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SHAMMITHA.S
Unstable angina/NSTEMI
UA
-New onset(< 2 months) angina.
- That is severe (angina with mild exertion) and or frequent(> 3
episodes/day).
- accelerating angina previously chronic stable angina which
becomes more frequent, severe,prolonged, or precipitated by less
exertion than before.
- angina at rest (>20min).
- development of unstable symptoms carries a 10-20% risk of
progression to AMI .
Definition(ACS)
Acute coronary syndrome (ACS) is the name given to several syndromes which are caused
by the sudden formation of blood clots (thrombosis) within a coronary artery.
These blood clots are generally caused by rupture of a plaque in the wall of the artery. The
clots produce partial or complete blockage of the artery, leading to ischemia (insufficient
blood flow to the heart muscle).
The type of ACS syndrome that occurs depends on the degree of blockage produced by the
clot, and how long the clot persists.
When ACS is diagnosed, further stratification into categories of ST-elevation myocardial
infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), and unstable angina
[SPECTRUM] guides therapeutic decision-making.
Continued..
Management of ACS
Beta-blocker contraindicated
Yes
No
Aspirin + Clopidrogel +
Heparin + IV nitrate +
statin + beta-blocker
Aspirin + Clopidrogel
+Heparin + IV nitrate +
Statin +Ca antagonist
Control in 24 hours
Yes
No
Risk factor ++
Exercise stress ECG
Consider coronary
angiography
Positive
Negative
Medical Therapy
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Continued.
General measures
admit CCU for observations. monitor cardiac rhythm for 24-48hour. Patient are encouraged
to report any recurrence of pain.
Bed rest, sedation and analgesics should be administered as in AMI.
IV morphine is recommended for patients with or recurrent symptoms despite anti ischaemic
therapy.
BP every 15-30 min for a few hr, then every 1-2 hr.
IV line for drug administration.
Oxygen via nasal prongs.
Serial ECG and cardiac enzymes to detect AMI and silent recurrent ischaemia
Other coronary risk factors (e.g. diabetes mellitus, hypercholesterolaemia) and precipitating
factors( e.g. anaemia) should be treated.
(aspirin)
-adenosine diphosphate
receptors antagonists:
( clopidogrel,ticlopidine)
Continued..
b)Anticoagulants
-IV unfractionated heparin (UFH) decreases incidence
of MI in patients with UA.
c)Platelet glycoprotein IIb/IIIa receptor antagonists
-Abciximab(reopro)
-Epitofibatide(intergrilin)
-tirofiban(aggrastat)
Continued..
3)Beta blocker.
Propranolol or metoprolol
4)Nitrates
Sublingual nitroglycerine
IV nitroglycerin
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Continued..
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A)RISK FACTORS.
Abnormal serum lipids (elevated total cholesterol, high LDL cholesterol, low HDL
cholesterol, smoking, hypertension, family history of premature CAD, age male>55, female>
65, DM
B) ANATOMICAL COLLERATIONS.
VESSELS OCCLUDED
-left ant desc.artery
-left circumflex artery
-right coronary artery
area of infarction
ant wall on the left vent. (LV), ant part of the
septum (affect intraventricular conduction).
lateral or inf. walls of the LV & post wall of
LV.
post and inf. Surface of the LV, post part of
the septum, RV.AV node 90% cases
SA node 60% cases
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Clinical features..
-pain:- retrosternal,>20mins, radiation to the
arms, neck and jaw.
-severe and crushing in nature not relieved
by GTN.
SYMPTOMS
-Sweating, nausea,vomiting,dyspnoea,weakness,
restlessness and anxiety
-25% are asymp.&detected by ECG
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INVESTIGATIONS
1)ECG..-provides valuable information on the size, extent, age of the MI and some
anatomical correlations of vessels occluded.
a)
STEMI( Q wave infarction)
ECG changes
onset
duration
ST elevation
within mins or hours
days or weeks
T inversion
immediate or hours
several months
Q wave
hours or days
remain indefinitely
b) NSTEMI (non Q wave infarction)
- Changes are prolonged ST depression and T inversions
- NSTEMI generally results frm incomplete occlusion or spontaneous lysis of
thrombus and is associated with higher incidence of reinfarction and recurrent
ischaemia.
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Continued..
Infarct site
Ant
-small
-extensive
Anteroseptal
Anterolateral
Lateral
Inf.
Post.
Subendocardial (non Q)
2) Cardiac enzymes
Ck: creatine kinase
AST:aspartate aminotransferase
LDH-lactic dehydrogenase
HBD-hydroxybutyrate dehydrogenase
Enzymes are measured in the first 3 days following a suspected MI.
TROPONIN T
-cardiac specific protein
- undetactable in healthy people
-appears in circulation as early as 2.5 hours after onset of chest pain and remains
elevated for > 7 days post-infract
- can be measured using rapid assay kit
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Continued
Troponin I
- Not detectable in healthy individuals.
- highly specific and sensitive for myocardial
tissue injury.
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Continued
Continued
CONTINUED
b)ECHOCARDIOGRAPHY
Images the cardiac structures, pericardium, and aorta
allowing identification of regional wall motion
abnormalities, valvular abnormalities as well as
global, left and right ventricular function
c)Coronary angiography
Interventional treatment is indicated then its
performed. In the peri -infarct period, thrombus is
known to appear and vanish with spontaneous
reperfusion.
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continued
d)General investigations
FBC,BUSE, blood sugar, cholesterol( within
24 hours or 3 months after MI) CXR, serum
creatinine, coagulation profile.
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Management STEMI..
Reperfusion therapy
Thrombolysis if no
contraindication
Beta-blocker if no contraindication
IV heparin if indicated
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THANK
YOU
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