AF & COPD Flashcards
what is atrial fibrillation
A type of supraventricular tachyarrhythmia. Characterized by uncoordinated atrial activity on the surface ECG with fibrillatory waves of varying shape, amplitude, and timing associated with irregularly irregular ventricular response when atrioventricular conduction is intact
pathophysiology of atrial fibrillation
- Rapidly firing ectopic foci located inside 1 or more pulmonary veins
- Abnormal atrial tissue substrate - ↑ atrial pressure, ↑ atrial muscle mass, atrial fibrosis, inflammation and infiltration of the atrium
- Only a proportion of electrical impulses in the atria reach the ventricles electrical re-entry which then results in atrial fibrillation
what are the different types of atrial fibrillation
initial episode - AF > 30 second diagnosed by ECG
paroxysmal - recurrent 2 or more episodes that terminate within 7 days
peristent - continuous > 7 days or AF > 48 in which a decision is made to perfrom CV
long standing - continuous AF for > 12 months
permanent - joint decision by patient and clinician to cease further attempts to restore or maintain sinus rhythm
aetiology of AF?
- in developed country most common HTN, coronary artery disease and MI
- in developing country most common congestive heart failure, HTN and rheumatic valvular disease
- Cardiac conditions Sinus sick syndrome (electrophysiological abnormalities), Wolff-Parkinson-White syndrome, Cardiac surgery, congenital heart disease, tumour near heart
- Infections pericarditis, amyloidosis, myocarditis
- Alcohol intoxication/Caffeine/Drugs
- Hyperthyroidism/thyrotoxicosis
- Lung cancer/PE
- Diabetes
- Obesity
- Idiopathic – 11%
clinical features of AF
palpitations tachycardia irregularly irregular pulse SOB chest pain dec exercise capacity/fatigue stroke as 1st presentation elevated JVP hypotension - AF induced haemodynamic instability
investigation for AF
feels for irregularly irregular pulse
ECG - if AF, will show fibrillation, irregular ventricular rate (RR intervals), no clear P waves, QRS rhythm is rapid and irregular
if paroxysmal AF is suspected and no AF recorded in initial ECG –> 24 hour ambulatory ECG
FBC, U&E, TFTs
CXR to exclude HF or resp. causes
Transthoracic echocardiography in those confirmed with AF - find any structural heart causes and baseline for long-term management
when will you admit a person with AF to hospital
if severe symptoms/serious complication
- pulse > 150
- BP < 90
- LOC / severe dizziness/ongoing chest pain/inc SOB
mx of acute AF
cardiovesion - electrical DC shock/IV drugs if - new-onset AF (<48 hours) - AF with a reversible cause - heart failure a cause \+ atrial flutter
- If unstable electrical DC shock + IV amiodarone after
- If stable either DC shock of IV amiodarone at a later stage
- A transesophageal echo is done to look for clots in heart before cardioversion otherwise it can dislodge and case a stroke or anti-coag for 4 weeks before cardioversion
Rate control - B-blocker, CCB or digoxin
Rhythm control - amiodarone
Anti-coag - after CHA2DS2-VASc and HAS-BLED
- DOAC as 1st line
- warfarin if mechanical valve, aortic stenosis or rheumatic fever
mx of chronic AF
- Rate controlling drugs – beta blockers, Ca channel blockers
- Antiarrhythmic drug – Quinidine, Beta blockers, amiodarone
- CHA2DS2-VASc for stroke assessment + HAS-BLED for bleeding risks
- Oral anticoagulant e.g. warfarin, NOACs – need to be calculated by the CHA2DS2-VASc scoring system
what is discussed in AF annual review
- Follow up 1 week after starting rate control treatment
- Check symptoms at rest and during exercise/assess HR
- If not controlled consider increasing dose/combining any 2 of beta blockers/digoxin/diltiazem (check this + beta blocker with specialist)
- If still not controlled refer within 4 weeks to cardiologist
- Side effects
- HR/BP
- Calculate TTR to ensure an INR of between 2 and 3 with warfarin
- Exclude measurements taken within the 1st 6 weeks of treatment
- Calculate over a maintenance period of at least 6 months
- If poor control then attempt to correct contributing factors/switch to NOACs
pathophysiology of COPD
poorly reversible airflow limitation that is usually progressive
associated with persistent inflammatory response of the lungs
chronic bronchitis
- airway narrowing
- hypertrophy and hyperplasia of mucus secreting glands
- bronchial wall inflammation
- mucosal oedema
- epithelial cell later may ulcerate
squmaous epithelium may replace columnar epithelium when ulcers heal –> squamour metaplasia
emphysema
- dilatation and destruction of the lung tissue distil to the terminal bronchioles
- loss of the elastic coil
- expiratory airflow limitation and air trapping
- smoking > 20 years
what scale is used to classify COPD
Medical Research Council Dyspnoea Scale
Grade 1 - breathless on strenuous exercise
Grade 2 - breathless on walking up hil
Grade 3 - breathless that slows walking on the flat
Grade 4 - stop to catch their breath after walking 100 meters on the flat
Grade 5 - unable to leave the house due to SOB
investigation of COPD?
MRC Dyspnoea Scale
spirometry - PEV1/FVC ratio < 0.7
CXR - hyperinflation and to exclude other diagnosis
FBC - anaemia, inc haematrocrit, polycythaemia, eosinophil count, sputum culture BMI ECG ECHO BNP Alpha 1 antitrypsin
what is used to assess the severity of COPD?
GOLD framework
what is the single most important diagnostic test for COPD
spirometry with bronchodilator reversibility test
- FEV1/FVC < 0.7
what are the different stages of COPD?
Stage 1, mild — FEV1 80% of predicted value or higher. With these values, a diagnosis of COPD can only be made on the basis of respiratory symptoms.
Stage 2, moderate — FEV1 50–79% of predicted value.
Stage 3, severe — FEV1 30–49% of predicted value.
Stage 4, very severe — FEV1 less than 30% of predicted value.
what is considered to be asthma features
previous diagnosis of asthma or of atopy, a higher blood eosinophil count, substantial variation in FEV1 over time (at least 400ml) or substantial diurnal variation in peak flow (at least 20%)
management of COPD without asthma features
1) SABA or SAMA PRN
2) LABA + LAMA
management of COPD with asthma features
1) SABA or SAMA PRN
2) ICS + LABA
3) if still exacerbations –> ICS + LAMA + LABA
what is pleura effusion
collection of fluid in the pleural cavity
what are the 2 types of pleural effusion
exudative - high protein count (>3g/L), protein leaking out of the tissues into the pleural space
transudative - relatively low protein count (< 3g/L protein), fluid moving across into the pleural space
aetiology of o exudative pleural effusion
local inflammation
- lung cancer
- penumonia
- TB
- PE
- post CABG
- systemic disease eg RA
aetiology of transudative pleural effusion
systemic shift in fluid
- congestive heart fialure
- cirrhosis, nephromatic syndrome
- Meig’s syndrome - R sided pleural effusion with ovarian malignancy
clinical features
SOB
cough - can be productive or not
dullness to percussion over the effusion
tracheal deviation away from the effusion - if massive
reduced breath sounds
improving pneumonia with a/onging fever - suspect empyema
investigation of pleural effusion?
CXR - 1st line • Blunting of the costophrenic angle • Fluid in the lung fissures • Larger effusions will have a meniscus • Tracheal and mediastinal deviation – massive effusion
USS - more sensitive than CXR
- Thoracentesis
- High protein count, pH<7.2, ↓ glucose, ↑ LDH = empyema
- Blood = malignancy, PE with infarction, trauma
- Light’s criteria is used when the pleural fluid is between 25-30g/L to differentiate between exudate and transudate
what is the light’s criteria for pleural effusions
it looks into protein and LDH to differentiate between exudate and transudate pleural effusion
Transudate
- protein (pleura/serum) < 0.5
- LDH (pleural/serum) <0.6
- pleura LDH < 2/3 of upper limit of normal serum LDH
Exudate
- protein (pleura/serum) > 0.5
- LDH (pleural/serum) >0.6
- pleura LDH > 2/3 of upper limit of normal serum LDH
management of pleural effusion?
small - conservative management
larger - pleural aspiration and chest drain
empyema (pH<7.2) - chest drina + ABx
what cancer most commonly mets to the lungs
breast colorectal renal bladder prostate
where does lung cancer most commonly mets to?
bone
liver
adrenals
brain
BLAB
clinical features of lung mets
enlarged axillary lymph nodes
bone pain
ascites
investigations of lung mets
CT chest abdo pelvis
PET-CT - for distant mets (not useful for brain, kidney or bladder)
MRI
what is mesothelioma
neoplasma arising from the lining of the lung
commonly caused by asbestos exposure, aged 60-85, male
what are the management of lung mets
bone - single fraction radiotherapy for bone mets, denosumab - prevent skeletal-related events from bone mets
Liver - peritoneal catheter drainage system for treatment resistant, recurrent malignant ascties
adrenal - surgical and replacemetn of cortisol and alderstone and androgen
brain - 1x met –> chemo/immuno otherwise stereotactic radiosurgery/radiotherapy
- if > 1x mets –> stereotactic radiosurgery/radiotherapy
what are the different types of lung cancer?
non small cell lung cancer
small cell lung cancer
what is sarcoidosis
granulomatous (nodules of macrophages) inflammatory condition commonly affecting the lungs, skin and eyes
aetiology of sarcoidosis
unknown
most commonly affect - women, black, young adulthood, > 60 yrs old
clinical faetures of sarcoidosis
CNS - diabetes inspidius, encepahlopathy
PNS - facial nerve palsy, mononeuritis multiplex
eye - uveitis, conjunctivitis, optic neuritis
lung - dry cough, SOB, wheeze, mediastinal lymphadenopathy, pulmonary fibrosis
heart - bundle branch block, heart block
liver - cirrhosis, cholestasis
skin - erythema nodosum, lupus pernio, granuloma development in scar tissues
systemic - fever, fatigue, weight loss
kidney - kidney stones, hypercalcaemia, nephrocalcinosis, interstitial nephritis
MSK - arthralgia, arthritis, myopathy
aetiology of sarcoidosis
unknown
most commonly affect - women, black, young adulthood, > 60 yrs old
management of sacroidosis
no/mild symptoms - no treatment
moderate symptoms
1) orla steriod - indicated for parenchymal lung disease/uveitis/hypercalacemia/neurological/cardiac involvment
2) bisophophonates for boen protection
3) methotrexate/azathioprien
severe lung transplant
what genetic mode of transfer is cystic fibrosis
autosomal recessive - gene mutation in the cystic fibrosis transmembrane conductance regulatory gene on chromosome 7
most common variant = delta F508
clinical features of cystic fibrosis
meconium ileus
recurrent LRTI
chronic cough
nasal polyps esp if bilateral
thick sputum production
crackles/wheeze on auscultation
salty sweat
finger clubbing
FFT abdo pain abdo distension pancreatitis steatorrhoea
what genetic mode of transfer is cystic fibrosis
autosomal recessive - gene mutation in the cystic fibrosis transmembrane conductance regulatory gene on chromosome 7
management of cystic fibrosis
MDT approach
chest physio with nebulised saline - twice daily
salbutamol
Nebulised DNase
ABx - prophylactic flucloxacillin
CFTR modulators eg ivacaftor (G551D mutation only)
vaccine - pneumococcal, influenza, varicella
transplants - lung, liver
high calorie diet, CREON tablets
investigation for cystic fibrosis
1) newborn screening via guthrie test (majority diagnosed here) + typical clinical symptosm/FHX of sibling
2) sweat test - gold standard - diagnostic if > 60 on 2 separate occasions
or genetic testing for CFTR gene during pregnancy by aminocentesis, CVS
clinical features of TB
persistent productive cough SOB Haemoptysis - late features weight loss fever night sweats malaise
extra-pulmonary involvement
- headache, vomiting, irritability, confusion, cranial nerve abnor - TB meningitis
- lymphadenopathy - cervical and supraclavicular lymph nodes
- SOB, chest pain, ankle swelling - TB pericarditis
- abdo/pelvic pain, constipation, bowel obstruction
sterile pyuria - renal TB
- skin lesions - erythema nodosum, lupas vulgaris - cutaneous TB
- bone/joint/back pains, joint swelling
investigation of TB
Active TB
• CXR
• 3x early morning sputum samples – acid fast bacilli +ve
• If active extrapulmonary, arrange scanning of the relevant areas
Latent TB
• Mantoux test – tuberculin injected and skin reaction after 2-3 days = +ve test
• Interferon gamma release assay (IGRA) test
• HIV/Hep B/Hep C testing
• CXR – calcified Ghon complex
management of TB
• Notifiable disease + immediate contact tracing
6 months (or 3 months if latent) of isoniazid with pyridoxine and rifampicin, supplemented in the first 2 months with pyrazinamide and ethambutol
