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A Fib

Atrial fibralation/flutter

arrhythmias abnormal rate/rhythm a rhythm other than normal (50-100BPM)
supraventricular arrhythmias originates above AV node not immediately life-threatening
types of supraventricular arrhythmias sinus tachy/bradycardias atrial fibralation/flutter paroxysmal supraventricular arrhythmia
paroxysmal supraventricular arrhythmia by pass tract reentry
ventricular arrhythmias originates below AV node can be life threatening (worsening cardiac output)
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)
atrial fibralation most common type of arrhythmia increased risk with age (2%>22 5%>65 10%>80y/o)
causes of A Fib HTN, valvular heart disease, HF, thyroidtoxicosis, hypoxia, pericarditis, post-cardiothoracc surgery, CAD(rare)
s/sx of a fib palpitations, dizziness/syncope, HF, SOB, cardiac arrest
SA + AV node drugs usually CCBs and BBs
atrial and ventricular muscle drugs usually Na and K channel blockers some BBs
SA + AV nodes slow conduction channels
atrial + ventricular muscle fast conduction channels
class 1 antiarrhythmics Na channel blockers
class 2 antiarrhythmics beta blockers
class 3 antiarrhythmics K channel blockers
class 4 antiarrhythmics Ca channel blockers
nodal drugs class II and IV
muscular drugs class I, II, and III
if patient is not hemodynamically stable electrocardioversion
fast rhythm countering drugs class I and IV
slow rhythm countering drugs atropine, isoproterenol or pacemaker
ventricular rate vs. ventricular rhythm CONTROL RATE FIRST!
ventricular arrhythmias control rhythm (class I or III)
digoxin effects on arrhythmias slows heart rate by enhancing PANS activity centrally
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
atrial flutter Tx same as atrial fibralation but pts. are more likely to undergo ablation (destruction/errosion of cells or tissue)
pharmacotheraputic goals of atrial fibralation Tx ventricular rate control prevention of thromboembolic events rhythm control (back to NSR)
ventricular rate control drugs reduce AV nodal conduction/prevent fast atrial beats from reaching the ventricles
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)
rate control in a fib needs to be achieved within 48 hours of onset
when is rhythm control initiated when we are sure the pt. is properly protected from thromboembolic events
digoxin adv. will treat CHF concurrently
digoxin disadv. slow onsset (several hours) ineffective with increase of sympathetic activity
CCB adv. fast onset, effective
CCB disadv. may worsen CHF may cause hypotension
BB adv. fast onset, effective effective in post-operative A fib
BB disadv. cantraindicated in pts. with asthma, COPD may worsen CHF symptoms may cause hypotension
rate control agent should be used until: patient restores normal sinus rhythm
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
amiodarone for ventricular rate control in pts. w/ LVD or HF in pts. that can not use other agents
amiodarone is primarily a K channel blocker but also has BB and CCB properties (BEWARE OF CONVERTING PT. TO NSR)
a FIB >48 HOURS high risk for thromboembolus Tx LMWH bridged w/ warfarin low risk pts. may not need bridging
warfarin therapy in a fib continued until NSR is restored then continue for an additional month
use anticoags 4 weeks before and after cardioversion back to NSR use anticoags 4 weeks before and after cardioversion back to NSR
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
after cardiversion use ___ to maintain NSR Na or K channel blockers
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)
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)
antiarrhythmic drug interactions anything prolonging QT causes Torsades amiodarone & digoxin, quinidine, verapamil dofetilide & HCTZ, cimetadine, triamterine, ketoconazole, megesterol, prochlorperazine, tromethoprim, verapamil
only use class 1c if: pt. has no other cardiac structural abnormality due to high risk of torsades
class 1a agents: no longer used due to high recurrence of a fib
antiarrhythmic therapy is continued until: cause of a fib is reversible
antiarrhythmic agents are usually more effective in: new onset a fib, not chronic a fib
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)
treatment endpoints NSR = 50-100BPM BP = 130/80 no thromboemolic events if on warfarin INR 2-3
monitoring for a fib pts. ECG, HR, BP, side effects of drugs used
Created by: lex86