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EP and Fetal Arrhythmias Flashcards

1
Q

Most common pediatric dysrhythmia

A

Paroxysmal SVT

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2
Q

Antibody associated with congenital lupus

A
  • Anti Ro/SSA
  • Anti La/SSB
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3
Q

Location of bundle of His in truncus arteriosus

A

Left aspect of the posterior/inferior rim of the VSD

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4
Q

Location of conduction fibers in ccTGA

A

Anterior superior rim

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5
Q

Most common fetal presentation of long QT

A

Sinus bradycardia with bursts of SVT

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6
Q

Incidence of fetal arrhythmias

A

1-3% but only 10% of these cause morbidity

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7
Q

Definition of fetal bradycardia

A
  • Rate < 110/min
  • If abnormal AV conduction have 50% risk of CHD
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8
Q

Definition of fetal tachycardia

A
  • Rate > 180/min
  • Baseline risk of CHD (1%)
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9
Q

Follow-up needed for fetal PACs

A
  • If frequent (every 3-5 beats) then weekly OB assessment
  • If infrequent, nothing special
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10
Q

Things to exclude for fetal PVCs

A

Myocarditis, cardiac tumors, maternal drug exposures

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11
Q

What types of CHD are at increased risk with fetal tachycardia

A
  • Ebsteins
  • Complete AV canal
  • HLHS
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12
Q

Fetal echo signs of tachyarrythmias

A
  • Early: atrial enlargement or AVV regurgitation
  • Late: ventricular dysfunction, effusion, hydrops, cardiomegayl
  • TACHY PLUS HYDROS = 50% mortality
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13
Q

1st and 2nd most common fetal tachyarrhythmias

A
  • AV reciprocating SVT with accessory pathway (70-90%)
  • Atrial flutter (10-30%)
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14
Q

1st line drug for fetal SVT

A

Digoxin - 50% termination
Oral load and higher doses
Direct IM is an option if hydrops
Check maternal levels and ECGs

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15
Q

2nd line drugs for fetal tachyarrhythmias

A
  • Sotalol: B blocker and K channel - daily ECG, some say better for A flutter
  • Flecainide - Na channel - daily ECG, some say better for SVT and not flutter
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16
Q

Things to rule out for fetal VT and treatment of fetal VT

A
  • Tumors, myocarditis, channelopathies, AV block
  • Tx: maternal IV mag or lido, oral propanolol or mexilitene
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17
Q

Percentage of congenital complete AV block that have CHD vs immune mediated

A
  • 50-55% have complex CHD (heterotaxy or L looping)
  • 40% are immune mediated with anti-Ro/SSA or anti-La/SSB antibodies
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18
Q

Percent risk of CCHB with known maternal antibodies

A
  • 3-5%
  • If prior then risk increases to 11-20%
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19
Q

Risks for death with CCHB

A

Structural CHD
HR < 55 at presentation
Hydrops
Decreased function

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20
Q

Difference between ORT vs ART

A
  • ORT has narrow QRS
  • ART has wide QRS with preexcitation
  • Both are accessory pathway mediated reentrant tachycardias with HR 200-250
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21
Q

Accessory pathway tachycardia associated with which CHD

A
  • Ebsteins
  • LTGA
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22
Q

Definition of PJRT

A
  • Permanent junctional reciprocating tachycardia
  • No preexcitation at baseline
  • Long VA during tachycardia, slower rates during SVT
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23
Q

Acute treatment of SVT

A
  • B block or CCB If normal EF and no preexcitation at baseline
  • Dig if no preescitation at baseline
  • DCCV
  • Amio if decreased EFC
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24
Q

Chronic treatment of SVT

A
  • If preexcitation: B blockers, Class Ia/Ic/III
  • No digoxin or verapamil due to risk for rapid anterograde conduction and VF if there is preexcitation
  • If no preexcitation can use digoxin, B blockers, Class Ia/Ic/III/IV
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25
Q

Risk for SCD with WPW

A
  • Risk is due to rapid conduction of AF
  • Risks are age < 30, male, CHD, hx syncope or arrest, familial WPW, shortest RR during AF < 220, shortest preexcited RR < 250, AP ERP < 250
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26
Q

Definition of AVNRT typical vs atypical and ECG findings

A
  • Typical is slow-fast
  • Atypical is fast-slow and can look like PJRT
  • HR 150-250, p often buried in QRS, rate can vary some
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27
Q

Differential for long RP tachycardia

A

Atypical AVNRT
PJRT
AET
Sinus tachy

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28
Q

Acute treatment of atrial tachycardia

A
  • Treat underlying cause
  • CCB, B blocker, dig, proc, amio
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29
Q

Where does typical atrial flutter originate

A

Cavotricusipd isthmus

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30
Q

Acute treatment of atrial flutter or fib

A
  • Rate control with B blocker or CCB if normal function, dig or amio if decreased function
  • Cardiovert pharm with ibutilide, amio or proc
  • DCCT if symptomatic but NOT IF DIG TOXICICTY
  • If > 48 hours have increased risk of clot so treat with rate control and anticoag for 3 weeks then DCCV with 4 weeks anticoag OR TEE plus anticoag bolus followed by DCCV immediately and then 4 weeks anticoag
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31
Q

Chronic treatment of atrial flutter or fib

A

B blocker
CCB
Class Ia/Ic/III
Chronic anticoagulation
Surgical maze

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32
Q

Acute treatment of WPW plus atrial fibrillation

A
  • Proc plus AVN blocker - dont use AVN blocker as single agent
  • DCCV
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33
Q

ECG findings for RVOT VT

A
  • LBBB morphology (bunny ears in V6) with inferior axis (positive QRS in 2, 3, aVF)
  • Occurs at rest or in recovery from exercise
  • Dx: AVRC, myocarditis, tumor
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34
Q

Treatment of RVOT VT

A

Verapamil
Responds to adenosine or vagal (cAMP mediated)
B blocker
DCCV or ablation

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35
Q

ECG findings of idiopathic or fasicular LV tachycardia

A
  • RBBB morphology (bunny ears in V1), superior axis (QRS negative in 2, 3, aVF)
  • Reeentrant from LV septum
  • Dx: myocarditis, tumor, CPVT
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36
Q

Treament of Fasicular VT

A

Verapamil
B blocker
Class Ia/Ic/III
DCCV or ablation

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37
Q

3 meds and ways they work for vasovagal syncope

A
  • Florinef (mineralocorticoid) - absorbs salt and volume expansion
  • B blocker - blocks B1/B2
  • Midodrine - alpha agonist - activates receptors on vasculature to increase tone
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38
Q

Most common etiologies of SCD in athletes

A

Ventricular arrhythmias from:
- HCM, LVH, coronary problem, commotio cordis

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39
Q

HCM risk factors for SCD

A
  • Wall thickness > 30 mm
  • Hx arrhythmia leading to syncope
  • Family history
40
Q

What does the murmur do in HCMD

A
  • Systolic murmur that increases with standing
41
Q

Genes associated with HCM

A
  • Autosomal dominant
  • TTN, MYH7, TNNT2, ACTC, MYBPC3
42
Q

What happens to the RV in ARVC

A

Myocardium gets replaced with fatty tissue which leads to electrical instability and risk for VT or SCD

43
Q

ARVDVC1 gene and association

A

TGFB3
Progressive RV myopathy

44
Q

ARVDVC2 gene and association

A

RYR2
Maybe associated with CPVT

45
Q

ARVDVC5 gene and association

A

LAMR1
Seen in New Foundland

46
Q

ARVDVC6 gene and association

A

Tyr phos
Early onset

47
Q

ARVDVC7 gene and association

A

DES
A/w myofibril myopathy

48
Q

ARVDVC8 gene and association

A

Desmolakin
Keratoderma and wooly hair

49
Q

Long QT type 1 gene, triggers and ECG finding

A

KCNQ1 - K channel loss of function
Broad based T waves
Triggers are exertion and swimming
Adolescent males and post partum females

50
Q

Long QT type 2 gene, triggers and ECG finding

A

KCNH2 - K channel loss of function
Low amplitude T waves and can have double notch
Triggers are startling (alarm clock)
Females > 13

51
Q

Long QT type 3 gene, triggers and ECG finding

A

SCN5A - Na channel gain of function
Long ST segment and late peaking T waves
Triggers are sleeping

52
Q

Treatment in long QT

A

If QTc > 470 use beta blockers or if symptomatic
Can use ICD if prior arrest or high risk

53
Q

CPVT definition

A
  • Catecholaminergic polymorphic VT
  • Polymorphic or bidirectional VT with sports or stimulus
54
Q

CPVT genetic mutations

A
  • AD RYR2
  • AR CASQ2, TRDN, CALM 1/2/3
55
Q

Brugada ECG apperance

A

RBBB with ST elevation in V1-V3
- Type 1 has downslowping ST segments and inverted T waves
- Type 2 has saddle back ST/T wave complex and biphasic T waves

56
Q

Mutation for Brugada

A

SCN5A
Loss of function in Na channels
Common in SE Asian males

57
Q

Treatment for Brugada

A

ICD if hx of arrest or high risk
Aggressive treatment of febrile illness
Can use quinidine

58
Q

How does vagal nerve regulate heart rate

A
  • Acetylcholine release, increases K permeability, decreases Ca permeability, slows pacemaker cells, slows AV node conduction
59
Q

How does sympathetic nerve regulate heart rate

A
  • Norepi release, increases Ca permeability, facilitates AVN conduction, accelerates pacemaker cells
60
Q

SA nodal artery origin

A

RCA in 60%, LCA in 40%

61
Q

AV nodal artery origin

A

RCA in 55%, LCx in 45%

62
Q

Right and left bundles get blood supply from where

A

Septal perforators of LAD

63
Q

Why no atropine for transplant patients with sinus brady

A
  • No response (denervated)
  • Risk for paradoxical response and leading to heart block
64
Q

Use for glucagon with sinus brady

A

B blocker or CCB overdose

65
Q

Causes of left axis deviation in infants

A
  • AV septal defect
  • Tricuspid atresia
66
Q

Is complete AV block more common in polysplenia or asplenia

A

Polysplenia due to underdevelopment of right sided structures

67
Q

Common training related changes on ECG

A
  • Sinus brady
  • First degree AV block
  • Incomplete RBBB
  • Early repolarization
  • Isolated QRS voltage criteria for LVH
68
Q

Treatment for fetal VT with hydrops

A

Sotalol

Digoxin is not good for hydropic fetus

69
Q

Primary electrolyte driver of depolarization

70
Q

Primary electrolyte driver of repolarization

71
Q

Class IA anti-arrhythmics

A
  • Sodium channel blockers
  • Delay depolarization and repolarization
  • Antivagal effects
  • Drugs: quinidine, procainamide, disopyramide
72
Q

Indications for quinidine

A

Brugada syndrome

73
Q

Side effect of class 1A anti-arrhythmics

A

Prolongs QT interval

74
Q

Procainamide indications and side effects

A
  • Indications: acute management of SVT and VT
  • Drug induced lupus but not an oral form anymore so less common
  • Prolonged QT
75
Q

Class 1B anti-arrhythmic drugs

A
  • Sodium channel blockers
  • Shorten action potential duration and repolarization
  • Drugs: lidocaine, mexiletine, phenytoin
76
Q

Lidocaine uses and side effects

A
  • Ventricular arrhythmias
  • SE: apnea and seizures (especially in infants)
77
Q

Mexiletine uses and side effects

A
  • PVCs or ventircular arrhythmias (oral lidocaine)
  • Long QT type III
78
Q

Class 1C anti-arrhythmics

A
  • Drugs: Flecainide, propafenone
  • Sodium channel blockers
  • Slow conduction
  • Minimal effect on repolarization
79
Q

Side effects of class 1C anti-arrhythmics

A

QRS widening

80
Q

Flecainide indications and side effects

A
  • No in LV dysfunction
  • Indication: SVT and VT
  • Can widen QRS
81
Q

Propafenone uses

A
  • Use for SVT and VT
  • Does have some beta blocker effect (cautious in asthma)
82
Q

Class 2 anti-arrhythmics

A

Beta blockers –> slow conduction

Selective: atenolol, metoprolol, esmolol

Non-selective: propranolol, nadolol

83
Q

Metabolism of different beta blockers

A

Liver: propranolol, metoprolol
Kidney: atenolol, nadolol

84
Q

Side effects/contraindications of beta blockers

A
  • Hypoglycemia (infants)
  • Contraindications: AV block, bradycardia, LV dysfunction
  • Cautious in asthma patients
85
Q

Class 3 anti-arrhythmics

A

STRONGEST
- Potassium channel blockers
- Prolong AP duration and repolarization
- Drugs: amio, sotalol, ibutilide, dofetilide

86
Q

Amiodarone uses

A
  • Has K, Na, Ca channel blocking
  • Also has beta and alpha blocker
  • Good for SVT and VT
  • LESS LV depression than others (so okay in dysfunction)
87
Q

Amio adverse effects

A
  • LFT dysfunction
  • Pulmonary interstitial fibrosis
  • Hypothyroidism
  • GI symptoms
  • Neurotoxicity
  • Hypotension with IV form
  • Photosensitivty
  • Corneal microdeposits
88
Q

Sotalol uses/function

A
  • K/Na channel blocker, non-selective beta blocker
  • Good for SVT and VT

*** Pay close attention to QT interval with initiation

89
Q

Uses of ibutilide

A

Very short acting IV form - acts in the atrium
- Good for atrial flutter or fibrillation
- Risk for QT prolongation and development of torsades

90
Q

Class IV anti-arrhythmics

A

Calcium channel blockers
- Affect slow response (in the atrium)

91
Q

Uses/contraindications for verapamil

A
  • Slows sinus/AV node, has some alpha effect
  • Good for SVT
  • Contraindicated for infants < 1 d/t calcium effects
  • Also no in WPW (can increase antegrade AP conduction)
92
Q

Uses for diltiaze

A
  • Calcium channel blocker
  • Very fast IV form for acute rate control of A fib or A flutter
93
Q

Adenosine mechanism of action and contraindication

A
  • K channel opener
  • Inhibits SA and AV node
  • Contraindication: asthma, heart transplant
  • Can cause acute onset of afib (hyperpolarizes the membrane potential)
94
Q

Use of ivabradine

A
  • Inhibits sinus node activity and decreases heart rate
  • Primary indication is to decrease heart rate in setting of heart failure
  • Slows down sinus rate
95
Q

Digoxin has effects with what other anti-arrhythmics

A

Frank Ate Pizza Very Quickly
- Flecainide
- Amiodarone
- Propafenone
- Verapamil
- Quinidine

96
Q

Wide complex tachycardia that is regular - why would you give adenosine

A

Could be SVT with baseline bundle branch block - will look like VT

97
Q

EKG for PJRT in tachycardia

A

Slower rates 150-200
P waves negative in II, III and aVF

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