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Atrial fibralation/flutter

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Question
Answer
arrhythmias   abnormal rate/rhythm a rhythm other than normal (50-100BPM)  
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supraventricular arrhythmias   originates above AV node not immediately life-threatening  
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types of supraventricular arrhythmias   sinus tachy/bradycardias atrial fibralation/flutter paroxysmal supraventricular arrhythmia  
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paroxysmal supraventricular arrhythmia   by pass tract reentry  
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ventricular arrhythmias   originates below AV node can be life threatening (worsening cardiac output)  
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types of ventricular arrhythmias   premature ventricular contraction non-sustained ventricular tachycardia sustained ventricular tachycardia (Torsades de Pointe) cardiac arrest (V fib, sudden cardiac death, asystole)  
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atrial fibralation   most common type of arrhythmia increased risk with age (2%>22 5%>65 10%>80y/o)  
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causes of A Fib   HTN, valvular heart disease, HF, thyroidtoxicosis, hypoxia, pericarditis, post-cardiothoracc surgery, CAD(rare)  
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s/sx of a fib   palpitations, dizziness/syncope, HF, SOB, cardiac arrest  
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SA + AV node drugs   usually CCBs and BBs  
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atrial and ventricular muscle drugs   usually Na and K channel blockers some BBs  
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SA + AV nodes   slow conduction channels  
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atrial + ventricular muscle   fast conduction channels  
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class 1 antiarrhythmics   Na channel blockers  
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class 2 antiarrhythmics   beta blockers  
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class 3 antiarrhythmics   K channel blockers  
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class 4 antiarrhythmics   Ca channel blockers  
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nodal drugs   class II and IV  
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muscular drugs   class I, II, and III  
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if patient is not hemodynamically stable   electrocardioversion  
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fast rhythm countering drugs   class I and IV  
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slow rhythm countering drugs   atropine, isoproterenol or pacemaker  
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ventricular rate vs. ventricular rhythm   CONTROL RATE FIRST!  
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ventricular arrhythmias   control rhythm (class I or III)  
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digoxin effects on arrhythmias   slows heart rate by enhancing PANS activity centrally  
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adenosine effects on arrhythmias   strong AV nodal blocker short half life rapid bolus followed by saline flush to ensure drug gets to heart as active drug  
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atrial flutter Tx   same as atrial fibralation but pts. are more likely to undergo ablation (destruction/errosion of cells or tissue)  
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pharmacotheraputic goals of atrial fibralation Tx   ventricular rate control prevention of thromboembolic events rhythm control (back to NSR)  
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ventricular rate control drugs   reduce AV nodal conduction/prevent fast atrial beats from reaching the ventricles  
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ventricular rate control drugs   BBs, CCBs(verapamil/diltiazem only), and digoxin (adenosine can work as well but is too short acting to be continuously effective)  
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rate control in a fib needs to be achieved within   48 hours of onset  
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when is rhythm control initiated   when we are sure the pt. is properly protected from thromboembolic events  
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digoxin adv.   will treat CHF concurrently  
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digoxin disadv.   slow onsset (several hours) ineffective with increase of sympathetic activity  
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CCB adv.   fast onset, effective  
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CCB disadv.   may worsen CHF may cause hypotension  
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BB adv.   fast onset, effective effective in post-operative A fib  
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BB disadv.   cantraindicated in pts. with asthma, COPD may worsen CHF symptoms may cause hypotension  
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rate control agent should be used until:   patient restores normal sinus rhythm  
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rate control agents should not be used indefinately if NSR is not achieved   rate control agents should not be used indefinately if NSR is not achieved  
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amiodarone for ventricular rate control   in pts. w/ LVD or HF in pts. that can not use other agents  
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amiodarone is   primarily a K channel blocker but also has BB and CCB properties (BEWARE OF CONVERTING PT. TO NSR)  
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a FIB >48 HOURS   high risk for thromboembolus Tx LMWH bridged w/ warfarin low risk pts. may not need bridging  
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warfarin therapy in a fib   continued until NSR is restored then continue for an additional month  
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use anticoags 4 weeks before and after cardioversion back to NSR   use anticoags 4 weeks before and after cardioversion back to NSR  
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CHADS2 score for ASA Px of thromboembolism (CHADS2 must be lower than 2 to treat with ASA)   CHF +1 HTN +1 age>70 +1 diabetes +1 stroke +2  
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after cardiversion use ___ to maintain NSR   Na or K channel blockers  
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choosing NSR restoring/maintaining agents   onset of action (IV or PO) duration of therapy (amiodarone is a lifetime drug with harsh side effects) liver/renal fxn (renal-procainamide, sotalol, dofetilide)  
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more NSR restoring/maintaining agent choices   left ventricular function (LVEF<40% use amiodarone, prefered, or dofetilide only 2 that don't inc. mortality) Hx of CAD or MI (use lidocaine or amiodarone only 2 that don't inc. mortality)  
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antiarrhythmic drug interactions   anything prolonging QT causes Torsades amiodarone & digoxin, quinidine, verapamil dofetilide & HCTZ, cimetadine, triamterine, ketoconazole, megesterol, prochlorperazine, tromethoprim, verapamil  
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only use class 1c if:   pt. has no other cardiac structural abnormality due to high risk of torsades  
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class 1a agents:   no longer used due to high recurrence of a fib  
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antiarrhythmic therapy is continued until:   cause of a fib is reversible  
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antiarrhythmic agents are usually more effective in:   new onset a fib, not chronic a fib  
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if recurrance of a fib/flutter   optimize dosing and compliance check risk factors cardiovert and continue therapy if all antiarrhythmic agents fail vontinue ventricular rate control and anticoagulation consider ablation therapy (eps in flutter)  
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treatment endpoints   NSR = 50-100BPM BP = 130/80 no thromboemolic events if on warfarin INR 2-3  
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monitoring for a fib pts.   ECG, HR, BP, side effects of drugs used  
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