04b: Arrhythmia Flashcards
Lifetime risk of developing A-fib in men and women at age 40 is (X)% and (Y)%, respectively.
X = 26 Y = 23
List the RFs for development of A-fib.
- Age
- HT
- Obesity
- Smoking
- Diabetes
- Low HDL
T/F: There are familial cases of A-fib, with an increasing number of genetic mutations identified.
True
Patient has had 3 episodes of AF. All lasted 5 days and stopped. Which category AF does she have?
Paroxysmal AF (2 or more episodes that terminate spontaneously within a week)
(X) AF is persistent AF lasting longer than 7 days. And (Y) is continuous AF lasting longer than 12 months.
X = persistent Y = longstanding persistent
What’s the difference between “longstanding persistent” AF and permanent AF?
Permanent AF refers to case in which either attempts to restore sinus rhythm have failed or decision has been made not to restore sinus rhythm
Highest relative risk of having thromboembolism in A-fib is if patient has (X) risk factor.
X = prior stroke/TIA
RR = 2.5
A-fib (X) risk score. What are the factors listed?
X = CHA(2)DS(2)VASc
- CHF or EF under 40%
- HT
- Age (65-75 or over 75)
- Diabetes
- Stroke (previous)
- Vascular disease
- Female
Which RFs on A-fib CHA(2)DS(2)VASc risk score deserve 2 points?
- Age over 75
2. Prior stroke
List the three mechanisms by which A-fib can be caused.
- Multiple random propagating wavelets
- Focal triggers
- Localized reentrant activity
(Slow/fast) atrial conduction, (short/long) refractory period, and (small/large) atria promote/perpetuate A-fib.
Slow, short, large
When AF is maintained for as little as (X) hours/days/months, cell level changes (atrial remodeling) promote electrical (reentry/triggers).
X = 24 hours
Both reentry and electrical triggers
AF therapy focuses on which two aspects?
- Stroke prevention
2. Symptom control
Deciding which stroke-prevention therapy to pursue with AF patient depends on (X).
X = CHA(2)DS(2)VASc risk score
Patients with AF should be on warfarin if CHA(2)DS(2)VASc score is (X). What is the other option for stroke-prevention meds?
X = 2 or higher
Aspirin if score less than 2
Treating AF symptoms is done by (rate/rhythm) control.
Either or
Rhythm control of AF is done by (X) therapies.
X = DC cardioversion and ablation
Rate control of AF is done by (X) therapies.
X = drug (B-blockers, CCBs, digoxin)
T/F: The risk of stroke is altered by rhythm control strategy.
False
T/F: Neither duration nor frequency of AF are factors attributed to stroke risk.
True
AF: Atrial remodeling promotes reentry by altering which key things?
- Shortening refractory period
- Slowing conduction (impaired connexins, fibrosis)
- Enlarging pathological space
List the three mechanisms of arrhythmogenesis.
- Enhanced automaticity
- Triggered activity
- Reentry
Arrhythmogenesis: what is the mechanism behind ‘enhanced automaticity’?
Increase in slope of Phase 4 depolarization (largely dependent on funny current, If)
Arrhythmogenesis: abnormal ‘triggered activity’ is a result of (X) states, such as in patients who are:
X = Ca-overloaded
Exercising, stressed, or have HF
List the two types of ‘triggered activity’ that can lead to arrhythmias. What differs between them?
- Delayed afterdepolarization (DAD) (during Phase 4)
2. Early afterdepolarization (EAD) (during Phase 2 or 3)**LETHAL
(X) arrhythmic state appears to be the initiating mechanism of the polymorphic ventricular tachycardia, torsades de pointes.
X = EAD (Early afterdepolarization)
Reentry: When conduction block occurs because a propagating impulse encounters (X), the block is said to be “functional”.
X = refractory cardiac cells
Reentry: When conduction block is caused by impulse encountering (X), the block is said to be “fixed”.
X = barrier imposed by fibrosis or scarring (that replaces myocytes)
Class I antiarrhythmic drugs (stimulate/block) (X).
Block
X = Na channels
Class II antiarrhythmic drugs (stimulate/block) (X).
Block
X = beta-adrenergic R
Class III antiarrhythmic drugs (stimulate/block) (X).
Block;
X = K channels
Class IV antiarrhythmic drugs (stimulate/block) (X).
Block
X = Ca channels
Which two drugs are used for their antiarrhythmic properties, but are not classified?
Adenosine and digoxin
List the subclassifications of Class I antiarrhythmics. What do these subclasses depend on?
Rate of dissociation from Na channels
IA (intermediate)
IB (fast)
IC (slow)
(X) subclass of Class I antiarrhythmics has the greatest affinity for (Y) channels.
X = IC (slowest dissociation, greatest affinity) Y = Na
Class I antiarrhythmics will block (higher/lower) percent of Na channels at greater HRs.
Higher
Procainamide is a(n) (X) drug used primarily for (Y).
X = Class IA antiarrhythmic Y = Pre-excited A-fib (WPW Syndrome)
(BUT RARELY USED!!!)
Procainamide mechanisms of action.
- Increases excitability threshold
- Decreases automaticity
- Prolongs conduction and repolarization
(X) anti-arrhythmic drug is known to have lupus-like syndrome as side effect. What’s another key side effect of this drug?
X = procainamide (Class IA)
Increased arrhythmias
Lidocaine is a(n) (X) drug used primarily for (Y).
X = Class IB antiarrhythmic Y = ventricular arrhythmias (esp in setting of ischemia)
Lidocaine mechanisms of action.
- Slows conduction (esp at rapid HR and ischemic tissue; little effect on normal tissue)
- Decreases slope of phase 4
Lidocaine is administered via (X) route(s) and has (slow/fast) onset of action.
X = IV only
Fast (45-90s)
T/F: Risk of increased arrhythmias is adverse effect of all Class I antiarrhythmics.
False - not Class IB
T/F: Risk of CNS effects is adverse effect of all Class I antiarrhythmics.
True
Flecainide is a(n) (X) drug used primarily for (Y).
X = Class IC antiarrhythmic Y = Atrial arrhythmias
ONLY in patients with structurally NORMAL HEARTS
Flecainide mechanisms of action.
SLOWS DOWN:
- Phase 0
- Conduction velocity
- Pacemaker activity
(X) antiarrhythmics should not be used in patients with underlying conduction problems due to its ability to cause:
X = Class IC (flecainide)
Functional BBB or AV Block (by slowing conduction in His bundle)
(X) is a common Class II Antiarrhythmic drug prototype used. It’s given (PO/IV/SC) and acts by which mechanism?
X = metroprolol
PO
NODAL effects: Reduces automaticity of SA node and conduction velocity of AV node
(X) antiarrhythmic drug can reduce “triggered” activity by (increasing/decreasing) (Y) currents.
X = metroprolol (Class II) and verapamil (Class IV)
Decreasing
Y = Ca currents
Metroprolol is used as antiarrhythmic in which cases?
Both supraventricular tachycardias (A-fib/atrial flutter) and ventricular tachycardias
(X) classes of antiarrhythmic drugs used for rhythm control and (Y) classes for rate control.
X = I, III Y = II, IV
(X) antiarrhythmic drug is given to treat (rhythm/rate) control of A-fib BEFORE (Y) drug given for (rhythm/rate) control.
X = metroprolol
Rate;
Y = Class IC (flecainide)
Rhythm
Metroprolol can cause serious (tachy/brady)-arrhythmia and is contraindicated in patients with (X). This is also true for Class (I/II/III/IV) antiarrhythmics.
Bradyarrhythmia (via heart block);
X = conduction abnormalities (AV conduction defect, SA Node dysfunction)
IV (verapamil)
Dofetilide is a(n) (X) drug that primarily works by which mechanism?
X = Class III antiarrhythmic
Blocks K channels (outward current), prolonging repolarization
Dofetilide used/indicated primarily for:
Atrial arrhythmias
Class III antiarrhythmic
Class (X) antiarrhythmics affect reentry; they (increase/decrease) excitable gap by (increasing/decreasing) (X) of tissue.
X = III
Decrease;
Increasing
X = refractory period
(X) antiarrhythmic drugs are more effective at slow HRs and less effective at fast HRs. This can result in torsaides due to (brady/tachy)-cardia with (short/long) (Y) interval.
X = Class III (Dofetilide)
Bradycardia
Long
Y = QT
Amiodarone is a(n) (X) drug that is drug of choice for:
X = Antiarrhythmic (primarily class III, but also I, II, IV characteristics)
Atrial/ventricular arrhythmias in patients with structurally abnormal heart
T/F: Risk of torsaides is high wth amiodarone
False
(X) drug used for antiarrhythmia is given (PO/IV) only. In the ED, it’s used for its ability to cause complete, transient (Y) block.
X = adenosine
IV;
Y = AV node (thus terminating atrial arrhythmias)
Digoxin antiarrhythmic effect is mediated by (increase/decrease) in vagal tone. It primarily allows (rate/rhythm) control by its actions on (X).
Increase;
Rate control
X = SA, AV nodes
Antidromic AVRT will present differently on EKG than orthodromic AVRT in which way?
Antidromic: wide QRS
Orthrodromic: narrow QRS
Antidromic AVRT: unidirectional block in (X) path and reentry travels up (Y) path.
X = Y = AV Node
Wolff-Parkinson-White (WPW) Syndrome affects (X)% of the population, and is defined by the presence of a(n) (Y) and associated arrhythmias.
X = 0.03 Y = antegrade (and retrograde) conducting bypass tract
Delta wave and (short/long) PR interval on EKG is hallmark of (X). Why does this wave occur?
Short PR
X = WPW Syndrome
Bypass tract conducts impulse antegrade, so ventricles depolarized via more than one, normal path (down septum)
T/F: The treatment of WPW is catheter ablation of the bypass tract.
True - to eliminate the anomalous AV connection
Why might A-fib be lethal in WPW Syndrome?
Accessory path doesn’t modulate conduction like AV node does (rapid conduction; HR can exceed 250 bpm)
It’s CRUCIAL to avoid giving (X) drugs to patients with WPW Syndrome experiencing pre-excited A-fib.
X = AV node blockers (B-blockers, CCBs, adenosine)!!!!
T/F: B-blockers can be given to WPW syndrome patients with SVT.
True - if not in pre-excited A-fib
Treatment of pre-excited A-fib requires (PO/IV/SC) administration of (X) drug or cardioversion.
IV
X = procainamide (slows conduction through accessory path)
How is pre-excited A-fib distinguishable from ventricular tachycardia on EKG?
Irregular rhythm and variable width of QRS complexes
WPW syndrome patients that are not amenable to ablation are treated with (X) drug.
X = flecainide
(X) antiarrhythmic drug is available only in IV and used to treat acute ventricular arrhythmia.
X = lidocaine
Key point to distinguish ventricular tachycardia from SVT on EKG.
WIDTH OF QRS (wide in VT)
