Pediatric Dysrhythmias

Related Conditions

Arrhythmias, tachycardia, bradycardia

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1. Description of the problem

Cardiac arrhythmias are relatively common in critically ill infants and children. Whether a primary rhythm disturbance or the effect of other associated/underlying conditions, cardiac rhythm disturbances can lead to significant hemodynamic compromise and should be treated accordingly.

The good news is that most children with arrhythmias in the setting of structurally normal hearts will ultimately do quite well. The bad news, on the other hand, is that even otherwise “normal” children can present critically ill in the setting of a cardiac rhythm disturbance.

In their most basic sense, pediatric arrhythmias can be divided into “too fast” (tachycardia) versus “too slow” (bradycardia). As the management of these entities will be vastly different, they will be addressed separately within each subsection.

Clinical features

Tachycardia symptoms

Young children who are non-verbal can present with significant hemodynamic compromise as tachycardia may have been present for several hours before coming to clinical attention. These children often present for evaluation of irritability, pallor and/or poor feeding and are then noted be tachycardic.

While young children with fever and dehydration can present with similar symptoms, it should be kept in mind that incessant SVT could be the cause of the clinical compromise in a small subset of children. In these cases, immediate attention should be given to restoring sinus rhythm.

Older children often present with intermittent palpitations and are less likely to present with significant hemodynamic compromise as they can communicate their discomfort and are generally brought to medical attention before symptoms progress.

However, there are rare instances where children with either known or unknown manifest pre-excitation/WPW present with hemodynamic collapse related to rapid antegrade conduction over their accessory pathway in the setting of atrial tachycardia/fibrillation. This is a rare, yet real, cause of sudden death in the young.

Reentrant arrhythmias are typically sudden in their onset and termination and can be more easily induced in settings of stress (increased intrinsic catecholamines).

Due to their relatively incessant nature, patients with automatic arrhythmias can present with symptoms of heart failure and do not necessarily recognize that they are in tachycardia.

Bradycardia symptoms

Children with clinically symptomatic bradycardia can present with fatigue, syncope, failure to thrive, and/or exercise intolerance. However, some children with AV block are asymptomatic and discovered during routine clinical evaluations.

Key management points

Management of pediatric arrhythmias can be divided into the acute and chronic categories.

In addition to treating the rhythm disturbance, it is important to treat any underlying associated conditions that could be contributing to arrhythmia susceptibility. These would include such things as fever, electrolyte imbalances, acidosis, and thyroid abnormalities.

Management of supraventricular tachycardia (SVT)


Focus is on restoring sinus rhythm. As noted in other sections, most of these children are hemodynamically stable, so vagal maneuvers can be tried while other providers are collecting IV supplies and drugs. If vagal maneuvers are unsuccessful, adenosine can be administered via rapid IV push. If at any point the patient appears hemodynamically compromised, emergent cardioversion should be performed. See details below in “Emergency Management” section.

As per 2010 AHA PALS guidelines:

  • Adhere to basic principles of CPR
  • Differentiate between sinus tachycardia and supraventricular tachycardiaSinus tachycardia:normal p-wave axis (upright in leads II, III and aVf)

    constant P-R interval, variable R-R interval

    warm up and cool down

    infants: rate typically <220 bpm

    children: rate typically <180 bpm

    Supraventricular tachycardia:

    p-waves either not visible or inappropriate axis

    fixed rate with sudden onset and termination

    infants: rate typically >220 bpm

    children: rate typically >180 bpm

  • Emergency principles/treatment outlined in next section


Choice of therapy is dependent upon the mechanism of tachycardia.

  • Infants with atrial flutter in the early days of life often require no long-term therapy once sinus rhythm is restored.
  • Older children with rare and/or single episodes of hemodynamically tolerated SVT can be managed with observation only and no medical therapy.
  • However, most patients who present to an ICU setting for management of SVT will likely require long-term therapy.
  • First line medications include digoxin, beta-blocker, calcium channel blockers (avoid calcium channel blockers in infants and any patient with WPW).
  • Other option in those patients refractory to medications, intolerant of medications, or uninterested in medications, is catheter ablation.
  • Consultation with a pediatric cardiologist/electrophysiologist will determine whether or not your patient is a candidate for ablative therapy.

Management of ventricular tachycardia (VT)


If the patient is hemodynamically unstable, proceed with cardioversion. Many pediatric patients with ventricular tachycardia are hemodynamically stable and can be medically managed.

As per 2010 AHA PALS guidelines:

  • Adhere to basic principles of CPR
  • Differentiate between SVT and VTConsider VT if QRS duration >90 msecVA dissociation typical in VT
  • Emergency principles/treatment outlined in next section


Depends upon the mechanism of tachycardia. Consultation with a pediatric cardiologist/electrophysiologist will determine choice of therapy and whether or not patient is a candidate for ablative therapy.

  • Right Ventricular Outflow Tract Ventricular Tachycardia (RVOT-VT) – if asymptomatic and normal cardiac function, could consider no therapy if burden of tachycardia is low.
  • Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) – associated with sudden cardiac death and exacerbated by activity. Treatment includes medical therapy with beta-blocker, calcium channel blocker, and/or sodium channel blocker (recent data). These patients may require ICD placement given the risk of sudden death.
  • Long QT syndrome (LQTS) – associated with sudden cardiac death related to polymorphic ventricular tachycardia. These patients are often treated medically, though ICD therapy can be utilized as primary or secondary sudden death prevention.
  • Fascicular ventricular tachycardia – often medically managed with calcium channel blockers, though also amenable to catheter ablation.

Management of AV block


Acute therapy depends upon symptoms.

  • Asymptomatic – no acute therapy
  • Symptomatic – treat as per 2010 AHA PALS guidelines (see below)


In general, pacing for AV block is a matter of when, not if. The following are guidelines for pacemaker implantation in pediatric patients:

  • Class IAdvanced 2nd or 3rd degree AV block associated with symptomatic bradycardia, ventricular dysfunction, or low cardiac outputPost-operative advanced 2nd or 3rd degree AV block that is not expected to resolve or that persists at least 7 days after cardiac surgery.

    Congenital complete AV block with a wide QRS escape rhythm, complex ventricular ectopy, or ventricular dysfunction.

    Congenital complete AV block in the infant with a ventricular rate <55 bpm or with congenital heart disease and a ventricular rate <70 bpm

  • Class IIaCongenital complete AV block beyond the first year of life with an average heart rate <50 bpm, abrupt pauses in ventricular rate that are 2 or 3 times the basic cycle length, or associated symptoms due to chronotropic incompetence.Unexplained syncope with prior congenital heart surgery complicated by transient complete AV block with residual fascicular block after a careful evaluation to exclude other causes of syncope.
  • Class IIbTransient post-operative complete AV block that reverts to sinus rhythm with residual fascicular block.Congenital complete AV block in asymptomatic children or adolescents with an acceptable rate, narrow QRS complex, and normal ventricular function.
  • Class IIINot indicated for transient post-operative AV block with return of normal AV conduction in the otherwise asymptomatic patient.Not indicated for asymptomatic bifascicular block with or without 1st degree AV block after surgery for CHD in the absence of prior complete AV block.

    Not indicated for asymptomatic type I 2nd degree AV block.

2. Emergency Management

Assume basic CPR principles (See AHA 2010 Guidelines) in the management of hemodynamic compromise in the setting of a cardiac rhythm disturbance

Supraventricular Tachycardia (SVT)
  • If patient significantly compromised, proceed with DC cardioversion or defibrillation as indicated (adequate sedation).
  • In the setting of SVT, most patients are hemodynamically stable. Step back, take your own pulse, get rhythm strip and ECG before intervening.Documenting the pattern of the tachycardia and pattern of termination are helpful in determining the tachycardia mechanism.
  • Try vagal maneuvers first:Ice-to-face in young children, mimicking a diving reflexValsalva or carotid massage in older children

    Massaging eyes contraindicated as can be associated with retinal detachment

  • Adenosine: 0.1-0.2 mg/kg/dose (IV or IO)Administer as central as possibleRapid bolus followed by 5-10 cc rapid flush

    If adenosine “doesn’t work”:

    check dose,

    check route (was IV central enough to deliver drug quickly to heart as it will be metabolized in seconds by red blood cells; half-life very brief),

    check rhythm strip (maybe it worked, blocking AV node and showing ongoing atrial tachycardia; thus, need to move to next line of therapy as adenosine will not be effective here)

  • Esmolol: 500 mcg/kg bolus, followed by continuous infusion at 50-300 mcg/kg/min
Ventricular Tachycardia (VT)
  • If the patient is hemodynamically unstable, proceed with cardioversion (0.5-1 J/kg, increase to 2 J/kg if ineffective).
  • Many pediatric patients with ventricular tachycardia are hemodynamically stable and can be medically managed.Consider SVT with aberrancy or antidromic SVT (pre-excited patient with antegrade limb of SVT being the accessory pathway) if patient hemodynamically stable in setting of wide complex tachycardia (>90 msec)Vagal maneuvers and/or adenosine bolus (dose as above for SVT) can be attempted

    2010 AHA PALS guidelines recommend amiodarone or procainamide for medical management of VT (see dosing below). However, many pediatric cardiologists continue to use lidocaine at 1mg/kg bolus for the acute management of VT

    Amiodarone – 5 mg/kg over 20-60 minutes. Infuse via central access in a monitored setting. Caution for bradycardia and/or proarrhythmia.

    Procainamide – 15 mg/kg over 30-60 minutes.

AV Block

Acute therapy depends upon symptoms.

  • Asymptomatic – no acute therapy
  • Symptomatic – treat as per 2010 AHA PALS guidelines:CPR if HR <60 bpm with poor perfusion despite adequate oxygenation and ventilationEpinephrine 0.01 mg/kg (0.1 mL/kg of 1:10,000 concentration IV/IO, may repeat every 3-5 minutes)

    Atropine (particularly if related to increase vagal tone or primary AV block) 0.02 mg/kg

    Temporary transvenous pacing if unable to achieve adequate cardiac output with pharmacologic intervention

    Temporary transcutaneous pacing – only use if critically ill while awaiting a more stable means of pacing, such as transvenous.

3. Diagnosis

  • Rhythm strip and 12-lead ECG to evaluate rate, QRS morphology, P-wave axis, AV relationship, onset and/or termination of tachycardia
  • Narrow vs. wide complex:If wide (>90 msec), assume ventricular origin, though may represent SVT with aberrancy, SVT in the setting of underlying bundle branch block, or antidromic tachycardia (SVT with manifest accessory pathway as antegrade limb).
  • Evaluating the A:V and V:A relationship (1:1, <1:1, >1:1) is critical in determining the tachycardia mechanism, which will then guide acute and chronic therapy.If AV relationship is <1:1 (fewer atrial depolarizations than ventricular depolarizations), assume ventricular or junctional in originIf AV relationship is 1:1, assume reentrant SVT (AV reentry or AV node reentry) or atrial tachycardia with 1:1 AV conduction. In young children with robust AV node conduction, however, 1:1 retrograde conduction can occur in ventricular tachycardia.

    If AV relationship is >1:1 (more atrial depolarizations that ventricular depolarizations), assume atrial tachycardia with variable AV conduction (atrial flutter, intra-atrial reentry tachycardia, atrial fibrillation).

  • Vagal maneuvers and adenosine can be diagnostic as well as therapeuticIn the setting of atrial tachycardia (atrial flutter, atrial fibrillation, chaotic atrial tachycardia), the transient AV dissociation will more clearly show the persistent atrial tachycardia despite loss of AV conduction.
  • Transesophageal pacing can also be helpful in the diagnosis and management of arrhythmias in the critical care settingBecause of the proximity of the atria to the esophagus, a lead placed into the esophagus can give a more pronounced atrial signal and allow for more accurate determination of frequency of atrial depolarization and AV relationship.The pacing probe can be used to pace terminate an atrial or supraventricular reentrant tachycardia as well (provided there is adequate sedation).
  • Echocardiogram should be performed to evaluate cardiac function and look for potential associated structural abnormality.
  • Invasive electrophysiologic testing might be indicated and will be determined in consultation with your pediatric cardiologist/electrophysiologist.

ECGs of patient in sinus rhythm and in SVT. In sinus rhythm the p-waves are clearly noted and with normal axis, whereas in SVT the p-waves are difficult to discern and buried retrograde in the t-wave.

Figure 1

Figure 2

Surface ECG suggests atrial flutter, which is confirmed by the transesophageal tracing . Atrial burst pacing via the transesophageal catheter results in conversion to sinus rhythm.

Figure 3

Figure 4

Figure 5

Figure 6

ECG of pediatric patient with ventricular tachycardia. Note fusion and capture beats, which are hallmarks of ventricular tachycardia.

Figure 7

  • It is important to determine the mechanism of tachycardia in order to guide therapy.
  • As noted above, sinus tachycardia can be differentiated from clinical SVT by looking at:Sinus tachycardia: normal p-wave axis, fixed P-R and variable R-R, rate <220 infants and <180 children, gradual onset and resolutionTreat underlying cause and see if resolves (i.e., fever, dehydration, fear).

    Supraventricular tachycardia: p-waves not visible or inappropriate axis, fixed rate, rate >220 infants and >180 children, sudden onset and resolution

    Ectopic atrial tachycardia may behave more like sinus tachycardia in that there is gradual onset and resolution with rates not as high as reentrant SVT. However, these automatic tachycardias are typically incessant and will not respond to maneuvers that might control sinus tachycardia (antipyretics, fluid bolus, relaxation). These tachycardias do not respond to atrial burst pacing or DC cardioversion, thus important to recognize and differentiate the mechanism when deciding upon medical therapy.

  • Ventricular tachycardia with QRS duration typically >90 msec, though SVT with aberrancy or antidromic tachycardia (SVT with antegrade limb being accessory pathway) can also result in wide complex tachycardia.Hallmark of VT are fusion and/or capture beatsVT typically demonstrates VA dissociation (<1:1 AV relationship)
  • As noted above, vagal maneuvers, adenosine, and transesophageal pacing are often helpful in determining the tachycardia mechanism (diagnostic in addition to being therapeutic).
Confirmatory tests
  • 12-lead ECG with rhythm strip is primary test to diagnose cardiac rhythm disturbances
  • Careful evaluation of ECGs looking at:AV and VA relationshipOnset and termination of tachycardia

    Fixed rate vs variable rate

4. Specific Treatment

  • Vagal maneuvers
  • Drugs:Adenosine – dose and route as outlined aboveEsmolol – bolus 250-500 microgram/kg, followed by continuous infusion

    Procainamide – as outlined above

    Amiodarone – as outlined above

  • Transesophageal Pacing (by pediatric cardiologist)
  • DC cardioversion anywhere along the line if hemodynamic compromise
Drugs and dosages

Class I antiarrhythmics (sodium channel blockers)

These agents block the voltage gated sodium channel, delaying phase 0 of the action potential. These agents can prolong refractory periods and suppress abnormal automaticity. They can depress myocardial contractility at higher serum concentrations. They are further subdivided into 3 group:

  • Class IA (prolong refractory periods)Procainamide – Useful in reentrant SVT, atrial tachycardia, JET and ventricular arrhythmias. Can be given po or IV (IV dose is 7-15 mg/kg load, followed by continuous infusion of 20-80 mcg/kg/min; oral dose is 15-50 mg/kg/day, divided tid or qid). ECG – prolongation of QRS and QTc.
  • Class IB (have more effect on diseased myocardium, slowing conduction velocity)Lidocaine – Useful in acute management of ventricular arrhythmias. IV load of 1 mg/kg, followed by continuous infusion at 20-50 mcg/kg/min (load may be repeated x3). No significant effect on ECG.Mexiletine – Useful in management of ventricular arrhythmias (and in patients with Long QT type 3, sodium channel mutation). Oral dose is 6-15 mg/kg/day, divided tid. No significant effect on ECG (may shorten QTc).
  • Class IC (decrease conduction velocityFlecainide – Most notable effect on His-Purkinje system and ventricular myocardium (also inhibits abnormal automaticity). Useful in treating atrial arrhythmias and reentrant SVT. Oral dose is 4-8 mg/kg/day, divided bid to tid. ECG – prolongation of PR and QRS.Propafenone – Similar effect as flecainide, though also with weak beta-blocking and calcium channel blocking properties. Useful in treating supraventricular and ventricular arrhythmias. ECG – prolongation of PR and QRS.

Class II antiarrhythmics (ß-blockers)

These agents competitively inhibit ß-adrenergic receptors.

  • Propranolol – 2-4 mg/kg/day, divided tid-qid.
  • Esmolol – 500 mcg/kg rapid bolus, followed by continuous IV infusion at 50-300 mcg/kg/min.
  • Atenolol – 1-2 mg/kg/day, divided q 12 hrs
  • Nadolol – 1 mg/kg/day

Class III antiarrhythmics

These agents prolong the action potential duration by delaying repolarization, and thus carry a risk of pro-arrhythmia (torsades de pointes).

  • Amiodarone – chronic dosing approximately 5 mg/kg/day, given once daily
  • Sotalol – pediatric dosing 90-180 mg/m2/day, monitor QTc given risk of torsades

Class IV antiarrhythmics

  • (calcium channel blockers). These agents block the slow inward calcium current, slowing conduction and increasing refractoriness in the AV node. They are useful in the management of SVT and VT, though are contraindicated in the immature myocardium.Verapamil
  • Others:AdenosineDigoxin
Refractory cases

Combinations of above infusions with the guidance of a pediatric cardiologist/electrophysiologist.

Discuss potential for urgent catheter ablation in patients with refractory tachycardia.

Consider ECMO in critically ill children that do not respond to medical therapy and/or are not candidates for catheter ablation.

5. Disease monitoring, follow-up and disposition

Expected results of treatment

The ultimate goal of treating cardiac rhythm disturbances is to restore sinus rhythm with 1:1 AV conduction, thus restoring hemodynamic stability.

In the setting of a structurally normal heart, cardiac arrhythmias typically carry a good long-term prognosis with adequate therapy. Infants with SVT have a reasonable chance of “outgrowing” their tachycardia in the first year of life.

For rhythms that are too slow, the goal is achieve adequate rate to support cardiac output. Long-term outcomes in patients requiring permanent cardiac pacing are quite good as well.

Incorrect mechanism

If your interventions are not having the expected result, consider the possibility that the suspected mechanism was/is incorrect.

For example, vagal maneuvers, adenosine, pacing and/or DC cardioversion are not likely to terminate automatic arrhythmias, though should have good success in treating reentrant tachycardia.

If the tachycardia persists despite adequate delivery of the chosen therapy, consider converting to a more potent anti-arrhythmic medication, which should be guided in consultation with a pediatric cardiologist/electrophysiologist.


Follow-up should be arranged through a pediatric cardiologist with detailed knowledge of the arrhythmia mechanism.

Titration of oral medications, if indicated, can be managed in the outpatient setting by the patient’s cardiologist.

Patients requiring long-term cardiac pacing should be managed by a pediatric cardiologist with specific interest and training in cardiac pacing.


Too Fast
  • Supraventricular tachycardia (SVT) differential diagnosis:Sinus tachycardiaAtrioventricular reentry tachycardia (AVRT), accessory pathway mediated (concealed vs. manifest)

    Atrioventricular node reentry tachycardia (AVNRT)

    Atrial tachycardia (ectopic atrial tachycardia, chaotic atrial tachycardia, atrial flutter, atrial fibrillation, intra-atrial reentry tachycardia)

    Junctional ectopic tachycardia (more commonly seen following CHD surgery, though can rarely be seen as a primary/isolated rhythm abnormality)

  • Ventricular tachycardia and ventricular fibrillation
Too Slow
  • Results either from a failure of the impulse generation or a failure of impulse conduction.
  • Bradycardia differential diagnosis:Sinus bradycardiaSick sinus syndrome (typically following surgery for complex congenital heart disease)

    Atrioventricular block [1st degree, Type I 2nd degree (Wenckebach), Type II 2nd degree, and 3rd degree]


    Acquired (surgical, infectious)

Mechanisms of Tachycardia


(most common mechanism of SVT in children)

  • AVRT (Atrioventricular reentry tachycardia)Concealed accessory pathway – narrow complex tachycardia with antegrade limb of circuit being the AV node and retrograde limb the accessory pathway. All or none phenomenon with sudden onset and termination. Often brought about by exercise or other activities with increased catecholamines (endogenous or exogenous).Manifest accessory pathway/WPW (Wolff-Parkinson-White syndrome) – narrow complex tachycardia when the AV node serves as the antegrade limb and the accessory pathway serves as the retrograde limb (ORT – orthodromic reciprocating tachycardia), though wide complex when the accessory pathway serves as the antegrade limb (ART – antidromic reciprocating tachycardia, less common).
  • AVNRT (Atrioventricular node reentry tachycardia)The reentrant circuit uses functionally and anatomically discrete regions of atrial inputs with different conduction propertiesTypical AVNRT – slow pathway serves as the antegrade limb and fast pathway as retrograde limb, resulting in short R-P tachycardia with retrograde P-wave buried in QRS. ECG in SVT demonstrates narrow complex tachycardia with absence of discrete P-waves.

    Atypical AVNRT – fast pathway serves as the antegrade limb and slow pathway as retrograde limb, resulting in a long R-P tachycardia. Differential diagnosis of long R-P tachycardia includes sinus tachycardia, atypical AVNRT, ectopic atrial tachycardia and PJRT.

Enhanced automaticity

  • Automaticity is the property of cells undergoing spontaneous depolarization in the absence of external stimulation
  • Normal in the setting of sinus rhythm (or sinus tachycardia in response to fever, hypovolemia, fear, etc.)
  • Automatic arrhythmias are often characterized by a “warm up” and “cool down” pattern, as opposed to the sudden onset/offset, all or nothing, pattern seen in typical reentrant arrhythmias. Additionally, these arrhythmias are generally not responsive to overdrive pacing and/or DC cardioversion.
  • Examples:Sinus tachycardiaEctopic atrial tachycardia

    Multifocal atrial tachycardia/chaotic atrial tachycardia

    Junctional ectopic tachycardia (JET)


(less common in children)

  • Result of oscillations in the membrane potential, which, if large enough, can lead to additional action potentials.


Supraventricular tachycardia

Occurs in approximately 1.5-4/1000 children

Most common mechanism is reentrant SVT (90%)

Most children with SVT have structurally normal hearts, though there is a higher incidence of SVT in children with cardiac structural abnormalities

Ventricular tachycardia

Most often related to cardiac structural abnormalities and cardiac channelopathies (congenital heart disease, hypertrophic cardiomyopathy, long QT syndrome, catecholaminergic polymorphic VT) and much less frequent than pediatric SVT.

Large pediatric referral centers typically see <10 patients with sustained VT annually.

AV block

Congenital complete atrioventricular block (CCAVB) has been estimated to occur in approximately 1 in 15,000-20,000 live births.

Some cases may be related to specific cardiac malformations (discordant atrioventricular connections, left atrial isomerism with atrioventricular septal defect) while others may be associated with maternal antibodies (anti-Ro and anti-La) that cross the placenta and presumably cross-react with fetal cardiac tissue at a critical stage of development, disrupting the normal conduction system.


Supraventricular Tachycardia (SVT) – long-term prognosis is favorable with options including no therapy (if brief, self-limited episodes), chronic medical therapy (patients generally able to function without cardiac restrictions), and curative catheter ablation (success rates in the current era approach 97%)

Ventricular Tachycardia (VT) – in the absence of structural heart disease, the prognosis of VT in children is often favorable (RVOT-VT, fascicular VT) and can be managed with no therapy, chronic medical therapy (often without restrictions), and curative catheter ablation.

If related to cardiac channelopathies, cardiomyopathy, or underlying structural heart disease, however, the long-term prognosis is less favorable and significant activity restrictions are often in order.

AV Block – in the current era, children with congenital or acquired AV block typically do quite well with chronic cardiac pacing. These children will require lifelong pacemaker follow-up with intermittent system upgrades, though typically lead active lifestyles.

Special considerations for nursing and allied health professionals.


What’s the evidence?

Clinical Cardiac Electrophysiology in the Young. 2006. (This book is a comprehensive overview of cardiac arrhythmias in young patients. Can be used as as practical guide to the evaluation and management of heart rhythm abnormalities in children.)

Cardiac Arrhythmias in Children and Young Adults with Congenital Heart Disease. 2001. (This book provides a detailed overview of cardiac arrhythmias, starting with basic electrophysiologic principles and progressing to invasive therapies. It serves as an excellent guide for trainees and seasoned practitioners involved in the care of children with congenital heart disease.)

Heart Disease in Infants, Children and Adolescents. 2001. (“Moss and Adams” is one of the primary texts for pediatric cardiologists. The section on electrophysiology is an excellent resource and provides a solid background for understanding heart rhythm disorders in children.)

Pediatric Intensive Care. 2008. pp. 1126-48. (Another good review of managing cardiac arrhythmias in the ICU setting.)

Pediatric Cardiac Pacing, Gillette. 1995. (Good review of the basic principles of pacing and children and adolescents)

Elswick. Ann Emerg Med. vol. 31. 1998 Mar. pp. 406-9. (Case report of ventricular arrhythmia used for ventricular tachycardia image in text.)