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PANUM KARDIO

CAD/PJK
• ANGINA PEKTORIS STABIL
• SINDROMA KORONER AKUT
ANGINA PECTORIS TIDAK STABIL
NON ST ELEVASI MIOKARD INFARK
ST ELEVASI MIOKARD INFARK
ANGINA PEKTORIS STABIL
• GEJALA : ANGINA TIPIKAL, SESAK NAPAS, TIDAK
NYAMAN DI DADA
• NYERI DADA  ANGINA TIPIKAL :
SENSASI TUMPUL, SEPERTI TERTEKAN, SEPERTI
DIREMAS, SEPERTI TERBAKAR
LOKASI SENTRAL/SUBSTERNAL
MENJALAR KE LENGAN KIRI, BAHU, RAHANG, LEHER
DIPICU OLEH AKTIVITAS/STRESS EMOSIONAL
MEMBAIK DENGAN NITRAT ATAU ISTIRAHAT
DURASI < 20MENIT
PEMERIKSAAN PENUNJANG
- ECG :
NORMAL
Gambaran iskemik  st depresi, t inverted

- TREADMILL STRESS TEST


POSITIVE ISCHEMIC RESPONSE
- NUCLEAR IMAGING
TERAPI
• KONTROL FAKTOR RISIKO SEPERTI DM, HTN,
DISLIPIDEMIA, OBESITAS, MEROKOK,
AKTIVITAS FISIK
• ANTIPLATELET  ASAM ASETIL SALISILAT 80
MG 1X1 ATAU TIENOPIRIDIN 1X1
• ANTI ANGINA  ISDN MG SUBLINGUAL
• BETA BLOKER
• CCB NONDIHIDROPIRIDINE
SINDROMA KORONER AKUT
• APTS
• NSTEMI
• STEMI
• KELUHAN : NYERI DADA, SESAK NAPAS,
PERASAAN TIDAK NYAMAM
• Karakteristik sama dengan APS, tapi durasi >
20 menit dan tidak hilang dengan istirahat
atau nitrat
Characters of anginal pain

• Localized usually at precordium


• Radiate to arm, neck, shoulder, back or
epicardium
• Feels like being pressed by heavy object, or
constricting or crushing.
• Concomitant systemic symptoms: dyspnea,
dizziness, nausea, diaphoresis

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ALUR DIAGNOSIS SKA
Diagnosis spectrum of ACS

Presentation
(Clinical, Initial ECG)

Working ST-Seg Elevation Non-STSeg Elevation


diagnosis Myocardial Infarction Acute Coronary Syndr

Time

Evolution of
ECG & Biomarker (+) Biomarker (-)
Biomarkers

Final ST-Seg Elevation Non-ST-seg- Unstable


diagnosis MCI Elevation MCI Angina
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National Heart Foundation Australia &The Cardiac Society of Australia and New Zealand, MJA 2006
Algorithm in Acute Coronary Syndrome

Admission CHEST PAIN

Performed in 10 min
Working Suspected ACS
diagnosis

Persistent No persistent {on serial


ECG
ST elevation ST elevation ECG}

Bio- Troponin, Troponin, - ACS unlikely


chemistry CKMB (+) - NSTEMI
CKMB (±)
- STEMI

Risk
Stratification
Risk: high / low

Initial management,
Management ±revascularization

Secondary Medical therapy,


prevention
coronary angiography Modified from ESC 2007
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ECG pattern in ACS

Transmural injury: ST ↑
Ischemia: ST ↓, tall T, inverted T

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ECG evolution

Important: check ECG serially; at least 2 times, 4-6 hours apart

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Biomarkers
• Recommendation: CKMB & Troponin upon admission and
serial in 6-12 hours
• LDH, SGOT/SGPT and other enzymes not recommended
• Increase of plasma CK plasma & CK-MB happens early, but
less specific
• Increase of TnI & TnT are more specific in diagnosing marker
MI; its level corresponds with prognosis (higher value, worse
prognosis).

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Biomarkers Early release myoglobin of
CKMB isoform
Trop
50 Cardiac troponin after “classical”
Multiple of the AMI cutoff limit

myocardial infarction

20 CK-MB after myocardial infarction

10 Cardiac troponin after “microinfarction”

5 CK-MB

2
1

0 1 2 3 4 5 6 7 8
Day after onset of AMI

Time-course of the different cardiac biochemical markers. From Wu AH et al. Clin Chem 1999 ; 45 : 1104,
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with permission
Initial management
• Monitor and support ABCs
• Check vital signs, incl oxygen saturation
• Establish IV access
• Administer
– Oxygen 4L/min
– Aspirin 160 mg chewed
– Clopidogrel loading dose 300 mg
– NTG (ISDN) sublingual
– Morphine if pain not relieved with NTG
• Caution: hemodynamic instability due to pump
failure &/ malignant arrhythmia

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Anticoagulation & reperfusion
• Heparin administration (LMWH or UFH)
– Enoxaparine 2x0.6 cc or fondaparinux 1x2.5 mg
– LMWH contraindicated in CKD
– UFH loading dose 60 unit/kg body weight (BW),
maintanance 12 u/kg BW/hour, target aPTT 1.5-2x
control
• Reperfusion in STEMI
– Fibrinolysis (onset <4 hrs) or primary percutaneous
coronary intervention (PCI) (onset ≤12 hrs), no
contraindication
– Door to needle time: 30 min
– Door to balloon time: 90 min
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Typical prescription of
ACS patients
• Aspirin 1x80 mg
• Clopidogrel 1x75 mg
• ISDN 3x5-10 mg
• Heparin UFH or LMWH
• Simvastatin 1x20 mg
• Tranquilizer diazepam 1x5 mg
• Laxative 1xCI

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Secondary prevention strategy
A Aspirin and Anticoagulants

B Beta blockers and Blood Pressure

C Cholesterol and Cigarettes

D Diet and Diabetes

E Education and Exercise

F Fun and Faith


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CONGESTIVE HEART FAILURE
CONGESTIVE HEART FAILURE
• PENYEBAB :SEMUA KELAINAN PADA JANTUNG
DAPAT MENYEBABKAN CHF
Etiologi
1. Penyakit pada miokard sendiri
PJK, Kardiomiopati, Miokarditis, PJR, Penyakit
infiltratif, Obat2an seperti Adriamisin, Radiasi
2. Gangguan Mekanik Pada miokard
a. Volume overload (Insufisiensi Aorta/mitral
PJB Left to right shunt, transfusi berlebihan )
b. Pressure overload ( HT, Stenosis aorta, KoA)
c. Hambatan pengisian ( Tamponade )
PATOFISIOLOGI
Faktor presipitasi

Hukum Laplace (+)


Regangan dinding ventrikel
Hukum Starling
(+)
Dilatasi 5 Hipertropi

Kontraktilitas
(-)
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Afterload 3 Curah Jantung
(+) Volume pengisian
Ventrikel
TD, Volume art

1 Simpatis,SRAA,Aldstrn,
(-)
ADH Preload
Vasokonstriksi (+) 2 (-)
Retensi Cairan
ANP &BNP
Dasar terapi
1. Vasodilator, untuk menurunkan after load
2. Venodilator dan diuretik, untuk menurunkan
preload
3. Inotropik untuk meningkatkan kontraktilitas
miokard
4. Aldosteron antagonis, untuk mencegah
hipertropi ventrikel kiri
5. Memperbaiki metab. Kardiak, untuk suplai
energi pada miokard
ALUR DIAGNOSIS CHF

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