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Myocardial infarction

Etiology - necrosis or irreversible damage of the myofibril caused by a prolonged ischemia, occlusion of coronary
artery due to thrombosis.
Classification - Acc investigation of ECG: ST elevation, Non-ST elevation
1. Acc etiology :
- caused by atherosclerosis 

- caused by other reasons such as trauma, embolism, atheritis 

2. Acc Clinical Pic 
- Typical 

- Atypical : Asthmatic form, Abdominal form, Cerebral form, Arrythmic form, Painless/Silent form
3. Location: Anterior, Posterior, Lateral, apex, septum 

4. Stages: Acutus, Acute, Subacute, Chronic 

5. Morphological: Transmural, Subendocardial 

6. Acc to square: Transmural, Q MI, Non Q MI 

Pathogenesis Pathogenesis : 

- coronary thrombosis/ stenotic coronary sclerosis spasm/ disruption of atherosclerotic plaque, vasospasm, 
platelet aggregation leading to coronary
artery occlusion. 

- no blood supply to the myocardium, necrosis of the myocardium. 

- 1st period: Moderate ischemia-activity decreased, slow. 

- 2nd period(After 30 minutes): Deep ischemia-no activity. Cells don‘t function. 

- 3rd period: Damage of myofibrils-Necrotic mass. Irreversible pathological stage. 

Stage MI dev
MI : Q type MI : Non Q-type Atypical variant
Clinical pict 1. Asthmatic Type :
- Pain is absent; attack of symptom like cardiac

- tachypnoe, cold sweat, palpitation, fear of
death, weakness, orthopnoe, apnoea & rales. 

- inspiratory dyspnea, tachycardia, dizziness,
peripheral cyanosis, intestitial edema 

- 1st Group: Old people 65-70 years, with

- 2nd Group: Previous MI. Secondary infarction 

2. Arrythmic Type :
- without pain. In some case, Accompanied by
pain at rest 

- Presence of palpitation, dizziness, fast &
irregular pulse. 

- Often in patient more than 40 years old. 

- sudden attack, ventricular arrhythmia,
tachycardia, extrabeats, transient arrythmias. 

- predispose to fibrillation 

3. Central/Brain Dependant Type :
- like stroke; loss of consciousness, weakness,
dizziness, vomiting, vertigo, nausea, headache.

- Impaired movement extremities one side,
impaired feeling of skin, paresis of muscle. 

- When infarction area is big, cause

4. Silent Infarction :
- No symptoms showing heart disorder 

- Might have discomfort in chest, pain in the
teeth or tip of finger. 

- necrosis isn‘t so large. 

- sudden weakness, soft vertigo, diminish
of heart 

- normally for pt with nerve insensitivity eg;

5. Abdominal variant:
- Abdominal(epigastric pain). GIT
dysfunctions (meteorism, diarrhea, nausea,

- Bradycardia. Paralysis of bowel. 

- Irritation of phrenic/vagus nerve 

- associated with irritation of intestine
(belching, distention, flatulence) 

- palpation in upper abdomen is painful. 

Investigation 1. Lab Test :

- creatine phosphokinase (MB fraction). after pain appear at the 1 6 hours & peak for the next 24hours. Next day, enzyme is

st rd th
- AST, ALT. It increases gradually in 1 6 hours & peak next day till 3 -4 day; then disappears. 

th th
- LDH. Max 5 -7 day after onset of infarction & disappear after 2weeks. 

st nd
- Troponins are elevated at end of 1 & 2 day. 

st st
- Leucocytosis Reactive – Max 1-2days; disappears at end of 1 week. ESR ↑ in 1 week, slowly 
disappears during 10-14 days.
↑ band leucocytes (in 1 1-3days). 

- C-rective proteins increases till 1 week 

st nd
- transmural infarction: Aneosinophilia in 1 /2 after infarction, it reappears again. ↑ myoglobin in 
blood. transient

3. ECG 

Transmural Type: ↑ ST
a. Acutus: 6 hours, increase ST with T wave 

b. Acute: 6 hours to 5th/7th day 

- R disappears. 

- ST elevation presence. 

- QS complex/syndrome. 

- Elevated T-wave. 

c. Subacute: QS, prominent –ve T
d. Chronic: QS wave, ST normalizes (after 8th week), +ve T Non Transmural Type :
- Subendocardial & intramural. 

- It can stay 2 days after onset of infarction. 

- Change in ST & T-wave only; Q-wave don‘t exist. (Last more than 30 minutes) 

- Comes quick, 2nd/3rd day S may disappear. (-T) till 8th week. 

- After 8 weeks, there is no trace of any changes. 

- So if it is transmural, after 8th week, we will not see (-T) 
non-Q wave MI - no ST elevation and no Q wave. Q wave MI - ST elevation,
and evolve Q wave 

Ultrasound :
- discoordination of myofibrils. No contraction 

- aneurysm of heart, dyskinesis or akinesis of myofibrils. 

Imaging methods :
- many changes in MI. using contrast 

- echocardiography: abnormality of wall motion, estimation of Left Ventricle function. 

- angiography abt the coronary vessels. 

Auscultation: S3, S4, Open-snap phenomenon. S2 Accentuation. Low S1. 

Treatment reduce the chest pain: - Nitrates

4. - beta blockers (Metoprolol/Esmolol) 

5. - morphine sulfate To stop pain: 

7. - Analgesic – Analgine 

8. - Sublingual Nitroglycerin 

9. - Narcotics: Morphine 

10. - Neuropeptic drug: Doperidole + Fentanyl 

Thrombolytic treatment / Fibrolytics:
- Streptokinase.
- Urokinase
- Tissue type plasminogen activator
antiplatelet /antiaggregant agents: Aspirin anticoagulating / antithrombin agents:
- Heparin (unfractioned heparin) 

- Enoxaparin (Lovenox). 

- Dalteparin (Fragmin) 

Antianginal Antiarrhythmic Fibrinolytic Anticoagulant Symptomatic therapy
6. morphine 
 10. sustained ventricular Anticoagulant Therapy:
7. nitroglycerin 
 tachycardia - Lidocaine 
 Heparin, Warfarin
8. 11. 

beta blockers -metoprolol ventricular fibrillation 

9. Opioid(synthetic 11. - prompt defibrillation - Unfractioned heparin -
alkaloid)+Neuroleptic (200-360 J) 
 initial dose is i/v 10000, then
Neuroleptanalgesia 12. -recurrences treated with 5000 or 2500 unit acc to
Fentanyl or Droperidol 
 lidocaine infusion 
 weight of the pt. 

c. atrial fibrillation -IV
digoxin or IV amiodarone, - low molecular weight
verapamil, cloradole heparin (LMWH).
d. sinus bradycardia - IV Fibrinolytic therapy: 

13. - tPA, streptokinase,
- Quinidine
tenecteplase, reteplase,
- Amiodarone/Sotalol
Treatment alteplase, urokinase,
12. - Ca-channel

antagonist: Verapamil (for
supraventricular arrhythmia)
14. -converts plasminogen to

 plasmin and lysis the
13. - Beta-blockers: thrombi. 

reduce chance of ventricular
arrhythmia, reinfarction. 15. - side effects like allergy,
Supraventricular arrhythmia. hemorrhage, arrhythmias,

Propanol, Metaprolol 
 relapsing of the thrombosis.
14. - AV Block – 
- Contraindications: 
Atropine, Euphiline or internal bleeding Aortic
hemorrhagic shock
Intracranial neoplasm 

Aneurysms of the heart Rupture of myocardium Pulmonary edema Dressler’s syndrome
symptom : dyspnea at rest.
- acute coronary failure, Tachypnea, tachycardia,
edema of the lung, wheezing, HT
cardiogenic shock, rupture Diagnosis :
of the aneurysm, 15. - Xray- diffuse haziness, and
arrhythmias, Kerley B lines of interstitial
thromboembolism of edema. 

pulmonary, acute LV insuff, 16. - echocardiography – to diff
acute pericardiatis betw cardiogenic or
noncardiogenic cause. 

17. - ballon flotation catheter –
measures diff betw high and
normal pressure causes of
pulmonary edema 

Types Pathophysiology Clinical picture Diagnostic criteria Prognosis

- Cardiogenic shock crisis
of microcirculation due
to the spread of
- systemic
depression of the
cardiac index, systolic

- Decreased ejection due to
- pale, cold extremities,
blocking in MI/spasm of
diffused acro-cyanosisle 

peripheral vessels. 

- True cardiogenic shock . 
 - spoor/stupor, Acute renal
- reduced coronary
18. - Reflex cardiogenic shock. 

Cardiogenic perfusion, hypoxemia and
19. - In permanent - Systolic BP less than 60;
shock lactic acidosis develop 

 diastolic less than 40 

- blood decrease in brain,
20. - Areactive shock 
 - psychosis 


- low cardiac output 

- blood move slow, stagnate
- poor cerebral function

in peripheral area,
decreased preload, liquid
blood come out to the

- After 6-12hrs, organ start
to die – Reduced liver
activity, etc. 

- After 12hrs, it changes to
irreversible organ type of

Regime Diet Physical activity 2ndary prophylaxis Prognosis
21. Emergency care: 
 22. - after infarct or post-infarct
24. - to stop progression of the
- Young patients, adequate
16. - complete rest 
- exercise test. conducted disease. 

treatment and with
17. - continuous oxygen with progressive - long term - antiplatelet (
secondary prophylaxis, good
 the hosp and after aspirin ) or clopidogrel 

Rehabilitation prognosis. 

18. - venous dilators - glyceryl discharge. Education. 
26. - ACEI for heart failure. 

- most patient can resume
trinitrate or sodium 23. - 3 weeks – when there27. is - routine of oral beta
working after abt 1 month
nitroprusside IVly 
 non-complicated MI 

after rehabilitation 

19. - cardiac inotropes - 30 28. - warfarin for at risk of
epinephrine, dobutamine 
 25. - pulse is weak and rapid 

20. - infusion therapy of 26. - severe bradycardia 
29. - Statins( lipid-lowering
vasopressors ( dopamine, 27. - tachypnea, Cheyne-stokes therapy ) 

dobutamine ) 
 resp, and jugular 
 30. - Amiodarone/Sotalol
21. - ballon aortic vein distension.
- S1 very (Tachyarrhythmias) 

 soft, and S3 may be audible.
31. - Heparin, Anticoagulants
22. - analgesic ( Analgine or - 5 weeks – when (For thromboembolism) 

Morphine), aspirin 
 complicated MI present.
23. - NTG 

24. - Arrhythmic: vent
extrabeat – Lidocaine 

supravent –
verapamil, beta blockers 

AV block –
atropine, euphiline 
fibrillation – verapamil,

- Thrombolytics:

Angina pectoris Myocardial infarction


Pain synd Present Absent

diagnosis NTG Effective
Not effective
ECG Changes disappears after NTG
Present changes.
Enzyme No changes
Changes present
Characteristics Stable Unstable
Occurrence Pain after/during phy exertion Pain at rest
Duration Pain 5-10 min Pain 45 min
Drug NTG effective NTG no effect
Mainly L part & apex of cardia d
Place of pain Other part but larger place
substernal area
Irradiate to L shoulder,
Irradiation of pain Other place of irradiation
shoulder,neck, jaw
After treatment pain
Character stops
pressing, heaviness, Pain do not stop
burning, squeezing