Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tachyarrhythmias are typically classified as:

2

A
  1. SVT.

2. VT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Brief ASYMPTOMATIC sinus pauses are …?

Pacemaker?

A

COMMON.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

200ms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Infranodal AV block may present w/ …

A

Syncope or cardiac arrest.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sinus node dysfunction in young, healthy pts?

A

Very rare.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Sinus node dysfunction — Acute management:

A

Treat only if sx.

==> Atropine, isoproterenol.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

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

Who require frequent ventricular pacing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Typical form of AVNRT (90%) conducts …

A

Antegrade down slow path.

Retrograde up the fast.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Atypical form of AVNRT conducts …

A

Antegrade down fast path.

Retrograde up the slow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

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

A

10%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

AVNRT is notable for

A

ABRUPT onset + termination of rapid, regular heart beat.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

AVNRT age of onset may range from …

A

Childhood to old age.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

AVNRT - What is the occasional associations?

A

Syncope or near-syncope but usually well tolerated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Atypical AVNRT findings on ECG:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

WPW syndrome - Definition:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

WPW - MC tachyarrhythmia?

A

AV reciprocating tachycardia (AVRT).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

WPW - 2nd MC tachyarrhythmia:

A

A-fib.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

The accessory pathway may be (2):

A
  1. Manifest.

2. Concealed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

The concealed accessory pathway conducts only in the …

A

Retrograde direction.

Baseline ECG appears normal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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 …

A

WPW ECG.

45
Q

WPW may present with tachycardia:

…% AVRT

…% A-fib.

A

70%.

30%.

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?

A

Very low.

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions