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KULIAH PENANGANAN MCI
The Management of Patients with Acute
Myocardial Infarction
Report of The American College of Cardiology/ American Heart Association
Task Force on Practice GuidelinesApril 2000
Emergency Department (ED) Algorithm/Protocol for Patients with Symptoms and Sign of AMI
Emergency nurse initiates emergency
nursing care in acute care area of ED
• Cardiac monitor • Blood studies
• Oxygen therapy • Nitroglycerin
• IV D5W • Aspirin
Ambulance presents patient
to ED lobby
Onset of symptom
s
Patient presents to ED lobby
Emergency physician evaluates patient
• History• Physical exam• Interpret ECG
ED triage or charge nurse triages patient
• AMI symptoms and signs• 12 lead ECG• Brief, targeted history
Other indicated treatment:
• Other drugs for AMI (beta-blockers, heparin, aspirin, nitrates)
• Transfer to cath lab for PTCA or surgery for CABG
AMIPatient ?
Evaluate furtherConsult
Candidate for fibrinolytic therapy ?
Fibrinolytic
therapy
Conduct education and follow-
up instruction
Admit Release
Consult
Yes No
Uncertain
YesNo
Uncertain
Differential Diagnosis of Prolonged Chest Pain
• AMI• Aortic dissection• Pericarditis• Atypical anginal pain associated with hypertrophic
cardiomyopathy• Esophageal, other upper gastrointestinal, or biliary tract
disease• Pulmonary disease
– Pneumothorax– Embolus with or without infarction– Pleurisy : infectious, malignant, or immune disease-related
• Hyperventilation syndrome• Chest wall
– Skeletal– Neuropathic
• Psychogenic
Algorithm for Initial Assessment and Evaluation of the Patient with Acute Chest Pain
Chest pain consistent with coronary ischemia
• Continue evaluation/monitoring in Emergency Department or Chest Pain Unit
• Serial serum cardiac marker levels-MB CK subforms
• Serial ECGs• Consider noninvasive
evaluation of ischemia• Consider alternative
diagnoses
Within 10 minutes• Initial evaluation • 12 lead ECG• Establish IV access • Establish continuous ECG
monitoring• Blood for baseline • Aspirin 160 – 325 mg chewed
serum cardiac markers
Therapeutic/Diagnostic tracking according to 12-lead ECG results
• Anti-ischemia Therapy
• Analgesia
Assess suitability for reperfusion :
• ? Contraindications for fibrinolysis
• Availability and appropriateness of primary angioplasty
Initiate anti-ischemia therapy• Beta-blocker• NitroglycerinAnalgesia
No evidence of MI or
ischemia
MI or demonstrable ischemia
Admit to unit of
appropriate intensity
Admission blood work
Discharge with follow-up as appropriate(Goal 8-12
hours)
Admission blood work
- CBC- Electrolytes, BUN,
creatinine- Lipid profile
Initiate fibrinolysi
s if indicated.Goal : 30 minutes
from entry to
ED
Primary PTCA, if
available and
suitable.(Goal : PTCA
within 90 30
minutes)
Admit - CCU
Enzymatic Criteria for Diagnosis of Myocardial Infarction
Serial increase, then decrease of plasma CK-MB, with a change > 25% between any two values
CK-MB > 10-13 U/L or > 5% total CK activity
Increase in MB-CK activity > 50% between any two samples, separated by at least 4 hrs
If only a single sample available, CK-MB elevation > twofold
Beyond 72 hrs, an elevation of troponin T or I or LDH-1 > LDH-2
Recommendations for the Management of Patients with ST Elevation
ST elevation
Eligible for
fibrinolytic therapy
Fibrinolytic therapy
contraindicated
Not a candicate for reperfusion
therapy
Persistent symptoms ?
Fibrinolytic therapy
Primary PTCA or CABG Other medical
therapy : ACE inhibitors? Nitrates
Anticoagulants
Consider Reperfusi
on Therapy
No Yes
12 h
> 12 h
Aspirin; Beta-blocker
Contraindications and Cautions for Fibrinolytic Use in Myocardial
Infarction
Absolute contraindications Previous hemorrhagic stroke at any
time : other strokes or cerebrovascular events within 1 yr
Known intracranial neoplasm Active internal bleeding (does not include
menses) Suspected aortic dissection
Contraindications and Cautions for Fibrinolytic Use in Myocardial
InfarctionCautions/Relative Contraindications Severe uncontrolled hypertension on presentation (BP >
180/110 mmHg) History of prior cerebrovascular accident or known
intracerebral pathology not covered in contraindications Current use of anticoagulants in therapeutic doses (INR
2-3); known bleeding diathesis Recent trauma (within 2-3 wks), including head trauma Noncompressible vascular punctures Recent (within 2-4 wks) internal bleeding For streptokinase/anistreplase : prior exposure (especially
within 5d-2y) or prior allergic reaction Pregnancy Active peptic ulcer History of chronic hypertension
Recommendations for the Management of Patients with Non-ST Elevation MI
ST depression/T-wave inversion :
Susptected AMI
Patients without prior beta-blocker therapy or who are
inadequately treated on current dose of beta-blocker
Heparin + Aspirin; Nitrates for recurrent
anginaAntithrombins : LMWH – high-risk
patientsAnti-Platelets : GpIIb/IIIa inhibitor
Persistent symptoms in patients with rpior beta-blocker therapy or who cannot tolerate beta-
blockersEstablish adequate beta-
blockadeAdd calcium antagonist
High-risk patient :1. Recurrent ischemia
2. Depressed LV function3. Widespread ECG
changes4. Prior MI
NoYes
Clinical stability
Assess clinical status
Catheterization : Anatomy suitable for
revascularization ?
Revascularization (PTCA, CABG)
Medical Therapy
Continued observation in hospital
Consideration of stress testing
Pharmacologic Management of Patients with MI
Heparin RecommendationClass I Recommendations
1. In patients undergoing percutaneous on surgical revascularization
Class IIa Recommendations
1. Intravenously in patients undergoing reperfusion therapy with alteplase/reteplase. See table below for dosing :
1999 Recommendations
Bolus Dose 60 U/kg
Maintenance 12 U/kg/hr
Maximum 4000 U bolus1000 U/h if > 70 kg
aPTT 1.5-2.0 x control(50-70 sec) for 48 hrs
Pharmacologic Management of Patients with MI
2. Intravenous unfractionated heparin (UFH) or low molecular weight heparin (LMWH) subcutaneously for patients with non-ST elevation MI.
3. Subcutaneous UFH (eg. 7.500 b.i.d) or low molecular weight heparin (eg. Enoxaparin 1 mg/kg b.i.d) in all patients not treated with fibrinolytic therapy who do not have a contraindication to heparin. In patients who are at high risk for systemic emboli (large or anterior MI, AF, previous embolus, or known LV thrombus), intravenous heparin is preferred.
4. Intravenously in patients treated with nonselective fibrinolytic agents (streptokinase, anistreplase, urokinase) who are at high risk for systemic emboli (large or anterior MI, AF, previous embolus, or known LV thrombus).
MI Management Summary
Initial Management in ED Initial evaluation with ECG in < 10 minutes O2 by nasal prongs, IV access, continual ECG
Sublingual TNG unless SBP < 90 or HR < 50 or > 100
Analgesia (MS or meperidine) Aspirin (160-325 mg chwed) Lipid panel, electrolytes, magnesium,
enzymes Fibrinolysis or PTCA if ST elevation > 1 mV
or LBBB (goal : door-needle < 30 minutes or door-dilatation < 90 minutes)
MI Management Summary
MI Management in 1st 24 hours Limited activity for 12 hrs, monitor 24
hrs No prophylactic antiarrhythmics IV heparin if : a) large anterior MI; b) PTCA;
c) LV thrombus; or d) alteplase/reteplase use (for ~ 48 hrs)
SQ heparin for all other MI (7,500 u b.i.d) Aspirin indefinitely IV TNG for 24-48 hrs if no / HR or BP IV beta-blocker if no contraindications ACE inhibitor in all MI if no hypotension
MI Management Summary
In-Hospital Management in Aspirin indefinitely Beta-blocker indefinitely ACE inhibitor (DC at ~ 6 wks if no LV
dysfunction) If spontaneous of provoked ischemia –
elective cath Suspected pericarditis – ASA 650 mg q4-6
hrs CHF – ACE inhibitor and diuretic as needed Shock – consider intra-aortic balloon pump
+ cath with PTCA or CABG RV MI-fluids (NS) + inotropics if hypotensive
The Management of
Patients with Chronic
Stable Angina
Report of The American College of Cardiology/ American Heart Association
Task Force on Practice GuidelinesMarch 2000
Clinical Assessmenta. Recommendations for History and PhysicalAngina is a clinical syndrome characterized by discomfort in the chest, jaw, shoulder, back, or arm. It is typically aggravated by exertion or emotional stress and relieved by nitroglycerin. Angina usually occurs in patients with CAD involving 1 large epicardial artery, but can also occur in individuals with other cardiac problems
Clinical Assessmentb. Recommendations for Initial Laboratory
Tests, ECG, and Chest X-Ray for Diagnosis1. Hemoglobin2. Fasting glucose3. Fasting lipid panel, including total cholesterol,
HDL cholesterol, triglycerides, and calculated LDL cholesterol
4. Rest electrocardiogram (ECG) in patients without an obvious noncardiac cause of chest pain
5. Rest ECG during an episode of chest pain6. Chest x-ray in patients with signs or symptoms
of congestive heart failure, valvular heart disease, pericardial disease, or aortic dissection/aneurysm
TreatmentRecommendations for Pharmacotherapy to prevent MI
and Death
and Reduce Symptoms
Class I1. Aspirin in the absence of contraindications
2. Beta-blockers as initial therapy in the absence of contraindications in patients with prior MI
3. Beta-blockers as initial therapy in the absence of contraindications in patients without prior MI
4. Calcium antagonists and/or long-acting nitrates as initial therapy when beta-blockers are contraindicated
5. Calcium antagonists and/or long-acting nitrates in combination with beta-blockers when initial treatment with beta-blockers is not successful
6. Calcium antagonists and/or long-acting nitrates as a substitute for beta-blockers if initial treatment with beta-blockers leads to unacceptable side effects
7. Sublingual nitroglycerin or nitroglycerin spray for the immediate relief of angina
8. Lipid-lowering therapy in patients with documented or suspected CAD and LDL cholesterol > 130 mg/dL with a target LDL of < 100 mg/dL
TreatmentRecommendations for Pharmacotherapy toprevent MI and Death and Reduce
Symptoms
Class IIa
1. Clopidogrel when aspirin is absolutely contraindicated
2. Long-acting nondihydropyridine calcium antagonists
instead of beta-blockers as initial therapy
3. Lipid-lowering therapy in patients with documented or
suspected CAD and LDL cholesterol 100 to 129 mg/dL,
with a target LDL of 100 mg/dL
Treatment
Basic Treatment /
Education
Aspirin and Anti-anginal
therapy
Beta-blocker and Blood
pressure
Cigarette smoking and
Cholesterol
Diet and Diabetes
Education and Exercise
TreatmentCoronary Disease Risk Factors and Evidence thatTreatment can Reduce the Risk for CoronaryDisease Events
1. Treatment of hypertension according to NHLBI
Joint National Conference VI Report on Prevention, Detection, and Treatment of High Blood PRessure
2. Smoking cessation therapy
3. Management of diabetes
4. Exercise training program
5. Weight reduction in obese patients in the presence of hypertension, hyperlipidemia, or diabetes mellitus
Clinical AssessmentChest Pain
History suggests intermediate to high probability
of CAD
Intermediate or high risk unstable
angina?
Low
probability
of CAD
History and appropriate
diagnostic tests demonstrate
noncardiac cause of chest pain
Reconsider probability or CAD. Initiate
primary prevention
No Yes No
Features of “intermediate- or high-risk” Unstable Angina :
• Rest pain lasting > 20 min
• Age > 65 years• ST and T wave change• Pulmonary edema
Treat Appropriately
Recent MI, PTCA, CABG ?
Conditions present that could cause
angina? e.g., severe anemia,
hyperthyroidism
See AHCPR Unstable Angina
GuidelineSee
appropriate ACC/AHA Guideline
Angina resolves with treatment of
underlying condition ?
Yes
Yes
Yes
No
No
Yes
Yes
Severe primary valvular lesion ?
Conditions present that could cause
angina? e.g., severe anemia,
hyperthyroidism
Enter Stress Testing/Angiograp
hy Algorithm
Angina resolves with treatment of
underlying condition ?
History and/or exam suggests valvular, pericardial disease
or ventricular dysfunction
See AHCPR ACC/AHA
Valvular Heart Disease
Guideline
Echocar-diogram
YesYes
LV Abnormality ?
High probability of CAD based on
history, exam, ECG
Indication for prognostic/risk assessment ?
Empiric therapy
Enter Treatment Algorithm
Yes No
Enter Stress Testing/Angiograp
hy Algorithm
Factors necessary to determine the need for risk assessment
• Comorbidity• Patient Preferences
No
No
No
Yes
Yes
No
Yes Yes
No
Stress Testing/ Angiography
Contraindications to stress testing ?
No
Yes
No
Need to guide medical
management ?
Yes
For diagnosis (and risk stratification) in patients with chest pain and an intermediate probability of CAD
ORFor risk stratification in pts with chest
pain and a high probability of CAD
Symptoms or clinical findings
warranting angiography ?
Patient able to exercise ?
Previous coronary
revascularization ?
Consider coronary
angiography
Pharmacological imaging study
Yes
Yes
No
No
Yes
Yes
No
No
Test results suggest high-risk
Resting ECG interpretable ?
Perform exercise test
No
Yes
Adequate information on diagnosis and
prognosis available?
Exercise imaging study
Consider coronary
angiography revascularization
Consider imaging study
angiography
Test results suggest high-risk
?
Adequate information on diagnosis and
prognosis available?
Consider coronary
angiographyEnter
Treatment Algorithm
Yes
No
Yes
Yes
No
No
Yes
No
Treatment
Anti-anginalDrug
Treatment
No
Yes
No
Chest pain• Intermediate to high probability of
CAD• High-risk CAD unlikely• Risk stratification complete or not
required
Yes
Sublingual NTG
History suggests Vasospastic angina?
(Prinzmetal)
Beta-blocker therapy if no contraindication (Espec. If prior
MI or other indication)
Successful Treatment ?
Yes
Yes
Yes
Medications or conditions that provoke or exacerbate
angina?*
Add or substitue CA channel blocker if no contraindication
Ca channel blocker, Long acting nitrate
therapy
Treat appro-priately
Successful Treatment ?
Successful Treatment ?Yes
Yes
Serious contraindication
Add long-acting nitrate therapy if no contraindication
Consider revas-cularization
therapy
Serious contraindication
Successful Treatment ?Yes
No
Yes
No
Education and Risk Factor Modification
Yes
Initiate educational program
Aspirin 81 to 325 mg OD if no
contraindication
Cigarette Smoking
Cholesterol High ?
Blood Pressure High ?
Routine Follow Up including (as appropriate) : Diet, Exercise program, Diabetes
management
Clopidogrel
Smoking Cessation program
See NCEP Guidelines
See JNC VI Guidelines
Serious adverse effect
or contraindicatio
n
No
No
Yes
Yes
Yes
Treatment* Conditions that exarcebate or provoke angina
Medications :
• Vasodilators
• Excessive thyroid replacement
• vasoconstrictors
Other medical problem
• Profound anemia
• Uncotrolled hypertension
• Hyperthyroidism
• hypoxemia
Other cardiac problems
• Tachyarrhythmias
• Bradyarrhythmias
• Valvular heart disease (espec AS)
• Hypertrophic cardiomyo-pathy
Clinical Classification of Chest Pain
Typical angina (definite)(1) Substernal chest discomfort with a characteristic quality and duration that is (2) provoked by exertion or emotional stress and (3) relieved by rest or nitroglycerin
Atypical angina (probable)Meets 2 or the above characteristics
Noncardiac chest painMeets of the typical angina characteristics
Pretest Likelihood of CAD in Symptomatic Patients According to Age and Sex
Nonanginal Chest Pain
Atypical Angina
Typical Angina
Age, y Men Women
Men Women Men Women
30 – 39 4 2 34 12 76 26
40 – 49 13 3 51 22 87 55
50 – 59 20 7 65 31 93 73
60 - 69 27 14 72 51 94 86
COR PULMONALE CHRONICUM (CPC)
Hipertrofi & dilatasi ventrikel kanan sebab hipertensi pulmonal akibat peny. parenkim dan/atau vaskuler paru (antara a. pulmonal utama dan masuknya vv pulmonal ke atrium kiri)
Etiologi UtamaPenyakit paru obstruktif khronis (PPOK) akibat bronkhitis khronis atau emfisema paru
ETIOLOGY OF PULMONARY HEART DISEASE (1)I. DISEASES AFFECTING THE PULMONARY VASCULATURE
A. Primary diseases of the arterial wall(1) Primary pulmonary hypertension(2) Granulomatous pulmonary arteritis(3) Toxin-induced pulmonary hypertension
a. Aminorex fumarateb. Intravenous drug abuse
(4) Chronic liver disease(5) Peripheral pulmonic stenosis
B. Thrombotic disorders(1) Sickle cell diseases(2) Pulmonary microthrombi
C. Embolic disorders(1) Thromboembolism (3) Other embolism (amniotic fluid, air)(2) Tumor embolism (4) Schistosomiasis and other parasitic
diseasesII. PRESSURE ON PULMONARY ARTERIES BY MEDIASTINAL TUMORS,
ANEURYSMS, GRANULOMATA, OR FIBROSISIII. DISEASES OF THE NEUROMUSCULAR APPARATUS AND CHEST WALL
A. Neuromuscular weakness D. Pleural fibrosisB. Kyphoscoliosis E. Sleep apnea syndromesC. Thoracoplasty F. Idiopathic hypoventilation
IV. DISEASES AFFECTING AIR PASSAGES OF THE LUNG AND ALVEOLI
A. Chronic obstructive pulmonary diseases
B. Cystic fibrosis
C. Congenital development defects
D. Infiltrative or granulomatous diseases
(1) Idiopathic pulmonary fibrosis
(2) Sarcoidosis
(3) Pneumoconiosis
(4) Scleroderma
(5) Mixed connective tissue disease
(6) Systemic lupus erythematosus
(7) Rheumatoid arthritis
(8) Polymyositis
(9) Eosinophilic granuloma
(10) Malignant infiltration
(11) Radiation
E. Upper airways obstruction
F. Pulmonary resection
G. High-altitude disease
ETIOLOGY OF PULMONARY HEART DISEASE (2)
PATHOGENESIS OF COR PULMONALEChronic lung disease
Reduction in pulmonary Hypoxia vascular bed
Acidosis andhypercapnia
Polycythemia and hyperviscosity Pulmonary hypertension
Hypertrophy and dilatationof the right ventricle
Right ventricular failure
PEMERIKSAAN PENDERITA CPC
Klinis :• Pemeriksaan fisik susah karena emfisema
pulm pada PPOK• Systolic parasternal heave• Tricuspid regurgitation• P2 >• Tanda gagal jantung kanan
EKG : Sangat spesifik, kurang sensitif
ELECTROCARDIOGRAPHIC CHANGES IN COR PULMONALE (1)ECG CRITERIA FOR COR PULMONALE WITHOUT
OBSTRUCTIVE DISEASE OF THE AIRWAYS
1. Right-axis deviation with a mean QRS axis to the right of + 110
2. R/S amplitude ratio in V > 1
3. R/S amplitude ratio in V < 1
4. Clockwise rotation of the electrical axis
5. P-pulmonale pattern
6. S Q or S S S pattern
7. Normal voltage QRS
o
1
6
1 3 1 2 3
ELECTROCARDIOGRAPHIC CHANGES IN COR PULMONALE (2)
ECG CHANGES IN CHRONIC COR PULMONALE WITH OBSTRUCTIVE DISEASE OF THE AIRWAYS1. Isoelectric P waves in lead I or right-axis deviation of the P
vector2. P-pulmonale pattern (an increase in P-wave amplitude in II,
III, AVf)
3. Tendency for right-axis deviation of the QRS
4. R/S amplitude ratio in V6 < 1
5. Low-voltage QRS
6. S1Q3 or S1S2S3 pattern
7. Incomplete (and rarely complete) right bundle branch block
8. R/S amplitude ratio in V1 > 1
9. Marked clockwise rotation of the electrical axis10. Occasional large Q wave or QS in the inferior or mid-
precordial leads, suggesting healed myocardial infarction
X-Thorax • Jantung dapat normal, atau membesar
dengan apeks terangkat• Dilatasi konus pulmonal + cabang besarnya,
sedangkan cabang-cabang kecil tak terlihat karena vasokonstriksi
• PPOK : kelainan paru-paru terlihat
Ekhokardiografi Doppler - ekho :
- Tek. a. pulmonalis- TR- RV dilatasi
HIPOKSIA• Sebab terpenting hipertensi pulmonal pada
PPOK• Vasokonstriksi pulmonal (langsung atau
lewat pelepasan zat vasoaktif)• Proliferasi sel endotel dan penebalan intima
arteriol• Hipertrofi tunica media a. pulmonal• Vasodilatasi terhambat
PENGELOLAAN
• OKSIGENDiberikan kontinu 1-2 l/menit, dapat memperbaiki prognosis karena mengurangi vasokonstriksi pulmonal dan memperbaiki hipoksia
• DIGITALISHanya bila juga ada gagal jantung kiri atau pada gagal jantung kanan akut
• THEOPHYLLINEBronkhodilatasi, fungsi RV - LV membaik
• BETA-ADRENERGIC AGONISTSBronkhodilator
• VASODILATOR ?• Atasi penyakit paru penyebabnya !!!
Dopamine
Effective renal plasma flow
Filtration fraction
Peritubular oncotic pressureTubular Na - Hexchange
+ +PCO
PCO
2
2
Plasma reninactivity
Angiotensin II
Plasmaaldosterone
Argininevasopressinlevel
Na retention:edema
+ ANP
Dopamine
Natriuresis
DopamineANP
ANP
ANPH O retention;
hyponatremia2
PRA
ANG II
AVP
RBF
Mechanisms of salt and water disturbance in patients with COPD
