbing, fractured rib
Iatrogenic - CT guided lung biopsy, TBLB, pleural aspiration
Spontaneous:
Primary - young patient, no underlying lung disease (often tall, thin young men)
Secondary - underlying lung disease (COPD (bullae rupturing), cystic fibrosis)
Pathophysiology of primary pneumothorax
Development of subpleural blebs/ bullae at lung apex
Possible additional diffuse, microscopic emphysema below the surface of the visceral pleura
Spontaneous rupture leads to tear in visceral pleura
Air flows from airways to pleural
space (pressure gradient)
Elastic lung then collapses
Pathophysiology of secondary pneumothorax
Inherent weakness in lung tissue (eg emphysema)
Increased airway pressure (eg asthma, ventilated patient)
Increased lung elasticity (eg pulmonary fibrosis)
Patient is generally much more symptomatic
(poor underlying lung function)
Management more complex, prognosis less good
More likely to require intervention
Symptoms and signs of pneumothorax
Pleuritic chest pain
Breathlessness (can be minimal if primary)
Respiratory distress (especially if secondary)
Reduced air entry on affected side
Hyper-resonance to percussion (?)
Reduced vocal resonance
Tracheal deviation if tension (+/- circulatory collapse)
Differential diagnosis: PTE, musculoskeletal pain, pleurisy/ pneumonia
Management of pneumothorax
Size less important than symptoms
Small pneumothorax very symptomatic if bad COPD
Can tolerate complete lung collapse very well if healthy
2cm rim of air at the axilla equates to 50% volume
<2cm defined as small, >2cm large
Options for management:
Observation (serial CXR) if small or not very symptomatic- can be as outpatient
Aspiration (small bore catheter 2nd intercostal space midclavicular line- aspirate air with syringe/ 3 way tap)
Intercostal drain with underwater seal
Good guideline developed by British Thoracic Society
What if a drain fails to work? (for Tx of pneumothorax)
VATS (Video Assisted Thoracic Surgery)
Considered if not resolved in 5 days
Can staple blebs
Talc pleurodesis (causes inflammatory reaction and pleural adhesion, highly effective)
Pleural abrasion/ stripping
Surgical pleurodesis considered if 2nd pneumothorax on same side, first contralateral event Professional considerations (eg airline pilots, scuba divers)
After a spontaneous pneumothorax has resolved on CXR, how long should the patient wait before flying
> = 7 days
After a spontenous pneumothorax has resolved on CXT, how long should they wait before diving?
Should not dive again
(as have at least 30% of having another pneumothorax) - the pressures on diving are far greater - can develop a tension pneumothorax)
Features of tension pneumothorax
A medical emergency
‘One way valve’ leads to increased intrapleural pressure
Venous return impaired, cardiac output and blood pressure fall
PEA arrest without intervention
Immediate management: insert venflon 2nd intercostal space midclavicular line to relieve pressure
Risk factors for spontanoeus pneumothorax
Smoking, male gender and height are risk factors
Underlying lung disease (secondary)
Recurrence rate 40-50% after first episode
Definitions of obstructive sleep apnoea and obstructive sleep apnoea syndrome
Obstructive Sleep Apnoea
Recurrent episodes of partial or complete upper (pharyngeal) airway obstruction during sleep, intermittent hypoxia and sleep fragmentation
Obstructive Sleep Apnoea Syndrome
Manifests as excessive daytime sleepiness
Mechanism of OSAS
Pharyngeal narrowing –>
Symptoms of OSAS
Snorer
Witnessed apnoeas (relative or partner has noticed)
Disruptive sleep – nocturia/choking/dry mouth/ sweating
Unrefreshed sleep
Daytime somnolence
Fatigue/ Low mood/ Poor concentration
Assessment of OSAS
History- history from partner is very important Clinical examination: Weight BMI BP - often hypertensive Neck circumference (>40cm) Craniofacial appearance (Retrognathia, Micrognathia - ENT issues) Tonsils Nasal patency
Questionairres:
The Epworth Sleepiness Score
The STOP-BANG Questionnaire
The Berlin Questionnaire
Investigations: Limited Polysomnography (Limited Sleep Study) 5 channel home study Oxygen Saturations Heart Rate Flow Thoracic and Abdominal effort Position
Investigation for more complex case:
Full polysomnography
ECG - sleep staging, position, flow, oxygen saturation, videoed, audio, limb leads, snore, eye movements (to tell what stage of sleep their at)
Transcutaenous Oxygen Saturations and Carbon Dioxide Assessment (TOSCA) - home or inpatient (looks at heart rate, saturations and CO2) - probe on your ear (gets to a high temperature)
Advantages of full polysomnography
Correct patient
Accurate assessment of sleep efficiency
Sleep staging via EEG
Parasomnic activity- acting out dreams, sleep talking
Sleep studies - looking at: Apnoea hypoapnoea Respiratory effort related arousals Apnoea - Hypopnoea Index (AHI) Oxygen desaturation index (ODI)
These are all looked at for diagnosis
Apnoea
the cessation, or near cessation, of airflow
4% oxygen desaturation, lasting ≥ 10 secs
Hypopnoea
Hypopnoea is a reduction of airflow to a degree insufficient to meet the criteria for an apnoea
Respiratory effort related arousals
arousals associated with a change in airflow that does not meet the criteria for apnoea or hypopnoea
Apnoea-Hypopnoea Index (AHI)
The apnoea-hypopnoea index (AHI) is calculated by adding the number of apnoeas and hypopnoeas and dividing by the total sleep time (in hours)
Oxygen desaturation index (ODI)
the number of times per hour of sleep that the SpO2 falls ≥ 4% from baseline
Diagnosis of OSA
AHI ≥15 is diagnostic of OSA
AHI 5-15 with compatible symptoms
AHI < 5 Normal
AHI 5-15 Mild
AHI 16-30 Moderate
AHI >30 Severe
Treatment of OSAS
Treat the symptomatic- OSAS (daytime sleepiness)
AIM: Improve daytime somnolence and QOL
Explain OSAS
Weight loss
Avoid triggering factors- alcohol
Treat underlying conditions- tonsils, hypothyroidism, nasal obstruction
Continuous Positive Airways Pressure (CPAP) - Splints airway open, stops snoring, stops sleep fragmentation, Improves daytime sleepiness + QOL
Compliance - >4 hours for >70% daysFixed vs Autoset CPAP
Nasal vs Full Face Mask (if breathe through mouth with need a full face mask)
For those who have mild-moderate OSAS and unable to tolerate CPAP –> Mandibular Advancement DEvicce –> pulls jaw forward to open airway
Sleep position trainers: Supine OSA Vibration when on back (wakes you up) Weeks to change sleeping position Appropriate in few patients with Supine OSA
