CV drugs

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trucle
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87450
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CV drugs
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2011-05-24 14:24:05
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CV drugs
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  1. Drugs for hyperlipid?
    • 1. statin (avartostatin)
    • 2. ezetimibe
    • 3. acid binding
    • a) nicotinic (Niacin)
    • b) bile sequestrants (cholestyramine)
    • c) fibric (gemfibrozil)
  2. SE of statin?
    • 1. liver toxic
    • 2. myopathy
    • 3. rabdomyolysis
    • 4. pregnancy X
    • 5. increase warfarin, digoxin
  3. SE of ezetimibe?
    • 1. liver
    • 2. respiratory
  4. SE of nicotinic acid?
    • 1.liver toxic
    • 2. flushing
    • 3. hyperglycemia
    • 4. gout
  5. SE of cholestyramine?
    • No.
    • just do not absorb into circulation.
    • mixed with fluid
    • do not take with other drugs
  6. SE of gemfibrozil?
    same as statin + gallstone
  7. 3 classes of lipids?
    • 1. triglycerides = most
    • 2. steroids => atherosclerosis
    • 3. phospholipid = build membrane
  8. Meds for antidysrhythmias?
    • 1. Sodium channel blocker (quinindine)
    • 2. Beta blocker (propranolol)
    • 3. potassium blocker (aminodarone)
    • 4. cacium channel blocker (verapamil)
    • 5. Others (digoxin & adenosine)
  9. what is dysrhythmias?
    • -abnormalities of conduction or rhythm
    • -harmless or deadly
  10. sx of dysrhythmias?
    dz, weakness, fainting, decreased exercise tolerance, sob. Skipped beat
  11. where Na & Ca? where K?
    • Na & Ca outside cell
    • -Na rush inside cell => depolarization
    • -Ca rush inside cell => depolarization/contraction

    • K inside cell
    • -K rush outside cell => back to polarized
  12. Action of Sodium channel blocker?
    • -block Na channel => slow rate of conduction
    • (similar to local anesthetics = lidocaine)
  13. Drugs of sodium blocker?
    • quinidine (protype)
    • lidocaine
    • phenytoin (dilantin)
  14. SE of sodium channel blocker?
    • -as slow conduction (rate) => H/B, dz, fainting.
    • -new dysrythmias or worsening
    • -anticholinergic (dry mouth, urine retention)
    • -double digoxin
    • -increase risk of heartblock with aminodarone
  15. Lidocaine (Na blocker)
    -action
    -SE
    -special intervention
    • -rapid control of Ventricular dysrthymias
    • -local anesthetic
    • SE = H/B, worsened dysrhythmias, heart block, respiratory (asthmaticus), confusion/sz/lightheadedness, lethargy, blurred vision.
    • -toxic if prolong => check level, mus be on cardiac monitor
  16. Action of beta blocker in dysrhythmias?
    • 1) reduce automaticity & conduction velocity => reduce heart rate
    • 3) reduce contractility =>reduce CO => reduce bp
  17. SE of beta blocker in dysrhy?
    • -H/B, dz, fainting (same as Na blocker)
    • -as also beta 2 (lung) => bronchospasm => asthma and COPD
    • -metoprolol = heart block, HF, alter insulin (diabetes), + digoxin => bradycardia
    • -propanolol = also tx migraine/ha. Do not give with MAO inhibitor
  18. Action of K channel blocker?
    slow conduction + prolong refractory period (resting) => stablizing dysrhythmias
  19. what meds used as CODE for dysrhythmias?
    • aminodarone (K channel blocker)
    • => V-tach, A-tach/fib (# v-fib = CPR, defri)
    • *also long half life
  20. SE of K channel blocker?
    • - H/B, dz, heart block, HF
    • -pulmonary toxic, pneumonia-like synd
    • - hepatic
    • -photosensitivity
    • -increase digoxin/anticoagulant/herbal
    • ***IV=continuous EKG
  21. 2 meds of CCC?
    • verapamil
    • diltiazem
  22. Action of CCC in dysrhyth?
    • -to treat supraventricular dysrhyth only
    • same as BAB
    • 1) reduce automaticity
    • 2) reduce conduction
    • 3) reduce contractility
    • => prolong refractory period
    • * verapamil = slow conduction, dilate coronary arteries (tx angina)
    • *Diltiazem = tx vasospastic angina = help coronary arteries relax, HTN, A-fib/flutter
  23. SE of CCC?
    • -H/B, ha
    • - increase digoxin (both have effect of slowing conduction)
    • -increase level with grapefruit

    * diltiazem = AV block, HF, insomnia, photosensitivity
  24. Action of digoxin in antidysrhythmias?
    same as BAB & CCC, except that instead of reduce contractility, it increase contractility => dysrhythmias if execess => take apical
  25. SE of digoxin in antidysrhythmias?
    • -dysrhythmias if excess
    • -interact with many common drugs
    • -hypotentsion, HF, anorexia
    • -hyperK
    • -toxic if pt with hypoK
  26. Action of adenosine?
    • -bolus IV to terminate serious A-tach by slowing conduction thru AV and automaticity SA.
    • -PSVT = paroxysmal supraventricular tachycardia
  27. why do we need to notify dentist, surgeons and eye doctor when taking propranolol?
    meds lower intraocular pressure
  28. what e-lyte produce depolarization?
    Na
  29. what meds in antidysrhythmias interact with digoxin?
    • -quinidine => need to reduce digoxin
    • -metoprolol, propanolol => + digoxin => increase digoxin=> bradycardia
    • -CCC => elevate digoxin
  30. what outcome to be expected when taking antidysrhythm?
    increased CO
  31. 2 CCC, besides treating dysrhythmias, what else are they used for?
    • -verapamil = tx angina
    • -diltiazem = HTN
  32. what meds for angia & MI?
    • 1) O2 & morphine
    • 2) nitrates (nitroglycerin)
    • 3) BAB (atenolol)
    • 4) CCC (diltiazem?? verapamil)
    • 5) thrombolytics (reteplase)
    • 6) antiplatelet
  33. SS of angina pectoris?
    sharp pain in heart region, moving to left side of neck, lower jaw, left arm
  34. Common cause of angina/MI?
    • -atherosclerosis
    • -mitral stenosis
    • -MI
    • -CAD
    • -DM
    • -peptic ulcer
    • -GERD
  35. what food rich in K and Mg
    banana, kidney bean, spinach, tomatoes, apricot, peanut butter, sweat potato, leafy green
  36. surgical procedures for angina/MI?
    • CABG
    • PTCA (areaof narrowing is opened using either balloon cath or laser)
  37. 4 mechanisms to reduce cardiac workload by pharmacological goal in angina/MI?
    • 1) slow heart rate
    • 2) reduce contractility
    • 3) dilate vein (so heart can receive less blood =reduced preload)
    • 4) lower bp (heart can push blood out of chamber = reduced afterload)
  38. Action and SE of morphine?
    antidote?
    • -dilate coronary arteries
    • -SE = H/B, cardiac/resp arrest, sedation, clouded sensorium, euphoria, sz, thrombocytopenia, urine retention
    • -Naloxone (Narcan)
  39. action of nitroglyceride?
    • 1) dilate vein => reduce preload returning blood => afterload CO
    • 2) dilate coronary artery => more O2 for myocardium, relax spasm
  40. Types and Meds of nitrates?
    • 1) short = SL, spray, cream = nitroglyeride
    • 2) long = oral, patch = isosorbide
  41. SE and contraindication of nitrates?
    • -H/B (may), reflex tachycardia (palpitation or skipped beat) ha, dz, flushing
    • -No = viagra, tidalafil (Cialis) => severe hypotension
  42. in angina/MI, BAB used with CCB may cause?
    excessive cardiac suppression
  43. In angina/MI, BAB used with digoxin may cause?
    slowed AV conduction => heartblock
  44. vasodilators?
    • 1) nitroglycerides (short nitrate)
    • 2) isosorbide (long nitrate)
    • 3) hydralazine (direct)
    • 4) nesiritide (IV in ICU only for HF)

    * used for chest pain
  45. cause of MI?
    plaque builup narrowing arteries => a broken piece goes to smaller vessel to lodge => block O2 supply => ischemic
  46. what meds for MI?
    • 1) thrombolytic (reteplase) = dissolve clot by activating plasminogen to bind to fibrin = effective w/in 30 minutes and not later 12 hrs
    • 2) antiplatelet = aspirin
    • 3) anticoagulant = heparin; glycoprotein IIb/IIIa, ADP receptor blocker
    • 4) BAB = effecitve w/in 24 hrs (reduce O2 demand by reduce rate/contractility/bp). H/r watch sx of dysrhyth b/c its ability to slow conduction
    • 5) ACE = w/in 1-2 days
    • 6) narcotic analgesic (morphine)
  47. what to know when taking anticoagulant? (SE)
    • SE = pt with active bleeding
    • -NO = consumption of food high K food (interfere with clotting time) eg. leafy green veg, herbal
  48. Meds for HF?
    • 1)digoxin
    • 2)diuretic (furosemide)
    • 3) ACE (lisinopril - used when pt also has HTN)
    • 4) phosphodiesterase (milrinone)
    • 5) vasodilator (isosorbide)
    • 6) BAB (carvedilol)
    • 7) natriuretic peptides (nesiritide - new, IV in ICU, vasodilation => cause severe hypotension)
  49. what and cause of HF?
    pathophysiology?
    • -inability of ventricle to pump enough blood for body's demand
    • -cause = weakened muscle.
    • - can be both, but normally left ventricle

    • -decreased contractility => decreased CO =>
    • 1) increased preload => lung congestion
    • 2) decreased bp =>
    • a- increased demand => increased rate => increased workload
    • b-decreased flow to kidneys => ADH & renin pathway activated => Na/water retention => increased blood volume => increased bp => increased afterload => increased work
  50. Drug of choice in HF?
    • first choice = mild to moderate
    • 1) ACE (esp with HTN which normally the case)
    • 2) diuretic
    • 3) digoxin (watch serious SE)

    • 2nd choice = severe & when 1st not effective =
    • 1) phosphodieterase
    • 2) vasodilator
    • 3) BAB
  51. 3 important factors of HF?
    • 1) preload (stretch)
    • 2) contractility (snap back)
    • 3) afterload (force of LV to pump against)
  52. action of digoxin?
    1) inhibit Na& K tapse => release Ca => increase force of contraction = increased CO (positive inotropic effect # BAB = negative) => increased UOP => relieve lung congestion & peripheral edema

    2)suppress SA & slow conduction AV (watch serious SE = excessive slow heart rate)
  53. SE of digoxin?
    • - most dangerous = create dysrhythmias (particularly pt w hypoK) even tho digoxin can also be used for dysrthythmias
    • - toxic if overdose (hypo and hyper K). hypoK predispose pt to toxic
    • -blurred vision, anorexia, sob, leg muscle cramp
  54. Action of ACE?
    • -inhibit ACE that cause conversion of angiotension I to II
    • -diate arterioles & veins => reduce blood volume and bp, peripheral edema
    • -prevent pathologic changes in cardiac structure
  55. SE of lisinopril (ACE)?
    • -caution in renal failure/insufficiency/DM
    • -dry cough
    • -hyperK
    • -angiodema (swelling of face/trachea/hand)
    • -hypotension
  56. action of diuretic?
    • inhibit transport of Na, K & Cl across loop of Henle = blocking NaCl (water) reabsorption => increase UOP => reduce blood volume => reduce bp, edema, congestion
    • * K-sparing (spironolactone) = inhibit aldosterone in distal tubule (far from loop => spare K)
  57. SE of furosemide?
    • -hypoK (cause lethal dysrhythmias), hypo e-lytes
    • -large dose => ototoxicity
    • -dehydration,
    • -hypotension
    • -pancreatitis
    • -leukopenia, thrombocytopenia
  58. most prescribed diuretic for HTN/HF?
    • -HCTZ
    • -act on different part of kidney to incresase UOP => less hypoK
  59. SE of K-sparing diuretics?
    • -HyperK!!! (#furosemide and HCTZ (less)
    • -angioedema
  60. action, use, SE of phosphodiesterase inhibitor?
    • -blocking phosphodiesterase => increase Ca => increaes contraction force (same as digoxin = positive inotropic)
    • - vasodilation
    • **short term (2-3 days) control of acute HF, toxic => only for pt who not respond to ACE & digoxin
    • -SE = ventricular dysrhythmias => EKG monitor
  61. action, use, SE of vasodilator (isosorbide) in tx of HF?
    • -act directly on vein to cause vedodilation => reduce venous return (preload) => reduce work for heart
    • -dilate coronary arteries => mroe O2 for myocardial tissue
    • -SE = hypotension, reflex tachycardia, ha
    • -contraindication = viagra
  62. pt with HF also experiencing angia, which meds?
    1) hydralazine
    2) HCTZ
    3) isosorbide
    4) milrinone
    isosorbide (b/c we have to take care of angia first)
  63. Meds for HTN?
    • 1) diuretic
    • 2) BAB (metoprolol)
    • 3) ACE (captopril, lisinopril)
    • 4) CCC (diltiazem)
    • 5) ARB(losartan)
    • 6) direct-acting vasodilator (hydralazine, nitroprusside)

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