CARDIOVASCULAR
DISEASES
SUPRAVENTRICULAR ON
TACHYCARDIA:
DIAGNOSIS AND MANAGEMENT
upraventricular tachycardia (SVT), by definition, includes all forms of tachycardia that either arise above
the bifurcation of the bundle of His or that have mechanisms dependent on the bundle of His. In patients with
SVT, the heart rate is at least 100 beats/min, but ventricular
rates can be lower as a result of atrioventricular (AV)
block. On electrocardiography (ECG), QRS morphology is
usually normal or supraventricular; however, it may be
widened or abnormal because of intrinsic conduction disturbance, myocardial disease, or rate-related bundle branch
block (BBB).
INCIDENCE OF SVT
The incidence of SVT in the general population remains
unclear. Published incidence data from studies vary widely
depending on the characteristics of the enrolled patients,
the diagnostic modality used to identify SVT, and specific
definitions incorporated into the studies.
In a short-term ambulatory monitoring study of 301 men
with a mean age of 56 years, the documented occurrence of
any form of SVT was 76%.1 The studys population had an
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other cases, has a ventricular rate that is faster than the atrial
rate, with ventriculoatrial block. Tachycardia myopathy has
been observed in cases in which the AV rate or rhythm has
not been adequately controlled.14,15
AV NODEINDEPENDENT ARRHYTHMIAS
Less commonly encountered forms of PSVT, including
atrial tachycardia, are independent of AV nodal conduction. These arrhythmias may persist during AV block. The
source of these arrhythmias is usually a small focus, and the
mechanism is usually abnormal automaticity or triggered
activity. The mechanism is usually microreentrant, especially in diseased atria.
Atrial tachycardias (commonly called flutters, if sufficiently rapid) may also occur as a result of a macroreentrant
mechanism. However, the reentrant circuit in these
tachycardias lies within the atrium (eg, a surgical atriotomy
scar) and is not dependent on the AV node. Although PSVT
may be related to reentry in and around the sinus node
region, this type of reentry is rarely observed as a clinically
relevant SVT.
Technically, multifocal atrial tachycardia, atrial flutter,
and atrial fibrillation are all AV nodeindependent arrhythmias. However, these conditions are not discussed further
in the current review.
INTERPRETATION OF ECG FINDINGS IN PSVT
Most PSVTs are represented on ECGs as narrow QRScomplex tachycardias, with the QRS duration being less
than 90 ms (ie, normal QRS duration). Tachycardia-contingent BBB (ie, aberrancy) is relatively frequent in patients
with PSVT. Many of these patients may have preexistent
BBB, interventricular conduction delays, or some other
QRS abnormality. These abnormalities carry over to the
tachycardia.
An initial analysis of ECG findings for a patient with
PSVT is best followed by a methodical approach to ECG
interpretation, in which the physician reviews the elements
of the differential diagnosis, either mentally or in writing,
and examines the evidence supporting each diagnostic possibility. A high-quality12-lead ECG is much more useful in
the clinical setting than limited presentations or individual
cardiac rhythm strips. The main ECG findings of interest
are compelling atrial activity and zones of transition, such
as ectopy, cycle length change, or intermittent aberrant
conduction.
Interventions may be helpful if the mechanism of the
tachycardia is unclear from examination of the routine
ECG or rhythm strips. Vagal stimulation maneuvers, such
as carotid sinus massage or Valsalva maneuver, are classic
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FIGURE 1. Schematic of typical atrioventricular nodal reentry. The panel on the left demonstrates
anterograde conduction from the atrium (ATR) to the ventricle (VTR) over both slow and fast pathways.
The ventricle is activated initially in sinus rhythm by the fast pathway. The panel in the center shows the
effect of a premature atrial complex (PAC). Although the fast pathway conducts rapidly, it repolarizes
slowly. In this hypothetical scenario, the fast pathway is refractory to the PAC, allowing the PAC to
proceed via the slow pathway, which has a shorter refractory period. In the panel on the right, conditions
are such that anterograde conduction of the PAC occurs via the slow pathway, with subsequent recovery
of the fast pathway. These conditions allow retrograde conduction into the atrium via the fast pathway,
thereby creating the first beat of typical slow-fast atrioventricular nodal reentrant tachycardia.
FIGURE 2. Schematic of 2 terminations of paroxysmal supraventricular tachycardia (PSVT) as recorded on electrocardiograms. The
top panel demonstrates PSVT terminating with a ventricular complex. The bottom panel shows PSVT terminating with an atrial
complex, indicating that this patient is highly unlikely to have atrial
tachycardia.
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QRS and T waves. If P waves are visible during tachycardia, comparison with P waves in sinus rhythm is useful.
Although all available ECG leads require inspection,
evaluation of the inferior ECG leads (particularly lead II),
as well as lead V1, is likely to be the most productive. A
normal P wave has a positive QRS morphology in the
inferior leads because normal atrial activation begins at the
sinus node during sinus rhythm, with a wave of electrical
propagation moving toward the AV node (ie, high to low
sequence). As this impulse moves toward the inferior leads,
it produces an upright P wave in leads II, III, and aVF. By
contrast, junctional-dependent rhythms, such as AVNRT
and AVRT, and atrial tachycardias with origins in the
lower atrium result in negative P waves in the inferior
leads. The negative P waves occur because these
tachycardias activate the atrium in the opposite direction
(ie, low to high sequence).
Careful analyses of other ECG leads can help physicians
to determine if the atria are being activated from left to
right or vice versa. This conclusion can be achieved by
examining the morphology of the P wave in leads I and
aVL. In right atrial tachycardia foci, the P wave is positive
or biphasic (ie, first negative, then positive) in lead aVL.
That is because the right atrium is activated first, with the
wave of depolarization moving toward the left atrium and,
thus, to lead aVL. In left atrial tachycardia foci, the P wave
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FIGURE 4. Electrocardiograms indicative of paroxysmal supraventricular tachycardia, with no visible P wave. Left, normal QRS morphology; right,
sudden development of right-sided bundle branch block (without any change in cycle length). The tachycardia shown in this electrocardiogram
was verified as atrioventricular nodal reentrant tachycardia during electrophysiologic testing.
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preexcited tachycardia (ie, antidromic AVRT) or from ventricular tachycardia. However, the most common wide
QRS tachycardia observed in patients with accessory pathways is orthodromic SVT with aberrant ventricular conduction. Preexcited tachycardia, in which the pathway conducts in an anterograde manner, occurs less frequently. The
most common form of preexcited tachycardia uses the
accessory pathway as the anterograde limb and the AV
node as the retrograde limb of the circuit (Figure 6). Because the ventricle is activated via myocardium rather than
specialized conduction tissue of the His-Purkinje system,
ventricular depolarization happens slowly, resulting in the
broad complex preexcited rhythm.
Electrocardiograms of patients with accessory pathway
arrhythmias may or may not show delta waves (ie, initial
slurring of the QRS) in sinus rhythm. The presence of a
delta wave in sinus rhythm usually suggests that the SVT is
related to the accessory pathway.
AP
AVN
QRS
MORPHOLOGY
IN
TACHYCARDIA
VENTRICULAR PREEXCITATION
Preexcitation of the ventricles is indicated by the presence
in the ECG of a shortened PR interval in association with
slurring of the upstroke of the QRS complex.25 Preexcitation occurs as the sinus impulse travels to the ventricle
via both the AV node and the accessory pathway, resulting
in a fusion of ventricular activation via both the conventional His-Purkinje system and the accessory pathway. Because AV nodal conduction is decremental and, hence,
relatively slow, the first part of the QRS is slurredthat is,
the anterograde accessory pathway conduction reaches the
ventricle first, forming a delta wave on the ECG. This
slurring persists until AV nodal conduction propagates into
the ventricle, activating the ventricles rapidly and resulting
in a terminal QRS complex that is closer to normal in
morphology. The greater the ventricular activation over an
accessory pathway, the more preexcitation occurs (thus,
the broader the QRS) and vice versa.
Many algorithms used in diagnosis allow approximate
localization of accessory pathways along the AV rings on
the basis of preexcited ECG morphology. These algorithms are more reliable when the preexcitation is predominant. A minimally preexcited ECG makes precise
localization difficult; however, such ECG results generally suggest a left lateral pathway that is much farther
away from the source of normal atrial activation than the
AV node.26,27 Accessory pathways are most commonly
located in the left lateral position (Figure 7), where the
ECG shows a delta wave that is positive in lead V1 and
negative in lead I. In right-sided pathways, the delta wave
is usually negative in lead V1 (with a QS pattern) and
positive in lead I.
Mayo Clin Proc.
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department and in the physicians office. In the emergency department setting, the physician should conduct a
thorough assessment of the patient, followed by close
inspection of all available ECGs or cardiac rhythm strips.
Comorbid conditions and current drug therapies should
be considered before any decision is made regarding
treatment for patients with arrhythmia. When sinus
rhythm is restored, the physician should consider the
long-term management options for the patient, including
conservative pharmacologic and ablative strategies.
REFERENCES
1. Hinkle LE Jr, Carver ST, Stevens M. The frequency of asymptomatic
disturbances of cardiac rhythm and conduction in middle-aged men. Am J
Cardiol. 1969;24(5):629-650.
2. Clarke JM, Hamer J, Shelton JR, Taylor S, Venning GR. The rhythm of
the normal human heart. Lancet. 1976;1(7984):508-512.
3. Harrison DC, Fitzgerald JW, Winkle RA. Contribution of ambulatory
electrocardiographic monitoring to antiarrhythmic management. Am J Cardiol.
1978;41(6):996-1004.
4. Manolio TA, Furberg CD, Rautaharju PM, et al. Cardiac arrhythmias on
24-h ambulatory electrocardiography in older women and men: the Cardiovascular Health Study. J Am Coll Cardiol. 1994;23(4):916-925.
5. Roche F, Gaspoz JM, Da Costa A, et al. Frequent and prolonged asymptomatic episodes of paroxysmal atrial fibrillation revealed by automatic longterm event recorders in patients with a negative 24-hour Holter. Pacing Clin
Electrophysiol. 2002;25(11):1587-1593.
6. Brembilla-Perrot B, Maron F, Bosser G, et al. Paroxysmal tachycardia
in children and teenagers with normal sinus rhythm and without heart disease.
Pacing Clin Electrophysiol. 2001;24(1):41-45.
7. Leitch J, Klein G, Tee R, Murdock C, Teo WS. Neurally mediated
syncope and atrial fibrillation [letter]. N Engl J Med. 1991;324(7):495496.
8. Nerheim P, Birger-Botkin S, Piracha L, Olshansky B. Heart failure and
sudden death in patients with tachycardia-induced cardiomyopathy and recurrent tachycardia. Circulation. 2004 Jul 20;110(3):247-252. Epub 2004 Jun
28.
9. Coumel P, Flammang D, Attuel P, Leclercq JF. Sustained intra-atrial
reentrant tachycardia: electrophysiologic study of 20 cases. Clin Cardiol.
1979;2(3):167-178.
10. Coumel P. Junctional reciprocating tachycardias: the permanent and
paroxysmal forms of A-V nodal reciprocating tachycardias. J Electrocardiol.
1975;8(1):79-90.
11. Huang SKS, Wood MA. Catheter Ablation of Cardiac Arrhythmias.
Philadelphia, PA: Saunders/Elsevier; 2006.
12. Garson A Jr, Gillette PC. Junctional ectopic tachycardia in children:
electrocardiography, electrophysiology and pharmacologic response. Am J
Cardiol. 1979;44(2):298-302.
13. Case CL, Gillette PC. Automatic atrial and junctional tachycardias in the
pediatric patient: strategies for diagnosis and management. Pacing Clin
Electrophysiol. 1993;16(6):1323-1335.
14. Villain E, Vetter VL, Garcia JM, Herre J, Cifarelli A, Garson A Jr.
Evolving concepts in the management of congenital junctional ectopic tachycardia: a multicenter study. Circulation. 1990;81(5):1544-1549.
15. Walsh EP, Saul JP, Sholler GF, et al. Evaluation of a staged treatment
protocol for rapid automatic junctional tachycardia after operation for congenital heart disease. J Am Coll Cardiol. 1997;29(5):1046-1053.
16. Kalbfleisch SJ, el-Atassi R, Calkins H, Langberg JJ, Morady F. Differentiation of paroxysmal narrow QRS complex tachycardias using the 12-lead
electrocardiogram. J Am Coll Cardiol. 1993;21(1):85-89.
17. Morton JB, Sanders P, Das A, Vohra JK, Sparks PB, Kalman JM. Focal
atrial tachycardia arising from the tricuspid annulus: electrophysiologic and
electrocardiographic characteristics. J Cardiovasc Electrophysiol. 2001;12(6):
653-659.
December 2008;83(12):1400-1411
www.mayoclinicproceedings.com
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
18. Tang CW, Scheinman MM, Van Hare GF, et al. Use of P wave configuration during atrial tachycardia to predict site of origin. J Am Coll Cardiol.
1995;26(5):1315-1324.
19. Tada H, Nogami A, Naito S, et al. Simple electrocardiographic criteria
for identifying the site of origin of focal right atrial tachycardia. Pacing Clin
Electrophysiol. 1998;21(11, pt 2):2431-2439.
20. Green M, Heddle B, Dassen W, et al. Value of QRS alteration in
determining the site of origin of narrow QRS supraventricular tachycardia.
Circulation. 1983;68(2):368-373.
21. Morady F. Significance of QRS alternans during narrow QRS tachycardias. Pacing Clin Electrophysiol. 1991;14(12):2193-2198.
22. Kay GN, Pressley JC, Packer DL, Pritchett EL, German LD, Gilbert MR.
Value of the 12-lead electrocardiogram in discriminating atrioventricular nodal
reciprocating tachycardia from circus movement atrioventricular tachycardia
utilizing a retrograde accessory pathway. Am J Cardiol. 1987;59(4):296300.
23. Coumel P, Attuel P. Reciprocating tachycardia in overt and latent
preexcitation: influence of functional bundle branch block on the rate of the
tachycardia. Eur J Cardiol. 1974;1(4):423-436.
24. Josephson ME. Clinical Cardiac Electrophysiology: Techniques and
Interpretations. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins;
2002.
25. Wolff L, Parkinson J, White PD. Bundle-branch block with short P-R
interval in healthy young people prone to paroxysmal tachycardia: 1930. Ann
Noninvasive Electrocardiol. 2006;11(4):340-353.
26. Szabo TS, Klein GJ, Guiraudon GM, Yee R, Sharma AD. Localization of
accessory pathways in the Wolff-Parkinson-White syndrome. Pacing Clin
Electrophysiol.1989;12(10):1691-1705.
27. Fitzpatrick AP, Gonzales RP, Lesh MD, Modin GW, Lee RJ, Scheinman
MM. New algorithm for the localization of accessory atrioventricular connec-
December 2008;83(12):1400-1411
www.mayoclinicproceedings.com
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