pharm - cardiac.txt

  1. ACEI drugs
    inhibit ACE, less angiotensin II produced (less vasoconstriction), less aldosterone secretion (less reabsorption), more bradykinin (vasodilation).
  3. ACEI kinetics (DOA)
    intermediate (12-24 hr) duration of action (except captopril).
  4. ACEI indication
    HTN, CHF, MI, diabetic neuropathy
  5. ACEI contraindications
    absolute hx of angioedema, pregnancy (cat D)
  6. ACEI interactions
    lithium (increased toxicity), azathioprine (increased toxicity). caution with NSAIDS in pts with poor kidney function (NSAIDS constrict, AA, ___ constrict EA).
  7. ACEI SE
    cough (>women), angioedema (>blacks, women, smokers), hyperkalemia, proteinuria, dysguesia
  8. lisinopril brand
    Prinivil, Zestril
  9. lisinopril class/dosing
    ACEI, 10-80mg PO qd (>40 rarely effective)
  10. benazepril brand
  11. benazepril class/dosing
    ACEI, 10-80mg PO qd (may give BID)
  12. enalapril brand
  13. enalapril class/dosing
    ACEI, 5-40mg PO qd (lower with diuretic)
  14. captopril class/info
    ACEI. dosed BID/TID on empty stomach, is not a prodrug (hepatic impairment). Additional SE rash.
  15. ACEI/ARB monitoring
    monitor K and SrCr as they begin or increase dose
  16. ARB drugs
  17. ARB MOA
    blocks binding of angiotensin II to AT1 receptor (less vasoconstriction)
  18. ARB kinetics (DOA)
    intermediate (12-24 hr) duration of action
  19. ARB indications
    HTN, CHF, pts who require an ACEI but cannot tolerate cough
  20. ARB contraindications
    absolute pregnancy (cat D). caution with volume depletion.
  21. ARB SE
    dizziness, hypotension, hyperkalemia, renal failure. [cough/angioedema less frequent]
  22. valsartan brand
  23. valsartan class/dosing
    ARB, 80-320mg PO qd (lower with diuretic)
  24. olmesartan brand
  25. olmesartan class/dosing
    ARB, 20-40mg PO qd
  26. Direct Renin Inhibitor drugs
    aliskiren (Tekturna)
  27. DRI MOA
    inhibit renin, less angiotensin I produced, less angiotensin II produced (less vasoconstriction), less aldosterone secretion (less reabsorption), more bradykinin (vasodilation).
  28. DRI kinetics (T1/2)
    long (40 hr) half life
  29. DRI indications
  30. DRI contraindications
    absolute pregnancy (cat D). caution with volume depletion, hyponatremia.
  31. DRI SE
    diarrhea, GERD, hyperkalemia.
  32. DRI misc
    renin concentrations will likely increase during administration (ATII negative feedback loop)
  33. Sodium Channel Blockers class
    class 1a - procainamide, disopyramide, quinidine. Class 1b - lidocaine, mexitetene. Class 1c - propafenone, flecainide.
  34. SCB - Class 1a
    moderate Na+ channel blockers, increased ERP
  35. SCB - Class 1b
    weak Na+ channel blockers, decreased ERB
  36. SCB - Class 1c
    strong Na+ channel blockers, no ERB effect
  37. SCB MOA
    block sodium channels, decreasing ion mvmt during phase 0. results in slower conduction, wider QRS. Phase 3 (and therefore QT interval) can be longer or shorter. also helps prevent after-depolarizations.
  38. SCB indications
    cardiac arrhythmia
  39. SCB contraindications
    pt does not have a life-threatening arrhythmia. lots of drug interactions (leading to QT prolongation, arrhythmias, other toxicities).
  40. SCB SE
    cardiac arrhythmias, including torsades de pointes
  41. procainamide class/SE
    SCB class 1a. SE drug-induced lupis.
  42. disopyramide class/SE
    SCB class 1a. SE anticholinergic.
  43. quinidine class/SE
    SCB class 1a. SE GI, bitter taste, cinchonism (vertigo, headache, tinnitus, psychosis)
  44. mexiletine class/info
    SCB class 1b. orally active form of lidocaine (lidocaine is IV due to short half life).
  45. propafenone class
    SCB class 1c
  46. flecainide class
    SCB class 1c
  47. Beta Blockers class/drugs
    class 2, "lols"
  48. BB MOA
    competitively antagonize the action of chatecholamines at beta receptors (beta-1 stimulation at SA/AV nodes leads to an increase in sodium currents/chronotropy/ionotropy). this reduces HR, contractility, and prevents after-depolarizations. can also block any compensatory increases in sympathetic activity.
  49. BB cardioselective (beta-1 only)
    atenolol, metoprolol selectivity
  50. BB non-cardioselective (beta-1 and beta-2)
    propanalol selectivity
  51. BB mixed alpha/beta
    labetalol, carvedilol selectivity
  52. BB least lipophilic, most water soluble, least CNS side effects
    atenolol, (labetalol) distribution
  53. BB most lipophilic, easily cross membranes, most CNS side effects (anhedonia, but could also help calm hyperenergetic brain)
    propranolol, (metoprolol) distribution
  54. BB indications
    HTN, CHF, angina, cardiovascular event protection, post-MI
  55. BB contraindications
    absolute non-selective + asthma, 2nd degree heart block, bradycardia, acute heart failure. many cautions/interactions.
  56. BB SE
    hypotension, Raynaud's, impotence, fatigue, hypoglycemia, insomnia, depression. **d/c taper (rebound HTN)
  57. atenolol brand
  58. atenolol class/dosing
    BB, 50-200mg PO qd
  59. metoprolol tartrate brand
  60. metoprolol tartrate (IR) class/dosing
    BB, 50-200mg PO BID
  61. metoprolol succinate brand
    Toprol XL
  62. metoprolol succinate (XL) class/dosing
    BB, 25-400mg PO qd
  63. carvedilol brand
  64. carvedilol (short-acting) class/dosing
    BB, 6.25-25mg PO BID
  65. carvedilol ER (Coreg CR) class/dosing
    BB, 20-80mg PO qd
  66. sotalol class/info
    BB with class 2 and class 3 antiarrhythmic properties. start in hospital due to potential for serious arrhythmias/interactions/issues. CrCl prior to start.
  67. Potassium Channel Blockers class/drugs
    class 3, amiodarone (also shows class 4 properties), dronedarone, ibutilide, dofetilide, azimilide
  68. PCB MOA
    blocking K channels in phase 3 of the action potential slows the efflux of K, increasing the refractory period.
  69. PCB EKG
    prolonged QT interval
  70. PCB interactions
    "darones" are inhibitors of CYP3A4/P-glycoprotein, so numerous interactions.
  71. amiodarone kinetics
    very long half-life (58 days), variable and slow elimination from plasma/tissues (so proarrhythmic effect, potential for interactions is prolonged). requires a loading dose.
  72. dronedarone kinetics
    shorter half-life than other "darone" (loading dose not needed). Is also less lipophilic, and lacks an iodine group.
  73. PCB indications
    treat/prevent a-fib/flutter, VF/VT
  74. PCB contraindications
    absolute with 2/3 degree heart block (suppresses conduction/escape beats). caution with amiodarone in pts with hypotension.
  75. PCB SE
    fatal pulmonary toxicity (report SOB/cough), eye issues, hepatotoxicity, blue-grey skin, thyroid issues. "beta blocker blues"
  76. Calcium Channel Blockers class/drugs
    class 4 = verapamil, diltiazem. also in this category are the "pines"(dihydropyridines)
  77. CCB MOA
    binds to various sites on L-type calcium channels (V, D, or N) blocking Ca influx. non-DHPs are cardiac depressants (chronotropy/ionotropy) with some vasodilator activity. DHPs are primarily vasodilators, which can lead to a potential reflex increased chronotropy/ionotropy.
  78. amlodipine kinetics (T1/2/info)
    much longer (40 hr) half life than nifedipine (4 hr), helping to mitigate reflex tachycardia.
  79. felodipine kinetics (info)
    has the highest affinity of the dipines, therefore causes the most dilation but also the most side effects
  80. CCB indications
    non-DHPs angina, tachycardia, HTN (diltiazem only). DHPs HTN, vasospasm (eg. Prinzmetal's).
  81. CCB contraindications
    non-DHPs end stage CHF. DHPs conditions where tachycardia might be undesirable.
  82. CCB interactions
    metabolized by CYP3A4, so numerous potential interactions. grapefruit is also an issue (except with amlodipine).
  83. CCB SE
    verapamil constipation (blocks Ca channels in bowel), diltiazem less so. DHPs HA, hypotension, peripheral edema.
  84. verapamil class/dosing
    CCB, 80-120mg PO TID
  85. diltiazem class/dosing
    CCB, 120-480mg PO qd
  86. amlodipine class/dosing
    CCB, 5-10mg PO qd
  87. cleviprex info
    IV CCB, avoid in pts allergic to soy/eggs
  88. anticholinergic drugs
    atropine (cardiac), glycopyrrolate (surgical), scopolamine (surgical, motion sickness)
  89. anticholinergic MOA
    block activity of ACh on parasympathetic muscaric receptors. in heart, SA/AV nodes increase pacemaker rate, sometimes increase conduction through blocks
  90. anticholinergic indications
    SB with hypotension, 2 degree heart block with bradycardia (can be tried in 3 degree).
  91. anticholinergic ACLS
    symptomatic bradycardia, slow PEA, asystole
  92. anticholinergic contraindications
    caution in situations where tachycardia can be dangerous
  93. anticholinergic side effects
    tachycardia, hyperthermia, delirium, other decreased parasympathetic issues
  94. atropine class/dosing
    anticholinergic, 0.5mg IV q5min max 3mg
  95. atropine OD
    quartet: red, hot, dry, confused
  96. adenosine MOA
    stimulates A1 receptors in AV note, decreasing K efflux, Ca influx, and Na influx. Hyperpolarization renders the cell refractory (essentially causing a 3 degree heart block for a few seconds).
  97. adenosine outcomes
    1) reentry circuits terminated and NSR resumes, 2) QRS eliminated so atrial tachycardias can be more easily diagnosed
  98. adenosine kinetics (T1/2)
    half life of 10 seconds, so double-push.
  99. adenosine interactions
    caffiene acts on the same receptors and can block its action.
  100. adenosine indications
  101. adenosine SE
    short-lived angina/extreme discomfort (endogenous adenosine is typically released with ischemia: decreased o2 --> decreased ADP change to ATP --> increased adenosine levels)
  102. adenosine dosing
    6-12 mg IV q1-2min, max 3 doses. pts taking carbamazepine, dipyridamole, heart transplant, central line initial dose is 3mg.
  103. Cardiac Glycoside drugs
    digoxin, digitalis (foxglove plant, longer T1/2)
  104. digoxin MOA1
    decreased Na/K pump action. Increased intracellular Na decreases electrochemical gradient for Na-Ca exchanger, less Ca exits cell and intracellular levels rise. Net result is increased contractility. Indirectly decreases need for sympathetic compensation.
  105. digoxin MOA2
    direct increase in parasympathetic tone via baroreceptors/brainstem vagal nuclei. net result is a decrease in HR (also useful in pts with a-fib due to increased PNS tone at AV node)
  106. digoxin kinetics (T1/2)
    half-life is 30 hrs
  107. digoxin toxicity
    therapeutic index 0.8-2ng/mL, 2.6 probable toxicity, 3 guaranteed toxicity (higher in children). Draw levels away from dose administration. 20% will experience toxicity, especially those with hypokalemia/electrolyte imbalances.
  108. digoxin indications
    CHF, a-fib
  109. digoxin contraindications
    absolute in pts with VF. relative in pt with ventricular arrhythmias/PVCs (exacerbate them).
  110. digoxin interactions
    diuretics (spironolactone), antiarrhythmics (quinidine), calcium antagonists (verapamil), statins (atorvastatin) increase levels
  111. digoxin SE
    GI (N/V/D, anorexia), CNS (confusion, dizziness, agitation), CV (arrhythmias/blocks), visual (orange-tinted vision, visual disturbances)
  112. digoxin EKG
    long PR interval, AV block, scooping of ST-segment, upslope into R wave
  113. statin MOA
    inhibit HMG-CoA reductase, mediator in the first step in the biosynthesis of cholesterol. reduced synthesis increases number of LDL receptors (via SREBPs), increasing catabolic rate of LDL and liver extraction of LDL precursors.
  114. statin effects
    major LDL. minor HDL/trigs.
  115. statin kinetics (prodrugs)
    lovastatin/simvastatin/atorvastatin/rosuvastatin have active metabolites
  116. statin interactions
    cyclosporine, macrolides, anti-fungals. pravastatin is the only one not metabolized by CYP450 enzymes (reduced risk of interactions)
  117. statin contraindications
    absolute pregnancy (cat X), liver disease
  118. statin SE
    generally well tolerated. myalgia 10%. rare include myositis/rhabdomyolysis, hepatotoxicity. possibly increase glucose.
  119. simvastatin brand
  120. simvastatin dose
    10-80mg PO qd
  121. atorvastatin brand
  122. atorvastatin dose
    10-80mg PO qd
  123. pravastatin brand
  124. pravastatin dose
    10-80mg PO qd
  125. lovastatin brand
  126. lovastatin dose
    20-80mg PO qd
  127. rosuvastatin brand
  128. rosuvastatin dose
    5-40mg PO qd
  129. simbastatin/ezetimibe brand
  130. simbastatin/ezetimibe (Vytorin) dose
    20-40mg/10mg PO qd
  131. statin monitoring
    monitor liver enzymes, blood sugar
  132. fibrates drugs
    gemfibrozil, fenofibrate, clofibrate
  133. fibrates MOA
    activate transcription factors (PPARs). reduces production of VLDL and speeds up removal of triglycerides, increases HDL levels (apo A1/A2 expression increased).
  134. fibrates effect
    major HDL/trigs. minor LDL.
  135. fibrates interactions
    gemfibrozil inhibits glucoronidation of statins (increased liklihood of muscle breakdown/pain with coadministration). Interact with warfarin (potentiate anticoag - monitor INR).
  136. fibrates SE
    rash, gallstones, liver enzyme elevation. rare pancreatitis, reversable decreased renal function, myositis/myopathy/rhabdomyositis.
  137. fenofibrate brand
  138. fenofibrate class/dose
    fibrate, 50-200mg PO qd
  139. gemfibrozil brand
  140. gemfibrozil class/dose
    fibrate, 600-1200mg PO qd
  141. Bile Acid Sequestrants drugs
    cholestyramine, colestipol, colesevelam
  142. BAS MOA
    bile acids facilitate fat digestion/absorption, and are normally enterohepatically recycled. sequestrants are large and carry a positive charge, so they bind negatively charged bile acids and are excreeted together. the body needs to create more bile acids (which takes cholesterol) and less fat is absorbed.
  143. BAS effect
    major LDL. no HDL. hurt trigs.
  144. BAS kinetics
    never leave GI tract, so are OK to use in disease/pregnancy. reduce absorption of fat-soluble vitamins (A,D,E,K)
  145. BAS contraindications
    hypertriglyceridemia (interruption of enterohepatic recycling increases enzyme activity of phospatidic acid phosphatase, which is involved in triglyceride formation)
  146. BAS interactions
    bind to negatively charged molecules, so interfere with absorption of thiazides, furosimide, propranolol, digoxin, warfarin, OCPs (can be overcome simply by seperating administration)
  147. BAS SE
    GI. rare hyperchloremic acidosis (bile acid resins are chloride salts, can result in increased chloride/decreased bicarb levels)
  148. cholestyramine brand
  149. cholestyramine class/dose
    BAS, 8g powder dissolved in liquid PO TID
  150. BAS combo
    most often used in combo with statins because their use alone results in upregulation of HMG-CoA reductase
  151. Nicotinic Acid (a B-complex vitamin)
  152. Niacin MOA
    unknown. does reduce liver synthesis of VLDL.
  153. Niacin effect
    major HDL/trigs. moderate LDL.
  154. Niacin contraindications
    arterial bleeding (can cause slight decrease in platelets/increased prothrombin times), hepatic issues (increased LFTs dose related)
  155. Niacin effects
    skin flushing, itching, dryness, rash (offset with ASA/ibuprofin 30 min prior). hyperglycemia, hyperuricemia, upper GI distress (offset by taking with food).
  156. Niacin class/dosing
    nicotinic acid, 0.5-2g PO TID
  157. Cholesterol Absorption Inhibitors drugs
  158. CAI MOA
    selectively inhibit absorption of cholesterol by small intestine (NPC1L1 transporter) by up to 50%
  159. CAI effect
    moderate LDL. no HDL/trigs.
  160. ezetimibe brand
  161. ezetimibe class/dosing
    CAI, 10mg PO qd
  162. Essential Fatty Acid drugs
    omega-3 fatty acids (eicosapentaenoic acid/docosahexaenoic acid; EPA/DHA)
  163. EFA MOA
    thought to inhibit triglyceride synthesis in the liver.
  164. EFA effect
    Major trigs. No HDL, hurt LDL.
  165. EFA contraindication
    caution with anticoagulation (can inhibit platelet aggregation)
  166. omega-3 fatty acid brand
  167. Lovaza class/dosing
    EFA, (EPA 465mg/DHA 375mg) 4g PO qd (can divide dose)
  168. Ionotrops/Pressors drugs
    dobutamine; norepinephrine, phenylephrine; epinephrine, dopamine
  169. I/P MOA
    act on adrinergic receptors. alpha-1 receptors increase IP3 which increases vascular tone (vasoconstriction). beta-1 receptors activate G proteins that increase cAMP levels, resulting in increased myocardial contractile force.
  170. beta1-selective ionotropes
    dobutamine (also a vasodilator)
  171. alpha1-selective pressors
    norepinephrine, phenylephrine (pure)
  172. combo pressors and ionotropes (alpha and beta)
    epinephrine, dopamine
  173. I/P kinetics (T1/2)
    very short half lives, so IV infusions (or boluses in ACLS)
  174. I/P indications
    hypotension, shock, acute CHF (dobutamine/dopamine)
  175. epinephrine dosing
    1mg IV q3-5min
  176. PDE-3 Inhibitors drugs
    amrinone/inamrinone, milrinone
  177. PDE-3 MOA
    PDE breaks down cAMP/cGMP. Inhibitors increase cAMP/cGMP, causing increased intracellular Ca. Cardiac tissue = stronger contraction, smooth muscle = decreased afterload due to smooth muscle relaxation. Also theoretically improves diastolic functioning (decreased end diastolic pressure).
  178. PDE-3 kinetics (T1/2)
    long half life even though administered IV, can make it tricky to find correct dose (often levels get too high) -- Swang Ganz monitoring of CO can help titrate to correct dose
  179. PDE-3 containdications
    CHF (increased risk of mortality)
  180. PDE-3 SE
    hypotension secondary to vasodilation (can last for hours due to long half life), thrombocytopenia (much less often with milrinone).
  181. PDE-3 vs. beta agonists
    PDE-3 not direct positive chronotropes (better for tachy pts/CAD). In CHF b-receptors are frequently down-regulated to to high endogenous chatecholamine compensatory mechanisms, so PDE-3 inhibitors are clinically much stronger.
  182. nitrates drugs
    nitroglycerin, isosorbide dinitrate (ISDN), isosorbide-5-mononitrate
  183. nitrates MOA
    release NO (EDRF), inducing vasodilation primarily on venous side (reduces venous return, preload, end diastolic pressure). Lower ventricle wall tension reduces stress/o2 demand; lower intraventricular pressure means higher coronary perfusion grandient and increased o2 supply. minor effects include coronary vasodilation, arterial vasodilation (decreased SVR) decreasing afterload.
  184. nitrates groups
    those that release NO spontaneously (sodium nitroprusside), those that require an enzymatic process (S-nitrosothiol; organic nitrates)
  185. nitrates kinetics (bioavailability)
    oral availability is low (10%) due to reductase enzyme in liver. sublingual route avoids this first pass effect, as does patch/ointment.
  186. nitrates kinetics (DOA)
    ISDN/IS5M have a longer duration of action, thus are useful for long-term prophylaxis.
  187. nitrates misc
    nitrate tolerance can develop particularly with long-acting agents, therefore they need a nitrate free period to remain effective (typically 12 on, 12 off)
  188. nitrates indications
    angina, acute coronary syndromes, CHF, hypertensive emergencies
  189. nitrates contrandications
    absolute concurrent use with PDE-5 inhibitors, increased ICP, severe anemia
  190. nitrates SE
    HA, flushing, hypotension, dizziness
  191. isosorbide mononitrate dosing
    20mg PO BID
  192. nitrates/beta blockers combo
    prevents reflex tachlycardia, nitrates prevent coronary vasospasm of b-blockers, nitrates prevent preload increases resulting from the negative ionotropic effects produced by b-blockers
  193. vasodilators drugs
    sodium nitroprusside, Hydralazine
  194. vasodilators MOA
    dilation of arterioles. SNP (prodrug) also slighly venodilates, Hydralazine is artery selective. exact mechanism is unknown.
  195. vasodilator kinetics (T1/2)
    very short half life, only available IV, rapid onset
  196. vasodilator indications
    severe hypertensive emergencies, severe heart failure
  197. vasodilator contraindications
    caution where reflex tachycardia/increased contractility would be harmful (CAD,AS,MS)
  198. vasodilator SE
    HA, flushing, tachycardia, lupus-like syndrome (~10%)
  199. Natriuretic Peptides drugs
    Nesiritide (recombinant form of BNP)
  200. NP MOA
    endogenous serve as a counter-regulatory system for RAAS, causing vasodilation, natriuresis, and inhibition of renin and aldosterone. This reduces preload/afterload.
  201. NP kinetics (T1/2)
    short half life (initial bolus followed by continuous infusion)
  202. NP indications
    advanced decompensated acute heart failure
  203. NP SE
    prolonged hypotension
  204. alpha-2 Agonists drugs
    clonidine, guanabenz, guanfacine, methyldopa (prodrug)
  205. alpha-2 agonsits MOA
    agonize central alpha-2 receptors (inhibits adenylyl cyclase activity), producing a decrease in peripheral resistance, HR, BP.
  206. alpha-2 agonists indications
    HTN (not first line)
  207. alpha-2 agonists SE
    sedation, dry mucus membranes, bradycardia, hypotension, constipation, nausea
  208. alpha-1 antagonists groups/drugs
    selective = prazosin, terazosin, doxazosin. non-selective (used in mgmt of pts w/ pheochromocytoma) = phentolamine, phenoxybenzamine
  209. alpha-1 antagonists MOA
    antagonize peripheral alpha-1 adrinergic receptors (stimulate phospholipase C activity), causing vasodilation
  210. alpha-1 antagonists indications
    HTN (not first line), benign prostatic hypertrophy
  211. alpha-1 antagonists SE
    orthostatic hypotension, HA, somnolence, palpitations (reflex tachycarda), nasal congestion, dizziness
Card Set
pharm - cardiac.txt
pharm - cardiac.txt