management of coronary artery diseases Flashcards
what are examples of stable ischemic heart disease
- chronic stable exertional angina
- ischemia without clinical symptoms
what are examples of acute coronary syndrome
- unstable angina
- NSTEMI
- STEMI
what are modifiable risk factors for CAD
- dyslipidaemia
- HTN
- DM
- smoking
- history of cerebrovascular or peripheral artery diseases
what are non-modifiable risk factors for CAD
- age
- sex
- family history
what are the signs and symptoms of angina
- diaphoresis
- nausea
- vomiting
- dyspnea
- tachycardia
- SOB
- light-headedness
what is the therapeutic management of CAD
- balance O2 supply and demand
- manage pain
- MONA (morphine, oxygen, nitroglycerin, aspirin)
what is the mechanism of action of GTN
- venous dilation to reduce preload
- reduces work needed on the heart
- reduces O2 demands
- coronary artery dilating increase O2+ flow to heart
how does GTN work in relationship to collaterals
- allows collaterals to dilate
- blood can flow to ischemic areas
how does GTN increase O2 supply and vasodilate
- GTN > nitrates > nitrites > NO
- absorbed into vascular smooth muscle cells
- monociliate enzymes activated
- GTP > cGMP
- relaxation and vasodilation
what are the adverse effects of GTN
- headache
- palpitations
- postural hypotension
what drug interactions does GTN have
PDE inhibitors - manage BPH and erectile dysfunction
how can b-blockers be used in CAD
- block beta1 receptors in the heart
- decreasing HR and contraction
- decrease CO
- lowers O2 demand
how does aspirin work
- antiplatelet
- opens the blocked arteries
- prevents reocclusion
why are b-blockers contraindicated in prinzmetal angina
- increase coronary artery spasm
- causes chest pain
what happens to O2 in atherosclerotic coronary stenosis
- imbalance in O2 demand and supply
- afterload and preload = stress on heart wall
what are collateral vessels
- side branches to coronary arteries
- formed when there is a shortage of blood supply to an area
- go around occlusion to supply O2
what causes vasospasm in CAD
absence of flow-obstructing atherosclerotic plaques
what is happening in vasospasm
- reduced production of vasodilators
- exaggerated response to endogenous vasoconstriction
precipitating factors of stable ischemic heart disease
- physical activity
- emotional stress/ excitement
- increased cardiac workload
what are the precipitating factors of unstable angina
minimal exertion or rest
what are the precipitating factors of NSTEMI and STEMI
rupture of atherosclerotic plaque
