# 17 - 256 Paroxysmal Supraventricular Tachycardias

### 256 Paroxysmal Supraventricular Tachycardias

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PART 6
Disorders of the Cardiovascular System
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FIGURE 255-2  Focal atrial tachycardia. In the right panel, a surface 12-lead electrocardiogram shows focal intermittent atrial tachycardia. Note the discrete P waves, with 
isoelectric segments between, as well as the sinus rhythm. The left panel shows an electroanatomic map of the same focal atrial tachycardia originating from the anterior 
interatrial septum, as viewed in an anterior-posterior (AP) view of the left atrium obtained during electrophysiology study and ablation. The colors represent the timing of 
local electrical activation during each tachycardia atrial activation, showing a focal early (red) site. Additional markers of white “flecks” represent conduction direction, 
demonstrating activation of the atrium dispersing from this focal site. Of note, the pink and red dots represent ablation lesions, in this case, for pulmonary vein isolation. 
(Adapted from J Brugada et al: 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. The Task Force for the management of patients with 
supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J 41:655, 2020.)
every other P wave may fall coincident with the QRS. Maneuvers that 
increase AV block, such as carotid sinus massage, Valsalva maneuver, 
or administration of AV nodal–blocking agents, such as adenosine, are 
useful to create AV block that will expose the P wave.
Acute management of sudden-onset, sustained AT is the same as 
for other forms of PSVT, but the response to pharmacologic therapy is 
variable, likely depending on the mechanism (Fig. 255-3).
For AT due to reentry, administration of adenosine or vagal 
maneuvers may transiently increase AV block without terminating 
tachycardia. Some ATs terminate with a sufficient dose of adenosine, 
consistent with triggered activity as the mechanism. Cardioversion can 
be effective in some but fails in others because of immediate recur­
rence, suggesting automaticity as the mechanism in these cases. Beta 
blockers and calcium channel blockers may slow the ventricular rate by 
increasing AV block, which can improve tolerance of the arrhythmias, 
but large doses are sometimes required. Potential precipitating factors 
Focal atrial tachycardia
Hemodynamic
instability
No
Yes
Adenosine
Cardioversion
Ineffective
Non-DHP CCB
and/or beta blocker
Recurrent
or incessant
Ineffective
Ineffective
Antiarrhythmic therapy
Catheter
ablation
(see Table 250-2)
Recurrent
or incessant
FIGURE 255-3  Clinical approach and treatment algorithm for management of focal 
atrial tachycardia. CCB, calcium channel blocker; DHP, dihydropyridine. (Adapted 
from J Brugada et al: 2019 ESC Guidelines for the management of patients with 
supraventricular tachycardia The Task Force for the management of patients 
with supraventricular tachycardia of the European Society of Cardiology (ESC) 
[published correction appears in Eur Heart J 41:4258, 2020]. Eur Heart J 41:655, 2020.)

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and intercurrent illness should be sought and corrected. Underlying 
heart disease should be considered and excluded.
For patients with recurrent episodes, beta blockers, calcium chan­
nel blockers such as diltiazem or verapamil, and antiarrhythmic drugs 
such as flecainide, propafenone, disopyramide, sotalol, and amioda­
rone can be effective, but potential toxicities and adverse effects often 
warrant avoidance of long-term use.
Catheter ablation targeting the AT focus is effective in >80% of 
patients and is recommended for recurrent symptomatic AT when 
drugs fail or are not desired or for incessant AT causing tachycardiainduced cardiomyopathy. Although AT is often a precursor to atrial 
fibrillation or atrial flutter, the associated risk for stroke and, hence, 
indications for long-term anticoagulation are unclear but not consid­
ered equivalent.
■
■FURTHER READING
Brugada J et al: 2019 ESC Guidelines for the management of patients 
with supraventricular tachycardia. The Task Force for the Manage­
ment of Patients with Supraventricular Tachycardia of the European 
Society of Cardiology (ESC) developed in collaboration with the 
Association for European Paediatric and Congenital Cardiology 
(AEPC). Eur Heart J 41:655, 2020.
Callans DJ: Josephson’s Clinical Cardiac Electrophysiology: Techniques 
and Interpretations, 7th ed. Philadelphia, Wolters Kluwer, 2024.
William H. Sauer, Paul C. Zei

Paroxysmal 

Supraventricular 

Tachycardias
In this chapter, sustained supraventricular tachycardias (SVTs) 
dependent on the atrioventricular (AV) node are discussed. These 
include AV nodal reentry tachycardia (AVNRT), junctional tachycar­
dia, AV reciprocating tachycardia (AVRT) utilizing an accessory path­
way, and a group of additional various SVTs that involve an accessory

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FIGURE 256-1  Atrioventricular (AV) node reentry. A. Leads II and V1 are shown. P waves are visible at the end of the QRS complex and are negative in lead II and may give 
the impression of S waves in the inferior limb leads II, III, and aVF and an R′ in lead V1. B. Stylized version of the AV nodal reentry circuit within the triangle of Koch 
(see Fig. 254-1) that involves AV node and its extensions along with perinodal atrial tissue. CS, coronary sinus.
pathway, termed preexcited tachycardias. The term SVT encompasses a 
broad group of tachyarrhythmias based on anatomic origin and techni­
cally includes sinus tachycardia, atrial tachycardia (AT), atrial flutter, 
and atrial fibrillation; however, for the purposes of describing an orga­
nized approach to diagnosis and treatment of SVT, a separate discus­
sion for these non-AV nodal–dependent SVTs are discussed elsewhere.
ATRIOVENTRICULAR NODAL REENTRY 
TACHYCARDIA
AVNRT is the most common form of paroxysmal supraventricular 
tachycardia (PSVT), representing ~60% of cases referred for catheter 
ablation. It most commonly manifests in the second to fourth decades 
of life, more often in women. It is usually well tolerated, but rapid 
tachycardia, particularly in the elderly, may cause angina, pulmonary 
edema, hypotension, or syncope. It is not usually associated with 
structural heart disease. In patients without associated heart disease, 
AVNRT is not a life-threatening arrhythmia; however, it may cause 
significant symptoms.
The mechanism is reentry involving the AV node and the perinodal 
atrium, made possible by the existence of multiple pathways for con­
duction from the atrium into the AV node that are capable of conduc­
tion in two directions (Fig. 256-1).
Most forms of AVNRT utilize a slowly conducting AV nodal path­
way (right inferior extension) that extends from the compact AV node 
near the His bundle, inferiorly along the tricuspid valve annulus to the 
floor of the coronary sinus. The reentry wavefront propagates up this 
slowly conducting pathway to the compact AV node and then exits 
from the fast pathway at the top of the AV node. The path back to the 
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FIGURE 256-2  Atrioventricular nodal reentry tachycardia with retrograde P waves before and after adenosine termination.

CHAPTER 256
Inferior AV node
extension:
Slow pathway
Compact AV node:
Fast pathway
Paroxysmal Supraventricular Tachycardias  
CS
Tricuspid
valve
slow pathway probably involves the left atrial septum, which has con­
nections to the coronary sinus musculature. More unusual forms of 
AVNRT utilize a left inferior extension that connects to the compact 
AV node through the roof of the coronary sinus or, in extremely rare 
cases, directly from the mitral valve annulus avoiding the coronary 
sinus musculature altogether. In typical forms, the conduction time 
from the compact AV node region to the atrium is similar to that from 
the compact node to the His bundle and ventricles, such that atrial 
activation occurs at about the same time as ventricular activation. The 
P wave is therefore inscribed during, slightly before, or slightly after the 
QRS and can be difficult to discern. Often the P wave is seen at the end 
of the QRS complex as a pseudo-r′ in lead V1 and pseudo-S waves in 
leads II, III, and aVF (Fig. 256-2).
More unusual forms of AVNRT have P waves falling later, any­
where between QRS complexes, in which case, an inverted P wave is 
seen in the inferior limb leads with the inverted P wave seen in the 
subsequent T wave. The rate can vary with sympathetic tone through 
its effect on the conduction time of AV nodal tissues. Simultaneous 
atrial and ventricular contraction results in atrial contraction against 
a closed tricuspid valve, producing a cannon A wave visible in the 
jugular venous pulse often perceived as a fluttering sensation in the 
neck. Elevated venous pressures may also lead to release of natriuretic 
peptides that cause post-tachycardia diuresis. In contrast to ATs, 
maneuvers or medications that produce AV nodal block terminate the 
arrhythmia. Acute treatment is the same as for other forms of PSVT 
(discussed below). Whether ongoing therapy is warranted depends on 
the severity of symptoms and frequency of episodes. Reassurance and 
instruction as to how to perform the Valsalva maneuver or other vagal 
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nerve–stimulating maneuvers to terminate episodes are sufficient for 
many patients. Administration of an oral beta blocker, verapamil, or 
diltiazem at the onset of an episode can be used to facilitate termina­
tion. Chronic therapy with these medications or flecainide is an option 
if prophylactic therapy is needed. Catheter ablation of the slow AV 
nodal pathway is recommended for patients with recurrent or severe 
episodes or when drug therapy is ineffective, not tolerated, or not 
desired by the patient. Catheter ablation is curative in >95% of patients. 
The major risk is AV block requiring permanent pacemaker implanta­
tion, which occurs in <1% of patients.

PART 6
Disorders of the Cardiovascular System
JUNCTIONAL TACHYCARDIA
Junctional ectopic tachycardia (JET) is due to automaticity within the 
AV node. It is rare in adults and more frequently encountered as an 
incessant tachycardia in children, often in the perioperative period 
of surgery for congenital heart disease. It presents as a narrow QRS 
tachycardia, often with ventriculoatrial (VA) block, such that AV dis­
sociation is present. JET can occur as a manifestation of increased 
adrenergic tone and may be seen after administration of isoproterenol, 
particularly after catheter ablation in the perinodal region. It may also 
occur for a short period of time after ablation for AVNRT. Accelerated 
junctional rhythm is a junctional automatic rhythm between 50 and 
100 beats/min. Initiation may occur with gradual acceleration in rate, 
suggesting an automatic focus, or after a premature ventricular con­
traction, suggesting a focus of triggered automaticity. VA conduction 
is usually present, with P-wave morphology and timing such that it 
resembles AVNRT at a slow rate. It can be related to increased sympa­
thetic tone and may produce palpitations. It usually does not require 
specific therapy.
ACCESSORY PATHWAYS AND THE 

WOLFF-PARKINSON-WHITE SYNDROME
Accessory pathways (APs) occur in 1 in 1500–2000 people and are 
associated with a variety of arrhythmias including narrow-complex 
PSVT, wide-complex tachycardias, and, rarely, sudden death. Most 
patients have structurally normal hearts, but APs are associated with 
Ebstein’s anomaly of the tricuspid valve and forms of hypertrophic 
cardiomyopathy including PRKAG2 mutations, Danon’s disease, and 
Fabry’s disease (Fig. 256-3).
APs are abnormal connections that allow conduction between the 
atrium and ventricles across the AV ring. They are present from birth 
and are due to failure of complete partitioning of atrium and ventricle 
by the fibrous AV rings. They occur across either an AV valve annulus 
or the septum, most frequently between the left atrium and free wall of 
the left ventricle, followed by posteroseptal, right free wall, and antero­
septal locations. If the impulse from the sinus node conducts through 
the AP to the ventricle (antegrade) before the impulse conducts 
through the AV node and His bundle, then the ventricles are preexcited 
during sinus rhythm, and the electrocardiogram (ECG) shows a short 
P-R interval (<0.12 s), slurred initial portion of the QRS (delta wave), 
and prolonged QRS duration produced by slow conduction through 
direct activation of ventricular myocardium over the AP. The mor­
phology of the QRS and delta wave is determined by the AP location 
and associated site of earliest ventricular activation, and the degree of 
fusion between the excitation wavefronts from conduction over the AV 
node and conduction over the AP (Fig. 256-4).
Right-sided pathways preexcite the right ventricle, producing a left 
bundle branch block–like configuration in lead V1, and often create 
marked preexcitation because of their relatively close proximity of the 
AP to the sinus node (Fig. 256-4). Left-sided pathways preexcite the left 
ventricle and may produce a right bundle branch–like configuration in 
lead V1 and a negative delta wave in aVL, indicating initial depolariza­
tion of the lateral portion of the left ventricle that can mimic Q waves 
of lateral wall infarction (Fig. 256-4). Because of the relatively large 
distance between the sinus node and left free wall APs, preexcitation 
may be minimal or absent on 12-lead ECG. Preexcitation due to an AP 
at the diaphragmatic surface of the heart, typically in the paraseptal 
region, produces delta waves that are negative in leads III and aVF, 

A
B
Sinus rhythm—
antegrade
AP conduction
Orthodomic AV
reentry—retrograde
AP conduction
Antidromic AV
reentry—antegrade
AP conduction
p
p
Delta-wave
C
FIGURE 256-3  Wolff-Parkinson-White (WPW) syndrome. A. A 12-lead 
electrocardiogram in sinus rhythm (SR) of a patient with WPW demonstrating 
short P-R interval, delta waves, and widened QRS complex. This patient had an 
anteroseptal location of the accessory pathway (AP). B. Orthodromic atrioventricular 
(AV) reentry in a patient with WPW syndrome using a posteroseptal AP. Note the P 
waves in the ST segment (arrows) seen in lead III and normal appearance of QRS 
complex. C. Three most common rhythms associated with WPW syndrome: sinus 
rhythm demonstrating antegrade conduction over the AP and AV node; orthodromic 
AV reentry tachycardia (AVRT) using retrograde conduction over the AP and 
antegrade conduction over the AV node; and antidromic AVRT using retrograde 
conduction over the AV node and antegrade conduction over the AP.
mimicking the Q waves of inferior wall infarction (Fig. 256-4). Preexci­
tation can be intermittent and disappear during exercise as conduction 
over the AV node accelerates and may take over ventricular activation 
completely.
Wolff-Parkinson-White (WPW) syndrome is defined as a preexcited 
QRS during sinus rhythm and episodes of PSVT. There are a number of 
variations of APs that may not cause preexcitation and/or arrhythmias. 
Concealed APs allow only retrograde conduction, from ventricle to 
atrium, so no preexcitation is present during sinus rhythm, but SVT

Left lateral
Right free wall
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AV
TV
MV
Coronary
sinus (CS)
Postero septal
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III
FIGURE 256-4  Potential locations for accessory pathways in patients with WolffParkinson-White syndrome and typical QRS appearance of delta waves that can 
mimic underlying structural heart disease such as myocardial infraction of bundle 
branch block. AV, aortic valve; MV, mitral valve; PV, pulmonary valve; TV, tricuspid 
valve.
can occur. Other unusual forms of APs exist. Fasciculoventricular 
connections between the His bundle and ventricular septum produce 
preexcitation but do not cause arrhythmia, probably because the circuit 
is too short to promote reentry. Atriofascicular pathways, also known 
as Mahaim fibers, probably represent a duplicate AV node and HisPurkinje system that connect the right atrium to fascicles of the right 
bundle branch and produce a wide-complex tachycardia having a left 
bundle branch block configuration.
ATRIOVENTRICULAR RECIPROCATING 
TACHYCARDIA
The most common tachycardia caused by an AP is the PSVT desig­
nated orthodromic AV reciprocating tachycardia. The circulating reentry 
wavefront propagates from the atrium anterogradely over the AV node 
and His-Purkinje system to the ventricles and then reenters the atria 
via retrograde conduction over the AP. The QRS is narrow or may 
have typical right or left bundle branch block, but without preexcita­
tion during tachycardia. Because excitation through the AV node and 
AP are necessary, AV or VA block results in tachycardia termination. 
During sinus rhythm, preexcitation is seen if the pathway also allows 
anterograde conduction. Most commonly, during tachycardia, the R-P 
interval is shorter than the P-R interval and can resemble AVNRT. 
Unlike typical AVNRT, P waves always follow the QRS and are never 
simultaneous with a narrow QRS complex because the ventricles must 
be activated before the reentry wavefront reaches the AP and conducts 
back to the atrium. The morphology of the P wave during tachycardia 
is determined by the pathway location, but it can be difficult to assess 
because it is usually inscribed during the ST segment. The P wave in 
posteroseptal APs is negative in leads II, III, and aVF, similar to that in 
AV nodal reentry, but P-wave morphology will differ from AV nodal 
reentry for pathways in other locations. Occasionally, an AP conducts 
extremely slowly in the retrograde direction, resulting in tachycardia 
with a long R-P interval, similar to most ATs. These pathways are 

usually located in the septal region and have negative P waves in leads 
II, III, and aVF. Slow AP conduction facilitates reentry, often leading 
to nearly incessant tachycardia, known as permanent junctional recip­
rocating tachycardia (PJRT). Tachycardia-induced cardiomyopathy can 
occur. Without an invasive electrophysiology study, it may be difficult 
to distinguish this form of orthodromic AV reentry from atypical AV 
nodal reentry or AT.

CHAPTER 256
PREEXCITED TACHYCARDIAS
Preexcited tachycardia occurs when the ventricles are activated by 
antegrade conduction over the AP. The most common mechanism is 
antidromic AV reciprocating tachycardia in which activation propagates 
from atrium to ventricle via the AP and then conducts retrogradely to 
the atria via the His-Purkinje system and the AV node (or rarely a sec­
ond AP). The wide QRS complex is produced entirely via ventricular 
excitation over the AP because there is no contribution of ventricular 
activation over more rapidly conducting specialized His-Purkinje 
fibers. This tachycardia is often indistinguishable from monomorphic 
ventricular tachycardia. The presence of preexcitation in sinus rhythm 
suggests the diagnosis.
Paroxysmal Supraventricular Tachycardias  
Preexcited tachycardia also occurs if an AP allows antegrade con­
duction to the ventricles during AT, atrial flutter, atrial fibrillation 
(AF), or AV nodal reentry, otherwise known as bystander AP conduc­
tion. AF and atrial flutter are potentially life-threatening if the AP 
allows very rapid repetitive conduction (Fig. 256-5).
Approximately 25% of APs causing preexcitation allow minimum 
R-to-R intervals of <250 ms during AF and are associated with a higher 
risk of inducing ventricular fibrillation and sudden death. Preexcited 
AF presents as a wide-complex, very irregular rhythm. During AF, the 
ventricular rate is determined by the conduction properties of the AP 
and AV node. The QRS complex can appear quite bizarre and change 
on a beat-to-beat basis due to the variability in the degree of fusion 
from activation over the AV node and AP, or all beats may be due 
to conduction over the AP. Ventricular activation from the Purkinje 
system may depolarize the ventricular aspect of the AP and prevent 
atrial wavefront conduction over the AP. Slowing AV nodal conduction 
without slowing AP conduction can thereby facilitate AP conduction 
and dangerously accelerate the ventricular rate. Administration of 
AV nodal–blocking agents, including oral or intravenous verapamil, 
diltiazem, beta blockers, intravenous adenosine, and intravenous 
amiodarone, is contraindicated during preexcited AF. Rapid preexcited 
tachycardia should be treated with electrical cardioversion or intrave­
nous procainamide or ibutilide, which may terminate the arrhythmia 
or slow the ventricular rate.
MANAGEMENT OF PATIENTS WITH 
ACCESSORY PATHWAYS
Acute management of orthodromic AV reentry is discussed below for 
PSVT. Patients with WPW syndrome may have wide-complex tachy­
cardia due to antidromic AV reentry, orthodromic AV with bundle 
branch block, or a preexcited tachycardia, and treatment depends on 
the underlying rhythm. Initial patient evaluation should include assess­
ment for aggravating factors, including intercurrent illness and factors 
that increase sympathetic tone. Examination should focus on excluding 
underlying heart disease. An echocardiogram is reasonable to exclude 
Ebstein’s anomaly, forms of hypertrophic cardiomyopathy that can be 
associated with APs, or tachycardia-mediated cardiomyopathy.
Patients with preexcitation who have symptoms of arrhythmia are 
at risk for developing AF and sudden death if they have an AP that 
allows rapid antegrade conduction. The risk of cardiac arrest is in the 
range of 2 per 1000 patients in adults but is likely greater in children. 
An invasive electrophysiology study is recommended to assess whether 
the pathway can support dangerously rapid heart rates if AF were to 
occur, and it is usually combined with potentially curative catheter 
ablation. Catheter ablation is warranted for recurrent arrhythmias 
when drugs are ineffective, not tolerated, or not desired by the patient. 
Efficacy is in the range of 95% depending on the location of the AP. 
Serious complications occur in <3% of patients but can include AV

PART 6
Disorders of the Cardiovascular System
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FIGURE 256-5  Preexcited atrial fibrillation (AF) due to conduction over a left free wall accessory pathway (AP). The electrocardiogram shows rapid irregular QRS 
complexes that represent fusion between conduction over the atrioventricular node and left free wall AP. Shortest R-R intervals between preexcited QRS complexes of <250 ms, as 
in this case, indicate a risk of sudden death with this arrhythmia.
block, cardiac tamponade, thromboembolism, coronary artery injury, 
and vascular access complications. The risk of AV block is higher when 
the AP is located near the AV node and/or His bundle, in the so-called 
anteroseptal or mid-septal locations. Procedure mortality is <1 in 1000 
patients. Ambulatory monitoring or exercise testing is often used to 
gain reassurance that the AP is not high risk, evaluating for abrupt loss 
of conduction (preexcitation) at physiologic heart rates consistent with 
a low-risk pathway, but this is not completely reliable. Gradual loss 
of AP conduction with increased sympathetic tone does not reliably 
indicate low risk since this can occur as AV nodal conduction time 
shortens, and therefore, the possibility of rapid antegrade AP conduc­
tion is not excluded definitively.
For patients with concealed APs or known low-risk APs causing 
orthodromic AVRT, chronic therapy is guided by symptoms and fre­
quency of events. Vagal maneuvers may terminate episodes, as may a 
dose of beta blocker, verapamil, or diltiazem taken at the onset of an 
episode. Chronic therapy with these agents or flecainide can reduce the 
frequency of episodes in some patients.
Adults who have preexcitation but no arrhythmia symptoms have a 
risk of sudden death estimated to be 1 per 1000 patient-years. Electro­
physiology study is usually advised for people in occupations for which 
an arrhythmia occurrence would place them or others at risk, such as 
police, military, and pilots, or for individuals who desire evaluation 
for risk. Routine follow-up without therapy is reasonable in others. 
Children are at greater risk of sudden death, ~2 per 1000 patient-years.

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TREATMENT
Paroxysmal Supraventricular Tachycardia
Acute management of narrow QRS PSVT is guided by the clinical 
presentation. Continuous ECG monitoring should be implemented, 
and a 12-lead ECG should always be obtained when possible, since 
this may be useful in determining the mechanism. In the presence 
of hypotension with unconsciousness or respiratory distress, QRSsynchronous direct current cardioversion is warranted, but this is 
rarely needed, because intravenous adenosine works promptly in 
most situations (see below). For stable individuals, initial therapy 
takes advantage of the fact that most PSVTs are dependent on AV 
nodal conduction (AV nodal reentry or orthodromic AV reentry) 
and, therefore, likely to respond to sympatholytic and vagotonic 
maneuvers and drugs. As these are administered, the ECG should 
be continuously recorded because the response can establish the 
diagnosis. AV block with only transient slowing of tachycardia 
may expose ongoing P waves, indicating AT or atrial flutter as the 
mechanism (Fig. 256-6).
Carotid sinus massage is reasonable provided the risk of carotid 
vascular disease is low, as indicated by absence of carotid bruits and 
no prior history of stroke. A Valsalva maneuver should be attempted 
in cooperative individuals, and if effective, the patient can be taught 
to perform this maneuver as needed. If vagal maneuvers fail or