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83 Cards in this Set
- Front
- Back
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Actions of Organic Nitrates
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-Release of NO activates guanylyl cyclase, which increases cGMP, which activates myosin LC phosphatase, which deactivates myosin LC
-Venodilation: decreases preload, and by decreasing filling they decrease O2 demand. -Mildly dilates arteriolar resistance vessels to decrease afterload -Mildy dilates epicardial arteries to increase blood flow |
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Side effects of Organic Nitrates
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-Hypotension
-Reflex tachycardia (add B blockers or Ca blockers to blunt) -Unavoidable tolerance after use for several hours: Need to withold drug for 10 hours to remove tolerance -Extensive cross tolerance between nitrates |
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Administration of Organic Nitrates
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-Bioavailability low because extensive first pass metabolism
-Take sublingually or buccally to avoid hepatic system -Inhale volatile nitrates -IV preparations -Their short half life and tolerance prevents nitrates from being used for long term |
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Administration of:
-Nitroglycerin -Isosorbide Dinitrite -Amyl nitrate |
-Nitroglycerin: Used for acute anginal attacks, taken sublingually, 1/2-1 hr. of relief; transdermal patches give few hours of relief
-Isosorbide Dinitrite: Time-released, 4 hrs. of relief, taken buccally -Amyl nitrate: aerosol |
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Actions of Calcium Channel Blockers (CCBs)
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-Block L-type Ca2+ channel on s.m. cells
-mostly reduce afterload by causes arteriolar dilation and increasing coronary blood flow -decrease preload by causing venodilation -verapamil and diltiazem also depress cardiac contractily, depress SA node automaticity, and depress AV node conduction |
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Dihydropyridine CCBs (-pine)
Ex. NifediPINE |
-More selective for vasodilation of arterioles and coranary blood vessels; don't decrease chronotropy and ionotropy
-Side effects: hypotension, bradycardia, and decreased cardiac contractility |
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Verapamil and Diltiazem mechanism of action
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-Non-DHP CCBs
-Cause arteriolar and coronary vasculature dilation -Also decrease chronotropy and ionotropy by decreasing contractility, decreasing SA node automaticity, and decreasing AV node conduction -Prevent reflex tachycardia from occuring in response to drug induced decrease in bp |
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Nimodepine
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-DHP CCB selective for dilation of cerebral vasculature
-used for subarachnoid hemmhorage to prevent regional vasoconstriction and ischemia |
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Beta Blockers used for treatment of Angina
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-Metaprolol, atenalol, and propanalol
-Decrease heart rate and contractility -Used with CCBs, esp. DHP CCBs, to offset any reflex tachycardia |
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Ranolazine
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-used as anti-anginal if nothing else works
-Blocks sodium channel permability, which increases the activity of the Na/Ca exchanger -Decreases contractility and calcium overload during ischemia -Also blocks fatty acid oxidation |
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Heparin
-Mechanism of Action |
-1/3 active mucopolysaccharides that increases ATIII binding to thrombin; increases inhibition of 8a, 9a, 10a, and 2a
-Direct inhibition of Xa |
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LMW Heparin (EnoxaPARIN, DaltePARIN)
-Mechanism of Action -Administration and monitoring -Toxicity |
-Mechanism of Action:
Fragments of heparin produced by enzymatic digestion; only increase ATIII binding and inhibition of Xa -Administration: Given SC once a day, do not need to monitor as much, greater bioavailability than heparin -Toxicity: Less toxicity than heparin and less risk of overdose; fewer bleeding side effects |
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Uses of Heparin and LMW Heparin
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After acute MI to prevent clot; Venous thromboembolism; unstable angina; anti-coagulation during prengnancy because not teratogenic
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Hirudin and Bivalirudin
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-non-clot specific, direct thrombin ihibitors
-used for unstale angina |
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Warfarin/Coumarin mechanism of action
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Vitamin K analogues that inhibit Vitamin K oxidoreductaqse; 8-12 hr. delay in onset and 1-3 day delay in appearande of peak effects because gamma-carboxylated factors already in blood stream
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Warfarin/Coumarin administration and monitoring
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-Taken orally
-need to monitor changes in pro-thrombin time via the INR (INR=ratio of patients PTT to a standard PTT and an index factor) -To increase recovery, stop administration, treat with Vitamin K and/or Factor IX concentrates (Proplex, Konyne80) |
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Warfarin/Coumarin Indications and Contraindications
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-Indications: atrial fibrillation and prosthetic heart valves
-Contraindications: TERATOGENIC; many drug interactions; VitK oxidoreductase hapolotype variations based on mRNA levels of enzyme (Asians=lower dose, A/A; Europens=A/B; African Americans =highest dose, B/B) |
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Ximelagartan
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-Drict thrombin inhibitor
-Orally active -not teratogenic -no drug interactions and don't need to monitor clotting times -taken off the market because killed too many people |
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Streptokinase and Anistreplase (APSAC)
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Activates plasminogen, not clot specific
-Anistreplase is complexs of plasminogen and streptokinase that becomes activated only in plasma |
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tPA and Urokinase
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-Clot specific protease that activates plasminogen
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Indications and Uses of Fibrolytic agents
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-Multiple pulmonary emboli
-Central deep venous thrombosis -Acute MI -Must give tPA during "Golden Hour" (first hour of MI) to see a huge reduction in mortality; streptokinase and tPA don't differt in effectiveness after Golden Hour |
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Aspirin
-Mechanism of Action |
-Irreversible COX-1 inhibitor, reduces TXA2 which prevents platelet aggregation
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Ticlopine and Clopidogrel (Clavix)
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-Inhibits adenosin-mediated platelet aggregation
-Used for patients who can't tolerate aspirin -Combination of Clopidogrel and aspirin reduces risk of reocclusion following MI than Aspirin alone |
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Eptifibatide
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Fibrinogen analog that binds GPIIb/EEa receptor and prevents platelet aggregation
-only IV and acute |
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Abciximab
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monoclonal Ab that blocks IIb/IIIa receptors
used with aspirin or heprin in angioplasty -only IV and acute |
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Actions of angiotensin II on blood vessels, adrenal cortex, CNS, and cell growth
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-blood pressure: strong vasoconstriction response 10 seconds upon IV infusion
-Adrenal cortex: acts on zona glomerulosa cells to increase aldosterone synthesis and release -CNS: resets baroreceptors so the increase in blood pressure doesn't induce reflexes; causes sympathetic-mediated pressor response; causes thirst; causes secretion of ADH and ACTH -cell growth: mitogen on vascular and cardiac cells, may contribute to cardiac hypertrophy |
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Classes of ACE inhibitors
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-Class I: Captopril only member, active as is and has some active metabolites
-Class II: majority in this class; are prodrugs requiring deesterification via hepatic metabolism -Class III: Lisinopril is only member; active as is and excreted unchanged by the kidney |
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Indications of ACE inhibitors
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-Hypertension, esp. if diabetic because doesn't effect insulin sensitivity
-Decreases mortality of congestive heart failure -Drugs of choice for diabetic nephropathy; decrease in bp prolongs kidney life -Post MI to reduce cardiac remodeling |
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Adverse effects and CIs of ACE inhibitors
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-Elevated bradykinin levels cause dry cough and skin rash
-Hyperkalemia, esp. in patients on K+ sparing diuretics -Acute renal failure-decreases golomerular filtration -Can't use if have bilateral renal stenosis because lowers bp too much to get blood into kidneys -Teratogin due to importance of AT2 receptors; don't give to patients in 2nd or 3rd trimester -Neutropenia -Will not work if have a high sodium diet because Na+ inhibits renin release; need to decrease salt intake to maintain sensitivity |
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Aliskerin
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Renin inhibitor; but causes reactive renin release so not used
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Captopril
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Class I ACE inhibitor; not a pro-drug; take 2-3 times a day
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Lisinopril
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Class III ACE inhibitor; not a pro-drug; only once a day
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Alacepril, benazepril, cilazepri, delapril, enalapril, fosinopril, perindopril, quinapril, ramipril, spirapril, trandolapril
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Class II ACE inhibitors; all pro drugs; take either once or twice a day
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Losartan
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ARB (AT1 receptor antagonist)
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Valsartan
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ARB (AT1 receptor antagonist)
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Indications of ARBs (AT1 Receptor Blockers)
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-If dry cough and skin rash unbearable from ACE inhibitor (because ARBs don't effect bradykinin levels)
-No more effective than ACE inhibitors |
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Contraindications for Diltiazem and Verapamil
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-Contraindication: Can cause sick sinus syndrome; Don't use if someone has AV node dysfunction; Use carefully with Beta blockers because have similar effects; Can cause heart failure because will lower cardiac output too much
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Mechanism of action and effects of Digitalis Compounds
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-inhibits Na/K ATPase, which decreases Na/Ca exchange activity in myocytes...The increase in intracellular Ca increases cardiac output
-Increases parasympathetic output...Decreases SA Node pacing and slows conduction at AV Node -Decreases sympathetic output...this decreases renin release and causes vasodilation |
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Drug interactions with Digitalis compounds
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-Quinidine reduces digoxin clearance, which increases digoxin concentration by 2
-Diuretics which are not K sparing and cause hypokalemia (thiazide and furosemide) increase digitalis compound potency |
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Manifestations of Digitalis toxicity
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-AV Junctional rhythm (due to greatly suppressed SA node)
-PVCs -AV Block -anorexia -nausea -color vision abnormaility (see yellow) -disorientation -rare gynecomastia [important because low therapeutic indices and long half lives of digitalis cmpds] |
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Digoxin
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-Digitalis compound used for CHF
-Also has weak vagomimetic activity, which slows SA and AV node conduction; used for CHF patients with atrial fib -Cleared by kidney; quinidine decreases clearance |
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Digitoxin
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-Digitalis compound used for CHF or [CHF + At fib]
-Hepatic clearance |
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Treatment for Digitalis toxicity
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-Decrease dose, but not very effective because of the long half life
-Elevate serum K+, because K+ is a competetive inhibitor -Give digibind, an Ab against Digoxin |
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Beta Blockers are used for which cardiac conditions?
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-Stable angina (often with DHP CCBs to counteract reflex tachycardia)
-Long term treatment of unstable angina -Congestive heart failure to reduce long term mortality (as long as not acutely decompensated) -atrial or ventricular premature beats -paroxysmal SVT -atrial fibrillation and atrial flutter -ischemia-related/reentry ventricular tachycardia |
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Dobutamine (Dobutex)
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B1 selective agonist used for acute IV treatment of CHF; positive chronotropy and ionotropy, but can't be used long term because of receptor desensitization
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Amrinone (Inocor)
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Phosphodiesterase inhibitor used for acute IV treatment of CHF; increases intracellular cAMP independently of B receptors; But hepatoxic and induces nausea
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Milrinone (Primacor)
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Phosphodiesterase inhibitor; increases intracellular cAMP independently of B receptors; But hepatoxic, induces nausea, and kills more people than digitalis
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IV Dopamine
-Indications -Mechanism of action |
-Used for acute IV treatment of CHF, esp. for patients with renal impairment
-Decreases peripheral NE release via presynaptic D2 receptors -Vasodilates peripheral vessels (B2) -Dilates renal vessels (D2) -Increases ionotropy and chronotropy |
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2 non-potassium sparing diuretics used for CHF
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-thiazides (ex. hydrochlorthazide), low ceiling
-forsemide, high ceiling |
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Why is spironolactone used for CHF?
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-spironolactone=aldosterone antagonist, K+ sparing
-Treats edema and excessive preload by reducing volume -Also decreases mortality because of its anti-aldosterone effects (blocks aldosterone induced myocardial fibrosis, increased vascular sensitivity to ang, and inhibtion of NO release) |
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Which venodilators are indicated for CHF?
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Nitrates in patients with high filling pressures and pulmonary congestions; Hydralazine to dilate arterioles in patients with low ventricular output
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Why are ACE Inhibitors and ARBs used for CHF?
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Reduces mortality by decreasing preload, afterload, and the mitogenic activity of ang. But do not give verapamil or diltiazem because they are negative ionotropes
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Which Beta Blockers are prescribed to reduce mortality from CHF?
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-Carvedilol(B1, B2, a1)
-Metoprolol (B1) -Bisprolol (B1) |
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Nesiritide
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Recombinant version of human B-type natiuretic peptide used for CHF
-activateds gunaylate cyclase and leads to vasodilation, esp. reducing RA pressure and pulmonary capillary wedgepressure; but there may be an increase in short term mortality |
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What is the standard step therapy for chronic CHF?
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1. Weight reduction and limiting of activity to decrease heart's workload
2. Restrict sodium intake to decrease volume 3. Diuretics to reduce volume 4. ACE inhibitors, sometimes before diuretics 5. Beta blockers 6. Digitalis compounds (may be moved up if have atrial fib) 7. Vasodilators |
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Quinidine
-Mechanism of action -Uses -Toxicity |
-Class Ia anti-arrhythmic (block Na and K channels), esp. used for atrial fib and flutter
-Has anti-muscarinic effect (increases HR and AV conduction) -Mild a1 receptor antagonist, which decreases bp -Has many drug interactions, including the impairment of digoxin removal -Quinidine syncope=torsades de pointes caused by quinidine use |
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Procainamide
-Mechanism of action -Uses -Toxicity |
-Class Ia anti-arrhythmic (blocks Na and K channels)used for ventricular arrhytmias associated with acute MI
-less anti-muscarinic activity than quinidine -given IV -1/3 of patients develop lupus-like symptoms only while takig drug |
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Disopyramide
-Mechanism of action -Uses -Toxicity |
-Class Ia anti-arrhythmic (blocks Na and K channels)used for ventricular arrhytmias only as a last resort
-has strongst anti-muscarinic effect |
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Class Ia anti-arrhytmics
-mechanism of action |
-Block Na+ channels and block K+ channels; mostly effect His/Purkinje and ventricles by delaying phase 0 and prolonguing repolarization (slows conduction and increases ERP)
-Also slows phase 4 depolarization of pace-makers (may increase or decrease SA and AV firing depending on how much anti-muscarinic activity drug possesses |
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Class Ia anti-arrhythmics
-indications |
Only used if other anti-arrhythmics don't work
-Ventricular tachycardia -Atrial fib and flutter -Paroxysmal supraventricular tachycardia |
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Class Ia anti-arrhytmics
-toxicity |
-Have anti-muscarinic activity, which can ncrease AV conduction, increase heart rate, and lead to arrhythmia
-Lengthen QT interval, which can cause torsades de pointes |
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Adenosine
-mechanism of action -use -side effects -administration |
-Opens K+ channels via adenosine receptor
-Inhibits funny current and Ca2+ current by inhibiting adenylate cyclase -Drug of choice for paraoxysmal supraventricular tachycardia becaus slows SA node and slows AV node conduction -side effects=hypotension, skin flushing, and bronchoconstriction (careful with asthmatics) -Given IV; Methylxanthine is a adenosine receptor antagonist; need to give more adenosine if patient had coffee |
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Class Ib anti-arrhythmics
-Mechanism of action -Indications -side effects |
-weak inhibitors of Na+ channels in state dependent manner; have highest affinity for inactivated state of Na channels and preferentially act on depolarized tissue (ischemic tissue, ectopic foci, or when have increased HR)
-Cause a small decrease in rate of phase 0 and decrease action potential duration -Used for acute suppression of ventricular tachycardia; also digitalis-induced arrhythmias -Have many CNS side effects: nausea, tremor, and light-headedness |
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Lidocaine
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-Class Ib anti-arrhytmic
-Also used as local anaesthetic |
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Mexiletine
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-Class Ib anti-arrhythmic
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Tocainide
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-Class Ib anti-arrhytmic
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Phenytoin
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-Class Ib anti-arrhytmic
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Class Ic antiarrhytmics
-mechanism of action -uses -toxicity |
-Most potent inhibitor of cardiac Na+ channels; decrease phase 0 rate but do not change action potential duration
-mostly work oon His-Purkinje system and widen QRS -used only as last resort for ventricular tachycardia, atrial fib, and paroxysmal supraventricular tachycardia -extremely pro-arrhythmic |
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Flecanide
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Class Ic anti-arrhythmic
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Propafenone
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Class Ic anti-arrhytmic
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Moricizine
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Class Ic anti-arrhytmic
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Class II anti-arrhythmics
-mechanism of actions -approved drugs -uses -side effect |
-Beta Blockers: decrease rate of phase 4 in SA and AV node, which decreases HR and increases AV refractory period; also prevents ischemia
-Prolongs PR interval because prolongs AV action potential -Propanolol, acebutalol, sotalol, metaprolol, and esmolol are approved -Avoid use in asthmatics and sudden withdrawal can lead to "rebound hypersensitivity" (receptor number upregulated from drug use) -used for: atrial premature beats, stress related ventricular premature beats, paroxysmal supraventricular tachy, atrial fib and flutter, ischemia-related ventricular tachycardia -reduce mortality of arrhythmias |
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Class IV anti-arrhythmics
-mechanism of action -approved drugs -uses -side effects |
-Calcium Channel blockers
-verapamil and diltiazem -Reduce SA node automaticity and reduce AV nodal conduction -Used for paraoxysmal supraventricular tachycardia, and to control ventricular rate in atrial fib, atrial flutter, and multi-focal atrial tachycardia -Do not use with beta blockers; systemic effects can lead to hypotension |
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Bretylium
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-Class III anti-arrhythmic (K+ channel blocker)
-Also blocks realease of catecholamines from nerve terminals after initial stimulation of release |
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Ibutilide
Dofetilide |
-Class III anti-arrhytmics
-Pure K+ channel blockers -used for atrial fib and flutter -elongate QT interval |
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The use of sotalol as an anti-arrhythmic
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The l isomer of sotalol is a Beta blocker, while both d and l isomers are K+ channel blockers; at clinical doses, the Beta blocking activity predominates, but also class III anti-arrhythmic
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Amiodarone
-mechanism of action -uses -toxicity |
-Class III anti-arrhytmic K+ channel blocker, but also blocks Na+ channels (class I), is a Beta blocker (class II), and blocks Ca2+ channels (class IV)
-Decreases SA node rate, Increases AV node refractiory period, increaes the PR interval, increases QRS duration, and increases QT interval -main use is for atrial fib and flutter; also used to stop reentry arrhythmias and supraventricular tachycardias; used as prophylaxis for ventricular tachycardias; used for bypass tract mediated ventricular tachycardia (WPW syndrome) -Has a lot of side effects: most common is photodermititis; prolongs QT interval, decrease SA or AV node function, and decrease contractility; hypotension; pulmonary fibrosis from pneumonitis; hypo- or hyperthyroid or silent thyroid changes; hepatic necrosis and elevated enzymes; peripheral neuropathy, headache, ataxia, tremors; corneal deposits; testicular dysfunction -need routine EKG tests and pulmonary function tests; 1/2 life is at least 1 month |
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Class III anti-arrhythmic
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-inhibit K+ channels
-Prolong repolarization of fast action potentials without affecting rate of conduction -decrease mortality from arrhythmias -increase QT interval |
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Heparin
-Administration |
-Administer either IV or SC because so large; immediate onset of action; must monitor aPTT to make sure ony 15-25% increase
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Heparin
-Side effects |
-Excessive bleeding; thrombocytopenia; long term treatment can cause osteoporosis and spontaneous fractures
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Proamine Sulfate
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Used to treat overdose of heparin
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Aspirin
-Uses |
-Used as prophylactic agent for MI at low doses
-At high doses, reduces mortality from MI -Reduces incidence of MI in patients with unstable and stable angina -Give after coronary bypass surgery to recude thrombotic graft closure and graft arteriosclerosis |
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Aspirin
-Toxicity |
-GI irritation and bruisi
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