Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
94 Cards in this Set
- Front
- Back
|
What defines CAD |
>50% stenosis of any epicardial cornoary artery |
|
|
how is CAD manifested |
chronic stbale angina |
|
|
other causes of angina |
vasospasms, anemia, cocaine, aortic stenosis, cardiac myopahties weather hypertrophic or diabetic, syndorme x, HCM prinzimentla angina aortic dissection pericarditis thyrotxicosis esophageal disease bilary colic respratory disease musculoskeletal |
|
|
what fall under the umbrella of CAD |
stbale angina, acute coronary syndrome heart failure sudden death adn silent ischemia |
|
|
what is included in acute coronary syndrome |
unstable angina nonstemi and stemi |
|
|
risk factors for CAD |
smoking, DM, dyslipidema, htn, bmi, dash diet, phsycial activity family history |
|
|
based on risk facotrs what is recommended to prevent CAD |
no smoking, keep fastic bs <100, kepe cholesteorl <200 without meds, keep htn <120/80 without meds, bmi <25kg/m2, DASH diet, >150 min a week of moderate activity or >75min week of high intensity activity |
|
|
based on family history risk facotr for CAD |
first degree male with CAD before 55 or female before 65 |
|
|
determinants of myocardial o2 demand |
wall stress heart rate and contractiltiy |
|
|
included in wall stress |
intravascular presure, ventircular volume wall thickenss |
|
|
detemrinants of blood flow and myocardial o2 supply |
coronary blood flow duration of diastole |
|
|
what detemrines coronary blood flow |
perfusion pressur and duration of diastole, inversely proprotional to coronary vasucalr bed resistance, increase resistance = decrease blood flow and vice versa |
|
|
detemrineants of vasculr tone |
arterial tone ( afterload) venous tone ( prelaod) |
|
|
arterial tone detemrines what |
systolic wall stress |
|
|
venous tone detemriens what |
diastolic wall stress |
|
|
ways drugs are used to relax smooth msucle |
increasecGMP, decrese intracellular calcium, stbalize or prevent deporlaiation of vascualr smooth msucle, increase cAMP |
|
|
these drugs increase cGMP |
nitrates |
|
|
these drugs decrease intrcellular calcium |
CCB, BBlockers |
|
|
these drugsstabalize or prevent depolazirng of vascualr smooth muslce |
minoxidil |
|
|
these drugs icrease cAMP |
b2 agonist but it is not used in angina |
|
|
features of stable and typical angina |
substenral discomfort, provoked by stress or exeriton and relieved by rest or nitro |
|
|
atypical angina |
has 2/3 symtoms of stable angina |
|
|
medica treatment for stbale anginal |
improve o2 supple decrease demand, limit furhter atherosclerosis controle xacerbating fctors lke pain and anemia |
|
|
drugs used in stbale angina |
anitpaltelte, beta antagonist, ccb, nitrate ranolazine statins |
|
|
in stbale angina this is going to be very beneficial |
medicaiton management. almsost similat to revascualrization |
|
|
when will PCI not be indicated |
low EF or high risk stress test have better outcomes with CABG |
|
|
who is CABG good for |
complex diffuse disease |
|
|
when do you consider surgicla treatment in stbale angina |
2-3 drug classess have failed |
|
|
class1 indication for cabg |
left main stenosis >50%, stenosis of proximal LAD and proximal circumflex >70%, 3 vessel and asymtpomatic with mild/stable angina, 3 vessl with proxmial LAD stenosis in pts with poor LV, 1-2 vessels and a large area of visible myocardium in high risk pts with stable angina, >70% proximal LAD with EF < or showing oischmeia on nninvasive testing |
|
|
othe rindications of CABG not included in class1 |
disabeling angina, ongoing ischemic in setting of NSTEMI that is not ersponding to meds, poor lv with viable nonfuncitoning myocardium above anatomic defect that can be revascularized |
|
|
qualities of unstbale angina |
rest pain >20 min, new onset nagina, progressive nagina 50% have ekg changes |
|
|
NSTEMI qualities |
elevation in caridac enzyme nit no ekg changes for MI, have t wave unversion normal st segment, may have transient ST elevation that you dont cnathch, elevation of CKMB OR Troponin, 50% have ekg changes |
|
|
these ekg changes suggest CAD |
q waves, st changes t wave inverisons |
|
|
management of ACs shoudl focus on what |
risk stratification based on history andgina characteirstic phsycial exam ekg and cardiac enzyes |
|
|
shoes dynamic ischemic changes |
serial ekg |
|
|
what is cardiac catheter indeicated for |
recurrent accelrated angina despite meds, S&S shock heart failrue or pulmoanry edema, new or worse MR, new lbbb, v tacy |
|
|
timi score |
risk for mortality with mi |
|
|
before performing a stress what should you ensure |
no angina atleast 12 hours and make sure positvie enzyes shoudl have pharm stress test72 hours after peak of enzymes |
|
|
initial conservative strategy |
low tim low grace intermediate risk maximize medical therapy coronary angiography in pts who deveop acs features |
|
|
coronary angiography test in which patients |
high risk stress test, angina at low levls of stress EF <40% |
|
|
initial invasive therapy |
plan for cornary angiogrpahy with intent to revasucalrize in 12-24hrs, elevated enzyes new st depress hx of cabg or reent pci within 6months, ef <40% DM mild -mod renal insufficiency, high timi high grace low intermediate risk who repreated acs presentaiton despite therapy |
|
|
medial treatemnt of ua / nstemi |
reduce iscemai by decreasing demands, improve perfusion prevent thrombus anitplatelte anticoagulant anitangila o2 |
|
|
CAGB in UA r NSTEMI |
significant left main cad, 3 vessels with lv dysfunciton 2 vessles with proximal LAD and complicated idsease |
|
|
this occues within 1 hour of symtooms onset |
vfib |
|
|
treatmetn if stemi |
rapid recognition and diagnosis, coordianted mobiization of resources prompr reprofusion ekj ithin 10 min, st elevation in 2 or more anatomically continguous leads, cardiac enzyes cbc coags bmp with mg ekg identify candidates for reprofusion relieve pain treat hpotension pulmoary edema or arrythmia, treat <sats, mechanical vent to decrease work of breahting and reduce o2 demand, serial ecg, tele |
|
|
mortlaity wiht acs is direclty related to what |
uschemic time |
|
|
med classes given in all stages of cad |
antiplatelet, beta blockers and nitrates are given in all stages |
|
|
* CAD/ stable angina
drug classes |
* Antiplatelet
* Bblocker * Cc blocker * Nitrate * Ace inhibitor * Ranolazine * Statin |
|
|
unstable angina and nstemi drug classes |
* Antiplatelet
* Anticoagulant * Beta blocker * Nitrate * Ace inhibitor * Cc blocker * Statin |
|
|
stemi drug classes |
* Antiplatelet
* Anticoagulant * Nitrate * Bblocker * Morphine * Thrombolytic- only under stemi |
|
|
antiplatelete quality |
* Within minutes and lasts the life of the platelet
* MOA - inhibit synthesis of thromboxane A2 |
|
|
aspirin qulaities |
* Aspirin naïve - give 325 than 81 daily
* Lowest dose to prevent MI is 75mg * For acute MI lowest dose is 160 * Also good for stroke |
|
|
clopidogrel qualities |
* For unstable angina or NSTEMI in combination with aspirin
* For NSTEMI- 300mg followed by 75 daily WITH aspirin 75-325 * For STEMI- 600mg loading than 75mg/day for 12 months WITH aspirin * Recent MI stroke or PVD- 75 daily |
|
|
prasurgrel dose |
60mg load than 10mg for 12 months |
|
|
ticagrelor qualities |
* Higher risk for bleeding
* Reduces risk of death MI CVA and stent thrombosis compared to clopidogrel * If given with ASA dose less than 100 |
|
|
GP2b3a drugs |
* Abciximab(reopro)
* Eptifibatide (integrelin) * Tirofiban (aggrastat) |
|
|
how do gp2b3a work |
* Blocks interaction between platelet and fibrinogen
* Targets final pathway for platelet aggregatio |
|
|
who should use gp2b3a |
* For high risk patients with refractory UA/NSTEMI
|
|
|
side effect of gp2b3a |
* Increased risk of major bleeding esp. in combination with clopidogrel
* Can cause thrombocytopenia |
|
|
bblocker qualities |
* First line therapy
* Reduces o2 demand by decreasing hr, bp, and contractility * Decrease HR= increase diastolic perfusion time = coronary perfusion * Decrease mortality in pts with stable angina and hx of MI * Selection is based on selectivity for b1 receptors |
|
|
carvedilol properties |
* Good for Low EF
|
|
|
b1 selective drugs |
metoprolol atenolol |
|
|
qualities of b1 selective drugs |
less oily to cause bronchospasms or exacerbate peripheral vascular disese titrate for resting hr 50-60 and exercise ate 90-100 |
|
|
bblocker adverse effect |
* Bronchospasms
* Postural hypotension * Claudication * Angina * Mi * Arrhythmia |
|
|
contraindication of bblcoker |
* Evidence of heart failure
* asthma * Av nodal block * Severe peripheral vascular disease * Sick sinus syndrome |
|
|
nitrates quality |
* MOA- increase venous capacitance which reduces ventricular volume and pressure
* Improves sub endocardial perfusion * Improves collateral flow afterload and coronary vasodilation * All patients should be prescribed sublingual or aerosol nitroglycerine to abort angina episodes * Includes nitroglycerine and isosorbide * Chronic therapy should incorporate asymmetric dosing with 12 hour nitrate free interval |
|
|
nitroglycicerin iv dosing |
* Initial 5mcg/min
* 10-200mcg * Titrate 5mcs/min with increase every 3-5 min until response * If no response seen in 20mcg increments of 10 and later 20 can be used |
|
|
adverse effect of nitroglycienr |
* With all nitrate preparation
* Nitrate free interval of at least 10-12 hrs can enhance treatment efficacy * Headache * Flushing * Hypotension * Syncope |
|
|
morphine qualities |
* Relief of anginal pain
* For refractory chest pain * By decreasing circulating catecholamine's * Catecholamine's speed everything up so by blocking this we decrease o2 consumption |
|
|
calcium channel blocker qualities |
* Antiangina from direct coronary vasodilation
* Reduces vascular resistance * Depresses contractility * Agent of choice for pts unable to tolerate bblocker * For stable angina unstable angina and NSTEMI * Not for stemi |
|
|
agent of choice for pt who cant tolerate bblocker |
ccblockers |
|
|
dihydropyridines |
pines line nifedipine nicardipine amlodipine |
|
|
non dihydropyridines |
verapamil and diltiazem |
|
|
dihydropyridine qualities |
blocks smooth msulce calcium channes and are less dependant on the heart potent coronary and peripheral vasodilators, peripheral edema palpitatios muscle cramps sexual dysfucntion |
|
|
nifedipine cautions |
* Nifedipine - immediate release preparation should be avoided in pts with CAD UA or prior MI because of concerns about excess cardiovascular morbidity and mortality
|
|
|
nondihydropyridine quality |
* Negative inotrope (contractility) choronotrope (rate) and dromotrope (conduction) effect
* More portent * Gingival hyperplasia * Constipation * Bradycardia * Hypotension * Peripheral edema * 1,2,3 av block |
|
|
ace inhibitor quality |
* Stable unstable and nstemi
* LV <40% particularly for these patients with lv dysfunction * Htn * Diabetes |
|
|
can be used in patients who cannot tolerate ace |
arbs |
|
|
anticoagulant quality |
* Not really for stable angina
* Antithrombotic effect by separating protein and antithrombin |
|
|
how does ufh and lmh work |
minimize thrombus formation by inhibiting face 2a and Xa |
|
|
ufh andlmwh qualities |
* Risk for HIT
* Heparin 60U/kg bolus than 12-14 units/kg/hr * Doesn’t need ptt checked * UFH preferred for pt going to cath lab can be turned off quickly |
|
|
fondaparinaux qualities |
synthetic polysaccharide that contianes the ame pentasaccaride ofund in ufh and lmwh. selective inhibitor of factor xa, hit unlikely, does teffect ptt, less risk of major bleeding, compared to lovnox less combined death mi or refactory ischemia, ass with catheter related thrombosis so pts going pci must get ufh |
|
|
bivalrudin qualitis |
* In conjunction with ASA and clopidogrel in pts presenting with UA/NSTEMI
* Given to pts with HIT * A direct thrombin inhibitor * Given with aspirin and clopidogrel |
|
|
who uses thrombolytic therapy |
* Only for STEMI
* For pts with MI clinically and by ecg and st elevation and LBBB have the best outcomes * Greatest benefit when it is given early within 6hours after symptomatic onset of acute MI |
|
|
streptokinase qualities |
protein that combines the proactivator plasminogen, catalyzs conversion of inactive plasminogen to active plasmin, load 25000-100000 u/hr for 24-72 hours, generalized thrombolytic, risk for hypotension which responds to volume |
|
|
urokinase |
* Human enzyme synthesized by kidney that directly converts plasminogen to active plasma
* Load 300,000u over 10 min than 300,000u/h for 12 hrs |
|
|
recombinant tissue plasminogen activator |
* Plasminogen can be activated endogenously by tissue plasminogen activator
* Activate plasminogen that is bound to fibrin which confines fibrinolysis to the formed thrombus and avoids systemic activation |
|
|
recombinant tissye plasminogen drugs |
alteplase tpa reteplase |
|
|
alteplase |
15mg iv bolus for first hour and then 0.75mg/kg over 30 min g max 50m |
|
|
reteplase |
10u iv x 2 separated by 30 min |
|
|
absolute contraindication for recombinant tissue plasminogen activator |
hx of ich/hemmorahging stroke, ischemic stokre <3 months, known cv lesiosn, chi <3months, aortic dissection,s evere uncontrolled htn, active bleeding or bleeding diathesis, acute pericaridits |
|
|
relative contraindication for tpa |
* Prior ischemic stroke >3 months
* Allergy or previous use of streptokinase >5day * Recent intracranial blood * Prolong traumatic cpr >10min * Active PUD * Non compressible vascular puncture * Severe menstrual bleeding * Hx intraocular bleeding * Pregnancy |
|
|
ranolazine |
metabolic moduator * Partial fatty acid oxidation inhibitor* Changes myocardial energy metabolism from fatty acid to glucose * Increase ATP efficacy in ischemic tissue |
|
|
direct bradycardia agent |
* Selective Ix sodium channel blocker
* Reduces cardiac rate by inhibiting the hyperpolarization- activated sodium channel in the sinoatrial node |
