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Cardiac Arrhythmias

Normal heart rate in children


- newborn 100-180/min
- 2-3 yr 100-130/min
- 4-8 yr 70-120/min
- 9-12 yr 65-100/min
- 13-15 yr 60-90/min

Sinus tachycardia
- HR exceeding with 20% the maximal for age
- tachycardia (>200/min in neonates, 150/min in infants, 120/min in older
children),
- physiologic factors: during effort, increased sympathic tonus (emotions)
- pathologic factors: hypoxia, electrolytic imbalance, intoxications,
bacterial toxins; fever, anemia, CHF, hyperthyroidism
- variable frequency difference with SVT
- each P wave followed by a QRS complex after a normal PR interval
- shortened TP intervals

Sinus bradycardia
- bradycardia - <90/min in neonates, <60/min thereafter
- physiologic factors: athletes, during sleeping, bradycardia with periodic
apnea in premature infants
- pathologic forms: systemic disease (myxedema), increased intracranial
pressure (tumors, hemorrhages), starvation, infectious diseases (thyphoid
fever, diphteria), rheumatic disease, hyperkaliemia, digitalis intoxication,
uremia
- P waves, QRS complexes, PR intervals normal
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- increased ST interval

Respiratory sinus arrhythmia


- normally pysiologic variation in impulse discharges from the sinus node
related to respirations
- slow rate during expiration, acceleration during inspiration
- exaggerated during convalescence from febrile illness, drugs that increase
the vagal tone (digitalis)
- abolished by exercise and atropine

Wandering atrial pacemaker


- an intermittent shift in the pacemaker of the heart from the sinus node to
another part of the atrium
- physiologic forms: usually represents a normal variant
- pathologic forms: myocardial lesions of any etiology, digitalis overdoses,
CNS disturbances (subarachnoid hemorrhage)
- ECG variable cardiac frequency, irregular R-R intervals, P waves before
each QRS complex, of different morphology (positive or negative), others
than the sinus node P wave

Extrasystoles (ectopic rhythms)


- premature cardiac beats of ectopic origin
- physiologic forms
- pathologic forms: miocardopathies, valvulopathies, acute and chronic cor
pulmonale, intoxications (digitalis, procainamide, ephedrine), cardiac
catheterism, surgical interventions
- isolated/coupled/systematized (bigeminus, trigeminus)
Premature atrial complexes/beats (PACs)

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- isolated in 20% of healthy children
- ECG: premature P wave (decreased distance between the preceeding and
ectopic P waves), of different morphology, normal QRS complex, the
following P wave, usually after normal interval (no compensatory pause)
Premature jonctional complexes/beats
- ECG: negative P wave followed by a normal QRS complex/included in a
normal QRS complex/preceeded by a normal QRS complex; shortened
PR interval, (postextrasystolic pause)
Premature ventricular complexes/beats (PVCs)
- benign - monomorphe (unifocal), <30/hr and disappear with effort
- pathologic: polytope (multifocal), >30/hr, bigeminus or couplets,
increased with effort, R on T phenomenon (premature ventricular
depolarization on the T wave of the preceeding beat), underlying heart
disease (myocarditis), digitalis intoxication, electrolyte imbalance,
hypoxia, intravenrticular catheter
- ECG: premature QRS complexes, widened, bizarre, not preceeded by a P
wave, followed by a compensatory pause (the interval between the beat
preceeding the extrasystole and the beat that follows the extrasystole is
equal to twice the normal sinus cycle length)

Paroxistic supraventricular tachycardia (SVT)


- the most frequent arrhythmia needing to be treated in childhood
- peak incidence in infancy and adolescence
- may be precipitated by acute infections, usually occurs at rest
- mechnism: AV re-entry mechanism through an accessory pathway
- 95% of patients have a normal heart/associated with a bypass tract in one
of the pre-excitation syndromes (Wolf-Parkinson-White WPW, Lown-
Ganong-Levine LGL), CHD (more common in Ebstein anomaly of the
tricuspid valve or corrected TGA), cardiomiopathies

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- attacks may last few second or hr
- many children tolerate the episodes very well
- if the HR is exceptionally rapid or if the attack is prolonged precordial
discomfort, CHF (tacypnea, hepatomegaly)
- infants usually diagnosed with CHF (tachycardia goes unrecognized for
a long time), restless, irritation, convulsions
- neonates when tachycardia occurs in the fetus, it can cause severe CHF
with hydrops fetalis (one of the major cardiac etiologies for hydrops
fetalis)
- very rapid HR, usually impossible to determine
- ECG: sudden beginning and ending; fixed HR 200-230/min, unmodified
by effort; equal atrial and ventricular rates; P-P intervals equal; modified P
wave (ectopic origin), often not recognizable (P on T phenomenon);
narrow QRS complexes; depressed ST segments and inverted T wave
(myocardial ischemia)
- 24 hr ECG (Holter) recordings for monitoring the course of therapy and
detecting brief runs of tachycardia that may be asymptomatic
- electrophysiologic studies (EP) by cardiac catheterization, in patients with
refractory SVT; multiple electrodes catheters are placed into different
locations in the heart, for the location of ectopic focuses or bypass tracts
- treatment of SVT attacks:
- vagal stimulation (facial submersion in iced saline or an icebag
over the face); older children vagotonic maneuvers (Valsalva
maneuver expiration with closed glottis, breath-holding,
drinking ice water, vomiting)
- urgent situations (symptoms of CHF), electroconversion with
0.5-1-2 J/kg
- in stable patients, antiarrhythmic agents: adenosine 0.1 mg/kg IV
bolus, rapid action and minimal effects on cardiac contractility;

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verapamil 0.1 mg/kg IV bolus over 2 min, in children >1yr,
may reduce cardiac output, produce hypotension and cardiac
arrest in children <1yr; propafenone 0.1 mg/kg IV infusion;
digoxin 0.04 mg/kg/dose, IV bolus
- long treatment therapy in children with several relapses with the same
drugs orally (except for adenosine), eg digoxin 0.01-0.02 mg/kg/24 hr,
divided 12 hr, propranolol
- radiofrequency ablation od an accessory pathway for patients in whom
multiple agents are required or if arrhythmia control is poor

Wolf-Parkinson-White Syndrome (WPW)


- accessory pathways bind the atria, the AV node or Hiss-bundle with the
ventricles, without the inclusion of any specialized condution tissue
- they are rapidly conducing ways
- WPW syndrome high incidence in the 1st yr of life, disappearance of
tachycardia from the 2nd yr
- ECG: typical pre-excitation pattern with short PR interval, delta wave,
larger QRS complex, variable episodes of SVT; atrial fibrillation,
ventricular fibrilation
- treatment: only children with symptomatic episodes of tachycardia,
propafenone, -blocking agents (propranolol, sotalol); digoxin not
recommended because of lenghtening the conduction through the normal
AV conduction system, facilitating the conduction through the accessory
pathway
- severe cases: radiofrequency ablation of the accessory pathway (after EP)

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