Abstract
A “supraventricular” origin of a tachycardia implies the obligatory involvement of one or more cardiac structures above the bifurcation of the His bundle (HB), including atrial myocardium, atrioventricular node (AVN), proximal HB, coronary sinus, pulmonary veins, venae cavae, or abnormal atrioventricular (AV) connections other than the HB (i.e., bypass tracts). Narrow complex supraventricular tachycardias (SVTs) include sinus tachycardia, inappropriate sinus tachycardia, sinoatrial nodal reentrant tachycardia, focal atrial tachycardia (AT), multifocal AT, atrial fibrillation (AF), atrial flutter (AFL), junctional tachycardia, AVN reentrant tachycardia (AVNRT), and AV reentrant tachycardia (AVRT).
Paroxysmal SVT is the term generally applied to intermittent SVT other than AF, AFL, and multifocal AT, and describes a clinical syndrome characterized by the presence of a regular and rapid tachycardia of abrupt onset and termination. The major causes are AVNRT (approximately 50% to 60% of cases), AVRT (approximately 30% of cases), and focal AT (approximately 10% of cases).
Most paroxysmal SVTs are generally benign and do not influence survival; therefore the primary indication for treatment is to alleviate symptoms and improve quality of life. The threshold for initiation of therapy and the decision to treat SVT with oral pharmacological therapy or catheter ablation depends on the frequency and duration of the arrhythmia, severity of symptoms, presence of concomitant structural heart disease, and patient preference. Given the high success rates and the low complication rate, catheter ablation is the treatment of choice in patients who desire to avoid or are unresponsive or intolerant to drug therapy.
Keywords
supraventricular tachycardia, atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, atrial tachycardia, bypass tract
Outline
Epidemiology and Natural History, 697
Clinical Presentation, 698
Initial Evaluation, 699
Principles of Management, 699
Electrocardiographic Features, 702
Regularity of the Tachycardia, 702
Atrial Activity, 702
Characterization of P/QRS Relationship, 703
QRS Morphology, 703
Effects of Interventions, 703
Electrophysiological Testing, 703
Baseline Observations During Sinus Rhythm, 704
Programmed Electrical Stimulation During Sinus Rhythm, 704
Induction of Tachycardia, 710
Tachycardia Features, 710
Diagnostic Maneuvers During Tachycardia, 714
Diagnostic Maneuvers During Sinus Rhythm After Tachycardia Termination, 722
Practical Approach to Electrophysiological Diagnosis of Supraventricular Tachycardia, 723
A “supraventricular” origin of a tachycardia implies the obligatory involvement of one or more cardiac structures above the bifurcation of the His bundle (HB), including the atrial myocardium, atrioventricular node (AVN), proximal HB, coronary sinus (CS), pulmonary veins, venae cavae, or abnormal atrioventricular (AV) connections other than the HB (i.e., bypass tracts [BTs]).
Narrow QRS complex supraventricular tachycardia (SVT) is a tachyarrhythmia with a rate greater than 100 beats/min and a QRS duration of less than 120 milliseconds. Narrow complex SVTs include sinus tachycardia, inappropriate sinus tachycardia, sinoatrial nodal reentrant tachycardia, focal atrial tachycardia (AT), multifocal AT, atrial fibrillation (AF), atrial flutter (AFL), junctional tachycardia, atrioventricular nodal reentrant tachycardia (AVNRT), and atrioventricular reentrant tachycardia (AVRT). These tachycardias can be divided into those that require only atrial tissue for their initiation and maintenance (sinus tachycardia, AT, AF, and AFL), and those that require the AV junction (junctional tachycardia, AVNRT, and AVRT).
Paroxysmal SVT is the term generally applied to intermittent SVT other than AF, AFL, and multifocal AT, and describes a clinical syndrome characterized by the presence of a regular and rapid tachycardia of abrupt onset and termination ( Fig. 20.1 ). The major causes are AVNRT (approximately 50% to 60% of cases), AVRT (approximately 30% of cases), and focal AT (approximately 10% of cases).
Epidemiology and Natural History
Paroxysmal SVT with sudden onset and termination is relatively common. In the United States, the estimated prevalence in the general population is 2.29 per 1000, with an incidence of 36 per 100,000 person-years. Paroxysmal SVT in the absence of structural heart disease can present at any age but most commonly first presents between ages 12 and 30 years. The risk of developing paroxysmal SVT is twofold greater in women than men.
In a large cohort of patients with symptomatic paroxysmal SVT referred for ablation, AVNRT was the most common mechanism (56%), followed by AVRT (27%) and AT (17%). However, the mechanism of paroxysmal SVT was significantly influenced by both age and gender. The majority of patients with AVRT are men (55%), whereas the majority of patients with AVNRT and AT are women (70% and 62%, respectively). As patients grew older, there was a significant and progressive decline in the number of patients presenting with AVRT, which was the predominant mechanism in the first decade, and a striking increase in AVNRT and AT ( Fig. 20.2 ). These trends were similar in both genders, although AVNRT replaced AVRT as the predominant mechanism much earlier in women.
AVNRT is the predominant mechanism overall in patients undergoing ablation, and after the age of 20 years it accounts for the largest number of ablations in each age group. AVNRT is unusual in children under 5 years of age, and typically initially manifests in early life, often in the teens. There is a striking 2 : 1 predominance of women in the AVNRT group, which remains without clear physiological or anatomical explanation. Female sex and older age (teens vs. early childhood years) favor the diagnosis of AVNRT over AVRT.
AVRT presents earlier in life than AVNRT (most commonly in the first two decades of life), with an average of more than 10 years separating the time of clinical presentation of AVRT versus AVNRT. The early predominance of AVRT is consistent with the congenital nature of the substrate. However, a minority of patients have relatively late onset of symptoms associated with AVRT and thus continue to account for a small proportion of ablations in older patients. Men account for a higher proportion of AVRT at all ages.
Focal ATs comprise a progressively greater proportion of paroxysmal SVT with increasing age, accounting for 23% of paroxysmal SVTs in patients older than 70 years. Although there is a greater absolute number of women with AT, the proportion of AT in both genders is similar. Age-related changes in the atrial electrophysiology (EP) substrate (including cellular coupling and autonomic influences) likely contribute to the increased incidence of AT in older individuals. In adults, focal ATs can occur in the absence of structural heart disease; nonetheless, the incidence of associated structural heart disease is higher in AT than other types of paroxysmal SVT. The long-term prognosis in patients with focal AT is generally benign, except for those with incessant ATs, which can precipitate tachycardia-induced cardiomyopathy.
Unlike AF and AFL, paroxysmal SVT does not appear to be a risk marker for stroke. In fact, unexplained stroke is rare in patients with SVT. Nonetheless, a strong link exists between SVT and atrial arrhythmias, particularly paroxysmal AF, even in patients with no ventricular preexcitation. The prevalence of a history of AF in the SVT patient population is approximately 2.6% compared to 0.4% to 2% in the general population. In addition, AVRT and, less frequently, AVNRT can serve as triggers for AF.
Clinical Presentation
The clinical syndrome of paroxysmal SVT is characterized as a regular rapid tachycardia of abrupt onset and termination. Episodes can last from seconds to several hours. Patients commonly describe palpitations and heart racing, frequently associated with complaints of dyspnea, weakness, chest pain, dizziness, or even frank syncope. The impact of SVT on quality of life varies according to the frequency and duration of episodes, and the severity of symptoms. Patients often learn to use certain maneuvers such as carotid sinus massage or the Valsalva maneuver to terminate the arrhythmia, although many require pharmacological treatment to achieve this.
Neck pounding can occur during tachycardia, which is related to pulsatile reversed flow when the right atrium (RA) contracts against a closed tricuspid valve. The physical examination correlate of this phenomenon is continuous pulsing cannon A waves in the jugular venous waveform (described as the “frog” sign). This clinical feature has been reported to distinguish typical AVNRT from orthodromic AVRT. Although the atrial contraction during orthodromic AVRT does occur against closed AV valves, the longer ventriculoatrial (VA) interval during the tachycardia results in separate ventricular and then atrial contractions and, hence, relatively lower RA and venous pressures. Therefore symptoms of “shirt flapping” or “neck pounding” are experienced less commonly in patients with AVRT than those with AVNRT (17% vs. 50%). In addition, polyuria, which related to higher RA pressures and elevated levels of atrial natriuretic protein, is more common in patients with AVNRT compared with patients who have AVRT.
Dizziness can occur initially because of hypotension, but it then disappears when the sympathetic response to the SVT stabilizes the blood pressure (typically within 30 to 60 seconds). Reductions of blood pressure and cardiac output (and the associated reflex sympathetic activity) are likely to be most prominent in SVTs with simultaneous atrial and ventricular activation (e.g., typical AVNRT) than those with short VA intervals (e.g., slow-slow AVNRT or orthodromic AVRT), and least prominent in long RP tachycardias (e.g., atypical AVNRT, permanent junctional reciprocating tachycardia [PJRT], and AT).
True syncope is rare but can occur, especially in elderly patients. Syncope at the initiation of SVT is commonly vagally mediated, especially in young patients, and is benign in nature. However, malignant ventricular arrhythmias as a cause of syncope should be considered in patients with manifest preexcitation. In these patients, AVRT can deteriorate into AF, which can be associated with very fast ventricular rates, with possible degeneration into ventricular fibrillation (VF).
In patients with underlying structural heart disease, symptoms can be more severe. Decompensation of underlying heart failure or ischemic heart disease can be precipitated by episodes of SVT. Truly paroxysmal SVT rarely leads to a tachycardia-induced cardiomyopathy. However, PJRT and focal AT can manifest as a frequently recurring or incessant tachycardia that can precipitate cardiomyopathy and heart failure. Elimination of the tachycardia results in normalization of left ventricular (LV) function within a few months in the vast majority of patients.
Initial Evaluation
History, physical examination, and an electrocardiogram (ECG) constitute an appropriate initial evaluation of patients presenting with symptoms suggestive of paroxysmal SVT. However, clinical symptoms are not usually helpful in distinguishing different forms of paroxysmal SVT. A 12-lead ECG during tachycardia can be helpful for defining the mechanism of paroxysmal SVT. Ambulatory 24- or 48-hour Holter recording can be used for documentation of the arrhythmia in patients with frequent (i.e., several episodes per week) but self-terminating tachycardias. A cardiac event monitor is often more useful than a 24-hour recording in patients with less frequent arrhythmias. Implantable loop recorders can be helpful in selected cases with rare episodes associated with severe symptoms of hemodynamic instability (e.g., syncope).
An echocardiographic examination should be considered in patients with documented sustained SVT to exclude the possibility of structural heart disease. Exercise testing is rarely useful for diagnosis unless the arrhythmia is clearly triggered by exertion. Further diagnostic studies are indicated only if there are signs or symptoms that suggest structural heart disease. Of note, troponin I and T levels (especially high-sensitivity Troponin T) are elevated in a significant proportion (more than 50%) of patients presenting with SVT, but this elevation does not constitute a clear biomarker of clinically significant coronary artery disease. Similarly, striking ST segment depression during SVT, that resolves quickly on cessation of tachycardia, is not uncommon but does not signify obstructive coronary artery disease.
Invasive EP testing is not indicated unless a decision to proceed with catheter ablation is undertaken. EP testing with subsequent catheter ablation may also be used for diagnosis and therapy in cases with a clear history of paroxysmal regular palpitations. It may also be considered in patients with preexcitation or disabling symptoms without ECG documentation of an arrhythmia.
Principles of Management
Acute Management
Most episodes of paroxysmal SVT require intact 1 : 1 AVN conduction for continuation and are therefore classified as AVN-dependent. AVN conduction and refractoriness can be modified by vagal maneuvers and by many pharmacological agents and thus are the weak links targeted by most acute therapies. Termination of a sustained episode of SVT is usually accomplished by producing a transient block in the AVN ( Fig. 20.3 ).
For acute conversion of SVT, vagal maneuvers (including Valsalva and carotid sinus massage) are the first-line intervention, although their success rate remains limited (less than 30%). Valsalva is the most effective technique in adults, but carotid sinus massage can also be effective. The so-called modified Valsalva (patient supine, with legs slightly elevated to increase venous return and decrease reflex sympathetic tone) has also been useful. Facial immersion in water is the most reliable method in infants. Vagal maneuvers are less effective once a sympathetic response to paroxysmal SVT has become established, so patients should be advised to try them soon after onset of symptoms.
When vagal maneuvers are unsuccessful, termination can be achieved with antiarrhythmic drugs whose primary effects increase AVN refractoriness or decrease AVN conduction. In most patients, the drug of choice is intravenous (IV) adenosine. In hemodynamically stable patients, IV diltiazem, verapamil, or beta-blockers are appropriate therapy for SVT that is refractory to adenosine or recurs after initial termination, and are successful in 64% to 98% of cases. Electrical cardioversion is recommended for acute treatment in patients with hemodynamically unstable SVT when vagal maneuvers or adenosine are ineffective or not feasible.
The advantages of adenosine include its rapid onset of action (usually within 10 to 25 seconds via a peripheral vein), short half-life (less than 10 seconds), and high degree of efficacy. The effective dose of adenosine is usually 6 to 12 mg, given as a rapid bolus over 1 to 2 seconds at a peripheral site, followed by a vigorous flush of normal saline. If a central IV access site is used, the initial dose should not exceed 3 mg and may be as little as 1 mg. Doses up to 12 mg terminate over 90% of paroxysmal SVT episodes (predominantly AVRT and AVNRT). Sequential dosing can be given at 60-second intervals because of adenosine’s rapid metabolism. In AVNRT, termination is usually caused by block in the slow pathway. In AVRT, termination occurs secondary to block in the AVN. Termination can also occur indirectly, that is, because of adenosine-induced premature atrial complexes (PACs) or premature ventricular complexes (PVCs). Adenosine also can terminate a significant proportion of focal ATs; therefore termination of an SVT in response to adenosine is not helpful in differentiating AT from other SVTs. Even when AT persists, adenosine can be useful diagnostically by producing transient AV block and unmasking the independent atrial activity during AT. Of note, adenosine is cleared rapidly; hence, reinitiation of paroxysmal SVT after initial termination can occur. Either repeated administration of the same dose of adenosine or substitution of a calcium channel blocker or beta-blocker typically is effective.
Importantly, adenosine shortens the atrial refractory period, and atrial ectopy can induce AF. This can be dangerous if the patient has a BT capable of rapid anterograde conduction, which can result in a rapid ventricular response that can degenerate into VF. In patients with Wolff-Parkinson-White (WPW) syndrome and AF, adenosine can result in a rapid ventricular response that can degenerate into VF. However, this problem has not been observed frequently, and the use of adenosine for diagnosis and termination of regular SVTs, including AVRT, is appropriate as long as close patient observation and preparedness to treat potential complications, such as with immediate electrical cardioversion/defibrillation, are maintained.
The AVN action potential is calcium channel–dependent, and the non–dihydropyridine calcium channel blockers verapamil and diltiazem are effective for terminating AVN-dependent paroxysmal SVT. The recommended dosage of verapamil is 5 mg IV over 2 minutes, followed in 5 to 10 minutes by a second 5- to 7.5-mg dose. The recommended dose of diltiazem is 20 mg IV followed, if necessary, by a second dose of 25 to 35 mg. Paroxysmal SVT termination should occur within 5 minutes of the end of the infusion, and more than 90% of patients with AVN-dependent paroxysmal SVT respond. As with adenosine, transient arrhythmias, including PACs, PVCs, AF, and bradycardia, can be seen after paroxysmal SVT termination with calcium channel blockers. Hypotension can also develop, particularly if the paroxysmal SVT does not terminate. Adenosine and verapamil have been reported to have a similar high efficacy in terminating paroxysmal SVT, with a rate of success ranging from 59% to 100% for adenosine and from 73% to 98.8% for verapamil, according to the dose and mode of administration. However, data also suggest that the efficacy of adenosine and verapamil is influenced by the arrhythmia rate. Adenosine appears to be more effective at terminating SVT with faster rates. In contrast, the efficacy of verapamil in restoring sinus rhythm was inversely related to the rate of paroxysmal SVT.
IV beta-blockers including propranolol (1 to 3 mg), metoprolol (5 mg), and esmolol (500 µg/kg over 1 minute and a 50-µg/kg per minute infusion) are also useful for acute termination. Digoxin (0.5 to 1.0 mg) is considered the least effective of the four categories of drugs available, but is a useful alternative when there is a contraindication to the other agents.
AVN-dependent paroxysmal SVT can present with a wide QRS complex in patients with fixed or functional aberration, or if a BT is used for anterograde conduction. Most wide complex tachycardias, however, are caused by mechanisms that can worsen after IV administration of beta-blockers and calcium channel blockers. Unless there is strong evidence that a wide QRS tachycardia is AVN-dependent, verapamil, diltiazem, and beta-blockers should not be used.
Limited data are available on the acute pharmacological therapy of ATs. Vagal maneuvers only rarely terminate AT, and the response to adenosine is variable. IV beta-blockers, diltiazem, or verapamil have modest efficacy (30% to 50%) in terminating the focal AT or slowing the ventricular rate. Class I or III antiarrhythmic drugs given orally or parenterally may be considered for refractory ATs. Adenosine does not slow or terminate microreentrant AT. In contrast, triggered activity ATs typically terminate abruptly in response to adenosine and do not spontaneously reinitiate. Automatic ATs are either slowed transiently by adenosine before gradual resumption of the AT rate or suppressed transiently before spontaneous reinitiation. Microreentrant ATs can terminate in response to carotid sinus massage and vagal maneuvers. Triggered activity ATs can also terminate in response to carotid sinus massage, vagal maneuvers, verapamil, beta-blockers, and sodium channel blockers. During automatic AT, carotid sinus massage can cause AV block and can slow the atrial rate; however, these interventions generally do not terminate the AT. Only beta-blockers have been useful in termination of paroxysmal (but not incessant) automatic AT. Termination of automatic AT is usually preceded by a cool-down phenomenon of the AT rate.
In general, most stable patients with SVT respond to pharmacological therapy, with conversion success rates of 80% to 98%. Electrical cardioversion is also recommended for patients with hemodynamically stable SVT when pharmacological therapy is ineffective or contraindicated. However, electrical cardioversion is inappropriate if the SVT is terminating and reinitiating spontaneously.
In patients with manifest preexcitation during normal sinus rhythm (NSR) presenting with AVRT (orthodromic or antidromic), vagal maneuvers are the first-line intervention for tachycardia termination. For persistent SVT, adenosine is recommended. Importantly, adenosine should be used with caution because it can induce AF with a rapid ventricular rate in the presence of an anterogradely conducting BT. This is unusual and should not be viewed as a contraindication to adenosine use, but one should be prepared for emergency cardioversion before administering adenosine to SVT patients. For refractory AVRT, IV diltiazem, verapamil, or beta-blockers may be considered to block conduction in the AVN, which represents the retrograde or anterograde limb in the AVRT circuit. AVN blocking drugs, however, are ineffective in patients with an antidromic AVRT that utilizes two separate BTs for anterograde and retrograde conduction. Drug treatment directed at the BT (ibutilide, procainamide, flecainide) may be considered. When drug therapy fails or hemodynamic instability is present, electrical cardioversion should be considered.
Chronic Management
Most paroxysmal SVTs are generally benign and do not influence survival; therefore the primary indication for treatment is to alleviate symptoms and improve quality of life. The threshold for initiation of therapy and the decision to treat SVT with oral pharmacological therapy or catheter ablation depends on the frequency and duration of the arrhythmia, severity of symptoms, presence of concomitant structural heart disease, and patient preference ( Fig. 20.4 ). The threshold for treatment is also influenced by whether the patient is a competitive athlete, a woman considering pregnancy, or someone with a high-risk occupation (e.g., pilots, bus drivers).
Catheter Ablation
Given the high success rates and the low complication rate, catheter ablation is the treatment of choice in patients who desire to avoid or are unresponsive or intolerant to drug therapy. Catheter ablation is also recommended for incessant SVT, even in asymptomatic patients, especially when tachycardia-induced cardiomyopathy has developed.
Pharmacological Therapy
For patients requiring therapy who are reluctant to undergo catheter ablation, drug therapy remains a viable alternative. Calcium channel blockers and beta-blockers may be considered in patients without ventricular preexcitation during NSR. Verapamil, propranolol, and digoxin likely have equivalent efficacy, and can improve symptoms in 60% to 80% of patients. However, verapamil, diltiazem, and beta-blockers are generally preferred to digoxin. The effective dose of digoxin is usually higher than that commonly used in clinical practice today. Given the risk of toxicity, digoxin should be reserved for patients who cannot take beta-blockers, diltiazem, or verapamil or a class IC agent (flecainide or propafenone) and must be used with caution in the presence of renal dysfunction.
In patients who do not respond, classes IC and III drugs may be considered. Flecainide and propafenone affect the AVN and BTs, reduce SVT frequency in 86% to 93% of patients, and may be considered in patients without ischemic or structural heart disease. Sotalol, dofetilide, and amiodarone are second-line agents. The probability of remaining free of SVT after 6 months of treatment is about 50% for dofetilide and 54% for propafenone, compared to 6% for placebo. However, the potential benefit should be balanced by the potential risks of proarrhythmia and toxicity. Because sympathetic stimulation can antagonize the effects of many antiarrhythmic agents, concomitant therapy with a beta-blocker can improve efficacy.
Pharmacological management of ATs has not been well evaluated in controlled clinical trials. Depending on the mechanism responsible for the arrhythmia, beta-blockers or calcium channel blockers may be considered as first-line drug therapy. Class IC agents in combination with an AVN blocking agent, or class III agents (sotalol and amiodarone) are second-line therapy ( see Chapter 11 ).
Patients with SVT should be educated on how to perform vagal maneuvers. Those with well-tolerated episodes of paroxysmal SVT that always terminate spontaneously or with vagal maneuvers do not require chronic prophylactic therapy. Selected patients may be treated only for acute episodes. Outpatients may use a single oral dose of verapamil, diltiazem, or propranolol to acutely terminate an episode of SVT. This so-called pill in the pocket is a reasonable treatment option for patients who have SVT episodes that are sustained but infrequent enough that daily preventive therapy is not desired. This approach necessitates the use of a drug that has a short onset of action (i.e., immediate-release preparations); crushing the drug tablet can potentially facilitate absorption. Candidate patients should be free of significant LV dysfunction, sinus bradycardia, and preexcitation.
For patients with ventricular preexcitation, antiarrhythmic drugs to block BT conduction are considered. Class IC agents (in patients without structural heart disease or ischemic heart disease), and class III drugs, such as sotalol and dofetilide, may be considered. Oral amiodarone is a last resort therapy, given the associated risks of long-term therapy. In general, antiarrhythmic drug therapy can offer symptomatic improvement in up to 90% of patients, although complete disappearance of symptoms is observed in only 30%. Chronic oral beta-blockers, verapamil, and diltiazem may be used for the treatment of patients with WPW syndrome, particularly if their BT has been demonstrated to be incapable of rapid anterograde conduction. However, these agents must be used with caution and after a discussion with the patient concerning the potential risk of rapid conduction over the BT if AF develops. Digoxin, on the other hand, should be avoided because it can shorten the refractory period of the BT and, hence, is potentially harmful in patients with manifest BTs.
Electrocardiographic Features
Regularity of the Tachycardia
Most SVTs are associated with a regular ventricular rate. If the rhythm is irregular, the ECG should be scrutinized for discrete atrial activity and for any evidence of a pattern in the irregularity (e.g., grouped beating typical of Wenckebach periodicity). If the rhythm is irregularly irregular (i.e., no pattern can be detected), the mechanism of the arrhythmia is multifocal AT, AFL with variable AV conduction, or AF ( Fig. 20.5 ). Multifocal AT is an irregularly irregular atrial rhythm characterized by more than three different P wave morphologies, with the P waves separated by isoelectric intervals and associated with varying P-P, R-R, and PR intervals ( see Fig. 11.2 ). On the other hand, AF is characterized by rapid and irregular atrial fibrillatory activity and, in the presence of normal AVN conduction, by an irregularly irregular ventricular response. P waves cannot be detected in AF, although coarse fibrillatory waves and prominent U waves can sometimes give the appearance of P waves. At times, the fibrillatory activity is so fine as to be undetectable. If the patient’s rhythm is regular or has a clearly discernible pattern, the ECG should next be assessed for P waves (atrial activity).
Atrial Activity
The P waves may be easily discernible; however, frequently, comparison with a normal baseline ECG is needed and can reveal a slight alteration in the QRS, ST segment, or T waves, suggesting the presence of the P wave. If the P waves cannot be clearly identified, carotid sinus massage or the administration of IV adenosine may help clarify the diagnosis. These maneuvers may also terminate the SVT.
Atrial Rate
An atrial rate greater than 250 beats/min is usually caused by AFL. However, overlap exists, and AT and AVRT can occasionally be faster than 250 beats/min, especially in youngsters. Although AVRT tends to be faster than AVNRT and AT, significant overlap exists and this criterion does not usually help in distinguishing among different SVTs.
P Wave Morphology
P waves indicate the result of atrial activation and may be broadly classified as concentric or eccentric. A P wave morphology identical to a sinus P wave suggests sinus tachycardia, inappropriate sinus tachycardia, sinoatrial nodal reentrant tachycardia, or AT arising close to the region of the sinus node. A nonsinus P wave morphology can be observed during AVNRT (P wave is concentric due to midline retrograde activation; see Fig. 17.8 ), AVRT (P wave can be eccentric or concentric due to retrograde conduction over the BT; see Fig. 18.12 ), AT (P wave can be eccentric or concentric), and AFL (lack of distinct isoelectric baselines between atrial deflections is suggestive of AFL, but can also be seen occasionally in AT; see Fig. 12.6 ). The P waves may not be discernible on the ECG, which suggests typical AVNRT or, less commonly, AVRT (especially in the presence of bundle branch block [BBB] contralateral to the BT). It is best to characterize P waves during SVT morphologically at the outset (concentric, eccentric) rather than attaching a mode of activation (i.e., retrogradely activated); for example, upright P waves in the inferior leads, though usually due to AT, may nonetheless be retrogradely conducted over an anterior BT, and although inverted P waves in inferior leads are often retrogradely conducted, focal AT from the coronary sinus ostium (CS os) can have an identical appearance. Thus not all retrograde P waves are inverted in the inferior leads, and not all inverted P waves in inferior leads are retrogradely conducted.
Characterization of P/QRS Relationship
RP-PR Interval Ratio
In general, SVTs are classified according to the RP interval as “short RP” (RP < PR) or “long RP” (RP > PR) tachycardias (see Fig. 20.5 ). The RP-to-PR ratio is not diagnostic of any tachycardia type but does help in creating a differential diagnosis of the possible tachycardia types. During short RP SVTs, the ECG will show P waves inscribed within the ST-T wave with an RP interval that is less than half the tachycardia R-R interval. Such SVTs include typical AVNRT (most common), orthodromic AVRT, AT with prolonged AV conduction, and slow-slow AVNRT. A very short RP interval (less than 90 milliseconds) is consistent with typical AVNRT and excludes AVRT. In typical AVNRT, the P wave is not usually visible because of the simultaneous atrial and ventricular activation. The P wave may distort the initial portion of the QRS (mimicking a q wave in inferior leads) or lie just within the QRS (inapparent) or distort the terminal portion of the QRS (mimicking an s wave in inferior leads or r′ in lead V 1 ; see Fig. 17.8 ).
Long RP SVTs (see Fig. 20.1 ) include AT (most common), atypical (fast-slow) AVNRT, and AVRT using a slowly conducting AV BT (e.g., PJRT). If the PR interval during the SVT is shorter than that during NSR, AT and AVRT are very unlikely, and atypical AVNRT, which is associated with an apparent shortening of the PR interval, is the likely diagnosis. ATs originating close to the AV junction are also a possibility.
The PR intervals during AT are appropriate for the AT rate and are usually longer than those during NSR. The faster the AT rate, the longer the PR interval. Thus the PR interval can be shorter than, longer than, or equal to the RP interval. The PR interval may also be equal to the RR, and the P wave may fall inside the preceding QRS, thus mimicking typical AVNRT.
Slow-slow AVNRT can be associated with RP intervals and P wave morphology similar to that during orthodromic AVRT using a posteroseptal AV BT. However, although both SVTs have the earliest atrial activation in the posteroseptal region, conduction time from that site to the HB region is significantly longer in AVNRT than in orthodromic AVRT. The results are a significantly longer RP interval in lead V 1 and a significantly larger difference in the RP interval between lead V 1 and inferior leads during AVNRT. Therefore ΔRP interval (V 1 –III) of more than 20 milliseconds suggests slow-slow AVNRT (sensitivity, 71%; specificity, 87%).
When the P wave is not visible, typical AVNRT is the most likely diagnosis, but AT with a long PR interval (P wave is obscured within the QRS) and junctional tachycardia are also possible.
Atrial-Ventricular Relationship
SVTs with an A/V ratio of 1 (i.e., equal number of atrial and ventricular events) include AVNRT, AVRT, and AT. On the other hand, an A/V ratio during the SVT of greater than 1 indicates the presence of AV block and that the ventricles are not required for the SVT circuit, thereby excluding AVRT and suggesting either AT (most common; see Fig. 11.7 ) or AVNRT (rare; see Fig. 17.9 ). AV dissociation (even complete AV block) can be observed during AT (most common) or AVNRT (rare). VA block during SVT is rare, but can occur in automatic junctional tachycardia with retrograde VA block and orthodromic AVRT using a nodofascicular or nodoventricular BT for retrograde conduction. Intra-Hisian reentry is another potential mechanism, but it is a theoretical entity whose clinical occurrence has not convincingly been demonstrated.
QRS Morphology
The QRS morphology during SVT is usually the same as in NSR. However, SVT can present as a wide complex tachycardia (QRS duration greater than 120 milliseconds) due to rate-related aberrant conduction, preexisting intraventricular conduction disturbance (IVCD), or ventricular preexcitation over an anterogradely conducting BT.
Functional aberration during SVT is much more common in orthodromic AVRT than AVNRT or AT (90% of SVTs with sustained left bundle branch block [LBBB] are orthodromic AVRTs). Thus the mere presence of LBBB aberrancy during SVT is suggestive of orthodromic AVRT, but can still occur in other types of SVTs.
Preexcited SVTs include antidromic AVRT, whereby the BT is an essential part of the tachycardia circuit, and AVNRT and AT with ventricular preexcitation over a bystander BT.
QRS alternans during fast SVTs is most commonly seen in orthodromic AVRT but can also be seen with other types of SVTs as well. However, when QRS alternans occurs during a relatively slow SVT, the diagnosis is almost always orthodromic AVRT.
Effects of Interventions
Carotid sinus massage or adenosine can result in one of four possible effects: (1) temporary decrease in the atrial rate in patients with sinus tachycardia or automatic AT; (2) slowing of AVN conduction and AVN block, which can unmask atrial electrical activity—that is, reveal P waves or flutter waves in patients with AT or AFL by decreasing the number of QRS complexes that obscure the electrical baseline; (3) terminating the SVT; or (4) no effect is observed.
Carotid sinus massage or adenosine can terminate the SVT, especially if the rhythm is AVNRT or AVRT by transient slowing and block of AVN conduction and interrupting the reentry circuit; termination of focal AT can occur but is much less common. A continuous ECG tracing should be recorded during these maneuvers because the response can aid in the diagnosis and changes can be subtle (rate slowing or transient AV block). Termination of the tachycardia with a P wave after the last QRS complex is most common in AVRT and typical AVNRT and is rarely seen with AT ( see Fig. 18.36 ), whereas termination of the tachycardia with a QRS complex is more common with AT, atypical AVNRT, and PJRT ( see eFig. 18.5 ). If the tachycardia continues despite development of AV block, the rhythm is almost certainly AT or AFL; AVRT is excluded and AVNRT is very unlikely.
Electrophysiological Testing
Discussion in this section will focus on differential diagnosis of narrow QRS complex paroxysmal SVTs, including focal AT, orthodromic AVRT, and AVNRT. The goals of EP testing in these patients include the following: (1) evaluation of baseline cardiac electrophysiology; (2) induction of SVT; (3) evaluation of the mode of initiation of the SVT; (4) definition of atrial activation sequence during the SVT; (5) definition of the A/V relationship at the onset and during the SVT; (6) evaluation of the effect of BBB on the tachycardia cycle length (TCL) and VA interval; (7) evaluation of the SVT circuit and requirement for the atria, HB, or ventricles in the initiation and maintenance of the SVT; (8) evaluation of the SVT response to programmed atrial and ventricular stimulation; and (9) evaluation of the effects of drugs and physiological maneuvers on the SVT.
Baseline Observations During Sinus Rhythm
The presence of preexcitation during NSR suggests AVRT as the likely diagnosis; however, it does not exclude other causes of SVT during which the BT is an innocent bystander. Furthermore, the absence of preexcitation during NSR does not exclude the presence of an AV BT or the diagnosis of AVRT.
Programmed Electrical Stimulation During Sinus Rhythm
The programmed stimulation protocol typically includes: (1) ventricular burst pacing from the right ventricular (RV) apex (down to the pacing cycle length [PCL] at which VA block develops); (2) single and double ventricular extrastimulus (VES; down to the ventricular effective refractory period [ERP]) at multiple PCLs (600 to 400 milliseconds) from the RV apex; (3) atrial burst pacing from the high RA and CS (down to the PCL at which 2 : 1 atrial capture occurs); (4) single and double atrial extrastimulations (AESs) (down to the atrial ERP) at multiple PCLs (600 to 400 milliseconds) from the high RA and CS; and (5) administration of isoproterenol infusion (0.5 to 4 µg/min) or epinephrine (0.05 to 0.2 µg/kg per minute) infusion as needed to facilitate tachycardia induction or sustenance.
Programmed Atrial Stimulation During Sinus Rhythm
Dual AVN physiology.
Although the demonstration of dual AVN physiology during programmed atrial stimulation favors AVNRT as the mechanism of SVT (positive predictive value greater than 80%), it is not an uncommon finding in patients with other types of SVTs. Furthermore, failure to demonstrate dual AVN physiology does not exclude the possibility of AVNRT, and might be related to similar fast and slow AVN pathway ERPs. Then, dissociation of refractoriness of the fast and slow AVN pathways can be necessary ( see Chapter 17 ).
Ventricular preexcitation.
Atrial stimulation can help unmask preexcitation if it is not manifest during NSR because of fast AVN conduction, slow BT conduction, or distant (left lateral) BT location. AES and atrial pacing from any atrial site result in slowing of AVN conduction and, consequently, unmask or increase the degree of preexcitation over the AV BT ( see Fig. 18.23 ). Moreover, atrial stimulation close to the BT insertion site results in maximal preexcitation and the shortest P-delta interval because of the ability to advance the activation of the AV BT down to its ERP from pacing at this site caused by the lack of intervening atrial tissue, whose conduction time and refractoriness can otherwise limit the ability of the AES to stimulate the BT prematurely ( see Fig. 18.24 ).
The failure of atrial stimulation to increase the amount of preexcitation can be caused by: (1) markedly enhanced AVN conduction; (2) the presence of another AV BT; (3) pacing-induced block in the AV BT because of a long ERP of the BT (longer than that of the AVN); (4) total preexcitation already present at the basal state caused by prolonged or absent AVN-His-Purkinje system (HPS) conduction; (5) decremental conduction in the BT; or (6) the presence of a fasciculoventricular BT rather than an AV BT.
Extra atrial beats.
AES and atrial pacing can trigger extra atrial beats or echo beats. Those beats can be caused by different mechanisms.
Intraatrial reentrant beats.
These beats usually occur at short coupling intervals, and can originate anywhere in the atrium. Therefore the atrial activation sequence depends on the site of origin of the beat. The more premature the AES, the more likely it will induce nonspecific intraatrial reentrant beats and short runs of irregular AT or AF.
Catheter-induced atrial beats.
These beats usually have the earliest activation site recorded at that particular catheter tip and have the same atrial activation sequence as the atrial impulse produced by pacing from that catheter. Portions of the catheter proximal to the tip usually do not elicit mechanically induced ectopic impulses.
AVN echo beats.
AVN echoes occur in the presence of anterograde dual AVN physiology ( see Fig. 4.23 ). Such beats require anterograde block of the atrial stimulus in the fast AVN pathway, anterograde conduction down the slow pathway, and then retrograde conduction up the fast pathway. AVN echo beats have several features: they appear reproducibly after a critical A 2 -H 2 interval; the atrial activation sequence is consistent with retrograde conduction over the fast pathway, with the earliest atrial activation site in the HB; and the VA interval is very short, but it can be longer if the atrial stimulus causes anterograde concealment (and not just block) in the fast pathway.
AV echo beats.
AV echo beats occur secondary to anterograde conduction of the atrial stimulus over the AVN-HPS and retrograde conduction over a BT (concealed or bidirectional BT). If preexcitation is manifest during atrial stimulation, the last atrial impulse inducing the echo beat will demonstrate loss of preexcitation because of anterograde block in the BT, and the atrial activation sequence and P wave morphology of the echo beat will depend on the location of the BT mediating VA conduction ( see Fig. 3.9 ). These beats have a relatively short VA interval (QRS onset to earliest atrial activation) but always longer than 70 milliseconds. Moreover, the VA interval of the AV echo beat remains constant, regardless of the varying coupling interval of the AES triggering the echo beat (“VA linking”). Of note, AV echo beats also can occur secondary to anterograde conduction of the atrial stimulus over a manifest BT and retrograde conduction over the AVN, in which setting the last paced beat is associated with anterograde block in the AVN and fully preexcited QRS complex.
Programmed Ventricular Stimulation During Sinus Rhythm
Retrograde VA conduction.
The absence of VA conduction (at ventricular PCLs greater than 600 milliseconds and despite isoproterenol administration) or the presence of decremental VA conduction makes the presence of a retrogradely conducting BT unlikely.
The normal AVN response to rate-incremental ventricular pacing or progressively premature single VESs is a gradual delay of VA conduction (manifest as gradual prolongation of the VA and His bundle–atrial [HA] intervals) as the PCL or VES coupling interval decreases. Nondecremental VA conduction suggests BT conduction, although fast pathway conduction in patients with AVNRT often shows minimal decrement. Nonetheless, some BTs with retrograde decremental conduction properties can also exhibit prolongation of conduction time and VA interval with ventricular pacing or VES. In addition, at short ventricular PCLs or VES coupling intervals, intramyocardial conduction delay can occur, resulting in prolongation in the VA interval; however, the local VA interval at the BT location remains unchanged. Furthermore, short ventricular PCLs or VES coupling intervals can encroach on the BT refractoriness, causing some decremental conduction, with a consequent increase in the surface VA interval and the local VA interval.
During the delivery of progressively premature single VESs, an abrupt increase in the VA conduction interval is often observed. This may be due to a variety of reasons including: (1) retrograde block in the AVN fast pathway and subsequent VA conduction over the slow pathway; (2) retrograde block in the right bundle branch (RB) and subsequent retrograde conduction over the left bundle branch (LB); or (3) retrograde block in the BT and subsequent VA conduction only over the AVN.
Retrograde atrial activation sequence.
VA conduction over the AVN produces a classic concentric atrial activation sequence starting in the anteroseptal or posteroseptal region of the RA because of retrograde conduction over either the fast or the slow AVN pathways, respectively. The duration of atrial activation is short because both atria are roughly simultaneously activated. Thus, if a normal P wave lasts 80 milliseconds (about 40 milliseconds for each atrium), a concentrically activated P wave (and total atrial activation time) approximates 40 milliseconds.
Eccentric retrograde atrial activation (i.e., lateral left atrium or RA earlier than AV junction and opposite chamber) can also occur. In the presence of a retrogradely conducting AV BT (whether manifest or concealed), atrial activation can result from conduction over the BT, over the AVN, or a fusion of both ( see Fig. 18.25 ). Conduction over the BT alone is the most common pattern at short PCLs or short VES coupling intervals. In this setting, the VA conduction time is fairly constant over a wide range of PCLs and VES coupling intervals (given the absence of intraventricular conduction abnormalities or additional BTs). On the other hand, retrograde conduction over both the BT and HPS-AVN is especially common when RV pacing is performed in the presence of a left-sided BT at long PCLs or long VES coupling intervals. This occurs because it is easier to engage the RB and conduct retrogradely through the AVN than it is to reach a distant left-sided BT. In this setting, the atrial activation pattern depends on the refractoriness and conduction times over both pathways and usually exhibits a variable degree of fusion. In addition, VA conduction can proceed over the HPS-AVN alone, resulting in a normal pattern of VA conduction, or can be absent because of block in both the HPS-AVN and BT, which is especially common with short PCLs and very early VES.
An eccentric atrial activation sequence in response to ventricular stimulation suggests the presence of an AV BT mediating VA conduction ( see Fig. 18.25 ). However, a concentric retrograde atrial activation sequence does not exclude the presence of a septal or paraseptal BT, or a free-wall BT located far from the pacing site, allowing for preferential VA conduction over the AVN. In addition, AVN slow pathway conduction can be associated with an eccentric atrial activation sequence in the CS. Accurate analysis of the atrial activation sequence frequently requires the use of multielectrode catheters around the tricuspid annulus and deep in the CS.
Retrograde dual AVN physiology.
Demonstration of retrograde dual AVN physiology during programmed ventricular stimulation suggests AVNRT (occurring most commonly during atypical AVNRT), but it can also be observed with other SVTs. Importantly, failure to demonstrate retrograde dual AVN physiology in patients with AVNRT can be the result of similar fast and slow AVN pathway ERPs, in which setting dissociation of refractoriness of the fast and slow AVN pathways is required ( see Chapter 17 ).
VA block at a ventricular PCL greater than 600 milliseconds or decremental VA conduction during ventricular pacing makes the presence of a retrogradely conducting BT unlikely, except for decrementally conducting BTs and the rare catecholamine-dependent BTs. In addition, development of VA block during ventricular pacing in response to adenosine suggests the absence of a BT.
VES during His bundle refractoriness.
A VES delivered when the HB is refractory (i.e., when the His potential is already manifest or within 35 to 55 milliseconds before the time of the expected His potential) that results in atrial activation is diagnostic of the presence of a retrogradely conducting BT. Because the HPS-AVN is already refractory and cannot mediate VA conduction, retrograde atrial activation from ventricular stimulation will necessarily be mediated by a BT.
Furthermore, an earlier VES that does conduct to the HB and results in an atrial activation that either precedes HB activation ( see Fig. 18.27 ) or is associated with an apparent HA interval shorter than that during drive complexes indicates “atrial preexcitation” via an AV BT.
Importantly, if a VES delivered when the HB is refractory does not result in atrial activation, this does not necessarily exclude the presence of a retrogradely conducting AV BT, because such a VES can be associated with retrograde block in the BT itself ( see Fig. 18.25 ). In addition, the lack of such a response does not exclude the presence of unidirectional (anterograde-only) AV BTs.
Differential-site RV pacing.
Differential-site RV pacing can help exclude the presence of a retrogradely conducting septal AV BT. The response to differential-site RV pacing can be evaluated by comparing two variables between RV basal and RV apical pacing: the VA interval (i.e., the stimulus-to-atrial [S-A] interval) and atrial activation sequence ( see Fig. 18.28 ).
VA interval.
In the absence of a septal BT, the RV apex, although anatomically more distant from the atrium than the RV base, is nonetheless electrically closer because of its proximity to the entrance to the HPS (i.e., RB terminus). Therefore the VA interval is shorter during pacing from the RV apex than that during RV basal pacing. In contrast, in the presence of a septal BT, the RV base is closer than the RV apex to the BT ventricular insertion site. As a result, the VA interval is shorter during RV basal pacing compared to apical pacing. Therefore, when the VA interval during RV apical pacing is longer than that during RV basal pacing, a retrogradely conducting AV BT is diagnosed ( see Fig. 18.28 ), and when the VA interval during RV apical pacing is shorter than that during RV basal pacing, a retrogradely conducting septal BT is excluded. Importantly, while this maneuver suggests AVN conduction, it may not exclude the presence of a free wall or a slowly conducting BT. It is important to ensure that the basal pacing site captures neither the HB or the RB, nor the atrium, which would yield spurious results.
Atrial activation sequence.
In the absence of a retrogradely conducting BT, the atrial activation sequence remains identical regardless of the RV pacing site because retrograde VA conduction propagates only over the AVN in both settings. In contrast, in the presence of a septal BT, atrial activation results from VA conduction over the BT during pacing at the RV base (because of its immediate proximity to the BT), and over the AVN, the BT, or a fusion of both during pacing at the RV apex. Therefore a change in retrograde atrial activation sequence in response to differential RV pacing (RV base vs. RV apex) indicates the presence of an AV BT, but a constant atrial activation sequence is not helpful in excluding the presence of a BT, because AVN-HPS conduction delay can allow retrograde VA conduction to occur over the BT during RV pacing from both the apex and the base.
Limitations.
This maneuver does not exclude the presence of a distant right or left free-wall BT because the site of pacing is far from the BT; as a consequence, pacing from the RV apex or RV base may result in preferential VA conduction exclusively over the AVN and a constant atrial activation sequence. This can be avoided by moving the basal pacing site closer to the putative BT location along the tricuspid or mitral annulus.
In addition, this maneuver does not exclude the presence of a slowly conducting BT. The VA interval criterion identifies the actual route of VA conduction and therefore the fastest path of this conduction; hence, a slowly conducting BT would be missed in the presence of fast VA conduction over the HPS-AVN.
The occurrence of right bundle branch block (RBBB) (but not LBBB) also can alter the significance of the VA interval criterion, especially when VA conduction propagates over the HPS-AVN. In the presence of retrograde RBBB, VA conduction occurs over the LB-HB; therefore the VA interval depends on the distance between the pacing site and the LB rather than the RB, and access of the paced wavefront to the LB can be faster for RV basilar or septal pacing compared with pacing from the RV apex ( Fig. 20.6 ).
Of note, the exact entrance to the HPS (i.e., the terminus of the RB) is difficult to identify; the entrance site can be located in the midseptum and not at the RV apex. In such situations, both the RV base and apex can be equidistant from the entrance to the HPS so that pacing at either location will produce a constant VA interval during retrograde conduction over the AVN. Therefore patient-to-patient variability with regard to the distance of the pacing catheter to the RB terminus can potentially introduce conflicting results. This problem is largely resolved by first pacing from the HB region (while avoiding HB capture) and then moving the pacing catheter in a stepwise fashion along the septum toward the RV apex. Pacing from sequential sites in this path brings the catheter closer to the RB terminus (entrance of the HPS), as reflected by shortening of the VA interval for AVN conduction, but not for BT conduction. As the pacing catheter is moved farther apically, the pacing sites become less useful diagnostically because the relative distance from the RB terminus to the insertion of the BT becomes less clear.
Retrograde RBBB during VES.
Retrograde RBBB occurs frequently during VES testing, and it can be diagnosed by observing the retrograde His potential during the drive train and its abrupt delay following the VES. Often, however, it is difficult to visualize the retrograde His potential during the pacing train; nevertheless, the sudden appearance of an easily distinguished retrograde His potential, separate from the ventricular electrogram following the VES, can be sufficient to recognize retrograde RBBB.
Prolongation of the VH interval is observed on development of retrograde RBBB because conduction must traverse the interventricular septum (which requires approximately 60 to 70 milliseconds in normal hearts), conduct retrogradely via the LB, and ascend to reach the HB. Although an increase in the VH interval necessarily occurs with retrograde RBBB, whether a similar increase occurs in the VA interval depends on the nature of VA conduction (over the AVN vs. BT).
Measurement of the effect of the development of retrograde RBBB during VES on the retrograde VH and VA intervals can help in distinguishing between retrograde AVN and BT conduction. In the absence of a BT, the AVN can be activated in a retrograde fashion only after retrograde activation of the HB; as a consequence, VA activation will necessarily be delayed with retrograde RBBB, and the increase in the VA interval will be similar to the increase in the VH interval. On the other hand, when retrograde conduction is via a BT, there will be no expected increase in the VA interval when retrograde RBBB is induced. Thus the increase in the VA interval is minimal and always less than the increase in the VH interval.
Extra ventricular beats.
Ventricular stimulation can trigger extra ventricular beats or echo beats. These beats can be caused by different mechanisms.
Bundle branch reentrant beats.
During RV stimulation at close coupling intervals, progressive retrograde conduction delay and block occur in the RB, so that retrograde HB activation occurs via the LB. At this point, the His potential usually follows the local ventricular electrogram. Further decrease in the VES coupling interval produces an increase in retrograde HPS conduction delay. When a critical degree of HPS delay (S 2 -H 2 interval) is attained, the impulse can return down the initially blocked RB and result in a QRS of similar morphology to the paced QRS at the RV apex—specifically, it will look like a typical LBBB pattern with left axis deviation because ventricular activation originates from conduction over the RB. The HV interval of the bundle branch reentry beat is usually longer than or equal to the HV interval during NSR. Retrograde atrial activation over the AVN, if present, follows the His potential ( see Fig. 4.26 ); if over a left-sided BT, atrial activation follows the QRS.
AVN echo beats.
AVN echoes are caused by reentry in the AVN in patients with retrograde dual AVN physiology ( see Fig. 17.13 ). The last paced beat conducts retrogradely up the slow AVN pathway and then anterogradely down the fast pathway to produce the echo beat. AVN echoes appear reproducibly after a critical H 2 -A 2 interval (or V 2 -A 2 interval, when the His potential cannot be seen), and manifest as extra beats with a normal anterograde QRS morphology and atrial activity preceding the His potential before the echo beat. This phenomenon can occur at long or short coupling intervals and depends only on the degree of retrograde AVN conduction delay. In most cases, this delay is achieved before the appearance of a retrograde His potential beyond the local ventricular electrogram (i.e., before retrograde block in the RB).
AV echo beats.
These beats occur secondary to retrograde block in the HPS-AVN and retrograde VA conduction over an AV BT, followed by anterograde conduction over the AVN. Alternatively, echo beats can result from retrograde block in the BT and retrograde VA conduction over the AVN-HPS, followed by anterograde conduction over the AV-BT. In the first setting, the echo beat displays a narrow QRS; in the latter setting, the echo beat is fully preexcited ( see Fig. 18.25 ).
Intraventricular reentrant beats.
This response occurs most commonly in the setting of a cardiac pathological condition, especially coronary artery disease, and usually occurs at short coupling intervals. It can have any QRS morphology, but more often RBBB than LBBB in patients with prior myocardial infarction. These responses are usually nonsustained (1 to 30 complexes) and typically polymorphic. In patients without prior clinical ventricular arrhythmias, such responses are of no clinical significance.
Catheter-induced ventricular beats.
Such beats usually have the earliest ventricular activation site recorded at that particular catheter tip and have the same QRS morphology as the QRS produced by pacing from that catheter.
Para-Hisian Pacing During Sinus Rhythm
Concept of para-Hisian pacing.
The para-Hisian pacing site is unique because it is anatomically close but electrically distant from the HB. Para-Hisian pacing at high output simultaneously captures the HB or proximal RB, as well as the adjacent ventricular myocardium. At lower output, direct HB-RB capture is lost and retrograde activation of the HB is delayed because the HB and RB are insulated from the adjacent myocardium and the peripheral inputs to the Purkinje system are located far from the para-Hisian pacing site. By maintaining local ventricular capture while intermittently losing HB-RB capture, retrograde VA conduction can be classified as dependent on the timing of local ventricular activation (BT), HB activation (AVN), or both (fusion).
Para-Hisian pacing can result in capture of the ventricle (indicated by a wide paced QRS), the atrium (indicated by atrial activation in the HB region immediately following the pacing artifact), the HB (indicated by narrow paced QRS), or any combination of these ( see Fig. 18.29 ). Careful attention must be given to minimize the atrial signal seen on the recording from the pacing electrode pair to ensure that local atrial capture does not occur during pacing.
Technique of para-Hisian pacing.
Ideally, two quadripolar catheters (one for pacing and another for recording) or a single octapolar catheter (for both pacing and recording) is placed at the distal HB-RB region. Alternatively, a single quadripolar HB catheter (which is typically used during a diagnostic EP study) is used, taking into account that such an approach would limit the ability to record the retrograde His potential and HA interval.
Overdrive ventricular pacing is performed (from the pair of electrodes on the HB catheter that records activation of the distal HB-RB) at a long PCL (greater than 500 milliseconds) and high output. During pacing, direct HB-RB capture is indicated by narrowing of the paced QRS width. The pacing output and pulse width are then decreased until the paced QRS widens, which is associated with a delay in the timing of the retrograde HB potential, indicating loss of HB-RB capture. The pacing output is increased and decreased to gain and lose HB-RB capture, respectively, while local ventricular capture is maintained. Occasionally, the HB can be captured uniquely (without myocardial capture), resulting in a QRS identical to the patient’s normally conducted QRS.
Response to para-Hisian pacing.
When the ventricle and HB are captured simultaneously, the wavefront activates the ventricles over the HPS and results in a relatively narrow QRS. The wavefront can also travel retrogradely over the AVN to activate the atrium with an SA interval (i.e., the interval from the pacing stimulus to the atrial electrogram) that represents conduction time over the proximal part of the HB and AVN (i.e., SA interval = HA interval) because the onset of ventricular activation and HB activation occur simultaneously (i.e., stimulus–His bundle [SH] interval = 0).
When the ventricle is captured but not the atrium or HB, the wavefront activates the ventricles by muscle-to-muscle conduction, resulting in a wide QRS with LBBB morphology caused by pacing in the RV. Once the wavefront reaches the RV apex, it conducts retrogradely up the RB and then over the HB and AVN to activate the atrium. In this setting, the SA interval represents the conduction time from the RV base to the HB (SH interval) plus the conduction time over the HB and AVN (HA interval). Thus, normally (in the absence of a retrogradely conducing BT), para-Hisian pacing results in a shorter SA interval when the HB (or HB plus RV) is captured than the SA interval when only the ventricle is captured.
In the presence of a septal AV BT, the SA interval usually remains fixed regardless of whether the HB is being captured, because in both situations the paced impulse travels retrogradely over the BT, with constant conduction time to the atrium as long as local ventricular myocardium is being captured. Atrial activation in this setting can be secondary to activation over the BT, especially when only the ventricle is captured, or a result of fusion of conduction over both the BT and AVN, especially when both the ventricle and the HB are captured. Nevertheless, because VA conduction time over the BT is faster than that over the AVN, the timing of the earliest atrial activation (i.e., the SA and local VA intervals) remains constant, regardless of whether HB-RB capture occurs and regardless of whether atrial activation occurs exclusively over the AV BT or as a fusion of conduction over both the AV BT and AVN.
Seven patterns of response to para-Hisian pacing can be observed ( Box 20.1 ; see Figs. 18.29 and 18.30 ). In patients with retrogradely conducing BTs, in whom retrograde conduction occurs over both the AVN and BT during para-Hisian pacing, the amount of atrial myocardium activated by each of the two pathways (atrial fusion) is dependent on four variables: (1) the magnitude of delay in retrograde activation of the HB (i.e., SH interval); (2) retrograde conduction time over the AVN (HA interval); (3) intraventricular conduction time from the para-Hisian pacing site to the ventricular end of the BT (SV BT ); and (4) retrograde conduction time over the BT (VA BT ). The first two variables (SH plus HA) form the SA interval resulting from retrograde VA conduction over the AVN, and the latter two variables (SV BT plus VA BT ) form the SA interval resulting from retrograde VA conduction over the BT. The amount of the atria activated by the AVN is greater during HB-RB capture, secondary to a minimal SH interval (i.e., SA interval = HA interval). Loss of HB-RB capture results in prolongation of the SH interval and, therefore, an increase in the amount of atria activated by the BT, resulting in a change in the retrograde atrial activation sequence. Consequently, a change in the retrograde atrial activation sequence with loss of HB-RB capture always indicates the presence of retrograde conduction over both the BT and AVN. There are four such patterns (patterns 4 through 7). In patterns 4 and 5, HB-RB capture is associated with activation of the atria exclusively by retrograde conduction over the AVN. In patterns 6 and 7, HB-RB capture results in atrial activation over both the AVN and the BT.
Pattern 1 (AVN/AVN Pattern)
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Retrograde conduction occurs exclusively over the AVN regardless of whether the HB-RB is captured.
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Loss of HB-RB capture results in an increase in the SA interval in all electrograms equal to the increase in the SH interval, with no change in the atrial activation sequence. The HA interval remains essentially the same.
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This response indicates that retrograde conduction is dependent on HB activation and not on local ventricular activation.
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This pattern is observed in all patients with AVNRT and is not observed in any patient with a septal or right free-wall BT. However, this pattern can be observed in some patients with a left free-wall BT or PJRT, in which case retrograde AVN conduction masks the presence of retrograde BT conduction.
Pattern 2 (BT-BT Pattern)
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Retrograde conduction occurs exclusively over a single BT.
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The SA interval is identical during HB-RB capture and noncapture, indicating that retrograde conduction is dependent on local ventricular activation and not on HB activation.
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This pattern does not exclude the presence of retrograde conduction over the AVN with longer conduction time or a second BT with longer conduction time or located far from the pacing site.
Pattern 3 (BT-BT L Pattern)
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Retrograde conduction occurs exclusively over a BT.
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Loss of HB-RB capture is associated with a delay in the timing of ventricular activation close to the BT. This results in an increase in the SA interval in all electrograms, with no change in the atrial activation sequence. The local VA interval, recorded close to the BT, remains approximately the same. The increase in the SA interval is less than the increase in the SH interval. Therefore the HA interval is shortened with loss of HB-RB capture, indicating that retrograde conduction cannot be occurring over the AVN. Two mechanisms have been identified accounting for the delay in timing of ventricular activation close to the BT.
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Activation of the HPS results in earlier ventricular activation near some BTs located far from the para-Hisian pacing site, such as left lateral or anterolateral BTs.
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Decreasing the pacing output to lose HB-RB capture occasionally results in a small delay in ventricular activation close to the pacing site.
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Pattern 3 is referred to as the BT-BT L pattern, where BT L refers to a lengthening of the SA interval with loss of HB-RB capture.
Pattern 4 (AVN-BT Pattern)
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Loss of HB-RB capture is associated with atrial activation exclusively over the BT.
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Loss of HB-RB capture results in an increase in SA and local VA intervals in all electrograms, with the least increase occurring in the electrogram closest to the BT.
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The HA interval shortens, indicating that the atrium near the AVN is activated by the BT before retrograde conduction over the AVN is complete.
Pattern 5 (AVN-Fusion Pattern)
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Loss of HB-RB capture results in activation of part of the atria by the AVN and part by the BT.
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Loss of HB-RB capture is associated with an increase in SA and local VA intervals in all electrograms.
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The HA interval remains constant, indicating that part of the atria was still activated by the AVN.
Pattern 6 (Fusion-BT Pattern)
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Loss of HB-RB capture results in atrial activation exclusively over the BT.
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Loss of HB-RB capture is associated with no change in the SA or local VA intervals recorded near the BT.
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In the HB electrogram, the SA interval increases, but not as much as the SH interval, leading to a decrease in the HA interval. This indicates that the atrial myocardium in that region is no longer activated by the AVN.
Pattern 7 (Fusion-Fusion Pattern)
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The atria continue to be activated by both the AVN and the BT during loss of HB-RB capture, with more of the atria activated by the BT than during HB-RB capture.
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Like pattern 6, loss of HB-RB capture is associated with minimal change in the SA or local VA intervals recorded close to the BT; however, the HA interval remains essentially the same, indicating that part of the atria is still activated by the AVN.
AVN, Atrioventricular node; AVNRT, atrioventricular nodal reentrant tachycardia; BT, bypass tract; HA, His bundle–atrial; HB-RB, His bundle–right bundle branch; HPS, His-Purkinje system; PJRT, permanent junctional reciprocating tachycardia; SA, stimulus-atrial; SH, stimulus–His bundle; VA, ventriculoatrial.
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