Appropriate Versus Normal Heart Rate

Normal heart rate ranges vary tremendously during childhood as a function of age and autonomic tone. Thus in a given clinical situation, “appropriate” heart rate is a more useful concept than “normal” heart rate. Critically ill patients typically manifest some degree of sinus tachycardia in response to pain, sepsis, shock, fever, or adrenergic agonist infusions, and the degree of tachycardia also serves as a gauge of pain or hemodynamic instability. Thus inappropriately fast or slow rates for a given circumstance warrant evaluation for underlying factors affecting the sinus rate or the possibility of a non-sinus mechanism.

Sinus Bradycardia and Sinus Pauses

Sinus bradycardia may result from high vagal tone, hypothermia, acidosis, increased intracranial pressure, drug toxicities, or direct surgical trauma to the sinoatrial (SA) node. In otherwise well patients, intermittent sinus bradycardia or prolonged sinus pauses may be caused by intense vagal episodes, such as those occurring during neurocardiogenic syncope. Whereas vagal stimulation may produce profound bradycardia, pauses, or even asystole lasting for several seconds, transient bradycardia should not be construed as an absolute indication for pacing. However, in the hemodynamically tenuous patient, persistent or recurring bradycardias, whether attributed to sinus node exit block (periodic loss of sinus impulse) or sinus arrest, often warrant intervention with vagolytic, sympathomimetic, or pacing therapies. It is important to recognize that blocked premature atrial depolarizations (where premature P waves may be obscured in the preceding T wave) may also mimic sinus pauses or even sinus bradycardia when occurring in a bigeminal pattern. In cardiac patients, sinus node dysfunction may be the result of surgical injury or heterotaxy syndromes. Primary sinus node dysfunction in childhood is rare but has been described.³

Conduction Abnormalities

First-degree, second-degree, and third-degree AV blocks are characterized by conduction delay, intermittent interruption, or complete interruption in AV conduction. As with sinus bradycardia, AV conduction delay may be the result of intense vagal tone, metabolic derangements, drug toxicity, or direct injury to the AV node. Second-degree block can be further characterized: Mobitz type I, also called Wenckebach conduction, displays progressively prolonged AV conduction prior to a single nonconducted atrial impulse, whereas Mobitz type II occurs abruptly without such delay. Wenckebach conduction is best recognized by comparing the PR interval prior to block to the conducted PR immediately after the blocked beat. Mobitz I usually represents block in the AV node and is less likely to progress suddenly to high-grade block. In some settings, such as in well-conditioned athletes, a Mobitz I block may be benign. Mobitz type II, characterized by abrupt failure to conduct without prior lengthening of the PR interval, usually is attributed to block within the His conduction system and may indicate greater potential for sudden progression to complete AV block. As such, type II block may be more ominous and may require more aggressive intervention (i.e., pacing).

Higher grades of second-degree AV block can occur as a progression from either Mobitz I or Mobitz II block and are best characterized by the ratio of atrial to ventricular depolarizations (2:1, 3:1, 4:1, etc.). The level of block cannot be inferred and may even occur physiologically in the setting of atrial tachyarrhythmias, including atrial flutter, which often result in second-degree AV block in the presence of normal AV nodal function. Likewise, vagally mediated AV block may result in transient high-grade block (although the sinus rate usually slows concurrently).

Complete or third-degree AV block represents complete loss of AV conduction, usually with a junctional or idioventricular escape rhythm that is regular but may be quite slow. Periodic shortening of the RR interval may be the only clue to distinguish complete AV block from high-grade second-degree block with intermittent conduction (Figure 28-1) or from a junctional rhythm with slower atrial rate and intermittent AV conduction.

Figure 28–1 Complete AV block, presumably congenital, in an asymptomatic 9-year-old with slow resting heart rate. Note the regular RR interval, which confirms complete rather than incomplete (second-degree) AV block.

Bundle branch block patterns occur when impaired conduction in the specialized intraventricular conduction system results in delayed right or left ventricular depolarization, resulting in an aberrant widened QRS complex. Bundle branch block and AV block sometimes represent normal physiologic responses to abrupt shortening of the cycle length (as with premature atrial systoles or tachycardia initiation) or may result from drug effects, surgical injury, or primary disease within the specialized conduction tissue.

Classification by Mechanism

As discussed earlier, some degree of sinus tachycardia is expected in most critical care patients as an appropriate response to the primary illness. The degree of sinus tachycardia for age may provide important insights into the level of sedation, pain, or hemodynamic stress of a given patient. However, exaggerated or persistent sinus tachycardia must be distinguished from other tachycardia mechanisms that may appear similar electrocardiographically.

Most abnormal tachycardias encountered clinically are caused by abnormal impulse propagation in the form of reentry. This may represent reentry using an accessory AV connection (AV reentry), the AV node and its adjacent tissues (AV nodal reentry), atrial myocardium (intraatrial reentry including atrial flutter and fibrillation), or ventricular myocardium (most ventricular tachycardias). Automatic tachycardias represent abnormal impulse formation arising from either ectopic foci or usual subsidiary pacemaker tissues (atrial, junctional, or ventricular) but at a significantly accelerated rate. These tachycardias may be due to an abnormally accelerated rate of depolarization of normally automatic tissues or to diseased atrial or ventricular myocardium with a propensity to abnormal spontaneous depolarization. Triggered tachycardias are thought to arise from abnormal secondary depolarizations (afterdepolarizations) following normal myocardial depolarizations, which may propagate to adjacent tissues. These tachycardias probably are important in several specific situations such as cardiac glycoside toxicity (delayed afterdepolarizations) and drug-induced long QT syndromes (early afterdepolarizations), and they also are important in many hereditary arrhythmias syndromes. Triggered activity is often dependent on the underlying heart rate, a feature that may sometimes be exploited therapeutically.

Classification by Site

Tachycardias usually are subdivided first according to the site of origin as supraventricular or ventricular. This anatomic distinction is the basis for most treatment algorithms. However, both supraventricular and ventricular tachycardias include a diverse group of arrhythmias with varying substrates, mechanisms, and electrocardiographic features that become increasingly important when simple treatment algorithms fail or when arrhythmias become recurrent and require repeated or ongoing therapies.

Supraventricular Tachycardias

“Supraventricular tachycardia” (SVT), “paroxysmal atrial tachycardia,” and “paroxysmal supraventricular tachycardia” (PSVT) are descriptive but nonspecific terms commonly used interchangeably to describe tachycardias with a regular rate (usually in excess of 200 to 220 beats/min), normal QRS morphology, and P waves that either are not discernible or follow the QRS complex. This phenotype represents the most common form of SVT seen in otherwise healthy neonates and children and usually can be attributed to AV nodal reentry or AV reentry using an accessory connection (see next section). However, these typical ECG features can be produced by a more diverse array of tachycardia mechanisms.⁵ Furthermore, intermittent AV block or QRS prolongation may be observed in certain types of “SVT,” such that the ECG distinction of “SVT” from other atrial arrhythmias becomes obscured. Likewise, some tachycardias of supraventricular origin are associated with a widened QRS, either because of rate-related bundle branch block or anomalous antegrade conduction through an accessory connection. Therefore it is most useful to include among SVTs all tachycardias originating from the atrium, the AV node, or both, regardless of whether the ventricles participate primarily (i.e., AV reentry) or merely as a secondary consequence of AV conduction. This broad and inclusive definition appropriately allows inclusion of nonreciprocating mechanisms that need to be included in the differential diagnosis of “SVT,” such as intraatrial reentry.

Atrioventricular Reciprocating Tachycardias

AV reciprocating tachycardias use one or more accessory AV connections to allow a reentrant circuit to develop involving both atrial and ventricular tissues. By definition, they display a fixed 1:1 AV relationship. Orthodromic reciprocating tachycardia (ORT) is the most common AV reentrant tachycardia and, in otherwise normal infants, also is the most common mechanism of SVT.^5,6 In ORT, antegrade conduction is over the AV node, whereas retrograde conduction to the atria occurs via an accessory AV connection. QRS morphology and duration usually are normal, with retrograde P waves often evident following each QRS complex. If the accessory connection conducts antegradely during sinus rhythm, ventricular preexcitation occurs prior to conduction over the AV node (Wolff-Parkinson-White [WPW] syndrome). The fusion of preexcited ventricular depolarization with the normal depolarization of the AV node and His-Purkinje system produces the characteristic short PR interval and Δ wave of WPW syndrome. Many patients experiencing ORT have normal QRS morphology during sinus rhythm. In these individuals the accessory pathway may only conduct retrogradely and is thus clinically evident only during tachycardia or during ventricular pacing.

Antidromic reciprocating tachycardia (ART) is a much less common AV reciprocating tachycardia in which the circuit is reversed: antegrade conduction occurs exclusively via the accessory connection and results in a “maximally preexcited” QRS. As a result, ART is not readily distinguishable from ventricular tachycardia by ECG features alone. Retrograde conduction occurs over the AV node (or a second accessory connection), producing a 1:1 ventricular-atrial (VA) relationship. By definition, patients with ART also have the ECG features of WPW syndrome during sinus rhythm. ART should be distinguished from ORT with aberrant conduction.

A specific form of antidromic AV reentry uses Mahaim fibers, which are accessory AV connections with decremental antegrade conduction. Most Mahaim fibers are located on the right ventricular free wall (atriofascicular connections), although some arise from the AV node itself (nodoventricular connections). Tachycardia using a Mahaim fiber should be considered in a young patient with a regular tachycardia and left bundle branch block QRS pattern. Typically, ART and tachycardia using Mahaim fibers have a 1:1 VA relationship. However, because retrograde conduction in either case may be supported over a second accessory connection, maneuvers typically resulting in AV nodal block may not terminate these tachycardias, further confusing clinical distinction between these wide QRS complex tachycardias and ventricular tachycardia.

Permanent junctional reciprocating tachycardia (PJRT) is a variant of ORT with retrograde conduction over a slowly conducting accessory AV connection that possesses decremental (“AV nodelike”) conduction.⁷ The relative conduction and refractory properties of the accessory connection and the AV node are such that the PR interval is short or normal and tachycardia is incessant. In a single-lead rhythm strip, PJRT may mimic sinus tachycardia, although a 12-lead ECG reveals atypical P wave morphology with P-wave inversion in the inferior leads. This tachycardia typically displays repeated spontaneous termination and prompt reinitiation, resulting in incessant tachycardia until it is adequately treated (Figure 28-2).

Figure 28–2 Supraventricular tachycardia resulting from the permanent form of junctional reciprocating tachycardia. Note the slow rate, long RP and short PR interval, and inverted P waves in ECG leads II and III. At rest, this rhythm often shows incessantly repetitive termination (with retrograde block), followed by immediate reinitiation (after single, isolated sinus complexes). With exercise, this rhythm often is faster and sustained, rendering it electrocardiographically indistinguishable from the atypical form of nodal reentry.

Atrioventricular Nodal Reentrant Tachycardia

AV nodal reentrant tachycardia (AVNRT) is the most common cause of SVT in older children and young adults without WPW syndrome or structural heart disease. It is seen less commonly in infants.^5,6 Occasionally it is precipitated for the first time by a serious illness or by other secondary factors associated with arrhythmias in the intensive care unit (ICU). This tachycardia can be attributed to so-called “dual AV nodal physiology.” Conceptually, one functional “limb” of the AV node typically displays slow conduction and a short refractory period, whereas the other limb typically displays more rapid conduction but a longer refractory period. The differential conduction between the two “limbs” of the AV node (slow and fast pathways) provides the functional substrate for reentry. In actuality, these “limbs” represent differential conduction properties of the fibers inputting the AV node from upper and lower approaches of the atrial septum, representing so-called “fast” and “slow” inputs.

Classically, two electrocardiographically distinct forms of AVNRT may occur. In the “typical” form of AV node reentry, antegrade conduction during tachycardia is over the slow AV node inputs, and the P waves often are obscured by the preceding QRS complex. In the “atypical” form of AV node reentry, antegrade conduction is via the fast inputs of the AV node and retrograde conduction is over the slow limb. This conduction results in a long RP and short PR with an inverted P wave. The typical form of AVNRT can be difficult to distinguish from ORT in which P waves also are often obscured. The atypical form of AVNRT may be indistinguishable from PJRT (see previous section), except that the tachycardia is paroxysmal rather than incessant. Like PJRT, atypical AVNRT must be carefully distinguished from other tachycardias with a normal PR interval, including sinus tachycardia, intraatrial reentry, or ectopic atrial tachycardias (see next section). Other atypical forms of AV nodal reentry using “intermediate” pathways can occur but are uncommon in children. Other variations of AVNRT can be characterized during the course of formal intracardiac electrophysiologic study.

Primary Atrial Tachycardias

Primary atrial tachycardias represent a diverse group of tachycardias originating solely from atrial tissue. They include tachycardias with discrete P waves (ectopic atrial tachycardia, intraatrial reentry), sawtooth flutter waves (atrial flutter), or disorganized atrial activity (atrial fibrillation, chaotic atrial tachycardia).⁸ The ECG appearance alone may not adequately distinguish the underlying mechanism.

In all cases, conduction to the ventricles is over the AV node (except in patients with associated WPW syndrome). The resulting ventricular rate determines the degree of clinical compromise during these tachycardias. If conduction is rapid or occurs over an accessory connection, the QRS morphology may be aberrant and difficult to distinguish from ventricular tachycardias. However, interventions that slow or block AV nodal conduction usually allow the ongoing and faster atrial rhythm to be revealed. It is useful and often necessary to directly record atrial depolarization (via esophageal, epicardial, or intraatrial recordings) to discern atrial activation. Despite the potential ECG similarities of the various primary atrial tachycardias, the varying mechanisms confer important differences in clinical behavior.

Most atrial tachycardias encountered in the intensive care setting are reentrant in nature. Most commonly these atrial tachycardias occur either in neonates, where the classic saw-toothed pattern of atrial flutter is observed, or in postoperative cardiac patients. In patients with congenital heart disease (CHD), the patterns of intra-atrial activation may be quite variable and depend upon the surgical anatomy and resultant scar and conduction slowing. As such, the tachycardia, often referred to as intra-atrial reentrant tachycardia (IART), often displays a slower atrial rate with more discrete and sometimes normal-appearing P waves (rather than classic “flutter” waves). Because of the slower atrial rate, 1:1 AV conduction may be especially common. The administration of an AV node–blocking agent may slow AV conduction, and especially if 2:1 AV conduction results, ongoing tachycardia may be mistaken as sinus tachycardia with first-degree AV block. Thus this arrhythmia should be considered with any monotonous and seemingly inappropriate sinus rate with PR prolongation in a patient with CHD. Careful inspection of any transient irregularities that may result from variations in the AV conduction ratio may reveal the diagnosis.

Atrial fibrillation, a very common arrhythmia among the elderly, is far less common in pediatric patients. It may occur as the result of atrial myocarditis,⁹ as a result of an underlying reentrant SVT,¹⁰ or sometimes as the result of central venous catheters (Figure 28-3). In patients with WPW syndrome, rapid conduction over the accessory pathway may be life-threatening. When atrial fibrillation is seen, the underlying basis should be sought, because the long-term implications and treatment measures are much different than in adult patients.

Figure 28–3 Sustained atrial fibrillation in a previously healthy 17-year-old placed on extracorporeal membrane oxygenation for pneumonia and acute respiratory distress syndrome. Review of stored telemetry revealed atrial ectopy soon after cannulation, eventually initiating atrial fibrillation. Following DC cardioversion to sinus rhythm, frequent ectopy persisted until the venous cannula was repositioned. Several months later, the patient remained free of further arrhythmias.

Ectopic atrial tachycardia is an automatic arrhythmia that typically presents as an incessant and chronically elevated atrial rhythm that may be mistaken for sinus tachycardia, depending on the site of the automatic focus. First-degree AV block may be seen as a result of the inappropriate rate. Patients often experience no overt palpitations but rather present with ventricular dysfunction and sometimes frank congestive heart failure. In such cases, careful scrutiny of the P wave morphology and evaluation of any abrupt changes in rate (as the result of transitions between sinus and the tachycardia) are necessary to establish the diagnosis. Adenosine may inhibit the automatic focus, making this diagnosis especially difficult.

Chaotic atrial tachycardia is an uncommon arrhythmia that is usually observed in infants and toddlers, often in association with a viral respiratory illness.¹¹ The hallmark features are a rapid and irregular atrial rate, often exceeding 300 bpm, and presence of multiple P-wave morphologies. The resulting ventricular response is irregularly irregular, simulating atrial flutter. However, this rhythm is probably the result of multiple triggered foci within the atria, and thus acute termination measures (i.e., DC cardioversion, adenosine, or pacing) are of little benefit. Usually this arrhythmia resolves within weeks or months of presentation.

Junctional Ectopic Tachycardia

Junctional ectopic tachycardia (JET) probably arises from an abnormal automatic focus or a protected microreentrant circuit in the region of the AV node or proximal His bundle. Antegrade conduction usually is over the normal His-Purkinje system with a narrow QRS. Retrograde (VA) block or complete VA dissociation with a slower atrial rate aids in the recognition of this mechanism. Variants include a congenital form, the more common postsurgical form, and paroxysmal JET described primarily in adults.^12,13 As in primary atrial tachycardias, atrial depolarization may be obscure, and direct atrial recordings aid the diagnosis. Occasionally JET is associated with 1:1 VA conduction, in which case additional pacing or pharmacologic maneuvers are necessary to distinguish it from other mechanisms of SVT.

Ventricular Tachycardias

Ventricular tachycardias include all tachycardias that arise exclusively within the ventricle(s) and require neither the atrium nor the AV node for perpetuation. Because ventricular depolarization is aberrant, the QRS duration is always prolonged for a given age and heart rate. The QRS morphology may be either uniform or changing (bidirectional, polymorphic). Classically, ventricular tachycardias are associated with VA dissociation (atrial rhythm at a slower rate). However, in children, VA conduction over the AV node (or an accessory connection) may be sufficient to allow intermittent or even 1:1 VA conduction. Thus VA dissociation, when present, is helpful, but when it is absent (or uncertain) it does not exclude ventricular tachycardia as the underlying mechanism. The presence of periodic fusion complexes (QRS morphology intermediate between tachycardia morphology and sinus morphology) is virtually pathognomonic for ventricular tachycardia with VA dissociation.

Although often regarded as a homogeneous group of arrhythmias, ventricular tachycardias actually constitute diverse rhythms, representing each of the underlying tachycardia mechanisms (reentry, automaticity, and triggered activity) with important therapeutic implications.¹⁴ Likewise, although they are sometimes lethal, they may range in complexity and severity from benign accelerated ventricular rhythm to rapid polymorphic ventricular tachycardia and ventricular fibrillation. Both the clinical setting and the QRS morphology during ventricular tachycardia may provide important clues to the mechanism and pathogenesis, anatomic origin or tachycardia focus (see incessant ventricular tachycardias), and treatment strategies, as discussed later.

Bradycardias

In the absence of AV block, bradycardias are characterized by the origin of the initiating impulse as sinus, atrial, junctional, or ventricular. It is important to distinguish junctional or ventricular bradycardia from sinus bradycardia with an underlying junctional or ventricular escape, respectively. Terms such as “nodal rhythm” and “dissociated” are imprecise and demand further characterization. When the atrial rate exceeds the ventricular rate, second-degree or third-degree AV block is present. In complete AV block, the resultant escape rhythm usually is regular; in second-degree AV block, the ventricular intervals vary (see Figure 28-1). Occasionally, sinus node disease and complete AV block coexist, so it is important in the setting of a slow atrial rate to note “sinus capture” complexes when appropriately timed P waves conduct to the ventricle. When atrial pacing is feasible (as in patients with recent cardiac surgery), temporary atrial pacing can be used to demonstrate normal AV conduction, and the maximum rate at which 1:1 conduction can be maintained can be easily determined and followed serially.

The distinction between bradycardia resulting from AV block and sinus nodal dysfunction may have important therapeutic implications. If AV nodal conduction is intact, it usually is most appropriate to pace the atrium only (see AAI mode) rather than perform dual-chamber pacing. In contrast, isolated AV block is best managed by sensing and tracking the intrinsic atrial rate (see DDD mode).

Extrasystoles

Extrasystoles, or premature beats, usually are defined as supraventricular (supraventricular premature beats or premature atrial complexes) or ventricular (premature ventricular complexes, ventricular premature beats [VPBs]) in origin. True junctional extrasystoles are uncommon. When the extrasystole results in an early QRS with normal morphology and duration, a supraventricular extrasystole may be presumed. Usually, an early P wave can be discerned, but it may be obscured by the preceding T wave in certain leads. The ensuing sinus beat usually is advanced by the atrial extrasystole, but entrance block can result in a “full compensatory pause,” usually attributed to a ventricular extrasystole.

Isolated premature QRS complexes with prolonged QRS duration may represent either ventricular extrasystoles or aberrantly conducted atrial extrasystoles. Distinguishing the two may be difficult from a single rhythm strip. Premature P waves often may be obscured in a particular lead, or the ventricular extrasystole morphology may appear similar to the sinus QRS in one lead (but totally dissimilar in another). The ECG features favoring ventricular extrasystoles over aberrantly conducted atrial extrasystoles include (1) wide QRS morphology, (2) a full compensatory pause, (3) presence of fusion beats, and (4) absence of a discernible premature P wave. In the setting of ventricular preexcitation, variable fusion can occur as a result of exaggerated preexcitation with premature atrial depolarizations. As noted earlier, ventricular extrasystoles usually are followed by a full compensatory pause because the sinus node is not reset by the ventricular depolarization. However, an atrial extrasystole may sometimes fail to reset the sinus node (because of entrance block) or a ventricular extrasystole may occasionally reset the sinus node because of retrograde (VA) conduction. The simultaneous occurrence of both narrow QRS and wide QRS extrasystoles usually favors normally and aberrantly conducted atrial extrasystoles, particularly when the QRS width varies with the degree of prematurity (excluding fusion complexes).

The distinction of atrial versus ventricular extrasystoles may be somewhat academic in otherwise asymptomatic individuals because neither generally warrants therapy. However, either might be a harbinger for underlying myocardial irritability and should prompt a search for underlying causes. Occasionally, measures to suppress ectopy may appear to improve cardiac output by “regularizing” filling time in an otherwise tenuous patient. The relative advantages and risks of any such measure, whether achieved with medications or temporary pacing, need to be considered individually.

Tachycardias with Normal QRS

By definition, all tachycardias with normal QRS represent either sinus tachycardia or a form of SVT. It should be noted that the terms supraventricular tachycardia, paroxysmal supraventricular tachycardia, and paroxysmal atrial tachycardia often are used in reference to tachycardias with normal QRS, a regular rate in excess of 200 bpm, and no readily discernible P waves. In otherwise healthy infants, children, and adolescents, these features usually result from either AV reentrant tachycardia or AVNRT (Figure 28-7). Further distinction between these two mechanisms has little impact on acute management. However, in the ICU setting, primary atrial tachycardias (including sinus tachycardia) and junctional tachycardias also must be considered (particularly following cardiac surgery). Abnormal P-wave morphology (determined by 12-lead ECG), PR interval greater than 50% of the RR interval, or completely obscured P waves favor a nonsinus mechanism. Finally, the QRS duration may appear normal by adult standards but be significantly prolonged for age.

Figure 28–7 Supraventricular tachycardia resulting from AV nodal reentry in an infant. Although considerably less common than orthodromic reciprocating tachycardia in this age group, the P wave on the terminal portion of the QRS complex results in a “pseudo rSr′ pattern.” During sinus rhythm, this terminal deflection on the QRS was absent, and the transesophageal recording confirmed the mechanism.

In young patients, intraatrial reentry, atrial flutter, and atrial fibrillation usually are seen following surgical treatment for congenital heart defects involving the atrium (atrial septal defects, atrial repair of transposition of the great arteries, or the Fontan operation).¹⁵ The sawtooth pattern typical of atrial flutter may be absent in these patients, and the term intraatrial reentrant tachycardia (IART) may be more appropriate when discrete P waves are present. Because the atrial rate often is relatively slow in comparison with “typical” atrial flutter, a high index of suspicion is required. In some cases, the atrial rate is slow enough that consistent 1:1 conduction (with discrete P waves) further obscures the diagnosis by simulating sinus tachycardia. Similarly, with 2:1 conduction, alternate P waves may be obscured by the T wave, giving the impression of sinus rhythm.

Distinguishing sinus tachycardia from various types of SVT may be difficult. The appropriateness and variation of the rate (or lack thereof) may be particularly helpful in differentiating sinus from nonsinus tachycardias. Observing the heart rate response to interventions such as volume expansion, analgesia, antipyretic agents, and catecholamine infusions often is helpful. Depending on the pattern of atrial activation, P waves may even simulate a normal sinus P-wave morphology during primary atrial tachycardias. In other cases, AV conduction may appear to be 1:1 on the surface electrocardiogram when, in fact, a second P wave is obscured by the QRS complex or T wave. Direct atrial recordings using transesophageal electrocardiography or temporary epicardial atrial pacing wires usually facilitate the diagnosis (see Figure 28-6, B). Vagal maneuvers or administration of adenosine to interrupt AV conduction transiently often helps characterize the true AV relationship and determine whether the AV node participates in the tachycardia mechanism.

Tachycardias with Prolonged QRS

Generally, tachycardias with prolonged QRS should be presumed to be ventricular tachycardias until or unless evidence of an alternative diagnosis is demonstrated. VA dissociation, the hallmark ECG feature of ventricular tachycardia, may not be seen in childhood because of rapid retrograde conduction over the AV node (see Figure 28-4). The distinction between ventricular tachycardia and SVT with aberrant conduction can be difficult and may require invasive electrophysiologic study. Prolonged attempts to differentiate the two at the bedside by noninvasive means often are fruitless and may delay treatment. The wrong conclusion may prompt inappropriate and potentially dangerous therapeutic maneuvers. In the acute setting, treatment based on a presumed diagnosis of ventricular tachycardia is rarely deleterious, even when the mechanism subsequently proves to be supraventricular. However, an erroneous presumption of “SVT with aberrant conduction” may have disastrous consequences. When feasible, a full 12-lead ECG may aid in the diagnosis, particularly when a baseline ECG in normal rhythm is available for comparison. Apparent hemodynamic stability should not be mistaken for evidence of SVT rather than ventricular tachycardia, whether in an otherwise healthy child or in a patient with known cardiac disease.