Although certain arrhythmias are more common in neonates and young infants compared to older children and adults, all types of arrhythmias can occur. Many are benign and do not cause hemodynamic compromise. Others may diminish cardiac output and cause decreased blood pressure and decreased perfusion. Sustained tachyarrhythmias may eventually cause myocardial dysfunction, which is known as tachycardia-induced cardiomyopathy. The purpose of this chapter is to review diagnosis and management of common arrhythmias in neonates and young infants.
MECHANISMS OF ARRHYTHMIAS
The electrical impulse normally originates in the sinoatrial (SA) node. The atrioventricular (AV) node, His bundle, and bundle branches provide the only normal pathway for transmission of impulses between the atria and ventricles. Generation of impulses from the SA node is modulated by many factors, including body temperature, blood pressure, autonomic nervous system, and circulating catecholamines. Abnormalities in any of these factors can result in bradycardia or tachycardia that are not related to any specific cardiac disorder.
Conduction through the AV node is slowed so that atrial contraction is complete before ventricular contraction occurs. If the SA node fails to depolarize, the AV node can function as an escape pacemaker.
Abnormal Impulse Formation
Abnormalities in impulse formation result in sinus bradycardia and tachycardia, premature atrial and ventricular contractions, and ectopic or automatic rhythms from the atria, AV node, or ventricles. Automatic tachycardias are usually incessant (ie, they are almost always present). Increased automaticity occurs when atrial, nodal, or ventricular cells display autonomous repetitive depolarization at a higher rate than is normal. This type of tachycardia is sometimes associated with fever, hypoxemia, electrolyte disturbances, or infusion of intravenous sympathomimetic agents. Sinus tachycardia can be considered an automatic tachycardia, but it is rarely spontaneous and characteristically resolves when the abnormal stimulus resolves. In contrast, other forms of automatic tachycardia, such as atrial ectopic tachycardia, junctional ectopic tachycardia, and the automatic form of ventricular tachycardia, may be spontaneous or triggered by the aforementioned stimuli. Regardless of site of origin, onset and termination are often gradual rather than abrupt. The rate of an automatic tachycardia is often sensitive to changes in autonomic tone. Therapies that produce only transient effects, such as direct current (DC) cardioversion and administration of adenosine, do not terminate automatic tachycardias.
Abnormal Impulse Conduction
Block within the normal conduction system is the most obvious form of abnormal impulse conduction. Block can occur at any location, but atrioventricular block is the most common site.
Re-entry, the other form of abnormal impulse conduction, is an important mechanism underlying supraventricular tachycardia in infants. The re-entrant circuit involves two functionally distinct pathways that have different conduction velocities and refractory periods (Figure 10-1). Under the right circumstances (often in response to a premature atrial contraction), an electrical impulse arrives when one of the pathways is refractory. The impulse ...