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Neonatal arrhythmias
Accepted Manuscript Title: Neonatal arrhythmias Author: Poonam Singh Anup Thakur Pankaj Garg Neelam Kler PII: DOI: Reference:
S2352-0817(16)30216-1 http://dx.doi.org/doi:10.1016/j.cmrp.2017.04.003 CMRP 264
To appear in: Received date: Accepted date:
23-12-2016 25-4-2017
Please cite this article as: Singh, P., Thakur, A., Garg, P., Kler, N., Neonatal arrhythmias, Current Medicine Research and Practice (2017), http://dx.doi.org/10.1016/j.cmrp.2017.04.003 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Neonatal Arrhythmias
Poonam [email protected], Anup Thakur*[email protected], [email protected], Neelam [email protected]
Pankaj
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Department of Neonatology, Sir Ganga Ram Hospital, New Delhi 110060
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Abstract
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Neonatal arrhythmia can be a life threatening emergency. Diagnosis of arrhythmias in newborns need high index of suspicion as signs and symptoms are non specific mimicking common neonatal problems like sepsis. Arrhythmias in neonates also need echocardiographic evaluation to exclude underlying structural heart disease. The review describes diagnosis and management of common neonatal rhythm disturbances.
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Abbreviations: ECG-Electrocardogram, SVT-Supraventricular tachycardia, AV node-Atrioventricular node, EAT-Ectopic atrial tachycardia, MAT-Multifocal atrial tachycardia, AVRT-Atrioventricular reciprocating tachycardia, WPW-Wolff Parkinson White Syndrome, AVNRT-Atrio ventricular nodal reentry tachycardia, AF Atrial fibrillation, VT- Ventricular tachycardia, VF- Ventricular fibrillation, PJRTPermanent junctional reciprocating tachycardia, LQTS-Long QT Syndrome.
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Introduction Arrhythmias in newborns are relatively common, occurring in up to 1-5% of the cases. (1) Arrhythmias are classified into benign and life threatening. Benign arrhythmias include sinus arrhythmia, nodal or junctional rhythm, wandering atrial rhythm, premature atrial contractions, and premature ventricular contractions. Benign arrhythmia do not pose serious threats and no additional treatment is immediately required. They do not need follow-up because prognosis is good. Life threatening symptomatic arrhythmias includes supraventricular tachycardia (SVT), sinoatrial node dysfunction, disorders of the atrioventricular conduction system, ventricular tachyacardia (VT), long QT syndrome (LQTS), ventricular fibrillation, as well as arrhythmias due to electrolyte disturbances. These types of arrhythmia can develop suddenly and need to be immediately recognized for optimal management of the patient. Diagnosis of arrhythmias is challenging in the neonatal period. Normal heart rate may vary markedly depending on the level of activity. Clinical features often overlap with sepsis. Diagnosing rhythm disturbances in the neonatal period begins with knowledge of normal newborn electrocardiogram (ECG). (2) Normal neonatal ECG parameters and classification of rhythm disorders In a normal infant, sino atrial node (SA node) acts as pacemaker of the heart as it has highest spontaneous depolarization rate. Thus in normal sinus rhythm every beat originates in the sinus node. The wave of depolarization spreads to the atrial fibres represented by “P” waves in ECG. The electrical activity conducts slowly in atrioventricular node (AV node) resulting in AV delay seen as isoelectric PR segment in ECG. This delay enables ventricles to be in a relaxed state when atria are propelling blood into the ventricles. Electrical activity spreads quickly across the ventricles via His Purkinje system allowing near simultaneous contraction of both the ventricles producing QRS complex. Repolarization of ventricles is characterized by T
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waves in ECG. Normal sinus rhythm produces upright P waves in leads I and aVF, followed by narrow QRS complexes. (3) The electrocardiogram (ECG) is the gold standard for identifying problems with heart rate and rhythm. Interpretation of ECG should take into account the normal values of various ECG parameters in neonatal period. Normal ECG and various waves and intervals are delineated in figure 1. Normal values are described in table 1. (4)
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Rhythm disturbances can be broadly classified into tachyarrhythmia or bradyarrhythmia. They can be benign or life threatening. Supraventricular tachycardia (SVT) is the commonest rhythm disorder in neonates. Depending upon the effect of rhythm disturbance on heart rate, arrhythmia is classified as in table 2.
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1. Tachyarrhythmia- These rhythm disorders are commonest and associated with abnormally increased heart rates. ECG and specific features of tachyarrhythmia are enlisted in table 3. The two main mechanisms of tachyarrhythmia include: reentry and increased automaticity. (3)
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Reentry- Three conditions should be fulfilled for reentry to take place and result in tachyarrhythmia. First, an anatomically distinct conducting pathway must be present. Secondly, reentrant pathway must provide unidirectional conduction block to the electrical wave approaching from one side but allows the impulse to cross the blocked area from other side and that further finds the pathway recovered from its refractory period allowing circus movement. Finally, there must be an area of conduction delay in the reentry circuit allowing whole of the circuit to recover from its refractory period before the arrival of the next electrical wave. The circuit for reentrant conduction is shown in figure 2. The peculiar feature of reentrant tachycardia is that they have a tendency to have an abrupt onset and cessation.
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Increased automaticity- It results from higher rate of spontaneous depolarization of the conduction system than the SA node as in ectopic focus.
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1.1 Sinus tachycardia Sinus tachycardia (ST) occurs as a result of systemic disturbances like fever, pain, hypoxia, dehydration, cardiac failure, drugs (e.g. isoproterenolol, xanthine therapy), and hyperthyroidism. Heart rate in ST slows down with the treatment of precipitating cause. ST needs to be differentiated from SVT which needs specific treatment. Clinically SVT is differentiated from ST by termination of SVT with maneuvers which increase vagal tone. ECG characteristics of ST and SVT also differ. In SVT, the heart rate usually exceeds 220 per min and it manifests as a narrow QRS complex (≤0.09 sec) with P waves visible on a standard electrocardiogram in only 50-60% of the cases. The heart rate in SVT tends to be unvarying. ECG criteria for ST include a heart rate less than 220 beats per minute which varies with changes in vagal and sympathetic tone, varying RR interval, constant PR interval, normal P wave axis and, a gradual onset and termination.(2) 1.2 Supraventricular tachycardia
The most common life-threatening arrhythmia of the newborn is SVT. It is defined as narrow complex tachycardia that requires atrial tissue or AV node as an integral part of arrhythmia substrate. In the neonate, SVT of 12 to 24 hours duration usually results in heart failure. ECG characteristics of SVT include (figure 3) (4) •
Rapid regular tachyarrhythmia (heart rate of 220-300 per min)
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Abrupt onset and termination
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Narrow QRS complexes
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Constant RR interval
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Absence of clearly discernible P waves
Clinical manifestation: The diagnosis of SVT in a newborn may be difficult because of the normally more rapid heart rate in infancy. Infants may be stable or hemodynamically unstable presenting with cardiac failure or shock. Usual presentation is poor feeding, tachypnea and irritability, with heart rates of 220 to 300 per min. These babies are often misdiagnosed as sepsis and SVT may be overlooked. Classification of SVT depending upon its mechanism has been illustrated in figure 4 and described below (2)
1.2.2
Atrioventricular reciprocating tachycardia (AVRT): AVRT uses a bypass tract which facilitates reentry. Conduction may be orthodromic or antidromic. Orthodromic conduction means there is antigrade conduction through AV node and retrograde through accessory pathway. Reverse is true for antidromic conduction. Depending upon the direction of transmission across accessory pathway SVT of AVRT type can be further classified into two:
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Concealed accessory connection: This accessory pathway allows only unidirectional retrograde electrical conduction from ventricle to the atria. Such pathways can only mediate orthodromic reentry. As these pathways do not disturb electrical transmission during sinus rhythm so during routine ECG they remain “concealed” or invisible.
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Wolf- Parkinson-White Accessory Connection: This may either be able to conduct bidirectionally (Wolff-Parkinson-White [WPW] syndrome) or retrograde only (concealed accessory pathway). Wolff–Parkinson–White (WPW) syndrome describes the combination of ventricular pre-excitation in sinus rhythm with paroxysmal tachycardia. The most common arrhythmia seen in WPW syndrome is orthodromic AV reentry tachycardia, but antidromic re-entry and atrial fibrillation also can occur. The typical electrocardiographic features of the Wolff-Parkinson-White syndrome are seen when the patient is not having tachycardia (in sinus rhythm). The hallmark of pre-excitation seen in WPW is a short PR interval (<0.1 msec in neonates) and a widened QRS with slow early activation – the delta wave (figure 5). 1.2.3
AV nodal re-entrant tachycardia (AVNRT) involves the use of two pathways within the AV node one fast and other slow. This involves re-entry using functional equivalent of an extra-connection within AV node. Neonatal AVNRT more commonly is associated with other cardio respiratory problems (e.g. congenital diaphragmatic hernia, congenital heart disease, sepsis) and is uncommon in an otherwise healthy infant.
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Management of SVT
Any baby presenting with narrow QRS complex tachycardia should be managed as a case of SVT after ruling out features suggestive of sinus tachycardia. Management begins with hemodynamic assessment which categorizes infants in three groups. First group includes symptom free infants picked up during routine clinical examination or by the parents in whom termination occurs spontaneously. Such infants who have self terminating SVT, no evidence of pre-excitation on ECG and normal cardiac structure do not require long term treatment. In cases presenting with poor activity during episode or when there is an increased risk for prolonged arrhythmia, long-term treatment is necessary. The second group of SVT infants is the seriously ill ones having features of congestive cardiac failures like tachypnea, sweating, poor feeding, hepatomegaly, rales in the chest, gallop rhythm and cardiomegaly on chest X ray with recordable BP and normal sensorium. These
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infants may be stable or unstable depending on the stage of congestive cardiac failure. The third group of infants with SVT is critically ill ones with rapid heart rates resulting in critically low blood pressure, non palpable pulses, altered sensorium or complete loss of consciousness. Treatment of SVT includes termination of tachycardia paroxysm and maintenance therapy. A. Termination of tachycardia paroxysm: Interventions for termination are illustrated in figure 6 for reverting SVT to sinus rhythm in an infant depending upon the hemodynamic status. Various options to abort SVT include following: Vagal stimulation Acetylcholine liberated at vagal endings by stimulating reflex vagal discharge depresses conduction in the atrial musculature and AV node. The increase in the degree of AV block abruptly lowers the ventricular rate by blocking atrial impulses to the ventricle. Vagal maneuvers should be tried with intravenous line in place and should not be continued for more than 5 minutes before trying other modalities in a seriously ill baby. Various maneuvers which can be tried include elicitation of gag with nasogastric tube or diving reflex by placing a bag filled with ice over the face and ears for 15 seconds. This maneuver successfully restores sinus rhythm in 30 to 60 percent of the cases. (5) Carotid massage or orbital pressure application should not be done in neonates.
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Adenosine Adenosine is the drug of choice for SVT where AV node is part of re-entry circuit. Adenosine causes a temporary AV nodal conduction block and interrupts re-entry circuit that involves the AV node. The drug has a wide safety margin because of its short half life of 10 seconds. Adenosine should be given only intravenously as close to the heart as possible followed by rapid saline flush to promote drug delivery to central circulation. The dose of Adenosine required to terminate SVT is 100 micrograms/kg, given by rapid IV infusion (not in umbilical artery). It can be repeated as 200 micrograms per kg and then 400 micrograms per kg if no effect is seen. When given by rapid IV injection, onset of effect is seen in 7 or 8 seconds. AV blockade is brief. The neonate should be under continuous ECG monitoring during therapy. This may show termination of SVT or may unmask other arrhythmias. Adenosine successfully aborts 80-95% of the cases of AVRT related SVT. (6) Early recurrence after termination of SVT may occur in up to 25-30% of cases. (7) Adenosine may fail to abort an attack of SVT if dose is inadequate or drug was administered too slowly. Adenosine is also ineffective if mechanism of tachyarrhythmia is VT or atrial tachycardia where adenosine blocks the AV node and reveals atrial flutter or atrial tachycardia as the cause of the problem. Other drugs: Other medications such as amiodarone, esmolol, and procainamide have been used to treat intractable SVT that either cannot be terminated with adenosine or cardioversion, or rapidly recurs. There are no controlled trials to guide the appropriate therapy but a retrospective review has found no difference in efficacy or safety between amiodarone or procainamide. (8) These medications are more often required in SVT associated with congenital heart diseases which tend to be more refractory.
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Cardioversion- Synchronized cardioversion is the treatment to abort SVT in a neonate who is critically or seriously ill and unstable.
B. Maintenance therapy Approximately 60% to 80% of the cases of SVT presenting in the neonatal period undergo spontaneous resolution during infancy leaving only few cases requiring long term treatment. (9) Choice of long term antiarrhythmic drugs is based on the severity of the presentation and the mechanism of the tachycardia, in particular the presence or absence of delta wave (pre excitation). Approach for maintenance therapy depends on level of sickness at the time of presentation. For
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Accelerated idioventricular rhythm (AIVR)
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mildly symptomatic babies with adenosine sensitive tachycardia that reverted easily maintenance therapy can be omitted as recurrence rates even with medication may vary between 40-80%. (5) For an infant presenting frequent attacks with circulatory collapse, or in whom cardioversion was difficult, beta blockers (propanolol 0.5 mg/kg PO every 6 hr) are used as these features predict refractory tachycardia in SVT. (10) Digoxin is used only if there is no evidence of pre-excitation in sinus rhythm in the dose of 5 micrograms/kg orally every 12 hr after initial load. Possibility of recurrence of SVT is similar with either digoxin or propranolol.(11) About 40% of newborns who have a treated episode of SVT do not have another episode when treated with antiarrhythmics for a minimum of 1 year after the first episode. If SVT persists beyond 1 year, spontaneous resolution is unlikely. Transcatheter ablation of the accessory pathway is of limited use in neonates due to the concerns like perforation, AV block and damage to the coronary arteries. Ablation is reserved for life-threatening, medically refractory cases. 1.3 Ventricular tachycardia Ventricular tachycardia presents as wide QRS complexes (QRS duration >0.09 sec) in ECG. It includes accelerated idioventricular rhythm, premature ventricular contractions and ventricular tachycardia. Supraventricular arrhythmias may also present as wide complexes in ECG e.g. SVT with bundle branch block and antigrade conduction through accessory pathway in WPW syndrome. Features of common ventricular tachycardia are described below.
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Accelerated idioventricular rhythm arises from accelerated discharge from an ectopic focus lying within bundle of His, Purkinje system or ventricular myocardium. ECG shows regular and wide QRS morphology with rates 20% or less of the sinus rate. If sinus and ectopic focus discharge at equal rates (isorhythmic) then fusion beats are visible in ECG. AVIR gradually appears as sinus rate slows down or ectopic rate accelerates above sinus rate. It is a benign arrhythmia, does not cause hemodynamic instability and requires no intervention. (12) Premature ventricular contractions- Refer table no 3.
1.3.3
Ventricular tachycardia (VT): It is also a wide QRS complex tachycardia with important causes being automatic focus in the ventricle, myocardial tumors like rhabdomyomas in association with tuberous sclerosis or fibromas, myocarditis and structural heart diseases. Presence of VT in a neonate prompts detailed echocardiography to assess structure and myocardial function to dictate duration of treatment and determine prognosis.
1.3.4
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1.3.2
Management of wide complex tachycardia Differentiation of wide complex tachycardia of ventricular or supraventricular origin is nearly impossible in neonates by ECG. Therefore, infants with wide QRS tachycardia are treated as if they have ventricular tachycardia. Method to restore sinus rhythm depends on hemodynamic status of the baby. Wide complex tachycardia in a non seriously ill infant is treated with intravenous procainamide or amiodarone. If wide complex tachycardia is discerned in an infant with collapse synchronized cardioversion is the intervention of choice.(13) 1.4 Algorithm for identifying tachycardia A sequential analysis of the ECG helps to classify the tachyarrhythmia. An easy approach is to look for QRS complex rate, regularity, and width followed by the relation of the P wave to the QRS and P wave morphology. Figure 7 provides an algorithm to diagnose tachyarrhythmia. (14) 2.
Bradyarrhythmia Transient bradycardia can occur in 20% to 90% of healthy newborns due to sinus bradycardia, sinus pauses, and junctional escape beats. Transient bradycardia may follow stressful labor or delivery but usually resolve within 48 to 72 hours. Rhythm disorder presenting with slowing of heart rate include following:
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Sinus bradycardia Newborn cardiac innervation has vagal dominance predisposing to episodic sinus bradycardia. Sinus bradycardia is characterized by regular slow atrial rate with normal P waves and 1:1 conduction. Pathologic causes of sinus bradycardia include hypoxia, acidosis, increased intracranial pressure, abdominal distention, hypoglycemia, apnea of prematurity and drugs such as digoxin and propranolol. 2.2 Heart blocks Heart block is basically of following 3 types. 1st-degree AV block: First degree heart block is characterized by prolonged PR interval but all the atrial impulses are conducted to the ventricle. 2nd-degree AV block: It is further classified into 2 types: • Mobitz type I (Wenckebach type): In this variant, the PR interval increases progressively until a P wave is not conducted. In the cycle following the dropped beat, the PR interval normalizes. Mobitz type is usually due to a functional suppression of AV conduction and it can usually be reversed with catecholamines or with vagolytic agents. It has better prognosis as compared to type II block. • Mobitz type II: In Mobitz type II second degree heart block, all atrial impulses are not conducted to the ventricles. Here a ventricular beat may follow every second or every third atrial beat referred as 2:1 block and 3:1 block respectively. This conduction defect is less common but has more potential to cause syncope and may be progressive. 2:1 conduction block seen in infants with markedly prolonged QT interval is an important risk factor for the development of torsades de pointes and sudden death. 3rd-degree AV block (complete heart block, CHB): In this type of heart block, none of the impulses from the atria reach the ventricles. Sinus impulses may be blocked either at the level of AV node (nodal block) or in the conducting system below the AV node (infranodal block). The escape rhythm for ventricular depolarization may be generated either in the healthy part of AV node or in the peripheral conducting system resulting in idioventricular rhythm much slower than atrial rate. ECG shows regular R-R intervals and regular P-P intervals (figure 8). The atrial rate is usually greater than the ventricular rate. CHB can be congenital or acquired. Congenital CHB is the most common congenital conduction defect. It is associated with structural heart disease in about half of the cases e.g. d-TGA. Congenital CHB can also occur as an isolated anomaly where it is strongly linked to transplacental passage of anti-Ro and anti-LA antibodies in the fetus. Acquired CHB may follow cardiac surgery, myocarditis or endocarditis.
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2.3 Complete heart block and lupus
When CHB occurs as an isolated anomaly, mother should be screened for anti Ro/SSA and anti LA/SSB antibodies. Risk of CHB in the infant of an anti Ro/SSA and anti LA/SSB antibody positive primipara or multipara mother with previously unaffected children is 2%. Recurrence risk in a previously affected pregnancy is 20%. The pathogenesis of CHB includes interference in clearance of apoptotic cardiocytes by healthy cardiocytes during development by anti Ro and La antibodies. This leads to phagocytosis of apoptotic cardiocytes by macrophages which secrete inflammatory and fibrosing cytokines resulting in conduction system and myocardial damage. Heart block most often develops between 18 to 24 weeks. Higher degrees of heart block may not be preceded by prolongation of PR interval and it can develop within a week of normal echocardiogram. Warning signs on echo suggestive of early signs of injury include echodensities and moderate to severe tricuspid regurgitation. Heart block of lesser degree may progress postnatally but conduction abnormality does not develop after a normal ECG at birth. Fetal treatment is based on suppression of inflammatory response by maternal administration of fluorinated steroids like dexamethasone or betamethasone and intravenous immunoglobulin. A non-randomized study showed variable effect of steroids on progression of lesser degrees of heart block to advanced one (15). Benefit with IVIG is also limited. Newborns with AV block are managed with cardiac pacing which is indicated if the heart rate is less than 55 beats per minute. CHB related to anti Ro/ anti La antibodies carries high mortality (20-30%) and morbidity with 67% requiring permanent pacemaker before adulthood (16, 17).
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3. Long QT syndromes
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Congenital long QT syndromes (LQTS) are genetic disorders of sodium and potassium channels resulting in prolongation of ventricular repolarization and QT interval. A typical ECG of LQTS is shown in figure 9. The rhythm disorder associated with this condition is polymorphic VT also called as torsades de pointes. The estimated incidence is about 1 per 10,000 births but variable penetrance makes precise assessment difficult. More than 400 different mutations have been identified in 10 LQTS susceptibility genes. Common drugs used in neonatal period which can prolong QT interval are mentioned in table 4. This arrhythmia may be asymptomatic if brief and self-limited, but if sustained beyond several seconds, usually results in ventricular fibrillation. LQTS may be detected during ECG done for other reasons. Manifestations include syncope provoked by exercise, fright, or a sudden startle, seizures, aborted cardiac arrest, or sudden death. Diagnosis of LQTS depends on accurate measurement of QTC interval (table 1). QTC interval of >0.47 sec is highly indicative, whereas a QTC interval of >0.44 sec is suggestive. Infants are screened for LQTS with an ECG due to a family history. Such screening should be delayed until the infant is 6 to 8 weeks of age because modest QT interval prolongation is relatively common (2.5%) among healthy infants and may cause undue family concern. Treatment of LQTS includes the use of β-blocking agents at doses that blunt the heart rate response to exercise. If drug therapy causes profound bradycardia then pacemaker needs to be implanted. Infants who are unresponsive to β-blockers and experienced cardiac arrest, an implantable cardiac defibrillator is indicated. β-blocking agents are not effective in patients with LQT3, hence implantable cardiac defibrillator is indicated.
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4. Salient details of drugs recommended for neonatal arrhythmias
These are listed along with their dosage and special comments in Table 5.
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5. Cardioversion
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Defibrillation is non synchronized random administration of shock during a cardiac cycle. Cardioversion is a synchronized administration of shock during the R waves of QRS complex of a cardiac cycle. During defibrillation and cardioversion, electrical current travels from the negative to the positive electrode by traversing myocardium. It depolarizes all of the heart cells simultaneously. This interrupts and terminates abnormal electrical rhythm. This, in turn, allows the sinus node to resume normal pacemaker activity. Non re-entrant rhythm disorders not responding to cardioversion include sinus tachycardia, automatic atrial tachycardia and junctional ectopic tachycardia Paddle size: Small paddles those used for direct delivery to epicardial surface of heart in older patients intraoperatively are appropriate for neonates. According to Pediatric advanced life support 2010 guidelines, “infant” size paddle or pad size is used for infants less than 10 kg (13). Interface: The electrode-chest wall interface is part of self adhesive pad, in contrast, electrode gel must be applied liberally on manually applied paddles. Saline soaked pads, ultrasound gel and bare paddles should not be used (13). Paddle position: Place manual paddles over the right side of upper chest, and the apex of the heart (13) or between the tip of the left scapula and the spine (3) so the heart is between the two paddles. Energy dose: Initial dose is 0.5-1.0 J/kg. This is followed by 1-2 J/kg if first shock is unsuccessful (4). Indications: Synchronized cardioversion is done for SVT and VT whereas for VF, cardioversion is used in asynchronous mode.
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CONCLUSIONS: Rhythm disorders can have variable presentation in neonatal period. All pediatricians and neonatologists should be able to interpret ECG in neonates and identify arrhythmias. Appropriate and timely management of such neonates is life saving with good long term outcomes in most of the cases. Conflicts of interest
References
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1. Dubin A. Arrythmias in the newborn. Neoreviews 2000; 1:e146–e151.
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The authors have nothing to declare.
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2. Cannon B, Kovalenko O, Snyder CS. Disorders of cardiac rhythm and conduction in newborns. In Richard J. Martin, Avroy A. Fanaroff, Michele C. Walsh, eds. Fanaroff and Martin's NeonatalPerinatal Medicine: Diseases of the Fetus and Infant. 10th ed. Elsevier Health Sciences, 2010, 12591274. 3. Barrett KE, Ganong WF. Ganong’s review of medical physiology. 23rd ed. New York: McGraw-Hill; 2010. 4. Killen AS, Fish FA. Fetal and neonatal arrhythmias. NeoReviews 2008; 9:242-252. 5. Kugler JD, Danford DA. Management of infants, children, and adolescents with paroxysmal supraventricular tachycardia. J Pediatr 1996; 129:324. 6. Ko JK, Deal BJ, Strasburger JF, Benson DW Jr. Supraventricular tachycardia mechanisms and their age distribution in pediatric patients. Am J Cardiol 1992; 69:1028. 7. Sherwood MC, Lau KC, Sholler GF. Adenosine in the management of supraventricular tachycardia in children. J Paediatr Child Health 1998; 34:53. 8. Chang PM, Silka MJ, Moromisato DY, Bar-Cohen Y. Amiodarone versus procainamide for the acute treatment of recurrent supraventricular tachycardia in pediatric patients. Circ Arrhythm Electrophysiol 2010;3:134–40. 9. Wu MH, Chang YC, Lin JL, et al. Probability of supraventricular tachycardia recurrence in pediatric patients. Cardiology. 1994;85:248-289. 10. Sanatani S, Hamilton RM, Gross GJ. Predictors of refractory tachycardia in infants with supraventricular tachycardia. Pediatr Cardiol 2002; 23:508. 11. Sanatani S, Potts JE, Reed JH, et al. The study of antiarrhythmic medications in infancy (SAMIS): a multicenter, randomized controlled trial comparing the efficacy and safety of digoxin versus propranolol for prophylaxis of supraventricular tachycardia in infants. Circ Arrhythm Electrophysiol 2012; 5:984. 12. Riera AR, Barros RB, de Sousa FD, Baranchuk A. Accelerated idioventricular rhythm: history and chronology of the main discoveries. Indian Pacing Electrophysiol J. 2010;10:40-8. 13. Kleinman ME, Chameides L, Schexnayder SM, et al. Part 14: pediatric advanced life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 Suppl 3):S876-908. 14. D S Kothari, J R Skinner. Neonatal tachycardias: an update. Arch Dis Child Fetal Neonatal Ed 2006;91:F136–F144. 15. Friedman DM, Kim, MY, Copel JA, Llanos C, Davis C, Buyon JP. Prospective Evaluation of Fetuses with Autoimmune Associated Congenital Heart Block Followed in the PR Interval and Dexamethasone Evaluation (PRIDE) Study. The American Journal of Cardiology, 2009; 103,1102– 1106.
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16. Buyon JP, Clancy RM, Friedman DM. Cardiac manifestations of neonatal lupus erythematosus: guidelines to management, integrating clues from the bench and bedside. Nat Clin Pract Rheumatol. 2009;5:139-48. 17. Kertesz NJ, Fenrich AL, Friedman RA. Congenital complete atrioventricular block. Tex Heart Inst J 1997; 24:301-7.
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Table 1: Normal values of ECG parameters in newborns Normal range
Events in the heart during intervals and comments
Heart rate
Average-120-160/min Range-90-230/min
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Sinus arrhythmia is variation in the heart rate during different phases of respiratory cycle due to reflex changes in vagal tone Heart rate increases during inspiration as vagal tone decreases
PR interval
70 -140 msec
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It extends from onset of the P wave to the Q or R wave in lead II Atrial depolarization and conduction through AV node
QRS axis
Term-55 to 200° Preterm-65 to 174° 20 to 80 msec
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Mean on postnatal day-4 -400±20 msec
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Ventricular depolarization and atrial repolarization Range described is measured in lead V5
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Ventricular depolarization plus ventricular repolarization Begins from onset of the QRS complex to the end of the T wave, is measured best in leads II, V5, and V6 As QT interval varies with heart rate so corrected, QTc interval is calculated by Bazett’s formula: QTc=QT(sec)/ (preceding RR interval in seconds) QTc is physiologically prolonged by 2 months with mean QTc= 410 msec) QTc reaches mean value of of 400 msec by 6 months of age
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QRS duration
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Parameter
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ST interval
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Ventricular repolarization (during T wave)
In the first postnatal week, T waves are variable but usually upright in lead V1 After the first postnatal week, the T wave is negative (downgoing) in lead V1 and positive in V5 and V6
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Table2. Classification of common arrhythmias in neonates Bradyarrhythmia
Sinus tachycardia
Sinus bradycardia
Atrial tachycardia
Heart Blocks
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Tachyarrhythmia
Atrial flutter
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First degree
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Atrial fibrillation
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Second degree
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Multifocal atrial tachycardia
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Wolff-Parkinson-White syndrome
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Permanent
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Ventricular tachycardia
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Table 3. Types and characteristics of various tachyarrhythmia ECG CHARACTERISTICS
COMMENTS
Premature atrial contractions (PAC)
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Ectopic atrial tachycardia
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Atrial flutter
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Mechanism: Automatic focus Common in healthy neonates If every sinus beat alternates with PAC then it is referred as atrial bigeminy If each PAC in atrial bigeminy is blocked then it can produce extreme bradycardia Prognosis is excellent Management- Observe for spontaneous resolution which usually occurs by 4 weeks
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P wave morphology is different from sinus P wave PAC conducted through conducting system of the heart produces narrow QRS If PAC finds AV node refractory then it remains non conducted called as “blocked” PAC If PAC crosses AV node but finds either right or left bundle branch refractory then conduction occurs via ventricular myocardium (aberrant conduction) producing wide QRS Aberrantly conducted PAC is differentiated from premature ventricular contraction by a preceding P wave Rate: Variable Usually upto 200 beats/min Gradually increases and decreases P waves: Precedes QRS Axis-abnormal
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TACHYARRHYTHMIA
Rate Upto 500 beats/min Ventricular rate is slower due to some degree of AV block Saw tooth flutter waves If P waves are masked by QRS complexes then diagnosis can
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Mechanism: Single automatic focus May be incessant Can lead to tachycardia induced cardiomyopathy May be difficult to control by pharmacotherapy or cardioversion Digoxin can be used as first line treatment, propranolol can be added if required If medical treatment fails then catheter ablation is an option with more than 90% success rate Mechanism: Reentry Treatment-Ttransesophageal overdrive pacing or synchronized DC cardioversion (0.5–2 J/kg) Recurrence is rare in the absence of congenital heart
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−
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Mechanism- Multiple irritable automatic foci in the atrium Medications which can be used to control the heart rate are digoxin, propranolol, flecainide, sotalol, and amiodarone Polytherapy may be required as this arrhythmia is more difficult to suppress Spontaneous resolution occurs in weeks or months following which medication can be withdrawn Commonest form of SVT in SVT Responds to Adenosine
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P wave follows QRS • overlapping upstroke of T wave •
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Atrioventricular re-entry tachycardia (Orthodromic)
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Multifocal atrial tachycardia
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disease so long term medication is not required Recurrent atrial flutter in the setting of atrial dilatation or structural heart disease is treated with digoxin
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complexes then diagnosis can be made by injecting adenosine which increases the AV block to unmask the flutter waves In contrast to atrial tachycardia flutter waves lack isoelectric period between P waves (figure 10) Defined as ≥3 different P wave morphologies Irregularly irregular heart rate resulting from frequently blocked P waves Variable PR interval No two RR intervals are same
Atrioventricular re-entry tachycardia Antidromic)
Atrioventricular nodal re-entry tachycardia
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Permanent junctional reciprocating tachycardia
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Superior P wave axis (inverted in lead II and aVF)
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Pre excitation (delta wave) and short PR interval is seen post termination in WPW Adenosine sensitive
P wave usually not visible superimposed on QRS Produces a small positive deflection at the end of the QRS in lead V1, which looks a bit like an r’ wave
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Adenosine sensitive
Inverted P waves in II, III, aVF appear to precede QRS complex P waves are characteristically deeply inverted in leads II, III, and aVF
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Incessant, slower rate than others-about 200 beats/min Typically restarts after electrical cardioversion or adenosine Maintenance antiarrhythmics such as flecainide is always
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•
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AV dissociation Narrow QRS complexes Ventricular rate faster than atrial rates
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QRS morphology of VPC is • different and wider than normal QRS •
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Mechanism-Increased automaticity in bundle of His or proximal bundle branches Causes − Congenital: Incessant, causes tachycardia induced cardiomyopathy and carries mortality of more than 50%. Amiodarone is used for the treatment − Post operative: Results from oedema, dyselectrolytemia, catecholamine surge, medications (dopamine, epinephrine) and it resolves as these factors are taken care of Mechanism: Spontaneous depolarization of ventricular myocardium Benign prognosis
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Ventricular premature contractions
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required Early catheter ablation may be required Can lead to tachycardia induced cardiomyopathy
Ventricular tachycardia (VT)
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Ventricular fibrillation
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Wide QRS complexes P wave may be dissociated from QRS complex “Capture” or “fusion” beats diagnostic
Chaotic irregular rhythm
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Rare in neonates
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VT is defined as an arrhythmia with three or more consecutive beats originating in the ventricles usually at a rate of 120/min or more Broad complex QRS always treated as VT unless proved otherwise Not terminated by Adenosine
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Rare in neonates
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Consider long QT syndrome or Brugada syndrome
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Table 4. Drugs that can prolong QT interval Erythromycin, Azithromycin, Trimethoprim/Sulfamethoxazole
Antifungals
Fluconazole, Itraconazole
Antihistamines
Astemizole, Terfenadine
Antipsychotics
Haloperidol, Risperidone, Chlorpromazine
Antiarrhythmics
Quinidine, Procainamide, Disopyramide, Amiodarone, Sotalol
Diuretics (Through K+ Loss)
Furosemide, Ethacrynic Acid, Bumetanide
Promotility agents
Cisapride
Dyselectrolytemia
Hypokalemia, Hypocalcemia, Hypomagnesemia
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Antibiotics
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Table 5: Antiarrhythmic drugs used in arrhythmias in neonates Dosage
Special comments
Esmolol
50-500 micrograms/kg/min
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1 10-15 mg/kg IV over 30-45 min
Digoxin
1 10 micrograms/kg IV as initial load; second dose in 6 hr and third at 24 hr
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Start IV dose of 100 micrograms/kg; double dose repeatedly until effect is seen, to maximum of 400 micrograms/kg
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Adenosine
Amiodarone
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Can cause hypotension Continuous blood pressure monitoring is essential
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Procainamide
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Monitor pulse, blood pressure Contraindicated in congestive heart failure • Do not give with verapamil
5 mg/kg IV over 15-30 min or as 5 separate 1 mg/kg aliquots
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Do not use in hypokalemia or if toxic reaction to digoxin is suspected
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Contraindicated in preexisting second- and third-degree AV block without pacemaker Use with caution in severe asthma; half-life is 10 sec in serum Occasionally induces atrial fibrillation
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Propranolol
0.25-1 mg/kg PO every 6 hr
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Atenolol
0.5-2 mg/kg/day PO divided every 12 hr
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Sotalol
2-8 mg/kg/day PO divided every 8 hr
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Given by central line diluted in D5W Can cause gasping syndrome in infants due to benzyl alcohol Observe for wheezing and symptoms of hypoglycemia
Torsades de pointes is likely with hypokalemia
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Figures:
Figure1. Waves and intervals of ECG in lead II.
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Figure2. Diagram showing re-entry phenomena. In re-entry, electrical signals generated from an appropriately timed premature beat find pathway B refractory, resulting in conduction block in this limb of the circuit. Meanwhile, conduction down pathway A proceeds unimpeded and subsequently the signal is conducted back via pathway B which has recovered leading to circus like movement.
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Figure 3. ECG of Supraventricular tachycardia
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Figure 4. Figure showing mechanism of Supraventricular tachycardia
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Figure 5. ECG showing pre-excitation as short PR interval and a widened QRS with slurred upstroke-Delta wave
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Figure 6.Treatment options for reverting SVT to sinus rhythm.
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Figure 7. Approach to tachyarrhythmia.
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Figure 8. Complete heart block
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Figure 9. Long QT syndrome
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Figure 10. Atrial flutter
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S2352-0817(16)30216-1 http://dx.doi.org/doi:10.1016/j.cmrp.2017.04.003 CMRP 264
To appear in: Received date: Accepted date:
23-12-2016 25-4-2017
Please cite this article as: Singh, P., Thakur, A., Garg, P., Kler, N., Neonatal arrhythmias, Current Medicine Research and Practice (2017), http://dx.doi.org/10.1016/j.cmrp.2017.04.003 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Neonatal Arrhythmias
Poonam [email protected], Anup Thakur*[email protected], [email protected], Neelam [email protected]
Pankaj
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Department of Neonatology, Sir Ganga Ram Hospital, New Delhi 110060
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Abstract
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Neonatal arrhythmia can be a life threatening emergency. Diagnosis of arrhythmias in newborns need high index of suspicion as signs and symptoms are non specific mimicking common neonatal problems like sepsis. Arrhythmias in neonates also need echocardiographic evaluation to exclude underlying structural heart disease. The review describes diagnosis and management of common neonatal rhythm disturbances.
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Abbreviations: ECG-Electrocardogram, SVT-Supraventricular tachycardia, AV node-Atrioventricular node, EAT-Ectopic atrial tachycardia, MAT-Multifocal atrial tachycardia, AVRT-Atrioventricular reciprocating tachycardia, WPW-Wolff Parkinson White Syndrome, AVNRT-Atrio ventricular nodal reentry tachycardia, AF Atrial fibrillation, VT- Ventricular tachycardia, VF- Ventricular fibrillation, PJRTPermanent junctional reciprocating tachycardia, LQTS-Long QT Syndrome.
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Introduction Arrhythmias in newborns are relatively common, occurring in up to 1-5% of the cases. (1) Arrhythmias are classified into benign and life threatening. Benign arrhythmias include sinus arrhythmia, nodal or junctional rhythm, wandering atrial rhythm, premature atrial contractions, and premature ventricular contractions. Benign arrhythmia do not pose serious threats and no additional treatment is immediately required. They do not need follow-up because prognosis is good. Life threatening symptomatic arrhythmias includes supraventricular tachycardia (SVT), sinoatrial node dysfunction, disorders of the atrioventricular conduction system, ventricular tachyacardia (VT), long QT syndrome (LQTS), ventricular fibrillation, as well as arrhythmias due to electrolyte disturbances. These types of arrhythmia can develop suddenly and need to be immediately recognized for optimal management of the patient. Diagnosis of arrhythmias is challenging in the neonatal period. Normal heart rate may vary markedly depending on the level of activity. Clinical features often overlap with sepsis. Diagnosing rhythm disturbances in the neonatal period begins with knowledge of normal newborn electrocardiogram (ECG). (2) Normal neonatal ECG parameters and classification of rhythm disorders In a normal infant, sino atrial node (SA node) acts as pacemaker of the heart as it has highest spontaneous depolarization rate. Thus in normal sinus rhythm every beat originates in the sinus node. The wave of depolarization spreads to the atrial fibres represented by “P” waves in ECG. The electrical activity conducts slowly in atrioventricular node (AV node) resulting in AV delay seen as isoelectric PR segment in ECG. This delay enables ventricles to be in a relaxed state when atria are propelling blood into the ventricles. Electrical activity spreads quickly across the ventricles via His Purkinje system allowing near simultaneous contraction of both the ventricles producing QRS complex. Repolarization of ventricles is characterized by T
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waves in ECG. Normal sinus rhythm produces upright P waves in leads I and aVF, followed by narrow QRS complexes. (3) The electrocardiogram (ECG) is the gold standard for identifying problems with heart rate and rhythm. Interpretation of ECG should take into account the normal values of various ECG parameters in neonatal period. Normal ECG and various waves and intervals are delineated in figure 1. Normal values are described in table 1. (4)
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Rhythm disturbances can be broadly classified into tachyarrhythmia or bradyarrhythmia. They can be benign or life threatening. Supraventricular tachycardia (SVT) is the commonest rhythm disorder in neonates. Depending upon the effect of rhythm disturbance on heart rate, arrhythmia is classified as in table 2.
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1. Tachyarrhythmia- These rhythm disorders are commonest and associated with abnormally increased heart rates. ECG and specific features of tachyarrhythmia are enlisted in table 3. The two main mechanisms of tachyarrhythmia include: reentry and increased automaticity. (3)
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Reentry- Three conditions should be fulfilled for reentry to take place and result in tachyarrhythmia. First, an anatomically distinct conducting pathway must be present. Secondly, reentrant pathway must provide unidirectional conduction block to the electrical wave approaching from one side but allows the impulse to cross the blocked area from other side and that further finds the pathway recovered from its refractory period allowing circus movement. Finally, there must be an area of conduction delay in the reentry circuit allowing whole of the circuit to recover from its refractory period before the arrival of the next electrical wave. The circuit for reentrant conduction is shown in figure 2. The peculiar feature of reentrant tachycardia is that they have a tendency to have an abrupt onset and cessation.
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Increased automaticity- It results from higher rate of spontaneous depolarization of the conduction system than the SA node as in ectopic focus.
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1.1 Sinus tachycardia Sinus tachycardia (ST) occurs as a result of systemic disturbances like fever, pain, hypoxia, dehydration, cardiac failure, drugs (e.g. isoproterenolol, xanthine therapy), and hyperthyroidism. Heart rate in ST slows down with the treatment of precipitating cause. ST needs to be differentiated from SVT which needs specific treatment. Clinically SVT is differentiated from ST by termination of SVT with maneuvers which increase vagal tone. ECG characteristics of ST and SVT also differ. In SVT, the heart rate usually exceeds 220 per min and it manifests as a narrow QRS complex (≤0.09 sec) with P waves visible on a standard electrocardiogram in only 50-60% of the cases. The heart rate in SVT tends to be unvarying. ECG criteria for ST include a heart rate less than 220 beats per minute which varies with changes in vagal and sympathetic tone, varying RR interval, constant PR interval, normal P wave axis and, a gradual onset and termination.(2) 1.2 Supraventricular tachycardia
The most common life-threatening arrhythmia of the newborn is SVT. It is defined as narrow complex tachycardia that requires atrial tissue or AV node as an integral part of arrhythmia substrate. In the neonate, SVT of 12 to 24 hours duration usually results in heart failure. ECG characteristics of SVT include (figure 3) (4) •
Rapid regular tachyarrhythmia (heart rate of 220-300 per min)
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Abrupt onset and termination
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Narrow QRS complexes
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Constant RR interval
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Absence of clearly discernible P waves
Clinical manifestation: The diagnosis of SVT in a newborn may be difficult because of the normally more rapid heart rate in infancy. Infants may be stable or hemodynamically unstable presenting with cardiac failure or shock. Usual presentation is poor feeding, tachypnea and irritability, with heart rates of 220 to 300 per min. These babies are often misdiagnosed as sepsis and SVT may be overlooked. Classification of SVT depending upon its mechanism has been illustrated in figure 4 and described below (2)
1.2.2
Atrioventricular reciprocating tachycardia (AVRT): AVRT uses a bypass tract which facilitates reentry. Conduction may be orthodromic or antidromic. Orthodromic conduction means there is antigrade conduction through AV node and retrograde through accessory pathway. Reverse is true for antidromic conduction. Depending upon the direction of transmission across accessory pathway SVT of AVRT type can be further classified into two:
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Concealed accessory connection: This accessory pathway allows only unidirectional retrograde electrical conduction from ventricle to the atria. Such pathways can only mediate orthodromic reentry. As these pathways do not disturb electrical transmission during sinus rhythm so during routine ECG they remain “concealed” or invisible.
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Wolf- Parkinson-White Accessory Connection: This may either be able to conduct bidirectionally (Wolff-Parkinson-White [WPW] syndrome) or retrograde only (concealed accessory pathway). Wolff–Parkinson–White (WPW) syndrome describes the combination of ventricular pre-excitation in sinus rhythm with paroxysmal tachycardia. The most common arrhythmia seen in WPW syndrome is orthodromic AV reentry tachycardia, but antidromic re-entry and atrial fibrillation also can occur. The typical electrocardiographic features of the Wolff-Parkinson-White syndrome are seen when the patient is not having tachycardia (in sinus rhythm). The hallmark of pre-excitation seen in WPW is a short PR interval (<0.1 msec in neonates) and a widened QRS with slow early activation – the delta wave (figure 5). 1.2.3
AV nodal re-entrant tachycardia (AVNRT) involves the use of two pathways within the AV node one fast and other slow. This involves re-entry using functional equivalent of an extra-connection within AV node. Neonatal AVNRT more commonly is associated with other cardio respiratory problems (e.g. congenital diaphragmatic hernia, congenital heart disease, sepsis) and is uncommon in an otherwise healthy infant.
1.2.4
Management of SVT
Any baby presenting with narrow QRS complex tachycardia should be managed as a case of SVT after ruling out features suggestive of sinus tachycardia. Management begins with hemodynamic assessment which categorizes infants in three groups. First group includes symptom free infants picked up during routine clinical examination or by the parents in whom termination occurs spontaneously. Such infants who have self terminating SVT, no evidence of pre-excitation on ECG and normal cardiac structure do not require long term treatment. In cases presenting with poor activity during episode or when there is an increased risk for prolonged arrhythmia, long-term treatment is necessary. The second group of SVT infants is the seriously ill ones having features of congestive cardiac failures like tachypnea, sweating, poor feeding, hepatomegaly, rales in the chest, gallop rhythm and cardiomegaly on chest X ray with recordable BP and normal sensorium. These
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infants may be stable or unstable depending on the stage of congestive cardiac failure. The third group of infants with SVT is critically ill ones with rapid heart rates resulting in critically low blood pressure, non palpable pulses, altered sensorium or complete loss of consciousness. Treatment of SVT includes termination of tachycardia paroxysm and maintenance therapy. A. Termination of tachycardia paroxysm: Interventions for termination are illustrated in figure 6 for reverting SVT to sinus rhythm in an infant depending upon the hemodynamic status. Various options to abort SVT include following: Vagal stimulation Acetylcholine liberated at vagal endings by stimulating reflex vagal discharge depresses conduction in the atrial musculature and AV node. The increase in the degree of AV block abruptly lowers the ventricular rate by blocking atrial impulses to the ventricle. Vagal maneuvers should be tried with intravenous line in place and should not be continued for more than 5 minutes before trying other modalities in a seriously ill baby. Various maneuvers which can be tried include elicitation of gag with nasogastric tube or diving reflex by placing a bag filled with ice over the face and ears for 15 seconds. This maneuver successfully restores sinus rhythm in 30 to 60 percent of the cases. (5) Carotid massage or orbital pressure application should not be done in neonates.
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Adenosine Adenosine is the drug of choice for SVT where AV node is part of re-entry circuit. Adenosine causes a temporary AV nodal conduction block and interrupts re-entry circuit that involves the AV node. The drug has a wide safety margin because of its short half life of 10 seconds. Adenosine should be given only intravenously as close to the heart as possible followed by rapid saline flush to promote drug delivery to central circulation. The dose of Adenosine required to terminate SVT is 100 micrograms/kg, given by rapid IV infusion (not in umbilical artery). It can be repeated as 200 micrograms per kg and then 400 micrograms per kg if no effect is seen. When given by rapid IV injection, onset of effect is seen in 7 or 8 seconds. AV blockade is brief. The neonate should be under continuous ECG monitoring during therapy. This may show termination of SVT or may unmask other arrhythmias. Adenosine successfully aborts 80-95% of the cases of AVRT related SVT. (6) Early recurrence after termination of SVT may occur in up to 25-30% of cases. (7) Adenosine may fail to abort an attack of SVT if dose is inadequate or drug was administered too slowly. Adenosine is also ineffective if mechanism of tachyarrhythmia is VT or atrial tachycardia where adenosine blocks the AV node and reveals atrial flutter or atrial tachycardia as the cause of the problem. Other drugs: Other medications such as amiodarone, esmolol, and procainamide have been used to treat intractable SVT that either cannot be terminated with adenosine or cardioversion, or rapidly recurs. There are no controlled trials to guide the appropriate therapy but a retrospective review has found no difference in efficacy or safety between amiodarone or procainamide. (8) These medications are more often required in SVT associated with congenital heart diseases which tend to be more refractory.
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Cardioversion- Synchronized cardioversion is the treatment to abort SVT in a neonate who is critically or seriously ill and unstable.
B. Maintenance therapy Approximately 60% to 80% of the cases of SVT presenting in the neonatal period undergo spontaneous resolution during infancy leaving only few cases requiring long term treatment. (9) Choice of long term antiarrhythmic drugs is based on the severity of the presentation and the mechanism of the tachycardia, in particular the presence or absence of delta wave (pre excitation). Approach for maintenance therapy depends on level of sickness at the time of presentation. For
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Accelerated idioventricular rhythm (AIVR)
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mildly symptomatic babies with adenosine sensitive tachycardia that reverted easily maintenance therapy can be omitted as recurrence rates even with medication may vary between 40-80%. (5) For an infant presenting frequent attacks with circulatory collapse, or in whom cardioversion was difficult, beta blockers (propanolol 0.5 mg/kg PO every 6 hr) are used as these features predict refractory tachycardia in SVT. (10) Digoxin is used only if there is no evidence of pre-excitation in sinus rhythm in the dose of 5 micrograms/kg orally every 12 hr after initial load. Possibility of recurrence of SVT is similar with either digoxin or propranolol.(11) About 40% of newborns who have a treated episode of SVT do not have another episode when treated with antiarrhythmics for a minimum of 1 year after the first episode. If SVT persists beyond 1 year, spontaneous resolution is unlikely. Transcatheter ablation of the accessory pathway is of limited use in neonates due to the concerns like perforation, AV block and damage to the coronary arteries. Ablation is reserved for life-threatening, medically refractory cases. 1.3 Ventricular tachycardia Ventricular tachycardia presents as wide QRS complexes (QRS duration >0.09 sec) in ECG. It includes accelerated idioventricular rhythm, premature ventricular contractions and ventricular tachycardia. Supraventricular arrhythmias may also present as wide complexes in ECG e.g. SVT with bundle branch block and antigrade conduction through accessory pathway in WPW syndrome. Features of common ventricular tachycardia are described below.
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Accelerated idioventricular rhythm arises from accelerated discharge from an ectopic focus lying within bundle of His, Purkinje system or ventricular myocardium. ECG shows regular and wide QRS morphology with rates 20% or less of the sinus rate. If sinus and ectopic focus discharge at equal rates (isorhythmic) then fusion beats are visible in ECG. AVIR gradually appears as sinus rate slows down or ectopic rate accelerates above sinus rate. It is a benign arrhythmia, does not cause hemodynamic instability and requires no intervention. (12) Premature ventricular contractions- Refer table no 3.
1.3.3
Ventricular tachycardia (VT): It is also a wide QRS complex tachycardia with important causes being automatic focus in the ventricle, myocardial tumors like rhabdomyomas in association with tuberous sclerosis or fibromas, myocarditis and structural heart diseases. Presence of VT in a neonate prompts detailed echocardiography to assess structure and myocardial function to dictate duration of treatment and determine prognosis.
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Management of wide complex tachycardia Differentiation of wide complex tachycardia of ventricular or supraventricular origin is nearly impossible in neonates by ECG. Therefore, infants with wide QRS tachycardia are treated as if they have ventricular tachycardia. Method to restore sinus rhythm depends on hemodynamic status of the baby. Wide complex tachycardia in a non seriously ill infant is treated with intravenous procainamide or amiodarone. If wide complex tachycardia is discerned in an infant with collapse synchronized cardioversion is the intervention of choice.(13) 1.4 Algorithm for identifying tachycardia A sequential analysis of the ECG helps to classify the tachyarrhythmia. An easy approach is to look for QRS complex rate, regularity, and width followed by the relation of the P wave to the QRS and P wave morphology. Figure 7 provides an algorithm to diagnose tachyarrhythmia. (14) 2.
Bradyarrhythmia Transient bradycardia can occur in 20% to 90% of healthy newborns due to sinus bradycardia, sinus pauses, and junctional escape beats. Transient bradycardia may follow stressful labor or delivery but usually resolve within 48 to 72 hours. Rhythm disorder presenting with slowing of heart rate include following:
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Sinus bradycardia Newborn cardiac innervation has vagal dominance predisposing to episodic sinus bradycardia. Sinus bradycardia is characterized by regular slow atrial rate with normal P waves and 1:1 conduction. Pathologic causes of sinus bradycardia include hypoxia, acidosis, increased intracranial pressure, abdominal distention, hypoglycemia, apnea of prematurity and drugs such as digoxin and propranolol. 2.2 Heart blocks Heart block is basically of following 3 types. 1st-degree AV block: First degree heart block is characterized by prolonged PR interval but all the atrial impulses are conducted to the ventricle. 2nd-degree AV block: It is further classified into 2 types: • Mobitz type I (Wenckebach type): In this variant, the PR interval increases progressively until a P wave is not conducted. In the cycle following the dropped beat, the PR interval normalizes. Mobitz type is usually due to a functional suppression of AV conduction and it can usually be reversed with catecholamines or with vagolytic agents. It has better prognosis as compared to type II block. • Mobitz type II: In Mobitz type II second degree heart block, all atrial impulses are not conducted to the ventricles. Here a ventricular beat may follow every second or every third atrial beat referred as 2:1 block and 3:1 block respectively. This conduction defect is less common but has more potential to cause syncope and may be progressive. 2:1 conduction block seen in infants with markedly prolonged QT interval is an important risk factor for the development of torsades de pointes and sudden death. 3rd-degree AV block (complete heart block, CHB): In this type of heart block, none of the impulses from the atria reach the ventricles. Sinus impulses may be blocked either at the level of AV node (nodal block) or in the conducting system below the AV node (infranodal block). The escape rhythm for ventricular depolarization may be generated either in the healthy part of AV node or in the peripheral conducting system resulting in idioventricular rhythm much slower than atrial rate. ECG shows regular R-R intervals and regular P-P intervals (figure 8). The atrial rate is usually greater than the ventricular rate. CHB can be congenital or acquired. Congenital CHB is the most common congenital conduction defect. It is associated with structural heart disease in about half of the cases e.g. d-TGA. Congenital CHB can also occur as an isolated anomaly where it is strongly linked to transplacental passage of anti-Ro and anti-LA antibodies in the fetus. Acquired CHB may follow cardiac surgery, myocarditis or endocarditis.
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2.1
2.3 Complete heart block and lupus
When CHB occurs as an isolated anomaly, mother should be screened for anti Ro/SSA and anti LA/SSB antibodies. Risk of CHB in the infant of an anti Ro/SSA and anti LA/SSB antibody positive primipara or multipara mother with previously unaffected children is 2%. Recurrence risk in a previously affected pregnancy is 20%. The pathogenesis of CHB includes interference in clearance of apoptotic cardiocytes by healthy cardiocytes during development by anti Ro and La antibodies. This leads to phagocytosis of apoptotic cardiocytes by macrophages which secrete inflammatory and fibrosing cytokines resulting in conduction system and myocardial damage. Heart block most often develops between 18 to 24 weeks. Higher degrees of heart block may not be preceded by prolongation of PR interval and it can develop within a week of normal echocardiogram. Warning signs on echo suggestive of early signs of injury include echodensities and moderate to severe tricuspid regurgitation. Heart block of lesser degree may progress postnatally but conduction abnormality does not develop after a normal ECG at birth. Fetal treatment is based on suppression of inflammatory response by maternal administration of fluorinated steroids like dexamethasone or betamethasone and intravenous immunoglobulin. A non-randomized study showed variable effect of steroids on progression of lesser degrees of heart block to advanced one (15). Benefit with IVIG is also limited. Newborns with AV block are managed with cardiac pacing which is indicated if the heart rate is less than 55 beats per minute. CHB related to anti Ro/ anti La antibodies carries high mortality (20-30%) and morbidity with 67% requiring permanent pacemaker before adulthood (16, 17).
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3. Long QT syndromes
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Congenital long QT syndromes (LQTS) are genetic disorders of sodium and potassium channels resulting in prolongation of ventricular repolarization and QT interval. A typical ECG of LQTS is shown in figure 9. The rhythm disorder associated with this condition is polymorphic VT also called as torsades de pointes. The estimated incidence is about 1 per 10,000 births but variable penetrance makes precise assessment difficult. More than 400 different mutations have been identified in 10 LQTS susceptibility genes. Common drugs used in neonatal period which can prolong QT interval are mentioned in table 4. This arrhythmia may be asymptomatic if brief and self-limited, but if sustained beyond several seconds, usually results in ventricular fibrillation. LQTS may be detected during ECG done for other reasons. Manifestations include syncope provoked by exercise, fright, or a sudden startle, seizures, aborted cardiac arrest, or sudden death. Diagnosis of LQTS depends on accurate measurement of QTC interval (table 1). QTC interval of >0.47 sec is highly indicative, whereas a QTC interval of >0.44 sec is suggestive. Infants are screened for LQTS with an ECG due to a family history. Such screening should be delayed until the infant is 6 to 8 weeks of age because modest QT interval prolongation is relatively common (2.5%) among healthy infants and may cause undue family concern. Treatment of LQTS includes the use of β-blocking agents at doses that blunt the heart rate response to exercise. If drug therapy causes profound bradycardia then pacemaker needs to be implanted. Infants who are unresponsive to β-blockers and experienced cardiac arrest, an implantable cardiac defibrillator is indicated. β-blocking agents are not effective in patients with LQT3, hence implantable cardiac defibrillator is indicated.
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4. Salient details of drugs recommended for neonatal arrhythmias
These are listed along with their dosage and special comments in Table 5.
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Defibrillation is non synchronized random administration of shock during a cardiac cycle. Cardioversion is a synchronized administration of shock during the R waves of QRS complex of a cardiac cycle. During defibrillation and cardioversion, electrical current travels from the negative to the positive electrode by traversing myocardium. It depolarizes all of the heart cells simultaneously. This interrupts and terminates abnormal electrical rhythm. This, in turn, allows the sinus node to resume normal pacemaker activity. Non re-entrant rhythm disorders not responding to cardioversion include sinus tachycardia, automatic atrial tachycardia and junctional ectopic tachycardia Paddle size: Small paddles those used for direct delivery to epicardial surface of heart in older patients intraoperatively are appropriate for neonates. According to Pediatric advanced life support 2010 guidelines, “infant” size paddle or pad size is used for infants less than 10 kg (13). Interface: The electrode-chest wall interface is part of self adhesive pad, in contrast, electrode gel must be applied liberally on manually applied paddles. Saline soaked pads, ultrasound gel and bare paddles should not be used (13). Paddle position: Place manual paddles over the right side of upper chest, and the apex of the heart (13) or between the tip of the left scapula and the spine (3) so the heart is between the two paddles. Energy dose: Initial dose is 0.5-1.0 J/kg. This is followed by 1-2 J/kg if first shock is unsuccessful (4). Indications: Synchronized cardioversion is done for SVT and VT whereas for VF, cardioversion is used in asynchronous mode.
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CONCLUSIONS: Rhythm disorders can have variable presentation in neonatal period. All pediatricians and neonatologists should be able to interpret ECG in neonates and identify arrhythmias. Appropriate and timely management of such neonates is life saving with good long term outcomes in most of the cases. Conflicts of interest
References
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1. Dubin A. Arrythmias in the newborn. Neoreviews 2000; 1:e146–e151.
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The authors have nothing to declare.
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2. Cannon B, Kovalenko O, Snyder CS. Disorders of cardiac rhythm and conduction in newborns. In Richard J. Martin, Avroy A. Fanaroff, Michele C. Walsh, eds. Fanaroff and Martin's NeonatalPerinatal Medicine: Diseases of the Fetus and Infant. 10th ed. Elsevier Health Sciences, 2010, 12591274. 3. Barrett KE, Ganong WF. Ganong’s review of medical physiology. 23rd ed. New York: McGraw-Hill; 2010. 4. Killen AS, Fish FA. Fetal and neonatal arrhythmias. NeoReviews 2008; 9:242-252. 5. Kugler JD, Danford DA. Management of infants, children, and adolescents with paroxysmal supraventricular tachycardia. J Pediatr 1996; 129:324. 6. Ko JK, Deal BJ, Strasburger JF, Benson DW Jr. Supraventricular tachycardia mechanisms and their age distribution in pediatric patients. Am J Cardiol 1992; 69:1028. 7. Sherwood MC, Lau KC, Sholler GF. Adenosine in the management of supraventricular tachycardia in children. J Paediatr Child Health 1998; 34:53. 8. Chang PM, Silka MJ, Moromisato DY, Bar-Cohen Y. Amiodarone versus procainamide for the acute treatment of recurrent supraventricular tachycardia in pediatric patients. Circ Arrhythm Electrophysiol 2010;3:134–40. 9. Wu MH, Chang YC, Lin JL, et al. Probability of supraventricular tachycardia recurrence in pediatric patients. Cardiology. 1994;85:248-289. 10. Sanatani S, Hamilton RM, Gross GJ. Predictors of refractory tachycardia in infants with supraventricular tachycardia. Pediatr Cardiol 2002; 23:508. 11. Sanatani S, Potts JE, Reed JH, et al. The study of antiarrhythmic medications in infancy (SAMIS): a multicenter, randomized controlled trial comparing the efficacy and safety of digoxin versus propranolol for prophylaxis of supraventricular tachycardia in infants. Circ Arrhythm Electrophysiol 2012; 5:984. 12. Riera AR, Barros RB, de Sousa FD, Baranchuk A. Accelerated idioventricular rhythm: history and chronology of the main discoveries. Indian Pacing Electrophysiol J. 2010;10:40-8. 13. Kleinman ME, Chameides L, Schexnayder SM, et al. Part 14: pediatric advanced life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 Suppl 3):S876-908. 14. D S Kothari, J R Skinner. Neonatal tachycardias: an update. Arch Dis Child Fetal Neonatal Ed 2006;91:F136–F144. 15. Friedman DM, Kim, MY, Copel JA, Llanos C, Davis C, Buyon JP. Prospective Evaluation of Fetuses with Autoimmune Associated Congenital Heart Block Followed in the PR Interval and Dexamethasone Evaluation (PRIDE) Study. The American Journal of Cardiology, 2009; 103,1102– 1106.
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16. Buyon JP, Clancy RM, Friedman DM. Cardiac manifestations of neonatal lupus erythematosus: guidelines to management, integrating clues from the bench and bedside. Nat Clin Pract Rheumatol. 2009;5:139-48. 17. Kertesz NJ, Fenrich AL, Friedman RA. Congenital complete atrioventricular block. Tex Heart Inst J 1997; 24:301-7.
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Table 1: Normal values of ECG parameters in newborns Normal range
Events in the heart during intervals and comments
Heart rate
Average-120-160/min Range-90-230/min
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Sinus arrhythmia is variation in the heart rate during different phases of respiratory cycle due to reflex changes in vagal tone Heart rate increases during inspiration as vagal tone decreases
PR interval
70 -140 msec
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It extends from onset of the P wave to the Q or R wave in lead II Atrial depolarization and conduction through AV node
QRS axis
Term-55 to 200° Preterm-65 to 174° 20 to 80 msec
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Mean on postnatal day-4 -400±20 msec
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Ventricular depolarization and atrial repolarization Range described is measured in lead V5
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Ventricular depolarization plus ventricular repolarization Begins from onset of the QRS complex to the end of the T wave, is measured best in leads II, V5, and V6 As QT interval varies with heart rate so corrected, QTc interval is calculated by Bazett’s formula: QTc=QT(sec)/ (preceding RR interval in seconds) QTc is physiologically prolonged by 2 months with mean QTc= 410 msec) QTc reaches mean value of of 400 msec by 6 months of age
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QRS duration
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ST interval
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Ventricular repolarization (during T wave)
In the first postnatal week, T waves are variable but usually upright in lead V1 After the first postnatal week, the T wave is negative (downgoing) in lead V1 and positive in V5 and V6
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Table2. Classification of common arrhythmias in neonates Bradyarrhythmia
Sinus tachycardia
Sinus bradycardia
Atrial tachycardia
Heart Blocks
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Tachyarrhythmia
Atrial flutter
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First degree
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Atrial fibrillation
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Second degree
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Multifocal atrial tachycardia
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Wolff-Parkinson-White syndrome
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Concealed accessory pathways
entry tachycardia •
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junctional reciprocating tachycardia
Ventricular tachycardia
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Table 3. Types and characteristics of various tachyarrhythmia ECG CHARACTERISTICS
COMMENTS
Premature atrial contractions (PAC)
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Atrial flutter
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Mechanism: Automatic focus Common in healthy neonates If every sinus beat alternates with PAC then it is referred as atrial bigeminy If each PAC in atrial bigeminy is blocked then it can produce extreme bradycardia Prognosis is excellent Management- Observe for spontaneous resolution which usually occurs by 4 weeks
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P wave morphology is different from sinus P wave PAC conducted through conducting system of the heart produces narrow QRS If PAC finds AV node refractory then it remains non conducted called as “blocked” PAC If PAC crosses AV node but finds either right or left bundle branch refractory then conduction occurs via ventricular myocardium (aberrant conduction) producing wide QRS Aberrantly conducted PAC is differentiated from premature ventricular contraction by a preceding P wave Rate: Variable Usually upto 200 beats/min Gradually increases and decreases P waves: Precedes QRS Axis-abnormal
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TACHYARRHYTHMIA
Rate Upto 500 beats/min Ventricular rate is slower due to some degree of AV block Saw tooth flutter waves If P waves are masked by QRS complexes then diagnosis can
• • • • • •
• •
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Mechanism: Single automatic focus May be incessant Can lead to tachycardia induced cardiomyopathy May be difficult to control by pharmacotherapy or cardioversion Digoxin can be used as first line treatment, propranolol can be added if required If medical treatment fails then catheter ablation is an option with more than 90% success rate Mechanism: Reentry Treatment-Ttransesophageal overdrive pacing or synchronized DC cardioversion (0.5–2 J/kg) Recurrence is rare in the absence of congenital heart
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−
•
Mechanism- Multiple irritable automatic foci in the atrium Medications which can be used to control the heart rate are digoxin, propranolol, flecainide, sotalol, and amiodarone Polytherapy may be required as this arrhythmia is more difficult to suppress Spontaneous resolution occurs in weeks or months following which medication can be withdrawn Commonest form of SVT in SVT Responds to Adenosine
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P wave follows QRS • overlapping upstroke of T wave •
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Atrioventricular re-entry tachycardia (Orthodromic)
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Multifocal atrial tachycardia
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disease so long term medication is not required Recurrent atrial flutter in the setting of atrial dilatation or structural heart disease is treated with digoxin
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complexes then diagnosis can be made by injecting adenosine which increases the AV block to unmask the flutter waves In contrast to atrial tachycardia flutter waves lack isoelectric period between P waves (figure 10) Defined as ≥3 different P wave morphologies Irregularly irregular heart rate resulting from frequently blocked P waves Variable PR interval No two RR intervals are same
Atrioventricular re-entry tachycardia Antidromic)
Atrioventricular nodal re-entry tachycardia
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Permanent junctional reciprocating tachycardia
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Superior P wave axis (inverted in lead II and aVF)
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Pre excitation (delta wave) and short PR interval is seen post termination in WPW Adenosine sensitive
P wave usually not visible superimposed on QRS Produces a small positive deflection at the end of the QRS in lead V1, which looks a bit like an r’ wave
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Adenosine sensitive
Inverted P waves in II, III, aVF appear to precede QRS complex P waves are characteristically deeply inverted in leads II, III, and aVF
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Incessant, slower rate than others-about 200 beats/min Typically restarts after electrical cardioversion or adenosine Maintenance antiarrhythmics such as flecainide is always
• •
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• • •
AV dissociation Narrow QRS complexes Ventricular rate faster than atrial rates
•
•
QRS morphology of VPC is • different and wider than normal QRS •
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Mechanism-Increased automaticity in bundle of His or proximal bundle branches Causes − Congenital: Incessant, causes tachycardia induced cardiomyopathy and carries mortality of more than 50%. Amiodarone is used for the treatment − Post operative: Results from oedema, dyselectrolytemia, catecholamine surge, medications (dopamine, epinephrine) and it resolves as these factors are taken care of Mechanism: Spontaneous depolarization of ventricular myocardium Benign prognosis
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Ventricular premature contractions
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Junctional ectopic tachycardia
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required Early catheter ablation may be required Can lead to tachycardia induced cardiomyopathy
Ventricular tachycardia (VT)
• • •
Ventricular fibrillation
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Wide QRS complexes P wave may be dissociated from QRS complex “Capture” or “fusion” beats diagnostic
Chaotic irregular rhythm
•
Rare in neonates
•
•
VT is defined as an arrhythmia with three or more consecutive beats originating in the ventricles usually at a rate of 120/min or more Broad complex QRS always treated as VT unless proved otherwise Not terminated by Adenosine
•
Rare in neonates
•
Consider long QT syndrome or Brugada syndrome
•
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Table 4. Drugs that can prolong QT interval Erythromycin, Azithromycin, Trimethoprim/Sulfamethoxazole
Antifungals
Fluconazole, Itraconazole
Antihistamines
Astemizole, Terfenadine
Antipsychotics
Haloperidol, Risperidone, Chlorpromazine
Antiarrhythmics
Quinidine, Procainamide, Disopyramide, Amiodarone, Sotalol
Diuretics (Through K+ Loss)
Furosemide, Ethacrynic Acid, Bumetanide
Promotility agents
Cisapride
Dyselectrolytemia
Hypokalemia, Hypocalcemia, Hypomagnesemia
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Antibiotics
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Table 5: Antiarrhythmic drugs used in arrhythmias in neonates Dosage
Special comments
Esmolol
50-500 micrograms/kg/min
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Drug
1 10-15 mg/kg IV over 30-45 min
Digoxin
1 10 micrograms/kg IV as initial load; second dose in 6 hr and third at 24 hr
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Start IV dose of 100 micrograms/kg; double dose repeatedly until effect is seen, to maximum of 400 micrograms/kg
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Adenosine
Amiodarone
• •
Can cause hypotension Continuous blood pressure monitoring is essential
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Procainamide
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Monitor pulse, blood pressure Contraindicated in congestive heart failure • Do not give with verapamil
5 mg/kg IV over 15-30 min or as 5 separate 1 mg/kg aliquots
•
Do not use in hypokalemia or if toxic reaction to digoxin is suspected
•
Contraindicated in preexisting second- and third-degree AV block without pacemaker Use with caution in severe asthma; half-life is 10 sec in serum Occasionally induces atrial fibrillation
• • • •
Propranolol
0.25-1 mg/kg PO every 6 hr
•
Atenolol
0.5-2 mg/kg/day PO divided every 12 hr
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Sotalol
2-8 mg/kg/day PO divided every 8 hr
•
Given by central line diluted in D5W Can cause gasping syndrome in infants due to benzyl alcohol Observe for wheezing and symptoms of hypoglycemia
Torsades de pointes is likely with hypokalemia
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Figures:
Figure1. Waves and intervals of ECG in lead II.
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Figure2. Diagram showing re-entry phenomena. In re-entry, electrical signals generated from an appropriately timed premature beat find pathway B refractory, resulting in conduction block in this limb of the circuit. Meanwhile, conduction down pathway A proceeds unimpeded and subsequently the signal is conducted back via pathway B which has recovered leading to circus like movement.
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Figure 3. ECG of Supraventricular tachycardia
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Figure 4. Figure showing mechanism of Supraventricular tachycardia
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Figure 5. ECG showing pre-excitation as short PR interval and a widened QRS with slurred upstroke-Delta wave
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Figure 6.Treatment options for reverting SVT to sinus rhythm.
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Figure 7. Approach to tachyarrhythmia.
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Figure 8. Complete heart block
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Figure 9. Long QT syndrome
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Figure 10. Atrial flutter
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