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CVD > 04b: Arrhythmia > Flashcards

04b: Arrhythmia Flashcards

1
Q

Lifetime risk of developing A-fib in men and women at age 40 is (X)% and (Y)%, respectively.

A 
X = 26
Y = 23
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2
Q

List the RFs for development of A-fib.

A
  1. Age
  2. HT
  3. Obesity
  4. Smoking
  5. Diabetes
  6. Low HDL
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3
Q

T/F: There are familial cases of A-fib, with an increasing number of genetic mutations identified.

A

True

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4
Q

Patient has had 3 episodes of AF. All lasted 5 days and stopped. Which category AF does she have?

A

Paroxysmal AF (2 or more episodes that terminate spontaneously within a week)

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5
Q

(X) AF is persistent AF lasting longer than 7 days. And (Y) is continuous AF lasting longer than 12 months.

A 
X = persistent
Y = longstanding persistent
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6
Q

What’s the difference between “longstanding persistent” AF and permanent AF?

A

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

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7
Q

Highest relative risk of having thromboembolism in A-fib is if patient has (X) risk factor.

A

X = prior stroke/TIA

RR = 2.5

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8
Q

A-fib (X) risk score. What are the factors listed?

A

X = CHA(2)DS(2)VASc

  1. CHF or EF under 40%
  2. HT
  3. Age (65-75 or over 75)
  4. Diabetes
  5. Stroke (previous)
  6. Vascular disease
  7. Female
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9
Q

Which RFs on A-fib CHA(2)DS(2)VASc risk score deserve 2 points?

A
  1. Age over 75

2. Prior stroke

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10
Q

List the three mechanisms by which A-fib can be caused.

A
  1. Multiple random propagating wavelets
  2. Focal triggers
  3. Localized reentrant activity
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11
Q

(Slow/fast) atrial conduction, (short/long) refractory period, and (small/large) atria promote/perpetuate A-fib.

A

Slow, short, large

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12
Q

When AF is maintained for as little as (X) hours/days/months, cell level changes (atrial remodeling) promote electrical (reentry/triggers).

A

X = 24 hours

Both reentry and electrical triggers

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13
Q

AF therapy focuses on which two aspects?

A
  1. Stroke prevention

2. Symptom control

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14
Q

Deciding which stroke-prevention therapy to pursue with AF patient depends on (X).

A

X = CHA(2)DS(2)VASc risk score

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15
Q

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?

A

X = 2 or higher

Aspirin if score less than 2

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16
Q

Treating AF symptoms is done by (rate/rhythm) control.

A

Either or

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17
Q

Rhythm control of AF is done by (X) therapies.

A

X = DC cardioversion and ablation

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18
Q

Rate control of AF is done by (X) therapies.

A

X = drug (B-blockers, CCBs, digoxin)

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19
Q

T/F: The risk of stroke is altered by rhythm control strategy.

A

False

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20
Q

T/F: Neither duration nor frequency of AF are factors attributed to stroke risk.

A

True

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21
Q

AF: Atrial remodeling promotes reentry by altering which key things?

A
  1. Shortening refractory period
  2. Slowing conduction (impaired connexins, fibrosis)
  3. Enlarging pathological space
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22
Q

List the three mechanisms of arrhythmogenesis.

A
  1. Enhanced automaticity
  2. Triggered activity
  3. Reentry
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23
Q

Arrhythmogenesis: what is the mechanism behind ‘enhanced automaticity’?

A

Increase in slope of Phase 4 depolarization (largely dependent on funny current, If)

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24
Q

Arrhythmogenesis: abnormal ‘triggered activity’ is a result of (X) states, such as in patients who are:

A

X = Ca-overloaded

Exercising, stressed, or have HF

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25
Q

List the two types of ‘triggered activity’ that can lead to arrhythmias. What differs between them?

A
  1. Delayed afterdepolarization (DAD) (during Phase 4)

2. Early afterdepolarization (EAD) (during Phase 2 or 3)**LETHAL

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26
Q

(X) arrhythmic state appears to be the initiating mechanism of the polymorphic ventricular tachycardia, torsades de pointes.

A

X = EAD (Early afterdepolarization)

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27
Q

Reentry: When conduction block occurs because a propagating impulse encounters (X), the block is said to be “functional”.

A

X = refractory cardiac cells

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28
Q

Reentry: When conduction block is caused by impulse encountering (X), the block is said to be “fixed”.

A

X = barrier imposed by fibrosis or scarring (that replaces myocytes)

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29
Q

Class I antiarrhythmic drugs (stimulate/block) (X).

A

Block

X = Na channels

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30
Q

Class II antiarrhythmic drugs (stimulate/block) (X).

A

Block

X = beta-adrenergic R

31
Q

Class III antiarrhythmic drugs (stimulate/block) (X).

A

Block;

X = K channels

32
Q

Class IV antiarrhythmic drugs (stimulate/block) (X).

A

Block

X = Ca channels

33
Q

Which two drugs are used for their antiarrhythmic properties, but are not classified?

A

Adenosine and digoxin

34
Q

List the subclassifications of Class I antiarrhythmics. What do these subclasses depend on?

A

Rate of dissociation from Na channels

IA (intermediate)
IB (fast)
IC (slow)

35
Q

(X) subclass of Class I antiarrhythmics has the greatest affinity for (Y) channels.

A 
X = IC (slowest dissociation, greatest affinity)
Y = Na
36
Q

Class I antiarrhythmics will block (higher/lower) percent of Na channels at greater HRs.

A

Higher

37
Q

Procainamide is a(n) (X) drug used primarily for (Y).

A 
X = Class IA antiarrhythmic
Y = Pre-excited A-fib (WPW Syndrome)

(BUT RARELY USED!!!)

38
Q

Procainamide mechanisms of action.

A
  1. Increases excitability threshold
  2. Decreases automaticity
  3. Prolongs conduction and repolarization
39
Q

(X) anti-arrhythmic drug is known to have lupus-like syndrome as side effect. What’s another key side effect of this drug?

A

X = procainamide (Class IA)

Increased arrhythmias

40
Q

Lidocaine is a(n) (X) drug used primarily for (Y).

A 
X = Class IB antiarrhythmic
Y = ventricular arrhythmias (esp in setting of ischemia)
41
Q

Lidocaine mechanisms of action.

A
  1. Slows conduction (esp at rapid HR and ischemic tissue; little effect on normal tissue)
  2. Decreases slope of phase 4
42
Q

Lidocaine is administered via (X) route(s) and has (slow/fast) onset of action.

A

X = IV only

Fast (45-90s)

43
Q

T/F: Risk of increased arrhythmias is adverse effect of all Class I antiarrhythmics.

A

False - not Class IB

44
Q

T/F: Risk of CNS effects is adverse effect of all Class I antiarrhythmics.

A

True

45
Q

Flecainide is a(n) (X) drug used primarily for (Y).

A 
X = Class IC antiarrhythmic
Y = Atrial arrhythmias

ONLY in patients with structurally NORMAL HEARTS

46
Q

Flecainide mechanisms of action.

A

SLOWS DOWN:

  1. Phase 0
  2. Conduction velocity
  3. Pacemaker activity
47
Q

(X) antiarrhythmics should not be used in patients with underlying conduction problems due to its ability to cause:

A

X = Class IC (flecainide)

Functional BBB or AV Block (by slowing conduction in His bundle)

48
Q

(X) is a common Class II Antiarrhythmic drug prototype used. It’s given (PO/IV/SC) and acts by which mechanism?

A

X = metroprolol
PO

NODAL effects: Reduces automaticity of SA node and conduction velocity of AV node

49
Q

(X) antiarrhythmic drug can reduce “triggered” activity by (increasing/decreasing) (Y) currents.

A

X = metroprolol (Class II) and verapamil (Class IV)
Decreasing
Y = Ca currents

50
Q

Metroprolol is used as antiarrhythmic in which cases?

A

Both supraventricular tachycardias (A-fib/atrial flutter) and ventricular tachycardias

51
Q

(X) classes of antiarrhythmic drugs used for rhythm control and (Y) classes for rate control.

A 
X = I, III
Y = II, IV
52
Q

(X) antiarrhythmic drug is given to treat (rhythm/rate) control of A-fib BEFORE (Y) drug given for (rhythm/rate) control.

A

X = metroprolol
Rate;
Y = Class IC (flecainide)
Rhythm

53
Q

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.

A

Bradyarrhythmia (via heart block);
X = conduction abnormalities (AV conduction defect, SA Node dysfunction)

IV (verapamil)

54
Q

Dofetilide is a(n) (X) drug that primarily works by which mechanism?

A

X = Class III antiarrhythmic

Blocks K channels (outward current), prolonging repolarization

55
Q

Dofetilide used/indicated primarily for:

A

Atrial arrhythmias

Class III antiarrhythmic

56
Q

Class (X) antiarrhythmics affect reentry; they (increase/decrease) excitable gap by (increasing/decreasing) (X) of tissue.

A

X = III
Decrease;
Increasing
X = refractory period

57
Q

(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.

A

X = Class III (Dofetilide)
Bradycardia
Long
Y = QT

58
Q

Amiodarone is a(n) (X) drug that is drug of choice for:

A

X = Antiarrhythmic (primarily class III, but also I, II, IV characteristics)

Atrial/ventricular arrhythmias in patients with structurally abnormal heart

59
Q

T/F: Risk of torsaides is high wth amiodarone

A

False

60
Q

(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.

A

X = adenosine
IV;
Y = AV node (thus terminating atrial arrhythmias)

61
Q

Digoxin antiarrhythmic effect is mediated by (increase/decrease) in vagal tone. It primarily allows (rate/rhythm) control by its actions on (X).

A

Increase;
Rate control
X = SA, AV nodes

62
Q

Antidromic AVRT will present differently on EKG than orthodromic AVRT in which way?

A

Antidromic: wide QRS
Orthrodromic: narrow QRS

63
Q

Antidromic AVRT: unidirectional block in (X) path and reentry travels up (Y) path.

A

X = Y = AV Node

64
Q

Wolff-Parkinson-White (WPW) Syndrome affects (X)% of the population, and is defined by the presence of a(n) (Y) and associated arrhythmias.

A 
X = 0.03
Y = antegrade (and retrograde) conducting bypass tract
65
Q

Delta wave and (short/long) PR interval on EKG is hallmark of (X). Why does this wave occur?

A

Short PR
X = WPW Syndrome

Bypass tract conducts impulse antegrade, so ventricles depolarized via more than one, normal path (down septum)

66
Q

T/F: The treatment of WPW is catheter ablation of the bypass tract.

A

True - to eliminate the anomalous AV connection

67
Q

Why might A-fib be lethal in WPW Syndrome?

A

Accessory path doesn’t modulate conduction like AV node does (rapid conduction; HR can exceed 250 bpm)

68
Q

It’s CRUCIAL to avoid giving (X) drugs to patients with WPW Syndrome experiencing pre-excited A-fib.

A

X = AV node blockers (B-blockers, CCBs, adenosine)!!!!

69
Q

T/F: B-blockers can be given to WPW syndrome patients with SVT.

A

True - if not in pre-excited A-fib

70
Q

Treatment of pre-excited A-fib requires (PO/IV/SC) administration of (X) drug or cardioversion.

A

IV

X = procainamide (slows conduction through accessory path)

71
Q

How is pre-excited A-fib distinguishable from ventricular tachycardia on EKG?

A

Irregular rhythm and variable width of QRS complexes

72
Q

WPW syndrome patients that are not amenable to ablation are treated with (X) drug.

A

X = flecainide

73
Q

(X) antiarrhythmic drug is available only in IV and used to treat acute ventricular arrhythmia.

A

X = lidocaine

74
Q

Key point to distinguish ventricular tachycardia from SVT on EKG.

A

WIDTH OF QRS (wide in VT)

CVD (8 decks)

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