CHAPTER 142 Dysrhythmias
ETIOLOGY AND DIFFERENTIAL DIAGNOSIS
Cardiac dysrhythmias or abnormal heart rhythms are uncommon in pediatrics, but may be caused by infection and inflammation, structural lesions, metabolic abnormalities, and intrinsic conduction abnormalities (Table 142-1). Many pediatric dysrhythmias are normal variants that do not require treatment or even further evaluation.
TABLE 142-1 Etiology of Dysrhythmias
DRUGS
INFECTION AND POSTINFECTION
METABOLIC-ENDOCRINE
STRUCTURAL LESIONS
OTHER CAUSES
SLE, systemic lupus erythematosus.
Sinus rhythm originates in the sinus node and has a normal axis P wave (upright in leads I and AVF) preceding each QRS complex. Because normal rates vary with age, sinus bradycardia and sinus tachycardia are defined based on age. Sinus arrhythmia is a common finding in children and represents a normal variation in the heart rate associated with breathing. The heart rate increases with inspiration and decreases with expiration, producing a recurring pattern on the electrocardiogram (ECG) tracing. Sinus arrhythmia does not require further evaluation or treatment.
Atrial Dysrhythmias
A wandering atrial pacemaker is a change in the morphology of the P waves with variable PR interval and normal QRS complex. This is a benign finding, requiring no further evaluation or treatment.
Premature atrial contractions are relatively common prenatally and in infants. A premature P wave, usually with an abnormal axis consistent with its ectopic origin, is present. The premature atrial activity may be blocked (no QRS following it), conducted normally (normal QRS present), or conducted aberrantly (a widened, altered QRS complex). Premature atrial contractions are usually benign and, if present around the time of delivery, often disappear during the first few weeks of life.
Atrial flutter and atrial fibrillation are uncommon dysrhythmias in pediatrics and usually present after surgical repair of complex congenital heart disease. They may also be seen in patients with myocarditis or in association with drug toxicity.
Supraventricular tachycardia (SVT) is the most common symptomatic dysrhythmia in pediatric patients. The rhythm has a rapid, regular rate with a narrow QRS complex. SVT in infants is often 280 to 300 beats/minute with slower rates for older children and adolescents. The tachycardia has an abrupt onset and termination. In a child with a structurally normal heart, most episodes are relatively asymptomatic other than a pounding heart beat. If there is structural heart disease or the episode is prolonged (>12 hours), there may be alteration in the cardiac output and development of symptoms of heart failure. Although most patients with SVT have structurally normal hearts and normal baseline ECGs, some children have Wolff-Parkinson-White syndrome or pre-excitation as the cause of the dysrhythmia.
Ventricular Dysrhythmias
Premature ventricular contractions (PVCs) are less common than premature atrial contractions in infancy but more common in older children and adolescents (Table 142-2). The premature beat is not preceded by a P wave and the QRS complex is wide and bizarre. If the heart is structurally normal, and the PVCs are singleton, uniform in focus, and disappear with increased heart rate, the PVCs are usually benign and require no treatment. Any deviation from the presentation (history of syncope or a family history of sudden death) requires further investigation and possibly treatment with antiarrhythmic medications.
TABLE 142-2 Dysrhythmias in Children
| Type | ECG Characteristics | Treatment |
|---|---|---|
| Supraventricular tachycardia | Rate usually >200 beats/min (range, 180–320 beats/min); abnormal atrial rate for age; ventricular rate may be slower because of AV block; P waves usually present and are related to QRS complex; normal QRS complexes unless aberrant conduction is present | Increase vagal tone (bag of ice water to face, Valsalva maneuver); adenosine; digoxin; sotalol; electrical cardioversion if acutely ill; catheter ablation |
| Atrial flutter | Atrial rate usually 300 beats/min, with varying degrees of block; sawtooth flutter waves | Digoxin, sotalol, cardioversion |
| Premature ventricular contraction | Premature, wide, unusually shaped QRS complex, with large inverted T wave | None if normal heart and if premature ventricular contractions disappear on exercise; lidocaine, procainamide |
| Ventricular tachycardia | ≥3 Premature ventricular beats; AV dissociation; fusion beats, blocked retrograde AV conduction; sustained if > 30 sec; rate 120–240 beats/min | Lidocaine, procainamide, propranolol, amiodarone, cardioversion |
| Ventricular fibrillation | No distinct QRS complex or T waves; irregular undulations with varied amplitude and contour, no conducted pulse | Nonsynchronized cardioversion |
| Complete heart block | Atria and ventricles have independent pacemakers; AV dissociation; escape-pacemaker is at atrioventricular junction if congenital | Awake rate < 55 beats/min in neonate or < 40 beats/min in adolescent or hemodynamic instability requires permanent pacemaker |
| First-degree heart block | Prolonged PR interval for age | Observe, obtain digoxin level if on therapy |
| Mobitz type I (Wenckebach) second-degree heart block | Progressive lengthening of PR interval until P wave is not followed by conducted QRS complex | Observe, correct underlying electrolyte or other abnormalities |
| Mobitz type II second-degree heart block | Sudden nonconduction of P wave with loss of QRS complex without progressive PR interval lengthening | Consider pacemaker |
| Sinus tachycardia | Rate < 240 beats/min | Treat fever, remove sympathomimetic drugs |
AV, atrioventricular; ECG, electrocardiogram.
Ventricular tachycardia, defined as three or more consecutive PVCs, is also relatively rare in pediatric patients. Although there are multiple causes of ventricular tachycardia, it usually is a sign of serious cardiac dysfunction or disease. Rapid rate ventricular tachycardia results in decreased cardiac output and cardiovascular instability. Treatment in symptomatic patients is synchronized cardioversion. Medical management with lidocaine or amiodarone may be appropriate in a conscious asymptomatic patient. Complete evaluation of the etiologic picture is necessary, including electrophysiologic study.
Heart Block
First-degree heart block is the presence of a prolonged PR interval. It is asymptomatic and when present in otherwise normal children requires no evaluation or treatment. Second-degree heart block is when some, but not all, of the P waves are followed by a QRS complex. Mobitz type I (also known as Wenckebach) is characterized by a progressive prolongation of the PR interval until a QRS complex is dropped. It is often seen during sleep, usually does not progress to other forms of heart block, and does not require further evaluation or treatment in otherwise normal children. Mobitz type II is present when the PR interval does not change, but a QRS is intermittently dropped. This form may progress to complete heart block and may require pacemaker placement. Third-degree heart block, whether congenital or acquired, is present when there is no relationship between atrial and ventricular activity. The ventricular rate is much slower than the atrial rate. Congenital complete heart block is associated with maternal collagen vascular disease (systemic lupus erythematosus) or congenital heart disease. The acquired form most often occurs after cardiac surgery, but may be secondary to infection, inflammation, or drugs.
TREATMENT
Most atrial dysrhythmias require no intervention. Treatment of SVT depends on presentation and symptoms. Acute treatment of SVT in infants usually consists of vagal maneuvers, such as application of cold (ice bag) to the face. Intravenous (IV) adenosine usually converts the dysrhythmia because the atrioventricular node forms a part of the reentry circuit in most patients with SVT. In patients with cardiovascular compromise at the time of presentation, synchronized cardioversion is indicated using 1 to 2 J/kg. In patients with palpitations, it is important to document heart rate and rhythm during their symptoms before considering therapeutic options. The frequency, length, and associated symptoms during the episodes, as well as what is required to convert the rhythm, determine the need for treatment. Some patients require only education regarding the dysrhythmia and follow-up. Ongoing pharmacologic management with either digoxin or a β-blocker is usually the first choice. However, digoxin is contraindicated in patients with Wolff-Parkinson-White syndrome. Additional antiarrhythmic medications rarely may be needed. In patients who are symptomatic or those not wanting to take daily medications, radiofrequency ablation may be performed.
A variety of antiarrhythmic agents are used to treat ventricular dysrhythmias that require intervention (Table 142-3). Management of third-degree heart block depends on the ventricular rate and presence of symptoms. Treatment, if needed, often requires placement of a pacemaker.
TABLE 142-3 Classification of Drugs for Antiarrhythmia
| Class | Action | Example(s) |
|---|---|---|
| I | Depression of phase of depolarization (velocity of upstroke of action potential); sodium channel blockade | |
| Ia | Prolongation of QRS complex and QT interval | Quinidine, procainamide, disopyramide |
| Ib | Significant effect on abnormal conduction | Lidocaine, mexiletine, phenytoin, tocainide |
| Ic | Prolongation of QRS complex and PR interval | Flecainide, propafenone, moricizine? |
| II | β blockade; slowing of sinus rate; prolongation of PR interval | Propranolol, atenolol, acebutolol |
| III | Prolongation of action potential; prolongation of PR, QT intervals, QRS complex; sodium and calcium channel blockade | Bretylium, amiodarone, sotalol |
| IV | Calcium channel blockade; reduction in sinus and AV node pacemaker activity and conduction; prolongation of PR interval | Verapamil and other calcium channel blocking agents |
AV, atrioventricular.