cardio Flashcards
(157 cards)
what is prinzmetals angina
non exertional chest pain due to coronary artery vasospasm
seen w brief st elevation and no raised biomarkers
seen in younger px esp w cocaine use
what is decubitus angina
chest pain brought on by lying flat
what is stable angina
central crushing chest pain (or to jaw, neck, l shoulder) brought on by exertion and relieved by rest <5min ir glyceryl trinitrate spray (GTN spray) mostly due to atheromous plaque
modifyable risk factors stable angina
obesity
smoking
poor diet
t2dm
hyperlipidaemia
sedentary lifestyle
htn
non-modifiable risk factors stable angina
FHX
male
ethnicity - south asian, afro-caribbean
incr age
signs and symptoms stable angina
central crushing chest pain due to exertion- relieved by stress
exertional dyspnoea
incr sweating
nausea
diagnosis stable angia
ecg- normal, may show st depression
normal biomarkers/ troponin
ct angiogram to show luminal narrowing
symptomatic treatment stable angina
glyceryl trinirate spray
long term treatment stable angina 1-3rd line
CCB or BB
ccb + bb
ccb+bb+ antianginal med eg long acting nitrate
non-pharmacological management stable angina
lose wt, incr exercise, stop smoking, better diet, control other co-morbidities
ddx for stable angina
acute coronary syndrom, heart failure pericarditis
ccb needed for stable angina + example
non rate limiting eg amylodipine not verapamil
can cause excessive brdycardia
tx if medicine isnt successful for stable agina
revascularisation
- pci (percutaneous intervention)
- cabg (coronary artery bypass grafting)
+/- cabg
- more invasive, incr risk of stroke, long recovery time
+ better outcome/ prognosis
-/+ pci
+ less invasive, short recovery time
- risk of stent thrombosis
what is pci
percutaneous intervention
- inflating a ballon in an atheromous vessel to dilate to help blood flow
what is cabg
coronary artery bypass grafting
- left internal mammary artery used to bypass left anterior descending artery to bypass occlusion/ atheroma
conditions of acute coronary syndrome
unstable angina
non stemi
stemi
general pathogenesis of acs
- atheroma formation
endothelial damage causes the entery of LDL into intima layer of artery - this oxidises causing inflam response -> macrophages
1. FATTY streak- 10yrs <
- lipid laden marcophages and t cells
- INTERMEDIATE LESIONS
- layers of smooth muscle, foam cells and t cells
- FIBROUS ADVANCED LESIONS
- lipid core w necrotic debis
- fibrous cap w smooth muscle, collagen and elastin
- tough fibrous cap - more stable - less chance of rupture
- protrudes into lumen -> stenosis can cause ischaemia and reduced perfusion
- PLAQUE RUPTURE
- cap needs to be maintained by reabsorption and redeposition of smooth muscle
- thins with damage eg enzymic activity causing it to haemorrhage and rupture
- contrnts released into lumen causing thrombus formation , which can cause ischaemia and infarction
- cap needs to be maintained by reabsorption and redeposition of smooth muscle
- INTERMEDIATE LESIONS
what % vessel occlusion does sx start to occur in stable angina
approx 70%
what is unstable angina
crushing central chest pain occurs spontanteously/ not due to exertion and not relieved by rest or gtn spray
due to partial occlusion of vessel
what is nonstemi
partial occlusion of a vessel leading to tissue necrosis and release of biomarkers eg troponin but not seen w st elevation
what is a stemi
st elevation myocardial infarct
complete occlusion of a coronary vessel causing cardiac tissue necrosis with raised biomarkers and ecg changes
are ecg changes seen in unstable angina
not commonly
- may see t wave inversion or st depression