Approach to Paroxysmal Supraventricular Tachycardias

Chapter 20 Approach to Paroxysmal Supraventricular Tachycardias




Clinical Considerations


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, the atrioventricular node (AVN), the proximal HB, the coronary sinus (CS), the pulmonary veins (PVs), the venae cavae, or abnormal atrioventricular (AV) connections other than the HB (i.e., bypass tracts, BTs).1



Epidemiology


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 QRS complex SVTs include sinus tachycardia, inappropriate sinus tachycardia, sinoatrial nodal reentrant tachycardia, atrial tachycardia (AT), multifocal AT, atrial fibrillation (AF), atrial flutter (AFL), junctional ectopic tachycardia, nonparoxysmal junctional tachycardia, atrioventricular nodal reentrant tachycardia (AVNRT), and atrioventricular reentrant tachycardia (AVRT).


Narrow QRS complex 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. The major causes are AVNRT (approximately 50% to 60% of cases), AVRT (approximately 30% of cases), and AT (approximately 10% of cases).


Paroxysmal SVT with sudden onset and termination is relatively common; the estimated prevalence in the normal population is 2.25/1000, with an incidence of 35/100,000 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. Women have a twofold greater risk of developing this arrhythmia than men.


The mechanism of paroxysmal SVT is significantly influenced by both age and gender. In a large cohort of patients with symptomatic paroxysmal SVT referred for ablation, 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. 20-1). These trends were similar in both genders, although AVNRT replaced AVRT as the predominant mechanism much earlier in women.2 The early predominance of AVRT is consistent with the congenital nature of the substrate and with the fact that symptom onset occurs earlier in patients with AVRT than AVNRT, most commonly in the first two decades of life. 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.



AVNRT is the predominant mechanism overall in patients undergoing ablation and after the age of 20 years 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. AVRT presents earlier, with an average of more than 10 years separating the time of clinical presentation of AVRT versus AVNRT. 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, that is, teens versus early childhood years, favor the diagnosis of AVNRT over AVRT.3


ATs comprise a progressively greater proportion of those with paroxysmal SVT with increasing age, accounting for 23% of 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 electrophysiological (EP) substrate (including cellular coupling and autonomic influences) can contribute to the increased incidence of AT in older individuals.



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 dizziness. Dizziness can occur initially because of hypotension, but it then disappears when the sympathetic response to the SVT stabilizes the blood pressure. Rapid ventricular rates can be associated with complaints of dyspnea, weakness, angina, or even frank syncope, and can at times be disabling. Neck pounding can occur during tachycardia because of simultaneous contraction of the atria and ventricles against closed mitral and tricuspid valves. The latter is more common in patients with typical AVNRT, occurring in approximately 50% of patients.


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. In patients without structural heart disease, the physical examination is usually remarkable only for a rapid, regular heart rate. At times, because of the simultaneous contraction of atria and ventricles, cannon A waves can be seen in the jugular venous waveform (described as the “frog” sign). This clinical feature has been reported to distinguish paroxysmal SVT resulting from AVNRT from that caused by orthodromic AVRT. Although the atrial contraction during AVRT will occur against closed AV valves, the longer VA interval results in separate ventricular and then atrial contraction and a relatively lower right atrial (RA) and venous pressure; therefore, the presence of palpations in the neck is experienced less commonly (up to 17%) in patients with AVRT.3 In patients with an AT exhibiting AV block, usually of the Wenckebach type, the ventricular rate is irregular.



Initial Evaluation


History, physical examination, and an electrocardiogram (ECG) constitute an appropriate initial evaluation 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-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.


Transesophageal atrial recordings and stimulation can be used in selected cases for diagnosis or to provoke paroxysmal tachyarrhythmias if the clinical history is insufficient or if other measures have failed to document an arrhythmia. Esophageal stimulation is not indicated if invasive EP investigation is planned. Invasive EP testing with subsequent catheter ablation may 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 transient block in the AVN.


Vagal maneuvers such as carotid sinus massage, Valsalva maneuvers, or the dive reflex are usually used as the first step and generally terminate the SVT. Valsalva is the most effective technique in adults, but carotid sinus massage can also be effective. 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. Vagal maneuvers present the advantage of being relatively simple and noninvasive, but their efficacy seems to be lower compared with pharmacological interventions, with the incidence of paroxysmal SVT termination ranging from 6% to 22% following carotid sinus massage.


When vagal maneuvers are unsuccessful, termination can be achieved with antiarrhythmic drugs whose primary effects increase AVN refractoriness, decrease AVN conduction (negative dromotropic effect), or both. These drugs can have direct (e.g., verapamil and diltiazem block the slow inward calcium current of the AVN) or indirect effects (e.g., digoxin increases vagal tone to the AVN). In most patients, the drug of choice is either adenosine or verapamil.


The advantages of adenosine include its rapid onset of action (usually within 10 to 25 seconds via a peripheral vein), short half-life (<10 seconds), and high degree of efficacy. The effective dose of adenosine is usually 6 to 12 mg, given as a rapid bolus. Doses up to 12 mg terminate over 90% of paroxysmal SVT episodes. 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 anterograde 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 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, and sometimes subsequently requires immediate electrical cardioversion. Because adenosine is cleared so rapidly, 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 will be effective.


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 intravenously 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 intravenously 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 over 90% of patients with AVN-dependent paroxysmal SVT respond. As with adenosine, transient arrhythmias, including atrial and ventricular ectopy, AF, and bradycardia, can be seen after paroxysmal SVT termination with calcium channel blockers. Hypotension can occur with calcium channel blockers, 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 affected by the arrhythmia rate. Increasing SVT rates are significantly associated with higher percentages of sinus rhythm restoration following treatment with adenosine. In contrast, the efficacy of verapamil in restoring sinus rhythm was inversely related to the rate of paroxysmal SVT.4


Intravenous beta blockers including propranolol (1 to 3 mg), metoprolol (5 mg), and esmolol (500 µg/kg over 1 minute and a 50-µg/kg/min 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 intravenous administration of adenosine and calcium channel blockers. Unless there is strong evidence that a wide QRS tachycardia is AVN-dependent, adenosine, verapamil, and diltiazem should not be used.


Limited data are available on the acute pharmacological therapy of ATs. Automatic or triggered tachycardias and sinus node reentry should respond to adenosine, verapamil, diltiazem, or beta-adrenergic blockers. Other ATs can respond to class I or III antiarrhythmic drugs given orally or parenterally.



Chronic Management


Because most paroxysmal SVTs are generally benign arrhythmias that do not influence survival, the main reason for treatment is to alleviate symptoms. The threshold for initiation of therapy and the decision to treat SVT with oral antiarrhythmic drugs or catheter ablation depends on the frequency and duration of the arrhythmia, severity of symptoms, and patient preference. The threshold for treatment will also reflect whether the patient is a competitive athlete, a woman considering pregnancy, or someone with a high-risk occupation. Catheter ablation is an especially attractive option for patients who desire to avoid or are unresponsive or intolerant to drug therapy.


For patients requiring therapy who are reluctant to undergo catheter ablation, antiarrhythmic drug therapy remains a viable alternative. For AVN-dependent paroxysmal SVT, calcium channel blockers and beta blockers will improve symptoms in 60% to 80% of patients. A comparison of verapamil, propranolol, and digoxin has shown equivalent efficacy in a small group of patients. However, in general, calcium channel blockers and beta blockers are preferred to digoxin. In patients who do not respond, class IC and III drugs can be considered. Flecainide and propafenone affect the AVN and BTs and reduce SVT frequency. Sotalol, dofetilide, and amiodarone are second-line agents. Because sympathetic stimulation can antagonize the effects of many antiarrhythmic agents, concomitant therapy with a beta blocker can improve efficacy.


Patients 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, propranolol, or propafenone to terminate an episode of AVRT or AVNRT effectively. This so-called “pill in the pocket” or “cocktail therapy” is a reasonable treatment option for patients who have tachycardia episodes that are sustained but infrequent enough that daily preventive therapy is not desired. Oral antiarrhythmic drug tablets are not reliably absorbed during rapid paroxysmal SVT, but some patients can respond to self-administration of crushed medications.


Pharmacological management of ATs has not been well evaluated in controlled clinical trials. Depending on the mechanism responsible for the arrhythmia, beta blockers, calcium channel blockers, and class I or III antiarrhythmic drugs may reduce or eliminate symptoms.



Electrocardiographic Features



Assessment of Regularity of the Supraventricular 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 to 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 either multifocal AT or AF (Fig. 20-2). 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. 11-1). 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.




Atrial Activity



Identification


If the patient’s rhythm is regular or has a clearly discernible pattern, the ECG should next be assessed for P waves (atrial activity).5 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 intravenous adenosine may help clarify the diagnosis. These maneuvers may also terminate the SVT.





Termination of the Arrhythmia


Carotid sinus massage or adenosine can terminate the SVT, especially if the rhythm is AVNRT or AVRT. A continuous ECG tracing should be recorded during these maneuvers, because the response can aid in the diagnosis.5 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. 18-22), whereas termination of the tachycardia with a QRS complex is more common with AT, atypical AVNRT, and permanent junctional reciprocating tachycardia (PJRT; see Fig. 18-19). 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.




Characterization of the P/Qrs Relationship






Electrophysiological Testing


Discussion in this section will focus on differential diagnosis of narrow QRS complex paroxysmal SVTs, including 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 relationship of the P wave to the QRS at the onset and during the SVT; (6) evaluation of the effect of BBB on the tachycardia cycle length (CL) and ventriculoatrial (VA) interval; (7) evaluation of the SVT circuit and requirement for the atria, His bundle (HB), and/or ventricles in the initiation and maintenance of the SVT; (8) evaluation of the SVT response to programmed electrical stimulation and overdrive pacing from the atrium and ventricle; and (9) evaluation of the effects of drugs and physiological maneuvers on the SVT.




Programmed Electrical Stimulation during Normal Sinus Rhythm


The programmed stimulation protocol should include (1) ventricular burst pacing from the right ventricular (RV) apex (down to pacing CL at which VA block develops); (2) single and double ventricular extrastimuli (VESs, down to the ventricular effective refractory period, ERP) at multiple CLs (600 to 400 milliseconds) from the RV apex; (3) atrial burst pacing from the high right atrium (RA) and coronary sinus (CS; down to the pacing CL at which 2:1 atrial capture occurs); (4) single and double atrial extrastimuli (AESs, down to the atrial ERP) at multiple CLs (600 to 400 milliseconds) from the high RA and CS; and (5) administration of isoproterenol infusion (0.5 to 4 µg/min) as needed to facilitate tachycardia induction.



Atrial Extrastimulation and Atrial Pacing During Normal Sinus Rhythm





Extra Atrial Beats


AES and atrial pacing can trigger extra atrial beats or echo beats. Those beats can be caused by different mechanisms.






Atrioventricular Nodal Echo Beats

These beats 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 AH 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.



Atrioventricular Echo Beats

AV echo beats occur secondary to anterograde conduction of the atrial stimulus over the AVN-HPS and retrograde conduction over an AV 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 AV BT, and atrial activation sequence and P wave morphology of the echo beat will depend on the location of the BT (see Fig. 3-10). These beats have a relatively short VA interval, 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). Alternatively, AV echo beats can occur secondary to anterograde conduction of the atrial stimulus over a manifest AV BT and retrograde conduction over an AVN, in which setting the last paced beat is associated with anterograde block in the AVN and fully preexcited QRS complex.



Ventricular Extrastimulation and Ventricular Pacing During Normal Sinus Rhythm




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. In the presence of a retrogradely conducting AV BT, atrial activation can result from conduction over the AV BT, over the AVN, or a fusion of both (see Fig. 18-16). An eccentric atrial activation sequence in response to ventricular stimulation suggests the presence of an AV BT mediating VA conduction (see Fig. 18-16). The presence of a concentric retrograde atrial activation sequence, however, does not exclude the presence of a retrogradely conducting BT that could be septal in location or located far from the pacing site, allowing for preferential VA conduction over the AVN.



Extra Ventricular Beats


Ventricular stimulation can trigger extra ventricular beats or echo beats. These beats can be caused by different mechanisms.









Right Bundle Branch Block during Ventricular Extrastimulation


During the delivery of progressively premature single VESs, an abrupt increase in the VA conduction interval is often seen. This may be due to a variety of reasons including a change in activation from a BT block to the AVN or a change from fast to slow pathway conduction, or it may be the result of an abrupt change when the refractory period of the RB has been reached.


Retrograde RBBB occurs frequently during VES testing, and can be diagnosed by observing the retrograde His potential during the drive train and its abrupt displacement with the VES. Often, however, it is difficult to visualize the retrograde His potential during the pacing train; even then, the sudden appearance of an easily distinguished retrograde His potential, separate from the ventricular electrogram, may be sufficient to recognize retrograde RBBB.


The VH interval prolongation occurs because, following RBBB, conduction must traverse the interventricular septum (which requires approximately 60 to 70 milliseconds in normal hearts), enter 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. Measurement of the retrograde VH and VA intervals on development of retrograde RBBB during VES can help the distinction 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 at least as much as the increase in the VH interval. In contrast, 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.8



Induction of Tachycardia



Initiation by Atrial Extrastimulation or Atrial Pacing



Inducibility


All types of paroxysmal SVTs can be inducible with atrial stimulation (except automatic AT). SVT initiation that is reproducibly dependent on a critical AH interval is classic for typical AVNRT (see Fig. 17-8). Atypical AVNRT is usually initiated with modest prolongation of the AH interval along the fast pathway with anterograde block in the slow pathway, followed by retrograde slow conduction over the slow pathway. Therefore, a critical AH interval delay is not obvious (see Fig. 17-10). AT initiation also can be associated with AV delay, but that is not a prerequisite for initiation. Orthodromic AVRT usually requires some AV delay for initiation; however, the delay can occur anywhere along the AVN-HPS axis. In patients with baseline manifest preexcitation, initiation of orthodromic AVRT is usually associated with anterograde block in the AV BT and loss of preexcitation following the initiating atrial stimulus, which would then allow that BT to conduct retrogradely during the SVT.9 Initiation may require catecholamines (isoproterenol) with any type of SVT, and this observation does not help for differential diagnosis.

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Jun 22, 2016 | Posted by in MUSCULOSKELETAL MEDICINE | Comments Off on Approach to Paroxysmal Supraventricular Tachycardias

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