CV_drugs

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Author:
simpson2209
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194243
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CV_drugs
Updated:
2013-01-22 00:00:43
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CV drugs
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CV drugs
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  1. Labetalol
    • Beta blocker with some alpha1 properties
    • Decrease myocardial O2 demand, slows HR, increases end diastolic volume
    • Nitrates can be coadministered to lower EDV
    • Used in stable post MI patients, HF, stable angina
    • Not in Prinzmetal's Angina: can worsen CA spasms
  2. Carvedilol
    • Beta blocker with some alpha1 properties
    • Decrease myocardial O2 demand, slows HR, increases end diastolic volume
    • Nitrates can be coadministered to lower EDV
    • Used in stable post MI patients, HF, stable angina
    • Not in Prinzmetal's Angina: can worsen CA spasms
  3. Organic Nitrates
    • Release NO or stimulate NO production
    • Converts Guanylyl cyclase to Guanylyl cyclase+
    • Converts GTP to cGMP
    • Converts Myosin LC-PO4 to Myosin LC which stimulates relaxation
    • Greatest affect on veins and large CA's
    • Autoregulation: normally dilates vessels in hypoxic areas
    • Non-selective dilation causes occluded vessels to lose flow to other ones (coronary steal). Does NOT occur with Nitroglycerin
    • Reduces platelet aggregation
    • Decreases preload (dilation of veins)
    • Decrease pulmonary pressures and heart size
    • Side effects: headache, reflex tachycardia, hypotension
    • When combined with beta blockers, block reflex tachycardia+increased FOC
  4. Isosorbide Dinitrate
    Oral organic nitrate, slow metabolism
  5. Ca Channel Blockers
    • Block L type calcium channels
    • DHP type: nifedipine: tonic block
    • verapamil/diltiazem: use dependent block
    • Used in exertional angina, vasospasm, arrhythmias, hypertension
  6. Nifedipine
    • DHP type, tonic block (non rapid depol tissues) of L type Ca channel
    • Act on peripheral vasculature-> vasodilitation
    • Small direct effect lowering HR+FOC
    • Pronounced reflex inc of HR and FOC by lowering afterload
    • Adding beta blockers can counter reflex tachy
    • Side effects: hypotension, headache, peripheral edema
    • Contraindicated in unstable angina
  7. Verapamil, diltiazem
    • Use dependent Ca channel block: binding sites are inside channel
    • Act on tissues that are more active/rapid
    • Directly decrease HR, conduction velocity, FOC
    • Beta blockers can cause excessive slowing of the heart
    • Can cause asystole, reduced CO, increased HF especially with beta blockers
    • Not to pts with sustained Vtach
    • Rapid toxicity
  8. Treatment guidelines for UA/NSTEMI
    • ASA/Asprin: immediately, indefinitely
    • Clopidogrel: if can't take ASAs
    • If underwent PCI: ASA+clopidogrel or IV GPIIb/IIIa inhibitor
    • Noninvasive: ASA+clopidogrel for 1-12 months + anticoags
  9. Dipyrimidole
    • Interferes with Ca accumulation, allows vasodilatation
    • Used in stress tests to induce vasodilatation
  10. Clopidogrel
    • Irreversible blocker of ADP receptor, inhibits ADP platelet activation pathway
    • Reduces risk of ischemic stroke, MI, vascular death in pts with prior MI
    • Better prevents arterial closure
    • Increased bleeding if combined with aspirin
    • Given post stenting 1-12 months
    • Long half life, avoid surgery for a few days after stopping
  11. Aspirin
    • Binds to COX, inhibitts production of thromboxane A2
    • Inhibits release of platelet granules and platelet aggregation
    • Side effects: bleeding, dizziness, ringing in ears
    • Increased ototoxicity if combined with furosemide or erythromycin
    • Used post MI, improves survival, also prevents re-occlusion after stenting
  12. Abciximab
    • Glycoprotein IIb/IIIa receptor inhibitor, final common pathway for platelet aggregation
    • Block binding of fibrinogen, VW factor, other adhesive ligands
    • Given after stenting/MI, preventing occlusions, unstable angina, acute coronary syndome, non Q wave/ST elevation MI
    • Given with thrombolytics to treat MI
  13. Unfractionated Heparin
    • Binds and increases activity of antithrombin
    • Antithrombin neutralizes: Thrombin (II), IXa, Xa, XIa, XXIIa, kallikrein
    • Given IV, rapid onset, continuous infusion
    • Monitor aPTT, heparin levels, Xa levels, active clotting time
    • Given for ACS, also to prevent DVT
    • Toxicity: bleeding, interactions with antihistamines, cephalosporins
    • Reversed with protamine
  14. Enoxaparin
    • Low molecular weight heparin
    • Selectively inhibits X, less effects on II (thrombin)
    • Equal efficacy as heparin, less frequent dosing, lower plasma binding: less need to monitor, dose independent clearance
    • Prevents DVT's PE's, given with aspirin, lower bleeding risk
  15. Warfarin
    • Inhibits synthesis of new II, VII, IX, X: inhibits synthesis by reducing oxidized vitamin K
    • Oral admin, long lasting 1/day
    • Highly protein bound, other drugs can displace it, cause toxicity/bleeding
    • Regular monitoring
    • Can't give a "loading dose"
    • Purple toe syndrome: protein C inhibition -> cutaneous necrosis from venous thrombosis
    • Dietary restrictions: keep vitamin K levels constant, changes can affect warfarin levels
    • Toxicity: give vitamin K/fresh frozen plasma
  16. Dabigatran
    • Directly inhibits thrombin, competitive, prevents thrombus formation
    • Oral, BID (2x/day)
    • Indicated for non-valvular afib to reduce stroke/emboli
    • Side effects: bleeding, GI pain
    • Unable to reverse effects
    • Contra: mechanical valves: can have strokes/thrombi
  17. Rivaroxaban
    • Indirectly inhibits thrombin
    • Oral, QD
    • Inhibits factor Xa, disrupts intrinsic and extrinsic coag pathways
    • Doesnt need monitoring
    • Used in DVT, PE, nonvalvular-Afib
    • Side effeccts: bleeding, hypersensitivity
    • No way to reverse effects
  18. tPA
    • Endogenously activates plasminogen -> plasmin to degrade fibrin
    • Needs to bind to plasminogen in presence of fibrin to have effect
    • More specific for breaking down existing clots
    • Early clots more than later clots with more platelets
    • Used in STEMI if cant get to cath lab
    • NOT in NSTEMI
  19. Streptokinase
    • Conformational change in plasminogen, makes it more accessible to TPA
    • Binds to any plasminogen even without fibrin: non specific fibrinolyitic
    • Contraindicated if active bleeding, CVA within 1 yr, previous streptokinase administration (antigenic rxn)
    • Side effects: reperfusion dysrrhythmias, antigenic, allergic rxns
  20. Furosemide
    • Loop diuretic, inhibits NaCl cotransporter in thick ascending limb, affects K concentrations
    • Given for Pulm edema, other edemas
    • Toxicities: Metabolic alkalosis, ototoxic, hyperuricemia
  21. Sprinolactone
    • K sparing diuretic, competitive aldosterone antagonist, similar to eplerenone
    • Interferes with Na/K exchange in distal tubule
    • Produces diuresis without compromising extracellular K levels, can cause hyperkalemia
    • Decrease mortality in pts with HF (given with B blockers, ACE inhibitors)
    • Not for pregnant women: Antiandrogenic, estrogenic effects
    • Eplerenone: more selective vs aldosterone
  22. Captopril, enalapril
    • ACE inhibitor
    • Prevents ANGI->ANGII conversion
    • Dec BP (Pre and afterload)
    • Enhances vascular endothelium patency, enhances bradykinin induced NO production
    • Prolong MI survival, reduce LV hypertrophy, improves LV function, reduce recurrent MI
    • Treat HTN, CHF, LV dysfunction post MI, atherosclerotic vascular disease
    • Side effects: cough/angioedema, hypotension, give ARB's instead
  23. Candesarten, Losarten, Irbesarten
    • ARBs: block ANG-II AT-1 receptor, AT-2 receptor still works
    • Well tolerated, no bradykinin vasodilitation benefit
    • Potent afterload reducer
    • Used for HTN, HF
    • Side effects: fetopathic potential (stop b4 2nd trimester), hyperkalemia
  24. Quinidinem Disopyramide Procainamide
    • Class 1A
    • Na Ca channel issues
    • Quinidine used in Brugada syndrome (genetic Na channel dysfunction in patients),
    • Can cause early afterdepol, cause torsades
  25. Lidocaine
    Class 1B: ischemic ventricular arrhythmias, Na channel blocker
  26. Propafenone
    1C Potent, not given to pts with structural heart disease
  27. Amiodarone
    • Class 2 and 3 effects, blocks K+ channels, serious side effects
    • Safe to use in damaged hearts, powerful antiarrythmic
    • Ventricular arrythmias IV, oral treatment of atrial
    • Blocks inactivated Na channels, K+ channels
    • Prolongs AP duration, prevents reentry
    • Weak Ca channel blocking
    • Decreases slope of phase 4 depol: inhibits abnormal automaticity
    • Highly toxic, long duration (2mos): pulm fibrosis, liver, thyroid, CNS, peripheral vasodilatation (blocks alpha and beta receptors), corneal deposits, blue-gray skin
  28. Adenosine
    • Naturally occurring, IV admin, rapid onset, short duration
    • 10s half life
    • enhances K conductance, inhibits cAMP induced Ca influx
    • Supresses Ca dependent AP's
    • Selectively inhibits AV nodal conduction, allows A flutter/fib to appear
    • Converts paroxysmal SVT, effective, short duration
    • Side effects: flushing, SOB, chest burning, depress SA node function
  29. Digoxin
    • Anti-arrhythmic, pro arrhythmic
    • used in CHF, increases Ca, improving contractility
    • inhibits Na/K pump, inc intra NA, reduces Ca extrusion via Na/Ca
    • Ca accumulation => myocardial contraction
    • Increases vagal tone, slows AV node, used in SVT
    • Reduces hospital visits in pts with HF
    • Narrow theraputic index before digitoxicity due to accumulation of calcium, interacts with other Ca modifying drugs
    • Side effects: AV junctional rhythm, delayed afterdepol, PVCs, AV blocks
  30. Sotalol
    • K+ blocker, B blocker, ionotropic effects
    • class 2 and 3, mostly 3
    • Increases QT
    • Used in Afib, SVT
    • Exacerbates asthma, can cause torsades

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