Disorders of rate and rhythm are fortunately rare in the pediatric population. The most common dysrhythmia is supraventricular tachycardia. Rhythm disturbances, such as sinus bradycardia, can be life-threatening, particularly in the neonate.

Dysrhythmias in children that are the result of cardiac lesions have a poorer prognosis than patients with a structurally normal heart. Noncardiac causes, such as hypoxia, electrolyte disturbances, toxins, and inflammatory disease, must be considered, as should cardioactive drugs, such as digoxin or over-the-counter cold remedies. The initial evaluation includes an electrocardiogram (ECG).

Age is an important consideration in the child presenting with a dysrhythmia. Age is also a factor in the clinical presentation of the dysrhythmia. A young infant may present with poor feeding, tachypnea, irritability, or signs of a low output state. Caregivers often note that their baby is “not acting right.” An older child often presents with more specific symptoms, such as syncope from decreased cerebral blood flow, chest pain from decreased coronary blood flow, or palpitations. The ventricular rate in third-degree heart block may be adequate for the 2-month-old child, but will not provide an adequate cardiac output for a 12-year-old child. Adolescents involved in competitive athletics who present with syncope, palpitations, or worrisome chest pain should be evaluated promptly. Normal ranges for heart rate and blood pressure are listed in Tables 43-1 and 43-2.

The initial emergency management of dysrhythmias is dependent on three factors: rate, QRS width, and clinical stability. Management decisions should be based on 12-lead ECG interpretation, since single-lead monitor strips can be misleading. Rapid rates may appear supraventricular in origin in the child with tachycardia. Children tolerate most rhythm disturbances well, providing ample time for precise interpretation.

Since dysrhythmias are relatively uncommon in the pediatric patient population, high-fidelity simulation has been shown to be useful for training purposes. Simulation training has been shown to decrease stress levels and increase levels of skill satisfaction in emergency care providers. Both technical and nontechnical skills showed significant improvement in those video-recorded, when compared with control groups.¹

SINUS BRADYCARDIA

Sinus bradycardia may be a manifestation of serious underlying disease or a normal physiologic variant; therefore, each child must be approached individually. Athletes commonly exhibit bradycardia, which is a normal finding. Serious causes of bradycardia include hypoxia, hypoglycemia, hypothyroidism, hypo- or hyperkalemia, tension pneumothorax, cardiac tamponade, toxins, coronary or pulmonary thrombosis, or increased intracranial pressure. Sinus bradycardia can be a manifestation of calcium-channel blocker, β-blocker, or digoxin toxicity. Treating the underlying condition often corrects the rate. If the cause is unclear and oxygenation and ventilation are adequate, compressions should be initiated in an unstable patient. In a recent multihospital cohort study, pediatric patients who had chest compressions initiated for bradycardia and poor perfusion prior to the onset of pulselessness, were more likely to survive to discharge.² Epinephrine should be given (1:10,000, at 0.01 mg/kg IV/IO or 1:1000, at 0.1 mg/kg via the endotracheal tube). The maximum dose of epinephrine is 1 mg IV or 2.5 mg by the endotracheal route. High-dose epinephrine via the intravenous route is no longer recommended unless there is concern for β-blocker overdose.³ Atropine, 0.02 mg/kg (minimum dose 0.1 mg), is reserved for patients with either vagally mediated bradycardia or first- and second-degree heart blocks. It is important to note that small doses <0.1 mg may produce a paradoxical bradycardia. Thus, minimum dose is 0.1 mg and the maximum dose for children is 0.5 and 1.0 mg for adolescents.^4–6

ATRIOVENTRICULAR BLOCKS

Complete atrioventricular (AV) block may be congenital or acquired. Congenital blocks associated with structural disease, such as an AV canal, have a poorer prognosis than blocks associated with maternal collagen vascular disease, such as Lupus. In the latter, maternal antibodies cause fibrosis and destruction of the conduction system. Complete AV block is suspected in utero in the setting of sustained fetal bradycardia, polyhydramnios, and congestive heart failure (CHF). Rates of 50 to 80 beats per minute (bpm) are typical in complete AV block. Symptoms are rate dependent, and most patients with rates >50 bpm are rarely symptomatic. An alternative explanation for instability must be pursued in patients with heart rates approaching 80 bpm. Treatment of neonatal symptomatic bradycardia due to AV block includes control of CHF, isoproterenol, and temporary transcutaneous, transthoracic, or umbilical transvenous pacing.

Acquired third-degree heart block is associated with myocarditis, endocarditis, rheumatic fever, cardiomyopathy, Lyme disease, or tumors. Additional reversible causes such as drugs of abuse, medications, and herbal supplements should be investigated.⁷ Postoperative blocks are less common today because of advances in intraoperative mapping. Postoperative blocks may last for years or occur years after surgery. Unlike congenital third-degree block, QRS complexes are usually wide. Treatment is similar, except patients with syncope must be paced immediately.

PACEMAKERS IN CHILDREN

The indications for pediatric pacemakers differ from indications in adults. The most common indication is for symptomatic bradycardia. Occasionally, an asymptomatic child with an extremely low heart rate needs pacing. Postoperative or acquired AV blocks require permanent pacing. Other indications include long QT syndrome (LQTS) and cardioinhibitory syncope lasting >10 seconds.

Advances in adult pacemakers have improved the management of children with dysrhythmias. Most permanent pediatric pacemakers are transvenous. Epicardial units are reserved for premature infants and those with right-to-left shunts. The choice of mode depends on the particular disease. For example, children with sinus disease require atrial pacing. Ventricular pacing is unnecessary because AV conduction is normal. Children with congenital or acquired AV block require dual-chamber pacing. Isolated ventricular pacing is employed in the very young. Most units can be programmed to sense, demand, or inhibit at the atrial or ventricular level, depending on the needs of the child. In addition, they may be programmed to sense motion or breathing.

Syncope or palpitations in a child with a pacemaker suggests malfunction. Chest radiography may reveal wire fracture or lead displacement. Most malfunctions are not mechanical, and require external reprogramming. If the issue is not easily resolved, the patient should be admitted to the hospital for observation and cardiologist consultation.

Temporary transvenous pacemakers are rarely necessary in children. Most temporary pacing is transcutaneous. Transthoracic pacing via pericardiocentesis catheter should be considered in the very unstable infant.

SINUS TACHYCARDIA

Sinus tachycardia is defined as a rate of sinus node discharge higher than normal for the patient’s age. In early versions of the Pediatric Advanced Life Support (PALS) resuscitation guidelines, sinus tachycardia was considered a dysrhythmia. However, sinus tachycardia is a common, normal presentation and is often caused by such benign conditions as fever, dehydration, pain, and anxiety. Sinus tachycardia may also be associated with pathologic conditions such as anemia, sepsis, hypoxia, hyperthyroidism, and drug ingestions. More serious, but less common causes include cardiac tamponade, tension pneumothorax, and thromboembolism. The treatment of sinus tachycardia is directed toward treating the underlying condition.⁸

SUPRAVENTRICULAR TACHYCARDIA

The most common dysrhythmia during childhood is supraventricular tachycardia (SVT). SVT is a narrow complex tachycardia (QRS ≤0.09 seconds), and is differentiated from sinus tachycardia by its abrupt onset, rates >220 bpm, the absence of normal P waves (Fig. 43-1), and little rate variation. SVT occurs with an estimated incidence of 1/250 to 1/1000 children. The prognosis for most pediatric patients is excellent. Previously, the fatality rate was poorly defined for SVT. A recent study of 1755 patients with SVT reported a fatality rate of 4%, with only 1% of deaths occurred without associated structural heart disease. Case fatality rate was higher in infants <1 month of age, in patients with structural heart disease, and in children with cardiomyopathy.⁹

Symptoms of SVT in infants include poor feeding, tachypnea, and irritability. They may appear ill or septic. Approximately 50% present within the first year of life, and likely present in congestive heart failure. Infants usually present within the first 24 hours. There are two mechanisms to consider: AV reciprocating tachycardia or AV nodal re-entry. Younger children are more likely to have accessory pathway tachycardia, which is very important in choosing treatment.

AV reciprocating tachycardia or accessory pathway tachycardia is most common in children. Conduction during SVT is usually orthodromic, with antegrade AV conduction and retrograde accessory pathway conduction (Fig. 43-2). Conduction during sinus rhythm can be via the accessory pathway, resulting in a short PR interval and appearance of a delta wave. This characterizes the Wolff–Parkinson–White (WPW) syndrome. Some accessory pathways only conduct retrograde during bouts of SVT and are termed “concealed” because they are not apparent on surface ECG.

The other mechanism, AV nodal re-entry, is more common in adults, but may be responsible for one-third of cases of SVT in adolescents. Within the AV node, fast pathways with long refractory periods are blocked during a premature atrial contraction (PAC), allowing for antegrade conduction down the slow tract. The impulse then propagates up the fast tract, initiating re-entry. Distinguishing nodal from accessory pathway SVT is often difficult during episodes of SVT. Negative P waves in II, III, and avF may indicate retrograde conduction through the accessory pathway, but they are usually buried in the QRS complex. Pointed or peaked T waves suggest retrograde P waves. In contrast, P waves are almost never seen in AV nodal re-entry. The lack of a delta wave during sinus rhythm does not rule out a concealed accessory tracts. Information from parents may be helpful, but first episodes of SVT or previously unstudied children make diagnosis difficult in the ED.