Cardiac & Resuscitation, Patient Care

Assessing and Managing Pediatric Cardiac Rhythm Disturbances

Issue 2 and Volume 40.

Key Terms

Arrhythmia: Absence or disruption of cardiac electrical activity resulting in abnormality in the heart’s normal rhythmic pattern.
Bradycardia: A heart rate below the normal limit for age.
Heart block: An interference with the normal conduction of electrical impulses that control activity of the heart muscle.
Tachycardia: A heart rate above the upper limit for age.
Torsades de pointes: Bidirectional v tach often indicating an underlying electrolyte, metabolic or pharmacological abnormality.


Learning Objectives
>> Identify the most commonly seen arrhythmias in pediatric patients.
>> Recognize the signs and symptoms of the most commonly seen arrhythmias in pediatric patients.
>> Understand how to manage commonly seen arrhythmias in pediatric patients.

 

You’re dispatched to a local park for an 8-year-old boy experiencing palpitations during his little league baseball game. Upon arrival, the patient appears anxious and pale. He states that all of a sudden his heart started beating very fast and he began feeling dizzy. The cardiac monitor confirms a heart rate in the 250s. He’s normotensive. You obtain a 12-lead ECG and see a narrow complex QRS that’s not preceded by P waves. You transport him to the nearest ED for management.

Pediatric cardiac rhythm disturbances are relatively common, especially after advances in cardiac surgery have resulted in survival of children with complex congenital heart disease.1

Cardiac arrhythmias become emergencies when they produce hemodynamic instability that leads to decreased cardiac output. The overall incidence of pediatric arrhythmias is 55.1 per 100,000 pediatric ED visits.2 The most commonly seen arrhythmias are sinus tachycardia (50%), supraventricular tachycardia (13%), bradycardia (6%) and atrial fibrillation (4.6%).2 This article reviews some of the commonly seen pediatric arrhythmias, with considerations for prehospital care.

Sinus Tachycardia

Sinus tachycardia is a rhythm in which the rate of impulses arising from the sinoatrial node is elevated. This is a special consideration in the pediatric population as the normal heart rate varies with age. (See Table 1 image above.) The heart rate is usually between 110 and 150 bpm in infants, with gradual slowing over the pediatric years and finally becoming equal to the heart rate of an adult in the adolescent years.

As with adults, the most common cause of sinus tachycardia is a normal response to exercise or stress. However, in a tachycardic child, other important etiologies to consider would be fever, volume depletion/shock, heart failure, anemia, hyperthyroidism, hypoxia or ingestions of stimulants.

Most verbal patients may complain of a rapid heartbeat or palpitations, shortness of breath, or dizziness. However, excessive sinus tachycardia is worrisome as it can lead to decreased cardiac output by shortening ventricular filling time and increased myocardial oxygen consumption. It’s most important to recognize treatable causes of sinus tachycardia by providing antipyretics for fever, IV fluid for volume depletion and supplemental oxygen for hypoxia.

Figure 1: ECG showing a regular rhythm without beat-to-beat variation and absence of P waves characteristic of SVT. Images courtesy Vanderbilt University School of Medicine

Supraventricular Tachycardia

Supraventricular tachycardia (SVT) is the most common pathologic rhythm disturbance in children, with an estimated prevalence of 1 to 250 per 25,000 children.3 Eighty percent of cases present in children younger than 1 year old.4 SVT is characterized by an abnormally rapid heart rate that originates above the ventricles. It’s frequently caused by a reentrant mechanism in which two distinct pathways for cardiac conduction exist, creating a circuit that can rapidly conduct electrical impulses. Heart rates are generally > 220 beats per minute in infants and young children and > 180 beats per minute in older children.4

Symptoms of SVT may include palpitations, chest pain, dizziness, lightheadedness, fatigue, diaphoresis, shortness of breath and exercise intolerance. Symptoms in infants are often more nonspecific and present as irritability, poor feeding and respiratory distress. If SVT persists for hours or days, signs of heart failure may develop.

Diagnosis is made by an ECG demonstrating a regular rhythm without beat to beat variation and the absence of P waves. (See Figure 1 image above.) Occasionally P waves may be seen retrograde (after the QRS complex). The QRS complex is generally narrow, but aberrant situations of wide complex QRS do exist.

Wolff-Parkinson-White (WPW) syndrome is a particular type of SVT in which an accessory pathway exists for propagation of conduction from atria to ventricles. ECG findings in WPW may be seen once SVT has been terminated, and include a shortened PR interval, a delta wave (slow upstroke of the QRS complex), and a widened QRS complex. Other potential causes for SVT include hyperthyroidism, infections (e.g., myocarditis), and some cough and cold medications.

Management depends on the hemodynamic stability of the patient. Patients without evidence of cardiovascular compromise may be transported to the nearest ED. Vagal stimulation such as Valsalva maneuver or application of ice to the face can result in spontaneous cessation of SVT. For the hemodynamically unstable patient, cardioversion is indicated. Support these patients with high-flow supplemental oxygen and continuous heart rate and pulse oximetry monitoring. Cardioversion may be accomplished with the administration of adenosine 0.1 mg/kg rapid IV push (max 6 mg) or with synchronized cardioversion 0.5–1 J/kg.1 When performing cardioversion, be prepared for further rhythm decompensation to v tach, v fib or asystole.

Sinus Bradycardia

Sinus bradycardia is a heart rate below normal range for age. The rhythm originates in the sinus node, and ECG demonstrates a normal P-wave axis (upright in leads II and aVF) with a QRS following every P wave and a P wave preceding every QRS complex. There are many etiologies, including respiratory disease (e.g., hypoxia), excess vagal stimulation, increased intracranial pressure, hypothyroidism, hypoglycemia, hypothermia, weight loss (e.g., anorexia) and many medications.1 It’s important to note that sinus bradycardia can also occur as a normal variant during deep sleep as well as in highly trained athletes.

Clinical manifestations are varied. Many patients are completely asymptomatic. In more severe cases, signs such as pallor, cyanosis, mottled skin, prolonged capillary refill time and weak pulses may be seen. Symptoms include irritability, lethargy, confusion and decreased level of consciousness. Severe bradycardia may progress to respiratory distress and hypotension.

The most immediate management strategy for prehospital providers is to assess and stabilize the ABCs (airway, breathing, circulation). Patients without evidence of poor perfusion may be transported to the nearest ED for evaluation. If cardiorespiratory compromise is present, establish an airway as needed and support breathing with 100% supplemental oxygen. It’s important to note the threshold for initiation of CPR is a rate < 60 in neonates and infants. Symptomatic bradycardia may be treated with epinephrine 0.01 mg/kg IV or atropine 0.02mg/kg IV (min 0.1 mg), with epinephrine being the initial drug of choice.5

AV Nodal Block

There are multiple types of heart block that result in impaired electrical conduction from the atria to the ventricles. An ECG confirms diagnosis of the specific type.

First-degree AV block is when there’s a delay in conduction through the AV node. ECG findings demonstrate a regular rhythm with a normal QRS morphology and prolonged PR interval beyond the normal range for age. Possible etiologies include increased vagal tone, untreated congenital heart disease (e.g., atrial or ventricular septal defect), medication therapy (e.g., beta-blockers, calcium channel blockers, digitalis), and electrolyte abnormalities.4 These patients are typically asymptomatic and generally don’t require any specific therapy.

Second-degree AV block (types I and II) results in intermittently failed conduction to the ventricles. This may result from infection (e.g., myocarditis, acute rheumatic fever), structural heart disease, drug toxicity (e.g., beta-blockers, digitalis), increased vagal tone, or post-operatively in children with previous cardiac surgery.4

Careful ECG reading and rapid transport to a pediatric ED are important factors for a successful outcome.

There are two distinct types of second-degree block. Type I (Mobitz I or Wenckebach) may occur as a normal variant in some children, or be transiently associated with infection (e.g., myocarditis). An ECG will demonstrate a PR interval that progressively prolongs with each beat, with an eventual “dropped” beat in which the P wave fails to conduct and there’s no QRS complex. After this dropped beat, the PR interval resets and the cycle repeats. These children generally have no hemodynamic compromise and require no specific therapy.

Type II (Mobitz II) is evidenced by intermittently failed AV conduction, with normal P waves and PR intervals, but only certain P waves followed by QRS complexes. The block may show a distinct pattern on an ECG, such as 2:1 when every other P wave is followed by a QRS complex, or 3:1 where every third P wave is followed by a QRS complex. This type is often permanent, frequently due to structural damage of the cardiac conduction system. Patients may present with syncope or heart failure, and this rhythm may progress to complete heart block.

Third-degree AV block, also termed complete heart block, is a total disruption of the AV nodal conduction system. In these patients, no atrial impulses reach the ventricles, and the ventricles are activated by an escape rhythm originating elsewhere in the AV nodal junction or ventricles. The ECG will demonstrate complete dissociation between P waves and QRS complexes. This type of block is rarely seen in pediatric patients, and is most often due to autoimmune disease or structural heart disease. Congenital cases may be seen in neonates born to mothers with systemic lupus erythematosus, rheumatoid arthritis or Sjogren syndrome.4 Patients may present with irritability, fatigue, significant bradycardia, syncope or sudden death. Cardiac monitoring is crucial during transport to emergency care, as these patients may develop worsening heart failure, hypotension or cardiac arrest. Patients frequently require placement of a pacemaker for definitive management.

Figure 2: ECG showing the inappropriately rapid rate and narrow QRS complexes characteristic of atrial fibrillation.

Atrial Fibrillation

Although atrial fibrillation is the most common chronic arrhythmia in adults, it’s very rare in the pediatric population and usually associated with structural heart disease, cardiomyopathy, WPW syndrome and thyroid disease.6 Atrial fibrillation is a rhythm with the absence of regular or organized atrial activity. Multiple circuits within the atrial myocardium generate multiple waves of activity, often competing with one another. These multiple waves generate rapid and localized impulses, suppressing the sinus node and preventing activation of the atrium. Absence of uniform activation of the atrium leads to absence of P waves on the surface ECG. The ECG also demonstrates an inappropriately rapid heart rate for age (i.e., greater than the 95th percentile) and narrow QRS complex. (See Figure 2.)

Initial management of atrial fibrillation is aimed at slowing the heart rate. In the stable patient, pharmacologic options such as beta-blockers, calcium-channel blockers and digoxin may be beneficial and cardiac pacing may additionally have some success in controlling the rate.7 Cardioversion may be considered in the unstable patient with evidence of heart failure or end-organ hypoperfusion.

Figure 3: ECG showing AV dissociation with characteristically wide QRS complexes.

Ventricular Tachycardia

V tach is additionally rare in children but easily confused with other types of tachycardia. It’s characterized by wide QRS complexes > 0.08–0.09 seconds (varies with age). Rates average 250 bpm and there’s AV dissociation with P waves completely independent from QRS.7 (See Figure 3.)

In pediatrics, v tach is most commonly associated with congenital heart defects, especially tetralogy of Fallot.8 Other causes to be considered in this dysrhythmia are electrolyte disturbance, toxins or myocarditis in addition to cardiomyopathy and long QT syndrome.

Although patients who experience slow v tach are hemodynamically stable at presentation, some patients present with rapid v tach that results in syncope or cardiac arrest. Unstable wide-complex tachycardia should be synchronously cardioverted with 0.5–1 J/kg. In stable v tach, conversion may be attempted with amiodarone 5 mg/kg over an hour.

Figure 4: ECG showing a prolonged QT interval, which may predispose a patient to development of torsades de pointe. 

Torsades de Pointes

Torsades de pointes (TDP) is a form of polymorphic v tach that occurs in the setting of acquired or congenital prolonged QT syndrome. (See Figure 4 image above.) TDP is also referred to as polymorphic v tach and is defined as a ventricular rhythm faster than 100 beats per minute with frequent variations of the QRS axis, morphology, or both. The variations take the form of a cyclic alteration of the QRS axis where the peaks of the QRS complexes appear to twist around the isoelectric line of the ECG recording, giving it the name “torsades de pointes” or “twisting of the points.”9

Typical features include a ventricular rate of 160–250 bpm, an antecedent prolonged QT interval, irregular RR intervals and a cycling of the QRS axis through 180 degrees every 5–20 beats.9 TDP may be short-lived and terminate spontaneously, but most patients experience multiple episodes of the arrhythmia, which may lead to v fib and sudden cardiac death.10

Drugs are a common cause of prolonged QT and TDP. Some common classes of drugs known to prolong the QT interval are antiarrhythmic drugs, macrolide antibiotics, certain psychotropic medications and gastric motility agents.

Hypokalemia and hypomagnesemia may also predispose a patient to TDP. Less commonly, hypocalcemia may also contribute. TDP should be immediately defibrillated in the unstable patient. Stable patients may be medically managed with IV magnesium sulfate, which is effective for both the treatment and prevention of recurrence of TDP.10

Case Conclusion

You correctly identify a supraventricular tachycardia arrhythmia in this patient and determine he’s stable. While vagal maneuvers have been unsuccessful en route to the pediatric ED, he’s quickly converted to a normal sinus rhythm with the use of rapid-push adenosine.

References

1. Fleisher GR, Ludwig, S, editors. Textbook of pediatric emergency medicine, sixth edition. Lippincott Williams & Wilkins: Philadelphia, 2010.

2. Sacchetti A, Moyer V, Baricella R, et al. Primary cardiac arrhythmias in children. Pediatr Emerg Care. 1999;15(2):95–98.

3. Dubin AM. (Nov. 6, 2013.) Supraventricular tachycardia in children: AV reentrant tachycardia (including WPW) and AV nodal reentrant tachycardia. UpToDate. Retrieved Nov. 29, 2014, from www.uptodate.com/contents/supraventricular-tachycardia-in-children-av-reentrant-tachycardia-including-wpw-and-av-nodal-reentrant-tachycardia.

4. Shah BR, editor. Atlas of pediatric emergency medicine, second edition. McGraw-Hill Medical: New York, 2013.

5. Doniger SJ, Sharieff GQ. Pediatric dysrhythmias. Pediatr Clin North Am. 2006;53(1):85–105.

6. Mills LC, Gow RM, Myers K, et al. Lone atrial fibrillation in the pediatric population. Can J Cardiol. 2013;29(10):1227–1233.

7. Strange GR, Ahrens WR, Lelyveld S, et al, editors. Pediatric emergency medicine, third edition. McGraw-Hill: New York, 2009.

8. Walsh EP, Cecchin, F. Arrhythmias in adult patients with congenital heart disease. Circulation. 2007;115(4):534–545.

9. Passman R, Kadish, A. Polymorphic ventricular tachycardia, long QT syndrome and torsades de pointes. Med Clin North Am. 2001;85(2):321–341.

10. Khan IA. Long QT syndrome: Diagnosis and management. Am Heart J. 2002;143(1):7–14.