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KK Paediatric Cardiology study > Arrhythmia > Flashcards

Arrhythmia Flashcards

1
Q

What are some complications of arrhythmias?

A
  • acutely decreased CO
  • degeneration into more dangerous arrhythmia such as VF
  • if incessant may lead to cardiomyopathy
  • may lead to syncope or to sudden death
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2
Q

Are single PACs or PVCs concerning?

A

These are common and in kids w/o heart disease, usually pose no risk to the patient

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3
Q

Describe broadly how class I antiarrhythmics work?

A

Block the sodium channel

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4
Q

Describe broadly how class II antiarrhythmics work?

A

Beta-blockers

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5
Q

Describe broadly how class III antiarrhythmics work?

A

prolong repolarisation by blocking potassium channels

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6
Q

Describe broadly how class IV antiarrhythmics work?

A

Calcium channel blockers

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7
Q

Give some examples of class IA (inhibit sodium fast channel, prolongs repolarisation) antiarrhythmics

A

Quinidine

Procainamide

Disopyramide

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8
Q

What are some indications for Quinidine?

A

SVT, AF, atrial flutter, VT

In artial flutter, an AV node-blocking drug (digoxin, verapamil, propranolol) must be given first to prevent 1:1 conduction

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9
Q

What are side effects of quinidine?

A

N/V, diarrhoea, fever, cinchonism, QRS and QT prolongation, AV nodal block, asystole syncope, thrombocytopenia, hemolytic anaemia, SLE, blurred vision, convulsions, allergic reactions, exacerbation of periodic paralysis

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10
Q

What are some drug interaction associated with quinidine?

A

enhances digoxin, may increase PTT when given with warfarin

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11
Q

What are indications for procainamide?

A

SVT, AF, atrial flutter, VT

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12
Q

what are side effects of procainamide?

A

PR QRS QT interval prolongation, anorexia, N/V, rash, fever, agranulocytosis, thrombocytopenia, coombs-positive hemolytic anaemia, SLE, hypotension, exacerbation of periodic paralysis, proarrhythmia

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13
Q

what are some drug interactions associated with procainamide?

A

toxicity increased by amiodarone and cimetidine

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14
Q

What are indications for disopyramide?

A

SVT, AF, atrial flutter

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15
Q

What are side effects of disopyramide?

A

anticholinergic effects, urinary retention, blurred vision, dry mouth, QT and QRS prolongation, hepatic toxicity, negative inotropic effects, agranulocytosis, psychosis, hypoglycaemia, proarrhythmia

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16
Q

Give some examples of class IB antiarrhythmics? (inhibits fast channel sodium, shortens repolarisation)

A

lidocaine, mexiletine, phenytoin

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17
Q

What are some indications for lidocaine?

A

VT, VF

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18
Q

what are some side effects of lidocaine?

A

CNS effects, confusion, convulsions, high-grade AV block, asystole, coma, paresthesias, respiratory failure

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19
Q

what are some drug interactions associated with lidocaine?

A

propranolol, cimetidine, increases toxicity

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20
Q

What are indications for mexiletine?

A

VT

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21
Q

What are some side effects of mexiletine?

A

GI upset, skin rash, neurologic

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22
Q

what drug interaction is associated with mexiletine?

A

cimetidine

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23
Q

what is an indication for phenytoin (arrhythmias)?

A

Digitalis intoxication

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24
Q

what are some side effects of phenytoin?

A

rash, gingival hyperplasia, ataxia, lethargy, vertigo, tremor, macrocytic anaemia, bradycardia with rapid push

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25
Q

what are some drug interactions associated with phenytoin?

A

amiodarone, oral anticoagulants, cimetidine, nifedipine, disopyramide –> increase toxicity

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26
Q

What are some examples of IC antiarrhythmics (inhibit sodium channel)?

A

flecainide, propafenone

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27
Q

what are some indication for flecainide?

A

SVT, atrial tachycardia, VT

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28
Q

what are some side effects of flecainide?

A

blurred vision, nausea, decrease in contractility, proarrhythmia

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29
Q

what drug interactions are associated with flecainide?

A

amiodarone increases toxicity

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30
Q

what are indications for propafenone?

A

SVT, atrial tachycardia, AF, VT

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31
Q

what are some side effects of propafenone?

A

hypotension, decreased contractility, hepatic toxicity, paresthesia, headache, proarrhythmia

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32
Q

what are some drug interactions associated with propafenone?

A

increases digoxin levels

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33
Q

give some exambes of class II antiarrhythmics (beta blockers)

A

propranolol, atenolol, nadolol

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34
Q

indications for propranolol?

A

SVT, long QT

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35
Q

side effects of propranolol?

A

bradycardia, loss of concentration, school performance problems, bronchospasm, hypoglycaemia, hypotension, heart block, CHF

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36
Q

what are some drug interactions with propranolol?

A

co-administration with disopyramide, flecainide, or verapamil may decrease ventricular function

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37
Q

indications for atenolol?

A

SVT

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38
Q

side effects of atenolol?

A

bradycardia, loss of concentration, school performance problems

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39
Q

drug interactions with atenolol?

A

co-admin with disopyramide, flecainide or verapamil may decrease ventricular function

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40
Q

indications for nadolol?

A

SVT, long QT

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41
Q

side effects of nadolol?

A

bradycardia, loss of concentration, school performance problems, bronchospasm, hypoglycaemia, hypotension, heart block, CHF

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42
Q

drug interactions with nadolol?

A

co-admin with disopyramide, flecainide, or verapamil may decreased ventricular function

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43
Q

example of class III antiarrhythmic (prolongs repolarisation)?

A

Amiodarone

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44
Q

indications for amiodarone?

A

SVT, JET (junctional ectopic tachycardia), VT

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45
Q

side effects of amiodarone?

A

hypothyroidism or hyperthyroidism, elevated triglycerides, hepatic toxicity, pulm fibrosis

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46
Q

drug interactions with amiodarone?

A

digoxin (increases levels), flecainide, procainamide, quinidine, warfarin, phenytoin

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47
Q

examples of class IV antiarrhythmics?

A

digoxin, verapamil, adenosine

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48
Q

indications for digoxin?

A

SVT (not WPW), atrial flutter, AF

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49
Q

side effects of digoxin?

A

PAC, PVC, bradycardia, AV block, nausea, vomiting, anorexia, prolongs PR interval

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50
Q

drug interactions with digoxin?

A

quinidine

amiodarone, verapamil increase digoxin levels

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51
Q

indications for verapamil?

A

SVT (not WPW)

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52
Q

side effects of verapamil?

A

bradycardia, asystole, high degree AV block, PR prolongation, hypotension, CHF

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53
Q

drug interactions with verapamil?

A

use with beta-blocker or disopyramide exacerbates CHF, increases digoxin level and toxicity

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54
Q

indications for adenosine?

A

SVT

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55
Q

side effects of adenosine?

A

chest pain, flushing, dyspnea, bronchospasm, AF, bradycardia, asystole

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56
Q

What is phasic sinus arrhythmia?

A

normal physiologic variation in impulse discharge from sinus node related to respirations. the HR slows during expiration and accelerates during inspiration. Occasionally if sinus rate is slow enough, an escape beat arises from the AV junction region

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57
Q

What drug may exacerbate sinus arrhythmia?

A

Drugs that increase vagal tone, such as digoxin, may exaggerate sinus arrhythmia

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58
Q

What is sinus bradycardia?

A

slow discharge of impulses from the sinus node. A sinu rate <90 beats/min in neonates and <60 beats/min in older children is considered sinus bradycardia

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59
Q

Sinus bradycardia may occur as part of what systemic diseases? what can it be associated with?

A

hypothyroidism, anorexia nervosa

associated with conditions with high vagal tone such as GI obstruction or intracranial processes

60
Q

What is a wandering atrial pacemaker?

A

intermittent shift in pacemaker from sinus node to another part of the atrium

not uncommon in childhood and usually represents a normal variant

may be seen in association with sinus bradycardia in which the shift in atrial focus is an escape phenomenon

61
Q

What is an extrasystole?

A

premature discharge of an ectopic focus that may be situated in the atrium, AV junction, or ventricle. Usually, isolated extrasystoles are of no clinical or prognostic significance. Under certain circumstances, premature beats may be caused by organic heart disease (inflammation, ischaemia, fibrosis) or drug toxicity

62
Q

what is a PAC?

A

Common

usually in absence of cardiac disease

may result in normal, prolonged, or an absent QRS complex

Absent QRS complex - premature impulse cannot conduct to the ventricle due to refractoriness of the AV node or distal conducting system

63
Q

what is a PVC?

A

can arise in any region of the ventricle

premature, widenned, bizarre QRS complexes that are not preceded by a premature p wave

ventricular extrasystoles are often, but not always followed by a full compensatory pause

when frequent, extrasystoles may assume a definite rhythm e.g. bigeminy or trigeminy

Most pts are unaware of a single PVC, although some may be aware of a ‘skipped beat’ over the precordium - sensation caused by increased SV of the normal beat after a compensatory pause

64
Q

what can exacerbate PVCs?

A

anxiety

febrile illness

ingestion of drugs or stimulants

65
Q

What are indications for further investigation of PVCs that could require suppressive therapy?

A
  • >2 PVCs in a row
  • multiform PVCs
  • increased ventricular ectopic activity with exercise
  • R-on-T phenomenon (premature ventricular depolarisation occurs on the T wave of the preceding beat)
  • extreme frequency of beats (e.g. >20% of total beats on holter monitoring)
  • presence of underlying heart disease, Hx of heart surgery, or both

best tx for benign PVCs is reassurance that the arrhythmia is not life threatening, although very symptommatic individuals may benefit from suppressive therapy

66
Q

What can cause malignant PVCs?

A

Usually seconday to another medical issue - electrolyte imbalance, hypoxia, drug toxicity, cardiac injury

67
Q

How to treat malignant PVCs?

A

correct underlying abnormality

IV lidocaine bolus and infusion is first line therapy, with more effective drugs such as amiodarone reserved for refractory cases or pts w/ underlying ventricular dysfunction or haemodynamic compromise

68
Q

What are the 3 major subcategories of SVTs?

A

reentrant tachycardias using an accessory pathway

reentrant tachycardias w/o an accessory pathway

ectopic or automatic tachycardias

69
Q

What is atrioventricular reciprocating tachycardia?

A

AVRT involves an accessory pathway and is the most common mechanism of SVT in infants

70
Q

At what ages is AV node reentry tachycardia seen?

A

AVNRT is rare in infancy, but there is an increasing incidence of AVNRT in childhood and into adolescence

71
Q

In what groups of children is atrial flutter seen?

A

rare in children with normal hearts

common in pts following cardiac surgery

72
Q

When are atrial and junctional ectopic tachycardias seen?

A

more often associated with abnormal hearts (cardiomyopathy) and the immediate postoperative period after surgery for CHD

73
Q

Clinical manifestation of SVT?

A

abrupt onset and termination

can occur when pt is at rest or exercising and in infants it may be precipitated by an acute infection

attacks can last a few seconds or can persist for hours

if HR exceptionally rapid or attack is prolonged, precordial discomfort and HF may occur

SVT exaverbated by caffeine, nonprescription decongestants, or bronchodilators

74
Q

How might SVT present in infants?

A

occasionally present with HF as tachycardia may go unrecognised for a long time

HR may be between 240-300bpm

if attack lasts 6-24hr or more, HF may be recognized and infant will have an ashen color and will be restless and irritable, with tachypnea, poor pulses, and hepatomegaly

Fetal tachycardia - can cause hydrops fetalis, the in-utero manifestation of HF

75
Q

How to differentiate between SVT and sinus tachycardia?

A

Important as sinus tachycardia requires treatment of the underlying problem (e.g. sepsis, hypovolaemia) rather than antiarrhythmic medication

If rate >230bpm with an abrnomal P-wave axis (normal P wave is positive in leads I and aVF), sinus tachycardia is not likely

HR in SVT also tends to be relatively unvarying, in sinus tachycardia the HR varies with changes in vagal and sympathetic tone

76
Q

What is wolf-parkinson white? What are they at risk of?

A

AVRT uses a bypass tract that may be able to conduct bidirectionally (WPW) or may be retrograde only (concealed accessory pathway)

Small but real risk of sudden death

if accessory pathway rapidly conducts in antegrade fashion, pt is at risk for AF begetting ventricular fibrillation

Risk stratification, including 24hr holter monitoring and exercise study, may help differentiate pts at higher risk for sudden death from WPW

Syncope is ominous symptom. Pt with WPW and syncope should have an electrophysiology study (EPS) and likely catheter ablation

77
Q

ECG findings of WPW?

A

short PR interval and slow upstroke of the QRS (delta wave)

78
Q

WPW syndrome can be associated with what anomaly?

A

May be associated with Ebstein anomaly of the tricuspid valve or hypertrophic cardiomyopathy

79
Q

Describe the electropathophysiology in WPW?

A

Critical anatomic structure is an accessory pathway consisting of a muscular bridge connecting atrium to ventricle on either the R or L side of the AV ring

in SR, impulse is carried over both the AV node and the accessory pathway –> produces a degree of fusion of the 2 depolarisation fronts that results in an abnormal QRS

during AVRT, an impulse is carried in antegrade fashion through the AV node (orthodromic tachycardia), results in a normal QRS complex, and in retrograde fashion through the accessory pathway to the atrium, thereby perpetuating the tachycardia

In these cases, only after cessation of tachycardia is the typical ECG features of WPW syndrome recognised

when rapid antegrade conduction occurs through the accessory pathway during tachycardia, and the retrograde reentery pathway to the atrium is by the AV node (antidromic tachycardia), the QRS complexes are wide, and potential for more serious arrhythmias (VF) is greater, esp if AF occurs

80
Q

What is AVNRT?

A

involves 2 functional pathways within the AV node, the slow and fast AV node pathways. More often seen in adolescense. One of few forms of SVT that is occasionally associated with syncope. Arrhythmia is often seen in association with exercise

81
Q

non-pharmacological treatment of SVT?

A

Vagal stimulation: face in ice water (older kids) or ice bag over face (infants)

Vagal maneuvers such as valsalva, straining, breath holding

Dont do ocular pressure

carotid sinus massage is rarely effective

82
Q

pharmacological management of SVT?

A

stable pts - adenosine by rapid IV push (0.1mg/kg, max 6mg)

As adenosine can initiate AF, DC cardioversion should be nearby just in case

verapamil - can be used as initial treatment in older kids. may reduce CO and produce hypotension and cardiac arrest in infants younger than 1yr and therefore is contraindicated in this age group

In urgent situations when sx of HF have already occurred, synchronised DC cardioversion (0.5-2J/kg) is recommended as initial management

83
Q

In children with WPW, what drugs may increase the rate of antegrade conduction of impulses through the bypass tract, with the possibility of VF, and are therefore contraindicated?

A

Digoxin, CCB

84
Q

Does management differ between SVT caused by AVNRT vs. AVRT?

A

Almost identical

85
Q

Are children with AVNRT at increased risk of sudden death?

A

No. They do not have a manifest accessory pathway

Episodes are more likely to be brought on by exercise or other forms of stress, and HR can be fast leading to chest pain, dizziness, and occasionally syncope

86
Q

Is atrial ectopic tachycardia common?

A

It is an unconnon tachycardia in childhood

87
Q

How is atrial ectopic tachycardia characterised?

A

Variable rate (seldom >200bpm), identifiable P waves with an abnormal axis, and either a sustained or incessant nonsustained tachycardia.

This form of atrial tachycardia has a single automatic focus

88
Q

How do you identify atrial ectopic tachycardia?

A

aided by monitoring ECG while initiating vagal or pharmacologic therapy. Reentry tachycardias “break” suddenly, whereas automatic tachycardias gradually slow down and then gradually speed up again

89
Q

Are atrial ectopic tachycardias easier to control than the more common reentrant tachycardias?

A

Atrial ectopic tachycardias are usually more difficult to control pharmacologically than the more common reentrant tachycardias

If pharmacological therapy with a single agent is unsuccessful, catheter ablation is suggested and has a success rate >90%

90
Q

What is chaotic or multifocal atrial tachycardia?

A

Atrial tachycardia with >3 ectopic P waves, frequent blocked P waves, and varying P-R intervals of conducted beats

91
Q

Multifocal atrial tachycardia occurs most often in what age group and is associated with?

A

Infants younger than 1 year, usually w/o cardiac disease, although some evidence suggests an association with viral myocarditis or pulmonary disease

92
Q

What is the goal of treatment for multifocal atrial tachycardia?

Prognosis?

A

Slowing of ventricular rate, because conversion to sinus may not be possible, and multiple agents are often required. When this arrhythmia occurs in infancy, it usually terminates spontaneously by 3yr of age

93
Q

What is junctional ectopic tachycardia (JET)?

A

automatic (non-reentry) arrhythmia in which the junctional rate exceeds that of the sinus node and AV dissociation results. Most often recognised in the early postoperative period after cardiac surgery and may be extremely difficult to control

94
Q

What are important adjunts to managment of juctional ectopic tachycardia?

A

Reduction of the infusion rate of catecholamines and control of fever and pain are important

95
Q

What are some possible sequale of congenital junction ectopic tachycardia?

How to treat?

A

May be seen in absence of surgery

Incessant and can lead to dilated cardiomyopathy

congenital JET can be cured by catheter ablation, but long-term AV block requiring a pacemaker is a prominent complication

96
Q

What can be used to treat postoperative junctional ectopic tachycardia?

A

IV amiodarone. Pts who require chronic therapy may respond to amiodarone or sotalol

97
Q

What is atrial flutter?

A

Atrial activity at a rate of 250-300 bpm in children and adolescents, and 400-600bpm in neonates.

Mechanism of common atrial flutter consists of a reentrant rhythm originating in the right atrium circling the tricuspid valve annulus

AV node cannot transmit such rapid impulses –> some degree of AV block is virtually always present, and the ventricles respond to every 2nd to 4th atrial beat

Occasionally the reponse is variable, and the rhythm appears irregular

98
Q

What setting does atrial flutter occur in older children?

A

congenital heart disease

99
Q

Do neonates with atrial flutter tend to have normal hearts?

A

Yes

100
Q

In what context does atrial flutter often present in?

A

acute infectious illnesses, but is most often seen in pts with large stretched atria, such as those associated with long-standing mitral or tricuspid insufficiency, tricuspid atresia, ebstein anomaly, or rheumatic mitral stenosis

also can occur after palliative or corrective intraatrial surgery

Uncontrolled atrial flutter may precipitate heart failure

101
Q

How to diagnose atrial flutter?

A

Vagal maneuvers or adenosine may produce a temporary slowing of the HR as a result of increased AV block, allowing diagnosis to be made

Diagnosis is confirmed by ECG, which demonstrates the rapid and regular atrial saw-toothed flutter waves

102
Q

How to treat atrial flutter?

A

DC cardioversion

Chronic flutter: increased risk for thromboembolism and stroke and should undergo anticoagulation before elective cardioversion

Beta-blockers or CCBs: slow ventricular response by prolonging the AV node refractory period

Class I agents: procainamide/propafenone

Class III agents: amiodarone and sotalol

Catheter ablation, particularly in pts with congenital heart disease with moderate success

After cardioversion, neonates w/ normal hearts can be ceased medications, or tx with digoxin/propranolol/sotalol for 6-12 months, after which can be ceased, as neonatal atrial flutter generally does not recur

103
Q

What is atrial fibrillation?

A

uncommon in children and is rare in infants

irregularly irregular ventricular response and pulse

often associated w/ atrial enlargement or disease

may be seen in older kids w/ rheumatic mitral valve stenosis

104
Q

in what setting is atrial fibrillation seen?

A

atrial enlargement or disease

older kids w/ rheumatic mitral valve stenosis

rarely as a complication of atrial surgery

L atrial enlargement secondary to L AV valve insufficiency

Pts w/ WPW syndrome

Thyrotoxicosis, PE, pericarditis, or cardiomyopathy may be suspected in previously well older child or adolescent with AF

Rarely AF may be familial

105
Q

Treatment of AF?

A

rate control - CCB

Digoxin not given if WPW present

NSR may be achieved with IV procainamide, ibutilide, or amiodarone

DC cardioversion is 1st choice in haemodynamically unstable pts

Pts w/ chronic AF are at risk for thromboembolosim and stroke and should under anticoagulation with warfarain

Pts have elective cardioversion should undergo anticoagulation

106
Q

What is the definition of ventricular tachycardia (VT)?

A

At least 3x PVCs at >120bpm

May be paroxysmal or incessant

107
Q

What might VT be associated with? In what setting of patient may it present?

A

myocarditis

anomalous origin of a coronary artery

arrhythmogenic cardiomyopathy

MVP

primary cardiac tumors

Dilated or hypertrophic cardiomyopathy

prolonged WT (either congenital or acquired - proarrhythmic drugs)

WPW

Drugs (cocaine, amphetamine)

can develop years after intraventricular surgery (esp TOF and related defects) or can occur w/o obvious organic heart disease

108
Q

How to treat VT?

A

should be treated promptly as hypotension and degeneration into VF may result

Haemodynamically stable: IV amiodarone, lidocaine, or procainamide is the initial drug of choice

Correct any underlying abn such as electrolyte imbalance, hypoxia, or drug toxicity

Amiodarone is Tx of choice during cardiac arrest

Haemodynamically unstable: DC cardioversion

Overdrive ventricular pacing, through temporary pacing wires, or permanent pacemaker may be effective, but can cause deterioration to VF

109
Q

In neonates, what might VT be associated with?

A

anomalous left coronary artery

myocardial tumour

110
Q

Unless a clear reversible cause of VT is noted, what needs to be done?

A

EPS study –> may need catheter ablation and/or ICD implantation

111
Q

What is ventricular accelerated rhythm?

A

Occasionally seen in infants

defined in same way as VT, but rate is only slightly faster than the coexisting sinus rate (within 10%)

generally benign and resolves spontaneously

112
Q

What is VF?

A

chaotic rhythm that results in death unless effective ventricular beat is rapidly established

113
Q

Treatment of VF?

A

CPR and DC cardioversion usually necessary

If defib ineffective or VF recurs –> amiodarone or lidocaine IV and defib repeated

After recovery, need to search for underlying cause

EPS indicated unless clear reversible cause is found

If WPW noted - catheter ablation should be done

If nil correctable abn - ICD is indicated due to high risk of sudden death

114
Q

What is Long QT syndrome? What is the incidence?

A

genetic abn of ventricular repolarisation

estimated incidence of 1 per 10, 000 births

115
Q

What is Long QT syndrome associated with?

A

Present as a long QT interval on ECG and associate with malignant ventricular arrhythmias (torsades de pointes and VF)

are a cause of syncope and sudden death and may be cause of some cases of SIDS, drowning, and IUFD

80% of cases - identifiable genetic mutation

asymptomatic but at-risk pts carrying the gene mutation may not all have a prolonged QT duration. QT interval prolongation may become apparent with exercise or during catecholamine infusions

116
Q

What are the 3 major genetic mutations associated with Long QT syndrome?

A

About 75% of clinically strong LQTS is caused by mutations in 3 genes (35% KCNQ1, 30% KCNH2, 10% SCN5A) encoding for ion channels responsible for cardiac action potential

Observed genotype-phenotype correlation include swimming/exertion/emotion with LQT1, auditory triggers/postpartum period with LQT2, and sleep/rest with LQT3

117
Q

What are some heritable arrhythmia syndromes?

A

Long QT syndrome

Triadin Knockout syndrome

Andersen-Tawl Syndrome

Timothy Syndrome

Short QT syndrome

Catecholaminergic polymorphic VT

Brugada Syndrome

Early Repolarisation Syndrome

Idiopathic ventricular fibrillation

progressive cardiac conduction disease/defect

Sick sinus syndrome (SSS)

Ankyrin-B syndrome

Familial AF

118
Q

In what order does the LQT syndromes (1, 2, 3) have highest associated with sudden death?

A

LQT3 –> LQT 2 –> LQT 1

119
Q

What are the classical event patterns for LQT 1?

A

Events induced by stress or exertion

120
Q

What are the classical event patterns for LQT 2?

A

Intermediate pattern, often occurring in the postpartum period or with auditory triggers

121
Q

What are the classical event patterns for LQT 3?

A

Occurs at rest, especially during sleep

122
Q

Clinical manifestations of LQTS?

A

most often a syncopal episode brought on by exercise, fright, or a sudden startle; some events occur during sleep (LQT 3)

Can initially present with seizures, presyncope, or palpitations

10% are initially in cardiac arrest

Dx made on ECG and clinical criteria

123
Q

What are some clinical indicators of LQTS?

A

HR corrected QT interval of >0.47s is highly indicative, whereas a QT interval of >0.44s is suggestive

notched T waves in 3 leads, T-wave alternancs, a low HR for age, a hx of syncope (esp with stress), and a FHx of either LQTS or unexplained sudden death

124
Q

In what percentage does genotyping identify the mutation in pts known to have LQTS by clinical criteria?

A

80%

Genotyping not useful in ruling out diagnosis in individuals with suspected disease, but when positive is very useful in identifying asymptomatic affected relatives of the index case

125
Q

How does short QT syndromes manifest? what mutations are they associated with?

A

Manifest with AF or VF

Associated with syncope and sudden death

Often caused by gain-of-function mutation in cardiac potassium channels

126
Q

Treatment of LQTS?

A

Beta-blockers at doses that blunt HR response to exercise

Propranolol and nadolol may be more effective than atenolol and metoprolol

Some pts need a pacemaker due to drug-induced bradycardia.

ICD indicated in pts with continued syncope despite tx with beta-blockers, and those who have had a cardiac arrest

Genotype-phenotype correlative studies suggest that beta-blockers are not effective in pts with LQT3, and an ICD is usually indicated

Recent studies show that mexiletine is helpful in pts with LQT3

127
Q

What is the difference between sinus arrest and sinoatrial block?

A

Both may cause a sudden pause in the heartbeat

Sinus arrest: failure of impulse formation within the sinus node

Sinoatrial block results from block between sinus pacemaker complex and surrounding atrium

These arrhythmias are rare in childhood except in pts who have had extensive atrial surgery

128
Q

What does sick sinus syndrome result from?

A

abnormalities in sinus node or atrial conduction pathways, or both

May occur in absence of CHD and has been reported in siblings, but it is most commonly seen after surgical correction of congenital heart defects, esp Fontan procedure and the atrial switch (Mustard or Senning) operation for TGA

129
Q

Clinical manifestation of sick sinus syndrome?

A

depend on HR

Most pts remain asymptomatic w/o treatment

Dizziness and syncope can occur during periods of marked sinus slowing with failure of junctional escape

May have episodes of SVT (tachy-brady syndrome) w/ symptoms of palpitations, exercise intolerance or dizziness

130
Q

Treatment of sick sinus syndrome?

A

Pacemaker therapy indicated in pts who experience symptoms such as exercise intolerance or syncope

Drug therapy to control tachyarrhythmias (propranolol, sotalol, amiodarone) may suppress sinus and AV node function to such a degree that further symptommatic bradycardia may be produced.

Pacemaker insertion in conjunction with drug therapy is usually necessay, even in absence of symptoms ascirbable to low HR

131
Q

What is first degree HB?

A

PR interval is prolonged but all atrial impulses are conducted to the ventricle

132
Q

What is second degree HB?

A

not every atrial impulse is conducted to the ventricle

133
Q

What is Wenckebach type (Mobitz type 1) heart block?

A

Variant of second degree HB

PR interval increases progressively until a P wave is not conducted

In the cycle following the dropped beat, the PR interval normalizes

134
Q

What is Mobitz type II HB?

A

Type of second degree HB

No progressive conduction delay or subsequent shortening of PR interval after a blocked beat. This conduction defect is less common but has more potential to cause syncope and may be progressive

Related condition is high-grade second-degree AV block, in which 2 or more P waves in a row fail to conduct - this is more dangerous

135
Q

What is third-degree AV block? (complete HB)

A

no impulses from the atria reach the ventricles. An independent escape rhythm is usually present but may not be reliable, leading to symptoms such as syncope

136
Q

What causes congenital complete AV block?

A

Presumed to be caused by autoimmune injury of fetal conduction system by maternally derived immunoglobulin G Ab (anti-SSA/Ro, anti-SSB/La) in a mother with overt or, more often, asymptomatic SLE or Sjogren syndrome

Autoimmune disease accounts for 60-70% of all cases of congenital complete AV block and 80% of cases in which the heart is structurally normal

Mutation in NKX2-5 is described in which congenital AV block is seen most often in association with ASDs

137
Q

In what settings might complete heart block be seen?

A

Seen in pts w/ complex CHD and abn embryonic development of the conduction system

Associated with myocardial tumours and myocarditis

known complication of myocardial abscess secondary to endocarditis

also seen in genetic abnormalities, including LQTS and Kearns-Sayre syndrome

Post-op AV block can be complication of CHD repair; in particular repairs involving VSD closure

138
Q

Incidence of congenital complete AV block?

A

1 per 20, 000 - 25, 000

139
Q

How is congenital complete AV block usually diagnosed?

A

Often diagnosed in the fetus (secondary to the dissociation between atrial and ventricular contractions seen on fetal echo) and may produce hydrops fetalis

Maternal treatment with corticosteroids to halt progression or reverse AV block is cotroversial

Infants w/ associated CHD and HF have a high mortality rate

In some infants of mother with SLE, complete AV clock is not present at birth but develops within the 1st 3-6 months after birth

140
Q

How might children present with complete AV block?

A

often asymptomatic in older children, although syncope and sudden death may occur

infants and toddlers may have night terrors, tiredness with frequent naps, and irritability

141
Q

How might children examine with complete AV block?

A

peripheral pulse is prominent due to compensatory large ventricular stroke volume and peripheral vasodilation; systolic BP is elevated

JVP occurs irregularly and may be large when the atrium contracts against a closed tricuspid valve (cannon wave)

Exercise and atropine may produce an acceleration of 10-20 bpm or more

systolic murmurs are frequently audible along the left sternal border, and apical mid-diastolic murmurs are not unusual

first heart sound is variable due to variable ventricular filing with AV dissociation

AV block results in enlargement of the heart based on increased diastolic ventricular filling

142
Q

How is complete AV block diagnosed?

A

Dx confirmed by ECG; P waves and QRS complexes have no constant relationship

QRS duration may be prolonged, or may be normal if heartbeat is initiated high in the AV node or bundle of His

143
Q

Prognosis for congenital complete AV block?

A

usually favourable

some pts observed to age 30-40 live normal, active lives

some pts have episodes of exercise intolerance, dizziness, and syncope (stokes-adams attacks)

syncope requires ICD

pacemaker should be considered for pts who develop sx such as progressive cardiac dilation, prolonged pauses, or daytime average HR of <50 bpm

prophylactic pacemaker implantation in adolescents is resonable considering the low risk of implant procedure and difficulty in predictitng who will develop sudden severe symptoms

144
Q

When is cardiac pacing indicated in neonates?

A

low ventricular rates (<55bpm)

evidence of HF

wide complex rhythms

CHD (with ventricular rates <70 bpm)

145
Q

What drugs can be used to increase HR temporarily until pacemaker placement is arranged in neonates?

A

isoproterenol, atropine, epinephrine

146
Q

What pacemakers are used in infants vs. young children?

A

Transthoracic epicardial pacemaker implants have traditionally been used in infants; transvenous placement of pacemaker leads is available for young children

147
Q

How is post-operative heart block managed?

A

initially managed with temporary pacing wires

likelihood of return to sinus rhythm after 10-14 days is low; permanent pacemaker is recommended after that time

KK Paediatric Cardiology study (8 decks)

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