Stable SVT susp AVRT dengan

WPW syndrome

Case based discussion

Oleh: dr. Imam Manggalya
Pembimbing: dr. Irsad Andi A, Sp.PD, Sp.JP(K)
 Ny. Suwarji, 48 thn

No CM : 01.30.24.56

Alamat : Samrirono, Yogyakarta

Pendidikan : SMA

Pekerjaan : Wiraswasta

Suku : Jawa

Agama : Islam

Dirawat di : Anggrek 1

Dokter Jaga : dr.Litha

Dokter bangsal : dr.Ratri

Indikasi rawat inap : Diagnosis dan Terapi

Keluhan utama :

Jantung berdebar-debar
RPS :

± 1 Jam SMRS, OS merasa jantung terasa erdebar-debar cepat saat aktivitas (memancing), sesak nafas (-), nyeri dada kiri (+), terasa

menusuk hingga ke punggung (+), dada terasa tidak nyaman, nyeri tidak menjalar ke tangan kiri, keluhan tidak hilang

dengan istirahat, keringat dinng (-)

Keluhan saat ini: jantung terasa berdebar-debar menurun, sesak nafas (-), nyeri dada (-).

Pada tahun 2006, OS pernah merasa keluhan yang sama. Tahun 2011, os pernah dirawat di ICCU dengan keluhan nyeri dada dilakukan

kateterisasi jantung, dkatakan belum perlu pasang ringkarena sumbaankecil.os kemudian diterapi dengan concord

1x25mg. 6 BSMRS OS dirujuk kepada senior Kardio direncaakan ablasi tapi OS menolak.
RPD :
• Riwayat alergi (-)
• Penggunaan obat2an (-)
• Riwayat operasi (-)
• Hasil pemeriksaan laboratorium sebelumnya (-)

RPK :
• Herediter (-)
• Familial (-)
• Infeksi (-)

Riwayat Pribadi :
• OS adalah seorang suami dengan 1 istri dan 1 orang anak, kesulitan ekonomi (-)
Anamnesis Sistem
 Keadaan umum

Kelemahan umum (-)

 Kulit

Tidak ada perubahan warna kulit, gatal (-), ruam (-), kelainan kuku (-), infeksi kulit (-)
 Kepala

Sefalgia (-), vertigo (-), nyeri (-), sinus (-), trauma kapitis (-)
 Mata

Tidak ada riwayat mata berwarna kuning

 Telinga

Tidak ada keluhan pendengaran, tinnitus (-), secret tidak ada kelainan, nyeri (-)
 Hidung

Pilek (-), obstruksi (-), epistaksis (-), bersin (-)

 Mulut dan tenggorokan

tidak ada keluhan sukar atau nyeri menelan atau mengunyah, tonsilitis (-), stomatitis (-), saliva tidak ada kelainan, suara serak (-)
Anamnesis Sistem (lanjutan)
 Leher

pembesaran gondok (-), pembengkakan kelenjar getah bening (-)

 Dada

Tidak pernah mengalami gejala asma, Batuk (-),dahak (-),sesak nafas (-), hemoptisis (-)
 Jantung

berdebar-debar
 Vaskuler

Tidak ada keluhan ataupun riwayat penyakit vaskuler

 Gastrointestinal

Tidak mual, tidak muntah, tidak ada riwayat penurunan nafsu makan maupun penurunan berat badan
 Genitourinaria

benjolan (-), nokturia (-), disuria (-), polakisuria (-), poliuria (-), retensi urin (-), anuria (-), hematuria (-)
Anamnesis Sistem (lanjutan)
 Muskuloskeletal

Nyeri sendi (-), bengkak sendi (-), nyeri otot (-), kejang otot (-), kelemahan otot (-), nyeri tulang (-), riwayat gout (-)
 Payudara

perdarahan (-), discharge (-), benjolan (-)

 Neurologik

Tidak ada penurunan kesadaran & kejang, gangguan saraf otak (-), paralysis (-), anastesi (-), parestesi (-), ataksia (-), gangguan fungsi luhur(-)
 Endokrin

Tidak ada keluhan pembesaran kelenjar gondok, gangguan pengaturan suhu, maupun perubahan rambut, tremor (-), diabetes (-), akromegali (-)
 Psikiatrik

Tidak ada gangguan perangai, orientasi, anxietas, depresi dan psikosis

Pemeriksaan Fisik

KU : sedang, CM

VS : TD 130/80 mmHg, tidur, manset di lengan kanan, large adult cuff

N 60 x/menit, irama teratur, isi dan tekanan cukup

R 20 x/menit, irama teratur, tipe pernapasan thorakoabdominal

T° 36,8 °C, suhu aksila

Kepala : Insp. : konj. anemis (-), sklera ikterik (-)

Palp. : tidak ada nyeri tekan, tak teraba massa

Leher : Insp. : JVP tak meningkat

Palp. : lnn ttb

Thorax :

Pulmo : Insp. : simetris, KG (-), retraksi (-)

Palp. : stem fremitus kanan = kiri

Perk. : sonor

Ausk. : vesikuler (+) N

Cor : Insp. : IC tak tampak

Palp. : IC teraba di SIC V LMCS

Perk. : kardiomegali (-), kesan konfigurasi dbn

Pemeriksaan Fisik

Abdomen : Insp. : DP > DD

Ausk. : peristaltik (+) N

Perk. : timpani di seluruh regio

Palp. : NT (-), H/L ttb

Extremitas : Insp. : edema − −

− −

Palp. : akral hangat, tidak ada nyeri tekan

 Pemeriksaan Penunjang

Darah rutin Coronografi 8/10 2011

Hb 17,1 LM normal

AL 11,1 LAD normal, low flow

AT 26 LCx normal

AE RCA stenosis 40% di mid

Hmt 51

Kesimpulan: CAD1VD unsignificant

S 35 Echo 8/8/2011

L 53 Dimensi ruang jantung N

M 8,3 EF 63%

E 2,6 Disfungsi diastolik LV

B 0.0 Fungsi sistolik RV normal

Katup-katup normal
Holter report 12/3/2012

Irama dasar sinus

SVES (-), VES (-)

Episode takikardi (+)

Bradikardi (-)’pause/arrest/gangguan konduksi (-)

ST/T changes (-), R wave (-)

Diagnosis Klinis :
• SVT stabil susp AVRT dengan WPW syndrome
• CAD 1 VD non signifikan
Terapi : Plan :
• Diet Janung II
• Monitor KU/VS
• O2 3 L /mnt
• EKG/24 jam
• Inf. NS 10 TPM mikro
• Echocardiography ulang
• Inj. ATP 20mg/24 jam
• Metoprolol 2x25mg

Co dr. LKD, Sp.PD, Sp.JP(K) :

• Acc diagnosis dan terapi

Subbagian terkait :
• Kardio
Supraventricular Arrhythmias
• Atrial arrhythmias (AT, AFL and AF)
• Atrioventricular nodal reentrant tachycardia
(AVNRT) and junctional ectopic tachycardia
(JET)
• Atrioventricular reentrant tachycardia (AVRT)
Wolf-Parkinson-White Syndrome
– Orthodromic AVRT
– Antidromic AVRT
SVT: Symptoms
• May be variable
– Palpitations, chest pounding, neck pounding
– Weakness/malaise
– Dyspnea
– Chest pain
– Lightheadedness
– Near syncope/syncope
• Symptoms usually abrupt in onset and termination
• May have history of symptoms since childhood or have a
positive FHx
SVT: Physical Exam

• In absence of tachycardia, usually normal

• Rapid heart rate (150-250)
– May be irregular or regular (mechanism)
• BP may be low or with narrow pulse
pressure
• Neck veins may reveal cannon waves.
Wolff-Parkinson-White Syndrome
• Second electrical connection
exists between the atria and
ventricles (accessory
pathway)
– Resemble atrial tissue
– Results in a short PR and
– Delta wave (pre-excitation)
• Some AP conducts only
retrograde (concealed)
Arrythmias in WPW
• The most common arrhythmia is orthodromic AV
reentrant tachycardia (narrow QRS)
• Less common are pre-excited tachcyardias (wide
QRS)
– Antidromic AV reentrant tachycardia
– Atrial tachycardia/flutter with pre-excitation
– AVNRT with pre-excitation
– Atrial fibrillation with pre-excitation (most life
threatening due to rapid ventricular response)
Orthodromic AVRT

Conduction down AV axis during tachycardia gives NARROW QRS complex

 Pre-excited Tachycardia

Mechanisms

AT
AVRT

AVNRT

Conduction down AP during tachycardia gives WIDE QRS complex

Atrial Fibrillation
RF Ablation in WPW
Supraventricular Arrhythmias
• Atrial arrhythmias (AT, AFL and AF)
• Atrioventricular nodal reentrant tachycardia
(AVNRT) and junctional ectopic tachycardia
(JET)
• Atrioventricular reentrant tachycardia (AVRT)
Wolf-Parkinson-White Syndrome
– Orthodromic AVRT
– Antidromic AVRT
 SUMMARY
Mechanisms of SVT

SP FP

Atrial Tachycardia AVNRT AVRT

Differential Diagnosis of NCT

• Short RP • Long RP • P buried in QRS

–
– AVRT – AT Typical AVNRT

– AT
– AT – Atypical – JET

– Slow- AVNRT
Slow – PJRT
AVNRT
SUMMARY
• Obtain a 12 lead ECG. The location of the P wave will
dictate the differential diagnosis
• If hemodynamically unstable (chest pain, heart failure,
hypotension) CARDIOVERSION
• If hemodynamically stable AV NODAL AGENT
• Long term therapy depends on mechanism and can be
conservative, pharmacologic or invasive
• EP study often needed for definitive characterization of
mechanism and can cure most SVTs with 90% success
rate
 Figure 4. Responses of narrow complex tachycardias to adenosine.

et al. Circulation 2003;108:1871-1909

Copyright © American Heart Association, Inc. All rights reserved.

Atrioventricular Reciprocating
Tachycardia (AVRT)
• Can be orthodromic (most
common) or antidromic
(very uncommon)
• Needs AV node to
perpetuate rhythm
• Always associated with an
AV bypass tract
• May mimic AVNRT and
atrial tachycardia
• Can be short or long RP
 Wolff Parkinson-White Syndrome
• Some patients have an accessory or additional
pathway to the AV Node from the SA Node.
• May be present all the time or intermittent.
• Depolarization from Atria to Ventricles travels two
paths – Bundle of His and now Kent Bundle (this
pathway is more RAPID). No Delay.
• They then join together at the beginning of
Ventricular depolarization.
Wolff-Parkinson-White
• Figure 12.10, Page 143
• Three characteristics:
– A: Short PR interval
– B: Wide QRS complex
– C: Delta Wave
• These characteristics are not
present in all leads.

Not in book
 INTRODUCTION

There are 02 types of accelerated conductions

from the atrium to the ventricles; viz.

• Wolff-Parkinson-White (WPW) Syndrome /

Pre-excitation Syndrome.

• Lown-Ganong-Levine (LGL) Syndrome.

 WPW SYNDROME
• Bundle of Kent by-pass the AV node or by
Mahaim fibes – which goes from Bundle of His
to Ventricular Septum. The pre-excitation of
‘Bundle of Kent’ is called WPW Syndrome.
• The atrial impulse passes through the normal
path of conduction and also through the anterior
intra-nodal fibre [Bachmann’s fibre / Bundle of
Kent], simultaneously.
CLASSIFICATION OF
WPW SYNDROME
WPW Syndrome is of 02 types ----

• Type A: where excitation travels along Left

accessory pathway – giving rise to RVH /
RBBB.
• Type B: where excitation travels along Right
lateral accessory pathways – giving rise to
LBBB. If it is associated with Cyanotic CHD –
Ebstein’s Anomaly is diagnosed.
 ECG OF WPW Syndrome

• Short P-R interval [less than 0.12 sec.].

• Wide QRS complex.
• Appearance of -wave / slurred upstroke of QRS.
• Normal P-wave axis.
 CAUSES OF WPW Syndrome
• Normal individuals.
• Myocardial Infarction.
• Acute Rheumatic Fever.
• CHD – Ebstein’s Anomaly.
• Cardiac catheterization / Surgical manipulation
of Heart.
• Hypertrophic Sub-aortic Stenosis.
• Idiopathic Cardiomyopathy.
• Thyrotoxicosis.
 WPW SYNDROME WITH
ATRIAL FIBRILLATION

• Irregularly irregular, wide complex tachycardia.

• Impulses from the atria are conducted to the ventricles via either
– both the AV node and Accessory pathway producing a broad
fusion complex.
– or just AV node producing a narrow complex (without -wave).
– or just Accessory pathway producing a very broad 'pure' - wave.
• People who develop this rhythm and have very short R-R intervals
are at higher risk of VF.
 WPW

• Can cause a rapid heart rate (tachycardia).

• Can be congenital but occurs mostly in adults age 30-40.
• Therapy can include the valsalva manuever, medications,
cardioversion, ablation or surgery.

Many people with this syndrome who have symptoms or episodes of tachycardia (rapid heart rhythm) may have dizziness, chest palpitations, fainting or,

rarely, cardiac arrest. Other people with WPW never have tachycardia or other symptoms.
What is an accessory pathway /
bypass tract?
• Tiny bands of myocardial tissue that most
commonly insert into the atrial muscle on one
end and in ventricular muscle on the other
• They behave much more like myocardial tissue
than AV node tissue – what does this mean?
• When stimulated rapidly they block suddenly not
gradually like the AV node (Wenkebach does not
occur)
• Invisible to the naked eye (surgeons can’t see
them when attempting surgical disruption
• This means they can only be located by their
electrophysiological effects
• They can occur anywhere along the AV groove
except in the space between the AV and MV
(continuous fibrous tissue)
• Can occur parallel to the AV node in the septum.
What causes an accessory
pathway to exist
• Anomalous embryonic development of
myocardial tissue which bridges the
annular fibrous ring
• Residual connections from the formation
of the AV node
Types of accessory pathways
• Dozens of pathway locations have been
described
• They are named according to their location
(where they come from and insert into) e.g.
• Atrioventricular, atriofasicular,
fasiculoventricular, internodal, nodoventricular
etc.
• However there are four main types
1. Atrioventricular (AV) bypass tracts – Track is
located along the AV groove and connects
atrial and ventricular muscle
2. Atriofasicular (aka AV nodal) bypass tracts –
connect low atrial myocardium to the His-
Purkinje system
3. Mahaim tracts – connect the distal atrial
myocardium (near AV node) to the RBB
4. Fasiculoventricular tracts - connect His or
Purkinje fibres to ventricular myocardium
Positions of the most common
accessory pathways

• A – atrioventricular
• B – atriofasicular
B

A D
• C – Mahaim (atrium to
RBB)
C
• D - fasiculoventricular
• A pathway that connects the atrium to the
ventricles is called a Kent bundle
• A pathway that connects the atrial fibres to the
upper part of the AV node is called a James
bundle
• Mahaim fibres connect atrial muscle to the RBB
or ventricular muscle but they display similar
properties to AV node tissue with accelerated
rates
• AV accessory pathways are by far the
most common!
• We can’t always tell from the ECG
exactly where the tract is coming
from or where it is inserting
 Antegrade or Retrograde
conduction
• Bypass tracts may conduct in a forwards
direction (called antegrade conduction)
• When they do the rapid conduction pre-
excites the ventricles
• This is seen on the ECG as a short PR
interval and a delta wave in the QRS
complex
Normal conduction and the ECG
Pre-excitation and the ECG

Delta wave

Bundle of Kent
Short PR interval
• The QRS complexes seen on the 12 lead
ECG are actually a fusion between
ventricular stimulation via the bypass tract
and ventricular stimulation via the normal
AV node conduction system
• They can be called fusion beats
• The degree of pre-excitation depends on several
factors
– AV node conduction time (slower conduction larger
delta wave)
– Conduction velocity and refractory period of the
bypass tract itself (rapid conduction and shorter
refractory period means more pre-excitation)
– Proximity of the bypass tract to the SA node (atrial
impulse reaches a right sided bypass tract earlier than
a left sided so pre-excites more)
• BUT, in many patients who present with SVT
mediated by bypass tracts the tracts can’t
conduct antegradely
• Instead they conduct in a retrograde direction
only
• These are called concealed bypass tracts
• They never generate delta waves or short PR
intervals when the patient is in normal sinus
rhythm
Why are bypass tracts
significant?
• They can confuse – delta waves can masquerade as Q
waves leading to false diagnosis of MI
• Marked pre-excitation during an atrial tachycardia can
have such slurred QRS complexes than it is mistaken for
ventricular tachycardia
• Bypass tracts can act as one limb of a macro-reentrant
circuit (normal AV conduction system acting as second
limb) so macro-reentrant SVT is common
• They bypass the normal protective mechanism of the AV
node during atrial tachyarrhythmias
• What might happen if a patient with a
bypass tract that conducts antegradely
develops atrial fibrillation?
• This is life threatening!!!!!!!
Figure 12.11, page 144
 Figure 5.4 Clinical Exercise Physiology Textbook
Wolff Parkinson-White Syndrome

http://medmovie.com/mmdatabase/mediaplayer.aspx?Message=VG9waWNpZD02ODQ7Q2xpZW50SUQ9NjU7VmVybmFjdWxhcklEPTE%3D%2DyHFV6XkUe9M%3D
Therapies II

• Some atrial tachycardias (about

40%) can be terminated with
adenosine
• Atrial flutter and fibrillation are
not terminated by changing AV
nodal conduction
– Consider rate control
– Electrical or chemical cardioverision
– RF ablation
 What’s the difference
between WPW and LGL?
Diagnostic criteria for Wolff-
Parkinson-White Syndrome
• Short PR interval (<0.12secs)
• +Evidence of pre-excitation on the ECG
(delta wave) and broader WRS
• +symptoms caused by supraventricular
tachycardia
• (If the patient does not have tachys we
can say they have WPW pattern on their
ECG but NOT the syndrome!)
Incidence of Wolff-Parkinson-White
syndrome
• International incidence is 0.15 – 0.20%
• Of these 60-70% have no other evidence of
heart disease.
• But also associated with MVP and Ebstein’s
• 60-70% of all those diagnosed are men
• Patients typically present as adolescents/ young
adults and are otherwise healthy
• Mortality has been estimated to be 0-4% and is
usually arrhythmogenic sudden cardiac death
Lown-Ganong-Levine syndrome
• Short PR interval (James Bundle)
• Normal QRS configuration (no delta wave)
• Recurrent paroxysmal tachycardia
• (If the patient does not have tachy’s we
say they have an LGL pattern on their
ECG)
Why no delta wave?
• Intranodal fibres bypass the main body of the AV
node and terminate near the Bundle of His
(James fibres)
• Therefore the major delay of the AV node does
not occur and there is a short PR interval
• However ventricular depolarization takes place
via the normal His-Purkinje system so the QRS
complex is normal