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for BOD

Quiz yourself by thinking what should be in each of the black spaces below before clicking on it to display the answer.
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Question
Answer
Left Anterior Descending Artery Supplies...   Anterior Wall & Some Septal Wall (Has "Diagonal Branches")  
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Left Circumflex Artery Supplies...   Lateral Wall (Has "Marginal Branches")  
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Right Coronary Artery Supplies...   Inferior Wall (Usually PDA off of it, which Supplies Infra-Septal and Inferior Wall)  
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Heart Blocks (1st, 2nd, 3rd Degree)   1st Degree: Consistent PR delay (>200 ms), No Skipped Beats. 2nd Degree: Increasingly lengthen PR w/ occasional PVC. 3rd Degree: Junctional (narrow) escape rhythm with complete AV. block  
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Alpha Receptors   Epi > NE (no isopreternol). Vasoconstriction, Mydriasis, Splenic Contraction. Gq --> PL-C --> DAG + IP3. DAG--> PKC + MAPK (Vasoconstrict, ^BP). IP3 --> Ca from SR (^ Cardiocontractility).  
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Beta Receptors   Iso > Epi > NE. Cardiostimulation, Bronchodilation, Vasodilation, Metabolic Acidosis. Gs --> Adenylyl Cyclase --> cAMP --> PKA --> Ca from SR --> Contractility  
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Epinepherine   Alpha Receptors: Vasoconstriction Beta Receptors: Vasodilation  
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Norepinepherine   Alpha Receptors (Mostly): Vasoconstriction Beta-1 Receptors (Cardiac): Cardiostimulation  
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Ispopreternol   Beta Receptors: Vasodilation and cardiostimulation  
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Ergotoxin   Blocks NE's Vasoconstriction (alpha) Blocks Epi's Vasoconstriction (alpha) Does NOT block Epi's Vasodlation (Beta) Alpha Blocker (The First!)  
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Dichloroisopreternol   Beta Blocker (The first!)  
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Dopamine   Inotropine (Similar to NE) Increase force of contraction Vasodilates renal arteries (but alpha effects & vasoconstriction at high doses) Indicated for shock with oliguria (increase CO via Beta Receptors & Increase renal blood flow via DA-ergic effects)  
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Dobutamine   (+) isomer: Beta-1 Agonist + Alpha-1 Antagonist (-) isomer: Alpha-1 agonist For: Short term for CHF, MI (increase CO, SV w/o HR increase)  
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Blood Vessels   Alpha-1 & Alpha-2 (Constrict to ^^BP). Beta-2 (Dilate in Skeletal muscle arterioles)  
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Bronchi   Alpha-1 (Constrict). Beta-2 (Relaxes)  
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Heart   Beta-1 & Beta-2 (increase HR, increase contractility). Target for beta-blockers!  
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Nerve Endings   Alpha-2 (neg feedback to lower NE Release). Beta-1 & Beta-2 (on nerve endings. Increase NE Release)  
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Mast Cells   Beta-2 (less histamine release)  
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Second Messengers for Alpha-1, Alpha-2, Beta-1, Beta-2 Receptors   A1 (IP3 + DAG). A2 (less cAMP). B1+B2 (more cAMP).  
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Ritodrine   B2 agonist. Delays uterine contraction att erm.  
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Salbutamol   B2 agonist. For asthma  
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Methoxamine & ****PHENYLEPHRINE*****   A1 agonist (vasoconstriction)  
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Alpha-Methylnorepinepherine & Clonidine   Alpha-2 agonist (neg feedback to stop vasoconstriction)  
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Butoxamine   B2 antagonist  
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Labetolol & Metoprolol   B1 antagonist  
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***Propanolol***   B1 & B2 antagonist  
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Yohimbine   A2 antagonist  
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Prazosin   A1 antagonist (for HTN)  
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***Phentolamine***   Short-acting A1/A2 antagonist (for shock)  
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***Phenoxybenzamine***   Long-Acting A1 & A2 antagonist (for shock)  
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Cocaine   Sympathomimetic. Blocks NET (more NE in synapse). Increase O2 demand (A + B adrenergic effect) w/ less O2 delivery. Result: ischemia, infarction, arrhythmia. Chronic: dilated or hypertrophic cardiomyopathy, atherosclerosis, myocarditis, necrosis.  
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Platelet Aggregation   Expose subendothelial Matrix. Thromboxane A2 + ADP recruit + activate platelets to form plug).  
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Anti-Platelet Drug Targets   Platelet Surface ADP Receptor P2Y12 (CLOPIDOGREL & PRASUGREL) & GPIIB/IIIa Receptors (ABCIXIMAB). Platelete dense granules: ThrombaxaneA2 (ASPIRIN via Cyclooxygenase inhibition. Irreversible) & ADP (CLOPIDOGREL + PRASUGREL).  
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Endothelial Cell Drug Targets (ANti-Clotting)    
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***Aspirin*** (Acetyl Salicyclic Acid)   Acetylates serine in COX-1. Irreversible inhibition. (Cannot become TxA2 which normally causes vasoconstriction and platelet agg). Toxicities: GI discomfort, bleeding, antiinflamm, Hypercapnia, Glucose intolerance, poison (reps alk, met acidosis, RD)  
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***Clopidogrel*** (Plavix)   P2Y12 Antagonist. Prodrug (CYP2C19 activates). (Omeprazole is a CYP2C19 inhibitor). Used to prevent occlusion after stunting coronary vessels.  
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***Prasugrel*** (Effient)   P2Y12 antagonist. Prodrug. MOre potent than plavix, more bleeding. Does not use CYP2C19, but DOES use Cyp3A5 + 2B6.  
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Ticagrelol (Brilanta)   Direct (no CYP450) reversible inhibitor of P2Y12  
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Abciximab, Tirofiban, Eptifibatide, Lamifiban   GPIIb/IIIa antagonist (block receptor). Inhibit platelet aggregation BUT risk intrinsic platelet activation & thrmbocytopenia (low platelet count). Used, bu limited.  
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Anticoagulants (note, different from antiplatet, these are anti-clotting)   Normally: tissue injury --> TF expressed, Phospholipid complex forms, Activates thrombin, Fibrin polymerization and clot formation  
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Pro-coagulation from Thrombin (IIa)   ADP, TXA2, Va, VIIa, XIa, TAFI (thrombin-activated thrombolysis inhibitor)  
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Anti-coagulation from Thrombin (IIa)   Prostocyclin, NO, tPA, Protein C+S (activate by IIa will inactivate Va, VIIIa)  
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Heparin (Anticoagulant)   Inactivates ACTIVE clotting factors oof INTRINSIC pathway. WOrks by accelerating ATIII 1000x  
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HIT   Heparin-Induced Thrombocytopenia: combo of bleeding AND thrombosis (30% mortality): activated platelets, removed by spleen macrophages (thrombocytopenia). Plaetelets also procoaglunant (thrombosis). Treat with thrombin inhibitors.  
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LMWH (***enoxaprin*** dalteparin, ___parin)   Low molecular weight heparin: more predictable effects, can give subQ, more bioavailable, longer half life, less HIT, less osteoporosis. does NOT inhibit IIa.  
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Thrombin Inhibitors (***Hirudin (leech derivative), Lepirudin, Argatroban, Bivalirdivin, **Rivaroxaban***(oral), ***Apixaban*** (oral)   Use for HIT (inactivates soluble and clot-bound IIa. WOrks if ATIII is deficient).  
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Warfarin   Oral anticoag. Inhibits FORMATION of active (acts @ IX, X, II). Prevents gamma carboxylation by inhib. vit K epoxide reductase. Takes ~1 week to kick in (circ clotting factors long 1/2 life). Monitor INR (2-3). CYP2C9. More vit K may lower INR. Teratogen.  
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Fibrinolysis (tPA, streptokinase, Reteplase, Tenecteplase)   tPA from endothelial cells, activates plasmin to degrade clot (more D-dimer in blood). Give for acute MI, thrombotic stroke, arterial thromboses, PE, DVTs, occlude catheters and shunts. Bleeding risk! Streptokinase: risk allergic rxn. Not fibrin-specific  
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Rose Criteria (is pain cardiac?)   1. Substernal Chest Pain 2. Temporal Relation to Stimulus (Exercise/Stress) 3. Relieved with discontinuation of stimulus 4. Relieved with Nitrates  
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Virchow's Triad   1. Hypercoaguability 2. Hemodynamic Changes (stasis/turbulence) 3. Endothelial cell injury/Dysfunction.......THROMBUS!!!  
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Risk Factors (For Pretty much Everything)   Male, Old, Smoker, HTN, Dislipidemia, Atherosclerosis, Family History  
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AAA (Abdominal Aortic Aneurism)   Saccular (one side) + Fusiform (all the way around. True (ALL layers) vs. False (Confined by adventitia but can still easily rupture)  
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Vasculitis   High ESR, High CRP, GIant cell arteritis, Sup temporal artery, common in elderly, often unilateral. Can go blind. Multinucleited giant cells.  
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Large Vessel Vasculitis   Giant cell arteritis if >50 YO, Takayasu if < 50 YO  
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Medium Vessel Vasculitis   Polyarteritis Nodosa (w/o MCLN) Lawasaki (w/ MCLN) (MCLN = mucocutaneous lymph node syndrome)  
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Small Vessel Vasculitis   Many! Immune complexes in vessels or paucity of vasc IgG  
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ST Depression   More global ischemia, cormobidities, coronary disease, hypertension, hyperlipidemia. A chronic thing.  
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Angina: General Treatment Strategies   1. Nitrates 2. Calcium Channel BLockers 3. Beta Blockers  
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Nitrates (Glyceryl Trinitrate/Nitroglycerine)   Venous capicitanse (more preload, less O2 demand). Release NO in vasc smooth muscle cells. Kidney excretion. Relzx blood vessel. Dosage! (vein-->arteries). Met by mito lad dehy. NO --> cGMP --> relax smooth muscle  
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Calcium Channel Blockers ***Verapamil***, ***NIfedipine***, Dilitiazem   Inhibit calcium entry. Verapiml + Dilitiazem suppress conduction (@ nodes) so less HR, more vasodilation, less contractility. Nifedipine, Nicardapine, Minodipine do NOT have effect on Conduction (vasodilator, less contractility).  
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Beta Blockers   Less contractility, less renin/angiotensein so lowers BP, anti-arrhythmic, less exercise tachycardia  
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1st Generation (Blanket) Beta Blockers   ***Propanolol*** (etc)  
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2nd Generation (B1) Beta Blockers (Cardioselective)   Atenolol, ***Metoprolol*** etc  
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3rd Generation (Vasodilating) Beta Blockers   Pindolol, ***Carvedilol*** etc  
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Mixed alpha/beta blocers   Labetalol  
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9 min half life beta blocker   Esmolol (to lower BP in ER)  
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Giant Cell Temporal Vasculitis   Large Vessel. Granulomatous vasculitis of aorta and extra cranial branches of carotid. Patients >50. May lead to blindness. Associated w/ polymyalgia rheumatica  
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Takyatsu Arteritis   Involves aortic arch and branches by granuloomatous arterities. Thickened intima. Female. Patients < 50  
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Polyarteritis Nodosa   Lesions of dif ages. 30% associated w/ HepB. Necrotizing inflammation w/o glomerulnephritis. Nodules on arterial wall, skin, viscera. Immune complex disease. Fibrinoid necrosis  
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Kawasaki Disease   Kids <4 yo, most common acquired heart disease in children. smooth muscle in arterial wall. Arteritis associated w/ MLNS  
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Wegener Granulomatosis   Granulomatous inflam. Resp tract, kidney , sinus, nasal mucosas. Necrotizing glomeruonephritis common. C-ANCA (anti-neutrophil cytoplasmic antibiodies) Low Ig.  
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Churg-Strauss Syndrome   Eosinophilia, Asthma, Granulomas. Glomerunophritis. p-ENCA  
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Microscopic Polyangitis/arteritis   Lesions of the same age. Nec glomeruonephritis common. Pulm capillaries involved. C-ANCA. Leads to hemorrhage.  
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Granulmoatous Vasculitis (Temporal Arteritis)   Intima Prolif, breaks in elastic stain. Biopsy need not be (+), elevated SED rate and CRP  
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Buerger Disease   Thromboangitis obliterans (in extremeties. Ven thromboses. With Tobacco!)  
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Rheumatic Fever   Pharyngitis, Skin absess (impetigo), group A strep pharyngitis precedes it. Antigen-mimic (M protein). Give prophylatic penicillin  
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Jones Criteria   2 Major or 1 Major + 2 Minor. Required: Evidence of Strep. Major: Carditis, Polyarteritis, Chorea, Erythema Marginatum, SubQ nodules. Minor: Fever, Arthralgia, Previous Rheum fever/heart disease, ESR up, CRP up, leukocytosis, PR interval up (heart blo  
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Fibrinous Pericarditis   From: End Stage Renal Disease, MI, Dressler's Syndrome (after MI), Radiation Pericarditis, Virus, Trauma, Drugs. UREMIA. "Bread & Butter." See fat, organization, fibrin (pink/amorphous)  
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Fibrous Pericarditis   Stiff, can't contract. TB, fungal, pericarditis, tumor, radiation, no-resolving fibrillin. Fibroblastic prolif. Create brididges pericardium to epicardium. KUSMALL sign: JVD  
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4 Factors Influencing Cardiac Performance   1. Preload (venous return) 2. Afterload (TPR) 3. Cotnractility 4. HR  
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Digitalis, Digoxin (longer), OUabain (shorter)   More contractility vía more intracellular sodium (inhibit the na/k atpase. Stops calcium extrusion. so more pumping.  
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DAD   Delayed after depolarization...more contractility, V. tach (toxicity of digitalis).  
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Beta Blockers in CHF   Metoprolol - B1 selective Carvedilol - Non selective  
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Systolic HF   "Fat and Short" P(V) curve  
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Diastolic HF   "Tall and Skinny" P(V) Curve  
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FACES   Heart failure symptoms: Fatigue, Angina, Congestion (Chest), Edema, SOB  
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NYHA Classification   I: Mid II Mild (slight limitation III Moderate (marekd limitation) IV: severe  
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ACC/AHA Classification:   A: High risk B: Asymptomatic LV dysfunction C: Past/current HF Sx D: End Stage HF  
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EAD (early after depolarizations)   Phase 2: prolonged or Phase 3 prolonged. Can mediate torsade de Pointes (polymorphic VT)  
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DAD (delayed after depolarization)   Impaired calcium handling (Na/Ca exchanger up, then depolarizing current). Occurs w/ digitalis and idiopathic c VTs. Sensitive to adenosine, Calcium channel blockers, beta blockade.  
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Class 1 Anti-Arrhythmics   Block Entry of Na (Phase 0). 1b (RAPID i.e. LIDOCAINE). 1a (med ie QUINIDINE). 1c (longer ie econide and flecanide).  
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Class 2 Anti-Arrhythmics   Beta Blockers -Main effect on L-type calcium channels and If phase 4 in nodal cells. PROPANOLOL: anti-arrhythmic, inhibits exercise tachycardia, alleviates angina, lowers renin. Use for increased sympathetic activity.  
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Class 3 Anti-Arrhythmics   K Blockers (slow depolarization) Amioderone, Sotalol, Bretylium. Prolong repolarization (may see EADs). Also photosensitivity with AMiderone.  
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Class 4 Anti-Arrhythmics   Ca Channel Blockers. 4a: L-type Ca block. Shorten repolarization (verapamil, dilitiazem). Depress phase 0 in SA cells, shorten plateau. 4B: K channel openers (ADENOSINE). SLOWING of AV conduction. DO NOT USE IN ASTHMA. for paroxysmal supra vent. tach.  
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Automaticity Arrhythmia?   Use Beta Blocker, Calcium Channel Blocker  
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Triggered Arrhythmia (EADs/DAD's)?   Use Beta blockers, Calcium Channel Blockers  
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Conduction (reentry) Arrythmias?   Sodium and Calcium blockers.  
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Imaging   X-ray, Cath, Nuclear, Echo, CTA, MR  
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