Arrhythmia: Presenter-Dr Praveen Kumar Moderator - DR Sandhya Chauhan

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ARRHYTHMIA

PRESENTER- DR PRAVEEN KUMAR


MODERATOR- DR SANDHYA CHAUHAN
ARRHYTHMIA:-

• The term arrhythmia refers to a disturbance in heart rate or rhythm.


• Such disturbances can lead to heart rates that are abnormally fast,
slow, or irregular.
• They may be transient or incessant, congenital or acquired, or
caused by a toxin or by drugs.
• They may be associated with particular forms of congenital heart
disease (CHD), may be a complication of surgical repair of CHD,
may be a result of certain genetic causes, or may be caused by fetal
inflammation, as in maternal connective tissue disease.
NELSON TEXTBOOK OF PEDIATRICS 21st
EDITION
 Arrhythmias, either slow or fast, may lead to acutely decreased
cardiac output, degeneration into a more dangerous arrhythmia
such as ventricular fibrillation, or if incessant may lead to
cardiomyopathy.
 Arrhythmias may lead to syncope or to sudden death. When a
patient has an arrhythmia, it is important to determine whether the
particular rhythm is likely to lead to severe symptoms or to
deteriorate into a life-threatening condition.

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


Tachyarrhythmias

 Classified as

Bradyarrhythmias
Atrial
Junctional
Ventricular
Heart Blocks
ELECTRICAL CONDUCTION
COMPONENTS:-
 Sinoatrial (SA) node
 Interatrial tract (Bachmann’s bundle)
 Internodal tracts
 Atrioventricular (AV) node
 Bundle of His
 Right and left bundle branches
 Purkinje fibres
CONDUCTION PATHWAY:-
Tachyarrhythmias - Symptoms

 General: palpitations, light headedness, syncope, fatigue, Shortness


of breath, chest pain
 Infants: poor feeding, tachypnoea, irritability, sleepiness, pallor,
vomiting
 Hemodynamic instability: respiratory distress/failure, hypotension,
poor end-organ perfusion, loss of consciousness, sudden collapse

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


Tachyarrhythmias - Causes

 Primary: Underlying conduction abnormalities


 Secondary: Reversible Hs & Ts
– Hypovolemia
– Hypoxia
– H+ ions (acidosis)
– Hypo/Hyperkalemia
– Hypothermia
– Hypoglycemia
– Toxins
– Tamponade
– Tension pneumothorax
– Thrombosis (coronary, pulmonary)
– Trauma
Tachyarrhythmias - Originating in the
atria
1. SINUS ARRYTHMIA
 Normal physiologic variation in impulse discharged from SA node
in relation to respiration
 HR slows during expiration, increases during inspiration
 Drugs like digoxin exaggerate it
 Abolished by exercise

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


Varied PP interval. No significant change in P wave morphology/PR
interval
2. SINUS TACHYCARDIA
 The sinus node sends out impulses faster than usual >>HR

 In response to body’s need for >>CO :exercise, anxiety, fever,


hypovolemia or circulatory shock, anaemia, CHF, administration of
catecholamines, thyrotoxicosis & myocardial disease.

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


P waves are present and normal , narrow QRS, beat to beat variability
3. PREMATURE ATRIAL CONTRACTIONS
• Benign in the absence of underlying heart disease
• Common in newborn period
• Depending on prematurity of the beat, PAC’s may result in a
normal/prolonged/absent QRS complex

Conducted to Not
ventricle with conducted
aberrant or to ventricle,
widened QRS apparent
complex pause NELSON TEXTBOOK OF PEDIATRICS 21st EDITION
Early p wave, sometimes with different morphology than a sinus p wave
4.WANDERING ATRIAL PACEMAKER
 Pacemaker shifts from sinus node to another atrial site
 Normal variant
 Irregular rhythm

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


5.SUPRA VENTRICULAR TACHYCARDIA
 Originating above the ventricles
 Most common abnormal tachycardia seen in pediatric practice
 Most common arrhythmia requiring treatment in pediatric
population
 Most frequent age presentation: 1st 3 months of life, 2nd peaks @
8-10 yrs and in adolescents

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


 Paroxysmal, sudden onset & offset
 Occurring at rest
 In infants, precipitated by infection and in children by
bronchodilators, decongestants
 Rates of SVT vary with age (>180 bpm)
 Short paroxysms usually are not dangerous
 Prolonged attack lasting for 6-24 hrs or HR > 300 bpm lead to heart
failure

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


 Older children present with palpitation
 Younger children – Basal HR higher for that age, HR >> greatly with crying

 P waves difficult to define, but 1:1 with normal QRS


 ECG similar to sinus tachycardia
Differentiating features :
 HR>230bpm, unvaryingNELSON
HR, abnormal
TEXTBOOK OFPPEDIATRICS
wave axis 21stifEDITION
seen
 • 3 major types
- re-entrant tachycardia with an accessory pathway
- Re-entrant tachycardia without an accessory pathway
- Ectopic/automatic tachycardias
AVRT
AVNRT
ATRIAL ECTOPICS
JUNCTIONAL ECTOPICS
ATRIAL FLUTTER
NELSON TEXTBOOK OF PEDIATRICS 21st EDITION
ATRIAL FIBRILLATION
ATRIOVENTRICULAR RECIPROCATING
TACHYCARDIA (AVRT):-
 Most common mechanism of SVT in infants
 Re-entrant tachycardia with an accessory pathway
 Flow of impulses may be bidirectional or retrograde only
• Wolff-Parkinson-White syndrome :
- Characterized by the presence of a muscular bridge connecting atria
and ventricles on either the right or left side of AV ring
- Flow of impulses is bidirectional

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


 Flow of impulses is antegrade through the AV node and retrograde
through the accessory pathway towards the atrium

SVT in a child with WPW showing normal QRS complexes with P waves
seen on upstroke of T waves NELSON TEXTBOOK OF PEDIATRICS 21st EDITION
 Typical features of WPW are apparent when tachycardia subsides
 Wide QRS complexes, delta waves, short PR interval
 Risk of sudden death NELSON TEXTBOOK OF PEDIATRICS 21st EDITION
Management of SVT:-

 Non pharmacological measures like:-


-Placing an ice bag over the face
-Valsalva maneuver
-Straining
-Breath holding
 If the child is hemodynamically stable, rapid iv push of adenosine (risk of
AF)
 In older children, CCB like verapamil can be given iv (C/I in <1year)

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


 If the child is not stable, synchronized DC cardioversion (1 J/kg)
 If the tachycardia is resistant, iv procainamide, quinidine, flecainide,
sotalol, amiodarone can be tried
 If SVT still persists, catheter ablation with success rate of 80-95%
-Radiofrequency
-Cryo
-Surgical
 Maintenance therapy
- When sinus rhythm is restored, for long term maintenance, DOC is beta
blockers in both WPW and Non WPW syndromes
- Digoxin can be given in infants with no accessory pathway NELSON TEXTBOOK OF PEDIATRICS 21st EDITIO
AV NODAL RE-ENTRANT
TACHYCARDIA:-
 Common form of SVT in adolescents Involves the use of 2
pathways within the AV node
 Precipitated by exercise
 Present with syncopal attacks
 Good control on antiarrythmic therapy
 Beta blockers remain the drug of choice for maintenance

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


ATRIAL ECTOPIC TACHYCARDIA:-

 Uncommon in children
 Variable HR, usually >200bpm
 Due to a single focus of automaticity
 On starting pharmacologic therapy, the tachycardia gradually slows
down only to speed up again
 ECG shows ectopic p waves with an abnormal axis

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


MULTIFOCAL ATRIAL TACHYCARDIA:-

 More common in infants than in older children


 Characterized by 3 or more ectopic P waves and varying PR intervals
 Spontaneous resolution occurs usually by 3 years of age

Chaotic ECG pattern with multiple ectopic P waves with abnormal axes
NELSON TEXTBOOK OF PEDIATRICS 21st EDITION
JUNCTIONAL ECTOPIC
TACHYCARDIA:-
 Due to an abnormal focus of automaticity
 The focus being a conducting tissue very close to the AV node
(junctional)
 Discharge of impulses from junctional tissue exceeds SA nodal discharge
leading to AV dissociation
 Occurs in early post op period or may be congenital
 IV amiodarone is the DOC for post-op JET
 Congenital JET requires catheter ablation
 Maintenance therapy with amiodarone/sotalol
NELSON TEXTBOOK OF PEDIATRICS 21st EDITION
ATRIAL FLUTTER:-
 Also called intra-atrial re-entrant tachycardia
 HR > 400-600 bpm in neonates, >250-300 bpm in children
 Due to re-entrant pathway located in the right atrium circling the tricuspid
valve annulus
 AV dissociation occurs and ventricles respond to 2nd - 4th atrial beat
 Occurs in neonates with normal hearts and in children with

 Rapid and regular saw-toothed flutter waves


NELSON TEXTBOOK OF PEDIATRICS 21st EDITION
 Temporary slowing of HR by vagal maneuvres/adenosine/CCB
 Synchronized DC cardioversion is the TOC
 Patients with chronic atrial fluttter are at >> risk for thromboembolism
and stroke
-require anticoagulants
 Maintenance therapy with type 1 and type 3 agents

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


ATRIAL FIBRILLATION:-

 Uncommon in infants and children


 HR > 400-700 bpm
 Irregularly irregular rhythm on ECG and pulse
 Post op, in CHD with enlarged atria, thyrotoxicosis, pulmonary
embolism, pericarditis, cardiomyopathy
 If stable, CCB, iv procainamide/amiodarone
 If unstable, DC cardioversion

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


Absence of clear P waves and an irregularly irregular ventricular response
(No two R-R intervals are the same)
Tachyarrythmias-Originating in the
ventricles:-
1.PREMATURE VENTRICULAR CONTRACTIONS –
• Uncommon in children
• Unifocal/multifocal
• Abolished on exercise
• If unifocal/disappearing with exercise/ associated with normal heart,
then considered benign, no therapy needed.
• Advise patients to avoid caffeine and other stimulants.

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


 Early, wide QRS complexes
 T waves in opposite direction of QRS
 Bigeminy, sinus beat followed by PVC, this repeating as a pattern also
frequently seen
2. VENTRICULAR TACHYCARDIA:-
•Defined as at least 3 PVC s at >120 bpm
•Paroxysmal/incessant
•Associated with myocarditis, anomalous LCA, MVP, primary cardiac
tumors, cardiomyopathy / Post-op
•Prompt treatment to prevent degeneration into VF

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


Wide QRS (>0.08 sec), P waves may be unidentifiable or not related to QRS

 If stable, treat with IV amiodarone/lidocaine/procainamide and correct the


cause
 If unstable, DC cardioversion NELSON TEXTBOOK OF PEDIATRICS 21st EDITION
3. VENTRICULAR FIBRILLATION:-
 Seen in children with long QT syndrome or Brugada syndrome
 Associated with cardiomyopathies, structural heart diseases causing
ventricular dysfunction
 Sudden death occurs unless an effective ventricular beat is reestablished.

 Treatment: immediate DC defibrillation, CPR


 If ineffective, give IV amiodarone, lidocaine and repeat defibrillation
 Treat the cause once sinus rhythm is established

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


NELSON TEXTBOOK OF PEDIATRICS 21st EDITION
LONG Q-T SYNDROMES:-

 Include genetic abnormalities of ventricular repolarization


 Long QT – interval on ECG
 Associated with malignant ventricular arrythmias leading to sudden death
 At least 50% are familial
 Precipitated by exercise
 LQT1 events are stress induced
 LQT3 occur during sleep
 LQT2 have an intermediate pattern
 LQT3 has highest probability of sudden death
NELSON TEXTBOOK OF PEDIATRICS 21st EDITION
• Diagnostic criteria
 Present with syncope, seizures, palpitations
 Corrected QT interval >0.47sec or a QT interval >0.44sec
 Notched T waves
 Low HR for age
 Familial history of LQTS/sudden death
• Treatment - Beta blockers which blunt the HR s response to exercise
• If drug induced profound bradycardia – pacemaker
• If drug resistant,LQT3- implantable cardiac defibrillator
NELSON TEXTBOOK OF PEDIATRICS 21st EDITION
Bradyarrhythmias:-

 Primary : Abnormal pacemaker/conduction system (congenital or


postsurgical injury), cardiomyopathy, myocarditis
 Secondary : Reversible Hs & Ts:
– Hypoxia
– Hypotension
– H+ ions (acidosis)
– Heart block
– Hypothermia
– Hyperkalemia
– Trauma (head)
– Toxins/drugs (cholinesterase inhibitors, Ca++ channel blockers, β blockers,
digoxin, α2 agonists, opioids)
SINUS BRADYCARDIA:-

 Physiological (ie: sleep, athletes)


 Pathological (ie: abnormal electrolytes, infection, drugs, hypoglycemia,
hypothyroidism, ↑ICP)

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


• SINUS ARREST - Failure of impulse formation within SA node

• SINOATRIAL BLOCK- Block between SA node and surrounding atrium


preventing conduction of impulses

 Rare in children
 Digoxin toxicity, extensive atrial surgery

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


• SICK SINUS SYNDROME
 Due to abnormalities in either the SA node / atrial conduction pathways /
both
 Post surgery for CHD (fontan, mustard, senning procedures) or even in
patients with normal heart
 Usually asymptomatic and don’t require treatment
 Periods of marked sinus slowing present with dizziness and syncope
pacemaker if symptoms recur

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


AV BLOCKS:-
NELSON TEXTBOOK OF PEDIATRICS 21st EDITION
NELSON TEXTBOOK OF PEDIATRICS 21st EDITION
CONGENITAL COMPLETE AV BLOCK:-

 Autoimmune injury to the fetal conduction system by maternally derived


anti-SSA/Ro, anti-SSB/La antibodies
 Maternal SLE or sjogren syndrome
 NKX2-5 gene mutation has congenital complete av block with asd
 High fetal loss rate
 May lead to hydrops fetalis
 Present with tiredness, frequent naps, irritability, symptoms and signs of
heart failure

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


NELSON TEXTBOOK OF PEDIATRICS 21st EDITION
VAUGHAN WILLIAMS
CLASSIFICATION:-
 Class 1a – sodium fast channel blockers, prolong
repolarization
(quinidine, procainamide, disopyramide)
 Class1b – sodium fast channel blockers, shorten repolarization
(lidocaine, mexiletine, phenytoin)
 Class 1c – sodium channel blockers (flecainide, propafenone)

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


 Class 2 – beta blockers (propranolol ,atenolol)
 Class 3 – potassium channel openers, prolong repolarization
(amiodarone)
 Class 4 – miscellaneous (verapamil, adenosine, digoxin)

NELSON TEXTBOOK OF PEDIATRICS 21st EDITION


HYPERKALEMIA:-

 Normal plasma potassium concentration is strictly regulated


between 3.5 to 5 mEq/L.
 Hyperkalemia, defined as serum potassium level above 5.5 mEq/L,
is a potentially life threatening condition.
 Severe hyperkalemia when serum potassium Levels are
>6.0meq/L.

decrease in renal excretion is the most frequent cause

PEDIATRIC NEPHROLOGY SIXTH EDITION, ARVIND BAGGA


CLINICAL FEATURES:-

 Most of Hyperkalemic individuals are asymptomatic.


 If present - symptoms are nonspecific and predominantly related to
muscular or cardiac functions.
 The most common - weakness and fatigue.
 Occasionally, frank muscle paralysis or shortness of breath.
 Patients also may complain of palpitations or chest pain.
 Arrythmias occur- Sinus Brady, Sinus arrest, VT, VF, Asystole
 Patients may report nausea, vomiting, and paresthesias

PEDIATRIC NEPHROLOGY SIXTH EDITION, ARVIND BAGGA


PEDIATRIC NEPHROLOGY SIXTH EDITION, ARVIND BAGGA
MANAGEMENT:-

 CALCIUM GLUCONATE 10%:- 0.5-1 ml/kg over 5-10 min under


EKG monitoring repeated q5-10 min (maximum total dose 30 ml)
 DEXTROSE/INSULIN:- Regular insulin 0.1units/kg with 2 ml/kg
of 25% dextrose over 30 min.
 Beta2 adrenergic agonist (Nebulization or IV)
 Sodium Bicarbonate:-1-2 mEq/kg over 30-60 min
 Furosemide:- 1-2 mg/kg
 Ion exchange resins:- Sodium Polystyrene Sulfonate 1g/kg q 8 hr
PO or PR
PEDIATRIC NEPHROLOGY SIXTH EDITION, ARVIND BAGGA
DIGOXIN TOXICITY:-

KDT PHARMACOLOGY 8TH EDITION


Ventricular bigeminy caused by digitalis toxicity. Ventricular ectopy is one of the most
common signs of digitalis toxicity. (A) The underlying rhythm is atrial fibrillation. (B)
Each normal QRS complex is followed by a premature ventricular complex.

 This digitalis toxic arrhythmia is a special type of ventricular tachycardia with QRS
complexes that alternate in direction from beat to beat. No P waves are present.
KDT PHARMACOLOGY 8TH EDITION
 Atrial fibrillation with an excessively slow ventricular rate because of digitalis toxicity.
Atrial fibrillation with a rapid ventricular rate is rarely caused by digitalis toxicity. 

KDT PHARMACOLOGY 8TH EDITION


SYMPTOMS:-

 The first symptoms of digoxin toxicity are gastrointestinal (abdominal


cramps, vomiting, diarrhea) and visual disturbances (green or yellow
halos, “fuzzy shadows”—like driving at night with dirty glasses).
 Confusion and yellow vision may occur with chronic toxicity,
followed by atrioventricular blockade, bradycardia, and
ventricular arrhythmias.
 Digoxin toxicity is also worsened by hypokalemia.
 Conversely, hyperkalemia diminishes digoxin's effectiveness.
 A number of other cardiovascular drugs predispose patients to digoxin
toxicity, including verapamil, diltiazem, quinidine, and amiodarone.
KDT PHARMACOLOGY 8TH EDITION
MANAGEMENT:-

 A- B - C
 Hydration with IV fluids, oxygenation and support of ventilatory
function, discontinuation of the drug, and, sometimes, the
correction of electrolyte imbalances.
 Fab antibody fragments are extremely effective in the treatment of
severe, acute digitalis toxicity.
 Cardiac glycosides undergo some degree of enterohepatic or
enteroenteric recirculation and are adsorbed to activated charcoal .
AC or multi-dose AC (MDAC) are recommended for digitalis
toxicity .
KDT PHARMACOLOGY 8TH EDITION
Management of arrhythmia:-
 In case of tachycardia: give lidocaine or phenytoin (No effect on AV
conduction).
 Life-threatening ventricular arrhythmias are treated according to the
algorithms of advanced cardiac life support (ACLS).
 In case of bradycardia: give atropine.
 Correct electrolyte disturbances
 In case of hyperkalemia: give EDTA and give insulin + glucose to shift
K+ intracellularly But Ca gluconate is contraindicated.
 However, hyperkalemia itself does not cause death, and treatment with
potassium-lowering agents does not reduce mortality.
KDT PHARMACOLOGY 8TH EDITION
DIGIFAB:-
THANK YOU

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