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Internal Medicine > JH IM Board Review - Arrhythmias I > Flashcards

JH IM Board Review - Arrhythmias I Flashcards

1
Q

Arrhythmias are classified as …?

A
  1. Bradyarrhythmias.

2. Tachyarrhythmias.

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2
Q

Bradyarrhythmias can result from abnormalities at any point along the conduction path because of … (3):

A
  1. Depressed automaticity.
  2. Conduction delay.
  3. Block.
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3
Q

Tachyarrhythmias are typically classified as:

2

A
  1. SVT.

2. VT.

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4
Q

Treatment options for arrhythmias vary depending on …?

4

A

The underlying cause. May encompass:

  1. Pharmacotherapy.
  2. Electrical conversion.
  3. Pacemaker or defibrillator insertion.
  4. Catheter or surgical ablation.
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5
Q

Bradyarrhythmias - Basic info - Arise from abnormalities in one or more of three locations:

(3)

A
  1. SA node.
  2. AV node.
  3. Infranodal.
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6
Q

SA node - Sinus node dysfunction (2 forms):

A
  1. SYMPTOMATIC sinus pauses (more than 2sec).
  2. CHRONOTROPIC INCOMPETENCE ==> Inability to attain 80% of the max predicted HR in response to exercise associated with fatigue or other symptoms.

==> Often coexists with A-fib (ie “tachy-brady” syndrome).

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7
Q

Brief ASYMPTOMATIC sinus pauses are …?

Pacemaker?

A

COMMON.

==> Permanent pacemaker therapy is generally indicated only in the presence of symptoms.

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8
Q

AV node and His-Purkinje system - 1o block - PR interval prolongation more than …

A

200ms.

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9
Q

AV node and His-Purkinje system - Mobitz I:

MC site of block is in the …

A

Progressive PR interval prolongation followed by single blocked P wave.

**MC site of block is in the AV node.

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10
Q

Mobitz II?

MC site of block is in the …

A

No progressive PR interval prolongation before blocked P wave.

==> MC site of block is in the His-Purkinje system.

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11
Q

3o AV block — Narrow QRS vs Wide QRS?

A

Narrow QRS (junctional) escape rhythm ==> Usually blocked in AV node.

Wide QRS (ventricular) escape rhythm ==> Suggests block in His bundle or below.

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12
Q

Some pts with Mobitz II and 3o AV block are asx.

Most present w/ …

(4)

A
  1. Fatigue.
  2. Dyspnea on exertion.
  3. Presyncope.
  4. Syncope.
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13
Q

AV node and His-Purkinje system pathology is often better tolerated than tachyarrhythmias b/c of their …

A

Slow progression.

**exception is INFRANODAL AV block.

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14
Q

Infranodal AV block may present w/ …

A

Syncope or cardiac arrest.

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15
Q

Sinus node dysfunction in young, healthy pts?

A

Very rare.

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16
Q

Sinus node dysfunction — Acute management:

A

Treat only if sx.

==> Atropine, isoproterenol.

==> Rarely, temporary pacer (if sx).

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17
Q

Permanent pacemaker implantation for chronic management of bradyarrhythmias — Indications:

(2)

A
  1. Sinus node dysfunction and Mobitz I in the presence of sx that correlate w/ the bradycardia.
  2. Mobitz II + 3o AV block, even when asx.
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18
Q

Device types:

3

A
  1. Dual-chamber pacemaker (DDD).
  2. Single-chamber ventricular pacemaker (VVI).
  3. Biventricular pacemaker, which provides cardiac resynchronization therapy (CRT).
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19
Q

DDD does what?

If A-fib is present …?

A

Senses and paces RA and RV.

**Unless permanent A-fib is present, in which case VVI is the most appropriate.

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20
Q

Biventricular therapy w/ CRT, increasingly used for pts with …

A

Chronic systolic HF (EF <50% or less).

Who require frequent ventricular pacing.

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21
Q

Narrow QRS complex tachycardias — 8 atrial rates:

A

Sinus tachy ==> 100-180.

AVNRT ==> 150-230.

Orthodromic AVRT ==> 150-250.

A-flutter ==> 240-320.

A-fib ==> 350-500.

A-tachy ==> 100-250.

Junctional tachy ==> 60-150.

MAT ==> 100-180.

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22
Q

Narrow QRS complex tachycardias — A to V?

A

Sinus tachy ==> 1:1.

AVNRT ==> 1:1.

Orthodromic AVRT ==> 1:1.

A-flutter ==> A > V.

A-fib ==> A&raquo_space; V.

A-tachy ==> A > V.

Junctional tachy ==> 1:1.

MAT ==> A > V.

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23
Q

Narrow QRS complex tachycardias — P wave morphology:

A

Sinus tachy ==> Sinus

AVNRT ==> Retrograde.

Orthodromic AVRT ==> Eccentric.

A-flutter ==> Sawtooth flutter waves.

A-fib ==> Fib (F) waves.

A-tachy ==> Eccentric.

Junctional tachy ==> Retrograde.

MAT ==> 3 or more different types.

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24
Q

Narrow QRS complex tachycardias — Response to carotid sinus pressure:

A

Sinus tachy ==> Slowing.

AVNRT ==> Termination.

Orthodromic AVRT ==> Termination.

A-flutter ==> Incr AV block.

A-fib ==> Decr ventricular rate.

A-tachy ==> Incr AV block.

Junctional tachy ==> Slight slowing.

MAT ==> Usually none.

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25
Q

Two functionally + anatomically distinct pathways within the AV node (“dual nodal physiology”):

(2)

A
  1. Slow-conducting pathway with short refractory period.

2. Fast-conducting pathway with long refractory period.

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26
Q

Typical form of AVNRT (90%) conducts …

A

Antegrade down slow path.

Retrograde up the fast.

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27
Q

Atypical form of AVNRT conducts …

A

Antegrade down fast path.

Retrograde up the slow.

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28
Q

Although up to …% of the general population may have dual nodal physiology, only a small proportion will experience AVNRT.

A

10%.

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29
Q

AVNRT is notable for

A

ABRUPT onset + termination of rapid, regular heart beat.

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30
Q

AVNRT age of onset may range from …

A

Childhood to old age.

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31
Q

AVNRT - What is the occasional associations?

A

Syncope or near-syncope but usually well tolerated.

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32
Q

Event monitor may be useful in pts with intermittent palpitations.

3 Typical AVNRT findings on ECG:

A
  1. 1:1 relationship of P wave to QRS complex.
  2. RP interval less than PR interval (“short PR tachycardia”), if P wave can be seen.
  3. Retrograde P wave at end of QRS complex (pseudo-R’ in lead V1, pseudo-S in lead II).
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33
Q

Atypical AVNRT findings on ECG:

A

RP interval more than PR interval (“long RP” tachycardia).

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34
Q

AVNRT — Acute management involves:

3

A
  1. Vagal maneuvers = Carotid sinus pressure, valsalva maneuver.
  2. IV adenosine (6-12mg rapid push) ==> Highly effective (90% conversion).
  3. IV verapamil (2.5-10mg) ==> Highly effective.
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35
Q

AVNRT — Chronic management:

A
  1. Catheter ablation (AV node modification, with ablation of slow AV nodal pathway).

==> 1st line tx — cures arrhythmia in more than 95% of pts.

  1. Medications if not a candidate for ablation:

==> Suppress AV node ==> Verapamil, diltiazem, or beta-blockers.

==> Slow conduction within the re-entrant circuit ==> Flecainide (Na channel blocker).

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36
Q

WPW syndrome - Definition:

A

Pt with both pre-excitation on ECG + an associated tachyarrhythmia.

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37
Q

WPW - MC tachyarrhythmia?

A

AV reciprocating tachycardia (AVRT).

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38
Q

WPW - 2nd MC tachyarrhythmia:

A

A-fib.

==> May be life-threatening in this setting because of rapid conduction down the accessory pathway.

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39
Q

What is the accessory pathway in WPW?

A

A congenital muscle fiber that connects the myocardium of the atrium to the ventricle outside of the AV node.

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40
Q

The accessory pathway may be (2):

A
  1. Manifest.

2. Concealed.

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41
Q

The manifest accessory pathway conducts in the …

A

Antegrade direction (atrium to ventricle) and usually the retrograde direction (ventricle to atrium) as well.

==> ECG shows pre-excitation (short PR + delta wave) + a slurred upstroke of the QRS complex.

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42
Q

The concealed accessory pathway conducts only in the …

A

Retrograde direction.

Baseline ECG appears normal.

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43
Q

What is the age of symptom onset in WPW?

A

Childhood through middle age.

44
Q

Some pts with accessory pathways may never develop sx tachycardia.

These pts technically do not have WPW syndrome, but rather …

45
Q

WPW may present with tachycardia:

…% AVRT

…% A-fib.

46
Q

AVRT in WPW is classified into (2):

A

Orthodromic or antidromic depending on the direction of conduction over the AV node.

47
Q

Orthodromic AV reciprocating tachycardia (ORT):

A

Tachycardia conducts antegrade down the AV node and retrograde up the accessory pathway.

48
Q

Orthodromic AV reciprocating tachycardia (ORT) is the …

A

MC form of AVRT (95%).

49
Q

ORT may occur with which type of pathway?

A

Both with manifest and with concealed accessory.

50
Q

ORT - ECG reveals a … tachycardia.

A

Narrow-complex.

51
Q

Antidromic AV reciprocating tachycardia (ART):

A

Tachycardia that conducts antegrade down the accessory pathway and retrograde up the AV node or a 2nd accessory path.

52
Q

ART - ECG reveals a … tachycardia.

May be mistaken for …

A

Wide-complex.

VT

53
Q

A-fib in WPW is …

A

Life-threatening!

54
Q

A-fib in WPW — Accessory pathways often conduct rapidly w/ small refractory periods.

May result in …

A

Extremely rapid transmission of A-fib impulses into the ventricles.

55
Q

What is the ECG in a-fib-WPW?

A

Shows wide, irregular QRS complex morphology.

56
Q

What is a possible consequence of A-fib in WPW?

A

May degenerate to V-fib and cardiac arrest.

57
Q

What are the ECG findings in WPW?

A
  1. Short PR <120ms.

2. Delta wave with widened QRS complex.

58
Q

What is the cause of the widened QRS complex in WPW?

A

Dual ventricular activation through both the accessory pathway and the normal AV node/His-Purkinje conduction system.

59
Q

What is the risk of sudden death for asx WPW pts?

60
Q

What are the guidelines for EP studies in asx WPW?

2

A
  1. Pts in high risk occupations (eg pilot, competitive athletes) may need EP testing for medical clearance.
  2. Some studies support EP testing in <35.
61
Q

What is the acute management of AVRT-WPW?

2

A
  1. Vagal maneuvers.

2. IV AV nodal blockers — adenosine, beta blockers, verapamil.

62
Q

What is the 1st line — acute management of A-fib with pre-excitation?

A

IV procainamide ==> slows accessory path + AV nodal conduction.

IV ibutilide ==> convert acute-onset AF to sinus rhythm.

63
Q

What should be avoided during the acute management of A-fib with pre-excitation?

A
  1. Digoxin.
  2. CCBs.

==> They cause even more rapid ventricular response via selective AV nodal blockade and shortening of atrial refractoriness.

64
Q

What is the acute management of a-fib with pre-excitation if pt is hypotensive or otherwise unstable?

A

Urgent/emergent electrical cardioversion.

65
Q

What is the chronic management of sx WPW pts?

A

Catheter ablation = 1st line.

66
Q

What is the time required for catheter ablation of the accessory path?

A

2-4h procedure to localize and ablate (cauterize) the path.

67
Q

What is the success rate of the cauterization of the accessory path?

A

90-95% depending on the site.

68
Q

What are the drugs that can be given to WPW pts who are managed chronically?

A
  1. Flecainide.
  2. Beta blockers.

==> To prevent further episodes of AVRT in pts awaiting catheter ablation OR if ablation is contraindicated OR not accepted by the pt.

69
Q

What are the 2 types of A-fib?

A
  1. Paroxysmal (<7days).

2. Persistent (>7days).

70
Q

What is the cause of the paroxysmal a-fib?

A

Initiated by PACs (premature atrial contractions) or by bursts of ectopic atrial activity (freq. originating in the pulm. Veins.).

**often no structural heart disease present.

71
Q

What is the cause of persistent a-fib?

2

A
  1. Structural heart disease (MS, atrial enlargement, HTN, CHF).
  2. Hyperthyroidism (1% of AF cases).
72
Q

What is the cause of a-flutter?

A

Reentrant circuit usually confined to the RA.

==> Typically proceeds COUNTER CLOCKWISE.

73
Q

What is the age of onset for a-flutter?

A

40 or older, similar to a-fib.

74
Q

What is the acute management of AF and A-fib?

A
  1. Rate control ==> beta blocker, CCB (verapamil, diltiazem).
  2. Digoxin (not for paroxysmal).
  3. Attempt cardioversion if hemodynamically UNSTABLE (hypotension, CHF, angina).
75
Q

What are the chronic management options for A-fib?

A
  1. Rate control ==> Beta blockers, CCBs, digoxin.
  2. If sx despite rate-controlling agents ==> antiarrhythmics.
  3. Consider electrical cardioversion to achieve sinus rhythm in sx pts.
  4. “Ablate and pace”.
  5. Consider pulm vein isolation.
  6. Chronic anticoagulation for stroke prevention.
76
Q

What are the antiarrhythmics for the chronic management of A-fib?

(4)

A
  1. Class IC ==> 1st line in structurally normal hearts (flecainide, propafenone).
  2. Amiodarone generally used in pts with systolic HF + severe LV hypertrophy.
  3. Sotalol + dofetilide ==> acceptable alternative in pts with CAD.
  4. Dronedarone ==> not in systolic HF or permanent a-fib.
77
Q

Chronic management options of AF — Can consider electrical cardioversion to achieve sinus rhythm in sx pts.

— What is that pts w/ AF or A-flutter should receive for more than 36 to 48h before the electrical cardioversion? (2)

A
  1. Therapeutic anticoagulation tx for at least 3wks before and 4wks after cardioversion.

Or

  1. Transesophageal echocardio to exclude atrial thrombus, followed by 4wks of continuous anticoagulation after cardioversion.
78
Q

What is the meaning of “ablate and pace” in the chronic management of A-fib?

A

In selected pts w/ refractory symptoms caused by rapid ventricular response, AV NODE ABLATION prevents conduction of rapid impulses to the ventricle and can decrease sx.

79
Q

What are the requirements of “ablate and pace” chronic management of AF?

(2)

A
  1. Chronic anticoagulation remains necessary, because the atria still fibrillate.
  2. Requires permanent ventricular pacemaker placement b/c of resulting complete AV block.
80
Q

What is the target group of “ablate and pace” chronic management of AF?

A

Older pts w/ sx refractory to other therapies.

81
Q

What is the target group in which we should consider pulmonary vein isolation?

A

Sx individuals w/ paroxysmal or short-duration persistent AF who are refractory to or intolerant of antiarrhythmic medications.

82
Q

What is the pulmonary vein isolation?

A

Catheter ablation procedure that does not involve AV node ablation.

83
Q

What is the criterion for chronic anticoagulation in order to prevent stroke in persistent + paroxysmal AF pts?

A

Depends on the risk score ==> CHA2DS2-VASc.

84
Q

What are the alternative anticoagulants in pts with nonvalvular AF?

A

NOACs ==> Dabigatran, rivaroxaban, apixaban, edoxaban.

85
Q

What are the 2 major contraindications for NOACs?

A
  1. Dose-adjustment depending on renal function and not recommended for use w/ ESRD.
  2. Pts with rheumatic valve disease or mechanical prosthetic valves.
86
Q

What is involved in the chronic management of A-flutter?

A
  1. Cardioversion (electrical or chemical).
  2. Catheter ablation of re-entrant circuit ==> 90-95% permanent elimination.
  3. Anticoagulation.
87
Q

What is the thromboembolic risk of atrial flutter?

A

Similar to A-fib.

88
Q

What are the characteristics suggestive of ventricular origin (vs supraventricular origin) in wide-complex tachycardias?

(6)

A
  1. Hx of structural or ischemic heart disease.
  2. Absence of an RS complex in all precordial leads (V1-V6).
  3. Peak of R wave to nadir of S interval >100ms in one precordial lead (V1-V6).
  4. Presence of AV dissociation (P waves unrelated to QRS complexes).
  5. Presence of fusion complexes (sinus QRS complex fuses with VT beats) or capture beats (sinus QRS complex appears between VT beats).
  6. QRS >0.16sec.
89
Q

What is the tx of sinus tachycardia?

2

A
  1. Identify and treat the underlying cause.

2. Beta blockade if caused by thyrotoxicosis, inappropriate sinus tachycardia, or if associated with cardiac ischemia.

90
Q

What is the cause of focal atrial arrhythmia?

2

A
  1. Enhanced atrial automaticity or triggered activity (rare).
  2. Digoxin toxicity.
91
Q

What is the acute management of focal atrial tachycardia?

A

Rate control or suppression with beta-blocker or verapamil.

92
Q

What is the chronic management of focal atrial tachycardia?

3

A
  1. Rate control.
  2. Suppression with flecainide, sotalol, amiodarone.
  3. Catheter ablation.
93
Q

What is the cause of multifocal atrial tachycardia?

A
  1. Multiple automatic or triggered atrial foci.

2. Occurs with elevated SNS tone, pulmonary disease (eg COPD), hypoxemia, stimulant, theophylline use.

94
Q

What is the ECG of MAT?

A

3 or more P wave morphologies are present, usually with varying PR intervals.

95
Q

What is the tx of MAT?

A

Treat underlying cause (eg hypoxemia).

==> Rate control w/ CCB or beta blockers.

96
Q

What is the tx to which MAT is generally NOT amenable?

A

Catheter ablation.

97
Q

What is a junctional tachycardia?

A

Automatic rhythm arising from the AV node.

98
Q

What is the cause of junctional tachycardia?

4

A
  1. Situations of enhanced automaticity (ie elevated SNS tone).
  2. Post-cardiac surgery.
  3. MI.
  4. Digoxin toxicity.
99
Q

What is the acute management of junctional tachycardia?

A

Treat the underlying cause.

100
Q

What is the chronic management of junctional tachycardia?

A

No tx is usually required.

101
Q

What is the chronic management of rare sx cases of junctional tachycardia?

A

Require antiarrhythmic drug therapy.

==> Catheter ablation may lead to AV block.

102
Q

What are the 4 major VTs?

A
  1. Sustained monomorphic VT.
  2. Idiopathic RVOT VT.
  3. V-fib.
  4. Torsades de pointes.
103
Q

What are the V-rates of the 4 major VTs?

A
  1. Sustained monomorphic VT ==> 140-250.
  2. Idiopathic RVOT VT ==> 140-230.
  3. V-fib ==> >300.
  4. Torsades ==> 200-300.
104
Q

What is the QRS morphology of the 4 major VTs?

A
  1. Sustained monomorphic VT ==> Any.
  2. Idiopathic RVOT VT ==> LBBB.
  3. V-fib ==> Polymorphic.
  4. Torsades ==> Polymorphic.
105
Q

What is the substrate for the 4 major VTs?

A
  1. Sustained monomorphic VT ==> Post-MI, cardiomyopathy.
  2. Idiopathic RVOT VT ==> Normal.
  3. V-fib ==> Ischemia, cardiomyopathy.
  4. Torsades ==> Long QTc interval.
106
Q

What is the medical tx of the 4 major VTs?

A
  1. Sustained monomorphic VT ==> Amiodarone, procainamide.
  2. Idiopathic RVOT VT ==> beta blockers, verapamil.
  3. V-fib ==> Amiodarone, lidocaine.
  4. Torsades ==> Mg, lidocaine.
107
Q

What are the 2 VTs in which ablation is possible?

A
  1. Sustained monomorphic VT.

2. Idiopathic RVOT VT.

Internal Medicine (106 decks)

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