Beruflich Dokumente
Kultur Dokumente
Departemen Kardiologi dan Kedokteran Vaskuler FKUI Pusat Jantung Nasional-RS Jantung Harapan Kita
Epidemiologi
Survei Kesehatan Rumah Tangga (SKRT) Departemen Kesehatan menunjukkan, penyakit jantung memberikan kontribusi sebesar 19,8 % dari seluruh penyebab kematian pada tahun 1993. Angka tersebut meningkat menjadi 24,4 % pada tahun 1998 Hasil SKRT tahun 2001, PJK telah menempati urutan pertama dalam deretan penyebab utama kematian di Indonesia.
Atherosclerosis Timeline
Foam Cells Fatty Streak Intermediate Atheroma Lesion Fibrous Plaque Complicated Lesion/ Rupture
Endothelial Dysfunction From First Decade From Third Decade From Fourth Decade
activated
Thrombus
Lipid core
Adventitia
Angina Pektoris terstabil Infark miokard non elevasi segmen ST (STEMI) Infark Miokard dengan elevasi segmen ST (NSTEMI)
Patofisiologi sama Persentasi sama Aturan2 pengelolaan awal sama STEMI perlu evaluasi untuk intervensi reperfusi akut
Type I Spontaneous MI related to ischemia due to a primary coronary event such as a plaque erosion and/or rupture, fissuring, or dissection Type 2 MI secondary to ischemia due to either O2 demand or decreased supply (coronary artery spasm, coronary embolism, anemia, HTN, hypotension, arrhythmia)
Type 3 Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia, accompanied by presumably new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood tests could be obtained, or at a time before the appearance of cardiac biomarkers in the blood.
Type 4a MI associated with PCI Type 4b MI associated with stent thrombosis as documented by angiography or at autopsy Type 5 MI associated with CABG
1. 2. 3. 4.
Lama oklusi (Ingat: door to balloon < 90 menit dan door to needle < 30 menit ) Kolateral Tingkat konsumsi oksigen miokard Keadaan metabolik Keseimbangan fibrinolitik
Diagnosis of Angina
Atypical angina
1 of the above
Unstable Angina
Non occlusive thrombus Non specific ECG Normal cardiac enzymes
NSTEMI
Occluding thrombus sufficient to cause tissue damage & mild myocardial necrosis ST depression +/T wave inversion on ECG Elevated cardiac enzymes
STEMI
Complete thrombus occlusion ST elevations on ECG or new LBBB Elevated cardiac enzymes More severe symptoms
4.
5.
Mengurangi luasnya infark Mempertahankan fungsi ventrikel kiri Mencegah kejadian kardiak atau komplikasi major Mengatasi komplikasi yang mengancam jiwa Mulai melakukan pencegahan sekunder
Acute Management
Initial evaluation & stabilization Efficient risk stratification Focused cardiac care
Evaluation
Occurs simultaneously
Emergent care
IV access Cardiac monitoring Oxygen Aspirin Nitrates
12 lead ECG Obtain initial cardiac enzymes electrolytes, cbc lipids, bun/cr, glucose, coags CXR
Focused History
Palliative/Provocative factors Quality of discomfort Radiation Symptoms associated with discomfort Cardiac risk factors Past medical history especially cardiac
Reperfusion questions
Timing of presentation ECG c/w STEMI Contraindication to fibrinolysis Degree of STEMI risk
Targeted Physical
Examination
Hypotension Tachycardia Pulmonary rales, JVD, pulmonary edema, New murmurs/heart sounds Diminished peripheral pulses Signs of stroke
Rekaman EKG harus secepatnya dilakukan dan diinterpretasi saat pasien tiba di IGD Standar waktu 10 menit
Presentation Working Dx
ECG
No ST Elevation NSTEMI
ST Elevation
ST-Segment Elevation MI
New LBBB
QRS > 0.12 sec L Axis deviation Prominent S wave V1-V3 Prominent R wave 1, aVL, V5-V6
50
Multiples of the URL
20 10 5 2 1 0 1
Upper reference limit
Cardiac troponin after classical AMI CK-MB after AMI Cardiac troponin after microinfarction
Modified from: ESC/ACC Comm MI redefined JACC 36: 959,2000 Wu AH et al. Clin Chem 1999;45:1104.
Cardiac markers
Troponin ( T, I)
CK-MB isoenzyme
Very specific and more sensitive than CK Rises 4-8 hours after injury May remain elevated for up to two weeks Can provide prognostic information Troponin T may be elevated with renal dz, poly/dermatomyositis
Rises 4-6 hours after injury and peaks at 24 hours Remains elevated 3648 hours Positive if CK/MB > 5% of total CK and 2 times normal Elevation can be predictive of mortality False positives with exercise, trauma, muscle dz, DM, PE
6 5 4 3 2 1 0
3.7 %
1.7 %
174 148 134 50 67
9.0
0 to <0.4 0.4 to <1.0 1.0 to <2.0 2.0 to <5.0 5.0 to <9.0 Cardiac troponin I (ng/ml)
Risk Stratification
Purposes Triage / Transfer for Tertiary Care Resource Allocation Selection of Rx Strategy Prognosis
Continuous Process Presentation: History, ACS features, Biomarkers, PEx In Hospital: Events, Response to Rx Discharge: LV Function, Arrhythmias, Ischemia
Risk Stratification
STEMI Patient?
Based on initial Evaluation, ECG, and Cardiac markers
YES
NO
UA or NSTEMI - Evaluate for Invasive vs. conservative treatment - Directed medical therapy
Fibrinolysis indications
ST segment elevation >1mm in two contiguous leads New LBBB Symptoms consistent with ischemia Symptom onset less than 12 hrs prior to presentation
Any prior ICH Known structural cerebral vascular lesion (e.g., AVM) Known malignant intracranial neoplasm (primary or metastatic) Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours Suspected aortic dissection Active bleeding or bleeding diathesis (excluding menses) Significant closed-head or facial trauma within 3 months
More universal access Shorter time to treatment Greater clinical trial evidence of:
33 33 50 20 20 20 20
Comparing outcomes
Morphine (class I, level C) Analgesia Reduce pain/anxietydecrease sympathetic tone, systemic vascular resistance and oxygen demand Careful with hypotension, hypovolemia, respiratory depression Oxygen (2-4 liters/minute) (class I, level C) Up to 70% of ACS patient demonstrate hypoxemia May limit ischemic myocardial damage by increasing oxygen delivery/reduce ST elevation
Nitroglycerin (class I, level B) Analgesiatitrate infusion to keep patient pain free Dilates coronary vesselsincrease blood flow Reduces systemic vascular resistance and preload Aspirin (160-325mg chewed & swallowed) (class I, level A) Irreversible inhibition of platelet aggregation Stabilize plaque and arrest thrombus Reduce mortality in patients with STEMI
Beta-Blockers (class I, level A) 14% reduction in mortality risk at 7 days at 23% long term mortality reduction in STEMI Approximate 13% reduction in risk of progression to MI in patients with threatening or evolving MI symptoms Reassess for therapy as contraindications resolve ACE-Inhibitors / ARB (class I, level A) Start in patients with anterior MI, pulmonary congestion, LVEF < 40% Start in first 24 hours ARB as substitute for patients unable to use ACE-I
Heparin (class I, level C to class IIa, level C) LMWH or UFH (max 4000u bolus, 1000u/hr) Indirect inhibitor of thrombin Adjunct to surgical revascularization and thrombolytic / PCI reperfusion 24-48 hours of treatment Coordinate with PCI team (UFH preferred) Used in combo with aspirin and/or other platelet inhibitors Changing from one to the other not recommended
Review guidelines for specific management of complications & other specific clinical scenarios
Decision making for risk stratification at hospital discharge and/or need for CABG
of actual ACS TIMI risk score ACS risk categories per AHA guidelines Low High
Intermediate
Low risk
Intermediate
risk
High risk
Conservative therapy
Invasive therapy
Coronary angiography and revascularization within 12 to 48 hours after presentation to ED For high risk ACS (class I, level A) MONA + BAH (UFH) Clopidogrel
20% reduction death/MI/Stroke CURE trial 1 month minimum duration and possibly up to 9 months
Early revascularization or PCI not planned MONA + BAH (LMW or UFH) Clopidogrel Glycoprotein IIb/IIIa inhibitors
Only in certain circumstances (planning PCI, elevated TnI/T) Serial ECGs Serial Markers
Surveillence in hospital
After adjusting for age, previous MI, CHF, Killip class, abnormal biomarker, ST deviation/BBB on presentation, the discharge use of the following medications was associated with lower 1-year mortality *: ASA [OR=0.48 (0.36 to 0.63), P<0.001] Beta-blocker [OR=0.72 (0.56 to 0.92), P<0.01] ACE inhibitor [OR=0.76 (0.60 to 0.96), P=0.02] Lipid lowering agent [OR=0.72 (0.57 to 0.92), P<0.01]
* OR= odds ratio (95% confidence interval)
Comprehensive Medical Therapy For 2nd Prevention for Patients with CHD or Other Vascular Disease
Risk Reduction
*The four medications every atherosclerosis patient should be treated with, unless contraindications exist and are documented
Pencegahan Sekunder
A : ASA, antikoagulan, ACE-I/ARB (LVD, HF, HTN, DM) B : Beta-blocker, BW reduction, BP Control (BP< 130/80 mmHg) C : Cigarette smoking cessation Cholesterol control (K-LDL<70 mg/dl) D : Diet ( AHA step 2 diet ) Diabetes management ( Ac<7%) E : Exercise regularly Education F : Family Support G : Go to Hospital
Primary Prevention
Subclinical Atherosclerosis Multiple Risk Factors Environmental, Genetic Factors that Produce Risk
Population Wellness
Prevention news
From 1994 to 2004 the death rate from coronary heart disease declined33%... But the actual number of deaths declined only18%
Getting better with treatment But more patients developing disease need for primary prevention focus
Kesimpulan
SKA mencakup APTS, NSTEMI, dan STEMI Fokus penatalaksanaan - penilaian dan intervensi segera ( MONA + BAH ) - stratifikasi resiko ( APTS/NSTEMI VS STEMI ) - reperfusi cepat pada STEMI (Fibrinolitik vs PCI ) - strategi konservatif vs invasif dini pada APTS/ NSTEMI Pencegahan sekunder agresif pada pasien SKA - BB, ACE-1/ARB, ASA, statin
FarahMutiaraSariHarmani
Objectives
Similar pathophysiology
Diagnosis of Angina
Atypical angina
Unstable Angina
Non occlusive thrombus Non specific ECG Normal cardiac enzymes
NSTEMI
Occluding thrombus sufficient to cause tissue damage & mild myocardial necrosis ST depression +/T wave inversion on ECG Elevated cardiac enzymes
STEMI
Complete thrombus occlusion ST elevations on ECG or new LBBB Elevated cardiac enzymes More severe symptoms
Acute Management
Initial evaluation & stabilization Efficient risk stratification Focused cardiac care
Evaluation
12 lead ECG Obtain initial cardiac enzymes electrolytes, cbc lipids, bun/cr, glucose, coags CXR
Focused History
Palliative/Provocative factors Quality of discomfort Radiation Symptoms associated with discomfort Cardiac risk factors Past medical history -especially cardiac
Reperfusion questions
Timing of presentation ECG c/w STEMI Contraindication to fibrinolysis Degree of STEMI risk
Targeted Physical
Examination
Superficial Erosion
Presentation Working Dx
ECG
No ST Elevation NSTEMI
ST Elevation
Cardiac troponin after classical AMI CK-MB after AMI Cardiac troponin after microinfarction
Modified from: ESC/ACC Comm MI redefined JACC 36: 959,2000 Wu AH et al. Clin Chem 1999;45:1104.
Risk Stratification
Purposes Triage / Transfer for Tertiary Care Resource Allocation Selection of Rx Strategy
Prognosis
Continuous Process Presentation: History, ACS features, Biomarkers, PEx In Hospital: Events, Response to Rx Discharge: LV Function, Arrhythmias, Ischemia
Goal = 10 min
Definite ACS
As Per Other Dx
Medical Rx
Symptoms Suggestive of ACS Possible ACS No ST elev. < 12h Lytic eligible Lytic
(D-N < 30 m)
Medical Rx
(ACEI)
Non dx ECG Neg. card. markers Observe f/u studies Neg Neg Outpt f/u Stress Pos Pos
Disadvantages
Risk Stratificaton Sens/Spec > CKMB Detect Recent MI Selection of Rx Detect Reperfusion
Low sens. early (< 6h) Repeat at 8-12 h if neg. Limited ability to detect late minor reinfarction
Recommendation Useful as single test to efficiently Dx NSTEMI Clinicians should familiarize themselves with Dx cutoffs in local lab
ECG assessment
ST Elevation or new LBBB STEMI
ST Depression or dynamic T wave inversions
NSTEMI
Non-specific ECG
Unstable Angina
ST-Segment Elevation MI
New LBBB
QRS > 0.12 sec L Axis deviation Prominent R wave V1-V3 Prominent S wave 1, aVL, V5-V6 with t-wave inversion
Cardiac markers
Troponin ( T, I)
CK-MB isoenzyme
Very specific and more sensitive than CK Rises 4-8 hours after injury May remain elevated for up to two weeks Can provide prognostic information Troponin T may be elevated with renal dz, poly/dermatomyositis
Rises 4-6 hours after injury and peaks at 24 hours Remains elevated 36-48 hours Positive if CK/MB > 5% of total CK and 2 times normal Elevation can be predictive of mortality False positives with exercise, trauma, muscle dz, DM, PE
3.7 %
1.7 %
174 148 134 50 67
9.0
0 to <0.4 0.4 to <1.0 1.0 to <2.0 2.0 to <5.0 5.0 to <9.0 Cardiac troponin I (ng/ml)
Risk Stratification
STEMI Patient?
Based on initial Evaluation, ECG, and Cardiac markers
YES
NO
UA or NSTEMI - Evaluate for Invasive vs. conservative treatment - Directed medical therapy
necrosis Preserve LV function Prevent major adverse cardiac events Treat life threatening complications
amount of myocardial
Fibrinolysis indications
ST segment elevation >1mm in two contiguous leads New LBBB Symptoms consistent with ischemia Symptom onset less than 12 hrs prior to presentation
Any prior ICH Known structural cerebral vascular lesion (e.g., AVM) Known malignant intracranial neoplasm (primary or metastatic) Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours Suspected aortic dissection Active bleeding or bleeding diathesis (excluding menses) Significant closed-head or facial trauma within 3 months
History of chronic, severe, poorly controlled hypertension Severe uncontrolled hypertension on presentation (SBP greater than 180 mm Hg or DBP greater than 110 mmHg) History of prior ischemic stroke greater than 3 months, dementia, or known intracranial pathology not covered in contraindications Traumatic or prolonged (greater than 10 minutes) CPR or major surgery (less than 3 weeks)
Recent (within 2-4 weeks) internal bleeding Noncompressible vascular punctures For streptokinase/anistreplase: prior exposure (more than 5 days ago) or prior allergic reaction to these agents Pregnancy Active peptic ulcer Current use of anticoagulants: the higher the INR, the higher the risk of bleeding
Fibrinolysis preferred if: <3 hours from onset PCI not available/delayed door to balloon > 90min door to balloon minus door to needle > 1hr Door to needle goal <30min No contraindications
Comparing outcomes
Morphine (class I, level C) Analgesia Reduce pain/anxietydecrease sympathetic tone, systemic vascular resistance and oxygen demand Careful with hypotension, hypovolemia, respiratory depression Oxygen (2-4 liters/minute) (class I, level C) Up to 70% of ACS patient demonstrate hypoxemia May limit ischemic myocardial damage by increasing oxygen delivery/reduce ST elevation
Nitroglycerin (class I, level B) Analgesiatitrate infusion to keep patient pain free Dilates coronary vesselsincrease blood flow Reduces systemic vascular resistance and preload Aspirin (160-325mg chewed & swallowed) (class I, level A) Irreversible inhibition of platelet aggregation Stabilize plaque and arrest thrombus Reduce mortality in patients with STEMI
Beta-Blockers (class I, level A) 14% reduction in mortality risk at 7 days at 23% long term mortality reduction in STEMI Approximate 13% reduction in risk of progression to MI in patients with threatening or evolving MI symptoms Reassess for therapy as contraindications resolve ACE-Inhibitors / ARB (class I, level A) Start in patients with anterior MI, pulmonary congestion, LVEF < 40% Start in first 24 hours ARB as substitute for patients unable to use ACE-I
Heparin (class I, level C to class IIa, level C) LMWH or UFH (max 4000u bolus, 1000u/hr) Indirect inhibitor of thrombin Adjunct to surgical revascularization and thrombolytic / PCI reperfusion 24-48 hours of treatment Coordinate with PCI team (UFH preferred) Used in combo with aspirin and/or other platelet inhibitors Changing from one to the other not recommended
Post-STEMI patients
no significant renal failure (cr < 2.5 men or 2.0 for women) No hyperkalemis > 5.0 LVEF < 40% Symptomatic CHF or DM
Review guidelines for specific management of complications & other specific clinical scenarios
Decision making for risk stratification at hospital discharge and/or need for CABG
cardiac
of actual ACS TIMI risk score ACS risk categories per AHA guidelines Low Intermediate High
Predicts risk of death, new/recurrent MI, need for urgent revascularization within 14 days
Low risk
Intermediate
risk
High risk
Conservative therapy
Invasive therapy
Smoking cessation
Cessation-class, meds, counseling Goal 30 - 60 minutes daily Risk assessment prior to initiation DASH diet, fiber, omega-3 fatty acids <7% total calories from saturated fats
Physical Activity
Diet
Patient education
In-hospital discharge outpatient clinic/rehab Depression/anxiety assessment & treatment Social support system
Antiplatelet agent
Aspirin* and/or Clopidorgrel Statin* Fibrate / Niacin / Omega-3 Beta blocker* ACE-I*/ARB Aldactone (as appropriate)
Antihypertensive agent
Summary
ACS includes UA, NSTEMI, and STEMI Management guideline focus Immediate assessment/intervention (MONA+BAH) Risk stratification (UA/NSTEMI vs. STEMI) RAPID reperfusion for STEMI (PCI vs. Thrombolytics) Conservative vs Invasive therapy for UA/NSTEMI Aggressive attention to secondary prevention initiatives for ACS patients Beta blocker, ASA, ACE-I, Statin
60
60
40
32
30
Patients* (%)
40
20
20
0 Inpatients Outpatients
0 Inpatients
IGT IFG
Outpatients
New DM
*n = 1920 without known diabetes OGTT = oral glucose tolerance test; IGT = impaired glucose tolerance; IFG = impaired fasting glucose
ICU patients
*P < 0.01 vs normoglycemia and known diabetes
Non-ICU patients
Stress hyperglycemia in AMI: Association with mortality risk in patients without known diabetes
Reference OSullivan 1991 Lewandowicz 1979 Soler 1981 Oswald 1986 Bellodi 1989 Ravid 1975 Sewdarsen 1989 Pooled 0 1 2 3 4 5 6 7 8 9 10 11 12 13
Hyperglycemia definition (mg/dL)
Admission glucose and glucose change within 24 hours predict mortality risk
N = 1469 with AMI (n = 1219 without DM)
12 10 30-day mortality (%) 8 6 4 2 0 0 <125 125<140 140<170 Baseline glucose (mg/dL) 170 9% in 30-day mortality per 11 mg/dL glucose in first 24 hr (P = 0.002)*
Increase
Superficial Erosion
Presentation Working Dx
ECG
No ST Elevation NSTEMI
ST Elevation
Disadvantages
Risk Stratificaton Sens/Spec > CKMB Detect Recent MI Selection of Rx Detect Reperfusion
Low sens. early (< 6h) Repeat at 8-12 h if neg. Limited ability to detect late minor reinfarction
Recommendation Useful as single test to efficiently Dx NSTEMI Clinicians should familiarize themselves with Dx cutoffs in local lab
Risk Stratification
Purposes Triage / Transfer for Tertiary Care Resource Allocation Selection of Rx Strategy
Prognosis
Continuous Process Presentation: History, ACS features, Biomarkers, PEx In Hospital: Events, Response to Rx Discharge: LV Function, Arrhythmias, Ischemia
Goal = 10 min
Definite ACS
As Per Other Dx
Medical Rx
Symptoms Suggestive of ACS Possible ACS No ST elev. < 12h Lytic eligible Lytic
(D-N < 30 m)
Medical Rx
(ACEI)
Non dx ECG Neg. card. markers Observe f/u studies Neg Neg Outpt f/u Stress Pos Pos
Electrocardiographic Changes
129
Acute myocardial infarction Benign early repolarization Left bundle branch block Left ventricular hypertrophy Ventricular aneursym Coronary vasospasm Pericarditis Brugada Syndrome Subarachnoid hemorrhage
130
Initial Management in ED
1. 2. 3. 4. 5. 6. 7.
Initial evaluation with ECG in < 10 min O2 by nasal prongs, IV access, continual ECG Sublingal NTG unless SBP<90 or HR <50 or >100 Analgesia (morphine or meperidine) Aspirin (325 mg po chewed) Lipid panel, electrolytes, magnesium, CIPs Thrombolysis or PCI if ST >1mV or LBBB (door-needle < 30 min or door-balloon < 90 min)
Thrombolytics
Mechanism of Action
Streptokinase Proactivator Activator Plasminogen tPA Reteplase Tenecteplase Plasmin
Fibrin
Thrombolytics
Mechanism of Action
Streptokinase Proactivator Activator Plasminogen tPA Reteplase Tenecteplase Plasmin
Fibrin
Thrombolytics
Absolute Contraindications
Precautions
Previous hemorrhagic stroke at any time; or other strokes within one year Known intracranial neoplasm Active internal bleeding Suspected aortic dissection
Severe uncontrolled HTN (BP>180/100mmHg) Current use of anticoagulants in therapeutic dose (INR 2-3) Recent trauma (within 2-4 weeks), including head trauma or traumatic or prolonged CPR or major surgery(<3 weeks) Noncompressible vascular punctures Recent internal bleeding (within 2-4 weeks) Active PUD H/O chronic severe HTN
Thrombolytics
Monitoring Parameters
GISSI-1
(1986)
GISSI-2
(1990)
ASSENT-2
(1999)
ASSENT-3
(2001)
ISIS-2
(1988)
GUSTO-I
(1993)
GUSTO-III
(1997)
GUSTO-V
(2001)
136
Comparing outcomes