1. ACUTE MYOCARDIAL INFARCTION
Dr. PRAVEEN PEDDI

2. DEFINITION
MI is the irreversible necrosis of heart muscle secondary to Prolonged ischaemia.

3. ARTERIAL SUPPLY OF THE HEART
LMCA RCA
LAD LCX.
Anterior & septal. Lateral Right heart &
inf wall of LV

4. PATHOPHYSIOLOGY
Myocardial ischaemia & its sequalae usually occur as a result of fixed atherosclerotic lesion .
Acute coronary syndrome is caused by SECONDARY reduction in myocardial blood flow due to
Coronary arterial spasm
Disruption / Erosion of athero plaque
Platelet aggregation
Thrombus Formation

5. Secondary causes:: Increase myocardial O2 demand reduced blood flow Decreased O2 delivery

6. In AMI the fundamental alteration is loss of functioning myocardiiam through 4 sequentially abnormal contraction pattern.
Dyssynchrony
Hypokinesis
Akinesis
Dyskinesis

7. CLINICAL PRESENTATION
Chest discomfort Pressure , heaviness, tightness, fullness, squeezing.. Location Radiation Ass symptoms

8. Physical Examination Deceptively well or Uncomfortable Pale Cyanotic
Respiratory distress
PR: N/tachy/Brady/irregular
BP : normal /high /low

9. CVS : heart sounds S3 gallop – 15% -20% The presence of new SYSTOLIC murmur is an ominous sign it may signify – Papillary muscle dysfunction Flail leaflet of the mitral valve Ventricular septal defect The presence of crepts – LVF / Left side CHF JVP raise , hepatic jugular reflex, peripheral edema – Right side CHF

10. DIAGNOSIS
STEMI --- ECG NSTEMI – BIO MARKERS USA– CLINICAL

11. ECG

15. RV INFARCTION
Rare Complication of IWMI 30% of inf wall MI Diagnosis  ST elevation in V4R in setting of Inf wall MI RV infarction with LV infarction has a devasting effect on hemodynamic function Treatment  Fluid balance and maintainance of adequate preload , Decreaseed RV afterload , 1-2 L of NS Inotropic support with Dobutamine

18. New onset LBBB is equivocal to MI

22. BIO MARKERS
STEMI
Serum MARKERS are useful in pt with non diagnostic ECG s for diagnosis of NSTEMI
Risk stratification of pt with STEMI / NSTEMI / USA

23. BIO MARKERS Bio MARKERS 1st Detection Peak Lasting for Troponin
2-6 hrs
12hrs
7-10 days
CK-MB
4-8 hrs
12-24 hrs
3-4days
Myoglobin
3hrs
4-9hrs
24 hrs

25. 2007 guidelines
Diagnosis of MI for those with Troponin elevation , at least one of the following must be present
Ischemic symptoms
New ST & T wave changes
New LBBB
New Q waves
New RWMA
Imaging evidence of a new loss of viable myocardium

26. TREATMENT
AIM --- To achieve immediate reperfusion and limit infarct Reperfusion :: Mechanical Angioplasty with or without stent Pharmacological Fibrinolytics Anti platelets Anti thrombins

27. GENERAL MEASURES
I.V access
Electrocardiac monitoring
O2 supply

28. PCI- PERCUTANEOUS CORONARY INTERVENTION
Preferred method of Reperfusion
Door to balloon inflation time < 90min
Acceptable delay -– > min
Angioplasty with or without stent
Atherectomy
Laser Angioplasty

29. Advantages ::: more effective in establishing flow and reducing reocclusion Decrease incidence of short and long-term death Intra cranial hemorrhage Complications ::: Excessive dissection Platelet deposition Thrombus Formation Plaque hemorrhage

30. FIBRINOLYTICS
INDICATIONS :: STEMI Time duration 6 hrs CONTRA INDICATIONS :: Any prior IC bleed cerebro Vascular malformations IC neoplasms Ischemic stroke within 3months Suspected Aortic Dissection Active internal bleeding

31. FIBRINOLYTICS NON SPECIFIC SPECIFIC
INDIRECT, ANTIGENIC DIRECT, NON ANTIGENIC Alteplase
Reteplase
Streptokinase Urokinase Tenecteplase
Anistreplase

32. INSOLUBLE FIBRIN PLASMINOGEN PLASMIN FIBRINOLYTICS SOLUBLE FIBRIN

33. STREPTOKINASE :: 1.5 million units over 60min ANISTREPLASE :: 30 units I.V over 2-5 min RETEPLASE :: 10 units I.V over 2 min, after 30 min 10 units I.V TENECTEPLASE :: <60 kg – 30 mg kgs - 35 mg kgs – 40 mg kgs – 45 mg > 90 kgs – 50 mg

34. ALTEPLASE :: Body weight >67 kgs  15mg I
ALTEPLASE :: Body weight >67 kgs  15mg I.v bolus | 50mg infused over next 30 min 35 mg infused over next 60 min Body weight <67 kgs  15 mg I.v bolus 0.75 mg / kg next 30 min 0.5 mg /kg next 60 min

35. FACILITATED PCI :: no benefits increased incidence of CHF, Shock, death RESCUE PCI :: Pt in cardiogenic Shock age < 75 y Severe heart failure Pulmonary edema Ventricular arrhythmias Moderate or large area of myocardium is at risk

36. Endothelial damage Decreased PGI2 release Increase TXA2 in platelets Decreased cAMP Degranulation of ADP Attach to the ADP receptors Activation of GP||a/ |||b receptors Fibrinogen helps to join to 2 platelets Thrombus Formation

37. Endothelial damage Decreased PGI2 release Increase TXA2 in platelets COX INHIBITORS ASPIRIN Decreased cAMP Degranulation of ADP Attach to the ADP receptors. ADA RECEPTOR BLOCKER CLOPIIDOGREL Activation of GP||a/ |||b receptors GP||a/GP|||b inhibitors Fibrinogen helps to join to 2 platelets Thrombus Formation

38. COX INHIBITORS :: ASPIRIN  325 mg po Prevents Formation of thromboxane A2 Inhibition for 8-12 days s/e GI and dose related ADP RECEPTOR ANTAGONIST :: CLOPIDOGREL  300 mg po,, 600 mg taking to PCI More rapid action Prasugrel  recently approved

39. GP ||b / |||a Inhibitors::: ABCIXIMAB  0. 25 mg/kg bolus | 0
GP ||b / |||a Inhibitors::: ABCIXIMAB  0.25 mg/kg bolus | micro gram /kg/min for hrs EFTIFIBATIDE 180microgram /kg bolus 2 microgram /kg/min for hrs TIROFIBAN  0.4 microgram /kg over 30 min 0.1 microgram /kg/miin for hrs

40. ANTI THROMBINS :::
UNFRACTIONATED HEPARIN  60 units /kg  12 units /kg/hr indusion
LMWH :: ENOXAPARIN  30mg iv bolus  1mg /kg s/c every 12 hr

41. OTHER ANTI ISCHEMIC THERAPIES
NTG  0.4 mg s/l every 5 min 10microgram /min I.V infusion MORPHINE 2 -5 mg every 5-15 min METOPROLOL  50 mg po every 12 hrs