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L/O/G/O

STEMI (ST elevation myocardium infarction) / NSTEMI(Non-ST elevation myocardium infarction)

Acute Myocardium

Infarction

Acute Myocardium

Infarction

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Risk factors

Abnormal serum lipids (elevated totalcholesterol, high LDL cholesterol, low

HDL cholesterol), smoking, HPT/HTN,

family history of premature CAD, age(male > 55, female > 65), male sex, and

DM.

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Management of STEMI (algorithm)

C l i n i c a l f e a t u r e s ,

E C G + / - b i o c h e m i c a l

m a r k e r s s u g g e s t i v e

o f S T E M I

Rapid examination to exclude

hypotension and acute pulmonaryoedema, ECG monitoring, Aspirin and

clopidogrel, statin, analgesia, sedation,

others.

ReperfusionTherapy Not for reperfusion therapy e

.g > 12hrs, contraindicated for thrombolysis

but primary PCI not available.

Thrombolysis if

no

contraindication

Primary PCI if

available

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Management of STEMI (algorithm)

Beta blocker if no contraindication, ACE

inhibitor especially anteriorMI, CCF, EF

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General Management of AMI

RIB for 2-3/7 in uncomplicated case.

ECG monitoring for at least 48hr.

Oxygen at 2-4 L/min for 2-3 hr &

continue thereafter if SaO2 remains

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General Management of AMI

Patient with recurrent symptoms after SLGTN and morphine should be started on

IVGTN.

Sedation with small oral doses ofdiazepam or lorazepam if necessary.

Diet and bowel care for the first day

afterMI, diet should be liquid or soft,stool softners or mild laxatives are

routinely given.

Potassium level should be maintained at

4-5 mmol/L.

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Specific Mx to reduce infarct size

and to improve mortality.

1. Thrombolytic therapy. Administration of fibrinolytic agents can

achieve early reperfusion in 50-70% of

patients (compared with a spontaneousreperfusion rate of

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Specific Mx to reduce infarct size

and to improve mortality.

a) All patient fulfilling the following criteriawithout CI should be given thrombolytic

therapy.

i. Clinical:

Chest pain or chest-pain-equivalent

syndrome consistent with acute MI 12 hr

from symptom onset with:

ii. ECG: 1 mm ST elevation in 2 contiguous limb

leads.

2 mm ST elevation in 2 contiguous

precordial leads.

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Specific Mx to reduce infarct size

and to improve mortality.

New bundle branch block.

True posteriorMI (tall R wave in V1 with

ST depression; exclude other causes of

tall R wave [ e.g RBBB, RVH, WPWsyndrome]; right ventricular infarction

[ST elevation V4R])

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Specific Mx to reduce infarct size

and to improve mortality.

iii. Time from onset of symptom: 12 hr : no significant benefit except inongoing ischemia manifested by persistent

chest pain and ST elevetion on ECG.

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Specific Mx to reduce infarct size

and to improve mortality.

b) Contraindications

i. Absolute CI:

Altered consiousness

Active internal bleeding

Prolonged or traumatic CPR (>10 min)

Known spinal cord or cerebral atriovenous

malformation or tumor.

Recent head trauma

Known previous haemorrhagic

cerebrovascular disease or stroke within

6/12.

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Specific Mx to reduce infarct size

and to improve mortality.

Intracranial or intraspinal surgery within2/12.

Trauma or surgery within 2/7, which could

result in bleeding in a closed space.

Persistent blood pressure > 200/120 mmHg.

Known bleeding disorder.

Pregnancy.

Suspected aortic dissection.

Previous allergic reaction to streptokinase

or APSAC (or prior use within 1 yr) use

rtPA instead.

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Specific Mx to reduce infarct size

and to improve mortality.

ii. Relative CI: Chronic uncontrolled HPT/HTN (diastolic

>100 mmHg), treated or untreated.

Ischaemic or embolic stroke in the past (>6month)

Major trauma or surgery > weeks and < 2

month.

Oral anti-coagulation, therapeutic.

Active peptic ulcer disease, or haem-

positive stool.

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Specific Mx to reduce infarct size

and to improve mortality.

ii. Relative CI: Acute pericarditis, infective endocarditis,

intracardiac thrombus.

Subclavian or intrajugular cannulation.

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Specific Mx to reduce infarct size

and to improve mortality.

c. Thrombolytic agent: Streptokinase

Recombinant tissue plasminogen activator

(rtPA/Alteplase) Anisoylated plasminogen streptokinase

activator complex (APSAC/Anistreplase)

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Specific Mx to reduce infarct size

and to improve mortality.

d. Choice of thrombolytic agents. Streptokinase

Recombinant tissue plasminogen activator

(rtPA/Alteplase)e. Monitoring.

Fibrinogen level and PTT should be

monitored 6 hr after the infusion.

Reperfusion is recognized by cessation or

reduction of pain, resolution of ST elevation, or

rapid evolution of ECG to Q waves, reperfusion

arrhythmias, early peak CK (by 12hr)

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Specific Mx to reduce infarct size

and to improve mortality.

f. Complications of thrombolytic therapy andmanagement.

i. Hypotension during striptokinase infusion.

ii. Allergic reaction to striptokinase.

iii. Uncontrollable bleeding.

iv. Reperfusion arrhythmias.

v. Invasive vascular procedures needed.

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Specific Mx to reduce infarct size

and to improve mortality.

2. Anti-platlet agents:

Aspirin.

Clopidogrel.

Ticlopidine.

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Specific Mx to reduce infarct size

and to improve mortality.

3. Beta blockers.

Propanolol.

Atenolol.

4. Nitroglycerin.

5. ACE inhibitors.

6. ARB, angiotensin receptor blocker.

7. Statin therapy.

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Specific Mx to reduce infarct size

and to improve mortality.

8. Calcium channel blocker.

9. Prophylactic anti-arrhythmics.

10.Anti-coagulants.

11.Primary percutaneous coronary

intervention:

For patients:

i. With CI to thrombolytic therapy.ii. Pressing within 4 hr of a large anteriorMI.

iii. In whom MI may be due to a vein graft occlusion

iv. With cardiogenic shock.

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Complications of AMI

1. Cardiac arrhythmias. Ventricular extrasystoles

VT

Vf Af

Sinus Bradycardia

Sinus Tachycardia Various conduction disturbances.

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Complications of AMI

2. Cardiac failure and cardiogenic shock

3. Thromboembolism.

4. Cardiac rupture.

5. Pericarditis.

6. Post-infarction angina.

7. Left ventricular aneurysm.

8. Other complications.

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L/O/G/O

Q u e s t i o n a n d A n s w e r S e s s i o n

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