Angina Flashcards
basis of ischemia
myocardium not getting the oxygen it demands. is an issue with oxygen delivery. coronary blood flow is the supply to the heart
angina
clinical syndrome characterized by discomfort in the chest, jaw, shoulder, back, and or arm. typically aggravated by exertion or emotional stress. relieved by nitroglycerin
metabolic effects of ischemia
anaerobic glycolysis is inadequate to maintain cell functions. ATP and creatine phosphate levels fall. Intracellular and extracellular acidosis develops. Extracellular levels of potassium, lactate, phosphate, and fatty acid levels rise.
most important contributor to elecrtophysiologic changes of ischemia
elevated extracellular potassium. causes the changes we see on ECG
injury currents (systolic current_
in subendocardial injury, the action potential of ischemic cells is more negative than that of normal cells in phase 2 and 3. during electrical systole, intracellular positive current flows from normal cells to ischemic cells
what is best way to diagnose ischemia?
stress test + imaging!
4 main risk factors for cardiovascular disease
lipid abnormalities, smoking, diabetes, hypertension
aspirin
irreversible inhibition of platelet cyclooxygenase (COX). COX is required for prostaglandin and thromboxane synth. adverse effect is bleeding. reduces mortality!
ticlopidine
not often used. inhibits platelet aggregation. reduces blood viscosity. not shown a decrease in adverse events in patients with stable angina. induces neutropenia and rarely TTP
clopidogrel
greater antithrombotic effect than ticlopidine. selectively and irreversibly inhibits the binding of adenosine diphosph to its platelet receptors. used in acute management.
prasugrel
thienopyridine class. irreversibly binds to the P2Y12 receptor. used to reduce thrombotic cardiovascular events during an acute coronary syndrome for those who have received a percutaneous coronary intervention (stent). good antiplatelet, but high risk of bleeding. must be less than 75 and lighter than 60kg in weight, with no stroke history
ticagrelor
similar in structure to adenosine. blocks ADP receptors. does not require hepatic activation. faster onset. also eliminated faster
dipyridamole
increases intracellular platelet cyclic adenosine monophosphate. use is limited because it vasodilates coronary arteries which can enhance exercise induced ischemia
cilostazol
inhibits cellular phosphodiesterase. causes increase in cAMP levels which results in inhibition of platelet aggregation. causes vasodilation, can cause increased mortality in heart failure patients
lipid lowering agents
decrease the risk of adverse ischemic events in patients with established CAD. side effects are muscle aches
ACE inhibitors
prevents angiotensin I -> angiotensin II. Angio II causes vasoconstriction. ACE also degrades bradykinin, a vasodilator. ACE inhibitors increase bradykinin levels. all end in -pril. dry cough, hypotension, hyperkalemia, angioedema side effects
beta blockers
prevent MI and sudden cardiac death. reduce angina and ischemia. bind to beta receptors and blunt effect of sympathetic system. decreases myocardial oxygen demand. increase survival post MI. end in -lol. side effects are fatigue, lethargy, insomnia, claudication, impotence
when to not use beta blockers
bradycardia, high degree AV block, sick sinus syndrome, unstable LV failure. Asthma, bronchospastic disease, severe depression, peripheral vascular disease
nitrates
endothelium independent vasodilators. activate smooth muscle guanylyl cyclase to form cGMP, which prevents calcium entry and muscle contraction. vasodilation reduces ventricular preload, reducing ventricular wall stress. inhibits platelet aggregation. inhibits leukocyte endothelial interactions (anti-inflamm). can develop nitrate tolerance with chronic use. headaches, hypotension, bradycardia due to Bezold Jarisch reflex
nitrates contraindications
hypertrophic cardiomyopathy, severe aortic stenosis, significant hypotension, use of phosphodiesterase inhibitors for ED
calcium channel blockers
reduce transmembrane flux of calcium via calcium channels. vasoselective dihydropyridines and non-dihydropyridines. vasoselective: dilatecoronary arteries and resistance vessels. negative inotropes. decrease conduction velocity and prolong repolarization in SA node and AV node, decreasing heart rate. hypotension, heart failure, peripheral edema, constipation side effects
