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70 Cards in this Set
- Front
- Back
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what are the class IA antiarrhythmics?
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Quinidine, Procainamide, Disopyramide
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what are the class IB antiarrhythmics?
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Lidocaine, Mexiletine
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What are the IC antiarrhythmics?
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Flecainide, Propafenone
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Which drug causes cinchonism?
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tinnitus, blurred vision HA
Quinidine |
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which class of drugs cause Torsades de pointes?
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IA anti-arrhythmic drugs, class III
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what is the MOA of class 1 antiarryhtmics?
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Na+ channel blocker - acting on open and inactivated NA channels and reduction of phase 0 velocity (non nodal tissues)
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MOA of class IA antiarrythmics
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Na+ block - intermediate depression of phase 0, strong K+ channel block -> increase ERP, prolong AP duration, increase QT, QRS on ECG
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What are class IA antiarrhythmics used for
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tx atrial and ventricular arrhythmias
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whose metabolite is NAPA?
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procainamide - class IA
has Class III actions metabolite form more in rapid acetylators (50% of Americans) |
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which drug causes bone marrow aplasia
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Procainamide
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which class IA drug has anti-cholinergic effects
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disopyramide - fewest SE in class IA
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what are anticholinergic SE
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dry mouth constipation urinary rention
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MOA of class IB anti-arrhythmics
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pure wk Na channel blocker - no K blockoade - decrease ERP, slight decrease in AP so slightly slower phase 0, shortens phase 3 repolarization
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Clinical use of IB antiarryth
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post -MI to prevent ventricular tach, preferentially affect ischemic or depolarized ventricular tissue, tx digitalis induced arrhythmias, PVCs, chronic pain
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which antiarrhytmic tx chronic pain (diabetic neuropathy)
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Mexiletine
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which IB causes drowsiness, dizziness, confusion, seizures
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Lidocaine
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SE of mexiletine
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CNS - tremor, blurred vision, orally, CV depression
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which IB is orally effective
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mexiletine
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MOA of IC
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storng Na channel blockage = strong depression of phase 0, little effect on ERP and no effect on AP, slight ability to block Ca channels - decrease AV nodal conduction (increased QRS)
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clinical use of IC
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SVT, vent tachycardia, A-fib (slow nodal conduction), PVC
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which class of antiarrythmics are CI in post MI patients
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IC
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which anti-arrythmic has pro-arrhythmic effects?
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flecainide don't give post MI
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Flecainide SE
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pro-arrhythmic, depression of LV preformance
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which class I anti-arrythmic is CI in asthmatics
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propafenone
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beta blockers MOA (antiarrythmic)
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block beta adrenorecpetors (so to decrease HR, contractility and conduction)
reduce nodal automaticity and conductance, block NE to bind so decrease cAMP -> decrease Ca -> suppress abnoraml pacemakers by decreasing slope of phase 4 (depolarization in SA/AV nodes), increase PR interval |
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which beta blockers are used as anti-arrythmic therapy
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Propranolol, metopropol, esmolol
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MOA of propranolol
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non selective B1 and B2 antagonist, inhibition of sympthatic stimulation of heart, may block Na channels at high doses
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MOA of metoprolol and Esmolol
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cardio selective for B1
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Use of beta blockers?
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A fib/flutter (decrease AV conduction for AVT-slow heart)
SOP to prevent ventricular arrhythmias post-MI |
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what is the standard protocol to prevent ventricular arrhythmias post MI
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beta blockers (propranolol, metoprolol and esmolol
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SE of propanool
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hypotension, AV block, severe bradycardia, possible HF, bronchospasm, acute w/drawal sydndrome predisposing to MI, increase TG and decrease HDL levels
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caution in which patients when prescribing propanolol
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asthamtic, diabetics (induce glucose intolerance)
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how is beta blocker (propanolol) toxicity reveresed
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glucagon or isoproterenol
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which beta blocker is best for acute managemet of ventricular rate in A fib/flutter
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Esmolol, b/c rapidly metabolized via IV
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SE of metoprolol
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dyslipidemia
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what are class II anti-arrythmics
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Beta blockers
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What are class III anti-arrythmics
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K channel blockers
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MOA of class III
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prolong phase 3 repolarizaton - leading to prolonged AP and ERP
prolongs refractory period by blocking outward K+ current needed to repolarize the cell after an AP no effect on phase 0 |
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is phase 0 effected by class III anti arrythmics
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no
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what are the class III antiarrythmics
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amiodarone, sotalol, dofetilide
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what is the most prescribed antiarrythmic
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amiodarone
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MOA of amiodarone
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block K channels - increase ERP, weak alpha and B blockers, Ca channel blocker (reduces automaticity - phase 4 slope, and decreases AV node conduction
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what is the first line tx of acute v-tach/fib
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amiodarone
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SE of amiodarone
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hyper/hypo thyroidism, blue skin discolaration (iodine), pulmonary fibrosis, hepatic dysfunction, QT prolongation (> risk for torsades than other class III)
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MOA of sotalol
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non selective B blocker that also has K channel blocking - increase APD and ERP, automaticity reduced by beta blocking acitions
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which anti arrythmic is approved for use in children
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sotalol
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SE of sotalol
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increase risk of torsades, can magnify SA node dysfunction
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MOA of dofetilide
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pure K + channel blocker, increase AP and ERP
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clinical use of dofetilide
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maintian NSR in A-fib/flutter
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SE of dofetilide
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use restricted to physicians who have undergone manufacturers training because of the risk of life-threatening vetnricular arrhythmias
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MOA of class IV anti-arrythmics
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Ca channel blockers ->block slow inward calcium current -> decrease depolarization (phase 4) in AV/SA nodes
increase ERP and PR interval |
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CCB classes
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nondihydropyridine, hydropyridine (greater affinity for vascular calcium channels)
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CCB used as anti-arrythmics
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nondihydropyridine agents
verapamil diltiazem |
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Clinical use of class IV
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SVT
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SE Class IV
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negative notropic effect so limit use in patients with LV dysfunction, hypotension, constipation (V>D), flushing and edema
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what are the other drugs used for arrythmias (non classified)
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Adenosine, digoxin, Mg
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which anti arrythmic produces transient asystole (5 secs)
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adenosine
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MOA of adenosine
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stimulate ACh - sensitive K current to increase phase 4 slope
antagonizes cCAMP effects to reduce Ca currents (increase nodal refractoriness and inhibits DAD) ctr-alt-del (rapid and transient cardiac depression) |
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clinical use of adenosine
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acute tx of SVT, drug of choice in dx/abolishing SVT
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CI of adenosine
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asthmatics/COPD - causes bronchoconstriction
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what blocoks the affects of adenosine
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theophylline
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MOA of digoxin
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inhibits Na/K ATPase -> indirect effect of increasing intracellular calcium (+ inotropic effect) -- have higher tendency for DAD
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clinical use of digoxin
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control of ventricular rate in A-fib/flutter
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SE of digoxin
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hypokalemia - increase risk of arrythmias, ventricular arrhythmias, low therapeutic index
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what is effective in treating torsades de pointes and digoxin toxicity
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Mg+
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which antiarrythmics are used for HTN
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propanolol - patients with high renin activity - youth, whites and BP control in patients with underlying heart disease
verapamil - HTN in low renin level pts Diltiazem - HTN in low renin levels |
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Na channel blockers
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decrease conduction velocity (phase 0)
suppress vetnricular and atrial muscle firing |
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K channel blockers
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increase time for repolarization (phase 2 and 3)
prolongs AP duration increases time to reset excitibility |
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K channel stimualtors
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increase repolarizing influence
decrease slope of phase 4 slow HR (Ach, PNS) |
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CCB
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nodal cells - decrease slope of phase 4
decrease excitibility of nodal cells not as effective in NA dependnent cells |
