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132 Cards in this Set
- Front
- Back
What is CAD defined as |
>50% stenosis of any epicaridal coronary artery |
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what is CAD manifested by |
in most cases its manifested by chronic stbale angina |
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other causes of angina |
vasospasms, anemia, cocaine, aortic stenosis, cardiac myopathy ( hypertrophic/ diabetic) syndorme x, prinzemental angina, aortic dissection, pericarditis, thyrotoxicosis, esophageal disease, respiratory disease, msuculoskeletal biliary colic |
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what is included under the umbrella of CAD |
stbale angina, acs, heartfailure, sudden death and silent ischemia |
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what is included under acute coronary syndrome |
unstbaleangina, nstemi, stemi |
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what is syndorme x |
angina with signs assiciated with decreased blood flow but with normal arteries |
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PRINZIMENTAL ANGINA |
aka variant angina occurs in cycles due to vasospasms |
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risk factors for CAD |
smoking, diabetes, dyslipdemai, htn, bmi >25, diet, physical activity, family history first degree male relatives with CAD before 55 or female >65 |
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based onr isk factors for cad what is recomended to decrease risk for cad
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stop smoking, keep fasting blood sugar <100, keep cholesterol <200 without treatment, kepe htn <120/80 without meds, keep bmi <25, adhere to a DASH diet, exercise >150min/wee of moerate instensity or >75 min/week of high intensity |
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this determines myocardial oxygen demandf |
wall stress, heart rate, contractility wall stres is based on intraventricular pressure, ventricular volume and wall thickness |
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wall stress is a determinant oof myocardial oxygen demand, what detemrines wall stress |
intraventricular pressure, ventricular volume, wall thickness |
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these are the determinants of blood flow and myocardial oxygen supply |
coronary blood flow, duration of diastole
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this determines coronary blood flow |
perfusion pressure and duration of diastole |
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coronary blood flow in relation to vasculr resistance |
cornary blood flow is inversly related to coronary vascular bed resisitance. increase resistance decreases blood flow |
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this is a detemrinant of vascular tone |
arterial tone and venous tone |
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arterial tone detmerines what |
systolic wall stress..aka afterload |
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venous tone determiens what |
diastolic wall stress..aka preload |
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what ways do drugs relax smooth muscle |
increasing cGMP, decrease intracellular ca, stabalize or prevent depolarization of vascualr smooth muscle cell, increase cAMP in vasuclar smooth msucle |
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these drugs increase cGMP |
nitrates |
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these drugs decrease intracellular calcium |
CCB and bblocker |
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stabalize or prevent depolarization of smooth msucle cell drugs |
monoxidil |
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increase cAMP |
beta agonsit which is not used in angina |
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features of stbale angina |
substernal discomfort, provoked by stres or exeriton, relieved byrest or nitro |
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what is atypical angina |
2/3 features of stable angina |
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noncardiac chest pain |
meets 1 criteria of stbale angina |
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goal of treatemnt of cad |
prevent mi, cardiac death, and reduce symptoms with lifestly changes medical therapy and revasuclrizing |
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goal of medical therapy |
improve o2 supply, decrease o2 demand, limit devleopment of further atherosclerotic disease control exacerbating facotrs ( pain anemia), drugs |
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what kind of management will be benficil in stable angina |
medical management will be beneficial |
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benefit of pci |
greater short term an dlong term relief |
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when is PCI not reccomended |
low EF or high risk stress test |
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when do you consider surgicla treatment |
when failure 2-3 classess of antianginals |
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class 1 indications for cabg |
left main stenosis >50%, stenosis of proximal LAD and proximal circumflex >70%, 3 vessel disease and asymptomatic with mild/stable angina, 3 vessel disease with proximal LAD stenosis in pts woth poor LV function, 1-2 vessel an dlarge area oof visible myocardium in high risk patients with stbale angina, >70% proximal LAD with low EF or showing ischemia on noninvasive testing |
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othe rindications ( not class1 ) for cabg |
disableing angina, ongoign ischemia in the setting of NSEMI that is not resposnive to medication, poor LV function but with viable nonfucnitonign myocardium above anatomic defect that can be revascualrized |
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unstbale angina quaities |
res pain >20min, new onset angina, progressive, 50% have ekg changes |
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NSTEMI qualities |
elevated cardiac enzymes but no ekg changes, may have t wave inversion normal ST segment, may have trnasient st segment elevation but you may not catch it, elevation of ckmb or troponins, 50% have ekg changes |
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these ekg changes suggest cad |
q wave, st changes, t wave inversions |
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management of acs should focus on what |
risk stratification based on history angina characterisitcs physica exam and cardiac ezymes |
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this shows dynamic changes of heart |
serial ekg |
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when is a cardiac cath indicated |
recurrant acclerated angina despite medication, S&S heart falure, pulmonary edema or shock, new or worse MR, new LBBB, v tach |
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timi score |
risk for mortality with MI |
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before you do a stress test what must you ensure |
no angina for atleast 12 hours, positive enzymes should have test 72 hours after peak value |
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who qualifies for initial conservative therapy for acs |
low timi score, low grace score, intermediate risk who are epected to have the same outcome at direct invasive strategies |
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what is included in conservative therapy |
maximize medical management, nonstress test before discharge, |
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when is coronary angiography indicated |
high risk stress test, angina at low levels, EF <40% |
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who qualifies for initial invasive therapy for acs managmenet |
if enzymes are elevated, new st depression, hx of cabg or recet pci within 6 months, ef <40 dm, mild - mod renal insufficicny, high timi high grace score,low intermediate risk who repeated acs presentation despite appropriate therapy |
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goal of medical treatment of UA/ NSTEMI |
reduce ischemia by decreasing demand, improve perfusion, prevnet thrombus |
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med classes for UA/NSTEMI |
antiplatelete, anticoagulant, antianginal, o2 |
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when would you do a cabg in UA/NSTEMI |
significalt left main, 3 vessels with lv dysfucniton, 2 vessels with proximal LAD and complicated disease |
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occurs within first hour of stemi |
v fib |
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treatment of stemi |
rapid recognition, ekg within 10 min, cardiac enzymes cbc coags bmp including magnesium, type and screen, ekg, identify candidates for reperfusion, relief pain, treat hypotension, pulmonary edema or arrythmias, treat sats <90, mecahnical vent to decrease work of breathing and decrease myocardial demad, serial ekg, |
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mortality is directly related to |
ischemia time |
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these medication classes are given in all stages of cad |
antiplatelt, bblocker, nitrate |
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CAD stable angina drugs |
anitplatelete, bblock, ccblock, nitrate ace inhibitor ranalozine statis |
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unstabel angina nstemi drug classess |
antilatelte anticoagulat bblock nitrate ace inhibitor ccblocker statin |
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stemi drugs classess |
antiplatete anticoagulat nitrates bblcok morphine thrombolytic |
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this medication is onl given in stemi |
thrombolytic |
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this medication is not given in stemo |
ccblockers |
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when do antiplateletes start working and how long do they last |
within minutes, last the life of the platelete |
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how do anitplateltes work |
block platelete aggregation by inhibiing synthesis of thomboxane a2 |
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how does aspirin work |
irreversibel inhibit platelete COX - lasts th elife of the platelete |
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aspirin naive dose |
325 than 81 daily |
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lowest aspirin dose that prevents mi |
75mg |
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aspirin doe for acute mi |
lowest dose is 160 |
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aspirin is also good in what disorder |
storke |
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psy12 inhibitor |
clopidogrel |
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what cad classess is clopidogrel used for |
unstbale angina, NSTEMI used iwth aspirin |
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plavix dose for NSTEMI |
300 followed by 75 WITH aspirin |
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plavix dose fot STEMI |
600 loading than 75 a day for 12 months WITH aspirin |
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plavix dose for recent MI or storke or PVD |
75mg |
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AE of prasurgrel |
causes more leeding |
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dose of prasurgrel |
60 loading than 10mg for 12 months |
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this medication reduces risk of death mi cva and stent thrombosis compared to clopidogrel |
ticagrelor |
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thises drugs are gp2b3a antagonist |
abciximab ( reopro), eptifibatide ( integrelin) tirofiban (aggrastat) |
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how do gp2b3a drugs work |
blocks interaction between platelte and fibronogren, targets final pathway in platelete aggregation |
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these drugs are for high risk patiens with refractory UA/NSTEMI |
gp2b3a antagonist |
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side effect of gp2b3a antagonist |
thrombocytopenia and increase drisk of major bleeidng esp with plavix |
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first line therapy |
bblocker |
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how do bblocker work |
reduce o2 demand by decreasing hr, bp, contractility |
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what happens when you decrease hr |
increas diastolic perfusion time which increases coronar perfusion |
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this drug ecreases mortality of patients with stbale andina and hx of mi |
bblockers |
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carvedilol property |
vasodilates as well |
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this drug is good for those with low ef |
carvedilol |
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low dose b1 selective drugs |
metoprolol atenolol |
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advantage of beta 1 antagonist |
less likly to cause bronchospasns or exacerbate peripheral vascular disease |
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when givin bblocker what shoudl your target hr be |
resitn g 50-60btm or exercise 90-100 |
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adver effect of bblcokers |
bronchospams posturla hypotension claudiction masking of hyperglycemia |
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abrupt wthdrawl of bblockers can cause |
angina mi arrythmias |
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contriindication to giving bblocker |
heart fialure, bronchospams, ashtma, av nodal block severe peripheral vascialr disease, sick sinus syndorme |
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how do nitrates wokr |
increase venous capacitance which reduces ventricular volume and pressure, |
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all patients should be presceribed htis medication to abort angina |
siblingual or aersol nitroglycerine |
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what to do with chornic therpay of nitrates |
12 hour nitrate free interval |
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dosage and titration of nitrate |
initial 5mc up to 10-200mcg, titrate 5mc every 3-5 minuts until response, if no resposne if no response in 20 mcg than increments of 1- or greater |
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continuus exposure of nitrates cancause what |
tacyphylaxis and decrease coronary eprufsion time that is why we need a nitrate free interval |
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adverse effect of nitrates |
headahce, flushign hypotension syncope |
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this medication is for refractory chest pain |
morphine |
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how does morphine work |
decrease o2 consption by decreasing catecholamines |
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what do ccbloeker do |
antianginal form direct coronary vasociation, redusces vascualr resistance decreases calcium avaiable in cells which depressess contractility |
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agent of choice for pts who can not toelrate bblcokers |
ccblockers |
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dihydropyridine ccblocker drugs |
nicardipines, amlodipine nifedipines end in pines |
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nondihydropyridine ccblocker |
verpimil and diltiazem |
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who is nifedipine contraindicated in |
immediate release is CI in pts with CAD UA or prior MI |
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side effect of dihydropyridine |
peripheral edema palpitations msucle crmaps sexual dysfucntion |
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potent coronary and peripherla vasodilators |
ccblcoekr esp dihydropyrdines |
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qalities of nondihydropyridines |
negative inotrpe (contractility) negative chronotrope (rate) negative domotrope ( conduction) |
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which class of ccblocker are more portent |
nondihydropyridies |
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qualities of nondihydropyridines |
negative inotrope, negative chronotrope, negative domotrope, mroe portnet, selective blocks tacycarida in av node |
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side effect of nondihydropyridines |
gingival hyperplasia, constiaption, bradycardia, hypotension, peripheral edema, 1,2,3 av block |
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ace inhibitors are used in what classess |
stabel unstable and nstemi |
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who will benefit from ace inhibitor |
acs and LV <40%, lv dysfuncito, htn, diabetes |
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these medications can be use dif pt cnat toelrate ace inhibitors |
ARBS - sartans |
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anticoagulant are used in which acs |
unstbael stemi and nontemi not for stable |
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indirect thrombin inhibitor drugs |
ufh, lmwh fondaparinaux, |
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hwo doe ufh and lmwh work |
minimize thormbus formaiton bu inhibiting factor 2a and xa |
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dose for herpatin |
60u/kg bolus than 12-14 u/kg/hr |
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benefit of lovenox |
doesnt need ptt |
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prefered for patients goign to cath lab |
can be turned off quickly |
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synthetic polusaccaride |
fondaparinaux atrixa |
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how doe sfondaparinaux work |
selective inhibitor of factor xa, HIT unliekly, doesnt effect ptt less risk fo major bleeding, less combined death from mi or refractory ischmea, |
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cons of fondaparinaux |
associated with catheter related thrombosis, pts undergoign pci must also get UFH |
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direct thrombin inhibitor |
bivalrudin angiomax |
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hwo is bivalrudin given |
in conjusntion with aspirina dn clopidogrel, given to pts with HIT only for STEMI |
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greatest benefit and use of bivalrudin |
for pts clinically and by ekg and st elevation and lbbb avebest outcmes esp when given within 6 hours after symtpomatic onset of acute mi |
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streptokinase moa |
protein that combines the proactive activator plasminogen catalyes conversion of inactive palsminogen to plasmin generlaized thormboytics |
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clot specific thombolytics |
recombinant tissye plasminogen acitvato like alteplase and reteplase |
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qualities of alteplase |
12mg iv bolu for first hour than 0.75mg/kg over 30 min, max is 50mg |
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how is reteplase given |
10u iv x 2 seperated 30 min apart |
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asolute contraindications to thormbolytics |
hx of ich, ischemic storke <3 months, known cv lesions, chi, aortic dissecton, severe uncontrolled htn, acite bleeding actue pericarditis |
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relative contraindications ot thrombolytics |
prior ischemc stroke >3 months, allergy or perioveiosu exposure to streptokinase >5 days, recent intracrnaial blood, prolong tauma cpr>10 min, active pud, noncomressible vascular puncture, severe menstural bleeding, Hx intraocular bleeding, pregnancy |
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metabolic modulators |
ranolazine |
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qualities of ranolazine |
changes in myocardial energy metbaolism form fatty acd to glucose, increase atp efficacy in ischemic tissue |
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direct bradycardia agents |
ivaradine |
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qualities of ivabradine |
selective Ix sodium channel blocker, reduces cardiac rate by inhibiting hyperpolarizaiotn - activated sodium channel in the SA Node |