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9
1
Supraventricular
Tachycardias
Hein J.J. Wellens
Classification of Supraventricular
Tachyarrhythmias . . . . . . . . . . . . . . . . . . . . . . . . . . . 1943
Other Findings Helpful in Making the Distinction
Between the Different Types of Supraventricular
Tachyarrhythmia . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1948
Key Points
• Supraventricular tachyarrhythmias (SVTs) are those
tachycardias in which structures above the division of
the bundle of His into the bundle branches are essential
for their occurrence.
• The width of the QRS complex during SVT ranges usually
from 80 to 100 ms. Supraventricular tachyarrhythmia
may present with a QRS complex of 120 ms or more when
(1) permanent bundle branch block is present; (2) functional bundle branch block develops because of the rate
of the tachycardia; (3) atrioventricular (AV) conduction
during the SVT goes over an accessory AV pathway.
• With atrial tachycardia, typically during the tachycardia,
the electrocardiogram (ECG) shows that the P wave precedes the QRS complex, and the atrial rate during the
tachycardia varies from 120 to 240 beats per minute.
• Atrial flutter is associated with macro reentry in the
right atrium with a regular atrial rate of 250 to 350 beats
per minute and a ventricular rate that depends on AV
nodal transmission characteristics. In most atrial flutter
patients, the cavo-tricuspid isthmus is part of the flutter
circuit. This is the area where catheter ablation is able to
interrupt the reentry mechanism and cure the patient.
• The most common type of atrial ventricular nodal reentry
tachycardia (AVNRT) typically shows simultaneous
activation of the atrium and the ventricle during the
arrhythmia.
• Accelerated atrioventricular junctional rhythms may
occur with myocardial ischemia, with inflammation,
after cardiac surgery, and in digitalis intoxication.
• Accessory connections between the atrium and ventricle
frequently participate in tachycardia circuits [atrioventricular reciprocating tachycardia (AVRT)].
• Alternating changes in the QRS complex during a narrow
QRS tachycardia are highly suggestive of AVRT.
• Adenosine given intravenously is the drug of choice for
patients with SVT unless the patient has a history of
bronchospasm.
The Practical Approach to Diagnosis . . . . . . . . . . . . . . 1951
Treatment of Supraventricular
Tachyarrhythmia . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1951
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1952
• Atrial flutter can best be terminated pharmacologically
by ibutilide.
• In most supraventricular tachycardias definitive cure is
possible by catheter ablation therapy.
Classification of Supraventricular
Tachyarrhythmias
Supraventricular tachyarrhythmias (SVTs) are those tachycardias in which structures above the division of the bundle
of His into the bundle branches are essential for their occurrence. They can be classified as to their site of origin and
mechanism as indicated in Table 91.1. As shown in that
table, also accessory atrioventricular (AV) pathways and the
ventricles may be incorporated in the tachycardia pathway.
However, when AV conduction occurs over the AV node–His
bundle branch system, they are classified as SVTs. When
atrial fibrillation (see Chapter 92) is excluded, it is common
to call the remaining SVTs supraventricular tachycardias.
Each of these different types of SVTs has its own characteristic electrocardiographic features.1–3 The width of the QRS
complex during SVT usually ranges from 80 to 100 ms.
Supraventricular tachyarrhythmia may present with a QRS
complex of 120 ms or more when (1) permanent bundle branch
block is present, (2) functional bundle branch block develops
because of the rate of the tachycardia, or (3) AV conduction
during the SVT goes over an accessory AV pathway. (See also
Chapter 96.)
The prevalence of SVT has been estimated to be 2.25/1000
persons and the incidence 35/100,000 person-years.4
Atrial Tachycardia
As shown in Table 91.1, different forms of atrial tachycardia
need to be recognized. Typically, during tachycardia the electrocardiogram (ECG) shows that the P wave precedes the
QRS complex (Fig. 91.1). The atrial rate during tachycardia
varies from 120 to 240 per minute. The polarity of the P
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Atrial tachycardia
Paroxysmal
Incessant
Atrial flutter
Atrial fibrillation
AVNRT
AV junctional accelerated
rhythm
Digitalis induced
Post cardiac surgery
Infectious
Ischemic
AVRT (circus movement
tachycardia)
Reentry
DAD
+
+
+
+ (mult.circ)
+
?
+
I
Abn Auto
II
+
+
III
V1
V6
+
+
+
+
Abn, abnormal; AP, accessory pathway; Auto, automaticity; AV, atrioventricular; AVNRT, AV nodal reciprocating tachycardia; AVRT, atrioventricular
reciprocating tachycardia; DAD, delayed after depolarization; multi.circ.,
multiple circuits.
or
AV nodal
tachycardia
(common
type)
15
TABLE 91.1. Classification of supraventricular tachyarrhythmias
according to site of origin and mechanism
91
atrial
tachycardia
circus
movement
tachycardia
CN 78295
800
ms
FIGURE 91.2. Example of a paroxysmal atrial tachycardia. Note
the sudden onset of the arrhythmia after three conducted sinus
beats with a P wave that precedes the QRS complex but has a different configuration from the sinus P waves. The arrhythmia stops
spontaneously after 11 tachycardia beats.
wave, the PR interval, and the ratio between P waves and
QRS complexes depend on the site of origin in the atrium,
the rate of atrial impulse formation, and the AV nodal transmission characteristics. The paroxysmal form is the most
common type of atrial tachycardia and is characterized by a
sudden onset and cessation of the arrhythmia (Fig. 91.2). The
behavior of this arrhythmia during programmed electrical
stimulation of the heart and its response to different antiarrhythmic drugs suggest that paroxysmal atrial tachycardia
is based either on reentry or on triggered activity. Triggered
activity is an arrhythmogenic mechanism resulting from
delayed afterdepolarizations.5 However, it is not always possible to identify the exact mechanism of paroxysmal atrial
tachycardia.
A relatively rare but serious arrhythmia is the incessant
(or permanent) form of atrial tachycardia (Fig. 91.3). In
patients with this rhythm disturbance, the arrhythmia is
present for more than 50% of the day. The rate of atrial
impulse formation, which is most likely caused by abnormal
automaticity, increases during exercise. The persistent nature
of the tachycardia and the inability to control the ventricular
rate by failure to prevent rate increase of the arrhythmia and
1 : 1 AV conduction may result in a dilated (tachycardiainduced) cardiomyopathy.6,7 Recognition that the arrhythmia
is the cause rather than the consequence of the cardiomyopathy is important. Destruction of the atrial area of abnormal
impulse formation by catheter ablation leads to cure of the
arrhythmia and improvement in pump function. Atrial
tachycardias may be uni- or multifocal. Multifocal tachycardias are usually accompanied by additional cardiac disease
or obstructive pulmonary disease.
Localizing Atrial Tachycardia
FIGURE 91.1. Three types of supraventricular tachyarrhythmia
(SVT) and the relation between QRS and P wave during tachycardia.
Note that in atrial tachycardia, P precedes QRS; P occurs simultaneously with QRS in the common type of atrioventricular (AV) nodal
tachycardia and follows QRS in circus movement tachycardia using
a fast-conducting accessory AV pathway, also called an atrioventricular reentrant tachycardia (AVRT).
CAR091.indd 1944
The ability to cure atrial tachycardia by catheter ablation
requires accurate identification of the site of origin of the
arrhythmia (in case of focal tachycardia), or a critical part of
the tachycardia pathway (in reentrant atrial tachycardia).
This should precede the catheter ablation procedure by
careful intraatrial activation mapping during the tachycardia. However, the 12-lead ECG can already give an indication
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s u p r av e n t r i c u l a r t a c h y c a r d i a s
I
V1
II
V2
III
V3
aVR
V4
aVL
FIGURE 91.3. Example of an incessant
atrial tachycardia. This patient, initially showing 2 : 1 and later 1 : 1 AV
conduction, has been continuously in
tachycardia for 12 years and presented
with a dilated cardiomyopathy.
V5
V6
aVF
where the atrial tachycardia is originating. This is done by
analyzing the P-wave axis and P-wave duration during atrial
tachycardia. Examples are given in Figures 91.4 to 91.6. The
ECG for localizing the site of origin of an atrial tachycardia
is helpful when the arrhythmia arises on the free wall of the
right or left atrium or low in the intraatrial septum, but it is
less helpful when the site of origin of atrial tachycardia is on
the right or left side of the intraatrial septum.
Atrial Flutter
Observations during atrial activation mapping indicate that
macro reentry in the right atrium is the common mechanism
in atrial flutter.8,9 The atrial rate is regular and varies between
250 and 350 per minute, with the ventricular rate depending
1 sec
7900
on AV nodal transmission characteristics. The flutter rate
may be slower in case of atrial enlargement, the use of drugs
that slow conduction velocity in the atrium, or following an
unsuccessful catheter ablation attempt. Atrial flutter is 2.5
times more prevalent in men than in women and very seldom
occurs before the age of 50 years, and the incidence increases
with aging, heart failure, and chronic obstructive lung
disease.10 The classic saw-toothed pattern of atrial activity is
the electrocardiographic hallmark of the arrhythmia. Carotid
sinus massage–induced AV block facilitates recognition of
the arrhythmia (Fig. 91.7). Figure 91.8 illustrates the two
most common types of atrial flutter. Occasionally, other
circuits in the right or left atrium may lead to ECG patterns
of atrial flutter.11 In most atrial flutter patients, the cavotricuspid isthmus (the area in between the tricuspid valve
II
II
I
I
I
p
p
I
II
II
III
III
III
III
V1
V1
V6
FIGURE 91.4. Example of an atrial tachycardia originating in the
lateral upper part of the left atrium. The negative P wave in lead I
indicates a left atrial origin. The P wave axis in the frontal plane,
pointing toward lead III, betrays a superior origin. The width of the
P wave (110 ms) tells that the arrhythmia is originating in the lateral
wall of the atrium with sequential activation of the left and right
atrium.
CAR091.indd 1945
V6
81537
FIGURE 91.5. Atrial tachycardia with an origin low in the
intraatrial septum. Note the superior axis (negative P waves in II
and III) and the short duration of the P wave. The latter indicates an
origin close to the septum with simultaneous activation of both
atria.
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91
II
I
II
I
p
III
I
II
V1
III
V5
III
V1
V6
400 ms
FIGURE 91.7. Carotid sinus massage reveals that atrial flutter is
the underlying rhythm at the atrial level.
V6
81537
FIGURE 91.6. Atrial tachycardia originating in the superior part of
the right atrium. Note the P wave axis in the frontal plane pointing
toward lead III.
pathway, and retrograde conduction over a rapidly conducting pathway (slow-fast AVNRT). During tachycardia, this
results in an ECG with the P wave either completely hidden
in the QRS complex or distorting the terminal portion of the
QRS complex. This pattern is represented in Figure 91.1, and
an ECG of the arrhythmia is shown in Figure 91.9. The P
wave can be hidden in the QRS, not only because of the
simultaneous activation of the atrium and the ventricle
during the common type of AVNRT, but also because the P
wave is very narrow (60–80 ms) since atrial activation starts
low in the intraatrial septum. The common type of AVNRT
occurs twice as often in women as in men. The arrhythmia
also develops on average 10 years earlier in women than in
men (29 ± 16 versus 39 ± 16, respectively).14 The uncommon
type of paroxysmal AVNRT is characterized by a P wave that
follows the QRS complex, the mechanism being retrograde
conduction over a slow pathway and anterograde AV nodal
conduction over either a rapid or a slow pathway. The RP
interval is long, and the P wave becomes located more in the
middle of two QRS complexes or in front of the next QRS
and the inferior caval vein) is part of the flutter circuit. This
is the area where catheter ablation is able to interrupt the
reentry mechanism and to cure the patient.9
Atrioventricular Nodal Reciprocating Tachycardia
The reproducible initiation and termination of paroxysmal
AV nodal reciprocating tachycardia (AVNRT) by programmed
stimulation of the heart suggests reentry as the underlying
mechanism. This is supported by the finding of “dual” AV
nodal conduction pathways in many of these patients.12,13
The common type of AVNRT typically shows simultaneous
activation of the atrium and the ventricle during the arrhythmia. Anterograde conduction in the AV node during tachycardia is considered to occur over a slowly conducting
A
B
01042
96D674
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
CAR091.indd 1946
400 ms
FIGURE 91.8. (A) “Counterclockwise” common atrial
flutter, with negative flutter waves in leads II, III, and
aVF, and positive flutter waves in V1. (B) “Clockwise”
common atrial flutter with positive flutter waves in
leads II, III, and aVF and negative flutter waves in V1.
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s u p r av e n t r i c u l a r t a c h y c a r d i a s
A
I
V1
I
V1
II
V2
II
V2
III
V3
III
V4
aVR
V5
aVL
V6
aVF
aVR
FIGURE 91.9. Example of the common
form of atrial ventricular nodal reentry
tachycardia (AVNRT). Note the pseudo–
S wave in leads II and III and the pseudo–
incomplete right bundle branch block
pattern in lead VI caused by the P wave
during tachycardia.
B
aVL
aVF
complex (a long RP tachycardia). This is a rare arrhythmia
that is seldom sustained and must be differentiated from an
AV reciprocating tachycardia using a slowly conducting
accessory pathway for ventriculoatrial conduction, a low
atrial tachycardia, and a His bundle tachycardia with retrograde conduction to the atrium (Fig. 91.10).
I
VR
VL
VF
99426/3
V3
V4
V5
V6
400 ms
Accelerated Atrioventricular Junctional Rhythm
Accelerated AV junctional impulse formation (of a nonparoxysmal type) may occur in ischemia, with inflammation, after
cardiac surgery, and in digitalis intoxication. The exact site
of origin in the AV junction (bundle of His?) is not known.
It is likely, however, as shown in Table 91.1, that the enhanced
impulse formation is based on delayed afterdepolarizations
(digitalis intoxication) or abnormal automaticity.
Atrioventricular Reciprocating Tachycardia
1
3
2
4
1 = CMT using slow AP
2 = AVNR (uncommon type)
3 = Low atrial tachycardia
4 = His bundle tachycardia
FIGURE 91.10. The four types of SVT resulting in an ECG during
tachycardia showing a negative P wave in front of the QRS complex
in lead II. Statistically most likely is an AVRT with AV conduction
over the AV node and ventriculoatrial (VA) conduction over a slowly
conducting accessory pathway (1). The other three possibilities are
the uncommon form (fast-slow) of AVNRT (2), a low atrial tachycardia close to the AV node (3), or a His bundle tachycardia with retrograde conduction to the atrium (4).
CAR091.indd 1947
Epicardial mapping and electrophysiologic investigations
have shown that accessory connections between atrium and
ventricle frequently participate in tachycardia circuits.15–17
An interesting subgroup of patients with SVT are those
with a so-called concealed accessory pathway.18,19 These
connections conduct the impulse only in the ventriculoatrial direction. They are often present in patients referred
for evaluation of an SVT. During atrioventricular reciprocating tachycardia (AVRT), also called circus movement tachycardia, two types of concealed accessory pathways may be
used (Figs. 91.11 and 91.12). Most common are patients using
a rapidly conducting accessory pathway for ventriculoatrial
conduction. The QRS is usually narrow, and characteristically the P wave is located shortly after the end of the QRS
(the RP interval being shorter than the PR interval). The Pwave axis and width will tell where the atrial end of the
accessory pathway is located. The group using a slowly conducting accessory pathway is small. Atrial activation follows
the QRS complex but with an RP interval that is longer
than the PR interval. This type of SVT must be differentiated from a low atrial tachycardia and an AVNRT of the
uncommon type (see Fig. 91.10). Atrioventricular reciprocating tachycardia using a rapidly conducting accessory AV
pathway is twice as common in men than in women. Concealed accessory pathways are about half as common as
overt anterogradely conducting accessory pathways (ventricular preexcitation). The mean age at onset of the first
attack of tachycardia in patients with overt or concealed
accessory pathways is 10 years younger than that in patients
with AVNRT.20
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91
Other Findings Helpful in Making the
Distinction Between the Different Types
of Supraventricular Tachyarrhythmia
Effect of Carotid Sinus Massage
As shown in Table 91.2, carotid sinus massage (CSM) may
induce changes during SVT that are helpful in differentiating between the different types. Before CSM is applied,
severe narrowing of the carotid arteries should be excluded
by checking pulsations and the absence of carotid bruits.
While recording the ECG, pressure should be applied on
the carotid bulb beneath the angle of the jaw, gradually
increasing the pressure, which should last no longer than 5
seconds. The elderly, especially, may be very sensitive to
CSM with a long period of asystole after termination of the
tachycardia.
CMT with “fast” AP
CMT with “slow” AP
FIGURE 91.11. Schematic representation of a circus movement
tachycardia using a “concealed” fast-conducting (left) or slowconducting (right) accessory AV pathway. The corresponding ECGs
during tachycardia with their characteristic RP/PR ratio are shown
in Figure 91.12.
A
B
94135
I
Mode of Initiation of Supraventricular
Tachyarrhythmia
Initiation of an SVT by a single atrial premature beat during
sinus rhythm after marked prolongation of the PR interval
suggests the presence of dual AV nodal pathways and AVNRT
as the mechanism of the arrhythmia (Figs. 91.13 and 91.14).
In contrast, initiation of an SVT during sinus rhythm
without prolongation of the PR interval suggests an AVRT
using an accessory pathway for ventriculoatrial conduction
(Fig. 91.15).
Initiation of an SVT by a single ventricular premature
beat argues in favor of an AVRT (Fig. 91.16).
II
III
aVR
aVL
aVF
V1
TABLE 91.2. Findings on carotid sinus massage in different types
of supraventricular tachyarrhythmias
Tachycardia
Effect of carotid sinus massage
Sinus tachycardia
Atrial tachycardia
Paroxysmal form
Gradual and temporary slowing in heart rate
V2
Incessant form
V3
V4
Atrial flutter
V5
Atrial fibrillation
V6
FIGURE 91.12. Two types of circus movement tachycardias. Circus
movement tachycardia due to rapid (A) and slow conducting (B)
accessory pathway (AP). The rapidly conducting AP (A) is associated
with a short RP, the slow conducting AP (B) with a long RP. The
P waves are relatively narrow, inverted in the inferior leads and
positive in leads aVR and aVL, suggesting a septal or paraseptal
location.
CAR091.indd 1948
AVNRT
AVRT (CMT)
Temporary slowing in ventricular rate
because of increase in AV block
Cessation of tachycardia
No effect
Temporary slowing in ventricular rate
because of increase in AV block
No effect
Temporary slowing in ventricular rate
because of increase in AV block
Transformation into atrial fibrillation
No effect
Temporary slowing in ventricular rate
because of increase in AV block
No effect
Cessation of tachycardia
No effect
Cessation of tachycardia
No effect
AVNRT, atrioventricular nodal reciprocating tachycardia; AVRT, atrioventricular reciprocating tachycardia; CMT, circus movement tachycardia.
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A
B
C
92426/1
I
atrium
s
f
II
AVN
III
His
aVR
aVL
aVF
PR 160
PR 240
PR 360
atrial echo
SR
APC
APC
common AVNT
FIGURE 91.13. Initiation of an AVNRT by an atrial premature
complex (APC) during sinus rhythm (SR). (A) During sinus rhythm,
the atrial impulse reaches the bundle of His by way of the most
rapidly conducting (the fast f) pathway. (B) An APC is conducted to
the bundle of His by way of the most rapidly conducting (the fast f)
pathway. This results in sudden prolongation of the PR interval
compared with sinus rhythm. (C) An even earlier APC with slower
conduction in the slow pathway is able to reenter the fast pathway
and to initiate the common form of AVNRT.
99574
V1
V2
V3
V4
V5
I
V6 920391
400 ms
FIGURE 91.15. Initiation of a SVT during sinus rhythm. Note that
an acceleration in rate during sinus rhythm is followed by a tachycardia with a narrow QRS complex. The RP interval exceeds the PR
interval during tachycardia with negative P waves in leads II, III, V2
to V6. These fi ndings indicate the presence of a circus movement
tachycardia using a slowly conducting accessory pathway for ventriculoatrial conduction.
II
III
aVR
aVL
aVF
V1
AV node
V2
Acc P
V3
His
V4
V5
VPB
V6
A
400 ms
FIGURE 91.14. Clinical example of initiation of the common form
of AV nodal tachycardia. After two sinus beats that are conducted
to the ventricle, an APC is conducted to the ventricle, with marked
PR prolongation indicating conduction over the slow AV nodal
pathway. This is followed by perpetuation of reentry in the AV node
and AVNRT. Six precordial leads were recorded simultaneously.
CAR091.indd 1949
B
FIGURE 91.16. (A) During sinus rhythm a circus movement tachycardia, using an accessory AV pathway, can easily be initiated by a
single ventricular premature beat (VPB) because the VPB fi nds the
distal conduction system refractory and is retrogradely conducted
to the atrium over the accessory pathway (ACC P). (B) In contrast,
because of refractoriness of the distal conduction system, a VPB
cannot get to the AV node to initiate AV nodal reentry.
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91
96536
I
II
III
aVR
AV node
aVL
aVF
Acc P
V1
His
V2
V3
VPB
A
V4
B
FIGURE 91.17. Differences for a ventricular premature beat (VPB)
to get into the tachycardia circuit (and to terminate tachycardia) in
AVNRT and in a circus movement tachycardia using an accessory
pathway for ventriculoatrial conduction. The VPB in AVNRT will
be blocked distal to the reentry circuit (B), whereas the VPB easily
invades the reentry circuit during circus movement tachycardia
(A).
V5
V6
960829
400 ms
FIGURE 91.18. Example of electrical alternans of the QRS complex
during a circus movement tachycardia using a “concealed” accessory AV pathway. Note that QRS alternation is best seen in leads II,
V3, and V4.
Mode of Termination of Supraventricular
Tachyarrhythmia
As shown in Figure 91.17, it is extremely unlikely for an
AVNRT to be terminated by a single ventricular premature
beat. However, this is quite common in an AVRT.
Electrical Alternans of the QRS Complex
Alternating changes in the QRS complex during a narrow
QRS tachycardia are highly suggestive for an AVRT.21 QRS
alternation as a clue to an AVRT can be used only when it
is present more than 5 seconds after the start of the tachycardia. Changes in QRS configuration are common at the
start of SVT because the sudden acceleration in ventricular
rate leads to different degrees of changes in refractoriness and
conduction velocity in the conduction system. In patients
with AVRT and a narrow QRS, the incidence of electrical
alternans increases with increasing heart rate during tachycardia. An example of electrical alternans is shown in Figure
91.18.
FIGURE 91.19. Increase in the length of the reentry circuit when
bundle branch block develops during circus movement tachycardia
using an accessory pathway that is on the same side as the bundle
branch block. (A) There is a right-sided accessory pathway. (B) The
tachycardia circuit is confi ned to the AV node. When right bundle
branch block develops in the patient with a right-sided accessory
pathway, the circuit becomes longer and the tachycardia rate slows;
compare V1 before and after right bundle branch block on the left.
In contrast (B), nothing happens to the tachycardia rate when bundle
branch block develops during AVNRT (measurements are in
milliseconds).
CAR091.indd 1950
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s u p r av e n t r i c u l a r t a c h y c a r d i a s
I
84041
II
III
V1
effects from antiarrhythmic drugs clearly diminish the
quality of life.
Supraventricular tachyarrhythmias can sometimes be
fatal or may lead to serious cardiac impairment when (1)
life-threatening trauma occurs during syncope, (2) SVT
precipitates acute pulmonary edema (in patients with
severe systolic or diastolic dysfunction), (3) thromboembolism occurs, or (4) incessant SVT leads to a dilated
cardiomyopathy.
Symptoms during SVT, frequency of recurrences, length
of episodes, and the presence or absence of additional heart
disease determine the type of treatment.
V4
Steps in diagnosis of narrow QRS tachycardia (QRS <0.12 sec)
V6
400 ms
FIGURE 91.20. The presence of a slower heart rate during SVT in
a case of left bundle branch block. As explained in Figure 91.20, this
indicates a circus movement tachycardia using an accessory AV
pathway on the same side as the blocked bundle branch. In this
example, therefore, the accessory pathway is between the left atrium
and the left ventricle.
1.
2nd degree AV block?
(spontaneous or after CSM)
no
yes
Atrial rate
>250/min
Slowing in Heart Rate During Tachycardia when
Bundle Branch Block Develops
Figures 91.19 and 91.20 illustrate the importance of careful
measurements of the rate of tachycardia when bundle branch
block develops and disappears during SVT. As shown in
Figure 91.20, a slowing in tachycardia rate during bundle
branch block indicates the presence of an AVRT using an
accessory AV pathway for ventriculoatrial conduction inserting into the free wall of the ventricle on the same side as the
blocked bundle branch.18,19
Atrial flutter Atrial T
2.
yes
AVRT
P wave location?
3.
PR > RP
P in R
AVRT with fast AP
AVNRT
Most patients with SVT have a normal life expectancy, but
their quality of life is often poor.22 The uncertainty of when
SVT may occur leads to social isolation. During SVT, symptoms such as palpitations, dizziness, syncope, chest pain, and
dyspnea; the need to seek hospital treatment; the feeling of
prolonged tiredness after an episode of SVT; and the side
CAR091.indd 1951
PR < RP
uncommon AVNRT
Atrial T
AVRT
P axis (frontal plane)
4a.
inferior-superior
Atrial T
AVRT
septal AP
other
Atrial T
AVRT
(right or left AP)
P axis (horizontal plane)
4b.
right
Treatment of Supraventricular
Tachyarrhythmia
AVNRT with 2:1 block
QRS alternation?
no
The Practical Approach to Diagnosis
A stepwise approach is advised for analyzing the 12-lead ECG
during SVT (Fig. 91.21). The steps include the relation
between atrial and ventricular events during SVT, the presence or absence of electrical alternans and the location and
configuration of the P wave. If that analysis does not facilitate a definitive diagnosis, an electrophysiologic study is
indicated, especially when the tachycardia is symptomatic,
leading to myocardial dysfunction, or because its frequent
occurrence is annoying and socially incapacitating for the
patient.
≤250/min
left
left
right
AVRT with right-sided AP
AVRT with left-sided AP
Atrial T
Atrial T
FIGURE 91.21. Four steps to be taken when analyzing the 12-lead
ECG of a regular SVT. As shown, information should be obtained
about the relation between atrial and ventricular events during SVT
[spontaneously and after carotid sinus massage (CSM)] followed by
a look for electrical alternans of the QRS complex. Thereafter, the
location of the P wave in relation to the QRS complex and the polarity of the P wave in the frontal and horizontal plane should be
studied.
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chapter
Vagal maneuvers (Valsalva, CSM, submerging the face in
cold water, etc.) can terminate SVT when they are applied
early after the start of the SVT, indicating that the patient
should be informed not only how but also when to perform
them.
In-hospital adenosine IV is the drug of choice in most
cases of SVT, unless the patient has a history of bronchospasm. Verapamil and diltiazem IV should be avoided in
patients using beta-blockers.
Atrial flutter can pharmacologically best be terminated
by ibutilide IV. It is important to stress that patients with
atrial flutter have a similar risk of thromboembolic events
as patients with atrial fibrillation, indicating the necessity
of adequate anticoagulation, also in relation to cardioversion
attempts.23,24
As discussed in the recent guidelines for the management of patients with supraventricular arrhythmias,25 antiarrhythmic drugs can be prescribed when the SVT is
relatively well tolerated, both for termination and prevention
of recurrences. As shown by Alboni et al.,26 in selected
patients, SVT can be safely terminated out-of-hospital by a
self-administered antiarrhythmic drug. However, chronic
antiarrhythmic drug treatment, because of side effects, often
impairs the patient’s quality of life more than the arrhythmia itself. Therefore, cure from SVT by catheter ablation is
increasingly used. It is efficacious and safe in the hands of
the experienced ablator.27 Obviously, as indicated in Chapter
102, an electrophysiologic study is required when catheter
ablation of the site of origin or part of the tachycardia pathway
is considered.
Summary
Supraventricular tachycardias are common and their significance may vary from being a nuisance to life-threatening.
Usually, the 12-lead ECG facilitates a correct diagnosis of the
type of arrhythmia. The mode of treatment depends on the
type of arrhythmia, its incidence and severity, and the presence or absence of additional heart disease that plays a role
in tolerance and risks.
In most supraventricular tachycardias, definitive cure is
possible by way of catheter ablation of the focus of the
arrhythmia or by interrupting the arrhythmia circuit (see
Chapter 102).
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