Respiratory Flashcards
Obstructive Spirometry
FEV1:FVC <70% indicates and obstructive airway defect. Reduced FEV1 vital capacity is preserved to an extent. Often pt have prolonged expiration
Causes of obstructive spirometry
COPD, Asthma (reversible), Bronchiestasis
Severity of Obstructive lung disease
Assessed by FEv1 usually applies to COPD Mild >80% Moderate 50-79% Severe 30-49% Very Severe <30%
Bronchodilator challenge
Reversibility >15% or increase in peak flow 200ml = asthma. Alternative = diurnal variation in serial peak flows
Restrictive Spirometry
FEV1:FVC maintained. FVC approx 50%, FEV1 usually maintained
Causes of restrictive spirometry
Obesity, neuromuscular, thoracic cage abnormality, pul fibrosis
Flow volume loops
Airflow (L/s) against volume (L) in contrast to spirometry which is airflow over time. Appropriate to lung volume. i.e. slower airflow due to reduced elastic recoil
Diffuse small airway disease
Highest flow rate achieved via forced expiration, due to loos of elastic recoil air fails to be expelled. Leading to ski slope shaped curve. Inspiratory curve normal/increases
FEV1:FIV1 is always <1 unless
Extra thoracic obstruction increasing tracheal resistance which makes inspiration harder than inspiration. At inspiration the trachea is compressed leading to proportionally greater reduction
Large airway obstruction
Leads to squashing of the flow volume loop
Lung volumes
Measured in an oxygen tank.
i) Obstructive = Increased RV and TVC
ii) Restrictive = reduced TVC due to restriction of lung expansion
V/Q
Better perfusion @ bases better ventilation @ apices
V/Q < 1 normal perfusion with reduced ventilation due to COPD, fibrosis, emphysema, consolidation = shunt
V/Q > 1 normal ventilation poor perfusion due to PE, pulmonary arteritis = physiological dead space leads to increased work of breathing
Transfer factor
Functionality of the alveolar capillary membrane. Breathe in fixed vol carbon monoxide and calculating how much diffuses into the blood
KCO
Assess functionality per unit volume of lung
COPD transfer factor
Reduced TCLO and KCO widespread destruction
Factors affecting TCLO
V/Q mismatch, pulmonary HTN, haemoglobin conc, increased alveolar membrane thickness, reduced alveolar area
Extrapulmoary restrictive defect
reduced TLCO, increased KCO - compensation of healthy tissue
Spiral CT
Done in continuum won’t miss any lesions good if suscpet cancer but unable to find source
HRCT
High resolution used for diffuse conditions such as IPF, EAA, bronchiestasis
CXR
minimal radiation, 1st line, can pick up large abnormalities
Pneumoconiosis
Restrictive lung disease caused by inhalation of fine particles of mineral dust
Caplans
Pneumoconiosis + RA nodules
Silicosis PC
slowly progressive from exposure usually 10-30 yrs ago
exposure - sand blasting, mining, stone mason
SOB, exertional cough
fatigue, wt loss can progress to cor pulmonate
Diagnosis of silicosis
Biopsy = gold standard onion skinned arrangement of collagen fibres, central hyalinisation, birefringent particles under polarised light
Pathogenesis pneumoconiosis
1-5 micrometre particles - silica and asbestos very reactive. Some impact @ alveolar bifurcations where they are engulfed by macrophages. IL-1 induces and inflammatory response, fibroblast proliferation and collagen deposition
Invx and Mx Silicos
CXR - small nodules in upper lobes, increased hilar size. can lead to progressive egg shell calcification and large patches @ apices
Mx - prevention at workplace -water spray, breathing masks, chest physic, O2 if needed. Transplant - cure
Coal workers
Long term exposure due to coal dust incidence falling due to closure of the mines.
Simple - 1-2mm nodular upper zone shadowing
Massive - large conglomerate masses of dense fibrosis . Lung grossly blackened on inspection post mortem, black sputum mixed obstructive and restrictive lung defect
Light asbestos exposure
pleural plaques, mesothelioma, pleural fibrosis
Heavy asbestos exposure
lung cancer, asbestosis
Asbestos
Used in insulation, roofing sheet and shipbuilding commonly. Increased risk of adenocarcinoma
Clubbing in resp disease
Lung cancer - squamous, bronchiectasis, CF, IPF, mesothelioma
Haemoptysis differntials
Infection, lung cancer, Vasculitis, COPD, TB
Fibrosis O/E and CXR
Increased vocal resonance, fine late inspiratory crackles, streaky shadowing, honeycomb appearance
Pleural effusion O/E and CXR
Dull to percussion, reduced vocal resonance, absent breathe sounds, blunting of costophrenic angle (500ml)
Spirometry needs
Height, age, sex
Risks of smoking
COPD, lung cancer, bladder cancer, HTN, IHD, infertility in males, increased neonatal mortality and IUGR
Pleural plaques
Seen in 58% of people with asbestos exposure. They are discrete areas of hyaline fibrosis in the parietal pleura often at the diaphragm. Usually asymptomatic.
CXR - holly leaf
Bilateral diffuse pleural thickening
Fibrous thickening of the visceral pleura with adherence to parietal and obliteration of the pleural space. Extends over 25% of chest wall. Restrictive lung defect and recurrent pleural effusions
CXR - continuous irregular pleural shadowing, loss of costophrenic angle
Asbestosis
Heavy exposure often 5-10 yrs after. Progressive SOB, diffuse basal interstitial fibrosis , severe restrictive defect
CXR - basal honeycomb lung/reticular shadowing
Smoking and asbestosis
Synergistic 5x
Mesothelioma
Cancer derived from the mesothelium. light asbestos exposure
PC long latency, SOB, pleural effusions, bloody sputum and chest pain. wt loss and night sweats. Mets to liver, adrenals and kidney
Imvx - pleural thickening on CT, calrectin stain on biopsy
Mx - 2yrs then death
Asthma
Reversible airway limitation, airway hyper responsiveness to many stimuli and bronchial inflammation - T lymphocytes, mast cells, oedema, SM hypertrophy, mucus plugging
PC Asthma
PC - diurnal variation in symptoms worse @ night and morning, triggers by cold weather, emotion and exercise. Wheeze cough and shortness of breathe
Occupational asthma vs work aggravated
Occupational - caused by an agent at work either new or substantial deterioration
Aggravated - increased symptoms but can be managed
Hallmarks of Occupational asthma
Better after holidays / 3 days off, onset within 1 year at work, associated with nasal and eye symptoms preceding the asthma.
Investigating work place asthma
Peak flow diary or OASYS. Plots and interprets serial peak flow readings
Allergen provocation testing - direct inhalation or work place challenge
Skin prick testing and serum IgE levels
Sputum eosinophils are collected using hypertonic saline with a deep cough often linked to HMW allrgens
Methacholine challenge
Pt inhales a bronchoconstrictor acts via M3 receptor to narrow the airways, those with pre-existing hyperresponsiveness will react to extremely low doses
High weight allergens
Proteins with specific IgE i.e. detergents, animals and pollen, antibiotic and latex, flour and organic dusts
Low weight allergens
Reactive chemicals isocyanates, wood dust, complex metal salts, dyes and metal salts
Fractional NO
Diagnostic test. NO produced by inflamed bronchial epithelial cells. Often done before and after treatment to assess response. Useful to assess who will be responsive for steroid treatment
Risk factors for occupational asthma
atopy - esp for MHW ie flour, fish extract - animal allergens
smoking - increased risk for flour, coffee
Mx occupational asthma
reduced exposure, protective equipement
health surveillance - IgE/skin prick monitoring
BTS guidlines
anti IgE specialist use for severe asthma - omalizumab
Pulmonary function test values
FEV1 = forced expiatory volume over 1 second FVC = volume of air that can be forcibly exhaled RV = residual volume of air left in lungs after expiration (increased with age and COPD due to gas trapping) VC = vital capacity is volume of air breathed out after deepest inhalation TLC = VC + RV TV = tidal volume is the volume of air moving in and out of the lung during quiet breathing
Mosaic CT pattern
Patches of radio dense lung parenchyma show areas of alveolar inflammation. Areas of radiolucent lung tissue (darker) show small airway narrowing bronchiolitis
Inflammatory reaction aims to prevent allergen reaching the alveolus causing gas trapping
EAA and health protection
Employee has no duty to inform anyone
Dr cant inform employer without employees permission
Employer has a duty to inform health protection england if they know about the problem
Pt needs to be disabled to receive compensation
Lung biopsy
SE = haemorrhage, infections pneumothorax, seeding of cancer through tumor wall
Crucially allows a histological diagnosis
Causes of tracheal deviation
Mediastinal lymphadenopathy, goitre, malignancy
lobe collapse - pull towards
tension pneumothorax, large pleural effusion - push away
Pleural effusion
Collection of fluid within the pleural space. Limits lung expansion and may become infected
Exudative causes
Infection - pneumonia, TB Malignancy - lung cancer, mesothelioma Asbestosis Inflammation - SLE, RA, PE
Protein >30g/l,
Transudative causes
Liver failure or nephrotic syndrome (low albumin), Heart failure or renal failure (increased hydrostatic pressure)
Meigs and hypothyroidism
Protein <30g/l, LDH<200 and fluid:serum LDH <0.6
Lights criteria
pleural fluid protein: serum protein > 0.5
pleural fluid LDH: serum LDH > 0.6
cloudy, protein > 2.9g/l
Interstitial Lung disease
Range of diseases which affect the lung parenchyma with cellular infiltrate of the alveoli, interstitium and distal airways
Function of interstitium
Provides structure between collagen and elastin. In disease it is thickened increasing diffusion distance and reducing efficacy
Causes of ILD
IPF, sarcoidosis,
drug induced - bleomycin, methotrexate,nitrofurantoin, amiodarone
Hypersensitivity pneumonitis, pneumoconiosis, TB, vasculitis
AI - SLE, RA, systemic sclerosis
CXR ILD
bilateral interstilial shadowing, reticular nodular pattern, shrunken lungs
Idiopathic pulmonary fibrosis PC
Chronic progressive and ultimately fatal ILD
Present in 50-60 2x more common in males
dry cough and progressive SOB
O/E pulmonary fibrosis
clubbing, central cyanosis, reduced chest expansion
fine late-end bibasal inspiratory crackles
Drug induced ILD
bleomycin, nitrofurantonin, amiodarone, methotrexate, sulfasalazine
Mx IPF
Prognosis approx 3 years from diagnosis. Supportive care 02 to prevent pulmonary HTN. Transplant = cure
Inv IPF
Crucial to exclude potentially reversible causes!!
Restrictive pattern of spirometry FEv1:FVC >70%, reduced TLCO and KCO
CXR - small lung volume, reticular shadowing at bases
HRCT = basal distribution, reticulation @ peripherys, honeycombing, bronchiestasis
Sarcoidosis
Multisystem granulomatous disease characterised by formation of multiple non caesating granulomas. Granuloma = mass/nodule of chronically inflamed tissue formed by response of macrophages to confine a pathogen and prevent surrounding tissue inflammation and destruction
Sarcoidosis epidemiology
20-40, 4x more common in black population, females
PC sarcoidosis
fatigue, weakness, wt loss, fever, poor appetite
lungs - dry cough, SOB, bilateral hilar lymphadenopathy, bilateral dry crackles
ENT - uveitis, Sjogrens
Neuro - (rare 2%)mononeuritis multiplex, CN palsys, seziures, peripheral neuropathy, cognitive dysfunction
Cardiac (Rare 3%) - arrhythmias, HB, cardiomyopathy
Hepatomegaly, deranged LFT’s splenomegaly
Erythema nodosum, lupus pernio
Lofgrens syndrome
bilateral hilar lymphadenopathy, arthralgia and erythema nodosum
Staging of sarcoid
I - bilateral hilar lymphadenopathy
II - bilateral lymphadenopathy and infiltrates
III - pulmonary infiltrates only
IV - fibrosis
Differential of bilateral hilar lymphadenopathy
sarcoidosis, TB, lymphoma, metastatic spread of bronchogenic cancer
Inv sarcoidosis
HRCT - nodules and beading along fissures, enlarged hilar lymph nodes
normocytic anaemia high ESR
hypercalcemia due to activated macrophages hydroxylating vit D independent of PTH
high ACE
Biopsy rules out cancer shows non caesating granulomas
Hypersensitivity pneumonitis
Allergic reaction affecting the small airways in response to an inhaled allergen
PC EEA
Acute - 4-6hrs post exposure fever, chills, malaise, SOB, rash
Chronic insidious onset progressive SOB and cough, wt loss and fatigue, finger clubbing, inspiratory crackles
Causes of EEA
Farmers lung - mouldy hay/vege
Bird fanciers - handling pigeons, cleaning lofts
Malt workers - germinating barley
Mushrooms workers, cheese washers, winemakers
Inv and Mx EEA
HRCT - ground glass opacity, air trapping, reticular shadowing
Mx - avoid exposure, steroids for acute exacerbations
Upper Zone fibrosis
Ank spon, TB, EEA, aspergillosis, coal workers pneumoconiosis
Lower zone fibrosis
Asbestosis, sarcoidosis, IPF, RA, SLE, systemic sclerosis
COPD define
Combination of emphysema and chronic bronchitis leading to irreversible obstructive airway disease characterised by FEV1:FVC <70%
Emphysema
Enlargement of air spaces distal to the terminal bronchiole accompanied by destruction of their walls without obvious fibrosis. Can lead to small airway collapse. This leads to expiratory airway limitation and gas trapping due to the loss of elastic recoil
Chronic bronchitis
Chronic inflammation of the bronchioles leading to increased mucus secretion. Can be improved by stopping smoking.
Mx of COPD
Crucial to stop smoking, doesnt reverse the damage but slows the rate of decline in lung function. LAMA, LABA and ICS has been shown to improve FEV1, reduce hospital admissions in those who frequently present and prevent severe exacerbations.
Pulmonary rehab has huge benefits, increasing psychological health, endurance and QoL.
CBT may be of benefit in those struggling to come to terms with diagnosis or coexisting depression/anxiety
COPD PC
Smoking Hx - passive? pubs etc
Urban pollution
PC - productive cough white clear sputum, progressive SOB and wheeze. Frequent exacerbations aggravated by winter
Chronic effects = cor pulmonate, wt loss, cachexia, osteoporosis
Alpha-1-antitrypsin
Inhibits proteolytic enzymes such as neutrophil elastase, in its absence destruction of alveolar capillary walls in the lung. 2% of emphysema never rule out esp if <40y/o or no smoking Hx
O/E COPD
tachypnoeic, prolonged expiratory phase, global wheeze, cyanosis centrally or peripherally, accessory muscle use and pursed lip breathing,
Hyperinflation of chest, reduced chest expansion, wheeze on expiration globally
Causes of pulmonary hypertension
- Left ventricular failure (MS,AS), MI, cardiomyopathy
- Lung disease - ILD, COPD, IPF, CF, bronchiectasis
- Hypoventilation - obesity, OSA, neuromuscular - MND/MG
- Pulmonary vascular disease - vasculitis, SLE, SS, idiopathic pulmonary hypertension
Causes of pulmonary hypertension
1 - arterial HTN - idiopathic pul HTN, vasculitis, CTD, drug induced, portal HTN, HIV, congenital heart
2 Left ventricular failure (MS,AS), MI, cardiomyopathy, congenital
3 Lung disease - ILD, COPD, IPF, CF, bronchiectasis, OSA, hypoventilation
Pathophysiology of pul HTN
2 - LV failure is due to inability of the LV to pump blood effectively to the body this leads to pooling of blood in the pulmonary vasculature causing increased resistance, pleural effusion and oedema
3 - Due to hypoxia or lung disease, hypoxia causes vasoconstriction of the pulmonary arteries. This shunting response is physiological to increase blood flow to areas of the lungs with improved ventilation. In global lung disease this leads to vasoconstriction globally,
PC pul HTN
fatigue, syncope, dyspnea, angina, abdo distention.
O/E - left parasternal heave, loud p2, tricuspid regurug
RHF = oedema, hepatomegaly, ascites and JVP distention
Mx cor pulmonale
In pt with RHF, pa02 <7.3 long term oxygen therapy (LTOT) is crucial to prevent hypoxia, this prevents the vasoconstriction of the capillaries and stop RV hypertrophy which will eventually degenerate in to RVF and congestive cardiac failure. Over 15hrs
Gold standard measure of pulmonary HTN
RA catherisation
Invx COPD
secondary polycythemia due to chronic hypoxia
ABG - resting hypoxemia,
ECG - P pulmonale evidence of RV hypertrophy
reduced TLCO, KCO and FEV1:FVC <70%
CXR - hyperinflation 6+ ant ribs, flattened diaphragm, huge bullae, signs of infective exacerbation
ABG - pH
If pH is abnormal = acute problem
<7.35 = acidosis
>7.45 = alkalosis
ABG - C02
If the pH is acidotic and co2 is low then the pt is hyperventilation to compensate and blow off co2. Therefore metabolic
If pH is alkotic is the CO2 indicating compensatory hypoventilation
ABG - HCO3
If huge bicarb loss think acute problem i.e. burns, D/V this would causes a metabolic acidosis
CPAP
Continous positive airway pressure. Helps with hypoexmia increases o2 delivery and intrathoracic pressure to reduced cardiac workload. Prevents alveolar collapse allowing co2 levels to fall.
Uses = OSA, RHF
T1RF
O2 < 8. Inadequate oxygenation due lung tissue damage either V/Q mismatch or right to left shunts
- poor o2 delivery PE, pneumonia, pul oedema,
T2RF
O2 < 8 and co2 > 6
Failure of ventilation co2 begins to accumulate in the blood. Very bad sign. Causes = fatigue life threatening asthma, COPD, reduced GCS, muscle weakness - myathesina
Respiratory acidosis
Due to abnormal hypoventilation leading to co2 retention
COPD, fatigued asthmatic, drug overdose = reduced GCS, neuromuscular disorders
Slow metabolic compensation by retention of bicarb
Respiratory alkalosis
Excessive loss of H+ ions due to hyperventilation
aspiring overdose, anxiety attack, PE. Often tachypnoeic and stressed
Slow metabolic compensation to retain H+ and excrete Hco3
Metabolic acidosis
Reduced HCO3 due to diarrhoea, DKA and strenuous activity, uremic acidosis
PC Kussmauls breathing - deep slow breathiest increase tidal volume or tachypnoea = resp compensation
Mx - IV sodium bicarbonate
Metabolic alklosis
Loss of H+ due to vomiting,
PC hypoventilation to compensate, weakness, polyuria, hypocalcaemia
Mx - IV KCL
Nocturnal hypoventilation detection
low 02 and high pco2 at night with transcutaneous co2 monitoring
PC of nocturnal hypoventilation
somnolence - excessive daytime sleepiness, fatigue
morning headache due to co2 retention
SOB on exertion, orthopnea, anxiety, poor appetite
Causes of hypoventilation
COPD, OSA, chest wall deformity, muscle disease
Inv hypoventilation
overnight transcutaneous co2 and o2 monitoring
venous bicarbonate
sleep studies
OSA
Recurrent nocturnal upper airway obstruction causing repetitive incidence of aponea during sleep. Due to reduced tone in pharyngeal muscles leading to collapse of airway. Reduction in REM sleep due to multiple awakenings
Risk factors for OSA
Obesity, DM/HTN, COPD, increasing age, tonsilar hypertrophy nasal polyps, acromegaly
respiratory depressive drugs - alcohol, opioids
PC OSA
loud snoring, daytime sleepiness, restless/unfreshed sleep, morning headache due to co2 retention over night
O/E OSA
large collar size, enlarged adenoids, nasal polyps, acromegaly
Inv OSA
Epworth sleepiness score
diagnostic - polysomnogram showing cyclical patterns of obstruction and breathing
Mx OSA
reduce wt and alcohol, stop medications, tonsillectomy
CPAP
Inform DVLA!
DMD and hypoventilation
Most common hereditary disorder causing resp failure.. X-linked needs NIV
Bronchiestasis
Abnormal and permanent dilation of the airways. Characterised by recurrent infection and damage leading to impaired mucocilary clearance and persistent inflammation
PC and O/E bronchiestasis
Persistant wet cough, large amounts of purulent sputum, SOB and haemoptysis . O/E = clubbing and coarse crackles
Causes of bronchiestasis
TB, sarcoidosis, CF, post infective brochial damage - bacterial/viral pneumonia, measles etc, immune deficiency
NIV
Positive pressure (non-cyclical) continusous positive airway pressure (CPAP) used for acute pulmonary edema, asthma, obstructive sleep apnoea (OSA)
Positive pressure (cyclical)
Bilevel positive airway pressure (BIPAP), inspiratory positive airway pressure (IPAP), pressure support ventilation (PSV) and positive pressure ventilation (PPV)
used for COPD, weaning, asthma, neuromuscular disease
CI NIV
Cardiac / respiratory arrest
Inability to protect airway – poor cough, excessive/ inability to clear secretions, decreased conscious state/ coma
upper airway obstruction
untreated pneumothorax
marked haemodynamic instability (e.g. shock, ventricular dysrhythmias, severe acute myocardial ischaemia GI bleeding)
Following upper GI surgery (some debate about this)
Maxillofacial surgery
base of skull fracture (risk of pneumocephalus)
patient refusal
staff inexperience
Intractable vomiting
