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Myocardial Infarction
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If ECG shows ST elevation, treatment approach would be revascularization. If within 2 hours patient
can have revascularization (balloon+stent, thrombolytic agents): ischemia is reversible. Later,
thrombus will be calcified, will be harder to treat.
Site of infarction will be reflected in leads (we didn’t really talk about this any further…)
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Q-wave infarcts:
• First area to suffer is endocardium. In less that 20-40 minutes, there is injury to the area of
ischemia.
• If pain lasts for 30 minutes or more, ischemia and injury extends, and necrosis begins. Moves
outwards towards pericardium. Longer pain (ischemia)? More extensive damage will be seen. In
24 hours, complete necrosis (pt. will not survive 24 hours of ischemia) to a large area of the
heart.).
• Collateral circulation: develops during physical activity, exercise. If this has developed in a
patient, the damage will be less, as the blood can bypass the blocked vessel.
(Know these!)
ECG findings:
Negative T: below baseline.
ST depression (down-sloping or horizontal): sign of ischemia. See this during stress test.
ST elevation: sign of injury
Q wave: sign of necrosis (transmural MI)
Most important in MI: Maintain cardiac output. Arrhythmia will cause damage. Time is essential.
DDX: Pericarditis:
Other cases where you might see ST elevation: pericarditis, but in pericarditis, don’t see Q-wave (no
necrosis).
DDX LECTURE 18, NOVEMBER 17TH – PAGE 2
Will also complain of central chest pain, but it is not associated with physical exertion. Not relieved
with rest. Pain will be worsened in supine position: alleviated by sitting and leaning forward.
Description of pain is different:
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Laboratory findings for MI: don’t need to know number of hours, but understand which markers
present when, for how long.
Troponins: remain elevated for up to two weeks (in contrast with other enzymes (CPK, MB))
If there is treatment but the patient still experiences pain, what does this mean? Continuing heart
damage: growing MI.
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Leukocytes are not a specific marker.
Myocardial imaging:
You will see cold spot in area of necrosis
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• Reperfusion:
• Thrombolytic therapy: IV admin of agents that can lyse coronary thrombus. Have to admin in
4-6 hours: reduces mortality by 25%. 50% if administered within 1 hour.
• TIME IS CRUCIAL!!!!!
• Emergency PTCA
• Coronary bypass surgery.
After treatment, patients should go for stress test in 6 months, then in a year. Stats show that re-
stenosis (stenosis again) may occur in this period. Want to see progression, what coronary tree looks
like.
See risks and CI for thrombolytic therapy.
Prognosis:
Depends on ventricle involved, other health concerns (diabetes: less positive outcome), other
systemic diseases of vessels.
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DDX LECTURE 18, NOVEMBER 17TH – PAGE 3
Cardiogenic shock
Extremely severe condition after transmural MI
Very small chance of survival (65% mortality: maybe even more)
Unconscious: not enough blood pressure to maintain consciousness
Decreased urine production: not enough blood supply to kidney: could cause acute renal failure.
2. Dressler’s syndrome
• Autoimmune: from damage to myocardium and pericardium.
• Benign disorder.
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See algorithm of chest pain. Help to rule out non-cardiac sources of chest pain.
See back page of note package for dietary suggestions.
See separate page for Cardiac and non-cardiac causes of chest pain
Case #1:
A 57-year old auto salesman who is hypertensive and a heavy cigarette smoker, describes a
pressure-like sensation that developed for the first tie 3 weeks before The discomfort which begins in
the retrosternal area, radiates to the left side of lower jaw, occurs when he walks rapidly in cold air,
and more recently develops at rest. Careful history reveals that it lasts for 10-15 minutes, but an
especially severe episode awakened him the night before and lasted nearly a half hour before
resolving spontaneously. Except for a blood pressure of 150/100mmhg the physical examination
findings are normal. An ECG obtained when pain had disappeared reveals deep and symmetrical T
wave inversion in leads V1 to V4. After admission and the iv administration of Nitroglycerin and
heparin, the patient’s condition stabilizes. An acute myocardial infarction is excluded.
DDX: Unstable Angina. Beginning to become worse at rest: he had it already. (Any changes in
previous patterns of angina = unstable.)
Risk factors: Smoking, hypertension, age, gender.
Case #2: (We saw this case on Nov. 15th. This is the complete version)
A 66-year old man complains of chest pain and shortness of breath for 2 days. His current problems
began abruptly after a “cold” 2 days ago. He noted shaking chills and a cough, productive of rust-
coloured sputum. The chest pain is right-sided, sharp, and much worse with deep breathing and
coughing. The medical history is significant for chronic alcoholism and smoking.
The patient appears acutely ill. His temperature is 104F and his breathing is rapid and shallow. A
DDX LECTURE 18, NOVEMBER 17TH – PAGE 4
lung examination reveals that the right lower lobe has decreased breath sounds with some crackles
in the periphery, dullness to percussion and increased vocal fremitus. Cardiac examination is normal,
and the rest of the physical examination reveals nothing abnormal.
DDX: Pneumonia: abrupt onset, association with cold, shaking chills, cough. This doesn’t fit picture
of angina. Chest pain worse with breathing and coughing: in angina, pain has nothing to do with
breathing and coughing. Fever. No elevation in angina.
Crackles: possible consolidation, accumulation of fluid in alveoli.
Dullness on percussion (consolidation, fluid): this is nothing to do with angina., increased vocal
fremitus increases over consolidated area. Amplifies sound transmission. Decreased or absent over
areas of fluid accumulation.