Flashcards in Pharm Ischemic Heart Disease Deck (28)
-Nitroglycerin (Nitrostat, Nitroquick)
-Isosorbide dinitrate (Isordil)
-Isosorbide mononitratae (Imdur)
-Transdermal patch (NitroDur)
-nitrates decrease the O2 demand of the heart by:
1. decreasing arteriolar and venous tone (systemic and coronary)
2. decrease preload
3. decrease afterload
4. incrase O2 supply to the heart
4. decrease BP
Short Acting Nitrates
-when do you use these?
-how are they taken?
-used fro immediate relief of acute anginal sx.
-sublingual nitro tablets or spray, repeat in 3-5min if needed x3. Not great advice for everyone, requires a lot of patient education. Best advice is to take one and call 911.
-Severe volume depletion
-acute RV infarction (rely on high preload during this time)
-Recent meds for ED (Viagra, Levitra, Cialis)
Long acting nitrates
-first line monotherapy? Why or why not?
-how long does the blood need to be free of free nitrates/day?
-Not used as first line, usually used as and add on to other anti-angina drugs. This is because over time tolerance is developed to this medication and it no longer works, so we save this for last.
-The blood needs to be free of free nitrates for 8-10hrs/day.
-Isosorbide mononitrate (Imdur)***
-Transdermal patch (NitroDur)
-Metoprolol (Lopressor, Toprol)
-Ischemic Heart disease
--NSTEMI (non-elevated ST elevation MI)
*negative inotrope and chronotrope
-decreases HR, force of contraction, AV conduction rate.
What is first line therapy for treatment of chronic angina?
What is the only anti-anginal agent proven to prolong life in patients with CAD post MI?
*most common: Metoprolol (Lopressor)
-decompensated heart failure (in midst of acute exacerbation)
-may worsent with Prinzmetals angina d/t leaving alpha 1 receptors unopposed. (normally, alpha and beta try to balance one another out, if you block the betas the alphas party b/c the betas are gone, this makes angina worse)
-mask hypoglycemia sx (tachycarida, sweating, confusion)
-abrupt withdrawl (3 days)
Calcium Channel Blockers
-Nifedipine (Adalat, Procardia)
-Calcium channel blockers decrease myocardial O2 demand by:
1. decrease preload
2. decrease heart rate (verapamil, diltiazem)
3. decrease blood pressure
4. decrease contractility (Verapamil, diltiazem)
5. increase O2 supply
6. cause coronary artery vasodilation
Which of the Ca2+ channel blocker medication is only approved for use in CHF? WHY?
-Dihydropyridines; Amlodipine (Norvasc)
-it does not have the negative inotropic(contractility) or chronotropic(rate) effects that the other calcium channel blockers have.
SE of Calcium CHannel Blockers
-Bradycardia (nondihydropyridines; cardizem & verapamil)
-CI to nondihydropyridines (verapamil, cardizem)
-CI for all calcium channel blockers
-systolic CHF d/t lower EF
-AV block or bradycardia.
CI All Ca2+:
-pt w/ peripheral edema or hx of hypotension
-multiple drug interactions* caution* (cleared through the liver, CYP enzymes)
Define each of the following:
Antiplatelets: drugs interfere either with platelet adhesion and/or aggregation. (prevent initial clot formation)
Fibrinolytic: degrade fibrinogen/fibrin (eliminate formed clots)
Anticoagulants: inhibit clotting mechanism ( prevent progression of thrombosis)
*last two are IV, used in setting of MI
-inhibits cyclooxygenase that then inhibits the synthesis of thromboxane A2, a potent stimulator of platelet aggregation.
*irreversible platelet inhibitor
Absorption peak is 1Hr
Dosing Recommendations of Aspirin
-primary prevention of CVA/MI
-Secondary prevention of CVA/MI (already had one)
-Acute coronary syndrome (in the midst of having an MI)
Primary prevention: 81mg/day
Secondary: 325mg/day acutely(several months)
Acute syndrome: 325mg chewed x1
SE of Aspirin
(H2 Blockers or proton pump inhibitors may decrease gastritis and GI bleeding, also administer with food to decrease GI disturbnace)
-tinnitus at high doses
-resistance (dont metabolize and has no effect on platelet aggregation)
How many days pre-op should you stop taking aspirin?
-inhibits the binding of fibrinogen to activated platelets by blocking P2Y12 receptor site, as a result the GP IIb/IIIa receptor is not activated. (which is the binding site for fibrinogen, von Willebrand factor)
-resulting in the blockage of platelet aggregation and prevention of thrombosis
-do these require loading dose?
-post intracoronary stent placement
*no indication for primary prevention of MI/CVA unless the patient is allergic to aspirin
-yes, these drugs require a loading dose. Plavix has the slowest time to detection in the blood of all three medications
-not recommended in whom?
-SOB w/ Ticagrelor
Not recommended in LOP. Greater than 75 or weigh less than 132lbs.
-No antidote for the reversal of the medication in the event of significant bleeding.
-Route of administration
examples: Platelet Antagonists
acute coronary syndrome, percutananeous coronary intervention
-onset of action
-yes Reversible, platelet function is restored to normal 4-8hrs after discontinuation of infusion
-thrombocytopenia (reversible once discontinuation of med_
Enoxaparin (Lovenox) (LMWH)
-acute MI situations only.
-what lab do we base our medication adjustments on?
-activation of anti-clotting factors (especially ATIII)
-indirect thrombin inhibitor
-Base med adjustments on the PTT
-anaphylaxis and recent major surgery
-bleeding, hypersensitivity rxn, transaminitis, heparin induced thrombocytopenia (HIT)
-route of admin
-inhibits Xa and ATIII
*indirect inhibitor of thrombin
used in MI, IV dose followed by SQ dose.
-Route of administration
-direct thrombin inhibitor (IIa), immediate onset of action.
-IV infusion only
-CI: Allergy or recent major surgery or trauma
-tPA: Alteplase (Activase); Reteplase (Retavase); Tenecteplase (TNKase)
-convert plasminogen into plasmin to break down fibrin strands.
-Limb threatening ischemia