Pengantar

Elektrokardiografi (EKG)
dan Aritmia

Andreas Arie
 Einthoven yang pertama merekam EKG
pada manusia
EKG saat ini 12 lead, 3 bipolar limb
lead, 3 unipolar limb lead, 6 unipolar
precordial lead
- EKG yang normal, belum tentu jantungnya normal
- Sebaliknya EKG yang abnormal, belum tentu pada
jantung yang abnormal
 Yang perlu diingat : EKG

Rekaman aktivitas listrik jantung

Tidak secara langsung menyatakan
abnormalitas struktur jantung, Hanya merekam
perubahan elektris akibat kelainan struktur
tersebut
Hanya merekam penjumlahan potensial
elektrik yang dihasilkan oleh sel-sel otot jantung
aliran listrik yg ditransmisikan ke area di
mana elektroda ditempatkan
 Tujuan merekam EKG
Analisis morfologi P-QRS-T
hipertrofi atrium (ka dan ki)
hipertrofi ventrikel (ka dan ki)
miokardial iskemi dan infark
intraventricular conduction defect
gangguan elektrolit
perikarditis dll
Analisis aritmia
menganalisis hubungan P dan QRS
bradikardia
takikardia
Anatomi Jantung
Anatomi Jantung
Elektrokardiografi
Normal Electrocardiogram (ECG)
 Electrical Activity of Myocardium
1)atria begin to
depolarize
2) atria depolarize
3)ventricles begin to
depolarize at apex;
atria repolarize
4)ventricles depolarize
5) ventricles begin to
repolarize at apex
6) ventricles repolarize
Prosedur perekaman EKG

PERSIAPAN
A. Alat
1. Mesin EKG lengkap
- Kabel untuk sumber listrik
- Kabel untuk bumi ( ground )
- Kabel elektroda
* Ekstremitas
* Dada
2. Jelly
3. Kertas tissue
4. Spidol
5. Gaas/kapas alkohol
6. Kertas EKG

B. Pasien
1. Penjelasan
- Tujuan pemeriksaan
- Hal hal yg harus diperhatikan selama
pemeriksaan
2. Dinding dada terbuka
CARA KERJA

1. Nyalakan mesin EKG

2. Baringkan pasien dg tenang di tempat tidur yg cukup luas,
tangan dan kaki tidak saling bersentuhan
3. Bersihkan dada, kedua pergelangan kaki & tangan dg kapas
alkohol
4. Keempat elektroda ekstremitas diberi jelly atau basahi dg
air yg mengandung elektrolit
5. Pasang keempat elektroda tersebut pada kedua
pergelangan tangan & kaki
6. Beri tanda elektroda dada & beri jelly untuk V 1 s/d V6
7. Pasang elektroda dada dg menekan karet hisapnya
8. Buat kalibrasi
9. Rekam setiap lead 3 4 beat
10. Setelah selesai perekaman semua lead, buat kalibrasi ulang
11. Semua elektroda dilepas
12. Jelly dibersihkan dari tubuh pasien
13. Beri tahu pasien bahwa perekaman sudah selesai
14. Matikan mesin EKG
15. Catat :
- Nama pasien
- Umur
- Jam, tanggal & tahun pembuatan
- Nama lead
- nama pembuat
16. Bersihkan dan rapikan kembali alat alat
 PEMASANGAN ELEKTRODE
PEMASANGAN ELEKTRODE EXTREMITAS
Lengan kanan dan lengan kiri
Kaki kanan dan kaki kiri
PEMASANGAN ELEKTRODE DADA
V1 = Parasternal kanan di ICS-4
V2 = Parasternal kiri di ICS-4
V4 = MCL kiri di ICS-5
V3 = Median antara V2 dgn V4
V5 = Para Axillair Line kiri di ICS-5
V6 = Median Axillair kiri di ICS-5
 SISTEM LEADS
STANDARD LIMB LEADS
I, II, III
AUGMENTED UNIPOLAR LIMB LEADS
aVR, aVL, aVF
UNIPOLAR CHEST LEADS
V1, V2, V3, V4, V5, V6
PQ interval = 0.12 0.20 sec
QRS interval = 0.06 0.10 sec
QT interval = 0.32 0.43 sec
 STANDARISASI EKG
Kecepatan kertas standard EKG
25 mm / s (10 25 50 mm / s)
Setiap kolom horizontal = 0.04 sec
Setiap kolom vertikal 10 mm = 1 mV
 MENGHITUNG DETAK JANTUNG (Rate)

Methods to determine heart rate:

1500/# small boxes between R waves.
o Most accurate; best for fast rhythms.
300/# large boxes between R waves.
o Good for slow rhythms.
o 300, 150, 100, 75, 60, 50 rule
# R waves in 6.0 s (30 large boxes) x 10
o Good for irregular rhythms.

Bahwa detak jantung tidak 100% teratur disebabkan

oleh pergerakan rongga thorax waktu bernafas,
sehingga akan diperoleh 2 angka frekwensi
 CARA MENGHITUNG HR
1. 300
Jumlah Kotak Besar R R

2. 1500
Jumlah Kotak Kecil R R

3. Ambil Rekaman EKG 6 detik, hitung jumlah gel QRS

Kemudian kalikan dengan 10
 MENENTUKAN AXIS EKG
Menghitung Axis:
Sudut yang dibuat oleh tingginya voltage R di I dengan
tingginya voltage R di aVF
Axis yg normal berada antara -30 dgn +90
Left Axis Dev berada antara -30 dgn -90
Right Axis Dev berada antara +90 dgn +180
axis jantung
 MENGENAL RITME
Bentuk : NORMAL ditandai oleh titik P-Q-R-S-T
Gelombang ritme : didahului P dan diikuti oleh QRS
komplex yang teratur = SINUS RITME
Setiap QRS komplex teratur yang tidak dimulai oleh
gelombang P atau gelombang P berada dibelakang
QRS komplex disebut sebagai NODAL RITME
Setiap irama QRS komplex yang tidak teratur dan
tidak mempunyai gelombang P disebut sebagai
irama ATRIAL FIBRILLASI
Irama Sinus ritme > 100 / m Sinus Takikardi
Irama Sinus ritme < 60 /m Sinus Bradikardi
 GELOMBANG P
Gambaran yang ditimbulkan oleh depolarisasi atrium

Normal
Tinggi : < 0,3 mvolt
Lebar : < 0,12 detik
Selalu positif di L II
Selalu negatif di aVR

Kepentingan
Mengetahui kelainan di Atrium
Gelombang P Mitral

Gelombang P Pulmonal
 GELOMBANG QRS
Gambaran yang ditimbulkan oleh depolarisasi ventrikel

Normal :
Lebar : 0,06 - 0,12 detik
Tinggi : Tergantung lead
Kepentingan :
Mengetahui adanya hipertrofi ventrikel
Mengetahui adanya Bundle branch block
Mengetahui adanya infark
Normal gelombang Q
Lebar : < 0,04 detik
Dalam : < 1/3 tinggi R

Gel Q yng lebar & dalam disebut Q pathologis

 Gelombang T
Gambaran yang ditimbulkan oleh repolarisasi ventrikel

Nilai normal :
* 1 MV di lead dada
* 0,5 MV di lead ekstrimitas
* Minimal ada 0,1 MV

Kepentingan :
* Mengetahui adanya iskemia/infark
* Kelainan elektrolit
 Interval PR
Diukur dari permulaan P s/d permulaan QRS

Normal : 0,12 - 0,20 detik

Kepentingan :
Kelainan sistem konduksi
 Segmen ST
Diukur dari akhir QRS s/d awal gel T

Normal : Isoelektris

Kepentingan : Elevasi Pada injuri/infark akut

Depresi Pada iskemia
 R V H

Kriteria :
- Gelombang R/ S di V 1 > 1
- RAD
- Strain pattern di V1 / V 2
 L V H
Kriteria
- Gel R/S di V5 atau V6 > 25 mm
- Gel R di V5/V6 + gel S di V1/V2 > 35
- Strain pattern di V5 / V6
Infark Miokard
 Infark miokard akut

Diagnosis
sakit dada yang khas
kenaikan enzym jantung
evolusi EKG
Evolusi Infark
 LOKASI INFARK

V1 V3 Anteroseptal
V3 V4 Apical
V1 V4 Anterior
I, aVL Lateral
I, aVL, V5 V6 High lateral
II, III, aVF Inferior
R tinggi di V1 V2 True Posterior
 TEHNIK INTERPRETASI ELEKTROKARDIOGRAM

Irama : reguler / irreguler

Frekuensi :
Gelombang P : sinus / ektopik / f / F
Interval PR :
Kompleks QRS :
Axis :
Durasi :
Zone transisi :
Konfigurasi :
Posisi elektrik :
Segmen ST :
Gelombang T :
Gelombang U :
Lain - lain :
 ATRIAL FIBRILLATION

AF is the most common sustained tachyarrhythmia

leading to substantial morbidity and mortality from
thromboembolism (stroke) and heart failure.
AF has been considered to be the epidemic of the
new millennium, its incidence increases with age and
with the presence of heart disease
AF is associated with a 2-fold increase in cardiac
mortality
It is associated with a 5-fold increased risk of stroke
in the absence of adequate anticoagulation therapy
AF
Sinoatrial
node

atrioventricular
node
Atrial
muscle

cartilage

Bundle
Of Mis

Left bundle
branch

Right bundle
branch

Ventricular
muscle

Electrical conduction system of the heart

Cardiac impulse and electrocardiographic patterns

AV

Septum

R SA
P T

SA Q
S
Atria AV

Plateau
septum
LV
repolarization
 Preventable
NEUROHORMONAL SUDDEN ELECTROLYTE
FACTORS DEATH ABNORMALITIES

Sympathetic tone K+
Renin-angiotensin system Mg2+
Catecholamines

HEMODYNAMIC CARDIAC IATROGENIC

FACTORS ARRHYTHMIAS FACTORS

Diuretics
End-diastolic pressure
Inotropes
Afterload
End-systolic volume Vasodilators
End-diastolic volume Antiarrhythmics

MECHANICAL SUDDEN
FACTORS DEATH

Stretch ?Nonpreventable
Myocardial length
Myocardial scars

Interrelationships of factors in the pathogenesis of arrhythmias in

heart failure culminating in the development of sudden death. (Singh,2002)
Leading Circle Reentry Ectopic Foci
50
30
10 1 2 Right Atrium Left Atrium
130 50 Septum
3 Superior
6 4 Vena
Cava
17
30 31
110
Pulmonary
Veins
5 Fossa 6 11
190 110 Ovails

Inferior
Vena
170 Cava Coronary
150 Sinus n = 45 pts
1 2 210

250 6 3 190
210 4
170

230 250
5
230

The Mechanisms Underlying Human AF

 Pathophysiology of Atrial Fibrillation
? Inflammation

LVH
Mitral compliance Diastolic
stenosis / Atrial dilatation/stretch
dysfunctio
regurgitati
n
on

stretch-activated channels
? Inflammation
dispersion of refractoriness
pulmonary vein
Increased vulnerability focal/discharges?
to atrial pathophysiology of AF
Hypothetical construct of the pathophysiology of AF.
(Gersh et al, 2004)
 Diseases Assosiated with Atrial
Fibrillation

Hypertension Pericarditis
Coronary artery disease Tumors
Cardiomyopathy Alcohol
Mitral valve disease Lung disease
Thyrotoxicosis
Sick sinus syndrome
Congenital heart disease
Cardiac surgery
Minimum work-up of the patient with atrial fibrillation

(1)History and physical examination

1.1. Define the presence and nature of symptoms
1.2. Define the clinical type of atrial fibrillation: paroxysmal,
chronic or recent onset
1.3. Define the onset of the first symptomatic attack and/or
date of discovery of atrial fibrillation
1.4. Define the frequency, duration (shortest and longest
episodes), precipitating factors and modes of termination
(self-terminating versus persistent) of symptomatic
episodes.
1.5. Define the presence of an underlying heart disease or
other possible identifiable cause (e.g. alcohol
consumption, diabetes, hyperthyroidism) which could be
cured.
Minimum work-up of the patient with atrial fibrillation
(2)Electrocardiogram
2.1. Left ventricular hypertrophy
2.2. Duration and morphology of the P waves in sinus rhythm
2.3. Evidence of repolarisation changes, bundle branch block,
old myocardial infarction and other abnormality.

(3)Echocardiogram (M mode and bidimentional)

3.1. Evidence and type of underlying heart disease
3.2. Size of the left atrium
3.3. Left ventricular size and function
3.4. Left ventricular hypertrophy
3.5. Intracavitary thrombus (poor sensitivity)

(4)Thyroid test function

If first discovery of atrial fibrillation, if the ventricular rate is
difficult to control or if amiodarone has been used in the past.
 Management of AF

The treatment of FA consists of

To suppress dysrhythmia
- Restorations and maintenance sinus
rhythm
- ventricular rate control
To reduce the risk of thromboembolism
To remove precipitating factors and
optimal treatment of underlying disease
 First detected

Paroxysmal1.4 Persistent2.4
(Self-terminating) (No self-terminating)

Permanent3

Patterns of atrial fibrillation. 1, episodes that generally last than or equal to 7 days (most less than 24 h);
2, usually more than 7 days; 3, cardioversion failed or not attempted; and 4 either paroxysmal or
persistent AF may be recurrent.
(Fuster et al, 2001)
 NEWLY DISCOVERED
AF

Paroxysmal Persistent

No therapy needed
unless severe
symptoms (e.g.,
hypotension, HF,
angina pectoris) Accept Rate control and
permanent AF anticoagulation
as needed
Anticoagulation
as needed
Anticoagulation Consider
and rate control antiarrhythmic
as needed drug therapy

Cardoversion

Long term
antiarrhythmic
drug therapy
unnecessary

Pharmacological management of patients with newly discovered AF.

(Fuster et al, 2001)
 Heart disease ?

No (or minimal*) Yes +

Flecainide
Propafenone HF CAD Hypertension
Sotalol

Amiodarone Sotalol LVH greater than or

Amiodarone, Dofetilide Dofetilide equal to 1.4 cm

Amiodarone
Dofetilide Yes No

Disopyramide Consider nonpharmacological

Procainamide options Disopyramide
Quinidine Procainamide Amiodarone Flecainide
Quinidine Propafenone

Amiodarone
Dofetilide
Sotalol

Disopyramide, Procainamide, Quinidine

Antiarrhythmic drug therapy to maintain sinus rhythm in patients with recurrent paroxysmal or persistent atrial fibrillation.
Drugs are listed alphabetically and not in order of seuggested use. *For adrenergic atrial fibrillation, beta-blockers or sotalol are
the initial drugs of choice. + Consider nonpharmacological options to maintain sinus rhythm if drug failure occurs.

(Fuster, dkk 2001)

 RECURRENT
PERSISTENT
PERMANENT
AF AF

Minimal or no Disabling Anticoagulation

symptoms symptoms in AF and rate control as
needed
Anticoagulation Anticoagulation
and rate control as and rate control
needed
Antiarrhythmic
drug therapy

Continue
Electrical anticoagulation as
cardioversion as needed and
needed therapy to sinus
rhythm

Pharmacological management of patients with recurrent

persistent or permanent AF. Initiate drug therapy before
cardioversion to reduce the likelihood(Fuster
of early
et al, 2001)