Download Rhythm disorders in neonates

Review article
Acta Pediátr Mex 2014;35:134-144.
Rhythm disorders in neonates
Luis Martín Garrido-García1
María de Guadalupe Delgado-Onofre2
1
Pediatric cardiologist. Head of Undergraduate and
Postgraduate Department.
2
Third year resident.
Instituto Nacional de Pediatría, México, D.F.
ABSTRACT
Arrhythmias are a variety of heart rhythm alterations which may occur
in fetuses and neonates considered healthy. The majority are benign. The
incidence reported varies from 1 to 10% in neonates in the first days of
extrauterine life. Arrhythmias in the neonatal stage entail high morbidity
and mortality, above all when they occur in patients with congenital
heart disease or lack of response to medical treatment. Opportune
pharmacological control of rhythm offers a good long-term prognosis.
The natural history of arrhythmias in the neonatal period differs from
arrhythmias in other pediatric age groups; they can be classified as:
sinus arrhythmia, tachyarrhythmias, long QT syndrome, and bradyarrhythmias. It is important that doctors in charge of treating this group of
patients recognize the causal factors of arrhythmias, and the diagnostic
and therapeutic options available.
Key words: arrhythmias, neonates, sinus dysrhythmia, tachyarrhythmias,
long QT syndrome, treatment, prognosis.
134
Received: August, 2013
Accepted: January, 2014
Correspondence
Dr. Luis Martín Garrido García
Insurgentes Sur 3700, Letra C
Col. Insurgentes Cuicuilco
CP 04530, México D.F.
Tel: 1084-0900
[email protected]
This article must be quoted
Garrido-García LM y Delgado-Onofre MG. Trastornos del ritmo en el recién nacido. Acta Pediat Mex
2014;35:148-158.
www.actapediatricademexico.org
Garrido-Garcia LM and Delgado-Onofre MG. Heart rhythm disorders in neonates
The electrocardiogram (ECG) is the reference
procedure to identify heart rhythm alterations in
neonates; however, it is necessary to ascertain
that an arrhythmia is not transitory. With the
development of neonatal intensive care units
and increased monitoring of patients, in both
the prenatal and postnatal stages, various rhythm
alterations have been identified in fetuses and
neonates considered healthy.1,2 The majority of
those arrhythmias are benign; however, detecting
them requires a thorough evaluation of them and
the risk factors for their genesis, such as maternal
illnesses or infections, fetal distress, or congenital
heart disease.
An incidence of heart rhythm alterations of between 1 and 10% has been described in healthy
neonates in the first days of extrauterine life;
notwithstanding, this figure is higher in patients
admitted to neonatal intensive care units.2-5
PATHOPHYSIOLOGY
Arrhythmias may occur as a result of various
mechanisms; the most important are: defects in
impulse generation with increase or reduction
of automaticity and defects in conduction of
stimulus with a simple block or one-directional
block and a reentry mechanism. However, for
these alterations to manifest clinically there
must be a pathophysiological substrate, in the
neonate, that predisposes him/her to rhythm
disorders. The most common are: 1) hydroelectrolytic alterations; 2) hypoxemia; 3) immaturity
of the autonomic nervous system; 4) myocarditis;
5) congenital heart disease; or 6) endovenous
catheters that irritate the endocardium.6
Evaluation of neonates with arrhythmias starts
with the search for maternal factors, which may
trigger rhythm alterations, in electrolyte intake
and blood sugar. A surface electrocardiogram is
sufficient to establish a diagnosis in most cases.
An echocardiogram is indicated in symptomatic
patients, in those with suspected congenital heart
disease and with persistent arrhythmias. A 24hour (Holter) electrocardiogram can establish
a diagnosis in patients with arrhythmias which
cannot be documented with a surface electrocardiogram.4,6
SINUS DYSRHYTHMIA
Sinus dysrhythmia is the most common form
of change in heart rhythm in neonates and is
considered a normal variant; the heart rate drops
during expiration and rises during inspiration.
This type of rhythm is more evident during episodes of fever.7
TACHYARRHYTHMIAS
This term means an abnormal increase in heart
rate. They are considered “benign” tachycardias
when there is no clinical hemodynamic repercussion and no treatment is required. This type
of phenomena do not require follow up because
they do not affect health.4,5
Depending on the site where these arrhythmias
are generated, they can be classified as: a) supraventricular tachyarrhythmias (when there is an
ectopic focus above the bundle of His or it participates in the circuit of the arrhythmia) and b)
ventricular tachyarrhythmias (when the abnormal
stimulus is generated below the bundle of His).
Finally, if the start and end of the abnormal
rhythm are sudden or gradual, tachyarrhythmias
are classified as paroxysmal or non-paroxysmal.
The most common form of non-paroxysmal
tachycardia is sinus tachycardia, in which case
the various factors that triggered the tachycardia
must be corrected: anemia, hydroelectrolytic
alterations, sepsis, respiratory problems, etc.5-9
(Figure 1).
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Acta Pediátrica de México
Figure 1. 12-lead electrocardiogram of a neonate of
8 days of extrauterine life and neonatal sepsis, with
fever of 39ºC and heart rate 200 bpm. We also observe
dilation of right auricle and ventricle.
Supraventricular tachyarrhythmias
Supraventricular extrasystoles
Are premature heartbeats originating in the atria.
They have been reported to exist in 5 to 30%
of neonates, a figure which is higher in preterm
neonates.10 Electrocardiographically there is premature atrial depolarization with an abnormal
morphology; if depolarization is conducted to the
ventricles it usually does so with a normal ventricular complex. If the supraventricular extrasystole is
capable of reactivating the sinus node it will have
an incomplete compensatory pause. (Figure 2). In
these heart rhythm disorders patients are usually
asymptomatic and they are considered benign
events in patients with structurally healthy hearts.
Supraventricular extrasystoles can be triggered by
several causes, among them: toxic concentrations
of sympathomimetic amines such as isoproterenol or dopamine, or by central catheters which
cause mechanical irritation. If supraventricular
extrasystoles are frequent, a chest x-ray and
an electrocardiogram are indicated to rule out
congenital heart disease or cardiomyopathy.
Such patients should be monitored for three or
four days and a 24-hour electrocardiographic
record is indicated. If there are no episodes of
136
Figure 2. Healthy neonate of 15 days of extrauterine
life with extrasystoles detected by auscultation. The
electrocardiogram shows supraventricular extrasystoles with incomplete compensatory pause.
supraventricular tachycardia the patients do not
require treatment; however, they are kept under
observation for a month. Cases in which atrial
extrasystoles trigger supraventricular tachycardia
with alteration of ventricular function should
receive treatment.6,7
Atrial ectopy
This arrhythmia is very common in fetuses and
neonates. It is produced by increased automaticity in a group of atrial cells which are not part
of the normal conduction system. In the ECG
they appear as tachycardias with a narrow QRS
complex and an abnormal P wave with variable
morphology (migratory pacemaker) or they may
have a single ectopic focus. It tends to accelerate and decelerate (“heating” and “cooling”
phenomenon). In most cases this arrhythmia
disappears over time and does not cause further
complications; however, when the ectopic atrial
rhythm has a frequency above 200 bpm and accelerated ventricular conduction, it can cause
heart failure and dilated cardiomyopathy.7,8
Atrioventricular reentry tachycardia
Occurs in one of every 1,700 neonates and is
the leading cause of supraventricular paroxysmal
Garrido-Garcia LM and Delgado-Onofre MG. Heart rhythm disorders in neonates
tachycardia in the neonatal period in up to 50% of
cases.2-5 For this arrhythmia to occur there must be
an accessory pathway that can allow anterograde
or retrograde conduction (Wolff-Parkinson-White
WPW syndrome) or a pathway with only retrograde conduction (occult pathway). In most cases
the tachycardia starts with an extrasystole which
may be atrial or ventricular; it causes a one-directional block, usually in the accessory pathway,
although it may also occur in the atrioventricular
node and the tachycardia is initiated by a reentry
mechanism.6-9 (Figures 3 and 4)
To distinguish an atrioventricular reentry tachycardia from other forms of supraventricular
tachycardia, it is important to locate the P wave
on the electrocardiogram during the tachycardia.
In atrioventricular reentry tachycardia there is a
retrograde P wave which is inscribed after the QRS
complex. For these arrhythmias atrial and ventricular tissue is required to maintain the reentry
circuit; therefore, there cannot be atrioventricular
block or disassociation during the arrhythmia.7,8
These arrhythmias occur more commonly in
patients with structurally healthy hearts; however, WPW syndrome may be associated with
Ebstein disease, corrected transposition of the
great vessels, or hypertrophic cardiomyopathy.3
It is well established that neonates with WPW
syndrome have a high probability of resolution
of supraventricular tachycardia in the first year
of life. However, it has also been shown that
up to one third of such patients with resolution
of symptoms have a probability of a relapse of
tachycardia at school age.3,6
Figure 3. 12-lead electrocardiogram of a patient of
1 month of age taken to the Emergency Service with
hemodynamic deterioration. Physical exploration
detected tachycardia with a narrow QRS complex;
ventricular heart rate of 300 bpm; retrograde P wave.
Lemler et al. conducted a study to identify risk
factors for reincidence of symptoms in patients
with WPW in subsequent stages of life. They
analyzed the following factors: heart failure during the arrhythmia, recurrence of the arrhythmia
during treatment in the first year of life, difficulty
controlling the arrhythmia in the initial period,
congenital heart disease and persistence of the
delta wave on the electrocardiogram. They found
that the only positive predictive factor for recurrence of the arrhythmia was persistence of the
delta wave despite treatment.11
Atrial flutter
Figure 4. 12-lead electrocardiogram of the same patient as Figure 3 after electric cardioversion. In sinus
rhythm with a short PR interval (90 ms) and delta wave.
Wolff-Parkinson-White Syndrome.
Although it is a common rhythm disorder in
fetuses (25% of tachycardias in fetuses) and in
neonates, it is very rare in pediatric age and does
not become common again until adult age. It
is associated with congenital heart diseases:
endocardial fibroelastosis or cardiomyopathies,
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Acta Pediátrica de México
chromosomal alterations, and other pathological
states in up to 30% of cases. Electrocardiographically it is characterized by a “sawtooth” shaped
pattern of P waves with frequencies ranging from
300 to 600 beats per minute; the ventricular
response may be regular or irregular, but with
lower frequency (Figure 5).
This arrhythmia has high morbidity and mortality
in the neonatal stage, especially if it is associated
with congenital heart diseases or lack of response
to medical treatment; however, if pharmacological control of the rhythm is achieved, the
long-term prognosis is good.7-9,12
Treatment of supraventricular tachyarrhythmias
Acute treatment. Depends on the patient’s
general condition. In cases of tachycardia with
narrow QRS complex, without hemodynamic
compromise, the initial treatment is to attempt
to suppress the arrhythmia with vagal maneuvers
like applying a cold compress on the patient’s
face for 10 to 20 seconds and even facial immersion in cold water for 5 seconds. Ocular
compression or carotid massage are not recommended. These maneuvers trigger the “diving
reflex,” which not only causes vagal stimulation
but also a drop in sympathetic activity. During
the procedure, the electrocardiographic record
and blood pressure should be monitored, due
to the possibility of asystole at the end of the
Volume 35, No. 2, March-April 2014
supraventricular tachycardia.7-9,13 If treatment
with vagal maneuvers is ineffective intravenous
adenosine is recommended in both term and
preterm neonates; initial dose 50 to 150 mg/
kg. The dose may be increased by 50 g/kg every
minute to a maximum dose of 250 to 500 mg/
kg. Side effects of large doses of adenosine are
bronchoconstriction, stridor, and low blood
pressure secondary to peripheral vasodilation.13
If the tachycardia persists despite treatment, with
hemodynamic instability of the patient, electric
cardioversion is indicated. The application of
current should be synchronized with the QRS
complex, starting with a dose of 0.5 joules per
kilogram of body weight. In the large majority
of cases cardioversion is effective to stop the
supraventricular tachycardia.7-9,11,13,14
Chronic treatment. In neonates with a history
of supraventricular tachycardia, when the acute
event is resolved, chronic treatment should be
initiated to prevent recurrence of the tachycardia.
Digoxin and b blockers are the first-line agents
for treating reentry tachyarrhythmias. Class 1A
(procainamide), IC (propafenone or flecainide)
and class 3 (amiodarone) antiarrhythmic drugs
have also been used successfully when digoxin
and b blockers are ineffective. Use of calcium
antagonists in neonates should be avoided as
a sudden drop in cardiac flow following their
administration has been reported13,14 (Table 1).
Ablation with radiofrequency in the neonatal
stage has been used in isolated cases where there
is recurrence of arrhythmia with hemodynamic
deterioration despite treatment which has also
had the side effects of antiarrhythmic drugs.14,15
Ventricular tachyarrhythmias
Figure 5. Rhythm strip from a neonate of 15 days
with diagnosis of transposition of the great vessels,
who underwent “arterial switch”. We can observe the
“sawtooth waves” typical of atrial flutter with heart rate
of 150 bpm and 2:1 conduction with mean ventricular
heart rate of 75 bpm.
138
Ventricular extrasystoles
Are defined as premature ventricular complexes.
The following criteria are used in electrocardio-
Garrido-Garcia LM and Delgado-Onofre MG. Heart rhythm disorders in neonates
graphic diagnosis: 1) early start of QRS complex;
2) duration of QRS complex greater than 80 ms;
3) abnormal morphology of QRS complex
with alteration in the ST segment and in the T
wave; and 4) no preceding P wave.3 Ventricular
extrasystoles are common in neonates with
structurally healthy hearts; their occurrence has
been reported in up to 18% of healthy neonates
who have undergone a 24-hour Holter in the first
day of extrauterine life.3,4 Premature ventricular
contractions have also been observed in patients with hypoxia, hypoglycemia, myocarditis,
ventricular hypertrophy, ventricular tumors, or
ventricular catheters3-6,9 (Figure 6).
Table 1. Antiarrhythmic drugs indicated in neonatology88 (continued on next page)
Drug
Oral Dose
IV Dose
Indications
Side effects
Remarks
Adenosine
0.05 mg/kg. The dose Reentry SVT
Dyspnea, arrhythmias, Administer rapidly
may be increased Diagnosis of atrial AV block, palpitations,
every 2 minutes by flutter
bradycardia
0.05 mg/kg
Amiodarone 10-20 mg/kg/day
(Class 3)
for 7 to 14 days
and then 5 mg/
kg/day
DI: 5 mg/kg in 1 h; Refractory SVT, VT, Proarrhythmia, brady- M o n i t o r p u l m o DM continuous in- and VF
c a r d i a , AV b l o ck , nary and thyroid
fusion 10-15 mg/kg/
hypothyroidism, in- functions
day
terstitial pneumonitis,
pulmonary fibrosis,
photosensitivity
Digoxin
DI: 15-20 μg/kg divi- SVT, atrial flutter
ded in 3 doses.
DM: 4-8 μg/kg/day
divided in 2 doses/
day
Maintenance
5-10 mg/kg/day
divided in 2 doses
F l e c a i n i d e 1-3 mg/kg/day in
(Class 1c)
3 doses.
May be increased
to up to 3-6 mg/
kg/day
Lidocaine
Bradycardia, arrhythmias, delayed conduction, lethargy, vomiting, diarrhea
Contraindication:
VT, hypokalemia,
AV block.
Use with caution in
WPW syndrome:
may cause VF
Refractory tachycar- Bradycardia, AV block,
dias: SVT, VT
a r r hy t h m i a s, h e a r t
failure, blood dyscrasias, liver dysfunction,
dyspnea
Contraindication:
retarded conduction, liver or myocardial dysfunction
1 mg/kg/dose in 1 to VT, VF
2 minutes.
Infusion 20-50 μg/
kg/min
Low blood pressure, Use after a cardiobradycardia, arrhyth- version
mias, lethargy, vomiting, paresthesia, respiratory depression
Procainami- 15-50 mg/kg/day DI. 3-6 mg/kg/dose SVT, WPW, VT
de
Divided in 4-8 in 5 minutes
(Class 1a)
doses/day
DM. Continuous
infusion 20-80 mg/
kg/min
Low blood pressure,
block, arrhythmias, vomiting, diarrhea, blood
dyscrasias, hepatomegaly, increase in liver
enzymes
Contraindication:
blockage in conduction, helical ventricular tachycardia
Propranolol 0.25 mg/kg/dose
(Class 2)
every 6-8 h; increase to a maximum of 5 mg/
kg/day
Low blood pressure,
heart failure, arrhythmias, alterations in
conduction, asystole,
lethargy, hypoglycemia, hyperglycemia,
bronchospasm, vomiting, diarrhea, agranulocytosis
Contraindication:
asthma, bradycardia, heart block,
cardiogenic shock
SVT, WPW, VT
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Acta Pediátrica de México
Table 1. Antiarrhythmic drugs indicated in neonatology8 (continuation)
Drug
Oral Dose
Quinidine
(Class 1a)
IV Dose
Indications
Side effects
Remarks
15-60 mg/kg/day
divided in 4 doses/day
SVT, VT
Low blood pressure, heart
block, ventricular fibrillation, fever, vomiting, diarrhea, blood dyscrasias,
respiratory depression
Contraindication:
WPW heart block
with propranolol
Reduce the dose of
digoxin in case of
combined use
Sotalol
(Class 2/3)
2-4 mg/kg/day in
2 doses
SVT, WPW, VT
Low blood pressure, helical ventricular tachycardia, blockage in conduction, bradycardia, fatigue,
hypoglycemia.
Contraindication:
structural heart disease, bronchospasm,
heart block
Verapamil
(Class 4)
4-8 mg/kg/day in
3 doses
Refractory tachycar- L ow b l o o d p r e s s u r e , Contraindication:
dias: SVT, VT
bradycardia, apnea
Children < 1 year and
WPW
ST: sinus tachycardia; SVT: supraventricular tachycardia; VT: ventricular tachycardia; VF: ventricular fibrillation; WPW: WolffParkinson-White.
Ventricular tachycardia
Figure 6. 12-lead surface electrocardiogram of a neonate with diagnosis of double right ventricle outlet.
Shows acuminate P wave and right ventricular hypertrophy. Bigeminal ventricular extrasystoles (normal
heartbeat and abnormal heartbeat).
In neonates with ventricular extrasystoles, a chest
x-ray and an echocardiogram are indicated to
rule out an underlying heart disease. Patients
with structurally healthy hearts and isolated ventricular extrasystoles do not require treatment. In
cases of underlying heart disease and frequent
ventricular extrasystoles (more than ten per
hour), of polymorphic ventricular extrasystoles
or when there are pairs of them, the initiation of
antiarrhythmic therapy is indicated.3-6,9
140
Is defined as the presence of three or more consecutive ventricular extrasystoles with a heart
rate above 120 bpm. This tachycardia may be
monomorphic, when the abnormal beats have
a single morphology, or polymorphic: different morphologies in the extrasystoles, which
means that there are multiple ectopic foci. It
may be nonsustained (less than 30 seconds of
arrhythmia) or sustained ventricular tachycardia.
Incessant ventricular tachycardia is arrhythmia
in more than 10% of a day.3-6,9,16 This type of arrhythmias are uncommon in the neonatal stage,
and when they appear their causes should be
investigated. Usually, antiarrhythmic therapy
is required. Conditions to consider as possible
causes of ventricular tachycardias include:
myocarditis, ventricular tumors, myocardial
infarction secondary to anomalies in the coronary arteries, electrolyte disorders, metabolic
diseases, drug use, and long QT syndrome3-6,9,16
(Figure 7).
Neonates with sustained ventricular tachycardia suffer hard-to-control heart failure and may
Garrido-Garcia LM and Delgado-Onofre MG. Heart rhythm disorders in neonates
long QT (corrected QT > 450 ms) on the surface
electrocardiogram.6,17,18 (Figure 8).
Figure 7. Male patient of two days’ extrauterine life
with severe neonatal asphyxia and hypoxic cardiomyopathy who developed ventricular tachycardia. 12lead electrocardiogram: ventricular tachycardia with
wide QRS complexes and mean ventricular heart rate
of 300 bpm.
develop cardiogenic shock; they have a poor
prognosis given that, even with antiarrhythmic
therapy, mortality near 50% has been observed.16
Treatment of ventricular tachycardias
In patients with ventricular tachycardia and hemodynamic compromise, it is indicated, initially
to perform electric cardioversion or defibrillation
with a dose of 2 joules per kilogram of body
weight. In patients with nonsustained ventricular
tachycardia, without hemodynamic deterioration, antiarrhythmic therapy with lidocaine or
amiodarone should be initiated. In cases of
incessant and recurrent ventricular tachycardia,
despite medical treatment, an electrophysiological study is indicated to locate the origin of the
ventricular tachycardia and attempt ablation with
radiofrequency6-9,13 (Table 1).
LONG QT SYNDROME
Long QT syndrome (LQT) is a hereditary disease and causes sudden death in the neonatal
stage; it is associated with both bradycardia
and helical ventricular tachycardia (torsade de
pointes)6,17,18 The diagnosis is based on a family history of sudden death and the finding of a
Figure 8. Rhythm strip from a patient with heart rate of
75 bpm. QT interval 460 ms. The QT interval corrected
by heart rate (Bazett formula = measured QT interval
(ms)/ÖR-R (ms) of 470 ms). Normal up to 450 ms.
Recently long QT syndrome has been associated
with three molecular abnormalities in transport
of electrolytes across the cell membrane: LQT 1
and LQT 2, related to potassium channels, and
LQT 3, which is accompanied by alterations in
sodium channels. A higher incidence of cardiovascular symptoms has been found in LQT 1 and
LQT 2; there is higher mortality in LQT 3.17,18
Treatment of long QT syndrome uses propranolol
at high doses to lower the adrenergic discharges
involved in the genesis of arrhythmias. If such
treatment proves unsuccessful, placement of a
permanent pacemaker or an implantable automatic defibrillator is indicated.13,17-19
BRADYARRHYTHMIAS
In neonates a drop in cardiac rhythm may be due
to alterations in impulse generation (function of
the pacemaker) or in conduction of the stimulus.
Sinus bradycardia
Is defined as a heart rate below 90 beats per
minute and has been described as the leading
cause of rhythm disorders in the neonatal stage.
This bradycardia may be primary, due to sinus
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Acta Pediátrica de México
node dysfunction; it is very rare in the neonatal
period and is associated with immaturity of the
central nervous system, and therefore is more
common in preterm neonates.10 The most common causes of pathological sinus bradycardia
are hypoxia and use of medications6,20 (Figure 9).
Volume 35, No. 2, March-April 2014
prolongation of the PR interval with eventual
failure of conduction and a blocked heartbeat.
This block is associated with medications or with
maternal connective tissue disease. In the Mobitz
2 block the alteration is located in the distal part
of the conduction system. It is characterized by
normal PR intervals interrupted by a blocked
heartbeat. This block has a more serious prognosis and in some cases may require placement
of a pacemaker.3,6,20
Congenital complete atrioventricular block
Figure 9. Female patient of 15 days’ extrauterine
life, asymptomatic. With sinus arrhythmia and sinus
bradycardia with ventricular heart rate of 80 bpm
during sleep.
First degree atrioventricular block
Is the presence of a PR interval above the normal
limit for the patient’s age. The normal PR interval
in the neonatal period varies from 0.06 to 0.14 s
(0.17 seconds in the first day of extrauterine life).
A prolonged PR interval may be due to alterations
in atrial conduction, in the atrioventricular node,
or in the His-Purkinje system. It is very commonly
associated with congenital heart diseases or with
inflammatory heart diseases. Medications that
raise vagal tone can also prolong the PR interval.
The majority of patients are asymptomatic and
do not require treatment.3,6
Congenital complete atrioventricular block
occurs in 15 000 to 20 000 live births. It is
characterized by failure of conduction of cardiac
stimulus from the atrium to the ventricles. The
atrial rhythm is higher than the ventricular and
the P waves have no relationship with the QRS
complexes2,6,21 (Figure 10).
Congenital complete atrioventricular block may
occur in a structurally healthy heart or be associated with congenital heart diseases. Patients with
congenital atrioventricular block and structurally
healthy hearts are very commonly associated
Second degree atrioventricular block
Is characterized by intermittent failure of conduction of stimulus to the ventricles. There are two
forms: Mobitz 1, with blockage in the atrioventricular node which produces the characteristic
Wenckebach phenomenon, consisting of gradual
142
Figure 10. Male patient of 40 days’ extrauterine life
with Holt-Oram syndrome. Interatrial communication
with signs of heart failure. 12-lead electrocardiogram
showing complete atrioventricular block, with atrioventricular disassociation. P waves with heart rate
of 150 bpm and QRS complexes with heart rate of
75 bpm.
Garrido-Garcia LM and Delgado-Onofre MG. Heart rhythm disorders in neonates
with exposure to anti-Ro (SS-A) and anti-La
(SS-B) antibodies. Such antibodies are common in women with connective tissue disease,
especially systemic lupus erythematosus and
Sjögren syndrome. These antibodies cause tissue
damage and fibrous degeneration of conductive
tissue.20,22 Congenital heart block in patients
with heart disease is associated with complex
congenital anomalies such as L-transposition
of the great vessels, left isomerism, and also in
patients with trisomy 18.6,20-22
Patients with congenital atrioventricular block
may be asymptomatic or develop left ventricular dysfunction and heart failure in early stages
of life and even in the prenatal stage. In such
cases an unstable ventricular escape rhythm is
observed, with heart rate below 50 bpm, and
a permanent pacemaker is indicated. Eronen
et al. studied 91 patients with congenital atrioventricular block. They observed that despite
early placement of permanent pacemakers in
symptomatic neonates, they developed heart
failure and dilated cardiomyopathy: risk factors
for this torpid evolution were hydrops, fetal and
neonatal bradycardias, low birth weight, male
patients with neonatal problems associated with
“prematurity” or with neonatal lupus.23,24
CONCLUSIONS
Arrhythmias in neonates are not common events.
However, the natural history of arrhythmias in the
neonatal period differs greatly from that of arrhythmias in other pediatric age groups. It is important
for physicians who attend to this group of patients
to know how to recognize rhythm disorders, the
factors for development of arrhythmias, and the
available diagnostic and therapeutic options.
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20. O’Connor M, McDaniel N, Brady WJ. The Pediatric Electrocardiogram Part II: Dysrhythmias. Am J Emerg Med
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