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132 Cards in this Set

  • Front
  • Back

What is CAD defined as

>50% stenosis of any epicaridal coronary artery

what is CAD manifested by

in most cases its manifested by chronic stbale angina

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

what is included under the umbrella of CAD

stbale angina, acs, heartfailure, sudden death and silent ischemia

what is included under acute coronary syndrome

unstbaleangina, nstemi, stemi

what is syndorme x

angina with signs assiciated with decreased blood flow but with normal arteries

PRINZIMENTAL ANGINA

aka variant angina occurs in cycles due to vasospasms

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

based onr isk factors for cad what is recomended to decrease risk for cad


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

this determines myocardial oxygen demandf

wall stress, heart rate, contractility


wall stres is based on intraventricular pressure, ventricular volume and wall thickness

wall stress is a determinant oof myocardial oxygen demand, what detemrines wall stress

intraventricular pressure, ventricular volume, wall thickness

these are the determinants of blood flow and myocardial oxygen supply

coronary blood flow, duration of diastole


this determines coronary blood flow

perfusion pressure and duration of diastole

coronary blood flow in relation to vasculr resistance

cornary blood flow is inversly related to coronary vascular bed resisitance. increase resistance decreases blood flow

this is a detemrinant of vascular tone

arterial tone and venous tone

arterial tone detmerines what

systolic wall stress..aka afterload

venous tone determiens what

diastolic wall stress..aka preload

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

these drugs increase cGMP

nitrates

these drugs decrease intracellular calcium

CCB and bblocker

stabalize or prevent depolarization of smooth msucle cell drugs

monoxidil

increase cAMP

beta agonsit which is not used in angina

features of stbale angina

substernal discomfort, provoked by stres or exeriton, relieved byrest or nitro

what is atypical angina

2/3 features of stable angina

noncardiac chest pain

meets 1 criteria of stbale angina

goal of treatemnt of cad

prevent mi, cardiac death, and reduce symptoms with lifestly changes medical therapy and revasuclrizing

goal of medical therapy

improve o2 supply, decrease o2 demand, limit devleopment of further atherosclerotic disease control exacerbating facotrs ( pain anemia), drugs

what kind of management will be benficil in stable angina

medical management will be beneficial

benefit of pci

greater short term an dlong term relief

when is PCI not reccomended

low EF or high risk stress test

when do you consider surgicla treatment

when failure 2-3 classess of antianginals

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

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

unstbale angina quaities

res pain >20min, new onset angina, progressive, 50% have ekg changes

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

these ekg changes suggest cad

q wave, st changes, t wave inversions

management of acs should focus on what

risk stratification based on history angina characterisitcs physica exam and cardiac ezymes

this shows dynamic changes of heart

serial ekg

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

timi score

risk for mortality with MI

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

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

what is included in conservative therapy

maximize medical management, nonstress test before discharge,

when is coronary angiography indicated

high risk stress test, angina at low levels, EF <40%

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

goal of medical treatment of UA/ NSTEMI

reduce ischemia by decreasing demand, improve perfusion, prevnet thrombus

med classes for UA/NSTEMI

antiplatelete, anticoagulant, antianginal, o2

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

occurs within first hour of stemi

v fib

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,

mortality is directly related to

ischemia time

these medication classes are given in all stages of cad

antiplatelt, bblocker, nitrate

CAD stable angina drugs

anitplatelete, bblock, ccblock, nitrate ace inhibitor ranalozine statis

unstabel angina nstemi drug classess

antilatelte anticoagulat bblock nitrate ace inhibitor ccblocker statin

stemi drugs classess

antiplatete anticoagulat nitrates bblcok morphine thrombolytic

this medication is onl given in stemi

thrombolytic

this medication is not given in stemo

ccblockers

when do antiplateletes start working and how long do they last

within minutes, last the life of the platelete

how do anitplateltes work

block platelete aggregation by inhibiing synthesis of thomboxane a2

how does aspirin work

irreversibel inhibit platelete COX - lasts th elife of the platelete

aspirin naive dose

325 than 81 daily

lowest aspirin dose that prevents mi

75mg

aspirin doe for acute mi

lowest dose is 160

aspirin is also good in what disorder

storke

psy12 inhibitor

clopidogrel

what cad classess is clopidogrel used for

unstbale angina, NSTEMI used iwth aspirin

plavix dose for NSTEMI

300 followed by 75 WITH aspirin

plavix dose fot STEMI

600 loading than 75 a day for 12 months WITH aspirin

plavix dose for recent MI or storke or PVD

75mg

AE of prasurgrel

causes more leeding

dose of prasurgrel

60 loading than 10mg for 12 months

this medication reduces risk of death mi cva and stent thrombosis compared to clopidogrel

ticagrelor

thises drugs are gp2b3a antagonist

abciximab ( reopro), eptifibatide ( integrelin) tirofiban (aggrastat)

how do gp2b3a drugs work

blocks interaction between platelte and fibronogren, targets final pathway in platelete aggregation

these drugs are for high risk patiens with refractory UA/NSTEMI

gp2b3a antagonist

side effect of gp2b3a antagonist

thrombocytopenia and increase drisk of major bleeidng esp with plavix

first line therapy

bblocker

how do bblocker work

reduce o2 demand by decreasing hr, bp, contractility

what happens when you decrease hr

increas diastolic perfusion time which increases coronar perfusion

this drug ecreases mortality of patients with stbale andina and hx of mi

bblockers

carvedilol property

vasodilates as well

this drug is good for those with low ef

carvedilol

low dose b1 selective drugs

metoprolol atenolol

advantage of beta 1 antagonist

less likly to cause bronchospasns or exacerbate peripheral vascular disease

when givin bblocker what shoudl your target hr be

resitn g 50-60btm or exercise 90-100

adver effect of bblcokers

bronchospams posturla hypotension claudiction masking of hyperglycemia

abrupt wthdrawl of bblockers can cause

angina mi arrythmias

contriindication to giving bblocker

heart fialure, bronchospams, ashtma, av nodal block severe peripheral vascialr disease, sick sinus syndorme

how do nitrates wokr

increase venous capacitance which reduces ventricular volume and pressure,

all patients should be presceribed htis medication to abort angina

siblingual or aersol nitroglycerine

what to do with chornic therpay of nitrates

12 hour nitrate free interval

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

continuus exposure of nitrates cancause what

tacyphylaxis and decrease coronary eprufsion time that is why we need a nitrate free interval

adverse effect of nitrates

headahce, flushign hypotension syncope

this medication is for refractory chest pain

morphine

how does morphine work

decrease o2 consption by decreasing catecholamines

what do ccbloeker do

antianginal form direct coronary vasociation, redusces vascualr resistance decreases calcium avaiable in cells which depressess contractility

agent of choice for pts who can not toelrate bblcokers

ccblockers

dihydropyridine ccblocker drugs

nicardipines, amlodipine nifedipines end in pines

nondihydropyridine ccblocker

verpimil and diltiazem

who is nifedipine contraindicated in

immediate release is CI in pts with CAD UA or prior MI

side effect of dihydropyridine

peripheral edema palpitations msucle crmaps sexual dysfucntion

potent coronary and peripherla vasodilators

ccblcoekr esp dihydropyrdines

qalities of nondihydropyridines

negative inotrpe (contractility) negative chronotrope (rate) negative domotrope ( conduction)

which class of ccblocker are more portent

nondihydropyridies

qualities of nondihydropyridines

negative inotrope, negative chronotrope, negative domotrope, mroe portnet, selective blocks tacycarida in av node

side effect of nondihydropyridines

gingival hyperplasia, constiaption, bradycardia, hypotension, peripheral edema, 1,2,3 av block

ace inhibitors are used in what classess

stabel unstable and nstemi

who will benefit from ace inhibitor

acs and LV <40%, lv dysfuncito, htn, diabetes

these medications can be use dif pt cnat toelrate ace inhibitors

ARBS - sartans

anticoagulant are used in which acs

unstbael stemi and nontemi not for stable

indirect thrombin inhibitor drugs

ufh, lmwh fondaparinaux,

hwo doe ufh and lmwh work

minimize thormbus formaiton bu inhibiting factor 2a and xa

dose for herpatin

60u/kg bolus than 12-14 u/kg/hr

benefit of lovenox

doesnt need ptt

prefered for patients goign to cath lab

can be turned off quickly

synthetic polusaccaride

fondaparinaux atrixa

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,

cons of fondaparinaux

associated with catheter related thrombosis, pts undergoign pci must also get UFH

direct thrombin inhibitor

bivalrudin angiomax

hwo is bivalrudin given

in conjusntion with aspirina dn clopidogrel, given to pts with HIT only for STEMI

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

streptokinase moa

protein that combines the proactive activator plasminogen catalyes conversion of inactive palsminogen to plasmin generlaized thormboytics

clot specific thombolytics

recombinant tissye plasminogen acitvato like alteplase and reteplase

qualities of alteplase

12mg iv bolu for first hour than 0.75mg/kg over 30 min, max is 50mg

how is reteplase given

10u iv x 2 seperated 30 min apart

asolute contraindications to thormbolytics

hx of ich, ischemic storke <3 months, known cv lesions, chi, aortic dissecton, severe uncontrolled htn, acite bleeding actue pericarditis

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

metabolic modulators

ranolazine

qualities of ranolazine

changes in myocardial energy metbaolism form fatty acd to glucose, increase atp efficacy in ischemic tissue

direct bradycardia agents

ivaradine

qualities of ivabradine

selective Ix sodium channel blocker, reduces cardiac rate by inhibiting hyperpolarizaiotn - activated sodium channel in the SA Node