Frequently underdiagnosed Life

threathening ECG patterns as a

cause for Syncope
dr Friska Anggraini Helena S SpPD – KKV
Division of Cardiology, Department of Internal Medicine
Dr. Kariadi Hospital
Syncope

• hilangnya kesadaran dan tonus postural

akibat hipoperfusi serebral .
• Kondisi ini sangat umum, dengan
perkiraan prevalensi seumur hidup
sekitar 20% dan kejadian tahunan 6,2 /
1000 orang/tahun pada orang dewasa
yang sehat.
• Salah satu alasan paling umum untuk
datang ke IGD.
Syncope
Diagnosis banding
Refleks atau hipotensi yang dimediasi oleh saraf ( 35% )
hipotensi ortostatik (10%)
Kardiogenik(20% -25%)
Penyakit serebrovaskular (1% -2%)
Psikogenik (2% -10%).
25% -40% kasus penyebab spesifik untuk sinkop tidak dapat
ditentukan.
Sinkop kardiogenik dikaitkan dengan prognosis terburuk
fokus evaluasi awal !
Syncope
• Syncope  FR SCD jika berkaitan dengan penyakit
jantung struktural
• ESC dan AHA  EKG sebagai inisial evaluasi
• EKG pasien dengan sinkop harus di periksa dengan
teliti untuk menemukan tanda penyakit jantung
- Gangguan sistem konduksi
bradyarhytmia, takiarrhytmia holter
- Primary electrical diseases
- kelainan struktural
 EKG pada sinkop akibat
Primary electrical diseases
Wanita 18 tahun diantar ke IGD karena sempat pingsan saat olahraga
Bagaimana cara meng asses?
1. Kesan umum : bradi/taki/normal
2. Reguler/ireguler ireguler/ireguler berkelompok
3. Analisis gelombang
- P : ada/tidak/identik?
- Sinus?
- Tanda pembesaran atrium
- Hubungan P dengan gelombang QRS
- PR interval
- QRS :durasi, axis, q patologis,R, (PRWP,tanda hipertrofi ventrikel) S
- ST segmen
- T wave
- U wave
- QT interval
 Kesan umum
1. Bradi/taki/normal?
 75x/m normal
2. Regularitas  slighly iregular
3. P?  ada,sinus
4. PR  memendek 0,08
5. QRS : 0,12, axis normal, slurred Rdelta
6. ST segmen depresi
6.T wave inversi hamper disemua lead
7. U wave tidak tampak
8. Qtc tidak memanjang

Sinus Rythm , short PR, delta wave, secondary ST T changes 

wpw pattern
 Wolff-Parkinson-White syndrome
• Although the ECG morphology varies widely, the classic ECG features are as
follows:
• A shortened PR interval (typically <120 ms in a teenager or adult)
• A slurring and slow rise of the initial upstroke of the QRS complex (delta
wave)
• A widened QRS complex
• ST segment–T wave (repolarization) changes, generally directed opposite the
major delta wave and QRS complex, reflecting altered depolarization
 KOMPLIKASI
Tachyarrhythmia
Syncopal attacks
Sudden cardiac death
Rekurens
 CAUTIO
N
Usual presentation is SVT

Sudden cadiac death possible

Digoxin, beta blockers,verapamil are

contraindicated

Underlying Ebstein’s anomaly, hypertrophic

cardiomyopathy should be evaluated
# kasus 2

• Seorang laki-laki 83 tahun pingsan Dia dilarikan ke UGD oleh

paramedis.pasien memiliki riwayat gagal ginjal dan cuci darah,

Kondisi mengancam jiwa apa yang ditunjukkan dalam penelusuran

EKG dan ritme apa yang berisiko muncul?

 Kesan umum
1. Bradi/taki/normal?
 60x/m normal
2. Regularitas  slightly iregular
3. P?  ada,sinus, P mitral, Ptf V1
4. PR  normal
5. QRS : sempit, axis normal,small R limb
lead, deep s V3,S persistent v5/6,
6.T wave
 different morf
7. U wave -
8. Qtc
memanjang
Sinus arrhythmia , T wave alternan, long QT, LVH by cornell,
LAE, limb lead low voltage , biventricular hypertrophy?
Life-Threatening Condition (II): Long QT Interval
and T-Wave Alternans.
How to measure the QT
interval
• 1. QT interval
2. Tentukan QTc
•Bazett formula: QTC = QT / √ RR  60-100
•Fridericia formula: QTC = QT / RR 1/3 <60 atau >100
•Framingham formula: QTC = QT + 0.154 (1 – RR)  <60 atau >100
•Hodges formula: QTC = QT + 1.75 (heart rate – 60)
RR interval = 60 / heart rate

Normal QTc values

•QTc is prolonged if > 440ms in men or > 460ms in women
•QTc > 500 is associated with increased risk of torsades de pointes
•QTc is abnormally short if < 350ms
•QT normal kurang dari setengah interval RR sebelumnya
Mekanisme pemanjangan QT interval
• Long QT syndrome may be present at birth or develop later in life.

• Onset later in life may result from certain medications, low blood potassium, low blood calcium,
or heart failure.

• Medications that are implicated include certain antiarrhythmics, antibiotics, and antipsychotics
• T-wave alternans  variabilitas "beat-to-beat"
• Variabilitas dalam repolarisasi ventrikel
• Jarang terlihat pada tingkat makroskopis, dan merupakan cerminan
dari jaringan miokard heterogen  re-entrant takikardia ventrikel
• Visible T-wave alternans in patients with
LQTS indicates an increased risk SCD because
of cardiac arrhythmias (ie, torsade de
pointes and ventricular fibrillation).
 Laki laki 30 tahun, memiliki riwayat sinkop, saat ini
tanpa keluhan, kelainan apa yang didapatkan dari EKG?
Kesan umum
1. Bradi/taki/normal?
 100x/m takikardi
2. Regularitas  regular
3. P?  ada,sinus
4. PR  normal
5. QRS : axis normal,lebar
6.ST : Coved STE >2mm in >1 of V1-
V3 followed by a negative T wave
7. U wave normal
8. Qtc nornal

Sinus takikardi ,brugada sign type 1

 • Discovered by the Brugada brothers
in 1992.
• Inherited defect of sodium

Brugada channels (SCN5A gene).

• Epicardial area of
Syndrome the RV has
repolarization
abnormality.
• Prone to spontaneous
Ventricular Arrhythmias.
 • Prevalent in Southeast Asian population
Epidemiology • Incidence of 5 of 10,000
• Clinical manifestations 9x more common
in men than women
• Symptoms often first occur in third of fourth
decade of life at rest or during sleep
Brugada Syndrome

• characterized by:
• ECG findings of RBBB and persistent ST elevation in V1 – V3
• structurally normal hearts
• propensity for life-threatening ventricular arrhythmias
• J point elevation
Life threathening ECG
Structural heart diseases
Laki laki 27 tahun, pusing dan deg2 an setelah aktivitas
Young patient, Voltage criteria for LVH.
Deep narrow Q waves < 40 ms wide in the lateral leads I, aVL and V5-6.

Hypertrophic Cardiomyopathy
Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy  most common genetic cardiomyopathy

• Prev 1:500 people across multiple geographies, ethnicities and races.

Symptoms from
LVOT obstruction
Impaired function
Diastolic dysfunction
Arrhythmia
Clinical features

• Exertional syncope or pre-syncope

• Symptoms of pulmonary congestion (e.g. exertional dyspnoea, fatigue,
orthopnoea, paroxysmal nocturnal dyspnoea) due to left ventricular
dysfunction.
• Chest pain — may be typical anginal pain due to increased demand (thicker
myocardial walls) and reduced supply (aberrant coronary arteries).
• Palpitations due to supraventricular or ventricular arrhythmias.
 1. Dynamic obstruction of the LVOT.
Processes 2. Left ventricular diastolic dysfunction resulting
responsible for from impaired relaxation and filling of the stiff
and hypertrophied left ventricle .
clinical 3. Abnormal intramural coronary arteries with
thickened walls and narrowed lumens.
manifestations 4. Chaotic, disorganised left ventricular
of HCM: architecture (“cellular disarray”) 
predisposing to abnormal transmission of
electrical impulses and thus serving as a
substrate for arrhythmogenesis.
Hypertrophic Cardiomyopathy

Diagnosis by ECG and Echo

MRI aids in diagnosis

Holter and Exercise stress in all patients

Risk stratification for sudden death

ECG features of Hypertrophic Cardiomyopathy

• LVH  increased precordial voltages and non-specific ST segment

and T-wave abnormalities.
• Asymmetrical septal hypertrophy 
Deep, narrow (“dagger-like”) Q waves in the lateral (V5-6, I, aVL)
and inferior (II, III, aVF) leads.
Mimic prior myocardial infarction, although the Q-wave
morphology is different:
Lateral Q waves are more common than inferior Q waves in HCM.
Asymmetrical septal hypertrophy
Apical HCM
- Uncommon form of HCM Most frequently in Japanese.
- There is localised hypertrophy of LV apex.
- The classic ECG finding is giant T-wave inversion in the precordial leads.
 • An inherited myocardial disease associated
with paroxysmal ventricular
arrhythmias and sudden cardiac death.
• Characterized pathologically by fibro-fatty
Arrhythmogenic replacement of the right ventricular
Right Ventricular myocardium.
• The second most common cause of sudden
Cardiomyopathy cardiac death in young people (after HOCM),
causing up to20% of sudden cardiac deaths in
patients < 35 yrs of age.
Clinical Features

• ARVC causes symptoms due to ventricular ectopic beats or

sustained ventricular tachycardia (with LBBB morphology) and typically
presents with palpitations, syncope or cardiac arrest precipitated by
exercise.
• The first presenting symptom may be sudden cardiac death.
• Over time, surviving patients also develop features of right ventricular
failure, which may progress to severe biventricular failure and dilated
cardiomyopathy.
• There is usually a family history of sudden cardiac death.
Electrocardiographic Features

ARVD is associated with characteristic ECG abnormalities:

• Epsilon wave (most specific finding, seen in 30% of
patients)
• T wave inversion in V1-3 (85% of patients)
• Prolonged S-wave upstroke of 55ms in V1-3 (95% of
patients)
• Localised QRS widening of 110ms in V1-3
• Paroxysmal episodes of ventricular tachycardia with LBBB
morphology (e.g. right ventricular VT).
The epsilon wave
• a small positive deflection (‘blip’ or ‘wiggle’) buried in the end of the QRS complex.

• Epsilon waves are caused by postexcitation of the myocytes in the right ventricle.

• Epsilon waves are the most characteristic finding in arrhythmogenic right ventricular
dysplasia (ARVD/C) myocytes are replaced with fat, producing islands of viable myocytes in a
sea of fat  This causes a delay in excitation of some of the myocytes of the RV and causes the
little wiggles seen during the ST segment of the ECG.
 Prolonged S-wave upstroke in V2 with localized QRS widening

• Epsilon wave in V1
Epsilon WAVE
PERKENALKAN LEAD FONTAINE
(bipolar precordial leads) (F-ECG) can be used to
1. increase the sensitivity of epsilon wave detection
2. search for AV dissociation in ventricular
tachycardia;
3. and to study abnormal atrial rhythms when the
P waves are too small on regular lead

•Right Arm (RA)  manubrium;

•Left Arm (LA)  xiphoid process;
•Left Leg (LL) standard V4 position (5th ICS MCL).