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Taquiarritmias Supraventriculares NEJM
Taquiarritmias Supraventriculares NEJM
clinical practice
This Journal feature begins with a case vignette highlighting a common clinical problem.
Evidence supporting various strategies is then presented, followed by a review of formal guidelines,
when they exist. The article ends with the authors clinical recommendations.
A 24-year-old woman presents to the emergency department with the sole symptom
of a racing heart, which began abruptly while she was eating dinner. She reports
having had prior episodes of palpitations that resolved spontaneously. In the emergency
room, her blood pressure is 84/60 mm Hg. An electrocardiogram (ECG) reveals a regu-
lar narrow-complex tachycardia at a rate of 190 beats
per minute without clear atrial activity (P waves). How
should this case be managed?
From Tufts Medical Center, Tufts Univer- Patients with symptomatic tachycardias require immediate medical attention. Al-
sity School of Medicine, Boston. Address though it is commonly believed that a precise diagnosis of the tachycardia is neces-
reprint requests to Dr. Link at Tufts Medi-
cal Center, 800 Washington St., Box sary before therapy is initiated, immediate treatment can usually be tailored to the
#197, Boston, MA 02111, or at mlink@ characteristics of the ventricular response. By focusing on the ventricular response,
tuftsmedicalcenter.org. one can assign the seven clinically relevant supraventricular tachycardias to diag-
N Engl J Med 2012;367:1438-48. nostic and therapeutic groups on the basis of the rapidity of onset, the heart rate,
DOI: 10.1056/NEJMcp1111259 and the regularity of the tachycardia (Fig. 1).1 This review focuses on the initial
Copyright 2012 Massachusetts Medical Society.
diagnostic and therapeutic approach to supraventricular tachycardias and the ways
of differentiating them from ventricular arrhythmias. Although atrial premature
contractions are technically not a supraventricular tachycardia, this abnormality is
included in the current discussion because it is often part of the differential diag-
nosis of supraventricular tachycardias.
The initial differential diagnosis of supraventricular tachycardias should focus on the ventricular response
characteristics of regularity, rate, and rapidity of onset, not on the atrial depolarization from the ECG.
The regular supraventricular tachycardias include sinus tachycardia, atrial flutter, atrioventricular nodal
reentrant tachycardia, atrioventricular reciprocating tachycardia, and atrial tachycardia.
The irregular supraventricular tachycardias are atrial fibrillation, atrial flutter with variable atrioventricular
block, and multifocal atrial tachycardia; multiple atrial premature contractions can cause a similar
presentation.
Sudden onset and termination are characteristic of acute atrial fibrillation and atrial flutter, atrioventricular
nodal reentrant tachycardia, atrioventricular reciprocating tachycardia, and atrial tachycardia. Gradual
onset and recession occur with sinus tachycardia, chronic atrial fibrillation and atrial flutter, multifocal
atrial tachycardia, and atrial premature contractions.
Adenosine blocks the atrioventricular node and is useful in distinguishing among supraventricular
tachycardias but should not be given in the case of irregular wide-complex tachycardias, since it may
render these rhythms unstable.
After administration of adenosine, slowing of the heart rate is consistent with a diagnosis of sinus
tachycardia, atrial tachycardia, atrial fibrillation, or atrial flutter, whereas termination of tachycardia
points to atrioventricular nodal reentrant tachycardia, atrioventricular reciprocating tachycardia, and
some atrial tachycardias.
jump from 60 beats per minute to 160 beats per tracing for this tachycardia difficult to distinguish
minute or more, and the patient is usually aware from that of other supraventricular tachycardias.
of this change. In contrast, in patients with However, a heart rate of 150 beats per minute is
chronic atrial fibrillation, the development of a highly suggestive of this tachyarrhythmia. In pa-
rapid heart rate is more gradual and occurs in tients who have atrioventricular node disease or
response to physical activity or other stressors who are receiving atrioventricular nodeblocking
similar to the case with sinus tachycardia. With medications, the rate in atrial flutter may be
all cases of atrial fibrillation, the ventricular slower than 140 to 150 beats per minute. In these
response is irregular, and the ventricular rate situations, the heart rate is irregular most of the
ranges from 60 to 220 beats per minute, de- time, although it is less chaotic than in atrial
pending largely on the patients age, whether fibrillation.
there is any underlying atrioventricular node dis- The three next most common supraventricular
ease, and whether the patient has received any tachycardias atrioventricular nodal reentrant
drugs that affect the atrioventricular node. tachycardia, atrioventricular reciprocating (re-
Atrial flutter, the second most common patho- entrant) tachycardia, and atrial tachycardia are
logic supraventricular tachycardia, results from a often considered to be a triumvirate because they
reentrant circuit around the tricuspid valve in the share many characteristics, including rapid on-
right atrium (although atypical flutters do occur, set, heart rates of 150 to 250 beats per minute,
primarily in persons who have undergone cardiac and regularity of the ventricular response (Fig. 2).
surgery or cardiac ablation) (Fig. 2). Atrial flutter Atrioventricular nodal reentrant tachycardia and
is an organized regular rhythm that is generally atrioventricular reciprocating tachycardia are
characterized by an atrial rate of 280 to 300 beats caused by the presence of abnormal electrical
per minute and that with 2:1 conduction in the circuits, whereas atrial tachycardia can be focal
atrioventricular node results in a ventricular rate of or caused by very small abnormal circuits. These
140 to 150 beats per minute. At a heart rate of supraventricular tachycardias occur in approxi-
150 beats per minute, the flutter waves are usu- mately 1 person per 500 in the United States.6
ally obscured by T waves, making the surface ECG Atrioventricular nodal reentrant tachycardia is
with a surface delta wave but no tachycardia have rhythmias are seen with bypass tracts: a narrow
ECG findings similar to those with the Wolff regular QRS complex (orthodromic; conduction
ParkinsonWhite syndrome but do not have the down the atrioventricular node and retrograde
syndrome. Nonetheless, these persons are still at conduction through the bypass tract), a wide regu-
risk for supraventricular tachycardias. Three ar- lar QRS complex (antidromic; conduction down
with conduction down the abnormal tissue and depolarize the ventricle through the HisPurkinje
back up to the atrium through the atrioventricu- system (and thus are, by definition, supraventricu-
lar node. lar tachycardias), wide-complex tachycardias can
be ventricular or supraventricular in origin (or
S t r ategie s a nd E v idence artifactual). Wide-complex tachycardias are caused
by ventricular arrhythmia (ventricular tachycardia,
Differential Diagnosis of Supraventricular ventricular fibrillation, and torsades de pointes or
Tachycardias polymorphic ventricular tachycardia) or supraven-
The initial differential diagnosis of supraventric- tricular tachycardias with aberrant conduction re-
ular tachycardias should focus on the ventricular sulting from one of the following conditions: dis-
response, not on atrial depolarization as observed ease in the HisPurkinje system, such as left or
on the ECG. The first step is to determine whether right bundle-branch block; a bypass tract (i.e., the
the QRS complex is narrow or wide. Then regu- WolffParkinsonWhite syndrome), with depo-
larity should be assessed (Fig. 1). Regularity is larization of the ventricle from the bypass tract;
defined as variation of less than 10% in beat-to- or a ventricular paced rhythm from a pacemaker.
beat timing, but most regular tachycardias actu- Wide-complex tachycardias can be regular or ir-
ally vary by less than 5%.8 After regularity is as- regular. Regular wide-complex tachycardias are
sessed, the rapidity of onset and offset should be either ventricular tachycardia or regular supraven-
determined, preferably by means of cardiac moni- tricular tachycardias (Fig. 3), whereas irregular
toring, although it can be assessed on the basis of wide-complex tachycardias are either the ventric-
the history. The heart rate should also be consid- ular arrhythmias of polymorphic ventricular tachy-
ered in the differential diagnosis of supraven- cardia, torsades de pointes, or ventricular fibril-
tricular tachycardias. lation or one of the irregular supraventricular
tachycardias (Fig. 4).
Narrow-Complex Supraventricular
Tachycardias
M a nagemen t
Only after the differential diagnosis has been
narrowed on the basis of the features mentioned Narrow-Complex Tachycardias
above should atrial activity be assessed. P waves
Vagal maneuvers and administration of adeno
immediately precede the QRS complex in sinus sine are useful in the diagnosis and treatment of
tachycardia, atrial tachycardia, multifocal atrial
narrow-complex supraventricular tachycardias.9
tachycardia, and multiple atrial premature con-
Vagal maneuvers including a Valsalva maneu-
tractions. P waves follow the QRS complex in ver, carotid sinus massage, bearing down, and
atrioventricular nodal reentrant tachycardia and
immersion of the face in ice water increase
atrioventricular reciprocating tachycardia. In tachy-
vagal tone and block the atrioventricular node.
cardias with very rapid heart rates (e.g., atrial
The resulting slowing of the heart rate often con-
tachycardia, atrioventricular nodal reentrant tachy-
firms the diagnosis of sinus tachycardia, atrial
cardia, and atrioventricular reciprocating tachy-
fibrillation, or atrial flutter and can frequently ter-
cardia), P waves may not be apparent owing tominate atrioventricular nodal reentrant tachycar-
overlap of the T wave. Atrial flutter with 2:1 con-
dia and atrioventricular reciprocating tachycardia.
duction block can easily be mistaken for sinus
Adenosine, a very short-acting endogenous nucleo-
tachycardia or atrial tachycardia because a flutter
tide that blocks atrioventricular nodal conduction,
wave is often buried in the T wave; however, a
terminates nearly all atrioventricular nodal reen-
rate of 150 beats per minute should lead one to
trant tachycardias and atrioventricular recipro-
suspect atrial flutter. Finally, the response to ad-
cating tachycardias as well as up to 80% of atrial
ministration of adenosine can assist in the diag-
tachycardias.10 Adenosine should be adminis-
nosis of a specific supraventricular tachycardia
tered quickly at a dose of 6 mg, followed by a
(Fig. 3) (see below for additional information re-
bolus of 20 ml of fluid. Since this drug may also
garding adenosine). excite atrial and ventricular tissue, causing atrial
fibrillation in up to 12% of patients and nonsus-
Wide-Complex Supraventricular Tachycardias tained ventricular tachycardia in rare cases,11 it
In contrast to narrow-complex tachycardias, should be administered only when a cardiac
which can be generated only by impulses that monitor is being used and a defibrillator is on
Narrow-complex tachycardia
Treat underlying
Termination No termination
cause
Rate control with
beta-blocker, vera-
pamil, diltiazem; if
unstable condition,
AT, AFL (ST, cardioversion, pro-
AVNRT, AVRT, AT cainamide, ibutilde
less frequently)
hand. A lower dose (3 mg) is recommended in mias that have caused hemodynamic instability
persons who have a cardiac transplant or in and that have not responded to electrical cardio-
whom the drug is administered through a central version. In these cases, procainamide and ibutilide
catheter. Adenosine should not be used in pa- can be used.10
tients with bronchospastic lung disease. Com-
mon side effects include chest tightness, flushing, Wide-Complex Tachycardias
and a sense of dread. Adenosine is also useful in the differential diagno-
Although intravenous verapamil and diltiazem, sis and treatment of wide-complex tachycardias,13
which also block the atrioventricular node, are but it should be given only when these tachycardias
of potential diagnostic and therapeutic use in are regular, since irregular wide-complex tachycar-
narrow-complex tachycardia, they may cause hy- dias may be rendered unstable after the administra-
potension and thus are not a first choice in the tion of adenosine. Potential risks include increasing
emergency setting.12 Electrical cardioversion is conduction through a bypass tract if the underlying
reserved for patients in unstable condition who arrhythmia is atrial fibrillation or (more worri-
are not having a response to adenosine. Antiar- some) terminating the supraventricular tachycardia
rhythmic agents are rarely necessary in the early but inducing atrial fibrillation with resultant rapid
management of supraventricular tachycardias, conduction down a bypass tract, leading to ven-
with the exception of the management of arrhyth- tricular fibrillation.11 Verapamil and diltiazem
Wide-complex tachycardia
No Yes
Ventricular
Termination No termination
tachycardia
should not be administered in patients with wide- plex tachycardias, as it is in the treatment of un-
complex tachycardias, since profound hypotension stable narrow-complex tachycardias. Procainamide
and death may occur.12 Electrical cardioversion is and ibutilide, as well as lidocaine, amiodarone, and
necessary in the treatment of unstable wide-com- sotalol, are useful in the treatment of wide-complex
tachycardias.10 Stable wide-complex irregular needed. Although the blood pressure of the wom-
tachycardias are usually atrial fibrillation with an in the vignette is 84/60 mm Hg, she is alert
aberrancy or the WolffParkinsonWhite syn- and has no signs of shock; thus, her condition is
drome; in the case of these arrhythmias, consul- not considered to be unstable. The initial assess-
tation with an expert is generally required. ment should distinguish between narrow- and
wide-complex tachycardia, determine whether the
A r e a s of Uncer ta in t y rhythm is regular or irregular, and consider the
rapidity of onset. This patient has a regular narrow-
Arrhythmias causing hemodynamic instability complex tachycardia with a sudden onset, as as-
(hypotension, heart failure, or coronary ischemia) sessed on the basis of the history. Possibilities
require urgent electrical cardioversion. However, it include atrial flutter, atrioventricular nodal reen-
is often unclear, especially in the case of atrial fi- trant tachycardia, atrioventricular reciprocating
brillation, whether the supraventricular tachycar- tachycardia, and atrial tachycardia. The narrow
dia is the cause or the result of the hemodynamic QRS complex rules out ventricular tachycardia;
instability.10 In many patients, rapid atrial fibrilla- the regular response rules out atrial fibrillation and
tion is a consequence rather than a cause of heart multifocal atrial tachycardia. The heart rate of
failure or cardiac ischemia. Atrial fibrillation is 190 beats per minute is inconsistent with atrial
rarely the cause of instability when heart rates are flutter. Furthermore, the suddenness of the onset
less than 150 beats per minute.10 of symptoms and the absence of clear P waves
suggest atrioventricular nodal reentrant tachy-
Guidel ine s cardia, atrioventricular reciprocating tachycardia,
or atrial tachycardia. Adenosine should be ad-
Guidelines for the early treatment of supraventric- ministered with the patient on a cardiac monitor,
ular tachycardias are included in the 2010 Amer- with a cardiac defibrillator at hand. Adenosine
ican Heart Association Advanced Cardiovascular would be expected to terminate the supraventric-
Life Support guidelines.10,14 The recommendations ular tachycardia. An ECG should be evaluated when
provided here are generally consistent with these sinus rhythm is restored; the presence of a delta
guidelines, including administration of adenosine wave would be consistent with a diagnosis of atrio-
as the initial treatment of choice for regular su- ventricular reciprocating tachycardia caused by the
praventricular tachycardias and as an important WolffParkinsonWhite syndrome.
aid in the differential diagnosis of regular wide-
Dr. Link reports receiving consulting fees from Lantheus
complex tachycardias. Medical Imaging and holding patents for a chest-wall protec-
tor for sports and a testing model for commotio cordis. No
other potential conflict of interest relevant to this article was
C onclusions a nd reported.
R ec om mendat ions Disclosure forms provided by the author are available with the
full text of this article at NEJM.org.
In a patient presenting with symptomatic tachy- I thank Dr. Bonnie L. Bermas for her careful review of an
earlier version of the manuscript, and Steven Moskowitz of Ad-
cardia, such as the woman described in the vi- vanced Medical Graphics for his assistance with earlier versions
gnette, prompt evaluation and treatment are of the figures.
References
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