Term
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Definition
| chest pain from the heart |
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Term
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Definition
| O2 debt due to stoppage of blood flow, 70-80% of O2 in arterial blood is extracted for the heart alone - needed b/c it uses fat as its main fuel source |
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Term
| which are the most important of the three antianginal drugs? |
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Definition
| organic nitrates - which immediately relieve pain associated with angina by dilating the vascular smooth muscle - particularly the veins, allowing blood to pool there and lower preload - keeping the heart from being overstressed. their effect on venous smooth muscle and preload differentiates them from the other 2 antianginals |
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Term
| how does the heart respond to oxygen debt? |
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Definition
| poorly, it cannot handle oxygen debt like skeletal muscle can |
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Term
| what does ischemia directly affect? |
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Definition
| ischemia quickly affects ATP production and contractile function which decreases L ventricular ejection, CO, and BP |
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Term
| how does ischemia appear on an EKG? |
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Definition
| ischemia: reversed T wave, MI: elevated S-T segment |
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Term
| what are the different types of angina? |
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Definition
| fixed, stable, unstable, and silent |
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Term
| what is the most common kind of angina? |
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Definition
| fixed/stable angina, which is precipitated by exercise and/or excitement. stable angina caused by obstruction of 1+ coronary arteries, usually due to arteriosclerosis and is relieved by rest |
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Term
| what is variant or prinzmetal's angina? |
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Definition
| variant/prinzmetals angina occurs at rest or even during sleep and is unpredictable. it is caused by *vasospasm of an artery that is probably injured |
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Term
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Definition
| this is used to categorize a variety of clinical presentations involving acute ischemic syndromes that are progressive, and in the initial stages, indistinguishable from an impending MI. this condition is believed to be caused by *thrombosis in a blood vessel |
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Term
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Definition
| ischemia of the myocardium w/out pain or symptoms |
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Term
| what drugs are good for fixed, stable angina? |
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Definition
| beta blockers, Ca+ channel blockers and nitrates |
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Term
| what drugs are good for unstable angina? |
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Definition
| beta blockers and nitrates |
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Term
| what drug is good for all three types of angina? |
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Definition
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Term
| what is the myocardial O2 supply dependent on? |
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Definition
| coronary blood flow, which is mainly dependent on local metabolites such as O2, pH, lactate, adenosine and endothelial factors (NO) |
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Term
| how is coronary flow related to coronary vascular bed resistance? |
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Definition
| inversely (relax vascular structure, increase flow and vice versa) |
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Term
| what does arteriolar tone control? |
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Definition
| vascular resistance and systolic wall stress |
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Term
| what does venous tone control? |
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Definition
| the amount of blood returned to the heart and diastolic wall stress |
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Term
| what is the number one factor determining O2 consumption? |
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Definition
| wall stress (myocardial fiber tension); which is composed of interventricular pressure, ventricular pressure, and wall thickness |
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Term
| what are other factors besides wall tension that determin O2 consumption? |
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Definition
| heart rate and contractility |
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Term
| what is the most potent vasodilator? |
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Definition
| ischemia, adenosine and NO are released as a natural response to encourage perfusion |
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Term
| why are Ca++ blockers used for variant angina and not beta-blockers? |
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Definition
| Ca++ blockers will dialate vasospastic arteries and help, but beta blockers do not help with this |
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Term
| why would you not want to use a Ca++ channel blocker with unstable angina? |
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Definition
| arterio/atherosclerotic vessels do not dialate like normal vessels, and if dilator drugs like Ca++ channel blockers are used, you may get a "coronary steal" effect (alteration of circulation patterns lead to a reduction in the blood directed to the coronary circulation). |
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Term
| what is the primary drug strategy for treatment of angina? |
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Definition
| reduction in preload/afterload to decrease cardiac work and O2 demand |
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Term
| what is preload? what decreases this? |
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Definition
| the workload presented to the heart, the blood coming back to the heart to be pumped - venous return. venodilators decrease this. |
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Term
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Definition
| the workload the heart must overcome to pump the blood out of the heart - peripheral resistance or the diastolic pressure. arteriodilators (Ca++ channel blockers) decrease this |
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Term
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Definition
| usually nitrate is released by eNOS (which uses arginine), in the endothelial cells and diffused to the smooth muscles where it activates guanylyl cyclase to produce cGMP that dephosphorylates the myosin light chain = relaxation (can have an additive effect with sildenafil - viagra) |
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Term
| how do nitrates affect angina? |
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Definition
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Term
| how does nitrate affect platelet aggregation? |
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Definition
| dilation due to nitrates disallows platelet aggregation - which is why it is used for all 3 kinds of angina |
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Term
| can nitrates also dilate arterioles? |
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Definition
| yes, nitrates do dilate arterioles as an effect that increases with dose. this *will decrease afterload and BP |
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Term
| what is one effect of excessive dilation? |
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Definition
| reflex increase in heart rate |
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Term
| what nitrate prep is good for acute attacks? |
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Definition
| sublingual prep, b/c it is short acting, incurs less tolerance and rebound |
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Term
| what are the potential benefits of nitrates in tx of angina? |
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Definition
| decreases ventricular volume (decreased myocardial O2 requirement), decreased arterial pressure, decreased ejection time, vasodilation of epicardial coronary arteries (relief of coronary artery system), increased collateral flow (improved perfusion to ischemic myocardium), and decreased L ventricular diastolic pressure (improved subendocardial perfusion) |
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Term
| what are the potential deleterious effects of nitrates in tx of angina? |
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Definition
| reflex tachycardia (increased myocardial O2 requirement), reflex increase in contractility, and decreased diastolic perfusion time due to tachycardia (decreased coronary perfusion) |
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Term
| what are the 2 types of Ca++ channel blockers? |
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Definition
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Term
| what is the main effect of verapamil? |
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Definition
| verapamil directly affects the heart to slow HR and AV conduction (good thing) - reducing O2 consumption by slowing the heart/decreasing afterload. verapamil possesses both cardiac and vasodilator activity. |
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Term
| what is the main effect of nifedipine? |
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Definition
| nifedipine (such as dihydropyridines) is mainly a vasodilator that relaxes smooth muscle, so it can possibly cause reflex tachycardia and needs to be given w/caution to people already on nitrates |
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Term
| what are Ca++ channel blockers used for? |
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Definition
| variant and stable angina by their main antianginal effect: decreased afterload |
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Term
| what do verapamil/diltiazem do? |
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Definition
| vasodilate, decrease afterload. they will decrease HR, AV conduction, and myocardial contractility |
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Term
| what ADRs are associated with verapamil/diltiazem? |
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Definition
| high dose/toxicity will cause CHF. *if used in conjunction with beta blockers, excessive reduction of contractility/CHF are possible |
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Term
| when are verapamil/diltiazem used? |
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Definition
| for variant and stable angina, as well as fast atrial/nodal arrhythmia to slow HR/AV conduction |
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Term
| what are the other dihydropyridine class drugs along with nifedipine? |
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Definition
| amlodipine and nicardipine |
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Term
| what do the dihydropyridines do? |
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Definition
| the dihydropyridines such as nifedipine are arterior dilators |
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Term
| what are the dihydropyridines used for? |
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Definition
| nifedipine and other dihydropyridines (amlodipine and nicardipine) are used in stable angina and *especially variant/vasospatic angina |
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Term
| what are ADRs associated with the dihydropyridines? |
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Definition
| excessive vasodilation, causing: nausea, lightheadedness, dizziness, headache, tachycardia, and peripheral edema |
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Term
| what is the main difference between the dihydropyridines and verapamil? |
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Definition
| the dihydropyridines can trigger reflex HR (tachycardia) w/excessive dilation |
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Term
| how do Ca++ channel blockers affect exercise performance in angina pts? |
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Definition
| Ca++ channel blockers such as diltiazem can increase performance w/out increasing HR or BP |
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Term
| what are the key beta blockers? which is used more? |
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Definition
| metoprolol (beta 1 blocker) and propanolol (beta 2 blocker), metoprolol is used more b/c a lot of skeletal muscle has beta 2 so blocking them could cause some peripheral vasoconstriction |
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Term
| what are beta blockers used for in terms of the other antianginals? |
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Definition
| beta blockers such as metoprolol can block tachycardia reflexed by nitrates and Ca++ antagonists (nidedipine class) |
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Term
| what are beta blockers used for? |
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Definition
| unstable and stable angina |
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Term
| what is the effect of beta blocker administration? |
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Definition
| B-1 effect decreases HR (increases diastole), SV, and O2 consumption |
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Term
| what is one effect of nitroglycerine through reflexes? |
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Definition
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Term
| why might nitroglycerine produce headaches? |
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Definition
| it can cause meningeal vasodilation |
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Term
| what is a good drug for exercise-induced angina prophylaxis when acute nitroglycerin is no longer an efficient tx? |
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Definition
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Term
| what should always be used for acute angina attacks? prophylaxis? |
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Definition
| acute: nitro prophylaxis: Ca++ channel blocker or beta blockers |
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Term
| what is the antianginal effect of propanolol attributed to? |
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Definition
| block of exercise/reflex-induced tachycardia |
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Term
| what would Ca++ channel blockers and beta-blockers have an additive effect on? |
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Definition
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Term
| what drug will help with both stable angina and clotting? |
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Definition
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Term
| would increased HR exacerbate the effects of variable angina? |
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Definition
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