This document defines and describes acute coronary syndrome, which includes unstable angina and myocardial infarction. It discusses the etiology, pathogenesis, clinical features, investigations, management, and prognosis of acute coronary syndrome. The key points are that acute coronary syndrome is caused by atherosclerosis and involves plaque disruption and thrombosis in the coronary arteries, leading to symptoms such as chest pain. Diagnosis involves electrocardiography, cardiac biomarker tests, and imaging. Treatment focuses on analgesia, antithrombotics, reperfusion therapy, and long-term secondary prevention. Prognosis depends on factors like the infarct location and timeliness of treatment.
3. INTRODUCTION
Acute 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
6. 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
8. 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% ]
9.
10.
11.
12.
13. CLINICAL FEATURES
SYMPTOMS
• Prolonged cardiac pain: chest, throat, arms, epigastrium or back
• Anxiety and fear of impending death
• Nausea & vomiting
• Breathlessness
• Collapse/syncope
14. PHYSICAL SIGNS
• Signs of sympathetic activation: pallor, sweating, tachycardia
• Signs of vagal activation: vomiting, bradycardia
• Signs of impaired myocardial function
Hypotension, oliguria, cold peripheries
Narrow pulse pressure
Raised JVP
S3
S1 –quiet
Apical impulse: diffuse
Lung crepitation
• Signs of tissue damage: fever
• Signs of complications: mitral regurgitation, pericarditis
15. Condition Duration Quality Location
Associated
features
Unstable
angina
10-20 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 stress
S4 gallop or mitral
regurgitation murmur
during pain
Acute MI
Variable;
often >30
min
Unrelieved with
nitroglycerin
May be associated
with heart failure
or arrhythmia
16. 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%)
19. 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
20. • 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
21. 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
22. 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
23.
24. MARKER ONSET PEAK DURATION NORMAL VALUE
CK-MB 3-6 hours 18-24 hours 36-72 hours 0-5.5 ng/ml
Troponins 4-10 hours 18-24 hours 8-14 days 0-0.1 ng/ml
Myoglobin 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/L
AST 24-36 hours 4-5 days 10-12 days 10-45 U/L
28. LATE MANAGEMENT IN MI
•Risk stratification and further investigation
•Lifestyle modification
•Secondary prevention drug therapy
•Rehabilitation
•Device
29. 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 year
75% for 5 years
50% for 10 years
25% for 20 years
31. 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
Patients who experience chest pain in the 24 hours preceding a heart attack
Tetrazolium chloride
-indicate cellular respiration
-redox indicator
-white compound reduced to triphenylformazan in living tissue (cz dehydrogenase)
Episodes of myocardial ischemia are due to an abrupt reduction in coronary blood flow caused by thrombosis or spasm (supply-led ischemia). In contrast, stable angina is related to a fixed obstruction and usually precipitated by an increase in myocardial oxygen demand (demand-led ischemia)
Other blood tests; leukocytosis peak 1st day, ESR and CRP increase
CXR; pul edema, heart size usually normal but cardiomegaly can be there due to pre-existing myocardial damage
Echo;
-assess vent f(x)
-detect complications; mural thrombi, cardiac rupture, vent septal defect, mitral regurgitation, pericardial effusion
T wave inverted persist even aftr ST-segment returned to normal so can IDENTIFY AGE OF INFARCT
Anteroseptal infarction: V1 to V4
Anterolateral infarction: V4 to V6, aVL, lead I
inferiorlateral: lead II, lead III, aVF, ‘reciprocal’ changes of ST depression on lead I, aVL and anterior chest lead
