the heart is a 4-chambered muscle that functions as a blood pump; the 2 upper chambers are called

the atria and the 2 lower chambers are the ventricles. The rhythm of the heart is normally controlled
by a natural pacemaker (the sinoatrial node) in the right upper chamber that beats about 60 times
per minute at rest and can increase with exercise. Electrical impulses travel from the natural
pacemaker through the atria, then pass through a filter called the atrioventricular node (AV)
between the atria and ventricles before running down specialized fibers that activate the ventricles.
(Figure 1) The atria are above the ventricles, hence the term supraventricular. The term tachycardia
refers to a rapid heartbeat of over 100 beats per minute. Supraventricular tachycardia is frequently
abbreviated as SVT (formerly paroxysmal atrial tachycardia or PAT). Supraventricular tachycardia
then is a rapid rhythm of the heart that begins in the upper chambers. When patients experience
change in the normal sequence of electrical impulses and an abnormal heart rhythm occurs, they are
said to be having an arrhythmia.
Jantung merupakan otot yang terdiri dari 4 ruangan dengan fungsi untuk memompakan darah.
Dua ruangan dibagian atas disebut atrium dan dua ruangan dibagian bawah disebut ventrikel.
Irama jantung dikendalikan oleh nodus sinoatrial. Cetusan listrik dari nodus sinoatrial untuk
mencapai otot ventrikel harus melewati filter yang disebut nodus atrioventrikuler (AV). Istilah
supraventriculer mengarah kepada ruangan di atas ventrikel yakni atrium, sedangkan takikardi
merupakan frekuensi jantung yang lebih cepat dari 100 denyut per menit. Supraventricular
tachycardia (SVT) merupakan frekuensi denyutan jantung yang cepat dan berasal dari rungan
atas jantung

SVTs are produced by disorders of impulse formation (causing

generation of rapid electrical impulses from a small area) and/or
disorders of impulse conduction, which result in re-entrant
tachycardias, where tachycardia is produced because the
electrical impulse repeatedly travels around a circuit. Re-entrant
tachycardias typically require an extrasystole to initiate them.
SVTs are among the few medical conditions that can be cured

SVT disebabkan oleh gangguan pembentukan atau konduksi impuls yang menyebabkan impuls
listrik bergerak berulangkali di sekitar sirkuit.

AVNRT
AVNRT is caused by a re-entrant circuit involving the posterior
and anterior inputs into the compact atrioventricular node.3 A
quarter of the population has two pathways that input into the
compact atrioventricular node, one of which is a rapidly
conducting pathway and the other a slower conducting pathway;
these two pathways form the circuit for AVNRT (fig 1⇓).
The extrasystole that triggers the tachycardia is critically timed
so that the faster pathway is still refractory from the last sinus
beat (that is, it is not yet ready to conduct an impulse because
it is still recovering from depolarisation). The electrical impulse
therefore propagates exclusively down the slow pathway, which
has a shorter refractory period (that is, it takes less time to
recover from depolarisation) and then returns up the fast pathway, which has by then recovered. The
circuit for typical
AVNRT is thus formed.
Less commonly, activation travels anterogradely down the fast
pathway and returns up the slow pathway, forming atypical
AVNRT. These different mechanisms result in very different
appearances on the surface electrocardiogram (ECG). In the
typical form, atrial and ventricular activation occur virtually
simultaneously (because the impulse returns up the fast pathway
at the same time as travelling down the His-Purkinje system),
so the P waves are invisible in the QRS complexes (a
pseudo-RSR’ pattern in lead V1 often provides a clue to the
presence of the P wave), whereas the delayed atrial activation
via the slow pathway in atypical AVNRT produces inverted P
waves typically in the middle of or late in the RR interval.
Typical AVNRT presents as a short RP tachycardia (the ECG
during tachycardia has a RP interval shorter than PR interval)
while atypical AVNRT produces a long RP tachycardia (RP
interval longer than PR interval)

AVRT (including Wolff-Parkinson-White

syndrome)
AVRT is also a re-entrant tachycardia; it requires the presence
of an accessory pathway, a small strand of myocardium that
bridges the normal insulation between atria and ventricles (fig
3⇓).
Some pathways can conduct impulses only from the ventricle
to the atrium and are known as concealed accessory pathways.
Others can conduct in both directions and usually produce
pre-excitation of the ventricle because they conduct more rapidly
than the atrioventricular node. This early ventricular activation
shows on the 12 lead ECG as a delta wave at the start of the
QRS (fig 3⇓). The terminal portion of the QRS complex is
narrow, reflecting the rapid conduction via the His-Purkinje
system once the atrioventricular node has been crossed. The
degree of pre-excitation varies depending on the time required
to cross the atrioventricular node and the location of the
accessory pathway. The diagnosis of Wolff-Parkinson-White syndrome describes
patients with a delta wave on the surface ECG who also
experience palpitations.
AVRT is usually triggered by a critically timed atrial
extrasystole that finds the accessory pathway refractory,
therefore antegrade conduction occurs exclusively down the
atrioventricular node. The accessory pathway is no longer
refractory by the time the wave front reaches its ventricular
insertion and it therefore conducts retrogradely to the atrium—
the re-entrant circuit is thus formed (fig 3⇓); this activation
pattern is termed orthodromic AVRT, and produces a narrow
complex tachycardia. Rarely, anterograde conduction travels
down the accessory pathway returning to the atrium via the
atrioventricular node, producing antidromic AVRT, which has
broad QRS complexes that exaggerate the pattern of
pre-excitation seen in sinus rhythm because ventricular
activation occurs exclusively via the accessory pathway

How does SVT present?

Common symptoms include palpitations, chest pain, anxiety,
lightheadedness, pounding in the neck, shortness of breath, and
uncommonly syncope.11
Sudden onset and offset of palpitations is typical for a re-entrant
arrhythmia, while for sinus tachycardia onset and offset is
usually gradual. Patients with AVNRT or AVRT may be able
to terminate palpitations with vagal manoeuvres such as the
Valsalva manoeuvre, breath holding, or coughing.
Some patients can identify triggers such as caffeine or alcohol
intake, which can initiate re-entrant tachycardia by increasing
the frequency of extrasystoles.
In the absence of an acute episode the examination is usually
normal. In a patient with tachycardia, prominent jugular venous
A waves caused by atrial contraction against the closed tricuspid
valve may be seen.12

Typically, patients have symptoms from SVT, but occasionally they may have no symptoms. A
common symptom during SVT is palpitations or a sensation that the heart is beating rapidly,
fluttering, or racing. This may last for a few seconds or several hours. Occasionally, patients may
have a sensation of shortness of breath or “air-hunger,” or chest pressure or pain. Sometimes
patients will feel lightheaded or dizzy, and rarely patients will feel like they are about to pass out.
Loss of consciousness (also known as syncope) during SVT is a rare occurrence. Although such
symptoms may raise concern, in general, SVT is not a serious or life-threatening condition.
Nonetheless, if any of these symptoms develops, immediate medical attention should be sought.

Gejala umum SVT adalah palpitasi, nyeri dada, rasa cemas, rasa pusing, berdebar di leher,
sesak nafas, dan sinkop. Gejala yang terjadi tiba-tiba biasanya khas pada re-enterant
arrhytmia. Gejala biasanya dicetuskan olehkafein dan alkohol.

What investigations are needed?

Electrocardiography
Attempts should always be made to capture the arrhythmia
during an episode of palpitations. We recommend giving the
patient a copy to ensure it is never lost and is easily available
to health professionals. A rhythm strip should be recorded if 12
lead electrocardiography is not available, and every effort should
be made to capture the termination of the tachycardia.
For patients with non-sustained episodes of palpitations, an
ambulatory electrocardiograph or an event monitor can be useful
in capturing an ECG during an episode.
Narrow complex tachycardia is most frequently seen (QRS <120
ms), but less commonly the QRS complexes are broad during
tachycardia. Even though supraventricular tachycardias can
present with broad QRS complexes, in the initial evaluation, a
broad complex tachycardia should be treated as a ventricular
tachycardia until proven otherwise.
A 12 lead ECG in sinus rhythm should also be recorded and
carefully examined for the presence of a delta wave. In figure
2⇓ we suggest how to analyse the 12 lead ECG during
tachycardia.
Upaya harus selalu dilakukan untuk menangkap aritmia
selama episode palpitasi. Kami merekomendasikan memberikan
rawat satu salinan untuk memastikan tidak pernah hilang dan mudah tersedia
untuk para profesional kesehatan. Irisan irama harus direkam jika 12
lead electrocardiography tidak tersedia, dan setiap usaha harus dilakukan
dibuat untuk menangkap penghentian takikardia.
Untuk pasien dengan episode palpitasi non-berkelanjutan, sebuah
elektrokardiograf ambulatori atau monitor acara dapat bermanfaat
dalam menangkap EKG selama suatu episode.
Takikardia kompleks yang sempit paling sering terlihat (QRS <120
ms), tetapi lebih jarang kompleks QRS luas selama
takikardia. Meskipun takikardia supraventrikular bisa
hadir dengan kompleks QRS yang luas, dalam evaluasi awal, a
takikardia kompleks luas harus diperlakukan sebagai ventrikel
takikardia sampai terbukti sebaliknya.
EKG 12 lead dalam irama sinus juga harus dicatat dan
hati-hati diperiksa untuk kehadiran gelombang delta. Dalam gambar
2⇓ kami menyarankan bagaimana menganalisis 12 lead ECG selama
takikardia.
Echocardiography
Echocardiography is an important investigation for patients
presenting with palpitations. The presence of structural heart
disease such as left ventricular impairment should prompt urgent
referral and investigation. Left ventricular impairment is
associated with an increased risk of sudden cardiac death,13 and
patients are less likely to tolerate tachycardia. Such patients
should not be prescribed class 1 antiarrhythmic drugs, such as
flecainide.1
Most patients with SVT have a structurally normal heart. In a
series of 145 patients referred for ablation, only 4% had heart

failure.14 However, certain types of structural heart disease are

associated with particular SVTs. Patients with Ebstein’s anomaly
(congenital displacement of the septal tricuspid valve leaflet
into the right ventricle) have an increased frequency of right
sided accessory pathways.15 Incisional atrial tachycardia occurs
as a result of re-entry around surgical scars and is a major source
of morbidity in the growing population of survivors of
congenital heart disease

Understanding the underlying mechanism is useful

in understanding the clues on ECG. Ventricular
rates in SVT may vary from 150 to 250 beats/min.
However, the rate may be slower in older patients and in patients taking AV nodal blocking medications
(i.e., calcium-channel blockers, β-blockers
and digoxin).7
Memahami mekanisme yang mendasarinya pada kasus SVT penting dalam memahami
petunjuk dari ECG. Frekuensi ventrikel pada SVT dari 150 hingga 250 denyut / menit. Namun,
angka ini mungkin lebih lambat pada pasien yang lebih tua dan pada pasien yang
mengkonsumsi obat penghambat nodal AV (blocker saluran kalsium, β-blocker dan digoxin)

In patients with AVNRT, two functionally

distinct pathways in the AV node — generally
referred to as fast and slow pathways — are involved
that may form an electrical circuit within
the AV node. Clues on ECG include a pseudo R1
wave in lead V1 and a pseudo S wave in the inferior
leads. These findings correspond to retrograde
P waves seen after the QRS complex

Pada pasien dengan AVNRT, terdapat dua jalur fungsional yang berbeda di AV node. Jalur cepat dan lambat,
bergantung pada sirkuit listrik yang terbentuk pada AV node. Hasil EKG memperlihatkan pseudo R1 pada
gelombang V1 dan gelombang pseudo S di inferior. Hasil ini bersamaan dengan gelombang P retrograde setelah
kompleks QRS

In patients with AVRT, the tachycardia involves both the AV node and an extranodal accessory pathway
(bypass tract) that connects the myocardium of the atrium to the ventricle. 10 In AVRT with a narrow QRS
complex, a circuit forms from the anterograde conduction through the AV node and retrograde conduction
through the accessory pathway. An ECG performed during the tachyarrhythmia may show retrograde P waves
following the QRS complex. Once terminated, the resting ECG may show signs of pre-excitation: a delta wave
with a widened QRS complex and a short PR interval. In Wolff– Parkinson–White syndrome, pre-excitation is
seen on the resting ECG (Figure 3) coupled with symptoms of palpitations (e.g., re-entrant tachycardia
involving the accessory pathway).
Pada pasien dengan AVRT, takikardia melibatkan jalur AV node dan jalur aksesori extranodal yang
menghubungkan miokardium atrium ke ventrikel. AVRT dengan kompleks QRS yang sempit, sebuah sirkuit
terbentuk dari konduksi anterograde melalui AV node dan retrograde melalui konduksi jalur aksesori. EKG
memperlihatkangelombang P retrograde mengikuti kompleks QRS. Setelah diterminasi, ECG pada saat istirahat
memperlihatkan tanda-tanda pra-eksitasi: gelombang delta dengan QRS yang lebar dan interval PR yang
kompleks dan pendek. Pada sindrom Wolff Parkinson White, terlihat pre-eksitasi pada EKG saat istirahat disertai
dengan gejala palpitasi.

Atrial tachycardia originates from a focal atrial site and is characterized by regular and organized atrial activity
(Figure 4). The mechanism of atrial tachycardia is a result of a micro– re-entrant circuit in the atrium or an
automatic focus.7 Depending on the atrial rate and the AV nodal conduction properties, 2:1 or variable
conduction may be seen. Diagnostic clues on ECG include a warm-up phenomenon in which the atrial rate
increases slightly over the first 5 to 10 seconds before stabilizing. On surface ECG, the P waves are usually seen
before every QRS complex and have a different axis than a sinus P wave. At high atrial rates, the P waves may
be embedded in the descending limb of the T wave or completely obscured by the T waves.7
Atrial flutter originates from an anatomic macro–re-entrant circuit in the atria. The most common (typical) atrial
flutter involves counterclockwise conduction in the right atrium along an anatomic circuit including the
cavotricuspid isthmus (the area between the inferior vena cava and the tricuspid annulus). Atrial flutter is
associated with many conditions, including heart failure, obstructive sleep apnea, chronic pulmonary disease,
previous stroke, hyperthyroidism, valvular heart disease, pericardial disease and postcardiac surgery.11,12 In
regular SVT due to atrial flutter, the atrial rate is typically 300 beats/min with a 2:1 ventricular rate of 150
beats/min.7 It can be identified on the ECG as a sawtooth pattern of flutter waves that are negative in the inferior
leads and positive in lead V1
Atrial tachycardia yang berasal dari fokal situs atrium ditandai dengan aktivitas atrium teratur dan
terorganisir. Mekanisme takikardia atrium adalah hasil dari sirkuit micro– re-entrant di atrium atau pada
fokus. Otomatis. Pada EKG terlihat warm-up phenomenon, frekuensi atrium meningkat sedikit selama 5
sampai 10 detik pertama sebelum stabil. Gelombang P biasanya tertanam di bagian bawah gelombang
T atau benar-benar dikaburkan oleh gelombang T.
Flutter atrial berasal dari sirkuit macro–re-entrant di atrium. Atrial flutter dikaitkan dengan banyak
kondisi, termasuk gagal jantung, obstructive sleep apnea, penyakit paru kronik, stroke, hipertiroidisme,
penyakit katup jantung, penyakit perikardial dan setelah operasi jantung. Pada EKG terlihat pola
gergaji gelombang flutter yang negatif pada sadapan inferior dan positif pada sadapan V1

What is the diagnostic approach in the emergency department

1. Assess hemodynamic status
When assessing a patient with suspected SVT, it
is essential to assess the patient’s hemodynamic
status quickly. Supraventricular tachycardias are
rarely fatal, but the annual risk of sudden cardiac
death is 0.02%–0.15% among patients with
Wolff–Parkinson–White syndrome.13 Nonetheless,
certain patients with cardiac comorbidities
may not tolerate the underlying rapid ventricular rate, which may lead to hemodynamic instability,
exacerbated congestive heart failure or
angina. If the patient is deemed unstable because
of the SVT, and a trial of vagal manoeuvres or
intravenous adenosine is ineffective or not feasible,
synchronized electrical cardioversion may
be warranted.5
Penilaian status hemodinamik secara cepat penting saat mendapatkan pasien dengan suspek SVT.
Pasien dengan komorbid penyakit jantung mungkin tidak dapat mentolerir frekuensi ventrikel yang
cepat sehingga menyebabkan ketidakstabilan hemodinamik, diperburuk gagal jantung kongestif atau
nyeri dada. Pada pasien tidak stabil, manuver vagal atau adenosin intravena tidak efektif dan tidak
disarankan. Pilihan yang disarankan adalah dengan kardioversi.
2. Assess the type of SVT
If the patient is hemodynamically and clinically
stable, the most important diagnostic step is to
obtain a 12-lead ECG. Once the ECG is obtained,
the four-step approach outlined in Figure 1 is
suggested to diagnose the underlying rhythm.
First, determine whether the QRS complex
is narrow (< 120 ms) or wide (≥ 120 ms). A
narrow complex confirms the supraventricular
origin of the arrhythmia; a wide complex may
represent ventricular tachycardia or SVT with
aberrancy.
Pada pasien dengan klinis dan hemodinamik stabil, langkah diagnostik yang paling penting adalah lakukan
pemeriksaan EKG 12 lead. Setelah ECG didapatkan, terdapat 4 langkah yanf harus dilakukan :
Pertama, tentukan apakah kompleks QRS sempit (<120 ms) atau lebar (≥ 120 ms). QRS yang sempit berarti
berasal dari supraventricular.

Second, if the QRS complex is narrow, assess

whether the rhythm is regular or irregular. An
irregular rhythm generally excludes AVNRT and
AVRT, and is more in favour of atrial fibrillation,
or atrial flutter or tachycardia with variable
conduction through the AV node. A narrowcomplex
tachycardia with a regular rhythm is
likely to be sinus tachycardia, AVRT, AVNRT,
atrial flutter or atrial tachycardia.
Kedua, jika kompleks QRS sempit, nilai apakah irama teratur atau tidak teratur. Irama tidak teratur umumnya
bukan AVNRT dan AVRT, lebih mengarah kepada fibrilasi atrium atau atrial flutter atau tachycardia dengan
variabel konduksi melalui AV node.

Third, to diagnose the mechanism behind the

narrow-complex tachycardia, look closely for
any sign of atrial activity or P waves. If a P wave is seen, the final step is to assess
its place in the cardiac cycle by comparing the
RP and PR intervals. If the RP interval is shorter
than the PR interval (i.e., the P wave is seen
immediately after the QRS complex), it is likely
a retrograde P wave, and the most likely diagnosis
is AVNRT or AVRT. If the RP interval is
longer than the PR interval (i.e., the P wave is
seen before the QRS complex), the most likely
diagnosis is sinus tachycardia or atrial tachycardia.
Atrial flutter may appear to fall in either category
when presenting as a regular tachycardia
with 2:1 conduction. Atrial flutter should be suspected
when the heart rate is near 150 beats/min
or when the P wave falls exactly in the middle of
the RR interval (i.e., the length of the RP interval equals that of the PR interval), in which case
another P wave (flutter wave) may be hidden in
the QRS complex.
Ketiga, jika gelombang P terlihat, langkah terakhir adalah menilai tempatnya di siklus jantung dengan
membandingkan Interval RP dan PR. Jika interval RP lebih pendek dari interval PR (yaitu, gelombang P
terlihat segera setelah kompleks QRS), itu mungkin gelombang P retrograde, dan diagnosis yang paling
mungkin adalah AVNRT atau AVRT. Jika interval RP adalah lebih lama dari interval PR (yaitu,
gelombang P adalah terlihat sebelum kompleks QRS), kemungkinan besar diagnosis adalah sinus
tachycardia atau takikardia atrium.

Atrial flutter harus dicurigai ketika denyut jantung mendekati 150 denyut / menit atau ketika
gelombang P jatuh tepat di tengah-tengah interval RR (yaitu, panjang interval RP sama dengan interval
PR), dalam hal ini Gelombang P lain (gelombang flutter) mungkin tersembunyi di dalamnya kompleks
QRS.

What is the initial treatment in hemodynamically stable patients?

In hemodynamically stable patients with SVT,
once the ECG is obtained, a diagnostic and therapeutic
trial of a vagal manoeuvre is recommended
under continuous ECG monitoring (Figure 6).5 In
patients with AVRT or AVNRT, the vagal manoeuvre
may terminate the circuit and restore normal
sinus rhythm. In patients whose tachycardia
does not involve the AV node (e.g., atrial flutter and atrial tachycardia), vagal manoeuvres or intravenous
use of adenosine may slow the ventricular
rate briefly and thus unmask the underlying atrial
rhythm. We recommend beginning with the nonpharmacologic
approach because it may obviate
the need for adenosine, and it may identify patients
who respond to the vagal manoeuvre and
who can be taught to use it in future episodes
Setelah EKG didapatkan pada pasien SVT dengan hemodinamik stabil, percobaan manuver vagal boleh
dilakukan dengan monitoringEKG. Manuver vagal dapat mengembalikan irama sinus pada pasien
dengan AVRT atau AVNRT. Pada pasien takikardia yang tidak melibatkan nodus AV (flutter atrium dan
takikardia atrium), manuver vagal atau intravena adenosine dapat memperlambat frekuensi
ventrikelsehingga bisa dilakukan penilaian dan mengetahui penyebab yang mendasari pada atrium.
Direkomendasikan untuk memulai dengan pendekatan non farmakologis, sehingga dapat mengurangi
kebutuhan adenosis dan bisa mengidentifikasi pasien mana yang respon dengan manuver vagal dan
mana yang butuh intervensi lanjutan.
Nonpharmacologic measures
pijatan pada sinus karotis dan manuver valsava dapat menyebabkan tonus vagal. Sebelum
melakukan pijatan sinus karotis dan manuver vagal, harus dilakukan auskultasi pada bruit karotis untuk
mencegah lepas plak arterosklerosis dan menyebabkan emboli. Kontraindikasi pijatan sinus karotis
diantaranya, bruit karotis, takiaritmia ventrikel, stroke atau infarkmiokard kurang dari 3 bulan.
Pharmacologic measures
Jika vagal manuver gagal, adenosin intravena dengan dosis inisial 6 mg dan dosis ulangan 12 mg
diberikan. Jika manuver vagal dan adenosin gagal, dapat diberikan nondihydropiridine calcium-channel
blocker (diltiazem dan verapamil) atau β-blocker. Jika pengobatan farmakologi gagal, dapat dilakukan
kardioversi, walaupun pada pasien stabil. Semua pasien AVNRT, AVRT, atrial flutter atau atrial
tachycardia simptomatik atau dengan serangan rekurens, dilakukan kateter ablasi radiofrekuensisebagai lini
pertama pengobatan.