Atrial premature beats
An atrial premature beat (APB) is characterized by a nonsinus P wave that occurs before the next anticipated sinus beat. Several electrocardiographic leads may be needed to distinguish P waves originating in the sinus node versus an ectopic focus. In the rare case of sinus nodal premature beats, the P wave will be identical. The post-extrasystolic cycle length is typically less than compensatory because of penetration and resetting of the sinus node by the premature depolarization, but suppression of sinus node automaticity may also occur and result in pauses equal to or longer than the sinus cycle. Intraventricular conduction may be normal or aberrant, whereas the PR interval can be longer than that of the normal sinus beat because of atrioventricular nodal delay. This especially occurs in the rare case of interpolated APBs, which do not depolarize the sinus node and do not affect the sinus rate. Blocked premature beats may masquerade as pauses or bradycardias when P waves are not seen. The T wave of those beats that precede a pause should be carefully inspected to detect any “hidden” premature P wave. Nonconducted APBs are a common cause of unexpected pauses. They can arise anywhere in the atria, including the sinus node.
Physiologic sinus tachycardia
Sinus tachycardia is defined as a nonparoxysmal increase in sinus rate to more than 100 beats per minute (bpm) in keeping with the level of physical, emotional, pathologic, or pharmacologic stress. ,
It is due to physiologic influences on individual pacemaker cells and from an anatomic shift in the site of origin of atrial depolarization superiorly within the sinus node.
In normal sinus rhythm, the P wave on a 12-lead electrocardiogram (ECG) in adults is positive in leads I, II, and aVF and V 3 to V 6 . It is negative in aVR and V 1 and V 2 . In sinus tachycardia P waves have a normal contour, but a larger amplitude may develop and the wave may become peaked.
Inappropriate sinus tachycardia
Inappropriate sinus tachycardia (IST) is a fast sinus rhythm (>100 bpm) at rest or minimal activity that is out of proportion with the level of physical, emotional, pathologic, or pharmacologic stress. The syndrome of inappropriate sinus tachycardia is also defined as a sinus heart rate greater than 100 bpm at rest (with a mean 24-hour heart rate >90 bpm not a result of primary causes) and is associated with distressing symptoms of palpitations. ,
The underlying mechanism of IST remains poorly understood and is likely to be multifactorial (dysautonomia, neurohormonal dysregulation, intrinsic sinus node hyperactivity). A gain-of-function mutation of the pacemaker hyperpolarization-activated cyclic nucleotide-gated (HCN) 4 channel has been reported in a familial form of IST. There is also evolving evidence that immunoglobulin G anti-β receptor antibodies are found in IST.
Diagnosis is based on the following:
The presence of a persistent sinus tachycardia, greater than 100 bpm at rest or greater than 90 bpm on average over 24 hours, during the day with excessive rate increase in response to activity and nocturnal normalization of rate.
The tachycardia and associated symptoms are usually nonparoxysmal with P-wave morphology and endocardial activation identical to sinus rhythm.
Exclusion of a secondary systemic cause (e.g., hyperthyroidism, physical deconditioning), and postural orthostatic tachycardia syndrome (POTS).
The limited and disappointing experience with catheter ablation reported in small observational studies suggests that catheter ablation should not be considered as part of the routine management of most patients with IST. It may be considered in very symptomatic patients who do not respond to therapy with both a beta blocker and ivabradine. It is aimed at modifying the sinus node with an unavoidable, concomitant risk of iatrogenic sinus nodal disease and the need for permanent pacing. Catheter modification of the sinus node is moderately effective (60%), but the benefits may be short term and can be complicated by the need of permanent pacing in 10% of the patients. Narrowing of the superior vena cava and phrenic nerve palsy may also occur.
Sinus nodal reentrant tachycardia
Sinus nodal reentrant tachycardia arises from a reentry circuit involving the sinus node and, in contrast to IST, is characterized by paroxysmal episodes of tachycardia. On the ECG, the polarity and configuration of the P waves are similar to the configuration of sinus P waves.
It is unclear whether the reentrant circuit is completely confined to the sinus node or if surrounding atrial tissue is involved.
Diagnosis is based on the following:
The tachycardia is paroxysmal.
P-wave morphology is almost identical to sinus rhythm.
Endocardial atrial activation is similar to that of sinus rhythm.
Induction and/or termination of the arrhythmia occurs with premature atrial stimuli.
Termination occurs with vagal maneuvers or adenosine.
Ιnduction of the arrhythmia is independent of atrial or atrioventricular (AV) nodal conduction time.
Catheter ablation should be considered in symptomatic patients who do not respond to drug therapy. The earliest atrial activation is the site of radiofrequency (RF) current applications, and results have been much better than those with IST, but clinical experience is limited.
Postural orthostatic tachycardia syndrome
POTS is defined as a clinical syndrome usually characterized by an increase in heart rate of 30 bpm or more when standing for more than 30 seconds (or ≥40 bpm in individuals aged 12 to 19 years), and absence of orthostatic hypotension (>20 mm Hg drop in systolic blood pressure). ,
A number of mechanisms have been described, including autonomic nervous system dysfunction, peripheral autonomic denervation, hypovolemia, hyperadrenergic stimulation, diabetic neuropathy, deconditioning, anxiety, and hypervigilance.
POTS is diagnosed during a 10-minute active stand test or head-up tilt test with noninvasive beat-to-beat hemodynamic monitoring. ,
Focal atrial tachycardia
Focal atrial tachycardia (AT) is defined as an organized atrial rhythm 100 bpm or greater initiated from a discrete origin and spreading over both atria in a centrifugal pattern. The ventricular rate varies, depending on AV nodal conduction. In asymptomatic young people (younger than age 50 years) the prevalence of focal AT has been reported to be as low as 0.34%, with an increased prevalence of 0.46% in symptomatic arrhythmia patients.
Atrial activation originates from a discrete focus (<1 cm in diameter) with centrifugal spread. Focal AT accounts for up to 10% of SVT referred for ablation. Microreentry, abnormal automaticity, and triggered activity are the possible mechanisms. Focal AT is usually not associated with underlying heart disease, with a prognosis that is benign unless a tachycardia-induced cardiomyopathy develops.
The P waves during focal AT are distinct, with intervening isoelectric intervals, in contrast to a continuous undulation typical of macroreentrant atrial tachycardia (MRAT). However, an isoelectric interval may not be present during very rapid rates and/or in the presence of atrial disease resulting in slowing of conduction.
Focal AT is characterized by a change in P-wave morphology and by 1:1 AV conduction or second-degree AV block. Most focal ATs arise in the right atrium, usually along the crista terminalis, and less commonly at sites along the tricuspid annulus. Other possible sites of origin include the coronary sinus ostium, mitral annulus, perinodal or para-Hisian region, ostia of the pulmonary veins, left atrial septum, and near the aortic coronary cusps. The morphology of the P wave assists in identifying the tachycardia origin. Foci arising from the superior crista terminalis display a negative or positive–negative P wave in lead V1. The P wave may be indistinguishable from that during sinus rhythm. A positive or negative–positive biphasic P wave in V1 and negative P wave in lead I indicates a left atrial focus, whereas a negative or positive–negative P wave indicates a right atrial focus ( Figs. 12.1 and 12.2 ).
The distinction between focal AT and AV nodal reentrant tachycardia or AV reentrant tachycardia can be made by analyzing the R-P relationship on the surface ECG. A variable R-P relationship strongly favors AT.
The diagnosis of focal AT at times can only be established with certainty in the electrophysiology laboratory (see Fig. 12.2 ).
Catheter ablation is the treatment of choice for recurrent focal AT, especially when the AT is incessant and has caused or may cause a tachycardia-induced cardiomyopathy. Distinguishing macroreentrant ATs from focal ATs is critical for the ablation strategy. Focal ATs display a centrifugal activation pattern that spreads throughout the atria. Mapping and ablation of focal ATs is based on determining the earliest activation site. In pulmonary vein (PV)–related AT, focal ablation may be performed but electrical isolation of both the culprit PV along with other PVs may be preferred. In contemporary studies, catheter ablation is reported to have average acute success rate 85% with a 20% recurrence rate; 1.4% of patients experiencing complications such as vascular complications, AV block, and pericardial effusion; and approximately 0.1% mortality.
Multifocal atrial tachycardia
Multifocal atrial tachycardia is an irregular tachycardia characterized by three or more different P-wave morphologies at different rates. Multifocal atrial tachycardia is commonly associated with underlying conditions, including pulmonary disease, pulmonary hypertension, coronary disease, and valvular heart disease, as well as hypomagnesaemia, theophylline therapy, and digitalis toxicity.
Macroreentrant atrial tachycardias
The mechanism of MRAT is a large reentry circuit. If the atrial rate is more than 250 bpm, the tachycardia is conventionally referred to as atrial flutter. There is no single point of origin of activation, and atrial tissues outside the circuit are activated from various parts of the circuit. ECGs with continuous regular electrical activity, most commonly but not invariably of the sawtooth pattern, mostly are due to macroreentrant atrial circuits, but microreentry is also possible. However, macroreentrant tachycardias with a significant part of the activation of the circuit in protected areas may display a focal AT pattern, with discrete P waves.
Cavotricuspid isthmus–dependent flutter (typical flutter)
Atrial flutter has an atrial rate of 250 to 330 bpm. Cavotricuspid isthmus (CTI)–dependent flutter represents a macroreentry circuit around the tricuspid annulus using the CTI as a critical passage at the inferior boundary. The crista terminalis and eustachian ridge are the functional posterior barriers, and the tricuspid annulus the anterior barrier ( Fig. 12.3 ). In typical counterclockwise atrial flutter, activation goes downward along the right atrium (RA) free wall, through the CTI, and upward along the right atrial septum. Activation of the left atrium (LA) is passive ( Fig. 12.4 ). The upper part of the circuit may be anterior or posterior to the superior vena cava. The activation pattern is counterclockwise (or anticlockwise) when viewed from a caudal left anterior oblique perspective.
Counterclockwise (common or typical) isthmus-dependent flutter is characterized electrocardiographically by a sawtooth pattern in the inferior leads and a positive flutter deflection in lead V1 with transition to a negative deflection at some point between V2 and V6. A less common pattern (10%) involves clockwise rotation around the tricuspid annulus. Clockwise (reverse) isthmus-dependent flutter shows the opposite pattern (see Fig. 12.4 )—that is, positive flutter waves in the inferior leads and wide, negative flutter waves in lead V1, transitioning to positive waves in lead V6).
The most common patterns of CTI-dependent atrial flutter include a tachycardia showing a counterclockwise rotation in the left anterior oblique view around the tricuspid valve (see Fig. 12.4 ). Typical atrial flutter (AFL) has a strong reproducible anatomic dependence, resulting in the morphologic reproducibility of the ECG ( Fig. 12.5 ). However, the classic ECG pattern may be significantly changed when atrial activation has been modified as it is in cardiac surgery involving atrial tissue, after extensive RF ablation, or advanced atrial disease. , Antiarrhythmic drugs (AADs) may also modify the typical ECG pattern ( Fig. 12.6 ). In these situations an atypical ECG does not rule out typical flutter using the CTI. Often there is 2:1 AV conduction with a resultant ventricular rate of approximately 150 bpm. Varying block produces an irregular rhythm, whereas 1:1 conduction may lead to hemodynamic instability. In some cases presenting with 2:1 AV block, the diagnosis of AFL may not be obvious on the ECG. In these situations intravenous adenosine increases the degree of AV block and reveals the typical ECG pattern. However, adenosine can produce a rebound increase in AV conduction to 1:1 and may also precipitate AF. ,
An electrophysiology study (EPS) ( Fig. 12.7 ) may be necessary to demonstrate the circuit of flutter and prove dependence of the CTI by entrainment. Entrainment mapping can be used to quickly confirm participation of the CTI in the reentrant circuit. The postpacing interval (PPI) measured on cessation of entrainment overdrive pacing is dependent on the distance between the pacing catheter location and the reentrant circuit, and a difference between the PPI and the tachycardia cycle length (TCL) of 20 ms or less indicates that the pacing site is part of the reentrant circuit. It should be noted, however, that a long PPI may be due to delayed conduction and does not exclude isthmus-dependent flutter ( Figs. 12.8 and 12.9 ). Localized capture without consistent advancement of the other atrial electrograms should be differentiated from true entrainment.