Which information would be used to determine the cause of premature atrial contractions

Premature Atrial Contractions

Premature atrial contractions (PACs) are common in children, and are defined as premature P waves with premature QRS complexes. There is an incomplete compensatory pause, making the premature beat less than two normal cycles. While most P waves have a subsequent QRS wave, rarely are PACs nonconducted.

The majority of children presenting with PACs are healthy children and neonates. Others include postoperative cardiac surgery patients and those with hypoxia, use of sympathomimetic drugs, hyperthyroidism, and digoxin toxicity. With the exception of treating the underlying disease or drug toxicity, no treatment is necessary for PACs.

Premature Atrial Contractions

Premature atrial contractions (PACs) arise from ectopic pacemakers located in the atrium. An abnormal P wave occurs earlier than expected in the cardiac cycle. This P wave may or may not be conducted through the AV node. PACs are one of the most common causes of pauses on the rhythm strip (Fig. 2‐1). Usually the QRS complex will appear normal. PACs are fairly common in all ages. Causes include stress, fatigue, alcohol, caffeine, nicotine, catecholamines, chronic obstructive pulmonary disease (COPD), theophylline, and digoxin toxicity. PACs rarely require treatment beyond removal of the precipitating agent or treatment of the underlying disease. Beta blockers and calcium‐channel blockers may be effective in reducing the frequency of PACs in a symptomatic patient.

Premature Atrial Contractions

Premature atrial contractions are observed frequently in normal subjects and patients with a variety of diseases. They are manifested as an interruption in the heart rhythm with a premature beat having a narrow QRS complex. Because the origin of the atrial impulse is ectopic, the appearance of the P wave is abnormal, denoting its abnormal early origin. There is quite a wide spectrum in the incidence and frequency of premature atrial contractions. Their nature is classified as follows: If the premature atrial contractions occur singly, they are classified according to their incidence per period of time. Therefore, an ambulatory ECG report commonly describes how many premature atrial contractions were observed in a given time, such as an hour, a minute, or 24 hours, according to how common they are. When premature atrial contractions are frequent, it is customary to further describe their nature (cyclic or noncyclic) and rate. For example, when premature atrial contractions occur cyclically, they may show a bigeminal pattern.

Premature atrial contractions

Premature atrial contractions (PACs) originate from ectopic pacemakers located anywhere in the atrium other than the SA node (Fig. 43.7). The ECG shows ectopic P waves that appear sooner than the next expected SA beat. The ectopic P wave has a different shape and/or direction to a normal P wave. The ectopic P wave will not be conducted if it reaches the AV node during the absolute refractory period but it will be conducted with delay (longer P–R interval) during the relative refractory period. PACs that are conducted through the AV node, bundle of His and the bundle branches will have typical QRS complexes. PACs may appear at any age and are often seen in the absence of heart disease. It is generally believed that stress, fatigue, alcohol, tobacco and caffeine may precipitate PACs, although nothing has been proven yet. Frequent PACs are seen in chronic lung disease, ischemic heart disease and digitalis toxicity. Treatment involves cessation of precipitating causes and management of underlying disorders. If the PACs produce symptoms or sustained tachycardias, drug therapy should be implemented, with the aim of suppressing the PACs (Weiderhold 1988, Hillegass 2001, Mammen et al 2004, Larry & Schaal 2006).

Premature Atrial Contractions

Premature atrial contractions are the most common atrial arrhythmias, occurring in 54% of patients with acute MI (see Table 20-1).8,11 These beats may result from heightened sympathetic activity owing to pain or anxiety, or they may result from atrial distention, pericarditis, atrial infarction, or atrial ischemia. Although premature atrial contractions may precipitate other atrial arrhythmias, they are usually asymptomatic and are of no hemodynamic significance. Because premature atrial contractions are not associated with increased mortality, medical therapy to suppress these beats is not indicated.11

6.33.1.1.2 Atrial arrhythmias

The atria are particularly subject to arrhythmias when age and disease have caused structural damage. Developments in atrial defibrillation have been recently reviewed.2

Types and Levels

On the basis of electrocardiogram (ECG) characteristics, AV block is classified as first-, second-, and third-degree AV block. Anatomically, block can occur at various levels in the AV conduction system; above the His bundle (supra-His), within the His bundle (intra-His), and below the His bundle within the bundle branches (infra-His).

First-degree AV block is defined as abnormal prolongation of the PR interval to greater than 200 ms and is commonly due to a delay in the AV node irrespective of the QRS width. Intracardiac recordings show an AH interval greater than 130 ms in the presence of a normal HV interval. Occasionally, a transition of AV nodal conduction from a fast to slow AV nodal pathway can manifest as first-degree AV block. Less commonly, first-degree AV block can also occur at or below the His bundle; in such cases the HV interval is prolonged beyond 55 ms (or 65 ms in the presence of left bundle branch block [LBBB]). First-degree AV block with a relatively narrow QRS due to His–Purkinje conduction delay is not an uncommon finding in cardiac amyloidosis, where diffuse amyloid infiltration into the myocardium can delay conduction equally in both right and left bundles (Fig. 106.1).2

Type I second-degree heart block on ECG refers to progressive PR prolongation before a nonconducted beat and a shorter PR interval for the next conducted beat (Fig. 106.2). This is the classical Wenckebach-type AV block, usually in conjunction with narrow QRS complexes, implying a more proximal level of block, usually in the AV node. Less commonly, Wenckebach-type AV block can also occur in a diseased His–Purkinje system. Intra-His Wenckebach phenomenon is manifested as a prolonged His electrogram (>30 ms) with splitting and progressive prolongation of the split before block (Fig. 106.3). Unlike Wenckebach block at the AV nodal level, intra-His AV block tends to worsen with exercise or with atropine. Rarely, Wenckebach block can be demonstrated below the His bundle, with progressive delay in the HV interval and with block and resumption of conduction with the shorter HV interval.

Type II second-degree heart block (Mobitz type II block) is characterized by fixed PR intervals before and after blocked beats (see Fig. 106.2). It is usually associated with a wider QRS complex, indicating distal levels of block in the conduction system with progression to complete AV block. Type II block cannot be diagnosed if the PR interval following a pause is shorter than the PR immediately preceding the nonconducted P wave. The PP interval remains constant, and the pause incorporating the nonconducted P wave is twice the PP interval. True Mobitz type II block is rare with normal QRS complexes, and atypical Wenckebach should be considered. This is particularly true during sleep when sinus slowing precedes nonconducted P waves due to vagotonia. When Mobitz type II block occurs in conjunction with a narrow QRS, the block is usually within the His bundle.

AV conduction in a 2:1 pattern can be due to proximal or distal block. Differentiation between proximal and distal levels of block can be difficult. In general, a narrow QRS implies block at the AV nodal level, whereas a wide QRS makes it more likely to be below the AV node. Fixed 2:1 AV block with a constant normal or relatively short PR interval suggests infranodal block, whereas a prolonged PR (>300 ms) or a preceding Wenckebach-type AV conduction implies block at the level of the AV node. Atropine and exercise tend to improve AV nodal block.

Advanced second-degree block (or “high-grade” AV block) refers to two or more nonconducted sinus P waves but with resumption of normal AV conduction in between. It is important to exclude retrograde invasion into the AV conduction system by ventricular or junctional beats. In the setting of AF or AFL, a prolonged pause (e.g., greater than 5 s) is often due to advanced second-degree AV block.

Third-degree AV block is defined as the complete absence of AV conduction, with P waves dissociated from the QRS. The atrial rate is always faster than the ventricular. In the case of AF, complete AV block is manifested as a regularized slow ventricular rate.

Supraventricular Arrhythmias

Supraventricular Arrhythmias

Atrial Arrhythmias

Isolated premature atrial contractions are common in the fetus and in infants and children.33 These ectopic beats, even when frequent, are usually benign. In one study approximately one in four term infants had more than five premature atrial contractions in 24 hours. The same infants, when monitored at 1 month of age, had no premature atrial contractions.34 Atrial ectopy in the fetus and child may have two different relationships with supraventricular tachycardia. The first is that atrial ectopy not associated with the tachycardia mechanism may initiate reentrant tachycardia.35 Several studies have confirmed that patients presenting with reentrant mechanisms of supraventricular tachycardia in early infancy have a high likelihood of resolution of episodes of clinical tachycardia at 1 year of age, despite the persistent ability to induce the tachycardia with provocative testing. This is likely due to a decreased frequency of premature atrial contractions that can initiate these arrhythmias.36,37 The second association with supraventricular tachycardia is present when the atrial ectopy is a manifestation of nonconducted accessory pathway echo beats.38 This pattern will have a fixed interval from the preceding ventricular beat to the atrial ectopy and may be a harbinger for as yet unidentified supraventricular tachycardia.

Primary atrial arrhythmias are a relatively uncommon cause of narrow QRS complex tachycardia in the fetus and in infants and children. They represent 10 to 15 percent of all narrow QRS complex tachycardias in children.39 The common mechanisms include enhanced or abnormal automaticity and reentry.

Automatic atrial tachycardia will typically resume immediately after atrial pacing or electrical cardioversion. Rate variability with “warm-up” at the initiation of tachycardia and “cool-down” just prior to termination are common. As the tachycardia is often not accompanied by an increase in sympathetic tone to enhance AV nodal conduction, there is frequently first-degree AV block and occasionally second-degree AV block.27 The P wave morphology on the surface ECG may be helpful in localizing the focus of the atrial tachycardia in children and adults.40 Kistler et al.40 showed that a P wave in lead V1 that was either negative or biphasic positive-negative was 100 percent specific for a right atrial focus, and P waves that were biphasic negative-positive, isoelectric, or positive were 100 percent specific for left atrial foci. Amiodarone is the most effective drug in treating automatic atrial tachycardia.41 Propafenone, flecainide, and occasionally β-adrenergic blockade may also be successful.42,43 Automatic atrial tachycardia in infancy is usually relatively persistent rather than paroxysmal. Children with ectopic atrial tachycardia may present with a tachycardia-induced cardiomyopathy, but this rhythm frequently undergoes spontaneous resolution over the course of years, both in pediatric and adult patients.44 Spontaneous resolution in children diagnosed at less than 3 years of age is more common (78 percent) than that in children diagnosed after 3 years of age (16 percent).45 The tachycardia can be cured with catheter ablation.45–47

Reentrant atrial tachycardia as a mechanism for primary atrial tachycardia in children is more common in patients with diseased or surgically damaged atria (see Figures 31-4 and 31-5).48 This mechanism can be terminated with pacing or cardioversion. Electrocardiographically, other than by its initiation and termination patterns, it is indistinguishable from atrial automatic tachycardia. This type of atrial tachycardia is also amenable to catheter ablation49 but may require placement of linear lesions, which result in conduction block in the reentrant circuit.50,51 Antitachycardia pacemakers have also been shown to be effective.52 Nonautomatic focal atrial tachycardia (likely micro-reentry) is seen in the pediatric and especially the adult congenital heart disease patient, commonly after repair of congenital heart disease.53 It is indistinguishable from other forms of atrial reentrant tachycardia clinically and on the ECG and is commonly mistaken for atrial flutter prior to electrophysiology study. It is often amenable to focal catheter ablation.53

Atrial flutter is a form of reentrant atrial tachycardia with rapid, regular undulations on the ECG, giving rise to a sawtooth appearance in some leads. The atrial rate during atrial flutter in the fetus and in infants and children is faster than the 250 to 350 beats/min seen in adults. Atrial flutter occurs in the pediatric population in two relatively distinct patterns. The first type occurs in the fetus and newborn infant (Figure 31-6).

In the fetus, atrial flutter accounts for approximately one quarter of all documented tachyarrhythmias and has a median atrial rate of 450 beats/min (range 370 to 500 beats/min).54 It is rarely seen before 27 weeks of gestation,55 probably because the atrial size required to maintain the tachycardia cycle length is not reached until that gestational age. There is typically 2:1 AV conduction.

Hydrops fetalis occurs in about 40 percent of all fetuses with atrial flutter, and the overall mortality for affected gestations is 8 percent, an incidence that is not significantly different from that of supraventricular tachycardia.54 Hydropic fetuses with atrial flutter have higher ventricular rates, but atrial rates are not significantly different than in fetuses with atrial flutter without hydrops.54

Texter et al. described a series of 50 infants with atrial flutter56 not associated with structural heart disease. Most were diagnosed within the first 2 days of life. The average atrial and ventricular rates were 424 beats/min (range 340 to 580 beats/min) and 208 beats/min (range 125 to 280 beats/min), respectively. Twenty percent of the infants had also either a supraventricular tachycardia or an automatic atrial tachycardia. An association with the Wolff-Parkinson-White (WPW) syndrome and concealed accessory AV connections has been described.57,58 In the study of Texter et al.,56 atrial flutter recurred after conversion in only 12 percent of infants, in all cases within 5 days, and in most cases within 24 hours after initial conversion. All infants with recurrence had an associated supraventricular arrhythmia mechanism. The majority of patients in this series (88 percent) received antiarrhythmic medication following conversion (most commonly digoxin) as in other series,59–61 although the reported risk for recurrence without drug therapy has been low.62,63 Conversion to sinus rhythm can either be accomplished with esophageal pacing64 or more reliably with synchronized cardioversion.56 Biphasic waveform cardioversion has been shown to be more effective at lower-delivered energy than monophasic waveform for the conversion of atrial flutter in infants.65

The second group of pediatric patients with atrial flutter includes the older infants, children, or adolescents. In a review by Garson, only 8 percent of these patients had structurally normal hearts.66 The vast majority had congenital heart disease,67 and some had cardiomyopathy.68 The ECG appearance and atrial rates during atrial flutter in these patients were similar to those in adults. In contrast to patients with atrial flutter in the newborn period or early infancy, recurrence of atrial flutter is common and as a rule requires catheter or surgical ablation or long-term drug therapy.

Chaotic atrial tachycardia is rarely seen in children. Unlike adults, in whom chaotic atrial tachycardia is usually seen with chronic obstructive pulmonary disease, most infants with this arrhythmia have structurally normal hearts,69 although frequently there are contributing noncardiac conditions.70 Coexisting respiratory infections were reported in one third of infants with this rhythm in one series and structural heart disease in a similar number in the same series.71 The ECG diagnosis requires three or more ectopic P wave morphologies, irregular PP intervals, an isoelectric baseline between p waves, and a rapid atrial rate.71 Chaotic atrial tachycardia is usually a well-tolerated and self-limited rhythm in most pediatric patients72 but has been reported to result in a tachycardia- induced cardiomyopathy in as many as one fourth of affected infants.71 This rhythm in infants frequently has an excellent outcome with spontaneous resolution by 1 year of age.71 If the ventricular rate can not be adequately controlled with digoxin, beta-blockade, or calcium channel blocker, conversion to sinus rhythm can usually be accomplished with amiodarone, flecainide, or propafenone. Electrical cardioversion is not effective.

Atrial fibrillation is seen more commonly in the adolescent or adult patient with congenital heart disease or cardiomyopathy.73 It often coexists with atrial reentrant tachycardia. Kirsh et al.74 reviewed a series of 149 patients with congenital heart disease undergoing cardioversion for reentrant atrial tachycardia or atrial fibrillation. They found that as many as one third of patients in this population had atrial fibrillation in addition to the more common reentrant atrial tachycardia. They did not find a tendency of progression of atrial tachycardia to atrial fibrillation, but they did find that both arrhythmias required intervention with increasing frequency over time. Patients with unoperated congenital heart disease or those with residual left ventricular valvular lesions appeared to be more prone to atrial fibrillation than those after a more adequate surgical repair or palliation. Rheumatic fever with severe mitral regurgitation was a more common cause of atrial fibrillation in the distant past but is now rarely seen.

Atrial fibrillation in the infant or child with a structurally normal heart is extremely rare.73 It has been reported with abuse of alcohol, inhalants, and other illicit drugs in children and adolescents75,76 and rarely in a familial form.77 In the adolescent with a structurally normal heart, atrial fibrillation is most commonly associated with WPW syndrome but can also be seen in patients with concealed accessory pathways (Figure 31-7). Atrial fibrillation in patients with accessory pathways with short refractory periods for anterograde conduction may cause hemodynamic collapse and cardiac arrest (see later discussion). In our experience, adolescents with WPW syndrome and frequent episodes of atrial fibrillation usually cease to have atrial fibrillation after successful radiofrequency catheter ablation of the accessory pathway.

Atrial fibrillation has been reported to result from administration of adenosine for treatment of supraventricular tachycardia.78,79 Adenosine is used when resuscitative facilities are available to abort hemodynamic collapse from rapid anterograde conduction over an accessory pathway during atrial fibrillation.80