Etapa 2. Identificación de criterios Neuroemocionales

Premature beats are common, but usually benign, arrhythmias and may arise in the atria, the atrioventricular junction, or the ventricles. By defi nition, premature beats are early and

Table 9-1

Bradycardia by Age and State

AGE HEART RATE

SURFACE ELECTROCARDIOGRAM

Neonates and infants ⬍100 beat/min, awake Children to 3 years _{⬍100 beats/min} Children 3–9 years ⬍60 beats/min Adolescents 9–16 years ⬍50 beats/min Adolescents ⬎16 years ⬍40 beats/min

AMBULATORY (HOLTER) MONITORING

Neonates and infants _{⬍60 beats/min, sleeping; 80 beats/min, awake, quiet} Children 2–6 years ⬍60 beats/min

Children 7–11 years ⬍45 beats/min Adolescents ⬎11 years ⬍40 beats/min

Cardiac Arrhythmias 99

thus are distinguished from escape or late beats occurring when higher pacemaker cells fail to produce an impulse at the expected interval. Two premature beats in a row constitute a couplet. If every second or third beat is a premature impulse, then a bigeminal or trigeminal rhythm is present.

Atrial Premature Contractions

Atrial premature contractions (APCs) are characterized by premature P waves with an axis and morphology that are diff erent from the sinus P waves. If an APC occurs when one of the bundle branches is refractory, then the premature beat will be conducted down the other bundle branch, resulting in an aberrant APC with a QRS morphology wider and diff erent from sinus QRS complexes (Figure 9-1). If both bundle branches are refractory, then the APC will not be conducted to the ventricles (blocked APC) but may reset the sinus node with a resultant pause greater than the previous RR interval. If every other beat is a blocked APC (blocked atrial bigeminy) in a newborn infant who is dependent on an adequate heart rate for normal cardiac output, then slowing of the heart rate suffi cient to alter feeding and arousal time may be present. T waves are usually smoothly inscribed, and consistent sharp defl ections in the T waves may represent P waves (Figure 9-2). APCs usually occur with normally conducted QRS complexes; but if wide beats are also noted, then the apparently prolonged QRS beats are likely to be aberrant APCs because premature atrial and ventricular contractions rarely occur together, especially in the newborn period.

Th e incidence of APCs is 50% to 75% in children on Holter monitoring. Most are benign and require no therapy; however, there are occasional associations with myocarditis, atrial stretch, sympathomimetic or other stimulant drugs, intracardiac catheters, and elec- trolyte disturbances. Th ey are most often without an obvious incitant and are usually not

0.84 0.48 0.97 200 150 100 50 Figure 9–1

Atrial premature contractions (arrows) with normal and aberrated conduction.

Figure 9–2

Every other beat is a blocked atrial premature contraction (blocked atrial bigeminy) represented by a consistent sharp defl ection in the T waves.

recognized by the child or adolescent. If suppressive therapy is required, then either digoxin or propranolol is suitable.

Premature Ventricular Contractions

Premature ventricular contractions (PVCs) are less common than APCs but may be present on Holter monitoring in up to 25% of healthy infants, children, and adolescents. PVCs are characterized by a QRS morphology that is diff erent from sinus QRS beats, occur before the next expected sinus beat, and are not preceded by a premature P wave. Th e QRS duration may be only slightly prolonged. Uniform PVCs have similar morphology to one another, and multiform PVCs have diverse morphology. Th e designations unifocal and multifocal are

no longer used, because the form of PVCs is now known not to correlate reliably with focus of origin. If a PVC occurs late, at the beginning of the next expected sinus beat, then it will produce a hybrid or fusion beat derived, in part, from the normal conduction pathways and, in part, from the PVC. Fusion beats have a morphology that is intermediate between the sinus QRS and PVC.

Although most PVCs are observed in healthy children and adolescents, PVCs can occur in patients with underlying heart disease, such as myocarditis, hypertrophic and dilated cardiomyopathies, and ventricular dysfunction in congenital cardiac malformations. Th e new appearance of PVCs in the setting of a febrile illness should raise the question of myocarditis. Other causes include sympathomimetic and street stimulant drugs, electrolyte imbalances, and intraventricular catheters. A 12-lead ECG should always be obtained to assess the premature beat morphology and to look for chamber enlargement but also to calculate the corrected QT interval.

QTc QT interval (seconds) Preceding RR inter

=

vval (seconds)

PVCs are considered benign if no evidence of heart disease exists, the QTc is normal (ⱕ0.44 second), the family history is not adverse (no sudden premature deaths or cardiac arrests, important arrhythmias, or cardiomyopathies), and the PVCs are uniform in appear- ance and are either suppressed or not aggravated with exercise. Conversely, the presence of any of these risk factors should prompt referral for further investigation. Because underlying heart disease may be subtle, an echocardiogram to assess cardiac structure and function is usually obtained in referred patients.

Benign PVCs do not require treatment or curtailment of exercise, even if a bigeminal rhythm is present. However, if frequent benign PVCs persist, then cardiology surveillance should be arranged to detect the unusual situation of arrhythmia-induced ventricular dila- tion or dysfunction, especially if the ectopy burden constitutes more than 5% of the total beats on a 24-hour ambulatory electrocardiogram.1 _{PVCs that are not clearly benign require} the expertise of a pediatric cardiologist to determine whether there is a need for therapy. Ventricular couplets are assessed in the same manner, but triplets represent ventricular tachy- cardia and are discussed later in this chapter.