A Fib Word Scramble
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| Question | Answer |
| 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
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