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Peds Cardiology > 6. EP > Flashcards

6. EP Flashcards

1
Q

What % of pregnancies have fetal arrythmias?

A

1-2

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2
Q

What is the most common type of arrhythmia in fetal life?

A

PACs

80-90%

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3
Q

What % of fetal arrhythmias are sustained?

A

10%

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4
Q

What can fetal SVT lead to?

A
  1. Hydrops
  2. Reduced ventricular function

(Limits diastolic filling time)

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5
Q

When is treatment indicated in fetal SVT?

A
  1. Sustained arrhythmia (>50% SVT burden)

2. Hydrops

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6
Q

What is the first line drug for fetal SVT if there is no evidence of hydrops?

A

Digoxin

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7
Q

What % of patients respond to digoxin for fetal SVT?

A

60-80%

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8
Q

What digoxin level do you need to have adequate fetal transfer?

A

2 (high)

This results in 60% fetal transfer

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9
Q

What happens to the fetal transfer rate of medications if the baby has hydrops?

A

Decreases by 50%

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10
Q

What are medication options for fetal SVT that is refractory to digoxin or if the baby is hydropic?

A
  1. Flecainide
  2. Sotalol
  3. Amiodarone
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11
Q

What are treatment options for fetal atrial flutter?

A
  1. Flecainide
  2. Sotalol
  3. Amiodarone
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12
Q

Which 2 drugs used for fetal arrhythmias have an excellent fetal transfer?

A

Flecainide and sotalol (80-100%)

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13
Q

What the fetal transfer of amiodarone

A

Poor, 10-30%

? role for this in infants with more severe hydrops

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14
Q

How early can a fetus with sustained tachycardia develop hydrops?

A

48 hours

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15
Q

Can adenosine be used in fetal SVT?

A

Yes, as an injection into umbilical vein

High risk to the fetus

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16
Q

Do isolated PACs require restriction from sports?

A

No

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17
Q

First line therapy for long QT?

A

Beta blockers

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18
Q

Risk factors for SCD in LQTS?

A
  1. Length of QT interval (>500 greatest risk)

2. Prior syncope

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19
Q

Can amiodarone be used in LQTS?

A

Relative contraindicated (prolongs QT)

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20
Q

Is a prophylactic ICD recommended in LQTS?

A

No

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21
Q

Best way to break flutter?

A

DC cardioversion

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22
Q

What effect does digoxin have on flutter?

A

Can slow ventricular response, but won’t often terminate the tachycardia

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23
Q

What are 3 drugs that can be used for flutter, but take time for effect and may not convert the rhythm?

A
  1. Sotalol
  2. B-blocker
  3. Amiodarone
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24
Q

What does a vagal maneuver do to flutter?

A

Slow ventricular rate so flutter becomes more visible

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25
Q

True or False: In infants, flutter has a low incidence of recurrence and won’t require short/long term anti-arrhythmics?

A

True

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26
Q

Strongest risk markers for sudden death in patients with HCM?

A
  1. FHx premature sudden death
  2. Septal thickness >30mm

Other RF:

  1. Non-sustained V-tach
  2. Syncope (not neurally mediated)
  3. BP decrease or inadequate increase during exercise testing
  4. LGE on MRI
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27
Q

What drugs does amiodarone increase effect/level/toxicity of any may need to have a decreased dose once starting amiodarone?

A
  1. Coumadin
  2. Digoxin
  3. Phenytoin
  4. Class I anti-arrhythmic
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28
Q

How is digoxin excreted?

A

Kidneys

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29
Q

True or false: Patients with WPW can have intermittent pre-excitation?

A

True

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30
Q

What are patients with WPW at risk for?

A

SVT

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31
Q

What % of patients with Lyme disease have cardiac involvement?

A

8%

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32
Q

When does cardiac involvement from Lyme disease usually present?

A

Within a few weeks of illness onset

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33
Q

What is the most common feature of Lyme carditis?

A

AV block

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34
Q

True or False: Most cases of Lyme carditis with AV block require pacemaker?

A

False- most resolve gradually with normalization of PR in 1-2 weeks… persistence needing pacemaker is unusual

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35
Q

Drug of choice for Lyme carditis?

A

Doxycycline

-Can also consider cephalosporin or amoxicillin

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36
Q

What may you need to due in Lyme carditis with AV block if the HR is too slow?

A

Temporary pacing

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37
Q

First step in neurocardiogenic syncope?

A

Increased fluids

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38
Q

Can an athlete with LVH and T-wave inversions on ECG still play?

A

Not until an echo is done

Worry about HCM

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39
Q

T wave inversions in which leads is almost always an abnormal finding?

A

V5
V6
I
aVL

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40
Q

Chronic opthalmoplegia, pigmentary retinal degeneration and at least 1 of ataxia/heart block/high protein in CSF

A

Kearns-Sayre syndrome

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41
Q

When does Kearns-Sayre usually present

A

Before 20

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42
Q

Cardiac issues in Kearns-Sayre?

A

BBB and prolonged QT often progressing to complete heart block

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43
Q

What should be done for a patient with Kearns-Sayre and bifasicular block on ECG?

A

Pacemaker (can rapidly progress to complete AV block)

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44
Q

Should all patients with Kearns-Sayre syndrome get a pacemaker?

A

Not necessarily… only if bifascicular block

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45
Q

What is % mortality in infancy for patients with LQTS with 2:1 AV block?

A

50

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46
Q

What is recommended therapy for an infant with bradycardia due to LQTS with 2:1 AV block?

A

Pacemaker and B-blocker (the B-blocker will enhance AV block, but decreases chance of ventricular arrhythmia)

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47
Q

Relationship of the conduction system to the VSD in patients with an AV canal?

A

Posterior/inferior to VSD

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48
Q

Why is there LAD in AC canal defects?

A
  • Initial QRS forces inferior/rightward

- QRS loop moves counterclockwise… superior/left causing LAD

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49
Q

Normal baseline HR of fetus?

A

120-160

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50
Q

Normal short term HR variability in a fetus?

A

2-3bpm around baseline

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51
Q

Normal long term HR variability in a fetus?

A

Baseline HR occurring 3-5 times per minute with an amplitude of 5-20bpm

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52
Q

What normally happens to HR when there is an increase in fetal BP?

A

Bradycardia (initiates vagal nerve reflex)

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53
Q

What effect can fetal hypoxemia have on HR?

A

Bradycardia or loss of HR variability

Hypoxia has a direct depressing effect on function of CNS and fetal myocardium

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54
Q

List predictors of poor long-term survival after ToF repair

A
  1. Older age at operation
  2. Significant residual hemodynamic abnormalities
  3. Use of outflow tract patch
  4. QRS >180msec
  5. Elevated LVEDP
  6. Poor LV function
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55
Q

True or False: Do PVCs increase risk of SCD in ToF patients?

A

False

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56
Q

What % of patients can have atrial tachycardia after ToF repair?

A

20-30% (may predispose to sudden death)

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57
Q

What ECG findings is a minor Jones criteria for acute rheumatic fever?

A

PR interval prolongation

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58
Q

How many major/minor Jones criteria for acute rheumatic fever?

A

2 major

1 major, 2 minor

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59
Q

Acute rheumatic fever follows an infection with that?

A

Group A strep

-After latency period of 3 weeks

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60
Q

What systems does rheumatic fever affect?

A
  1. Heart
  2. Joints
  3. Brain
  4. Cutaneous/subcutaneous tissues
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61
Q

What % of patients with RF have carditis?

A

50%

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62
Q

True or false, complete heart block usually isn’t seen in rheumatic carditis?

A

True

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63
Q

What is an early sign of myocarditis?

A

Tachycardia

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64
Q

What disease does Choreiform movements go with?

A

Rheumatic fever (rapid jerking movements of hands, face, feet)

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65
Q

Coronary artery aneurysms

A

Kawasaki

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66
Q

Dilated ascending aorta

A

Marfan

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67
Q

Bifid Uvula

A

Loeys-Dietz

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68
Q

True or False: SLE and scleroderma may be associated with a prolonged PR interval

A

True

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69
Q

True or False: PACs are common in fetal life and don’t warrant therapy

A

True

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70
Q

In a fetus with PACs, what can cause temporary decreases in HR?

A

Blocked PACs

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71
Q

What intervention is needed for blocked PACs in fetal life?

A

None if fetus has good ventricular function and no hydrops

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72
Q

What is the incidence of premature beats detected in utero?

A

2%

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73
Q

What % of fetuses with premature beats in utero have arrhythmias that persist in the newborn?

A

<10%

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74
Q

What % of premature beats in fetuses are PACs?

A

80-90%

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75
Q

First line therapy for SVT in WPW?

A

Propranolol

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76
Q

What 2 drugs are relatively contraindicated for SVT in presence of WPW?

A

Digoxin and verapamil

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77
Q

What is a second line agent for SVT in WPW if the patietn does respond to beta blocker?

A

Flecainide

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78
Q

What anti-arrhythmic class does mexiletine fall into?

A

IB

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79
Q

What causes the + T wave in V1 in a neonate?

A

Early appearance of repolarization in LV and late termination of depolarization in RV (overall LV to RV sequence)
-Change to negative T waves happens during 1st week of life

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80
Q

What happens to P waves in episode of PJRT?

A

Deeply negative in II, III, aVF

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81
Q

What is an accessory pathway mediated tachycardia due to a slowly conducting accessory pathway typically located in the right posterior septum?

A

PJRT

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82
Q

Due to the position of the pathway in PJRT, the P-wave axis is usually what?

A

-90 degrees… negative P-waves in II, III, aVF

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83
Q

True or False: P waves are usually easily visible on ECG in PJRT

A

True

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84
Q

True or False: PJRT often has 1:1 relationship of ventricles to atria

A

True

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85
Q

Describe PJRT

A
  • Incessant form of tachycardia
  • May cause a cardiomyopathy
  • Rates tend to be slower (150-200bpm)
  • Harder to detect clinically
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86
Q

What happens to ECG with K of 5.5-6.5?

A

T waves become tall and peaked

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87
Q

What happens to ECG with K >6.6?

A

QRS widening with ST segment elevation

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88
Q

What happens to ECG with K >8.5?

A

P waves disappear

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89
Q

Above what K level do you typically see arrhythmias?

A

9

*AV block, v-tach, v-fib

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90
Q

What are Q waves often indicative of?

A

Infarction

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91
Q

Most common arrhythmia in the acute post-op period following surgery?

A

JET

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92
Q

What is a focal tachycardia with gradual warm-up/cool down and rate variability?

A

JET

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93
Q

Where are P-waves in JET?

A
  • Terminal portion or shortly after QRS

- Can be completely dissociated

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94
Q

Describe the rate in JET

A

Constant or fluctuate with increases/decreases in catecholamine state

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95
Q

True or False: JET has VA dissociation with ventricular rate being faster than atrial rate

A

True

*Know it’s not flutter/EAT because ventricular rate is faster than atrial rate

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96
Q

Describe relationship between atria/ventricles in re-entrant SVT

A

1:1

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97
Q

How to distinguish between tachycardia with V-A dissociation?

A

Narrow QRS: JET

Wide QRS: V-tach

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98
Q

Most common coronary anomaly?

A

Left circumflex from right main (1/3 of all)

*Usually incidental finding with no clinical significance

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99
Q

Name a coronary anomaly that is often of greater clinical significance

A

Left main from right sinus of Valsalva

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100
Q

What are the 4 pathways a left coronary artery from the right sinus of Valsalva can take?

A
  1. Posterior to aorta
  2. Anterior to RVOT
  3. Within ventricular septum beneath RV infundibulum
  4. Between aorta and pulmonary artery
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101
Q

What type of coronary anomaly most commonly causes sudden cardiac death?

A

Left main coronary artery from right sinus of Valsalva passing between aorta and PA

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102
Q

Most likely result of maternal treatment with amiodarone during pregnancy?

A

Neonatal hypothyroidism

*No significant impact to neonatal liver, lungs, eyes or kidneys

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103
Q

What defect should you consider with LAD on ECG?

A

Primum ASD

-80 degrees

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104
Q

Common findings on ECG with primum ASD?

A

LAD, RVH, RAE

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105
Q

What type of ASD has a prolonged PR?

A

All

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106
Q

Which ASD types have a normal to right axis?

A

Secundum, sinus venosus, unroofed CS

*Can have an rSR’ pattern in V1

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107
Q

What % of the population has a PFO?

A

20-30%

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108
Q

True or False: Erythromycin is associated with QT prolongation

A

True

*Others include some anti-arrhythmic, tricyclic antidepressants, erythromycin, ondansetron, chloral

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109
Q

Half life of adenosine?

A

2-10 seconds

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110
Q

What drug is excellent for acute termination of re-entrant SVT or diagnosis of flutter?

A

Adenosine

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111
Q

What is done for SVT if patient is hemodynamically unstable?

A

DC cardioversion

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112
Q

What anti-arrhythmics are relatively contraindicated under 1 year?

A

CCB- Verapamil

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113
Q

First line therapy for neonatal atrial flutter?

A

DC cardioversion

  • 0.5-1 J/kg
  • High doses often needed in neonates due to the energy not being delivered as efficiently via neonatal pads
  • If 1J/kg unsuccessful, increase energy and cardiovert again
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114
Q

What type of cardioversion if there is a stable rhythm with a pulse?

A

Synchronized

*Unsynchronized can cause shock on T-wave = V-fib

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115
Q

What may be needed if flutter cardioversion is successful, but re-starts immediately after?

A

Antiarrhythmic (like amiodarone)

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116
Q

Class I recommendations for permanent pacing in children, adolescents and patients with congenital heart disease?

A
  1. Advanced second or third degree AV block associated with symptomatic bradycardia, ventricular dysfunction, or low CO
  2. Sinus node dysfunction with correlation of symptoms during age-inappropriate bradycardia. The definition of bradycardia varies with the patient’s age and expected HR
  3. Post-operative advanced 2nd or 3rd degree AV block that isn’t expected to resolve or persists at least 7 days after cardiac surgery
  4. Congenital 3rd degree AV block with a wide QRS escape rhythm, complex ventricular ectopy or ventricular dysfunction
  5. Congenital 3rd degree AV block in the infant with a ventricular rate <50-55bpm or with congenital heart disease and a ventricular rate <70bpm
  6. Sustained pause-dependent VT, with or without prolonged QT, in which the efficacy of pacing is thoroughly documented
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117
Q

True or False: Complex ventricular ectopy is an indication for pacemaker placement

A

True

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118
Q

What type long QT presents as syncope or arrhythmia with exercise?

A

1

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119
Q

What is the most common form of long QT

A

Long QT 1

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120
Q

Genetic testing can reveal a cause in what % of patients with high index of suspicion for long QT?

A

75%

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121
Q

What is the gene mutation in Long QT 1?

A

KCNQ1

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122
Q

True or False: There is often no conduction disease of AV node (no abnormalities of AH or HV intervals) in long QT

A

True

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123
Q

What testing can be helpful in bringing out Brugada?

A

Procainamide challenge

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124
Q

True or False: Proxainamide can prolong the QT

A

True

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125
Q

In order for reentry to occur in cardiac muscle and to result in dysrhythmia, what must also be present?

A

Area of conduction delay

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126
Q

What is needed for SVT to occur?

A

2 pathways with difference in conduction properties and refractory periods separated by an area of nonconduction

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127
Q

What is entrainment?

A

Form of mapping reentry tachycardias

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128
Q

Name 2 properties of focal tachycardias

A
  1. Triggered activity

2. Increased automaticity

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129
Q

True or False: Patient can develop AV block years after heart surgery

A

True

  • More common in patients who had temporary AV block in immediate post-operative period
  • Late development of AV block may play a role in sudden cardiac death
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130
Q

Which patients with 2nd degree heart block need a pacemaker?

A
  • Mobitz I (Wenckebach): Only if slow underlying rate or symptoms
  • Mobitz II: All patients, there is conduction system disease and patient is at risk even without symptoms and with good underling HR
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131
Q

What is a macro re-entrant arrhythmia with atrial rates between 240-400bpm?

A

Atrial flutter

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132
Q

ECG with regular rhythm and saw-tooth P-waves?

A

Atrial flutter

  • AV node can’t conduct at the same rate as the atrial activity
  • Typically some type of conduction block (2:1 or 4:1)
  • Block can be variable and cause flutter to appear as an irregular rhythm
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133
Q

True or False: Flutter is common in patients who have undergone atrial surgery

A

True

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134
Q

What is the most effective way to terminate flutter?

A

DC cardioversion

*Especially if hemodynamic instability

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135
Q

What is an alternative to DC cardioversion for hemodynamically stable flutter?

A

Atrial overdrive pacing

*With atrial pacing wires post-op

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136
Q

Temporary overdrive pacing can work to terminate what type of tachycardias?

A

Re-entrant

  • Flutter
  • SVT
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137
Q

For temporary overdrive pacing, what do you typically set the pacing rate at?

A

10-20bpm faster than tachycardia

*Can try progressively faster rates, but there is a risk of inducing a-fib

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138
Q

What is the effect of adenosine and digoxin on flutter?

A

Blocks the ventricular response, but doesn’t terminate rhythm

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139
Q

What is elective replacement indicator or ERI?

A
  • Set when the battery voltage drops below a certain limit on pacemaker
  • Paces at a rate lower than the set rate
  • Pacemaker may change from dual chamber to a single chamber pacing mode as well to conserve battery life
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140
Q

How long will a pacemaker operate on ERI conditions from the point the ERI is set?

A

At least 3 months

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141
Q

What happens after 3 months in ERI for a pacemaker?

A
  • End of life mode
  • Erratic pacing
  • Pacemaker further conserves battery life by disabling all pacemaker features except pacing
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142
Q

When should a patient be scheduled for pacemaker replacement due to battery?

A

When ERI first reached

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143
Q

What is rate-responsive pacing?

A

Increases the pacing rate in response to increased patient activity

*Can also set pacemaker to decrease rate at night during sleep and pace at set rate otherwise

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144
Q

What dysrhythmia occurs in 10-15% of patients with hyperthyroidism?

A

A-fib

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145
Q

How does thyroid hormone contribute to arrhythmogenic activity?

A

Alters the EP characteristics of atrial myocytes by shortening the AP duration and enhancing automaticity and triggered activity in the pulmonary vein cardiac tissue

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146
Q

What does hypothyroidism due to ECG voltages?

A

Decreases them

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147
Q

True or False: Hyperthyroidism can cause heart block

A

False- Typically doesn’t affect conduction

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148
Q

In peds, sick sinus syndrome is most likely associated with what?

A

Surgery for CHD

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149
Q

What type of surgery can cause damage to sinus node?

A

Anything within the atrium

*Risk for sinus node dysfunction is directly related to the extent of surgery in the atrium

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150
Q

Which two surgical patients are at the highest risk for sinus node dysfunction?

A
  1. Atrial switch

2. Fontan

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151
Q

Name 3 conditions associated with AV block

A
  1. Lyme
  2. Maternal SLE
  3. Myocarditis
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152
Q

Most common arrhythmia after sinus venosus ASD repair?

A

Sinus node dysfunction

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153
Q

Why do sinus venosus ASDs have a higher incidence of sinus node dysfunction?

A

Proximity to the sinus node with the potential for direct damage or injury to the sinus node artery during repair

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154
Q

What do the 3 letters represent in pacemakers?

A
  1. Chamber paced
  2. Chamber sensed
  3. Response to sensed event
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155
Q

What is inhibit mode for a pacemaker?

A
  • When pacemaker senses an intrinsic cardiac event, it inhibits pacing
  • Allows intrinsic cardiac events to happen without pacing
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156
Q

What is triggered mode for a pacemaker?

A

-Pacemaker actively paces in response to sensed event -Senses an intrinsic atrial contraction then paces ventricle in response

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157
Q

What does DDD pacemaker setting do?

A
  • Paces both atrium and ventricle
  • Senses both atrium and ventricle
  • Inhibits and tracks in response to sensed event
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158
Q

If a person with a DDD pacemaker has a higher HR than the set rate, what is happening?

A

Device is sensing native higher atrial rate and triggering the ventricle to pace at same rate

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159
Q

What type of patients would DDI be a helpful pacemaker setting?

A
  • Atrial arrhythmias
  • Avoid pacemaker tracking rapid atrial rates with subsequent rapid pacing in the ventricles

-Sense/pace in both atrial ventricles, but only inhibits…can’t track an atrial rate above the lower rate limit of the pacemaker

160
Q

What is DOO pacing?

A

Pace the atrial and ventricle at lower rate limit with no sensing (pace atria and ventricles without regard to intrinsic cardiac activity)

161
Q

3 most common side effects of B-blockers in children?

A
  1. Behavioral changes
  2. Depression
  3. Mood swings
162
Q

Less common side effects of beta blockers in children (besides behavioral changes, depression and mood swings)?

A
  1. Lightheadedness
  2. Tiredness
  3. Headache
  4. Nightmares
  5. Difficulty sleeping
  6. Heartburn
  7. Diarrhea
  8. Constipation

*Rarely can cause rash or hypoglycemia

163
Q

What underlying condition can beta-blockers exacerbate?

164
Q

Why do beta-blockers need to be used cautiously in patients with diabetes?

A

Can block hypoglycemia symptoms

165
Q

ECG findings in Pompe?

A
  • Marked ventricular hypertrophy (QRS complexes off the page)
  • Short PR interval
  • Strain with ST segment changes and T-wave inversion in limb leads
166
Q

What results from an inherited deficiency of lysosomal enzyme alpha-glucosidase (responsible for breakdown of glycogen to glucose)?

A

Pompe disease- Glycogen storage disease type II

167
Q

Glycogen storage disease type II

168
Q

What results in intralysosomal accumulation of glycogen (primarily in muscle cells) which leads to progressive loss of muscle function?

169
Q

What is one of the most severe/lethal forms of HCM with death in the 1st 2 years of life?

170
Q

Baby clinically well at birth, but within 6 months starts
to develop hypotonia, severe cardiomegaly, hepatomegaly, poor weight gain, difficulty sucking, enlarged protruding tongue…?

171
Q

What EP issue is a patient with unrepaired L-TGA most at risk for?

A

Complete AV block

  • 10% may present with heart block
  • Occurs at a rate of up to 2% per year
172
Q

Why is there an increased risk for AV block in L-TGA?

A

Displacement of AV node and abnormal course of conduction tissue which runs very superifical

173
Q

What 2 EP issues are patients with L-TGA at risk for?

A
  • Complete heart block (highest risk)

- WPW

174
Q

True or False: Patients with L-TGA are not at high risk for atrial flutter, sinus node dysfunction, junctional tachycardia or torsades

175
Q

A normal HV interval is usually between what?

176
Q

A shorter HV interval is seen in what?

A

Ventricular preexcitation (WPW)

177
Q

A longer HV interval is seen in what?

A

AV node or His-Purkinje disease (BBB)

178
Q

What should happen during an EP study if you deliver a premature atrial stimuli after a pacing train?

A

Small decremental change in AH interval

179
Q

What is an AH jump?

A

When there is a large change (>50msec) in the AH interval with a 10msec change in premature atrial stimulus

180
Q

What does an AH jump suggest?

A

Dual AV node pathways (fast and slow)

*This may be a substrate for AV nodal re-entry tachycardia

181
Q

What is it called during an EP study when you deliver a premature atrial stimuli after a pacing train and it captures the atrium, but doesn’t conduct to the ventricles?

A

AV node effective refractory period

182
Q

What is it called during an EP study when you deliver a premature atrial stimuli after a pacing train and it fails to capture the atrium?

A

Atrial effective refractory period

183
Q

True or False: Wenckebach is demonstrated during an extrastimulus protocol?

A

False- During atrial pacing

184
Q

True or False: The lengthening of the AV conduction time represented by the AH interval is a normal finding (decremental property of the AV node) and doesn’t indicate AV conduction disease

185
Q

What is it called during an EP study when you deliver a premature ventricular stimuli after a pacing train and it fails to capture the ventricle (pacing spike, but no QRS)?

A

Ventricular effective refractory period

*Failure of output if there was no pacing spike

186
Q

What is it called during an EP study when you deliver a premature ventricular stimuli after a pacing train and is captured the ventricular beat, but blocked going to the atria (ventricular signal on ventricular catheter and QRS on surface ECG, but no atrial conduction)?

A

AV node retrograde effective refractory period

187
Q

True or False: VA Wenckebach occurs during ventricular pacing and not during a ventricular extrastimulus protocol?

188
Q

Paced ECG with P waves that have no relationship to the QRS complex (completely dissociated)… what modes are possible?

A

VOO or VVI

189
Q

What mode represents asynchronous dual chamber pacing?

190
Q

Electrogram with complete AV dissociation and ventricular rate faster than atrial?

A

Ventricular tachycardia

191
Q

In an accessory pathway mediated tachycardia, what is the relationship between the atria and ventricle?

192
Q

In a wide complex rhythm with rapid ventricular rate, how do you diagnose antegrade complete AV block?

A

The atrial rate would have to be faster than ventricular

193
Q

What is the AV relationship in AVNRT?

194
Q

What form of CHD should you consider with RVH and ST segment elevations consistent with ischemia in V1/V2?

195
Q

What causes RVH and RV ischemia seen in PA + IVS?

A

RV dependent coronary circulation

*High pressure in the RV creates sinusoidal connections between the RV and coronary artery circulation that can predispose to ischemia

196
Q

What is typically seen on ECG in ToF and Truncus?

197
Q

What is typically seen on ECG in TAPVR?

A

RVH + RA enlargement

198
Q

What pacemaker settings would have atrial sensing followed by ventricular tracking and resultant ventricular pacing?

A

Dual chamber

DDD or VDD

199
Q

What is a VDD pacemaker setting?

A

Can sense in the atria, but not pace

200
Q

True or False: Most patients have atrial and ventricular leads placed with a dual chamber pacemaker?

A

True

*There are leads which have the capability in a single lead to sense both atrium and ventricle as well as pace the ventricle achieving AV synchrony using a single lead set VDD

201
Q

If a pacemaker was set VVI or VOO, how would it pace?

A

At the lower rate limit set

202
Q

How does DOO pacing work?

A
  • Pace atria/ventricles without sensing

- Atrial and ventricular pacing spikes would be present and pace without any regard to existing P waves or QRS complexes

203
Q

AV conduction block is a complication of what % of surgical operations for CHD?

204
Q

Unless treated with an implanted pacemaker, post-op complete heart block is associated with what % mortality?

205
Q

True or False: Permanent placement implantation is a class I indication for surgically induced complete AV block regardless of the ventricular escape rate and condition of the patient

206
Q

How long should wait to determine whether AV nodal conduction will return following post-op heart block?

A

At least 7 days

  • Usually resolves after 7-10 days if it will resolve
  • Patients need long-term monitoring for conduction abnormalities
207
Q

Progressive PR prolongation, usually due to changes in AH interval (AV node delay) with eventual failure of conduction to ventricle

A

Mobitz type I 2nd degree AV block (Wenckebach)

208
Q

Abrupt failure of AV conduction of 1 or more atrial impulses without prior PR prolongation

A

Mobitz type II 2nd degree AV block

209
Q

Where does Mobitz type II 2nd degree AV block usually occur?

A

Below AV node

210
Q

Why is Mobitz type II 2nd degree AV block an indication for a pacemaker even in the absence of symptoms?

A

May abruptly progress to 3rd degree heart block without an adequate escape rhythm

211
Q

When would you place a pacemaker in the setting of sinus bradycardia, Wenckebach or prolonged PR interval?

A

If there are significant symptoms associated with the rhythm

212
Q

True or False: LBBB is an indication for a pacemaker?

A

False

*Not an indication, regardless of QRS duration

213
Q

What should you consider with bidirectional v-tach with QRS changing in every other beat during VT?

214
Q

What should you consider with ventricular tachyarrhythmias which occur with exercise or emotion?

215
Q

True or False: The resting ECG in CPVT can be normal?

A

True

*Heart often structurally normal as well

216
Q

What mutations cause CPVT?

A
  1. RYR2 (ryanodine receptor)
  2. CASQ2 (calsequestrin 2)

+ many more

217
Q

What often triggers dysrhythmias in long QT or Brugada?

A

Early afterdepolarization with a PVC at the end of the T-wave leading to torsades

218
Q

What tachydysrhythmia is often seen with long QT or Brugada?

219
Q

What kind of rhythm issues are seen in ARVC?

A

VT from RV

220
Q

True or False: HCM patients are at increased risk of VT?

221
Q

Intermittent capture of the ventricles by a pacemaker is consistent with what issue in the lead?

A

Partial fracture of ventricular lead

222
Q

What measure on interrogation would be a clue that there is a partial lead fracture of a ventricular pacemaker lead?

A

Lead impedance abnormal

223
Q

Inability of a pacemaker to sense spontaneous myocardial depolarization… get paced complexes in presence of intrinsic rhythm

A

Undersensing

224
Q

What does undersensing lead to?

A

Inappropriate pacing complexes after native QRS beats

225
Q

What can happen when native ventricular escape beats don’t reset the pacemaker timing cycle?

A

Pacemaker continues to pace at lower rate limit- Undersensing

226
Q

True or False: Undersensing can be a marker that something is wrong with a pacing lead?

227
Q

Pacemaker sensing artifact and not pacing when indicated

A

Oversensing

228
Q

Point in pacemaker battery life where replacement is needed, but pacemaker will continue to operate and will result in ventricular capture

A

ERI

*At end of life when battery voltage extremely low, pacemaker may not be able to generate enough energy to capture the heart

229
Q

What happens if you put a magnet over a pacemaker?

A

Causes it to pace asynchronously

*Shouldn’t lose capture

230
Q

List adverse effects of amiodarone

A
  1. Photosensitivity
  2. Thyroid dysfunction
  3. Weakness
  4. Peripheral neuropathy
  5. Corneal microdeposits
  6. Elevated hepatic enzymes

*Less common: Proarrythmic, pulmonary fibrosis

231
Q

What tests need followed with someone on amiodarone?

A

TFTs, PFTs, LFTs

Yearly optho visits (corneal microdeposits)

232
Q

What side effect is common when starting amiodarone, but usually resolves with time?

233
Q

What do you need to counsel patients about regarding sun exposure when starting amiodarone?

A

Photosensitivity common

234
Q

What should an ECG with marked RAE, RBBB and pre-excitation make you consider?

235
Q

Ebstein, HCM and cc-TGA are associated with what?

236
Q

True or False: 30% of patients with Ebstein have pre-excitation, 50% of those with an accessory pathway will have more than 1 accessory pathway

237
Q

What dysrhythmias are patients with Ebstein at risk for?

A
  1. Re-entrant SVT (accessory pathway)
  2. Atrial tachycardia/flutter (dilated atrium)
  3. Atrial fibrillation
238
Q

True or False: Isolated PS often results in RAE on ECG?

239
Q

What are 1st steps in treatment of neurocardiogenic or vasovagal syncope?

A
  1. Fluids

2. Behavior modifications- exercise, etc.

240
Q

When should tilt-table testing be used in the diagnosis of neurocardiogenic syncope?

A

Only if diagnosis can’t be made by history alone

241
Q

When does digoxin toxicity commonly occur?

A

Acute or chronic renal failure

242
Q

What electrolyte imbalance increases the cardiac sensitivity to digoxin?

A

Hypokalemia and hypomagnesemia

*Can become cardiotoxic even with therapeutic digoxin levels

243
Q

Management of digoxin toxicity?

A
  • ICU
  • Hydration
  • O2
  • Temporary transvenous pacemaker (severe bradycardia)
  • Dig immune Fab
  • Lidocaine
244
Q

What is a big problem with digoxin toxicity?

A

Arrhythmias

245
Q

How should beta-blocker be used in digoxin toxicity?

A
  • Can be helpful for supraventricular tachycardias with rapid ventricular rates
  • Cautious if sinus node suppression or AV block, can cause further bradycardia
  • Use shorter acting like esmolol
246
Q

What anti-arrhythmics can help with ventricular arrhythmias in digoxin toxicity?

A
  1. Lidocaine

2. Phenytoin

247
Q

What causes ventricular arrhythmias from digoxin?

A

Result from early afterdepolarization (depolarization of the ventricular myocardium during early repolarization)

*Same as long QT

248
Q

What is Dig immune Fab made from?

A

Immunoglobulin fragments from sheep which have been exposed to a digoxin derivative

249
Q

How does Dig immune Fab work?

A

Irreversibly binds to digoxin and makes it unable to act on its target cells

250
Q

What do you have to monitor for closely when giving Dig immune Fab?

A

Anaphylaxis

251
Q

What is the timeframe for onset of action and complete response with Dig immune Fab?

A
  • Onset of action: 20-90 minutes

- Complete response: 4 hours

252
Q

Ventricular tachycardia with varying QRS morphology?

A

Torsades de Pointes

253
Q

What is the treatment for Torsades de Pointes?

A

Mg Sulfate

*5-10mg/kg IV (1-2g adults) as bolus over 30-60 seconds, repeat dose in 5-15 minutes and start drip at 0.3-1mg/kg/hr

254
Q

True or False: Mg Sulfate can be effective even in patients with normal Mg levels in the setting of Torsades?

255
Q

What should be done in patients with sustained torsades (especially is Mg isn’t available)?

A

Defibrillation

*But Mg may prevent further recurrences

256
Q

How does adenosine work?

A
  • Via specific adenosine receptor linked to K channel

- Results in shortening of AP duration and sinus bradycardia/AV block

257
Q

What is the half-life of adenosine?

A

1-5 seconds

*Metabolized by erythrocytes and endothelial tissue

258
Q

How should adenosine be given?

A
  • Rapid push
  • Large vein close to heart
  • Saline flush following to ensure entire dose quickly administered in blood stream
259
Q

True or False: Adenosine should be effective regardless of the duration of tachycardia?

260
Q

What is the 4th letter of NBG pacing code represent?

A

Rate response pacing

261
Q

What is rate response pacing?

A
  • Pacemaker uses some type of sensor to detect activity and increases the lower rate limit of pacing in conjunction with the level of activity
  • When activity ceases, pacing returns to set basal rate
262
Q

What does rate response allow for?

A

Patients pacemaker can vary the HR when the sinus node can’t provide appropriate rate for body’s demands

263
Q

When is rate-response pacing indicated?

A

Patients who have chronotropic incompetence (HR can’t reach appropriate levels during exercise, etc)

264
Q

What is the 5th letter in NBG code used to signify?

A

Biventricular pacing

*Pacing both left and right ventricles

265
Q

When would you use AAIR pacemaker settings?

A

Sinus node dysfunction

266
Q

What does AAIR pacing mean?

A

It can only sense and pace in the atria

267
Q

AAIR pacing is only indicated when?

A

Problem with sinus node

*To correct any degree of heart block, a lead in ventricle is needed

268
Q

A patient will get a defibrillation shock if the ventricular rate goes above what rate?

A

Programmed shock rate or v-fib zone

269
Q

True or False: In the v-fib zone, patients will receive a shock if the ventricular rate is above the set rate, even if the rhythm is sinus?

A

True

*Separate v-tach zone can be set with discriminators to try to determine if the arrhythmia is a sinus tachycardia or atrial tachycardia and can be programmed to withhold shock therapy if the device determines patient isn’t in v-tach… in v-fib zone, discriminators aren’t available and the device will deliver therapy purely base on the ventricular rate

270
Q

True or False: A patient who is in slow v-tach might not receive a shock?

A

True- if V-tach occurs at a rate lower than the set shocking rate

271
Q

What is one of the most common reasons for inappropriate shocks in patients with ICD?

A

Sinus tachycardia in the VT zone

272
Q

Why do you need to be cautious with someone who has a pacemaker and is getting a surgery where electrocautery will be used?

A

Electrocautery can create inappropriate noise and sensing within the pacemaker thus causing it to oversense and prevent necessary pacing

273
Q

How do you prevent oversensing due to electrocautery from a surgery?

A

Place a magnet over the pacemaker to cause asynchronous pacing

274
Q

What happens if you place a magnet over a pacemaker/ICD?

A
  • Asynchronous pacing in a programmed mode
  • Disables all shock therapy –Avoids inappropriate shocks due to oversening from electrocautery during surgery
  • Stops appropriate shock delivery due to v-tach
  • Over ICD: Disables shock therapy, but pacing isn’t affected
  • Over Pacemaker: Asynchronous pacing
275
Q

In the absence of a known reversible or treatable cause of sudden cardiac arrest, what is the treatment of choice?

A

ICD

*Class I indication

276
Q

Newborn with an ECG showing LAD, LVH, RAE and decreased right sided forces?

A

Tricuspid atresia

*Can also see short PR w/o preexcitation

277
Q

CAVC, primum ASD, tricuspid atresia and WPW can all cause what on ECG?

278
Q

True or False: LVH only rarely causes LAD in pediatrics?

279
Q

HLHS, truncus and ToF may show what on ECG?

A

RAD/RVH

*Could be normal in newborn period though

280
Q

What are some potential ECG findings in a baby with truncus?

A
  • RAD/RVH

- Normal axis, combined ventricular hypertrophy

281
Q

Complete heart block in utero is strongly associated with that?

A

Maternal antibodies to SSA/SSB

282
Q

What is the common maternal history in a baby with complete heart block?

A

-Often asymptomatic, but with underlying autoimmune diseases like SLE or Sjogrens

283
Q

How does maternal SLE/Sjogren’s cause neonatal heart block?

A

Unknown… presumed due to transplacental passage of IgG autoantibodies from Mom to baby

284
Q

What screening should be done for Mom and baby when baby has complete heart block?

A

Anti-SSA

Anti-SSB

285
Q

True or False: 22q11 deletions are a rarely reported in some patients with complete heart block?

286
Q

What can cause a wide complex rhythm with sine wave pattern and no differentiation between QRS and T wave

A
  • Hypoxia
  • Acidosis
  • Hyperkalemia
287
Q

What happens to the ECG with hyperkalemia?

A
  • Initially tall peaked T-waves
  • T waves become more peaked
  • Intraventricular conduction delay
  • Widened QRS
  • PR prolongation
  • ECG looks like sine wave or wide v-tach
288
Q

At K concentrations above what does atrial standstill, AV block or v-fib occur?

289
Q

Increased Ca causes what on ECG?

A

Shortened QT interval

290
Q

What is represented by the HV time on an EP study?

A

The time it takes for the signal to get through the AV node and bundle of his (His to ventricle time)

291
Q

What is a normal HV time?

292
Q

How is the HV interval calculated?

A

Measure the distance from His deflection to earliest QRS deflection on any lead on surface ECG

293
Q

What does a short HV (<25-35msec) indicate?

A

Alternative method of conduction other than the AV node… only possible in presence of an accessory pathway

294
Q

What does it mean if the HV interval is negative?

A

Accessory pathway with the ventricular myocardium in close proximity to the site of the accessory pathway being activated prior to bundle of His

295
Q

What effect do BBB and infra-Hisian conduction delay have on the HV interval?

A

Prolongs it

296
Q

What change in the AH interval is seen with 1st degree AV block?

297
Q

What is seen during an atrial extrastimulus protocol which results in prolongation of the AH interval?

A

Dual AV node physiology

298
Q

What is the classic arrhythmia seen in patients with long QT?

299
Q

What characterizes Torsades?

A

QRS complexes change morphology

300
Q

What effect does erythromycin have on the QTc?

A

Prolongs it

301
Q

What is the treatment of choice for atrial flutter?

A

Cardioversion

302
Q

Why should CCB be avoided in newborns?

A

Newborn heart sensitive to Ca… CCB can result in long pauses and have been associated with sudden death with longer term use

303
Q

True or False: Majority of neonates who present in atrial flutter have no underlying structural heart disease and a low incidence of recurrence

A

True

  • Newborn myocardium has unique properties which allow it to conduct very rapidly
  • Rates over 400bpm can be maintained with no structural heart disease
  • Need to echo these patients
304
Q

Irregularly irregular rhythm?

305
Q

What does a-fib increase the risk of?

306
Q

Why does a-fib increase risk of stroke?

A
  • No organized atrial contractions
  • Stasis in atria
  • Predisposes to thrombi/potential strokes
307
Q

True or False: The risk for stroke can persist for a period of time in a-fib even after sinus rhythm is restored

308
Q

Progressive prolongation of the PR interval followed by a dropped beat?

A

Mobtiz type 1 second degree AV block (Wenckebach)

309
Q

True or False: Mobitz type 1 second degree AV block is not uncommon in teens and older adults while sleeping?

A

True (rare while awake)

310
Q

What is the management for asymptomatic Mobitz type 1 second degree AV block?

A

If isolated in an asymptomatic person while sleeping, likely no clinical significance with no therapy or further evaluation

311
Q

What finding on exercise stress testing in someone with pre-excitation indicates an accessory pathway that won’t rapidly conduct to the ventricle in a-fib and is low risk for sudden death?

A

Loss of preexcitation in a single beat (go from a wide/pre-excited QRS to a narrow QRS)

312
Q

True or False: Risk of SVT can be assessed by a baseline ECG in someone with preecitation?

A

False- Antegrade conduction seen on resting ECG has no definitive relationship with the retrograde conduction that causes SVT

313
Q

What are 2 signs indicative of atrial lead dysfunction?

A
  • Intermittent atrial undersensing

- Atrial pacing with no evidence of capture

314
Q

What ECG findings are seen in anorexia?

A
  • Sinus bradycardia
  • Low voltage QRS
  • Low amplitude T-waves
315
Q

What is the body’s response to nutritional deprivation?

A

Decreased HR

316
Q

What is the classic pattern seen in typical AVNRT on an EP study?

A

Activation via Bundle of His to Atrium followed by ventricle

317
Q

What causes pattern of His deflection, ventricle followed by an atrial activation at least 20-40msec following QRS?

A

Accessory pathway mediated tachycardia

*Goes down AV node through ventricle up accessory pathway to atrium and back down AV node

318
Q

Atypical AVNRT is what type of tachycardia?

319
Q

CAVC, primum ASD and tricuspid atresia all have what in common on ECG?

320
Q

List forms of CHD which may have a RAD?

A

Truncus
TAPVR
ToF
CoA

321
Q

Extreme left axis deviation (northwest axis)?

322
Q

An ECG with S wave > R wave in I and aVR gives an axis between what?

A

-90 to -180 (northwest)

323
Q

What are clues to a northwest axis?

A
  • LAD with S wave > R wave in leads I and aVF
  • Small Q in I and aVL…. Axis went through a counterclockwise vectorcardiogram loop to get to final axis (If axis went clockwise (through RAD), there would be Q waves in II, III and aVF)
324
Q

What should you consider with extreme biatrial enlargement on ECG?

A

Restrictive cardiomyopathy

*Patients are at risk for Pulmonary HTN

325
Q

Massive biventricular hypertrophy and short PR interval should make you consider what?

A

Glycogen storage disorder (type 2- Pompe)

*Patients often present with hepatomegaly

326
Q

RBBB with ST segment elevation in V1/V2?

327
Q

What causes Brugada?

A

Channelopathy affecting Na transport

328
Q

What are the clinical manifestations of Brugada?

A
  • Ventricular tachyarrhythmias
  • Recurrent syncope
  • SCD
329
Q

What should be done for someone with Brugada and syncope or ventricular arrhythmias?

330
Q

True or False: Amiodarone can exacerbate ventricular arrhythmia in Brugada?

331
Q

True or False: Patients with spontaneous ECG for Brugada are thought to be at risker risk for arrhythmia

332
Q

Genetic defect associated with Brugada?

333
Q

Brugada results from a mutation in what type of electrolyte channel?

334
Q

HERG and KCNQ1?

335
Q

What drug can bring out a Brugada pattern on ECG?

A

Class I- Procainamide

336
Q

Progressive prolongation of the AH interval with PR interval followed by a non-conducted beat?

A

Wenckebach (Mobitz Type 1 2nd degree AV block)

337
Q

Diffuse ST segment elevation and PR segment depression?

A

Pericarditis

338
Q

What is one of the most common causes of pericarditis?

339
Q

What changes can be seen on ECG with cocaine abuse?

A

ECG changes localized to one segment… appears abnormal without true acute infarction

340
Q

What effect does cocaine have on the heart?

A

Can cause coronary vasospasm and ischemia

341
Q

Myosin heavy chain mutation?

342
Q

What can be seen on ECG in HCM?

A
  1. LVH with strain
  2. Short PR interval (pre-excitation or pseudo-preexcitation)

*Rapid AV nodal conduction seen in HCM

343
Q

What changes can increased intracranial pressure cause on ECG?

A

T-wave changes and QT prolongation

344
Q

What effect does erythromycin have on the QT interval?

345
Q

What should you consider with an irregular wide complex tachycardia?

A

A-fib in the presence of either pre-existing BBB or pre-excitation (WPW)

346
Q

Why is a-fib of concern in someone with WPW?

A

Patient can have rapid conduction through an accessory pathway and is at risk for v-fib

347
Q

What should be done for someone with an irregular wide complex tachycardia and pulses?

A

Cardiovert

348
Q

What needs done for someone with WPW and a-fib?

A

Ablation- Eliminate conduction in accessory pathway since it could conduct very rapidly

*If that isn’t possible, should be treated with an antiarrhythmic (flecainide or amiodarone) to slow conduction in accessory pathway

349
Q

What rhythm issue is classically associated with Ebstein, cc-TGA and HCM?

350
Q

Patients with Ebstein are at risk for what rhythm issue?

A

WPW and a-fib (due to dilated atria)

351
Q

What drug is relatively contraindicated in A-fib + WPW?

A

Anything that blocks the AV node (adenosine, dig, CBB)

352
Q

Why are AV nodal blockers relatively contraindicated in WPW?

A

If a-fib, may cause preferential conduction down accessory pathway resulting in rapid conduction to the ventricle and subsequent v-fib

353
Q

No relationship between P waves and QRS complexes?

A

Complete AV block

354
Q

When is a pacemaker indicated with complete AV block?

A
  • Symptoms
  • Wide complex escape rhythm
  • Complex ventricular ectop
  • HR <50 without CHD
  • HR <70 with CHD
355
Q

List conditions associated with complete AV block

A
  1. Chagas
  2. cc-TGA
  3. Maternal Ro/La antibodies
  4. Endocarditis with abscess formation
356
Q

What should you consider for a long RP tachycardia?

A

PJRT

Atypical AVNRT

357
Q

Describe the P waves in PJRT or atypical AVNRT?

A

Deeply negative in II, III and aVF

358
Q

What is PJRT?

A

-Accessory pathway-mediated tachycardia due to a slowly conducting accessory pathway typically located in the right posterior septum

359
Q

Where is the accessory pathway typically located in PJRT?

A

Right posterior septum

360
Q

Why is the there a long RP interval in PJRT?

A

-Accessory pathway conducts slowly so atrial activation is seen a significant time following QRS

361
Q

True or False: PJRT and AVNRT should break with adenosine?

A

True- But both tend to be incessant and may reinitiate quickly after termination with adenosine

362
Q

What happens after adenosine is given in flutter?

A

It will continue with the P-waves in a saw-tooth pattern

363
Q

What happens after adenosine is given in sinus tachycardia?

A

Slows transiently, then speeds back up

364
Q

What might happen after adenosine is given in a sinus or atrial tachycardia in the presence of preexcitation?

A

QRS may widen transiently as AV node blocks and there is preferential conduction down AV node

365
Q

What is the differential diagnosis of long RP tachycardia:

A

Atrial tachycardia
PJRT
Atypical AVNRT

*Flutter can also present as a long RP tachycardia

366
Q

Describe a Mahaim fiber

A

Accessory pathway which conducts only antegrade

367
Q

How does a Mahaim fiber present?

A

Wide complex tachycardia

368
Q

How to you determine location of an accessory pathway on an EP study?

A

Look for area of earliest atrial activation once in SVT

369
Q

Where does the CS catheter run in an EP study?

A

In the CS- so along the AV groove between LA/LV

370
Q

Where would an accessory pathway be located if the earliest atrial activation was in the mid-CS?

A

Left-sided pathway

371
Q

What ECG finding is a poor prognostic sign in someone with Long QT?

A

QRS alternans or alternating pattern of the appearance of the T-waves

372
Q

What does an alternating pattern of appearance of the T-waves increase risk for in someone with long QT?

A

2:1 AV block and sudden death

373
Q

True or False: Methadone does not prolong the QT interval

374
Q

What screening needs done with long QT?

A

Other family members need to be screened… most cases familial

375
Q

The underlying mutation which causes long QT most often involves which channels?

376
Q

Ca channel mutations are a common cause of what dysrhythmia?

377
Q

What is rate responsiveness on a pacemaker?

A
  • Allows pacemaker to increase pacing rate in response to patient activity
  • Denoted by 4th letter of NBG pacing code
378
Q

How does rate responsiveness work in a pacemaker?

A

Accelerometer which senses motion and increases patient’s pacing rate in response

379
Q

True or False: Electromagnetic interference may inhibit rate responsiveness on a pacemaker?

A

True

*Also can cause it to pace asynchronously

380
Q

How would oversensing affect heart rate?

A

Decrease- From inhibition of pacing

381
Q

What happens when a magnet is placed over a pacemaker?

A

Asynchronously paces at a set rate determined by the pacemaker manufacturer (AKA Magnet rate)

382
Q

What are classic ECG findings of Brugada?

A

ST segment elevation

RBBB in V1 and V2

383
Q

What type of ECG pattern carries the highest risk for arrhythmias in Brugada?

A

Spontaneous Brugada ECG pattern

384
Q

True or False: Some patients with Brugada may have a normal ECG at rest?

385
Q

What can trigger the ECG findings in Brugada?

A

Fever… patients can have increased incidence of arrhythmias during febrile illness

386
Q

What adjustment in ECG lead position can bring out ECG findings of Brugada?

A

“High-lead” placement of V1/V2…Involves moving 2 leads up one or two intercostal spaces in attempt to bring out characteristic changes in J-point ad ST segments of leads V1/V2

387
Q

What drug can be infused to bring out the typical ECG findings of Brugada?

A

Procainamide

388
Q

What is a typical trigger for LQTS type 2?

A

Emotional stress

389
Q

What can exacerbate symptoms in patients with HCM?

A

Dehydration

390
Q

True or False: HTN can cause LVH with strain?

391
Q

The majority of events in LQTS type 3 happen when?

392
Q

What is the purpose of chronic resynchronization therapy (CRT or biventricular pacing)?

A

Try to promote ventricular synchrony in patients with HF and a wide QRS

393
Q

What are the indications for CRT?

A
  • LVEF less than or equal to 35%
  • Sinus rhythm
  • LBBB with QRS duration greater than or equal to 150msec and NYHA class III, III or ambulatory IV symptoms on guideline directed medical therapy (only class I indication)?
394
Q

What is the only class I indication for CRT?

A

LBBB with QRS duration greater than or equal to 150msec and NYHA class III, III or ambulatory IV symptoms on guideline directed medical therapy (only class I indication)?

395
Q

When is CRT beneficial?

A

Usually only in EF < 35% and after medical therapy has been optimized

396
Q

True or False: CRT decreases incidence of arrhythmias?

A

False- CRT only improves symptoms, doesn’t decrease incidence of arrhythmias or increase survival

397
Q

True or False: There is some evidence that CRT may be beneficial with narrower QRS duration and in patients with RBBB pattern

A

True- But tends to have lower success rate in these patients and isn’t a class I indication

Peds Cardiology (20 decks)

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