CAD Flashcards
what is coronary artery disease
the narrowing of coronary arteries due to atherosclerosis (lipid deposition, inflammation, thrombosis)
chronic and acute coronary syndrome (4)
STEMI, NSTEMI, unstable angina, chronic angina
atherosclerotic plaque development steps
- fatty streak - endothelial dysfunction allows cholesterol to enter the bv wall, it is recognised as a foreign body which drives leukocyte modification and recruitment, foam cells form;
- plaque progression - smooth muscle cells migrate and there is altered matrix synthesis and degradation, due to inflammation and cholesterol levels driving it;
- plaque disruption - disturbed plaque integrity due to unstable/thin surface, thrombus forms due to rupture into bv which can occlude the artery
why is smoking a risk factor for CAD
the toxins damage the bv wall
main trigger factors for bv wall inflammation (4)
cholesterol crystals; neutrophil extracellular traps; atheroprone flow (turbulent); hypoxia
risk factors for atherothrombosis (12)
hypertension; hypercholesterolemia; diabetes; smoking; FH; obesity/metabolic syndrome; male; old age; ethnicity; socio-economic status; genetic profile; inflammatory markers
what is used to calculate the future risk of CVD event
QRISK2 - increased by 10% indicates treatment for cholesterol should be given
what areas of arteries are at particular risk from atherosclerosis
branch points and bifurcations due to turbulent flow
what areas of arteries are at a particularly high risk of atherosclerosis
branches and bifurcations due to turbulent flow
what is ischaemia due to
fixed vessel narrowing and abnormal vascular tone
what determines myocardial O2 supply (7)
coronary blood flow; coronary perfusion pressure; coronary vascular resistance; external compression; intrinsic regulation; local metabolites; endothelial factors; neural innervation
what determines myocardial O2 demand (3)
wall stress (Pr/2h); heart rate; contractility
what determines the effect n blood flow of stenosis (2)
the degree of narrowing; the amount of compensatory vasodilation the arterioles can achieve
what can abnormal vascular tone result in? (2)
inappropriate vasoconstriction of coronary arteries; loss of normal antithrombotic properties
why does angina occur
metabolic hyperaemia can no longer match myocardial perfusion to myocardial oxygen demand in exercise due to restricted blood flow
4 characteristics of angina (location, character, relieving/exacerbating factors, duration)
location - retrosternal, diffuse, may involve both sides + chest;
character - pressure, tightness, heaviness, occasionally burning sensation or chocking if in the neck, toothache if in jaw;
relieving/precipitating - provoked by exertion, more easily provoked after a heavy meal or cold weather, rapid relief w GTN;
duration - attacks last a few minutes only
features of a normal lumen (3)
patent lumen; normal endothelial function; platelet aggregation inhibited
features of stable angina lumen (2)
lumen narrowed by plaque; inappropriate vasoconstriction
features of unstable angina (4)
plaque rupture; platelet aggregation; thrombus formation; unopposed vasoconstriction
features of variant angina (2)
no overt plaques; intense vasospazam
chest pain differentials (11)
cardiac - angina, pericarditis;
GI - reflux(GORD), peptic ulcer, oesophageal spasm, biliary colic;
msk - costochondral syndrome (sharp pain, rib fractures, cervical radiculitis
other - pneumonia, PE (stabbing pain), anxiety, aortic dissection
symptoms of PE
sudden SOB; chest pain; anxiety; palpitations
diagnostic tests for CAD (4)
stress ECG; myocardial perfusion imaging, stress echo; stress MRI
imaging for CAD (2)
CT coronary angiogram; coronary angiogram
what does a depressed ST segment in an ECG stress test indicate
ischaemia
shape of RCA on angiogram
‘c’ shaped
4 main coronary arteries
right coronary; left anterior descending; circumflex; left coronary
what is the first region to be damaged by ischemia
subendothelial region as it is furthest from blood supply
subendothelial vs transmural ischaemia ECG
subendothelial - ST depression
transmural - ST lelevation
stable vs vulnerable plaques
stable - thick fibrous cap, small lipid pool
vulnerable - think fibrous cap, large lipid pool, many inflammatory cells
what happens to a ruptured plaque
thrombogenic extracellular matrix exposed to lumen, thrombus formed; this can either be reabsorbed resulting in a narrower lumen and fibrous intima or in occlusion of the lumen
what marker is key in identifying if an MI has occured
troponin - cardiac specific troponin can be identified, this elevates if the heart is damaged
what can raised troponin indicate other than ACS
exercise; renal failure/other severe illness
what is a pathological Q wave
a Q wave that is >3mm, it often appears post MI due to wall damage, it persists in the ECG after other changes have reverted
NSTEMI ECG appearance
ST depression or T wave inversion; no pathological Q wave
post MI complications (7)
A -arrythmia
C-congestive HF/cardiogenic shock
T- thromboembolism
R - rupture (V free wall, papillary muscle, septum)
A - aneuyrsm
P - pericarditis
I - ischaemia
D - dresslers syndrome/detah
what is Dressler’s syndrome
inflammation of the sac surrounding the heart (pericarditis); the immune system responding to damage to heart tissue or damage to the pericardium
how does endothelial dysfunction contribute to ACS
reduced vasodilator and antithrombotic effect
dressler’s syndrome symptoms
fatigue; weakness; pain worse on lying down; pleural effusion; increased WCC
what is pericardial friction rub (what does it sound like and why)
occurs due to the inflammation of the pericardium post MI and so the two layers rub against each other; grating, scratching, or rasping sound systolic and diastolic; best heard between the apex and sternum but may be widespread
