PENYAKIT JANTUNG

KORONER

Dr.NINIEK PURWANINGTYAS SpJP, FIHA

KARDIOLOGI & KEDOKTERAN VASKULAR
FK UNS RSUD Dr MOEWARDI
SURAKARTA
 Worldwide Statistics

Each year:
> 4 million patients are admitted with
unstable angina and acute MI
> 900,000 patients undergo
Percutaneous Coronary Intervention
(PCI) incl. PTCA with or without stent
 Penyakit Jantung Koroner dan Stroke
Penyebab Kematian No. 1 di Dunia

Penyakit Paru 6.3

Kecelakaan 9

AIDS 9.7

Kanker 12.6

Penyakit Infeksi 19.3

Peny. Jantung Koroner 22.3

dan Stroke
0 5 10 15 20 25 30

Penyebab Kematian (%)

1
The World Health Report 2001. Geneva. WHO. 2001.
The Coronary
Arteries
Left
Coronary
Artery
A Right
C Left main
Coronary
Artery
D circumflex
B posterior artery (Cx)
descending
artery E intermediate
marginal
F left anterior
descending
(LAD)
 7
Risk Factors for Atherothrombosis

Hypercoagulable states Life-style (e.g., Hyperlipidemia

smoking, diet,
Homocysteinemia lack of exercise) Hypertension

Diabetes Infection?

Obesity Age
Atherosclerosis
Genetics Gender
Atherothrombotic Manifestations
(MI, Ischemic Stroke, Vascular Death)
American Heart Association. Heart and Stroke Facts: 1997 Statistical Supplement; Wolf. Stroke 1990;21(suppl
1990;21(suppl 2):
II-4II -6; Laurila et al. Arterioscler Thromb Vasc Biol 1997;17:2910-2913; Grau et al. Stroke 1997;28:1724-1729;
Graham et al. JAMA 1997;277:1775-1781; Brigden Brigden.. Postgrad Med 1997;101(5):249-262.
9
ATHEROSCLEROSIS LESION
1. Fatty streak
2. Fibrous plaque
3. Advance (complicated) plaque
 Myocardial Ischemia

General spectrum of presentation

silent ischemia
exertion-induced angina
unstable angina
acute myocardial infarction
ACS
( NSTEMI & STEMI )
 Stable Angina Pectoris
GEJALA :
1. SAKIT DADA DENGAN GEJALA SEPERTI
DITUSUK- TUSUK
2. NYERI DADA SUBSTERNAL/ DIDAERAH
EPIGASTRIUM, MENJALAR KEPUNDAK, LEHER
ATAU LENGAN KIRI
3. LAMANYA < 5-10 MENIT
4. FREKWENSI : JARANG
5. HILANG DENGAN ISTIRAHAT
6. HILANG DENGAN PENGOBATAN VASODILATOR :
Nitrat
Acute Coronary Syndrome
( ACS )
 Acute Coronary Syndrome

The spectrum of clinical conditions

ranging from:
unstable angina
non-Q wave MI
Q-wave MI
characterized by the common
pathophysiology of a disrupted
atheroslerotic plaque
 Spectrum of Acute Coronary Syndromes

Presentation Ischemic Discomfort

at Rest

Emergency No ST-Segment ST-Segment

Department Elevation Elevation

+ +
+ +
In-Hospital

Unstable Non-Q-wave MI Q-wave MI

Angina ( : positive cardiac biomarker)
ST elevation injury miocard
Q wave infarction
PATOGENESIS OF UNSTABLE ANGINA / NSTEMI

Causes of Unstable Angina :

1.Nonocclusive thrombus on pre-existing
plaque
2.Dynamic obstruction (coronary spasm
or vasoconstriction)
3.Progressive mechanical obstruction
4.Secondary UA

Imbalance between myocardial oxygen

supply & demand
PRINCIPLE PRESENTATIONS OF
UNSTABLE ANGINA

REST ANGINA
NEW-ONSET ANGINA
INCREASING ANGINA
POST INFARCTION
 Coronary Heart Disease
Evaluation

Based on the patients

history / physical exam
electrocardiogram
Patients are categorized into 4 groups
non-cardiac chest pain
stable angina
unstable angina
myocardial infarction
 TYPICAL ANGINA

Retro sternal
Quality : Heavy pain
Compressing
Constricting
Crushing
Squeezing
Choocking
Precipitating factor (+) / (-)
Radiating to left neck, ear, jaw, back
ACUTE MYOCARDIAL INFARCTION
 Clinical History :

Characteristics of chest paint in MI :

Severe chest pain at rest for usually > 30 minutes
Same character and location as previous anginal pain but
more severe in intensity
Not relieved by nitroglycerine
Three anginal equivalent : (symptoms due to CAD other than
chest pain)
1. Dyspnea
2. Cardiac arrythmia
3. Exhaustion
Pathophysiology of MI

1. Acute thrombosis
2. Rupture of unstable plaque
3. Vasospasm
4. Embolism
5. Non-thrombotic MI (e.g. related
to shock or arrhythmia)
 General Guidelines to Differentiate Chest Pain of
Myocardial Infarction, Unstable and Chronic
Stable Angina

Chest Pain Myocardial infarction Unstable Angina Chronic Stable Angina

Severity Very severe Moderate severe Mild
Duration > 30 minutes 15 - 30 minutes < 15 minutes
Frequency Persistent pain Increasing frequency Stable, less frequent
Timing At rest At rest or with exertion With exertion
Relief With No Usually no yes
Nitroglycerine
Other anxiety, diaphoresis, Less than MI Less than MI
symptoms dyspnea, nausea
 Criteria for Diagnosis

Modified WHO Criteria : Two Out of 3 of the

Following Establishes the Diagnosis

1. Prolonged chest discomfort or chest pain

2. ECG evidence of myocardial infarction or
ischemia
3. At least a 2 fold rise in CK-MB, Troponin
 A. Normal B. Acute C. Recent D. Late E. Old
(<24 hours) (1-3 days) (3 days-6wks) (> 6 weeks)

II

III

aVR

aVL

aVF

V1-2

V3-4

V5-6

A B C D E
 Cardiac Marker - Release Kinetics
Cardiac Spesificity Increase Peak Returns
Durationto of
Marker Specificity
action Appears At Peaks At Normal
Myoglobin Non-specific 1- 3 hours 6 - 9 hours 24 hours
CK-MB Moderately 4 - 6 hours 12 - 24 hours 72 hours
Troponin I Specific 4 - 6 hours 12 - 24 hours 5- 10 days
6
Blood Level of Marker Above

Blood Myoglobin
Upper Limit of Normal

5 CK-MB
level of Troponin I
Marker 4

above

upper 3
limit of
normal 2



1

0 4 8 12 16 20 24 48 72 96 120

Time After
TimeOnset Post post
of onset AMI MCI
( Hours )
(hours)
( Peter ,2001 )
 Complications of MI :
Cardiac arrhythmias and sudden death (usually within 24 hours of MI)
Congestive heart failure or ventricular dysfunction
Cardiogenic shock
Deep venous thrombosis and pulmonary embolism
Pericarditis (Dresslers syndrome)
Rupture of papillary muscle
Rupture of ventricular septum
Rupture of cardiac wall
Systemic arterial embolism
Ventricular aneurysm
Immediate Assessment in
ED
Vital signs, including blood pressure
Oxygen saturation
IV access
12-leads ECG
Brief, targeted history and physical exam (to identify
reperfusion candidates)
Fibrinolytic check list; check contraindications
Obtain initial cardiac markers
Portable Chest X-ray < 30 min.
Assess for the following :
-Heart rate > 100 bpm and SBP < 100 mmHg
-Pulmonary edema/rales or
-Signs of shock
If any of these conditions is present, consider triage to a
facility capable of cardiac catheterization and
revascularization
 Emergency Department
(1)
AMI Protocol
-ECG screening within 10 minutes
-Door-to-drug time < 30 minutes
-Door-to-balloon time inflation < 90 minutes

For all patients with ischemic-type chest

pain, provide supplementary oxygen, IV
access, and continuous ECG monitoring
 Emergency Department
(2)
Prompt aspirin (160-325 mg) for all patients
with AMI who are reperfusion candidates.

Reperfusion therapy for ST-segment

elevation MI (STEMI)
- Rule out contraindications and assess risk-
benefit ratio.
-Consider PCI if ineligible for fibrinolytics
-angiography for cardiogenic shock
(angioplasty or CABG if indicated)
 Emergency Department
(3)
Beta-blockers for all patients without
contraindications.

IV nitroglycerin for initial 24-48 hrs

in patients with AMI and CHF, large
anterior infarction, persistent
ischemia, or hypertension.
 Blok Cabang Berkas Kiri
(BCBKi)
Gambaran EKG pada BCBKi :

Interval QRS melebar 0.10 detik

Gelombang R yang lebar, sering berlekuk di I, V5
dan V6 dengan WAV > 0.08 detik.
rS atau QS di V1, disertai rotasi searah jarum
jam.

Bila interval QRS 0.10 0.12 detik : BCBKi

inkomplit.

Bila interval QRS 0.12 detik : BCBKi komplit.

Infark Non ST Elevasi Inferior dan
Anterior Ekstensif
 Fibrinolytics

Absolute Contraindications :

-Any prior intracranial hemorrhage (ICH)

-Known structural cerebral vascular lesion (eg. AVM)
-Known malignant intracranial neoplasma
-Ischemic stroke within 3 month EXCEPT acute
ischemic stroke within 3 hrs
-Suspected aortic dissection
-Active bleeding or bleeding diasthesis
-Significant closed head trauma or facial trauma
within 3 months
Percutaneous Coronary Intervention (
Percutaneous Transcutaneous Coronary Angioplasty (PTCA)
Stenting
Coronary Bypass Surgery
ETIOLOGI :
Sering tidak dapat ditentukan
SECARA PASTI
PENYAKIT DASAR yang
menyertai aritmia

Aritmia tindakan EMERGENSI :

1. Keadaan hemodinamika :
TDS < 90 mmHg dengan hipoperfusi
2. Keluhan nyeri dada ,sesak presinkop,
kesadaran menurun
3. Tanda Gagal jantung
DERAJAT KEGAWATAN tergantung :
1. Jenis aritmia
2. Kelainan dasar jantung
3. Kelainan diluar jantung

TUJUAN PENGOBATAN :
1. Mengkonversi ke arah sinus
2. Tujuan alternatif : mengendalikan
frekwensi ventrikel optimal: 60-100x/m
3. Mengobati etiologi / penyakit penyerta
SARANA :
1. Obat antiaritmia
2. Direct Current Shock
3. Implantable Cardioverter Defibrilator
4. Pemacu jantung
5. Pengobatan ablasi dengan frekwensi
radio

PROGNOSIS :
Dipengaruhi derajat disfungsi ventrikel kiri
Batasan :

- ARITMIA :
Gangguan pembentukan dan atau
penghantaran impuls
- IRAMA SINUS normal : 60 100x/menit
- PEMBAGIAN :
- Gangguan pembentukan impuls : sinus ,
atrium penghubung AV ,ventrikel
- Gangguan penghantaran impuls :
blok SA, AV, intra ventrikel
- PEMBAGIAN SECARA KLINIS :
- Taki, bradi, bradi-taki-aritmia
 ALGORITMA ARITMIA
Keluhan :
Nyeri dada , sesak nafas , berdebar ,sinkop
Kesadaran menurun , hipotensi / shock
Curiga aritmia

EKG ,hemodinamika

Aritmia jantung gawat

Takiaritmia Bradiaritmia
Cardiac arrest
Sinus bradikardi Asistol
Henti kardiopulmoner
Blok AV/Frekw.ventr lambat
Fibrilasi ventrikel (VF)
QRSsempit
QRS lebar
Reguler Irreguler Reguler Irreguler
1. VT 1. AF + WPW 1. Sinus takikardi 1. AF
2. SVT+RBBB 2. Torsade depointes
2. A. fluter 2. A. fluter
3. LBBB 3. TSVP (PAT)
1. Obat obat anti-aritmia dalam klasifikasi
Vaughan - Williams ialah sebagai berikut :
Kelas I : Golongan penyekat Natrium
(Sodium Blockers )
1a. - Quinidine
- Procainamide
- Disopyramide
1b. - Lidocaine
- Mexiletine
- Phenytoin
- (Tocainide , Moricizine ,
jarang dipakai )
1c. - Propafenone
- Flecainide
Kelas II : Golongan penyekat beta
( beta-blockers )
- Contoh : Propanolol , atenolol ,
bisoprolol dsb
Kelas III: Golongan obat obatan yang
memperpanjang potensial aksi
dan repolarisasi
- Amiodarone
- Sotalol
- Bretylium tosylate
 Kelas IV : Golongan Calcium
antagonist
- Verapamil
- Diltiazem
Selain obat obatan tersebut diatas
masih terdapat 2 obat anti takiaritmia
lain yang tak dapat dimasukan dalam 4
kelas tersebut diatas , yaitu :
- Adenosin
- Digoxin (preparat digitalis)

2. Obat-obat anti-bradiaritmia
Tak banyak obat-obat yang dipakai untuk
pengobatan bradiaritmia karena telah beralih pada
pacu jantung
 KARDIOVERSI LISTRIK
KARDIOVERSI = upaya mengkonversi irama jantung
yang abnormal (bukan sinus) menjadi irama sinus
METODE:
1.KARDIOVERSI LISTRIK
2.KARDIOVERSI FARMAKOLOGIS

INDIKASI KARDIOVERSI LISTRIK:

taki aritmia yang tidak stabil

KONTRAINDIKASI KARDIOVERSI:
irama sinus
atrial fibrilasi yang lebih dari 48 jam, kecuali dalam
antikoagulan yang adekuat atau terbukti tidak ada
thrombus di dalam jantung.
 CARA KARDIOVERSI LISTRIK
1. Berikan sedasi adekuat dan jaga ventilasi
2. Letakkan pad pada sternum dan apex
3. Tekan SYNC pada alat
4. Perhatikan MARKER gelombang R oleh alat
5. Pastikan keadaan CLEAR
6. SHOCK

alat mengenali setiap

gelombang R, sehingga kejut
listrik diberikan jauh dari
gelombang T yang
merupakan daerah rentan
terjadi VT akibat shock
KARDIOVERSI LISTRIK

VT Shock irama menjadi sinus

Perhatikan diberikan
marker
 DOSIS KARDIOVERSI
AF : 120 200 J
Atrial flutter atau SVT lainnya: 50 100 J
VT monomorfik : 100 J
VT polimorfik dianggap VF defibrilasi
 Defibrilasi segera
Defibrilasi segera merupakan penentu penting
keberhasilan ACLS
RJP segera sebelum dan sesudah defib, tanpa
mengecek irama atau pulsasi setelah defib.
1 menit 7
10%tertunda Defib =
mortalitas meningkat
 Mekanisme Defibrilasi
Memberikan sejumlah
energi listrik melalui
miokardium untuk
mendepolarisasi
sejumlah massa otot,
sehingga impuls listrik
kembali normal.
POSISI STANDAR
pad STERNUM di
bawah klavikula kanan
pad APEX di midaxilla
kiri
 DOSIS ENERGI

MONOFASIK : 360 J
BIFASIK : 120 200 J (sesuai
rekomendasi alat) atau dosis maksimal
yang tersedia (jika tidak tahu)

Pada anak/bayi (<8 tahun):

percobaan pertama : 2 J/kg
percobaan selanjutnya : 4 J/kg
Hati - Hati

Pad diletakkan minimal 5

cm dari generator
pacemaker
 KEAMANAN
Pastikan keadaan pasien (terutama
toraks) tidak basah
Pastikan rekan2 aman dan tidak
menyentuh pasien: "Im clear, you are
clear, everybody clear?
PACU JANTUNG TRANSKUTAN

INDIKASI:
bradikardia simptomatis, tidak respons
dengan obat

KONTRAINDIKASI:
asistol
 PACU JANTUNG TRANSKUTAN
KEUNTUNGAN:
dapat dilakukan segera
mudah
tidak perlu kanulasi akses vena
dapat menjadi terapi sementara hingga ahli datang untuk
pacu transvena

KERUGIAN:
tidak nyaman untuk pasien
 CARA PENGGUNAAN
1. Jelaskan pada pasien (bila sadar) tentang efek
yang tidak nyaman (jika perlu sedasi/analgesik)
2. Tempelkan pad pacu pada sternum dan pada
apex
3. Berikan pacu pada laju nadi tertentu (>60
x/min) dan output listrik yang di-captureoleh
miokard
4. Konsultasi ahli untuk pacu jantung transvena
TERIMAKASIH 64