Cardiology Flashcards
what is angina pectoris?
chest pain arising from the heart as a result of myocardial ischaemia
name 3 types of angina
classic/stable, unstable/crescendo, Prinzmetal’s.
decibitus, nocturnal.
what are the differences between stable and unstable angina
stable angina is induced by effort + relieved by rest.
unstable angina occurs at rest.
what is Prinzmetal’s (variant) angina?
angina that occurs without provocation, usually at rest - due to coronary artery spasm.
what causes angina?
atheroma of coronary arteries leading to myocardial ischaemia
give 5 risk factors for angina
diabetes, smoking, hyperlipidaema, hypertension, family history, lack of exercise
list the differential diagnoses of central chest pain
angina, ACS, pericarditis, myocarditis, aortic dissection, massive PE, musculoskeletal, GORD
describe the presentation of angina
central, crushing, retrosternal chest pain - comes on with exertion, relieved by rest.
may radiate to arms and neck
list some things that can exacerbate angina
exercise, cold weather, anger, excitement, heavy meals
give some clinical features, apart from pain, of angina
dyspnoea, nausea, sweating, faintess
what investigation would you carry out on a patient with angina? what would you find?
exercise ECG test - ST depression, flat/inverted T waves
how would you manage stable angina?
modify risk factors.
secondary prevention - aspirin, statins.
symptomatic treatment - GTN spray, CCBs, beta blockers, nitrates.
how does aspirin work as a method of secondary prevention in angina?
inhibits COX2 and formation of thromboxane A2 - a platelet aggregating agent.
reduces risk of coronary events.
name an alternative to aspirin in secondary prevention of coronary events.
clopidogrel
give some examples of beta-blockers
bisoprolol, atenolol, propranolol, metoprolol
describe the mechanism of action of beta blockers in improving symptoms of angina
by acting on beta1 receptors in the heart, they reduce the force of contraction and speed of conduction in the heart - relieves myocardial ischaemia by reducing cardiac work and oxygen demand
what is the major contra-indication of beta-blockers? why?
asthma - beta blockers also act on beta2-receptors which are found in the smooth muscles of airways - cause bronchoconstriction!
give some examples of calcium channel blockers
diltiazem, amlodipine, nifedipine, verapamil
describe the mechanism of action of calcium channel blockers in controlling symptoms of stable angina
they decrease calcium entry into vascular and cardiac cells. they reduce myocardial contractility and suppress cardiac conduction - reduce heart rate, contractility and afterload - reduces myocardial oxygen demand - prevents angina.
what are the major side effects of calcium channel blockers?
postural hypotension/dizziness, headache, ankle oedema - due to systemic vasodilation
describe the mechanism of action of short-acting (GTN) nitrates and long-acting nitrates in acute angina
Nitrates are converted to NO, which increases cGMP and reduces intracellular calcium in vascular smooth muscle cells - vasodilation of venous capacitance vessels reduces preload and LV filling.
reduced cardiac work and myocardial oxygen demand - relieve angina
what interventions may be used in worsening angina?
Percutaneous coronary intervention (PCI) - balloon used to dilate atheromatous arteries (stents can be placed) - via catheter.
Coronary artery bypass grafting (CABG)
what is involved in a coronary artery bypass graft (CABG)?
internal mammary artery used to bypass stenosis in the LAD or RCA.
what does the term acute coronary syndromes (ACS) include?
unstable angina.
NSTEMI.
STEMI.
how would you differentiate between NSTEMI and unstable angina?
NSTEMI involves enough occlusion to cause myocardial damage - elevation of serum troponin and creatinine kinase.
unstable angina doesn’t cause myocardial damage.
describe the common pathology behind acute coronary syndromes
1) rupture/erosion of fibrous cap of an atheroma plaque in a coronary artery
2) platelet-rich clot forms
3) vasoconstriction due to chemicals released by platelets
name 3 non-modifiable risk factors for ACS
age.
male gender.
FHx of IHD
name 3 modifiable risk factors for ACS
smoking, hypertension, DM, hyperlipidaemia, obesity, sedentary lifestyle, cocaine use
list 3 symptoms and 3 signs of ACS
symptoms - central chest pain, sweating, dyspnoea, palpitations.
signs - sweating, anxiety, tachycardia, pallor.
what biochemical markers would you test for in ACS?
troponin, creatinine kinase, myoglobin
what would you expect to see on a 12 lead ECG in ACS?
hyperacute (tall) T waves
ST elevation (STEMI) or ST depression (NSTEMI/unstable angina).
new LBBB.
after hrs-days - T wave inversion, Q waves.
what would be your immediate management of ACS?
MONA:
Morphine, Oxygen, Nitrates, Aspirin
± clopidogrel/ticragelor
what drugs might a patient be put on after an ACS, for secondary prevention?
beta-blockers, ACE inhibitors, statins, aspirin
what might the non-medical management of ACS be?
PCI - percutaneous coronary intervention
list some possible complications following a MI
heart failure, rupture of interventricular septum, mitral regurg, arrhythmias, heart block, pericarditis, thromboembolism, ventricular aneurysm
give 3 causes of heart failure
ischaemic heart disease; valvular disease; pericarditis; pericardial effusion; alcohol; cocaine; myocarditis; arrhythmias; cardiomyopathies; anaemia; pulmonary hypertension
what are the types of heart failure?
systolic/diastolic, low output/high output, left/right
what compensatory mechanisms are activated as the heart begins to fail?
sympathetic nervous system, RAAS, ventricular dilatation, ventricular remodelling
what causes the oedema and dyspnoea seen in heart failure?
activation of the RAAS by decreased renal perfusion (due to low CO) - salt/water retention - peripheral/pulmonary congestion
describe the ventricular remodelling seen in heart failure
initial dilatation.
hypertrophy, loss of myocytes, increased interstitial fibrosis.
what is the difference between systolic and diastolic failure?
systolic = inability of ventricles to contract normally
diastolic = inability of ventricles to relax and fill normally
give 3 symptoms of heart failure
exertional dypnoea, orthopnoea (SOB on lying down), paroxysmal nocturnal dyspnoea, fatigue, oedema, weight loss, wheeze
give 5 signs of heart failure
cold peripheries, cyanosis, displaced apex, wheeze, RV heave, valve disease, hypotension, pleural effusion, oedema, ascites
what are 5 features of heart failure seen on CXR?
ABCDE:
Aleveolar oedema (bats wings)
Kerly B lines (interstitial oedema)
Cardiomegaly
Dilated upper lobe vessels
pleural Effusion
list 2 major criteria on the Farmingham criteria for heart failure diagnosis
SAW PANIC
S3 heart sound - gallop.
Acute pulmonary oedema.
Weight loss
Paroxysmal nocturnal dyspnoea
Abdominojugular reflux
Neck vein distension
Increased cardiac shadow on CXR (cardiomegaly)
Crepitations (crackles heard in lungs)
list 2 minor criteria on the Farmingham criteria for heart failure diagnosis
HEART ViNo:
Hepatomegaly
Effusion, pleural
Ankle oedema bilaterally
exeRtional dyspnoea
Tachycardia
Vital capacity decrease by 1/3rd
Nocturnal cough
describe the NHYA classification of heart failure
class I = no limitation
class II = mild limitation (comfort at rest, fatigue and dyspnoea on normal physical activity)
class III = marked limitation (comfort at rest, dyspnoea on gentle physical activity)
class IV = symptomatic at rest, exacerbated by any physical activity
what investigations would you do in heart failure?
ECG - underlying cause.
CXR.
Bloods - BNP (B type natriuretic peptide - if normal, HF is excluded).
echocardiography.
describe the medical management of heart failure
loop diuretics (furosemide) ± spironolactone ± thiazide.
ACE inhibitors (or ARB).
beta blockers.
± digoxin, vasodilators (e.g. hydralazine)
name 2 ACE inhibitors
ramipril, lisinopril
what causes the common cough side effect of ACE inhibitors? what drug class are a good alternative?
increased levels of bradykinin, which is usually inactivated by ACE.
ARBs
how do ACE inhibitors act?
prevent conversion of angiotensin I to angiotensin II.
Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion - blocking this reuces afterload, lowering BP.
name 2 angiotensin receptor blockers (ARBs)?
losartan, candesartan
how do angiotensin receptor blockers work?
block action of angiotensin II on the AT1 receptor. similar effects as ACE inhibitors.
give 3 causes of mitral stenosis
rheumatic heart disease (most), congenital, cardial fibroelastosis, malignant carcinoid, prosthetic valve.
what is mitral stenosis?
thickening and immobility of valve leaflets - leads to obstruction of blood flow from left atrium to left ventricle.
give 3 symptoms of mitral stenosis
exertional dyspnoea, fatigue, palpitations, chest pain, systemic emboli, haemoptysis
what is the heart murmur heard in mitral stenosis?
rumbling mid-diastolic murmur
what diagnostic tests would you perform in mitral stenosis? what would you see?
ECG - AF, bifid P waves.
CXR - LA enlargement, pulmonary oedema, mitral valve calcification.
Echo - diagnostic.
how would mitral stenosis be treated?
diuretics - decrease pre load.
balloon valvuloplasty / valve replacement.
give 2 complications of mitral stenosis
pulmonary hypertension.
emboli (dilated LA).
pressure from large LA on local structures e.g. hoarseness due to compression of L recurrent laryngeal
give 3 causes of mitral regurgitation
prolapsing mitral valve + rheumatic heart disease = most common.
infective endocarditis, annular calcification, LV dilatation, ruptured chordae tendinae, papillary muscle rupture.
connective tissue disorders (Ehlers-Danos, Marfan’s).
cardiomyopathy, congenital.
give 3 symptoms of mitral regurgitation
dyspnoea, fatigue, palpitations, infective endocarditis
what murmur is heard in mitral regurgitation?
pansystolic murmur
what does a bifid P wave indicate on ECG?
bifid P waves = p mitrale - mitral valve disease
what investigations would you perform in valvular heart disease?
ECG, CXR, echo ± cardiac catherization
what would you see on CXR in mitral regurgitation?
enlarged LA and LV, mitral valve calcification, pulmonary oedema
how would you treat mitral regurgitation?
asymptomatic = echo every 1-5yrs.
anticoagulate with warfarin if - AF, hx of embolism, prosthetic valve, additional mitral stenosis.
diuretics.
surgery - valve replacement or repair.
give 3 causes of aortic stenosis
degeneration and calcification of normal valve (in the elderly).
calcification of congenital biscuspid valve (middle age).
rheumatic heart disease.
what is the classical triad of symptoms in aortic stenosis?
SAD:
Syncope
Angina
Dyspnoea - heart failure
what murmur is heard in aortic stenosis?
ejection systolic murmur
what would you expect to see on an ECG in aortic stenosis?
p mitrale, LVH with strain pattern (depressed ST and T wave inversion in I, AVL, V5 and V6)
what would you see on a CXR of a patient with aortic stenosis?
normal heart size, prominent ascending aorta, valvular calcification
how would you treat aortic stenosis?
prompt valve replacement
what are the most common causes of aortic regurgitation?
rheumatic fever and infective endocarditis
give 3 causes of acute aortic regurgitation
infective endocarditis, acute rheumatic fever, dissection of the aorta, AAA dissection, prosthetic valve failure
give 3 causes of chronic aortic regurgitation
chronic rheumatic heart disease, syphilis, rheumatoid arthritis, severe hypertension, biscupid aortic valve, aortic endocarditis, Marfan’s, osteogenesis imperfecta
give 3 symptoms of aortic stenosis
exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, palpitations, angina, syncope, CCF
what murmur is heard in aortic regurgitation?
early diastolic murmur.
“at L sternal edge in 4th intercostal space”
what would you see on CXR/ECG in aortic regurgitation?
CXR - cardiomegaly and dilatation of the ascending aorta, pulmonary oedema.
ECG - LVH.
how would you treat aortic regurgitation?
reduce systolic hypertension - ACE inhibitors.
echo every 6-12/12.
valve replacement.
what are the 3 main cardiomyopathies?
hypertrophic (HCM), dilated (DCM) and restrictive
what is hypertrophic cardiomyopathy?
ventricular hypertrophy in absence of abnormal loading conditions - LV outflow tract obstruction.
what causes hypertrophic cardiomyopathy?
50% = autosomal dominant
50% = sporadic.
what is the major consequence of hypertrophic cardiomyopathy?
sudden cardiac death in young people
name 2 clinical features of hypertrophic cardiomyopathy
can be asymptomatic.
angina, syncope, sudden death, systolic thrill.
what investigations might you carry out in cardiomyopathy?
CXR, ECG, echo.
cardiac MR.
how would you treat hypertrophic cardiomyopathy?
beta blockers/CCBs to control symptoms.
anticoagulate to prevent emboli.
implantable defib.
give 3 causes of dilated cardiomyopathy
alcohol, hypertension, haemachromatosis, viral infection, autoimmune, congenital.
give 3 clinical features of dilated cardiomyopathy
dyspnoea, emboli or arrhythmia, displaced apex beat, S3 gallop, pleural effusion, oedema, jaundice, ascites.
how would you treat dilated cardiomyopathy?
bed rest.
diuretics, digoxin, ACE inhibitors.
biventricular pacing/implantable cardiac defibs.
heart transplant.
what is restrictive cardiomyopathy?
rigid myocardium restricting diastolic ventricular filling.
give 2 causes of restrictive cardiomyopathy
amyloidosis. haemachromatosis. sarcoidosis. scleroderma. idiopathic.
give 3 clinical features of restrictive cardiomyopathy
constrictive pericarditis. raised JVP. oedema, ascites, features of RVH.
what investigation would you perform in order to diagnose restrictive cardiomyopathy?
cardiac catheterisation.
what are the 2 causes of ventricular septal defect?
congenital.
acquired post-MI.
how might a ventricular septal defect present?
severe heart failure in infancy.
OR - asymptomatic, detected later in life
does a smaller ventricular septal defect produce louder or quieter murmurs?
louder
what murmur is heard in VSD?
harsh pansystolic murmur at left sternal edge, with systolic thrill
give 2 complications of a ventricular septal defect
aortic regurgitation, infundibular stenosis, IE, pulmonary hypertension, Eisenmenger’s complex.
what is seen on a CXR of someone with a ventricular septal defect?
Small VSD - normal sized heart ± enlarged pulmonary blood vessels.
Large VSD - cardiomegaly, large pulmonary arteries, marked enlargement of pulmonary vessels.
how would you manage a ventricular septal defect?
medical support until spontaneous closure.
OR - surgical patch repair or device closure.
what are the different types of atrial septal defect?
ostium secundum defects - most common - present in adulthood.
ostium primum defects - associated with AV valve abnormalities - present early.
give 3 clinical features of an atrial septal defect
pulmonary hypertension, cyanosis, arrhythmia, haemoptysis, chest pain, AF, raised JVP.
pulmonary ejection systolic murmur.
what investigations are used to diagnose most structural heart defects?
echo.
cardiac catheter.
how would you treat an ASD?
transcatheter or surgical closure
what genetic disorder is associated with atrioventricular septal defects?
Downs syndrome
what structures are involved in an atrioventricular septal defect?
atrial septum, ventricular septum, mitral and tricuspid valve
what are the clinical features and management of a complete AVSD?
breathless neonate, failure to thrive, poor feeding, torrential pulmonary blood flow.
repair with PA band.
what are the clinical features and management of a partial AVSD?
presents in adulthood, similar to small ASD/VSD.
treatment not necessary.
what is a patent ductus arteriosus?
persistent communication between left pulmonary artery and descending aorta - L to R shunt.
normally the ductus arteriosus closes within hrs of birth.
what are the clinical features of a PDA?
3 classic signs: bounding pulse, ‘machinery murmur’, pulmonary hypertension.
also - breathless, poor feeding, failure to thrive, Eisenmenger’s syndrome
how would you treat a PDA?
indometacin (prostaglandin) can stimulate closure.
if large - surgical or percutaneous closure.
what is Eisenmenger’s syndrome?
cyanosis - clubbed and blue toes, pink not clubbed fingers.
what is coarctation of the aorta?
congenital narrowing of the descending aorta
what are the clinical features of coarctation of the aorta? name 2 complications.
radiofemoral delay, weak femoral pulse, high BP, systolic murmur.
heart failure + IE.
how would you treat coarctation of the aorta?
surgery or balloon dilation ± stenting
what are the consequences of a biscupid aortic valve?
go on to develop aortic stenosis - requiring valve replacement.
higher risk of IE.
give some clinical features of pulmonary stenosis
RV failure as neonate. collapse. poor pulmonary blood flow. RVH. tricuspid regurg.
how would you treat pulmonary stenosis?
ballon valvuloplasty.
open vavlotomy.
what are the 4 features of tetralogy of Fallot?
1 - VSD.
2 - pulmonary stenosis.
3 - RVH.
4 - aorta overriding the VSD
what causes tetralogy of Fallot?
abnormalities in separation of truncus arteriosus into the aorta and pulmonary arteries early in gestation
describe the presentation of tetralogy of Fallot
acyanotic at birth. gradually become cyanotic.
Fallow (hypoxic) spells - go blue, restless, inconsolable crying - toddlers may squat.
what is the characteristic feature of a CXR in tetralogy of Fallot?
boot shaped heart
how is tetralogy of Fallot managed?
oxygen. knee-chest position. morphine.
long-term beta blockers.
surgery at less than 12 months.
list 3 viral causes of acute pericarditis
Coxsackie B
Influenza
EBV
Mumps
Varicella
HIV
list 3 bacterial causes of acute pericarditis
Pneumonia
Rheumatic fever
TB
Streps
Staphs
list 5 causes, other than bacterial/viral infection, of acute pericarditis
Fungi, MI, uraemia, rheumatoid arthritis, SLE, myxoedema, trauma, surgery, malignancy, radiotherapy, sarcoidosis, idiopathic + drugs
describe the pain seen in acute pericarditis
sharp, central chest pain - worse on inspiration or lying flat, relieved by leaning forward
what might be heard on auscultation of a patient with pericarditis?
pericardial friction rub
what investigation would you carry out to diagnose acute pericarditis? what would you see?
ECG - concave upwards (saddle-shaped) ST segment elevation in all leads
how would you treat acute pericarditis?
treat underlying cause.
NSAIDs for analgesia.
colchicine if relapsing.
what is constrictive pericarditis?
heart is encased in a rigid fibrotic pericardium - prevents diastolic filling of ventricles.
what causes constrictive pericarditis?
most common in UK = idiopathic.
globally = TB.
also occurs after any pericarditis.
what are the clinical features of constrictive pericarditis?
those of right-sided heart failure - raised JVP, oedema, hepatomegaly, ascites, pulsus paradoxus, diffuse apex beat
what two investigations would you carry out in constrictive pericarditis and what would you find?
CXR - normal/small heart + pericardial calcification.
CT/MRI - pericardial thickening/calcification
how would you treat constrictive pericarditis?
surgical excision of pericardium
what is the definition of hypertension?
> 140/90mmHg based on 2+ readings on separate occasions
what are the criteria for treating hypertension?
ALL with sustained >160/100mmHg.
those with sustained >140/90 that are at high risk of coronary events, have diabetes or end-organ damage
list 3 causes of secondary hypertension
renal disease - diabetic nephropathy, chronic glomerulonephritis, PKD, chronic tubulointerstitial nephritis.
endocrine disease - Conn’s, phaeochromocytoma, Cushing’s, acromegaly.
Coarctation of the aorta.
pregnancy.
steroids.
the Pill.
give 3 risk factors for hypertension
age, FHx, male gender, African or Caribbean origin, high salt intake, sedentary lifestyle, overweight/obese, smoking, excess alcohol intake.
what investigations would you carry out on a patient presenting with a high blood pressure reading?
take blood pressure again, on at least 1 other occasion.
24h ambulatory BP monitoring (ABPM) - exclude white coat effect
give 3 examples of non-pharmacological measures you would encourage a patient with hypertension to take
weight reduction.
Mediterranean diet - oily fish, low saturated fat, low salt.
limit alcohol consumption.
exercise.
smoking cessation.
increase fruit and veg intake.
what drug would you prescribe for a 45yo caucasian patient with hypertension with no other medical history?
ACE inhibitor - ramipril.
if CI (cough) - ARB - losartan
what drug would you prescribe a 67yo Afro-Caribbean man with hypertension?
calcium channel blocker - amlodipine
if first line treatment is failing to control a patient’s hypertension, what drug regime would you prescribe them? and if this fails?
ACE inhibitor + CCB or ACE inhibitor + thiazide.
all 3 if a combination of 2 fails to control.
how do calcium channel blockers work to reduce hypertension?
decrease calcium entry into vascular smooth muscle cells - vasodilation of arterial smooth muscle, lowering arterial pressure.
what are the side effects of CCBs?
bradycardia, headaches, flushing
what is the most common cardiac arrhythmia?
atrial fibrillation
what is AF?
chaotic, irregular atrial rhythm at 300-600bpm.
AV node is conducting some of the atrial impulses - irregular ventricular response.
irregularly irregular pulse.
list 4 causes of atrial fibrillation
heart failure/ischaemia, hypertension, MI, PE, mitral valve disease, pneumonia, hyperthyroidism, caffeine, alcohol, hypokalaemia, hypomagnaesaemia
what ECG features would you see in atrial fibrillation?
absent P waves
irregular QRS complexes
atrial rate 300bpm
give 3 forms of treatment you would give a patient with atrial fibrillation
warfarin - anticoagulation.
beta blockers/CCBs - rate control.
Cardioversion - rhythm control.
describe what you would see on an ECG trace in atrial flutter
saw tooth flutter waves between QRS complexes
what is the difference between atrial fibrillation and atrial flutter?
atrial fibrillation = irregular ventricular conduction of atrial beats.
atrial flutter = atrial rate of 300bpm (same as AF), but ventricles conduct every other atrial beat - 150bpm
name 2 common causes of heart block
coronary artery disease, cardiomyopathy, fibrosis of conducting tissue
what is first degree AV block? how does it appear on ECG?
delayed AV conduction.
prolonged PR interval (>0.22s).
how does Mobtiz type I (second degree) AV block appear on ECG? aka Wenckebach phenomenon
progressive PR interval prolongation until a P wave fails to conduct - PR interval then returns to normal, then begins to get longer again.
how is Mobitz type II (second degree) AV block seen on ECG?
dropped QRS waves aren’t preceded by progressive PR prolongation. wide QRS complex.
what is 2:1 or 3:1 advanced second degree AV block?
every second or third P wave conducts to ventricles
what is third degree AV block? how are ventricular contractions maintained?
all atrial activity is failing to conduct to ventricles - atrial and ventricular activity completely dissociated (shown in P and QRS waves).
ventricular contractions are being maintained by spontaneous escape rhythms from below site of block.
describe the ECG features seen in RBBB
secondary R waves in V1.
slurred S in V5 and V6
list 2 causes of RBBB
PE, RVH, IHD, congenital heart disease, idiopathic
describe the ECG features seen in LBBB
opposite to RBBB.
secondary R waves in left ventricular leads (I, AVL, V4-V6).
slurred S in V1 and V2.
list 2 causes of LBBB
IHD, LVH, aortic valve disease, post-op
give 3 causes of sinus tachycardia
physiological - exercise/excitement.
fever, anaemia, heart failure, thyrotoxicosis, acute PE, hypovolaemia, drugs.
what causes atrioventricular junctional tachycardias?
re-entry circuits - two separate pathways for impulse conduction
what are the ECG changes seen in supraventricular tachycardia?
absent or inverted P wave after QRS
name 2 things that may aggravate a supraventricular tachycardia
exertion, coffee, tea, alcohol
what is the 1st line management of a supraventricular tachycardia?
vagal manoeuvres - breath holding, valsalva manoeuvre, carotid massage
what drugs may be used to treat a supraventricular tachycardia?
IV adenosine.
if fails - verapamil/atenolol.
what is the long-term management of a supraventricular tachycardia?
radiofrequency ablation of accessory pathway via catheter.
what are ventricular ectopic premature beats?
a premature beat arising from an ectopic focus in the ventricles - this focus depolarises before the SAN, leading to a premature and inefficient beat.
describe the clinical and ECG features of a premature ventricular ectopic beat
broad, abnormal QRS complex before you would expect it.
patient complains of extra/missed beats/heavy beats - palpitations
how would you treat a symptomatic ventricular ectopic beat? what are patients with ventricular ectopic beats at a higher risk of?
beta blockers.
ventricular fibrillation.
what are the ECG features of a ventricular tachycardia?
rapid ventricular rhythm with broad abnormal QRS complexes
list 3 causes of prolonged QT
congenital, hypokalaemia, hypocalcaemia, hypomagnesaemia, tricyclics, macrolides
what causes Wolff-Parkinson-White?
congenital accessory conduction pathway between atria and ventricles
describe the features of a resting ECG in a patient with WPW
short PR interval, wide QRS complex due to slurred upstroke (delta wave)
what is an aneurysm? how might they cause symptoms?
permanent localised dilation of an artery.
pressure effects on local structures, or vessel rupture.
can be a source of emboli.
how might an abdominal aortic aneurysm be discovered?
a pulsatile mass palpated on abdo exam.
calcification on a plain XR.
rupture.
epigastric or back pain due to pressure effects.
what is the difference between a true and false aneurysm?
true aneurysm has the wall of the artery forming a capsule around the aneursym.
false aneurysm wall is made up of surrounding tissue.
how would a ruptured AAA present?
sudden severe epigastric pain radiating to back leading to hypovolaemic shock - collapse
how would a ruptured AAA be repaired?
endovascular repair with stent insertion, or surgical replacement of aneurysmal section
describe the pain of a dissecting aortic aneurysm
abrupt onset of severe, tearing central chest pain radiating through back
how is a dissecting aortic aneurysm managed?
urgent BP control - lanetalol IV.
surgical repair.
give 3 risk factors for peripheral arterial disease
hypertension, smoking, diabetes, diet, sedentary lifestyle, obesity, hyperlipidaemia, age, male gender, FHx
what causes peripheral artery disease?
atherosclerosis causing stenosis of arteries
describe the clinical features of intermittent claudication
cramping pain in calf/thigh/buttock after walking a given distance (shorter=more severe) - relieved by rest
describe the clinical features of critical ischaemia
ulceration, gangrene, pain at rest.
burning foot pain at night relieved by hanging legs over the side of the bed
what are the 4 stages in the Fontaine classification of peripheral artery disease?
asymptomatic - intermittent claudication - ischaemic rest pain - ulceration/gangrene (critical ischaemia)
give 3 signs of peripheral artery disease
absent femoral, popliteal or foot pulses.
cold, white leg(s), atrophic skin, punched out ulcers, postural colour change, capillary refill prolonged
what are the 5 Ps of acute limb ischaemia?
Paraesthesia
Perishingly cold
Pallor
Paralysis
Pain
what diagnostic tests would be performed in peripheral artery disease?
Ankle-brachial pressure index (ABPI) - ratio of ankle and brachial systolic pressures.
colour duplex USS.
MR/CT angiography.
describe conservative treatment of limb ischaemia
exercise, quit smoking, lose weight, manage diabetes and hypertension.
clopidogrel (antiplatelet) to prevent progression and reduce risk.
how would intermittent claudication be managed, beyond conservative risk reduction treatments?
revascularisation - percutaneous transluminal angioplasty (PTA) or surgical reconstruction/arterial bypass graft.
what are some risk factors for infective endocarditis?
congenital - valve defects, VSD, PDA.
prosthetic valves.
IVDU.
poor dental hygiene.
soft tissue infections.
name the most common causative organism in infective endocarditis?
Streptococcus viridans
give 3 organisms (apart from Strep viridans) that can cause infective endocarditis
enterococci, staph aureus/epidermidis, diphtheroids, Haemophilus, actinobacillus, Coxiella burnetii, chlamydia.
fungi - Candida, aspergillus, histoplasma.
what is an infective endocarditis patient at risk of?
stroke - vegetations.
destruction of valve - regurgitation - worsening heart failure.
describe the clinical features of infective endocarditis
systemic features of infection - malaise, fever, night sweats, weight loss, anaemia.
heart failure + new murmurs.
vascular events - embolism ± metastatic abscesses.
immune complex deposition - petechial haemorrhages under skin, splinter haemorrhages under nails, Roth’s spots, arthrlagia, acute glomerulonephritis.
what investigations should you carry out in suspected endocarditis?
3 sets of blood cultures, at different times and sites.
bloods - anaemia, neutrophilia, high ESR/CRP.
transthoracic echocardiography (TTE) - just standard echo.
describe the Duke criteria for diagnosis of IE
2 major or 1 maj + 3 min, or 5 min.
Major criteria - persistently +ve blood culture. endocardium involvement seen on +ve echo, new murmur.
Minor criteria - fever, vascular/immunological signs, +ve blood culture/echo that doesn’t meet major.
how would you treat infective endocarditis?
before results of culture - IV benzylpenicillin + gentamicin.
then tailor to cultures and sensitivity.
what is shock?
acute circulatory failure with inadequate or inappropriately distributed tissue perfusion - prolonged oxygen deprivation leads to necrosis, organ failure and death
list the different types of shock
hypovolaemia, cardiogenic, sepsis, anaphylaxis, neurogenic shock
give 3 causes of hypovolaemia shock
haemorrhages - GI bleed, trauma, AAA dissection etc.
fluid loss - burns, diarrhoea, intestinal obstruction.
give 3 causes of cardiogenic shock
(= pump faillure).
ACS, arrhythmias, aortic dissection, PE, tension pneumothorax, cardiac tamponade, endocarditis
give 3 signs of hypovolaemic shock
pale grey skin, slow capillary refill, sweating, weak pulse, tachycardia
name 2 precipitating factors of anaphylactic shock
penicillin, contrast, latex, dairy, nuts, insect stings
describe the clinical features of anaphylactic shock
onset within 5-60mins of exposure.
warm peripheries, hypotension, urticarial, angio-oedema, wheezing, upper airway obstruction.
how would you manage septic shock?
take blood cultures before abx - then co-amoxiclav and tazocin IV
how would you manage anaphylactic shock?
remove cause. O2. IM adrenaline. IV chlorphenamine and hydrocotisone.
how would you manage hypovolaemic shock?
raise legs. fluid bolus - repeat if shock improves.
what risk score is used to determine stroke risk in AF patient?
CHA2DS2-VASc score:
Congestive heart failure.
Hypertension.
Age >75yrs. (2 points, that’s why it’s A2).
Diabetes mellitus.
S2 - prior stroke (2pts).
V - vascular disease
Age - 65-74.
Sex category - female sex.
what is the enzyme that breaks down bradykinin?
angiotensin converting enzyme - excess bradykinin (since it’s not being broken down) is the reason why some patients on ACEi get a persistent dry cough
explain how ACE inhibitors work
ACE inhibitors inhibit conversion of angiotensin I to angiotensin II in the lungs - this prevents it from acting on the adrenals to increase aldosterone secretion and thus cause water and sodium retention at the kidneys.
angiotensin II is also a vasoconstrictor, so ACEi act as vasodilator, and causes sodium and water excretion - lower blood volume, lowers BP.
how do angiotensin receptor blockers produce a similar effect to ACEi? give two examples of ARBs
by blocking angiotensin II receptors, so its actions cannot be exerted.
losartan, candesartan.
give 2 examples of ACEis
ramipril, lisinopril
why do you get hyperkalaema as a side effect of angiotensin 2 receptor blockers?
ARBs cause a direct effect on aldosterone production in the adrenals - aldosterone works on the distal convoluted tubules of kidney by causing sodium to be reabsorbed in return for potassium excretion - ARBs reverse this transfer, so there’s potassium retention.
calcium channel blockers are negatively inotropic and negatively chronotropic, what does this mean?
inotropic - reduces the contraction.
chronotropic - lowers the heart rate.
how do calcium channel blockers work? give some examples.
decrease calcium entry into vascular and cardiac cells. intracellular calcium is lower - relaxation and vasodilation of arterial smooth muscle.
reduce myocardial contractility and suppress cardiac conduction, particularly at AV node.
this reduces myocardial oxygen demand - important in angina.
dihydropyridines (amlodipine, nifedipine) - selective for vasculature.
non-dihydropyridines (diltiazem, verapamil)- selective for heart
what clotting factors does warfarin work on?
2, 7, 9, 10 by inhibiting vitamin K synthesis - so anticoagulates by inhibiting coagulation factor synthesis
statins are given to correct hyperlipidaemia, what enzyme do they act on? name 2 statins.
HMG-CoA reductase - involved in making cholesterol.
so they reduce the cholesterol production in liver and increase clearance of LDL-cholesterol from blood.
simvastatin, atorvastatin, pravastatin.
amiodarone is used for pharmacological cardioversion, but it also chemically resembles a hormone made naturally by the body - what is this and what can this cause?
thyroxine - can cause hyperthyroidism
in supraventricular tachycardia, adenosine is administered IV to bring the heart back into normal rhythm, how does it work on the heart? what type of arrhythmias should it be used for?
it works via the A1 receptor, which reduces cAMP - so causes cell hyperpolarisation by pushing potassium out of the cell.
also relaxes the smooth muscle of the heart causing vasodilation.
only used for ventricular tachycardias.
why do you need to warn the patient that they may get a sense of ‘impending doom’ after you administer adenosine?
because it induces transient heart block in the AV node so the heart stops for a beat or so
atropine is derived from the deadly nightshade, but what heart arrhythmia is it used for and how does it help?
it is used for any severe bradycardia - it blocks the action of the vagus nerve/parasympathetic system by being a competitive antagonist of muscarinic ACh receptors.
dilates pupils, increases heart rate and reduces salivation.
if you have a patient that comes in with unstable angina but tells you he is allergic to aspirin, what is then your first line of treatment after giving GTN?
clopidogrel monotherapy
give an example of a short and a long acting nitrate
short - glyceryl trinitrate (GTN).
long - isosorbide mononitrate
how do nitrates work to reduce the pain of angina?
converted to NO, which is a vasodilator - relaxation of capaticance vessels reduces cardiac preload + LV filling, which reduces cardiac work and myocardial oxygen demand.
give 2 possible side effects of nitrates
flushing, headaches, light headedness, hypotension
name 3 beta blockers
bisoprolol, atenolol, propranolol, metoprolol
how do beta blockers work to improve symptoms of ischaemic heart disease?
they reduce force of contraction and speed of conduction in the heart via beta 1 receptors - reducing cardiac work and oxygen demand.
how do beta blockers work as a treatment for AF?
slow the ventricular rate by prolonging the refractory period at the AV node
list the indications for beta blockers
IHD - symptoms and improve prognosis.
chronic heart failure.
AF and other SVTs - reduce rate, maintain sinus rhythm.
hypertension - only if other medicines are insufficient.
how do beta blockers work as a treatment for hypertension?
reduce renin secretion from the kidney, which is mediated by beta1 receptors.
give some possible SEs of beta blockers
fatigue, cold extremities, headache, nausea, sleep disturbance, ED in men.
what major disease is a contraindication to the use of beta blockers?
ASTHMA - can cause life-threatening bronchospasm due to blockade of beta2 adrenoreceptors in airways
name an aldosterone antagonist
spironolactone, epleronone
what cardiac indication do aldosterone antagonists treat?
chronic heart failure - as an addition to beta blocker and ACEi/ARB
name a LMWH. name a drug that is very similar to LMWHs
dalteparin, enoxaparin.
similar drug - fondaparinux.
how do LMWHs work?
inhibit factor Xa by inhibiting antithrombin
how does fondaparinux work?
inhibits factor Xa.
how does aspirin work in prevention of thrombosis?
it irreversibly inhibits cyclooxygenase (COX) to reduce production of pro-aggregation factor thromboxane from arachidonic acid - reduces platelet aggregation and risk of arterial occlusion.
give some examples of antiplatelet drugs, apart from aspirin
clopidogrel, new oral anticoagulants, glycoprotein IIb/IIIa inhibitors
how does clopidogrel work?
prevents platelet aggregation by binding irreversibly to adenosine diphosphate receptors on surface of platelets
- independent of COX pathway, so can be taken with aspirin
how do glycoprotein IIb/IIIa inhibitors work?
prevent platelet aggregation by inhibiting the GPIIb/IIIa receptor on platelet surface
name 2 fibrinolytic (thrombolysis) drugs
alteplase, streptokinase
how do fibrinolytic drugs work?
catalyse the conversion of plasminogen to plasmin which acts to dissolve fibrinous clots and re-canalise occluded vessels.
- allows reperfusion of tissues, preventing/limiting tissue infarction.
name a loop diuretic
furosemide, bumetanide
give a cardiac indication of loop diuretics
symptomatic treatment of fluid overload in chronic heart failure
describe the mechanism of loop diuretics
act on ascending limb of loop of Henle to inhibit the Na/K/2CL cotransporter that transports the ions into the cell - water follows these ions, so they have a potent diuretic effect.
also - cause dilation of capaticance vessels - reduces preload + improves contractile function of the heart.
what are potassium sparing diuretics used for? name an example.
used as part of combination therapy, to treat hypokalaemia arising from loop/thiazide diuretic use.
amiloride.
how do potassium sparing diuretics work?
weak diuretics.
act on distal convoluted tubules in kidney - inhibit sodium and water reabsorption by acting on epithelial sodium channels - causes potassium retention.
give an example of a thiazide/thiazide like diuretic
bendroflumethiazide, indapamide, chlortalidone
describe the mechanism of action of thiazide diuretics
inhibit the Na/Cl cotransporter in the distal convoluted tubule of the nephron, preventing reabsorption of sodium and water.
also cause vasodilation.
how does digoxin work in AF/atrial flutter?
reduces heart rate and increases force of contraction (-vely chronotropic, +vely inotropic).
works via indirect pathway - increased vagal tone, reduced contraction at AVN and preventing dome impulses travelling to the ventricles.
for what cardiac problem might sildenafil be prescribed? what class of drug is this?
primary pulmonary hypertension.
phosphodiesterase type 5 (PDE5) inhibitor
how does sildenafil work as a treatment of pulmonary hypertension?
causes arterial vasodilation by increasing cGMP (normally broken down by PDE5).
<p>What HR is considered sinus tachycardia?</p>
<p>>100bpm</p>
<p>Name some causes of sinus tachycardia</p>
<p>Anxiety, dehydration, recent exercise, sepsis, pneumonia etc etc</p>
<p>What lead(s) would you look in to assess sinus bradycardia/tachycardia?</p>
<p>any - rhythm strip is best</p>
<p>What HR is considered sinus bradycardia?</p>
<p><60bpm</p>
<p>List some causes of left axis deviation</p>
<p>left anterior hemiblock</p>
<p>WPW syndrome</p>
<p>inferior MI</p>
<p>ventricular tachycardia</p>
<p>LVH</p>
<p>What is the most likely cause of right axis deviation? List any alternative causes</p>
<p>RVH is most likely</p>
<p>normal variant - tall thin people</p>
<p>lateral MI</p>
<p>WPW syndrome</p>
<p>dextrocardia or R/L arm lead switch</p>
<p>left posterior fascicular block</p>
<p>How would you detect left axis deviation?</p>
<p>Look for lead I and II "Leaving" each other - small lead I, negative lead II and III</p>
<p>What is a more likely cause of left axis deviation, conduction issues orLVH?</p>
<p>conduction issues</p>
<p>What is the mechanism of atrial flutter?</p>
<p>a re-entry circuit within right atrium</p>
<p>List some causes of AF</p>
<p>ischaemic heart disease</p>
<p>thyrotoxicosis (hyperthyroidosis)</p>
<p>sepsis</p>
<p>valvular heart disease</p>
<p>alcohol excess</p>
<p>PE</p>
<p>hypokalaemia/hpomagnesaemia</p>
<p>What is the mechanism of atrial tachycardia?</p>
<p>A single ectopic focus, outside the SAN that's triggering rapid depolarisation of the atria</p>
<p>List causes of atrial tachycardia</p>
<p>digoxin toxicity</p>
<p>atrial scarring</p>
<p>catecholamine excess</p>
<p>congenital abnormatlities</p>
<p>What is the mechanism of junctional tachycardia?</p>
<p>AV junctional pacemaker rhythm exceeds that of SAN. There is increased automaticity in AVN coupled with decreased automaticity in SAN.</p>
<p>List causes of first degree heart block</p>
<p>increased vagal tone</p>
<p>athletic training</p>
<p>inferior MI</p>
<p>mitral valve surgery</p>
<p>Myocarditis (Lyme disease)</p>
<p>electrolyte disturbances (e.g. hyperkalaemia)</p>
<p>AV nodal blocking drugs:</p>
<p>beta blockers</p>
<p>CCBs</p>
<p>digoxin</p>
<p>amiodarone</p>
<p>Describe the ECG trace in Mobitz type I 2nd degree heart block (Wenckebach phenomenon)</p>
<p>progressive lengthening of PR interval, followed by absent QRS (a non-conducted P wave), then cycle repeats</p>
<p>PR interval is longest just before dropped beat, and shortest just after</p>
<p>What is the mechanism of Mobitz I 2nd degree heart block?</p>
<p>usually due to reversible conduction block at AVN - malfunctioning AVN cells progressively fatigue until they fail to conduct an impulse (dropped beat)</p>
<p>List causes of Mobitz I 2nd degree heart block</p>
<p>Drugs: beta blockers CCBs digoxin amiodarone</p>
<p>Increased vagal tone (e.g. athletes)</p>
<p>inferior MI</p>
<p>myocarditis</p>
<p>cardiac surgery</p>
<p>Describe the ECG trace in Mobitz type II 2nd degree heart block</p>
<p>intermittent non-conducted P waves without progressive prolongation of PR interval</p>
<p>P waves 'march through' at constant rate</p>
<p>What is the mechanism of Mobitz II 2nd degree heartblock?</p>
<p>usually due to failure of conduction at His-Purkinje system</p>
<p>generally due to structural damage to conducting system "all-or-nothing"</p>
<p>- no progressive fatigue like in Mobitz I, instead His-Purkinje cells suddenly and unexpectedly fail to conduct</p>
<p>List causes of Mobitz II 2nd degree heart block</p>
<p>Anterior MI (septal infarction wiht necrosis of bundle branches)</p>
<p>Idiopathic fibrosis of conducting system</p>
<p>cardiac surgery</p>
<p>inflammatory conditions (rheumatic fever, myocarditis, Lyme disease)</p>
<p>autoimmune (SLE, systemic sclerosis)</p>
<p>infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis)</p>
<p>hyperkalaemia</p>
<p>Drugs: beta blockers CCBs digoxin amiodarone</p>
<p>List causes of complete heart block</p>
<p>inferior MI</p>
<p>AVN blocking drugs - CCBs, beta blockers, digoxin</p>
<p>Idiopathic degeneration of conducting system</p>
<p>In what lead(s) is complete heart block best seen?</p>
<p>II and V1</p>
<p>What is the mechanism of complete heart block?</p>
<p>there is complete absence of AV conduction - end point of second degree heart block.</p>
<p>Either progressive fatigue of AVN cells (mobitz I) or due to sudden onset of complete conduction throughout His-Purkinje system (mobitz II)</p>
<p>What is the clinical significance of complete heart block? How would it be treated?</p>
<p>high risk of sudden cardiac death - urgent admission for cardiac monitoring, backup temporary pacing followed by permanent pacemaker insertion</p>
<p>Describe what is seen:</p>
<p><strong>Complete heart block.</strong></p>
<p>atrial rate is 60bpm</p>
<p>ventricular rate is 27bpm</p>
<p>slow ventricular escape rhythm</p>
<p>Describe what is seen:</p>
<p>2:1 heart block</p>
<p>Describe what is seen:</p>
<p>3:1 heart block</p>
<p>Describe what is seen:</p>
<p>Mobitz II second degree heart block</p>
<p>Intermittent P waves without progressive lengthening of PR interval</p>
<p>Describe what is seen:</p>
<p>Mobitz I second degree heart block</p>
<p>aka Weckebach phenomenon</p>
<p>progressive lengthening of PR interval until a QRS fails to conduct (dropped beat)</p>
<p>Describe what is seen:</p>
<p>First degree heart block</p>
<p>PR >0.2s (5 small squares)</p>
<p>Describe what is seen:</p>
<p><strong>R</strong>ight axis deviation</p>
<p>leads I and II <strong>r</strong>eaching towards each other</p>
<p>Describe what is seen:</p>
<p><strong>L</strong>eft axis deviation</p>
<p>Leads I and II are <strong>l</strong>eaving each other</p>
<p>Describe what is seen:</p>
<p>atrial fibrillation</p>
<p>irregularly irregular, absent P waves</p>
<p>Describe what is seen:</p>
<p>Atrial fibrillation</p>
<p>irregularly irregular</p>
<p>absent P waves</p>
<p>Describe what is seen:</p>
<p>Atrial flutter</p>
<p>"saw tooth P waves" at c300bpm</p>
<p></p>
<p>Describe what is seen:</p>
<p>atrial tachycardia</p>
<p>narrow complex tachycardia at 120bpm</p>
<p>each QRS is preceded by an abnormal p wave</p>
<p>Describe what is seen:</p>
<p>junctional tachycardia</p>
<p>narrow QRS</p>
<p>retrograde P waves before, during or after QRS</p>
<p></p>
<p>Describe what is seen:</p>
<p>RBBB</p>
<p>broad QRS</p>
<p>M complex in V1-3</p>
<p>W complex in V6 (slurred S waves)</p>
<p>Describe what is seen</p>
<p>LBBB</p>
<p>broad QRS</p>
<p>dominant S in V1 - W</p>
<p>broad R in lateral leads- M</p>
<p>Describe what is seen:</p>
<p>ST elevation in I and aVL (high lateral leads)</p>
<p>reciprocal ST depression in III and aVF (inferior leads)</p>
<p></p>
<p>acute MI localised to superior part of lateral wall -</p>
<p><strong>high lateral STEMI</strong></p>
<p>occluded first branch of LAD</p>
<p>Describe what is seen</p>
<p>ST elevation in inferior (II, III, aVF) leads and lateral (I, V5-V6) leads</p>
<p>ST depression in V1-V3 suggests associated posterior infarction</p>
<p><strong>acute anterolateral STEMI with posterior extension</strong></p>
<p>occlusion of proximal circumflex</p>
<p>Describe the ECG changes seen in right bundle branch block</p>
<p>broad QRS >120ms</p>
<p>RSR pattern in V1-3 ('m' shaped complex)</p>
<p>wide, slurred S waves in lateral leads (I, aVL, V5-6) giving a 'W' shaped complex in V6</p>
<p>(MarroW - M in V1, W in V6, rr = right)</p>
<p>possible ST depression in precordial leads (V1-3)</p>
<p>Describe what is seen:</p>
<p>ST elevation in leads II, III and aVF</p>
<p>Q-wave formation in III and aVF</p>
<p>reciprocal ST depression and T wave inversion in aVL</p>
<p><strong>inferior STEMI</strong></p>
<p>circumflex occlusion - ST elevation in lead II = lead III</p>
<p>Describe what is seen:</p>
<p>marked ST elevation in leads II, III and aVF</p>
<p>reciprocal changes in aVL</p>
<p><strong>inferior STEMI</strong></p>
<p>RCA occlusion as ST elevation in lead III> lead II</p>
<p>What is the mechanism in RBBB?</p>
<p>activation of R ventricle is delayed as depolarisation has to spread across septum from left ventricle due to blockage of R bundle of Purkinje fibres</p>
<p></p>
<p>left ventricle is activated normally, so early part of QRS is unchanged, but delayed R ventricle activation produces a secondary R wave in V1-3 and a slurred S wave in lateral leads</p>
<p>What does this V2 lead trace suggest?</p>
<p>posterior MI</p>
<p>horizontal ST depression</p>
<p>upright T wave</p>
<p>dominant R wave (R/S ratio >1)</p>
<p>List causes of RBBB</p>
<p>RVH / cor pulmonale</p>
<p>PE</p>
<p>IHD</p>
<p>rheumatic heart disease</p>
<p>myocarditis or cardiomyopathy</p>
<p>degenerative disease of conduction system</p>
<p>congenital heart disease</p>
<p>Describe the ECG changes seen in left bundle branch block</p>
<p>broad QRS >120ms</p>
<p>dominant S wave in V1 - W</p>
<p>broad, notched R wave in V6 - M</p>
<p>(WilliaM - W in V1, M in V6, ll = left)</p>
<p>no Q waves in lateral leads (I, V5-6, small Q waves in aVL)</p>
<p>prolonged R wave peak time >60ms in V5-6</p>
<p>List causes of LBBB</p>
<p>aortic stenosis</p>
<p>ischaemic heart disease</p>
<p>dilated cardiomyopathy</p>
<p>anterior MI</p>
<p>primary degnerative disease (fibrosis) of the conducting system</p>
<p>hyperkalaemia</p>
<p>digoxin toxicity</p>
<p>Describe the mechanisms in LBBB?</p>
<p>septum is activated R to L instead of L to R</p>
<p>spreads via right bundle branch, and then via septum to left bundle branch</p>
<p>this extends the QRS duration and removes Q waves in lateral leads</p>
<p>as the venrticles are activated sequentially, broad R waves are produced</p>
<p>Describe what is seen:</p>
<p>ST elevation is maximal in anteroseptal leads (v1-V4)</p>
<p>Q waves present in septal leads (V1-2)</p>
<p>hyperacute (peaked) T waves in (V2-4)</p>
<p><strong>hyperactute anteroseptal STEMI</strong></p>
<p>Describe what is seen:</p>
<p>ST elevation in V1-6 + I and aVL</p>
<p>minimal reciprocal depression in III and aVF</p>
<p><strong>anterior STEMI</strong></p>
<p>Describe the ECG changes seen in junctional escape rhythms</p>
<p>no p waves, or p waves completely unrelated to QRS</p>
<p>normal QRS, maybe slightly narrow</p>
<p>slow HR</p>
<p></p>
<p>What is the mechanism of junctional escape rhythms?</p>
<p>there are pacemaker cells at various points in the conduction system</p>
<p>junctional escape rhythm occurs when the rate of AV node depolarisation is less than the intrinsic rate of an ectopic pacemaker</p>
<p>list causes of junctional escape rhythms</p>
<p>severe sinus bradycardia</p>
<p>sinus arrest</p>
<p>sino-atrial exit block</p>
<p>high-grade second degreeheart block (4:1, 5:1 etc)</p>
<p>complete heart block</p>
<p>hyperkalaemia</p>
<p>drugs:</p>
<p>beta blockers</p>
<p>CCBs</p>
<p>digoxin poisoning</p>
<p>Describe the ECG changes seen in a ventricular escape rhythm</p>
<p>ventricular rhythm of 20-40bpm</p>
<p>broad QRS complexes, possibly with a LBBB or RBBB morphology</p>
<p>Describe what is seen:</p>
<p>ventricular fibrillation</p>
<p>what arteries are likely to be blocked in a lateral STEMI</p>
<p>LAD and LCx</p>
<p>Describe what is seen:</p>
<p>sinus rhythm</p>
<p>broad QRS with slurred upstroke - delta wave</p>
<p>dominant R wave in V1</p>
<p><strong>Wolff-Parkinson-White</strong></p>
<p>Describe the ECG changes seen in a lateral STEMI</p>
<p>ST elevation in the lateral leads</p>
<p>(I, aVL, V5-6)</p>
<p>reciprocal ST depression in inferior leads (III and aVF)</p>
<p>Describe what is seen</p>
<p><strong>Digoxin effect</strong></p>
<p>"sagging" ST segements</p>
<p>hockey stick T waves</p>
<p>Describe the ECG changes seen in an inferior MI</p>
<p>ST elevation in II, III and aVF</p>
<p>progressive development of Q waves in II, III and aVF</p>
<p>reciprocal depression in aVL (±lead I)</p>
<p></p>
<p>Describe what is seen:</p>
<p><strong>pericarditis</strong></p>
<p>widespread concave ST elevation and PR depression throughout V2-V6 and I, II, aVL, aVF</p>
<p>reciprocal ST depression and PR elevation in aVR</p>
<p>Which artery most commonly causes an inferior STEMI?</p>
<p>right coronary artery</p>
<p>(more ST elevation in lead III than II)</p>
<p>LCx can cause it less commonly</p>
<p>(ST elevation in lead II = lead III)</p>
<p></p>
<p>Describe the ECG changes seen in posterior MI</p>
<p>In V1-V3:</p>
<p>horizontal ST depression</p>
<p>tall, broad R waves</p>
<p>upright T waves</p>
<p>dominant R wave in V2</p>
<p>Occlusion of what artery causes an anterior STEMI?</p>
<p>LAD</p>
<p>Describe the ECG changes seen in anterior STEMI</p>
<p>ST elevation with Q wave formation in the precordial leads (V1-6) ± the high lateral leads (I and aVL)</p>
<p>reciprocal ST depression in the inferior leads (mainly III and aVF)</p>
<p>In what leads would ST elevation be maximal in a septal STEMI?</p>
<p>V1-2</p>
<p>In what leads would ST elevation be maximal in an anterior STEMI?</p>
<p>V2-5</p>
<p>In what leads would ST elevation be maximal in an anteroseptal STEMI?</p>
<p>V1-4</p>
<p>In what leads would ST elevation be maximal in an anterolateral STEMI?</p>
<p>V3-6, I + aVL</p>
<p>What is seen in an NSTEMI?</p>
<p>pathological Q waves only</p>
<p>Describe the ECG changes that may be seen in a ventricular tachycardia</p>
<p>very broad QRS (>160ms)</p>
<p>no p waves</p>
<p>T waves difficult to identify</p>
<p>rate > 200bpm</p>
<p></p>
<p>Describe the ECG changes seen in ventricular fibrillation</p>
<p>chaotic irregular deflections of varying amplitude</p>
<p>no identifiable P waves, QRS complexes or T waves</p>
<p>rate 150-500bpm</p>
<p></p>
<p>Causes of VF</p>
<p>myocardial iscahemia/infarction</p>
<p>electrolyte abnormalities</p>
<p>cardiomyopathy (dilated, hypertrophic, restrictive)</p>
<p>Long QT</p>
<p>Brugada syndrome</p>
<p>Drugs</p>
<p>environmental - electrical shock, drowing, hypothermia</p>
<p>PE</p>
<p>cardiac tampnoade</p>
<p>blunt trauma</p>
<p></p>
<p>Describe the ECG changes seen in Wolff-Parkinson-White syndrome</p>
<p>sinus rhythm</p>
<p>right axis deviation</p>
<p>short PR interval</p>
<p>sluured upstroke of the QRS complex, best seen in V3 and V4 - wide QRS due to this delta wave</p>
<p>dominant R wave in V1</p>
<p></p>
<p>what is the mechanism in Wolff-Parkinson-White?</p>
<p>accessory pathway, usually from left atria, allows direct transmission of signal, bypassing AVN (hence short PR)</p>
<p></p>
<p></p>
<p>Describe the "digoxin effect"</p>
<p>downsloping ST depression with "sagging" appearance</p>
<p>flattened, inverted or biphasic T waves - hockey stick</p>
<p>shortened QT</p>
<p>What is the mechanism behind the digoxin effect?</p>
<p>shortening of atrial and ventricular refractory periods - producing short QT</p>
<p>increased vagal effects at AVN - prolonged PR interval</p>
<p>Describe the ECG changes seen in pericarditis</p>
<p>widespread concave ST elevation and PR depression</p>
<p>Reciprocal ST depression and PR elevation in aVR</p>
<p></p>
<p>What is P Pulmonale?</p>
<p>peaked P waves</p>
<p>What is seen in p mitrale?</p>
<p>bifid p waves</p>
<p>list causes of p pulmonale</p>
<p>anything that cause right atrial enlargement</p>
<p>e.g. tricuspid stenosis, pulomnary hypertension</p>
