Blomström-Lundqvist
ET AL., MANAGEMENT OF PATIENTS WITH Supraventricular
Arrhythmias
J
Am Coll Cardiol 2003;42:1493–531
ACC/AHA/ESC
Guidelines for the Management of Patients With Supraventricular
Arrhythmias
A
Report of the American College of Cardiology/American Heart Association
Task Force on Practice Guidelines and the European Society of Cardiology
Committee for Practice Guidelines (Writing Committee to Develop
Guidelines for the Management of Patients With Supraventricular
Arrhythmias)
IV.
CLINICAL PRESENTATION, GENERAL EVALUATION, AND MANAGEMENT OF PATIENTS
WITH SUPRAVENTRICULAR ARRHYTHMIA
A.
General Evaluation of Patients Without
Documented Arrhythmia
1. Clinical History and Physical Examination
Patients with paroxysmal arrhythmias are most often asymptomatic
at the time of evaluation. Arrhythmia-related symptoms include palpitations;
fatigue; lightheadedness; chest discomfort; dyspnea; presyncope;
or, more rarely, syncope.
A
history of arrhythmia-related symptoms may yield important clues
to the type of arrhythmia. Premature beats are commonly described
as pauses or nonconducted beats followed by a sensation of a strong
heartbeat, or they are described as irregularities in heart rhythm.
Supraventricular tachycardias occur in all age groups and may be
associated with minimal symptoms, such as palpitations, or may present
with syncope. The clinician should distinguish whether the palpitations
are regular or irregular. Irregular palpitations may be due to premature
depolarizations, AF, or MAT. The latter are most commonly encountered
in patients with pulmonary disease. If the arrhythmia is recurrent
and has abrupt onset and termination, then it is designated paroxysmal.
Sinus
tachycardia is, conversely, nonparoxysmal and accelerates and terminates
gradually. Patients with sinus tachycardia may require evaluation
for stressors such as infection or volume loss. Episodes of regular
and paroxysmal palpitations with sudden onset and termination (also
referred to as PSVT) most commonly result from AVRT or AVNRT. Termination
by vagal maneuvers further suggests a re-entrant tachycardia involving
AV nodal tissue (eg, AVNRT, AVRT). Polyuria is caused by release
of atrial natriuretic peptide in response to increased atrial pressures
from contraction of atria against a closed AV valve, which is supportive
of a sustained supraventricular arrhythmia.
With
SVT, syncope is observed in approximately 15% of patients, usually
just after initiation of rapid SVT or with a prolonged pause after
abrupt termination of the tachycardia (55).
Syncope may be associated with AF with rapid conduction over an
accessory AV pathway or may suggest concomitant structural abnormalities,
such as valvular aortic stenosis, hypertrophic cardiomyopathy, or
cerebrovascular disease. Symptoms vary with the ventricular rate,
underlying heart disease, duration of SVT, and individual patient
perceptions. Supraventricular tachycardia that is persistent for
weeks to months and associated with a fast ventricular response
may lead to a tachycardia-mediated cardiomyopathy (56-58).
Of
crucial importance in clinical decision making is a clinical history
describing the pattern in terms of the number of episodes, duration,
frequency, mode of onset, and possible triggers.
Supraventricular
tachycardia has a heterogeneous clinical presentation, most often
occurring in the absence of detectable heart disease in younger
individuals. The presence of associated heart disease should, nevertheless,
always be sought and an echocardiogram may be helpful. While a physical
examination during tachycardia is standard, it usually does not
lead to a definitive diagnosis. If irregular cannon A waves and/or
irregular variation in S1 intensity is present, then a ventricular
origin of a regular tachycardia is strongly suggested.
2.
Diagnostic Investigations
A
resting 12-lead ECG should be recorded and evaluated for the presence
of abnormal rhythm, pre-excitation, prolonged QT interval, sinus
tachycardia, segment abnormalities, or evidence of underlying heart
disease. The presence of pre- excitation on the resting ECG in a
patient with a history of paroxysmal regular palpitations is sufficient
for the pre- sumptive diagnosis of AVRT, and attempts to record
spontaneous episodes are not required before referral to an arrhythmia
specialist for therapy (Fig. 2). Specific
therapy is discussed in Section V–A clinical history of irregular
and paroxysmal palpitations in a patient with baseline pre-excitation
strongly suggests episodes of AF, which requires immediate electrophysiological
evaluation because these patients are at risk for sudden death (see
Section V–D). The diagnosis is otherwise made by careful analysis
of the 12-lead ECG during tachycardia (see Section IV). Therefore,
patients with a history of sustained arrhythmia should always be
encouraged to have at least one 12-lead ECG taken during the arrhythmia.
Automatic analysis systems of 12-lead ECGs are unreliable and commonly
suggest an incorrect arrhythmia diagnosis.
Indications
for referral to a cardiac arrhythmia specialist include presence
of a wide complex tachycardia of unknown origin. For those with
narrow complex tachycardias, referral is indicated for those with
drug resistance or intolerance as well as for patients desiring
to be free of drug therapy. Because of the potential for lethal
arrhythmias, all patients with Wolff-Parkinson-White (WPW) syndrome
(ie, pre-excitation combined with arrhythmias) should be referred
for further evaluation. All patients with severe symptoms, such
as syncope or dyspnea, during palpitations also should be referred
for prompt evaluation by an arrhythmia specialist. An echocardiographic
examination should be considered in patients with documented sustained
SVT to exclude the pos- sibility of structural heart disease, which
usually cannot be detected by physical examination or 12-lead ECG.
An
ambulatory 24-hour Holter recording can be used in patients with
frequent (ie, several episodes per week) but transient tachycardias
(59-61). An event or wearable loop
recorder is often more useful than a 24-hour recording in patients
with less frequent arrhythmias (62).
Implantable loop recorders may be helpful in selected cases with
rare symptoms (ie, fewer than two episodes per month) associated
with severe symptoms of hemodynamic instability (63).
Exercise testing is less often useful for diagnosis unless the arrhythmia
is clearly triggered by exertion.
Transesophageal
atrial recordings and stimulation may 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
electrophysiological investigation is planned (64,65).
Invasive electrophysiological investigation with subsequent catheter
ablation may be used for diagnoses and therapy in cases with a clear
history of paroxysmal regular palpitations. It may also be used
empirically in the presence of pre-excitation or disabling symptoms
(Fig. 2).
3.
Management
The
management of patients with symptoms suggestive of an arrhythmia
but without ECG documentation depends on the nature of the symptoms.
If the surface ECG is normal and the patient reports a history consistent
with premature extra beats, then precipitating factors, such as
excessive caffeine, alcohol, nicotine intake, recreational drugs,
or hyperthy- roidism, should be reviewed and eliminated (Table
3). Benign extrasystoles are often manifest at rest and tend
to become less common with exercise.
If symptoms and the clinical history indicate that the arrhythmia
is paroxysmal in nature and the resting 12-lead ECG gives no clue
for the arrhythmia mechanism, then further diagnostic tests for
documentation may not be necessary before referral for an invasive
electrophysiological study and/or catheter ablation. Patients should
be taught to perform vagal maneuvers. A beta-blocking agent may
be prescribed empirically provided that significant bradycardia
(less than 50 bpm) have been excluded. Due to the risk of proarrhythmia,
antiarrhythmic treatment with Class I or Class III drugs should
not be initiated without a documented arrhythmia.
B.
General Evaluation of Patients With Documented Arrhythmia
1.
Diagnostic Evaluation
Whenever
possible, a 12-lead ECG should be taken during tachycardia but should
not delay immediate therapy to terminate the arrhythmia if there
is hemodynamic instability. At a minimum, a monitor strip should
be obtained from the defibrillator, even in cases with cardiogenic
shock or cardiac arrest, before direct current (DC) cardioversion
is applied to terminate the arrhythmia.
a.
Differential Diagnosis for Narrow QRS-Complex Tachycardia
If
ventricular activation (QRS) is narrow (less than 120 milliseconds
[ms]), then the tachycardia is almost always supraventricular and
the differential diagnosis relates to its mechanism (Fig.
3) (66,67). If no P waves or
evidence of atrial activity is apparent and the RR interval is regular,
then AVNRT is most commonly the mechanism (Fig.
4). P-wave activity in AVNRT may be only partially hidden within
the QRS complex and may deform the QRS to give a pseudo-R wave in
lead V1 and/or a pseudo-S wave in inferior leads (Fig.
4). If a P wave is present in the ST segment and sepa- rated
from the QRS by 70 ms, then AVRT is most likely. In tachycardias
with RP longer than PR (Fig. 5), the most
typical diagnosis is atypical AVNRT, permanent form of junctional
reciprocating tachycardia (PJRT) (ie, AVRT via a slowly conducting
accessory pathway), or AT (see Sections V–B, V–D, and
V–E). Responses of narrow QRS-complex tachycardias to adenosine
or carotid massage may aid in the differential diagnosis (Fig.
6) (68-70). A 12-lead ECG recording
is desirable during use of adenosine or carotid massage. If P waves
are not visible, then the use of esophageal pill electrodes can
also be helpful.
b.
Differential Diagnosis for Wide QRS-Complex Tachycardia
If
the QRS is wide (greater than 120 ms), then it is important to differentiate
between SVT and ventricular tachycardia (VT) (Fig.
7). Intravenous medications given for the treatment of SVT,
particularly verapamil or diltiazem, may be deleterious because
they may precipitate hemodynamic collapse for a patient with VT
(71-73). Stable vital signs during
tachycardias are not helpful for distinguishing SVT from VT. If
the diagnosis of SVT cannot be proven or cannot be made easily,
then the patient should be treated as if VT were present. Wide-QRS
tachycardia can be divided into three groups: SVT with bundle-branch
block (BBB) or aberration, SVT with AV conduction over an accessory
pathway, and VT.
SUPRAVENTRICULAR
TACHYCARDIA WITH BUNDLE-BRANCH BLOCK. Bundle-branch block may be
pre-existing or may occur only during tachycardia when one of the
bundle branches is refractory due to the rapid rate. Most BBBs are
not only rate-related, but are also due to a long-short sequence
of initiation. Bundle-branch block can occur with any supraventricular
arrhythmia. If a rate-related BBB develops during orthodromic AVRT,
then the tachycardia rate may slow if the BBB is ipsilateral to
the bypass tract location.
SUPRAVENTRICULAR
TACHYCARDIA WITH ATRIOVENTRICULAR CONDUCTION OVER AN ACCESSORY PATHWAY.
Supra- ventricular tachycardia with AV conduction over an accessory
pathway may occur during AT, atrial flutter, AF, AVNRT or antidromic
AVRT. The latter is defined as anterograde conduction over the accessory
pathway and retrograde conduction over the AV node or a second accessory
AV pathway. A wide-QRS complex with left bundle-branch block (LBBB)
morphology may be seen with anterograde conduction over other types
of accessory pathways, such as atriofascicular, nodofascicular,
or nodoventricular tracts.
VENTRICULAR
TACHYCARDIA. Several ECG criteria have been described to differentiate
the underlying mechanism of a wide-QRS tachycardia.
VENTRICULAR
ARRHYTHMIA DISSOCIATION. Ventricular arrhythmia dissociation
with a ventricular rate faster than the atrial rate generally proves
the diagnosis of VT (Fig. 8) but is clearly
discernible in only 30% of all VTs (74).
Fusion complexes represent a merger between conducted sinus (or
supraventricular complexes) impulses and ventricular depolarization
occurring during AV dissociation. These complexes are pathognomonic
of VT. Retrograde VA block may be present spontaneously or brought
out by carotid massage. The demonstration that P waves are not necessary
for tachycardia maintenance strongly suggests VT. P waves can be
difficult to recognize during a wide-QRS tachycardia. Therefore,
one should also look for evidence of VA dissociation on examination:
irregular cannon A waves in the jugular venous pulse and variability
in the loudness of the first heart sound and in systolic blood pressure
(75). If P waves are not visible,
then the use of esophageal pill electrodes can also be useful.
WIDTH
OF THE QRS COMPLEX. A QRS width of more than 0.14 seconds with
right bundle-branch block (RBBB) or 0.16 seconds during LBBB pattern
favors VT (74). The QRS width criteria
are not helpful in differentiating VT from SVT with AV conduction
over an accessory pathway. A patient with SVT can have a QRS width
of more than 0.14 (RBBB) or 0.16 (LBBB) in the presence of either
pre-existing BBB or AV conduction over an accessory pathway, or
when class Ic or class Ia antiarrhythmic drugs are used. CONFIGURATIONAL
CHARACTERISTICS OF THE QRS COMPLEX DURING TACHYCARDIA. Leads V1
and V6 are helpful in differentiating VT from SVT (74,76,77).
•
An RS (from the initial R to the nadir of S) interval longer than
100 ms in any precordial lead is highly suggestive of VT (78).
• A QRS pattern with negative concordance in the precordial
leads is diagnostic for VT (“negative concordance” means
that the QRS patterns in all of the precordial leads are similar,
and with QS complexes). Positive concordance does not exclude antidromic
AVRT over a left posterior accessory pathway (79).
• The presence of ventricular fusion beats indicates a ventricular
origin of the tachycardia.
•
QR complexes indicate a myocardial scar and are present in approximately
40% of patients with VTs after myocardial infarction (80).
The
width and morphologic criteria are less specific for patients taking
certain antiarrhythmic agents and those with hyperkalemia or severe
heart failure. Despite ECG criteria, patients presenting with wide
QRS-complex tachycardia are often misdiagnosed (71,72,81).
A positive answer to two inquiries, namely the presence of a previous
myocardial infarct and the first occurrence of a wide QRS-complex
tachycardia after an infarct, strongly indicates a diagnosis of
VT (82).
2.
Management
When
a definitive diagnosis can be made on the basis of ECG and clinical
criteria, acute and chronic treatment should be initiated on the
basis of the underlying mechanism (see the sections on specific
arrhythmias). If the specific diagnosis of a wide QRS-complex tachycardia
cannot be made despite careful evaluation, then the patient should
be treated for VT. Acute management of patients with hemodynamically
stable and regular tachycardia is outlined in Fig. 9. The most effective
and rapid means of terminating any hemodynamically unstable narrow
or wide QRS-complex tachycardia is DC cardioversion.
a.
Acute Management of Narrow QRS-Complex Tachycardia
In
regular narrow QRS-complex tachycardia, vagal maneuvers (ie, Valsalva
[83], carotid massage, and facial
immersion in cold water), should be initiated to terminate the arrhythmia
or to modify AV conduction. If this fails, IV antiarrhythmic drugs
should be administered for arrhythmia termination in hemodynamically
stable patients. Adenosine or nondihy- dropyridine calcium-channel
antagonists are the drugs of choice (Fig.
7). The advantage of adenosine relative to IV calcium-channel
or beta blockers relates to its rapid onset and short half-life.
Intravenous adenosine is, therefore, the preferred agent except
for patients with severe asthma. Patients treated with theophylline
may require higher doses of adenosine for effect, and adenosine
effects are potentiated by dipyridamole. In addition, higher rates
of heart block may be seen when adenosine is concomittantly administered
with carbamazepine. Longer-acting agents (eg, IV calcium-channel
blockers or beta blockers [ie, verapamil/diltiazem or metoprolol])
are of value, particularly for patients with frequent atrial premature
beats or ventricular premature beats, which may serve to trigger
early recurrence of PSVT. Adenosine or DC cardioversion is preferred
for those with PSVT in whom a rapid therapeutic effect is essential.
Potential adverse effects of adenosine include initiation of AF
(1 to 15%), which is usually transient, and may be particularly
problematic for those with ventricular pre-excitation. Adenosine
should be avoided in patients with severe bronchial asthma. It is
important to use extreme care with concomitant use of IV calcium-channel
blockers and beta blockers because of possible potentiation of hypotensive
and/or bradycardic effects. An ECG should be recorded during vagal
maneuvers or drug administration because the response may aid in
the diagnosis even if the arrhythmia does not terminate (Fig.
6). Termination of the tachycardia with a P wave after the last
QRS complex favors AVRT or AVNRT. Tachycardia termination with a
QRS complex favors AT,which is often adenosine insensitive. Continuation
of tachycardia with AV block is virtually diagnostic of AT or atrial
flutter, excludes AVRT, and makes AVNRT very unlikely.
b. Acute Management of Wide QRS-Complex Tachycardia
Immediate
DC cardioversion is the treatment for hemodynamically unstable tachycardias.
If the tachycardia is hemodynamically stable and definitely supraventricular,
then management is as described for narrow QRS-complex tachycardias
(Fig. 6). For pharmacologic termination
of a stable wide QRS-complex tachycardia, IV procainamide and/or
sotalol are recommended on the basis of randomized but small studies
(84,85). Amiodarone is also considered
acceptable. Amiodarone is preferred, compared to procainamide and
sotalol, in patients with impaired left ventricular (LV) function
(86,87) or signs of heart failure.
These recommendations are in accord with the current Advanced Cardiovascular
Life Support guidelines (88). Special
circumstances may require alternative therapy (ie, pre-excited tachycardias
and VT caused by digitalis toxicity). For termination of an irregular
wide QRS-complex tachycardia (ie, pre-excited AF), DC cardioversion
is recommended. Or, if the patient is hemodynamically stable, pharmacologic
conversion using IV ibutilide, flecainide, or procainamide is appropriate.
c.
Further Management
After
successful termination of a wide QRS-complex tachycardia of unknown
etiology, patients should be referred to an arrhythmia specialist.
Patients with stable narrow QRS-complex tachycardia, normal LV function,
and a normal ECG during sinus rhythm (ie, no pre-excitation) may
require no specific therapy. Referral is indicated for those with
drug resistance or intolerance as well as for patients desiring
to be free of lifelong drug therapy. When treatment is indicated,
options include catheter ablation or drug therapy. Finally, because
of the potential for lethal arrhythmias, all patients with WPW syndrome
(ie, pre-excitation and arrhythmias) should be referred for further
evaluation (89). |
