Acute Coronary Syndrome (ACS), Medicine
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Transcript of Acute Coronary Syndrome (ACS), Medicine
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ACUTE CORONARY SYNDROME
MARYAM JAMILAH BINTI ABDUL HAMID082013100002
IMS BANGALORE
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LEARNING OUTCOME•Definition•Etiology•Pathogenesis•Clinical features• Investigation•Management•Prognosis
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INTRODUCTIONAcute coronary syndrome: Encompasses both
unstable angina and myocardial infarction (MI)
Unstable angina: Characterized by new-onset or rapidly worsening angina (crescendo angina),
angina on minimal exertion or angina at rest in the absence of myocardial damage
MI: Symptoms occur at rest and there is evidence of myocardial necrosis, as demonstrated by an
elevation in cardiac troponin or CK-MB isoenzyme
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ETIOLOGY•Atherosclerosis•Arteritis•Coronary dissection• Embolism•Coronary mural thickening•Causes of coronary luminal narrowing•Congenital coronary artery disease
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PATHOGENESIS
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UNSTABLE ANGINA• Pattern of pain that is progressive with increasing frequency
• Precipitated by less effort
• Often occurs at rest. Tends to be long duration.• Induced by disruption of atherosclerotic plaques, with
superadded thrombosis, embolization & vasospasm.• Pre Infarction Angina
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MYOCARDIAL INFARCTION
TYPES•TRANSMURAL •SUBENDOCARDIAL
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LOCATION OF INFARCT
•LAD Anterior & Apical LV& 2/3 IV Septum [40--50%]
•RCA Post & Basal LV & Post 1/3 of IV Septum [30--40%]
•LCA Lateral wall of LV [15 - 20% ]
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CLINICAL FEATURESSYMPTOMS
• Prolonged cardiac pain: chest, throat, arms, epigastrium or back
• Anxiety and fear of impending death
• Nausea & vomiting
• Breathlessness
• Collapse/syncope
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PHYSICAL SIGNS• Signs of sympathetic activation: pallor, sweating,
tachycardia• Signs of vagal activation: vomiting, bradycardia• Signs of impaired myocardial function
Hypotension, oliguria, cold peripheriesNarrow pulse pressureRaised JVPS3S1 –quietApical impulse: diffuseLung crepitation
• Signs of tissue damage: fever• Signs of complications: mitral regurgitation,
pericarditis
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Condition Duration Quality Location Associated features
Unstable
angina10-20 min Pressure,
tightness, heaviness, burning
Retrosternal, often with radiation to or isolated discomfort in neck, jaw, sholders, or arms- freq. left
Precipitated by low exertion, at rest, exposure to cold, psychologic stressS4 gallop or mitral regurgitation murmur during pain
Acute MI
Variable; often >30 min
Unrelieved with nitroglycerinMay be associated with heart failure or arrhythmia
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KILLIP CLASS• 1967, Acute myocardial infarction
• Focus on physical examination & development of heart failure to predict risk
• Class I: No evidence of heart failure (mortality 6%)
• Class II: Mild to moderate heart failure (S3 gallop, rales < half-way up lung fields or elevated JVP)
• Class III: Pulmonary edema (mortality 38%)
• Class IV: Cardiogenic shock defined as SBP <90 mmHg, signs of hypoperfusion; oligouria, cyanosis, swelling (mortality 67%)
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RISK STRATIFICATION
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INVESTIGATION• Electrocardiography
•Plasma cardiac biomarkers
•Other blood tests
•Chest X-Ray
• Echocardiography
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ECG
• Confirming diagnosis
• To be repeated
• Limitation: difficult to interpret if bundle branch block (BBB) or
previous MI present
• Best seen in the leads ‘face’ ischaemic or infected area
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• Anteroseptal infarction: V1 to V4
• Anterolateral infarction: V4 to V6, aVL, lead I
• Inferior infarction: lead II, lead III, aVF, ‘reciprocal’ changes of ST depression on lead I, aVL and anterior chest lead
if involve RV– need additional leads on right pericardium• Posterior wall infarction: no ST elevation or Q waves in
standard leads, ‘reciprocal’ changes (ST-segment depress), tall R wave V1-V4
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Transmural MI
1. Proximal occlusion of a major coronary artery; ST-segment elevation (or new BBB)
2. Diminution size of R wave
3. Transmural develop Q wave
4. T wave inverted; change in ventricular repolarisation
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Subendocardial MI
• Non ST-segment elevation
• Partial occlusion of a major vessel or complete occlusion of a minor vessel
• Unstable angina, subendothelial MI
• T wave inversion
• Loss of R wave
• Absence of Q wave
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MARKER ONSET PEAK DURATION NORMAL VALUE
CK-MB 3-6 hours 18-24 hours 36-72 hours 0-5.5 ng/mlTroponins 4-10 hours 18-24 hours 8-14 days 0-0.1 ng/mlMyoglobin 1-4 hours 6-7 hours 24 hours 10-95 ng/ml (M)
10-65 ng/ml (F)LDH 6-12 hours 24-72 hours 6-8 days 125-220 U/LAST 24-36 hours 4-5 days 10-12 days 10-45 U/L
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IMMEDIATE MANAGEMENT- FIRST 12 HOURS
•Analgesia
•Antithrombotic therapy
•Anti-angina therapy
•Reperfusion therapy
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COMPLICATIONS OF ACUTE CORONARY
SYNDROME• Arrhythmias• Ischemia• Acute circulatory failure• Pericarditis• Mechanical complication• Embolism• Impaired ventricular function, remodeling and ventricular aneurysm
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LATE MANAGEMENT IN MI•Risk stratification and further investigation•Lifestyle modification•Secondary prevention drug therapy•Rehabilitation•Device
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PROGNOSIS• ¼ cases, death within few minutes without medical care• ½ death within 24 hours of onset• 40% affected patients die within first month• Reach hospital & receive medication; 28-day survival >85%• Worse prognosis with anterior and inferior infarction• Who survive acute attack;>80% live a further year75% for 5 years50% for 10 years25% for 20 years
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CONCLUSION
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REFERENCES•BRIAN R. WALKER, NICKI R. COLLEDGE, STUART H. RALSTON, IAN D. PENMAN, Davidson’s Principles & Practice of Medicine, 22nd Edition
•MICHAEL GLYNN, WILLIAM DRAKE, Hutchinson’s Clinical Methods, 23rd Edition
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THANK YOU