Case
Hi, I’m calling to let you know about a newborn infant that is full-term but transferred to the NICU because of a persistent tachycardia that was noted after delivery. The heart rate seems to remain high regardless of what the baby is doing. The baby seems stable to me, but the heart rate is definitely higher than I would expect. We have an ECG of it but, I have to admit, it’s a bit hard for me to interpret.
What am I thinking?
Usually, when I get a call like this, I am thinking about a few different types of tachycardia. A few of the key points in this call are as follows: (1) the baby is stable, (2) the baby is a full-term newborn, (3) the tachycardia has persisted since delivery. Perhaps a bit more subtle are the comments made by the caller that often strikes me as telling. Stating that a heart rate is “higher than I would expect” usually clues me in to consider heart rates that could be considered within the normal range. Often, when a patient has a more typical accessory pathway-mediated, reentrant, supraventricular tachycardia, the heart rate is what the caller leads with (i.e., heart rate is 220 bpm). Here, I am receiving the clue that the heart rate is not that high. Another comment is that the ECG is a “bit hard for me to interpret” suggesting that the ECG does not look entirely normal but it is not obvious that it is abnormal. These types of cases can be exciting for an electrophysiologist (EP) as we rely heavily on our diagnostic capabilities, utilizing our knowledge of arrhythmias, diagnostic maneuvers, and ECG tracings.
| Differential diagnosis |
|---|
| Likely |
| Atrial flutter Atrioventricular reentrant tachycardia, accessory pathway-mediated Sinus tachycardia secondary to sepsis or hypovolemia |
| Possible |
| Automatic atrial ectopic tachycardia Multifocal atrial tachycardia Congenital junctional ectopic tachycardia Atrioventricular nodal reentrant tachycardia Persistent junctional reciprocating tachycardia |
| Rare |
| Ventricular tachycardia Sinus tachycardia secondary to hyperthyroidism |
History and physical
As with any newborn tachycardia, it is important to establish the onset of the tachycardia. Was the tachycardia noted in fetal life? Immediately after delivery? Sudden onset later in the newborn period? Fetal tachycardias often reflect atrial arrhythmias but can also represent pathway mediated tachycardias and others. On many occasions, the fetal atrial arrhythmia resolves and does not recur after delivery—but this is not always the case. If the arrhythmia was noted only immediately after delivery, the possibility of atrial flutter should be strongly considered. In general, arrhythmias that have a sudden onset later in the newborn period are more suggestive of a reentrant form of tachycardia. History should also elicit any history of maternal infection or fever to evaluate for potential sepsis. Feeding history and assessment of urine output can be helpful to determine volume status and a compromise of the cardiac output.
Characteristics of the arrhythmia itself can assist in determining its etiology. At this time, it would be prudent to review some basic concepts of arrhythmias to further assist in the understanding, diagnosis, and management of pediatric arrhythmias.
Pediatric arrhythmias can be categorized by the arrhythmia mechanism: namely reentrant, automatic, or triggered. The most common mechanism in the pediatric patient is reentry (>90%), followed by automatic (∼10%) and triggered as a distant third. Reentrant arrhythmias can be reflected by the circuitous nature of the propagation of the arrhythmia, usually around an anatomic or electrophysiologic barrier (see Fig. 3.1 ). Given a specified path of the reentrant arrhythmia, there is often minimal to no variation in arrhythmia rate and is reflected clinically as a persistent rate with sudden start and stop. Automatic tachycardias, in contrast, originate as the insidious firing of a group of myocardial cells. As there is no specified path for the arrhythmia to propagate, the rate can vary and often can be subject to the influence of the catecholamine state. This typically presents clinically as a “warm up” or “cool down” variation in heart rate that can be exacerbated by physiologic stress and alleviated with a resolution of physiologic stress (i.e., sedation).
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