Cardiac arrhythmias are due to abnormalities in the heart rhythm or conduction that can range in clinical significance from benign to life threatening. The frequency with which these occur varies with age and comorbid conditions, and true cardiac arrhythmias are rare in young people. It is important for the clinician to identify the arrhythmia and determine whether further evaluation or treatment is required. In general, the principle of treatment in this population is to minimize or alleviate symptoms, reduce associated risks (ie, cardiac dysfunction), prevent hemodynamic compromise, and/or prevent mortality.
Proper identification of cardiac arrhythmias in the young requires a clear understanding of the normal physiologic changes in heart rate that occur with age and activity. It is also important to understand the average expected resting heart rate for a given age (Table 12-1).1,2 Identification of clinically relevant arrhythmias requires assessment of the patient’s heart rate, a basic understanding of electrocardiogram interpretation in the context of the patient’s age, a focused clinical history, and awareness of the patient’s current hemodynamic state. This provides a framework for appropriate evaluation and management.
This chapter will outline basic pediatric arrhythmias and focus on several important cardiac conditions that may result in malignant arrhythmias or syncope. Each cardiac arrhythmia will be described based on electrocardiographic findings, causes, clinical features, and management options.2-6
A slow heart rate that is below the lower limits of normal for age but regular and originating from the sinus node. This is characterized by (1) a P wave preceding every QRS complex with a normal PR interval and (2) a normal P-wave morphology and axis (upright/positive in leads I and aVF).
Sinus bradycardia can be due to increased parasympathetic (vagal) tone as seen in well-conditioned athletes; withdrawal of sympathetic tone as seen during sleep and obstructive sleep apnea; drugs such as sedatives, parasympathomimetics, sympatholytics, and many antiarrhythmics agents; increased intracranial pressure; hypothyroidism; hypothermia; prolonged hypoxia; or sinus node dysfunction.
Most patients with sinus bradycardia are asymptomatic. However, symptoms of bradycardia include lightheadedness, dizziness, fatigue, exercise intolerance, presyncope, or syncope.
Generally, no therapy is required, but in symptomatic patients, the primary management is to diagnose and treat the underlying cause. In rare cases of symptomatic bradycardia with or without sinus pauses, patients may require short-term treatment with atropine (a vagolytic) or long-term treatment with a permanent atrial pacemaker to increase the atrial heart rate.
See Figure 12-1.
A slow heart rhythm, below the lower limits of normal for age, that originates from the atrioventricular (AV) junction. This is characterized by (1) a regular, narrow QRS rhythm with no P waves preceding the QRS complexes and (2) P waves that are totally absent, unrelated to the QRS complexes, or inverted and following QRS complexes.
Junctional bradycardia is often benign and due to excessive vagal tone in a structurally normal heart. Other causes include increased intracranial pressure, sequelae of cardiac surgery, sinus node dysfunction, and digitalis toxicity.
As with sinus bradycardia, most patients are asymptomatic, but symptoms of bradycardia may occur.
Generally, no therapy is required, but as with sinus bradycardia, atropine and/or pacemaker therapy may be needed in symptomatic patients.
See Figure 12-2.
A slow to low-normal heart rate that is below or at the lower limits of normal for agethat originates from a nonsinus location in the atrium. This is characterized by (1) a regular rhythm with P waves preceding every QRS complex and a normal PR interval and (2) an abnormal P-wave morphology and axis (ie, P waves are not upright in leads I and aVF). Commonly, low right atrial rhythms show an upright/positive P wave in lead I and inverted/negative P wave in lead aVF.
Ectopic atrial rhythm is often benign but can also occur in the setting of sinus node dysfunction.
As with sinus bradycardia, most patients are asymptomatic, but symptoms of bradycardia may occur.
Generally, no therapy is required, but as with sinus bradycardia, atropine and/or pacemaker therapy may be needed in symptomatic patients.
See Figure 12-3.
A slow to normal heart rhythm that originates from 2 alternating sites in the atrium. Most commonly, low atrial rhythm may alternate with sinus rhythm to produce this effect. This is characterized by (1) a P wave occurring before every QRS complex and (2) a gradual or abrupt change in the P-wave morphology and axis, which may result in a change in the PR interval.
Wandering atrial pacemaker is a benign finding due to alterations in vagal tone. Increases in vagal tone may result in suppression of sinus node function shifting the site of the natural atrial pacemaker to another focus in the atrium that has inherent automaticity.
Patients are asymptomatic with no clinical manifestations related to the wandering location of atrial activity.
No therapy is required.
See Figure 12-4.
A premature beat originating from a nonsinus location in the atrium. This is characterized by (1) a P wave occurring prematurely that is usually followed by a QRS, (2) an abnormal P-wave morphology, and (3) a PR interval that is usually prolonged. If the P wave occurs early enough, there may be AV block.
Premature atrial contractions (PACs) are usually idiopathic and not associated with any heart disease. However, causes should be considered and include electrolyte derangements, fever, hyperthyroidism, drug toxicity, infection, and foreign body in the atrium (ie, catheter or wire).
Patients are usually asymptomatic. Occasionally, PACs produce palpitations.
No therapy is required. In rare cases when patients are clearly symptomatic, β-blocker therapy may be used.
See Figure 12-5.
A premature beat originating from the ventricle. This is characterized by a wide QRS beat occurring prematurely. The premature ventricular contraction (PVC) may or may not perturb the normal atrial rhythm.
PVCs are usually idiopathic and not associated with any heart disease. Benign PVCs are usually suppressed during exercise, and PVCs that increase in frequency with activity are more ominous. However, causes should be considered and include electrolyte derangements, fever, hyperthyroidism, drug toxicity, infection, or foreign bodies in the ventricle (ie, catheter or wire).
Patients are usually asymptomatic. Occasionally PVCs produce palpitations.
No therapy is required. Although most PVCs are benign, the incidence of underlying heart disease is slightly more than with PACs. Echocardiography is usually advised to assess for underlying structural heart disease or cardiomyopathy. In rare cases when patients are clearly symptomatic, β-blocker therapy may be used.
See Figure 12-6.
First-degree heart block is a sinus rhythm with prolonged conduction from the atrium to the ventricle. This is characterized by (1) a P wave preceding every QRS complex, (2) a QRS complex following every P wave, and (3) a PR interval greater than the upper limits of normal. A PR interval of greater than 200 ms is considered first-degree heart block in adults. However, the PR interval is age and heart rate dependent, with shorter PR intervals for younger age and faster heart rates. A PR interval greater than 120 ms for an infant, 150 ms for a toddler, and 180 ms for a young child is considered prolonged for heart rates below 100 beats per minute (bpm).
The PR interval will be prolonged if there is delayed conduction above the AV node, through the AV node, or below the AV node in the His-Purkinje system. Causes include inflammatory processes (ie, Lyme myocarditis), congenital heart defects (ie, Ebstein anomaly), medication exposure (ie, digitalis toxicity), postsurgical injury to the native conduction system, and increased vagal tone in anotherwise healthy child.
First-degree block typically does not result in symptoms but can progress to more advanced heart block that could result in symptomatic bradycardia.
Assessment of secondary causes should be identified to allow for appropriate treatment, which may result in resolution of the first-degree block (ie, treatment of digitalis toxicity or treatment of Lyme myocarditis with appropriate antibiotics).
See Figure 12-7.
Sinus rhythm with progressive prolongation of conduction from the sinus node to the ventricle until the sinus impulse is blocked from conducting to the ventricle. This is characterized by progressive prolongation of the PR interval until there is a P wave that is not followed by a QRS. The PR interval of the next beat is short, and the cycle may repeat. Progressive delay in conduction with eventual block is referred to as Wenckebach phenomenon.
Mobitz I block usually occurs within the compact AV node and is typically a benign finding that occurs in healthy patients, especially well-conditioned athletes with increased vagal tone. Additional causes include inflammatory processes such as myocarditis, medication exposure such as digitalis toxicity, and postsurgical injury to the conduction system.
Mobitz I block typically does not result in symptoms or progress to more advanced heart block.
Generally, no therapy is required.
See Figure 12-8.
Second-degree heart block is a sinus rhythm with intermittent “all or none” conduction to the ventricle and no alteration in the preceding PR interval. This is characterized by intermittent P waves that are not followed by a QRS and without prolongation in the PR interval of the preceding conducted beats.
The causes of Mobitz II block are similar to the causes of Mobitz I block; however, Mobitz II block typically occurs below the AV node at the level of the His bundle. This is more ominous and may progress to complete heart block.
Mobitz II block usually does not produce symptoms unless there are significant pauses or bradycardia. It may progress to more advanced heart block.
Assessment of secondary causes should be identified to allow for appropriate treatment, which may result in resolution of the second-degree block. Pacemaker therapy may be required for symptomatic bradycardia or symptomatic pauses due to intermittent loss of ventricular activation.
See Figure 12-9.
High-grade AV block is characterized by several consecutive nonconducted P waves occurring in a row. Conduction may occur with every third or fourth beat.
High-grade AV block, like Mobitz II block, typically occurs below the AV node at the level of the His bundle. Causes include postsurgical injury, myocarditis, drug toxicity, and congenital heart block.
Symptoms depend on the rate and reliability of the ventricular heart rate. Patients with significant bradycardia or sinus pauses can have symptoms that include lightheadedness, dizziness, fatigue, exercise intolerance, presyncope, or syncope.
Management includes assessment for secondary causes and appropriate treatment. Pacemaker therapy may be required for symptomatic bradycardia or symptomatic pauses due to intermittent loss of ventricular activation.
See Figure 12-10.
Third-degree heart block is defined as blocked conduction in the AV node or His-Purkinje system, resulting in independent atrial and ventricular rhythms. This is characterized by (1) a regular ventricular rhythm with regular QRS complexes that are not related to the P waves and (2) a ventricular rate that is slower than the atrial rate (ie, more p waves than QRS complexes). The QRS complex can be narrow or wide depending whether the escape rhythm originates from the AV junction or the ventricle.
Third-degree AV block can be congenital or acquired. Fetal exposure to maternal autoantibodies related to lupus or Sjögren syndrome is the most common cause of congenital complete heart block. Over half of congeni-tal heart block cases are “idiopathic” and do not have any specific identifiable cause. Complete heart block can occur in the setting of congenital heart disease, especially congenitally corrected transposition of the great vessels. Acquired complete heart block occurs in conditions that injure the AV node, including myocarditis, Lyme carditis, rheumatic fever, cardiomyopathies, cardiac tumors, drug toxicity (ie, calcium channel blockers or digoxin), myocardial infarction, or direct trauma as a complication of cardiac surgery.
Symptoms depend on the rate and reliability of the ventricular heart rate. Surprisingly, many children with congenital heart block are completely asymptomatic despite heart rates that are well below the “lower limits” for age. Patient with significant bradycardia or sinus pauses may experience lightheadedness, dizziness, fatigue, exercise intolerance, presyncope, or syncope. In very rare cases, prolonged asystolic pauses may precipitate ventricular fibrillation and sudden death.
Assessment for secondary causes and appropriate treatment is paramount. Short-term management of complete heart block that results in low cardiac output and associated symptoms is focused on increasing the effective ventricular rate. This may be accomplished with medications like atropine, isoproterenol, or epinephrine. Temporary transvenous or transcutaneous pacing is indicated for symptomatic patients when medications fail. Permanent pacemaker therapy may be required for children with symptomatic bradycardia or prolonged sinus pauses.
Supraventricular tachycardia (SVT) is the most common tachyarrhythmia in infants and children after sinus tachycardia. SVT is a broad term that describes any arrhythmia originating from above the AV node or ventricles. The term is often synonymous with paroxysmal SVT of which AV nodal re-entrant tachycardia (AVNRT) and atrioventricular re-entrant tachycardia (AVRT), more specifically orthodromic re-entrant tachycardia, compose more than 90% of SVTs encountered in children and infants.7,8 Other less common forms of SVT in children include ectopic atrial tachycardias, atrial fibrillation, atrial flutter, and other rare SVTs.
Although not a true supraventricular “arrhythmia,” sinus tachycardia is defined as a rapid heart rate, above the upper limits of normal for age (Table 12-1), originating from the sinus node. This is characterized by (1) a regular, narrow QRS rhythm; (2) a P wave that precedes every QRS complex with a normal PR interval; and (3) normal P-wave morphology and axis (upright/positive in leads I and aVF). The heart rates tend to be below 200 bpm, but some infants and small children may be able to generate sinus rates up to 230 bpm.
Sinus tachycardia can be a result of increased sympathetic tone; withdrawal of parasympathetic tone; endogenous catecholamines in the setting of fever, pain, fear, distress, or dehydration; exogenous catecholamines like epinephrine, norepinephrine, and β-agonists (ie, albuterol); and dehydration. In addition, metabolic disorders that increase the body’s metabolic state such as hyperthyroidism or brain injury that results in dysregulation of the autonomic nervous system can result in tachycardia. Finally, compensatory sinus tachycardia can be seen in cardiac dysfunction to maintain cardiac output.
Sinus tachycardia usually presents with a gradual increase in heart rate that may or may not cause symptoms of palpitations. It is important to consider the underlying cause because sinus tachycardia is rarely an isolated finding.
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