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Askep Pada Acute Coronary Syndrome Acs

1. Acute coronary syndrome (ACS) describes a range of conditions caused by reduced blood flow in the coronary arteries that supply the heart, including unstable angina and myocardial infarction. 2. Pathogenesis is usually due to atherosclerosis where rupture of a coronary plaque forms a thrombus that occludes the lumen, restricting blood flow. The severity of occlusion determines if it is unstable angina, NSTEMI, or STEMI. 3. Diagnosis involves history, physical exam, electrocardiogram, and cardiac enzyme levels. ST elevation on ECG indicates STEMI while ST depression or T wave changes suggest NSTEMI or unstable angina. Cardiac tropon

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0% found this document useful (0 votes)
124 views62 pages

Askep Pada Acute Coronary Syndrome Acs

1. Acute coronary syndrome (ACS) describes a range of conditions caused by reduced blood flow in the coronary arteries that supply the heart, including unstable angina and myocardial infarction. 2. Pathogenesis is usually due to atherosclerosis where rupture of a coronary plaque forms a thrombus that occludes the lumen, restricting blood flow. The severity of occlusion determines if it is unstable angina, NSTEMI, or STEMI. 3. Diagnosis involves history, physical exam, electrocardiogram, and cardiac enzyme levels. ST elevation on ECG indicates STEMI while ST depression or T wave changes suggest NSTEMI or unstable angina. Cardiac tropon

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defi rh
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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ASKEP PADA ACUTE

CORONARY SYNDROME
(ACS)
{
Overview of ACS

Acute Coronary
Syndromes*

1.57 Million Hospital Admissions - ACS

UA/NSTEMI† STEMI

1.24 million 0.33 million


Admissions per year Admissions per year

*Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA.
Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69–171.
DEFINISI

Suatu sindroma klinik yang menandakan

adanya iskemia miokard akut, terdiri dari :


Infark miokard akut Q wave (STEMI)
Infark miokard akut non-Q (NSTEMI)

Angina pektoris tidak stabil (UAP)

Spektrum ischemia akut


STEMI
NSTEMI
UAP
3
PATOGENESIS
• Umumnya disebabkan oleh aterosklerosis
koroner
• Plak aterosklerosis ruptur  terbentuk
trombus diatas ateroma yang secara akut
menyumbat lumen koroner
• Apabila sumbatan terjadi secara total 
hampir seluruh dinding ventrikel akan
nekrosis
4
The cardiovascular continuum of events

Ischemia = oxygen supply


and demand imbalance
Myocardial
Ischemia

CAD
plaque
Atherosclerosis

Risk Factors
( DYSLIPIDEMIA , BP, DM,
Insulin Resistance, Platelets,
Fibrinogen, etc)
Adapted from
Dzau et al. Am Heart J. 1991;121:1244-1263
The cardiovascular continuum of events

Coronary
Thrombosis

Myocardial
Ischemia

CAD

Atherosclerosis

Risk Factors
( DYSLIPIDEMIA , BP, DM,
Insulin Resistance, Platelets,
Fibrinogen, etc)
Adapted from
Dzau et al. Am Heart J. 1991;121:1244-1263
The cardiovascular continuum of events
ACS

Coronary
Thrombosis

Myocardial
Ischemia

CAD

Atherosclerosis

Risk Factors
( DYSLIPIDEMIA , BP, DM,
Insulin Resistance, Platelets,
Fibrinogen, etc)
Adapted from
Dzau et al. Am Heart J. 1991;121:1244-1263
Coronary
Plaque
Stable
UA/NSTEMI
STEMI
thrombosis
rupture
angina
Penyempitan
Pembuluh darah
Clinical Spectrum of Acute Coronary Syndrome
Acute Coronary Syndrome

Non-ST Segment ST Segment


Elevation Elevation

STEMI

NSTEMI
Unstable Non-Q-wave Q-wave
Angina Pectoris Acute Myocardial Infarction
Pathophysiology of Stable Angina and ACS
Pathophysiology ACS

Penurunan suplai O2

Asymptomatic
•Stenosis

Myocardial Infarction
•Anemia
•Plaque rupture/clot

Peningkatan O2 Demand

Angina
Suplai dan demand tidak seimbang →Ischemia

Myocardial ischemia→necrosis
ACS PATHOPHYSIOLOGY

 Distruption of coronary artery


plaque -> platelet
activation/aggregation
/activation of coagulation
cascade -> endothelial
vasoconstriction ->intraluminal
thrombus/embolisation ->
obstruction -> ACS
 Severity of coronary vessel
obstruction & extent of
myocardium involved
determines characteristics of
clinical presentation
Unstable
NSTEMI STEMI
Angina
Non-occlusive
thrombus Complete thrombus
Non occlusive sufficient to cause occlusion
thrombus tissue damage &
mild ST elevations on
Non specific myocardial necrosis ECG or new LBBB
ECG
ST depression +/- Elevated cardiac
Normal cardiac T wave inversion on enzymes
enzymes ECG
More severe
Elevated cardiac symptoms
enzymes
Diagnosis

Anamnesis
Pemeriksaan Fisik
Pemeriksaan Penunjang :
1. Laboratorium
2. Elektrokardiografi
3. Thoraks Foto
HISTORY
PRODROMAL SYMPTOMS
History very valuable to establish D/. Prodoma : chest discomfort –
unstable angina
1/3 symptoms for 1 – 4 wks
20% symptoms for < 24 hrs
Malaise, exhaustion

NATURE OF PAIN
• Most patients
severe prolonged,  30 minutes - hours
• Constricting, crushing, oppressing, compressing
heavy weight or squeezing in chest
• Choking, vise-like, heavy pain or stabbing, knife-like, boring or
burning discomfort
• Location : retrosternal, spreading frequently to both sides of the
chest with predilection to the left side
• Often pain radiates down ulnar aspect of left arm, producing
tingling sensation in left wrist, hand and fingers
15
NATURE OF PAIN
• SOME INSTANCES : pain begins in epigastrium, and simulates
abdominal disorder
• Sometimes pain radiates to shoulders, upper extremities, neck, jaw and
interscapular region favoring the left side
• Elderly : no chest pain but acute left ventricular failure and chest
tightness or marked weakness or syncope
• Pain arises from nerve endings in ischemic or injured, but not necrotic,
myocardium

OTHER SYMPTOMS
50% nausea or vomiting in transmural infarcts
Occasionally diarrhea, profound weakness, dizziness, palpitation, cold
perspiration, sense of impending doom
Occasionally : cerebral embolism or systemic arterial embolism

16
Pain Patterns with Myocardial Ischemia

17
Anamnesis untuk UAP

• 3 kategori presentasi klinik UAP:


 Angina saat istirahat (resting angina)
 Angina awitan baru (new onset angina)
 Angina yang bertambah berat (increasing
angina)

• Riwayat penyakit dahulu :


 Riwayat angina on effort, infark atau
operasi pintas
 Riwayat penggunaan nitrogliserin
 Identifikasi faktor-faktor risiko
18
PHYSICAL EXAMINATION
GENERAL APPEARANCE
Anxious, considerable distress, restless, fist on chest
(Levine sign)
LV failure & symp. stimulation : cold perspiration, pallor,
dyspnea, cough with frothy pink or blood-streaked
sputum.
Shock : cool, clammy skin, facial pallor, cyanosis,
confusion or disorientation

HEART RATE
Variable depending on underlying rhythm and degree or
ventr. failure
Most commonly, HR 100 – 110/min; > 95% patients :
VPB’s within first 4 hours
19
BLOOD PRESSURE
Majority normotensive, but syst. BP may decline and diast.
BP may rise
 Half of pts with inferior MI  parasympathetic stimulation
: hypotension, bradycardia or both (Bezold – Jarisch
reflex)
 half of pts with anterior MI,  sympathetic excess :
hypertension, tachycardia or both

TEMPERATURE AND RESPIRATION


Most pts with extensive MI  fever within 24-48 hrs, fever
resolves by 4th or 5th day
Respiration  due to anxiety and pain, in LV failure : resp.
rate correlates with degree of heart failure

20
JUGULAR VENOUS PULSE
JVP usually normal
RV infarction : marked jug. venous distension

CAROTID PULSE
Small pulse  reduced stroke volume
Pulse alternans : severe LV dysfunction

21
CHEST
LV failure and/or LV compliance ↓ : moist rales
Severe failure : diffuse wheezing, cough + hemopthysis
1967 : Killip & Kimball : prognostic classification

Class I : patients free of rales or S3


II : rales < 50% lung fields +/- S3
III : rales > 50% lung fields, frequently
pulm. edema
IV : cardiogenic shock

22
Pemeriksaan Penunjang
• Pemeriksaan EKG

Gambaran EKG infark miokard akut Q-wave (STEMI) :

 Elevasi segmen ST  1 mm pada  2 sadapan


extremitas

 Atau  2 mm pada  2 sadapan prekordial yang


berurutan

 Atau gambaran LBBB baru atau diduga baru


23
ST-segment elevation
Gambaran EKG infark miokard akut non-Q-wave (NSTEMI) atau
angina pektoris tidak stabil (UAP) :

 Depresi segment ST atau gelombang T terbalik pada  2 sadapan


berurutan

 Inversi gelombang T minimal 1 mm pada 2 sadapan atau lebih


yang berurutan.

 Perubahan segment ST saat keluhan dan kembali normal saat


keluhan hilang  sangat menyokong UAP

27
ST-segment depression
T-wave inversion
ELEKTROKARDIOGRAM

Current-of-injury patterns with acute ischemia

30
• Pemeriksaan Penanda Jantung/Enzim jantung
(Cardiac Markers):

Yang lazim adalah CKMB, dapat pula troponin T (TnT)


atau troponin I (TnI)

Peningkatan marka jantung akan terlihat pada infark


miokard akut Q-wave (STEMI) dan non-Q-wave
(NSTEMI)

31
Plot of the appearance of cardiac markers in
blood versus time after onset of symptoms

32
A myoglobin C CK-MB
B troponin D troponin in UA
TIMI RISK SCORE –increase in mortality with increasing score
~40% all cause mortality at 14 days for patients requiring urgent
revascularisation
Diagnosis Banding
1. Diseksi aorta
2. Perikarditis
3. Nyeri angina atipikal pada kardiomiopati
hipertrofi
4. Penyakit esofageal, GI atas atau traktus biliaris
5. Penyakit paru-paru : pneumotoraks, emboli,
pleuritis
6. Sindroma hiperventilasi
7. Gangguan dinding dada : muskuloskeletal,
neurogen
35
8. Psikogen
 Gangguan perfusi jaringan jantung b.d.
obstruksi (aterosklerosis, spasmus, trombus)
 Nyeri b.d. ischemia mioakrdium
 Cemas b.d. ancaman kematian
 Resiko penurunan CO b.d aritmia, penurunan
kontraktilitas jantung

DIAGNOSA
KEPERAWATAN
Manajemen
The cardiovascular continuum of events
ACS
Coronary
Thrombosis Arrhythmia and
Loss of Muscle

Myocardial
Ischemia Remodeling

Ventricular
CAD Dilatation

Atherosclerosis Congestive
Heart Failure

Risk Factors End-stage Heart


( DYSLIPIDEMIA , BP, DM, Disease
Insulin Resistance, Platelets,
Fibrinogen, etc)
Adapted from
Dzau et al. Am Heart J. 1991;121:1244-1263
DELAY TO THERAPY

1. From onset of symptoms to patient recognition

2. Out-hospital transport

3. In-hospital evaluation
ISCHEMIC CHEST PAIN ALGORYTHM
Chest pain suggestive of ischemia
ISCHEMIC CHEST PAIN

TYPICAL ANGINA EQUIVALENT ANGINA

1. NO CHEST DISCOMFORT
1. CHEST DISCOMFORT 2. LOCATION
2. LOCATION 3. INDIGESTION
3. RADIATION 4. UNEXPLAINED WEAKNESS
4. UNLIKELINESS 5. DIAPORESIS
6. SHORTNESS OF BREATH
Acute coronary syndrome algorithm

Chest discomfort suggestive of ischemia

Immediate ED assessment and immediate ED general treatment

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90
Chest discomfort suggestive of ischemia

Immediate ED assessment ( 10 min) Immediate ED general treatment


• Vital sign • O2 at 4 L/min (maintain O2 sat 90%)
• Oxygen saturation • Aspirin 160-325 mg
• Obtain IV access • Nitroglycerin SL, spray, or IV
• Obtain ECG 12 lead • Morphine IV 2-4 mg repeated every
• Brief history and physical exam 5-10 minutes (if pain not relieved
• Check contraindication for fibrinolytic with nitroglycerine)
• Initial serum cardiac markers
• Initial electrolyte and coagulation Memory: “MONA” greets all patients
study
• Portable chest x-ray ( 30 minutes)

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90
Acute coronary syndrome algorithm

Chest discomfort suggestive of ischemia

Immediate ED assessment and immediate ED general treatment

Review initial 12 lead ECG

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90
Acute coronary syndrome algorithm

Chest discomfort suggestive of ischemia

Immediate ED assessment and immediate ED general treatment

Review initial 12 lead ECG

ST elevation or new or
presumably new LBBB
strongly suspicious for
injury

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90
Acute coronary syndrome algorithm

Chest discomfort suggestive of ischemia

Immediate ED assessment and immediate ED general treatment

Review initial 12 lead ECG

ST elevation or new or ST-depression or


presumably new LBBB dynamic T-wave
strongly suspicious for inversion strongly
injury suspicious for injury

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90
Acute coronary syndrome algorithm

Chest discomfort suggestive of ischemia

Immediate ED assessment and immediate ED general treatment

Review initial 12 lead ECG

ST elevation or new or ST-depression or Normal or non-


presumably new LBBB dynamic T-wave diagnostic changes
strongly suspicious for inversion strongly in ST-segment or T-
injury (STEMI) suspicious for injury waves (intermediate/
(UA/NSTEMI) low-risk UA)

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90
Acute coronary syndrome algorithm

Chest discomfort suggestive of ischemia

Immediate ED assessment and immediate ED general treatment

Review initial 12 lead ECG

ST elevation or new or ST-depression or Normal or non-


presumably new LBBB dynamic T-wave diagnostic changes
strongly suspicious for inversion strongly in ST-segment or T-
injury (STEMI) suspicious for injury waves (intermediate/
(UA/NSTEMI) low-risk UA)
Start adjunctive treatment

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90
ADJUNCTIVE TREATMENT
(Do not delay reperfusion)

1. Beta-adrenergic receptor blocker

2. Clopidogrel

3. Heparin (UFH or LMWH)

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90
Acute coronary syndrome algorithm
Chest discomfort suggestive of ischemia

Immediate ED assessment and immediate ED general treatment

Review initial 12 lead ECG

ST elevation or new or ST-depression or dynamic Normal or non-


presumably new LBBB T-wave inversion strongly diagnostic changes in
strongly suspicious for suspicious for injury ST-segment or T-
injury waves

Start adjunctive treatment

Time from onset of


symptoms
 12 hours
- Reperfusion strategy: PCI (90
min) or fibrinolysis (30 min)
- ACE-I/ARB
- Statin

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90
Acute coronary syndrome algorithm
Chest discomfort suggestive of ischemia

Immediate ED assessment and immediate ED general treatment

Review initial 12 lead ECG

ST elevation or new or ST-depression or dynamic Normal or non-


presumably new LBBB T-wave inversion strongly diagnostic changes in
strongly suspicious for suspicious for injury ST-segment or T-
injury waves

Start adjunctive treatment Start adjunctive treatment

Time from onset of


symptoms
 12 hours
- Reperfusion strategy: PCI (90 min) or
fibrinolysis (30 min)
- ACE-I/ARB within 24 hours of onset
- Statin

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90
Adjunctive treatment

• Heparin (UFH/LMWH)

• Glycoprotein IIb/IIIa receptor inhibitors

• -Adrenoreceptor blockers

• Clopidogrel

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90
Chest discomfort suggestive of ischemia

Immediate ED assessment and immediate ED general treatment

Review initial 12 lead ECG

ST elevation or new or ST-depression or dynamic Normal or non-


presumably new LBBB T-wave inversion strongly diagnostic changes in
strongly suspicious for suspicious for injury ST-segment or T-
injury waves

Start adjunctive treatment Start adjunctive treatment

Time from onset of  12 hrs Admit to monitored bed


symptoms Assess risk status
 12 hours
- Reperfusion strategy: PCI (90 - High risk: early invasive
min) or fibrinolysis (30 min) strategy
- ACE-I/ARB within 24 h of - Continue ASA, heparin,
symptom onset) ACE-I, statin
- Statin

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90
VERY HIGH-RISK PATIENT

1. Refractory chest pain

2. Recurrent/persistent ST deviation

3. Ventricular tachycardia

4. Hemodynamic instability

5. Sign of pump failure

6. Shock within 48 hours

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90
Chest discomfort suggestive of ischemia

Immediate ED assessment and immediate ED general treatment

Review initial 12 lead ECG

ST elevation or new or ST-depression or dynamic Normal or non-


presumably new LBBB T-wave inversion strongly diagnostic changes in
strongly suspicious for suspicious for injury ST-segment or T-
injury waves

Start adjunctive treatment Start adjunctive treatment Develops high or


intermediate risk criteria
or troponin-positive
Time from onset of  12 hrs Admit to monitored bed
symptoms Assess risk status
Monitored bed in ED
 12 hours
- Reperfusion strategy: PCI (90 - High risk: early invasive
strategy Develops high or
min) or fibrinolysis (30 min)
- ACE-I/ARB within 24 h of - Continue ASA, heparin, intermediate risk criteria
ACE-I, statin or troponin-positive
symptom onset)
- Statin
No evidence of ischemia and MI: discharge with follow-up
2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90
Early Invasive

Conservative
 Evaluate for conservative vs. invasive strategy based upon:
 Likelihood of actual ACS
 Risk stratification by TIMI risk score

 ACS risk categories per AHA guidelines

Low High
Unstable angina/NSTEMI
Intermediate cardiac care
                                                                                                                                                 
Pengobatan Pasca Perawatan
 Obat-obat untuk mengontrol keluhan iskemia
harus dilanjutkan
 Aspirin
 Beta-blocker
 ACE inhibitor

Modifikasi Faktor Risiko


 Berhenti merokok
 Pertahankan BB optimal
 Aktivitas fisik sesuai dengan hasil treadmill
 Diet
 Rendah lemak jenuh dengan kolesterol, bila perlu
dengan target LDL < 100 mg/dL
 Pengendalian hipertensi
60
 Pengendalian ketat gula darah pada penderita DM
Terima Kasih
Selamat Belajar
•Get regular medical checkups.
•Control your blood pressure.
•Check your cholesterol.
•Don’t smoke.
•Exercise regularly.
•Maintain a healthy weight.
•Eat a heart-healthy diet.
•Manage stress.

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