i went through all the ECG books i could have access to, none of them included a full classification of myocardial infarction. since few of its types, such as: transmural, non- transmural, Q-wave MI, non-Q wave MI are no longer recommended. many books didn't mention them at all, and the ones which did, excluded others such as STEMI & NSTEMI or the classification by anatomical sites. so it's rather a stumbling rock when it comes to finding everything about its classification. well, i gathered data from a lot of sources: books, websites, my college notes, etc. and combined them up into this. btw, it is detailed. (and i made this two years back, so forgive me if they found some new information) if you'd like a PDF, drop a comment.

1. MYOCARDIAL INFARCTION
BY: FARHEEN ANSARI
(BCLT)

2. CONTENTS
1. INTRODUCTION TO MYOCARDIUM
A. ANATOMY
B. PHYSIOLOGY
2. DEFINITION OF MYOCARDIAL INFARCTION
3. RISK FACTORS
4. PATHOPHYSIOLOGY
5. CLINICAL MANIFESTATIONS
6. UNIVERSAL CLASSIFICATION OF MYOCARDIAL INFARCTION (ETIOLOGICAL )
7. ECG INTERPRETATION OF MYOCARDIAL INFARCTION

3. CONTENTS
8. CLASSIFICATION:
A. ANATOMICAL/ MORPHOLOGICAL :
i. ACC. TO THE DEGREE OF THICKNESS OF VENTRICULAR WALL INVOLVED
a. TRANSMURAL
b. SUBENDOCARDIAL
II. ACC. TO THE ANATOMIC REGION OF THE LEFT VENTRICLE INVOLVED
a) ANTERIOR
b) POSTERIOR
c) INFERIOR
d) LATERAL
e) SEPTAL
f) CIRCUMFERENTIAL AND THEIR COMBINATIONS LIKE, ANTEROLATERAL, POSTEROLATERAL AND ANTEROSEPTAL
B. DURATION:
I. HYPERACUTE (WITHIN MINS.)
II. FULLY EVOLVED PHASE (WITHIN HOURS)
III. RESOLUTION PHASE (OLD)

4. CONTENTS
C. DIAGNOSTIC CLASSIFICATION OF MYOCARDIAL INFARCTION
I. ST ELEVATED MYOCARDIAL INFARCTION (STEMI)
II. NON ST ELEVATED MYOCARDIAL INFARCTION (NSTEMI)
III. DIFFERENCE BETWEEN UNSTABLE ANGINA, NSTEMI & STEMI.
IV. DIFFERENCE BETWEEN STEMI & NSTEMI.
9. DIAGNOSIS BY SERUM CARDIAC BIOMARKERS
10. COMPLICATIONS
11. MANAGEMENT
A. PHARMACOLOGICAL
B. SURGICAL
12. PREVENTION
A. PRIMARY PREVENTION
B. SECONDARY PREVENTION

5. INTRODUCTION TO
MYOCARDIUM

6. ANATOMY
IT IS THE MUSCULAR MIDDLE LAYER OF THE HEART WALL.
IT IS CHIEFLY COMPOSED OF SPONTANEOUSLY CONTRACTING CARDIAC MUSCLE TISSUE.
IT IS THICKEST OF THE THREE HEART WALL LAYERS AS THIS VENTRICLE IS RESPONSIBLE FOR GENERATING THE
POWER NEEDED TO PUMP OXYGENATED BLOOD FROM THE HEART TO THE REST OF THE BODY.
THE MYOCARDIUM IS SURROUNDED BY THE EPICARDIUM (OUTER LAYER OF THE HEART).

7. PHYSIOLOGY
PROVIDE A SCAFFOLDING TO THE HEART CHAMBERS.
ASSIST IN CONTRACTION AND RELAXATION OF THE CARDIAC WALLS SO THAT THE BLOOD CAN
PASS BETWEEN THE CHAMBERS.
CONDUCT ELECTRO-STIMULATION THROUGH ITS OWN TISSUES AND INTO THE EPICARDIUM
(THE CONDUCTING SYSTEM OF THE HEART.
HEART CONTRACTION IS AN AUTONOMIC (INVOLUNTARY) FUNCTION OF THE PERIPHERAL
NERVOUS SYSTEM.
THESE CONTRACTIONS PRODUCE WHAT IS KNOWN AS A HEARTBEAT.
THE BEATING OF THE HEART DRIVES THE CARDIAC CYCLE WHICH PUMPS BLOOD TO CELLS
AND TISSUES OF THE BODY.

8. CORONARY ARTERIES AND
THEIR SUPPLY

10. DEFINITION OF MYOCARDIAL
INFARCTION
THE TERM “ MYOCARDIAL INFARCTION “ FOCUSES ON THE MYOCARDIUM (THE HEART
MUSCLE) AND THE CHANGES THAT OCCUR IN IT DUE TO SUDDEN DEPRIVATION OF
CIRCULATING BLOOD.
THE MAIN CHANGE IS NECROSIS (DEATH) OF THE MYOCARDIAL TISSUE.
IT IS ALSO KNOWN AS HEART ATTACK.

11. THIRD UNIVERSAL DEFINITION
MYOCARDIAL INFARCTION (MI) IS DEFINED WHEN THERE IS DETECTION OF A RISE AND/OR FALL OF CARDIAC
BIOMARKER VALUES (PREFERABLY CARDIAC TROPONIN WITH AT LEAST ONE VALUE ABOVE THE 99TH PERCENTILE
UPPER REFERENCE LIMIT [URL]) AND WITH AT LEAST ONE OF THE FOLLOWING:
SYMPTOMS OF ISCHEMIA
DEVELOPMENT OF PATHOLOGIC Q WAVES IN THE ECG
NEW OR PRESUMED NEW SIGNIFICANT ST-SEGMENT-T WAVE (ST-T) CHANGES OR NEW LEFT BUNDLE
BRANCH BLOCK (LBBB)
IDENTIFICATION OF AN INTRACORONARY THROMBUS BY ANGIOGRAPHY OR AUTOPSY
IMAGING EVIDENCE OF NEW LOSS OF VIABLE MYOCARDIUM OR A NEW REGIONAL WALL MOTION
ABNORMALITY.

12. RISK FACTORS
NON MODIFIABLE:
AGE
GENDER
FAMILY HISTORY
 MODIFIABLE:
SMOKING
ALCOHOL AND DRUG ABUSE
STRESS
DIABETES
HYPERTENSION
HYPERLIPIDEMIA
OBESITY
PHYSICAL INACTIVITY
ATHEROSCLEROSIS
HYPERTHYROIDISM
ANEMIA
ISCHEMIA

13. PATHOPHYSIOLOGY

14. CLINICAL MANIFESTATIONS
 CHEST PAIN DESCRIBED AS HEAVINESS, PRESSURE, FULLNESS AND CRUSHING SENSATION
WITH AN EPISODE OF MORE THAN 20 MINUTES
 ANXIETY
 NAUSEA AND VOMITING
 DYSPNEA
 SYNCOPE
 WEAKNESS
 LIGHT-HEADEDNESS
 PALPITATIONS
 FATIGUE

15. • INITIALLY THE BP AND PULSE MAY BE ELEVATED. DUE TO INCREASED SYMPATHETIC TONE, OR THE BP
CAN BE LOW DUE TO CARDIOGENIC SHOCK DEPENDING ON THE EXTENT OF THE STEMI
• LATER, BP WILL DROP DUE TO DECREASED CARDIAC OUTPUT.
• URINE OUTPUT WILL DECREASE
• A S4 HEART SOUND MAY BE PRESENT DURING MYOCARDIAL ISCHEMIA DUE TO THE LACK OF ADENOSINE
TRIPHOSPHATE PRODUCTION IMPAIRING LEFT VENTRICULAR RELAXATION. [RECALL THAT MYOCARDIAL
RELAXATION IS AN ACTIVE PROCESS REQUIRING ATP, WHICH IS REDUCED DURING ISCHEMIA, AND A S4
HEART SOUND OCCURS WHEN THE NONCOMPLIANT, STIFFENED LEFT VENTRICLE IS NOT ABLE TO RELAX
ADEQUATELY WHEN IT RECEIVES BLOOD DURING ATRIAL CONTRACTION. THE S4 SOUND IS FROM THE
BLOOD ITSELF STRIKING THE NONCOMPLIANT VENTRICLE.]

16. • WHEN THE LEFT VENTRICULAR END-DIASTOLIC PRESSURE, OR LVEDP, INCREASES DURING MYOCARDIAL
ISCHEMIA, THAT PRESSURE CAN BE TRANSMITTED BACKWARD TO THE PULMONARY VEINS AND INTO THE
PULMONARY VASCULATURE, CAUSING TRANSIENT PULMONARY EDEMA THAT RESULTS IN DYSPNEA AND
RALES ON LUNG EXAMINATION.
• DURING INFERIOR ISCHEMIA, POSTEROMEDIAL PAPILLARY MUSCLE DYSFUNCTION CAN CAUSE MITRAL
REGURGITATION, RESULTING IN A HOLOSYSTOLIC MURMUR AT THE CARDIAC APEX RADIATING TO THE
AXILLA. THIS RARELY OCCURS DURING ANTERIOR OR LATERAL ISCHEMIA BECAUSE THE ANTEROLATERAL
PAPILLARY MUSCLE HAS DUAL SUPPLY FROM THE LEFT ANTERIOR DESCENDING AND CIRCUMFLEX
CORONARY ARTERY.
• JUGULAR VEINS MAY BECOME DISTENDED AND HAVE OBVIOUS PULSATIONS.

17. UNIVERSAL CLASSIFICATION
OF MYOCARDIAL INFARCTION
(ETIOLOGICAL)

19. ECG INTERPRETATION OF
MYOCARDIAL INFARCTION

20. BEFORE DIAGNOSING MYOCARDIAL INFARCTION, REMEMBER TO MENTION THE
FOLLOWING POINTS:
1. CRITERIA OF INFARCTION BY LOOKING FOR ST ELEVATION, Q WAVE AND T INVERSION
 Q WAVE: MYOCARDIAL NECROSIS
 ST SEGMENT: MYOCARDIAL INJURY
 ST ELEVATION : MYOCARDIAL INFARCTION
 ST DEPRESSION: MYOCARDIAL ISCHEMIA
 T WAVE: ISCHEMIA
2. SITE OF INFARCTION & CORONARY ARTERY INCLUDED
(WHETHER ANTERIOR, INFERIOR, SEPTAL, LATERAL)
3. RECENT OR OLD.

22. ARRANGEMENT OF LEADS ON ECG

23. LOCALISATION ST elevation Reciprocal ST depression Coronary artery
Anterior MI V3-V4 II, III, aVF LAD
Lateral MI I, aVL, V5- V6 II,III, aVF LCx or MO
High lateral LI & aVL II, III, aVF
Inferior MI II, III, aVF I, aVL & sometimes V5-V6 RCA (80%) or
RCX(20%)
Posterior (true) MI None [in II, III, aVF if inferior MI is
present]
high R in V1-V3 with ST
depression V1-V4 > 2mm
(mirror view)
RCX
Septal MI ST elevation, Q wave formation, & T
wave inversion in leads V2 & V3
none LAD- septal
branches
Anteroseptal MI V1 to V4 (mainly V2 to V4)
Anterolateral MI LI, aVL, V3 to V6
Right ventricular MI V1, V4R I, aVL RCA
Subendocardial MI Symmetric T inversion in all chest
leads (non Q wave MI)
Transmural MI (Q wave MI) no ST changes
Atrial MI PR segment in I,V5,V6 PR segment in I,II, or III RCA

24. ANATOMICAL/ MORPHOLOGICAL
CLASSIFICATION:

25. 1. ON THE BASIS OF DEGREE OF THICKNESS OF VENTRICULAR WALL INVOLVED:
TRANSMURAL
SUBENDOCARDIAL

26. TRANSMURAL MYOCARDIAL INFARCTION:
 TRANSMURAL INFARCTS INVOLVE THE WHOLE THICKNESS OF MYOCARDIUM FROM EPICARDIUM TO
ENDOCARDIUM AND ARE USUALLY CHARACTERIZED BY ABNORMAL Q WAVES ON ECG. [FULL
THICKNESS MYOCARDIAL INJURY— Q WAVE]
 ST ELEVATION: THE CURRENT OF THE INJURY GOES TOWARDS THE INJURED SITE, THAT’S WHY THESE
CURRENTS GOES TOWARDS THE CHEST LEADS LEADING TO ST ELEVATION.

27. SUBENDOCARDIAL MYOCARDIAL INFARCTION:
 NON-TRANSMURAL OR SUBENDOCARDIAL INFARCTS DO NOT EXTEND THROUGH THE VENTRICULAR
WALL AND CAUSE ONLY ST-SEGMENT AND T-WAVE (ST-T) ABNORMALITIES. [70% MYOCARDIAL
INJURY — NON Q WAVE]
 SUBENDOCARDIAL INFARCTS USUALLY INVOLVE THE INNER ONE THIRD OF MYOCARDIUM, WHERE
WALL TENSION IS HIGHEST AND MYOCARDIAL BLOOD FLOW IS MOST VULNERABLE TO CIRCULATORY
CHANGES.
[THE ENDOCARDIAL AND SUBENDOCARDIAL ZONES OF THE MYOCARDIAL WALL ARE THE LEAST
PERFUSED REGIONS OF THE HEART AND ARE MOST VULNERABLE TO CONDITIONS OF ISCHEMIA.]
 ST DEPRESSION: THE CURRENT OF THE INJURY TRAVELS INWARDS THAT’S WHY THESE CURRENTS GO
AWAY FROM THE PRECORDIAL LEADS WHICH LEADS TO ST DEPRESSION.

28. 2. ACC. TO THE ANATOMIC REGION OF THE LEFT VENTRICLE INVOLVED:
 AN ANTERIOR WALL MYOCARDIAL INFARCTION — ALSO KNOWN AS ANTERIOR WALL MI, OR AWMI, OR
ANTERIOR ST SEGMENT ELEVATION MI, OR ANTERIOR STEMI — OCCURS WHEN ANTERIOR MYOCARDIAL
TISSUE USUALLY SUPPLIED BY THE LEFT ANTERIOR DESCENDING CORONARY ARTERY SUFFERS INJURY DUE TO
LACK OF BLOOD SUPPLY.
 IT IS LOCALIZED TO THE LEFT VENTRICULAR FREE WALL BETWEEN THE INTERVENTRICULAR GROOVE AND THE
LATERAL MARGIN OF THE ANTERIOR PAPILLARY MUSCLE.
ANTERIOR WALL MI

29.  ECG CRITERIA IN ACUTE ANTERIOR MI:
 ST SEGMENT ELEVATION IN THE ANTERIOR LEADS (V3 AND V4) AT THE J POINT AND SOMETIMES
IN THE SEPTAL OR LATERAL LEADS, DEPENDING ON THE EXTENT OF THE MI. THIS ST SEGMENT
ELEVATION IS CONCAVE DOWNWARD AND FREQUENTLY OVERWHELMS THE T WAVE. THIS IS CALLED
“TOMBSTONING” FOR OBVIOUS REASONS; THE SHAPE IS SIMILAR TO THAT OF A TOMBSTONE.
 RECIPROCAL ST SEGMENT DEPRESSION IN THE INFERIOR LEADS (II, III AND AVF).

31. LATERAL WALL MI
THE LATERAL MI IS LOCALIZED IN THE REGION BETWEEN THE LATERAL MARGIN OF THE ANTERIOR
PAPILLARY MUSCLE AND THE LATERAL MARGIN OF THE POSTERIOR PAPILLARY MUSCLE.
THE LATERAL WALL OF THE LV IS SUPPLIED BY BRANCHES OF THE LEFT ANTERIOR DESCENDING (LAD) AND
LEFT CIRCUMFLEX (LCX) ARTERIES.
ECG CRITERIA IN ACUTE LATERAL MI:
 ST ELEVATION IN THE LATERAL LEADS (I, AVL, V5-V6). ST ELEVATION PRIMARILY LOCALIZED TO LEADS
I AND AVL IS REFERRED TO AS A HIGH LATERAL STEMI.
 RECIPROCAL ST DEPRESSION IN THE INFERIOR LEADS (III AND AVF).

33. INFERIOR WALL MI
 THE INFERIOR MI IS LOCALIZED IN THE REGION BETWEEN THE LATERAL BORDER OF THE POSTERIOR PAPILLARY
MUSCLE AND THE POSTERIOR SEPTUM.
 AN INFERIOR WALL MYOCARDIAL INFARCTION — ALSO KNOWN AS IWMI, OR INFERIOR MI, OR INFERIOR ST
SEGMENT ELEVATION MI, OR INFERIOR STEMI — OCCURS WHEN INFERIOR MYOCARDIAL TISSUE SUPPLIED BY
THE RIGHT CORONARY ARTERY, OR RCA, IS INJURED DUE TO THROMBOSIS OF THAT VESSEL. WHEN AN INFERIOR
MI EXTENDS TO POSTERIOR REGIONS AS WELL, AN ASSOCIATED POSTERIOR WALL MI MAY OCCUR.
 ECG CRITERIA IN ACUTE INFERIOR MI:
 ST SEGMENT ELEVATION IN THE INFERIOR LEADS (II, III AND AVF)
 RECIPROCAL ST SEGMENT DEPRESSION IN THE LATERAL AND/OR HIGH LATERAL LEADS (I, AVL, &
SOMETIMES IN V5 AND V6).

34. NOTE:
IF THE RECIPROCAL ST SEGMENT DEPRESSIONS ARE NOT PRESENT, CONSIDER ALTERNATIVE CAUSES
OF ST SEGMENT ELEVATION, SUCH AS PERICARDITIS.

35. SEPTAL MI
THIS KIND OF MI IS LOCALIZED TO THE INTERVENTRICULAR SEPTUM.
SUPPLY OF BLOOD BY THE SEPTAL BRANCHES OF LAD.
ECG CRITERIA IN ACUTE SEPTAL MI:
 ASSOCIATED WITH ST ELEVATION, Q WAVE FORMATION, & T WAVE INVERSION IN
LEADS V2 & V3.
 NO RECIPROCAL ST DEPRESSION.

37. POSTERIOR WALL MI
THE ECG FINDINGS OF A POSTERIOR WALL MYOCARDIAL INFARCTION ARE DIFFERENT THAN THE TYPICAL
ST SEGMENT ELEVATION SEEN IN OTHER MYOCARDIAL INFARCTIONS. A POSTERIOR WALL MI OCCURS
WHEN POSTERIOR MYOCARDIAL TISSUE (NOW TERMED INFEROBASILAR), USUALLY SUPPLIED BY THE
POSTERIOR DESCENDING ARTERY — A BRANCH OF THE RIGHT CORONARY ARTERY IN 80% OF INDIVIDUALS
— ACUTELY LOSES BLOOD SUPPLY DUE TO INTRACORONARY THROMBOSIS IN THAT VESSEL. THIS
FREQUENTLY COINCIDES WITH AN INFERIOR WALL MI DUE TO THE SHARED BLOOD SUPPLY.

38.  ECG CRITERIA IN ACUTE POSTERIOR WALL MI:
 ST SEGMENT DEPRESSION (NOT ELEVATION) IN THE SEPTAL AND ANTERIOR PRECORDIAL LEADS (V1-
V4). THIS OCCURS BECAUSE THESE ECG LEADS WILL SEE THE MI BACKWARDS; THE LEADS ARE
PLACED ANTERIORLY, BUT THE MYOCARDIAL INJURY IS POSTERIOR.
 A R/S WAVE RATIO GREATER THAN 1 IN LEADS V1 OR V2.
 ST SEGMENT ELEVATION IN THE INFERIOR LEADS (II, III AND AVF) IF AN INFERIOR MI IS ALSO
PRESENT.

40. CLASSIFICATION ON THE BASIS
OF DURATION

41. ACC. TO DURATION, MI ARE OF 3 TYPES:
HYPERACUTE (WITHIN MINS.)
FULLY EVOLVED PHASE (WITHIN HOURS)
RESOLUTION PHASE (OLD)

42.  HYPERACUTE PHASE:
 THE HYPER ACUTE PHASE CHANGES ARE OBSERVED WITHIN MINUTES AFTER THE ONSET OF THE
EPICARDIAL VESSEL OCCLUSION.
 THE FOLLOWING ECG CHANGES ARE OBSERVED IN TWO OR MORE LEADS ORIENTED TO THE INFARCTED
SURFACE:
 LEADS FACING THE INFARCTED SURFACE: ST SEGMENT ELEVATION.
 LEADS FACING THE UNINJURED SURFACE: ST SEGMENT DEPRESSION (RECIPROCALS)
 T WAVES BECOME TALL, WIDENED AND MIGHT BE TALLER THAN THE R WAVE.
 R WAVE- INCREASED AMPLITUDE [VENTRICULAR ACTIVATION TIME IS INCREASED TO >45 MS,
SOMETIMES >60 MS]
 Q WAVE- ABSENT.

43.  SIGNIFICANCE OF HYPERACUTE PHASE:
IT IS THE MOST CRITICAL PHASE. V-FIB IS COMMON IN THIS PERIOD. THERE’S MYOCARDIAL INJURY, BUT
NO INFARCTION OR NECROSIS OCCURS. THIS PHASE MAY PERSIST FOR FEW HOURS. IF TREATED PROPERLY,
MYOCARDIAL BLOOD SUPPLY IS IMPROVED.

44.  MECHANISM OF TALL T WAVE IN HYPERACUTE MI:
IT IS DUE TO NECROSIS OF MYOCARDIUM RELEASING K+ LEADING WHICH CAUSES LOCALIZED HYPERKALEMIA,
LEADING TO TALL T WAVES.
 TALL T WAVES IN HYPER ACUTE MI VS. TALL T WAVES IN HYPERKALEMIA:
• T WAVES IN HYPER ACUTE MI ARE TALL, BROAD, AND ASYMMETRICAL.
• T WAVES IN HYPERKALEMIA ARE TALL, NARROW, AND SYMMETRICAL.
DIFFERENT CAUSES OF TALL T WAVES

45.  FULLY EVOLVED PHASE:
 CHANGES IN THIS PHASE EVOLVE WITHIN HOURS AFTER THE ONSET OF INFARCTION.
 THE FOLLOWING ECG CHANGES ARE OBSERVED IN TWO OR MORE CONTIGUOUS LEADS ORIENTED TO THE
INFARCTED SURFACE:
 NEW S-T SEGMENT ELEVATION REFLECTS MYOCARDIAL INJURY
 CUT-OFF FOR NEW S-T SEGMENT ELEVATION TO DIAGNOSE MI:
• >0.1 MV IN ALL LEADS OTHER THAN V2-V3
• ≥0.2 MV IN MEN ABOVE 40 YEARS IN LEADS V2-V3
• ≥0.25 MV IN MEN BELOW 40 YEARS IN LEADS V2-V3
• ≥0.15 MV IN WOMEN IN LEADS V2-V3
 PATHOLOGICAL Q WAVE DEVELOPMENT REFLECTS MYOCARDIAL NECROSIS

46. ECG OF T WAVE INVERSION IN
LEAD V3
ST SEGMENT ABNORMALITIES
ATTENUATION OF R WAVE AMPLITUDE WITHOUT THE ASSOCIATED PATHOLOGICAL Q WAVES
INVERTED, SYMMETRICAL, AND POINTED T WAVES OF AMPLITUDE ≥0.1 MV ARE OBSERVED — REFLECTS
MYOCARDIAL ISCHEMIA.

47. RESOLUTION PHASE:
 WEEKS AFTER THERE WILL BE A GRADUAL RETURN OF ST SEGMENTS TO BASELINE.
 T WAVES WILL GRADUALLY RETURN TO NORMAL BUT ARE THE LAST TO CHANGE BACK (MAY STILL BE
INVERTED).
 PATHOLOGICAL Q WAVE.

48. AN OLD MI (RESOLUTION PHASE)

49. DEFINITION OF A PATHOLOGICAL Q WAVE
 ANY Q-WAVE IN LEADS V2–V3 ≥ 0.02 S OR QS COMPLEX IN LEADS V2 AND V3
 Q-WAVE ≥ 0.03 S AND > 0.1 MV DEEP OR QS COMPLEX IN LEADS I, II, AVL, AVF, OR V4–V6 IN
ANY TWO LEADS OF A CONTIGUOUS LEAD GROUPING (I, AVL,V6; V4–V6; II, III, AND AVF)
 R-WAVE ≥ 0.04 S IN V1–V2 AND R/S ≥ 1 WITH A CONCORDANT POSITIVE T-WAVE IN THE
ABSENCE OF A CONDUCTION DEFECT.

51. DIAGNOSTIC CLASSIFICATION
OF MYOCARDIAL INFARCTION

52. STEMI
‘ST SEGMENT ELEVATION MYOCARDIAL INFARCTION’ MOST COMMONLY OCCURS WHEN THROMBUS
FORMATION RESULTS IN COMPLETE OCCLUSION OF A MAJOR EPICARDIAL CORONARY VESSEL. [IN STEMI,
THERE IS EPICARDIAL CORONARY INJURY LEADING TO TRANSMURAL INFARCTION.] THE MOST SERIOUS FORM
OF ACUTE CORONARY SYNDROMES, STEMI IS A LIFE-THREATENING, TIME-SENSITIVE EMERGENCY THAT
MUST BE DIAGNOSED AND TREATED PROMPTLY VIA CORONARY REVASCULARIZATION, USUALLY BY
PERCUTANEOUS CORONARY INTERVENTION.
UNLIKE DURING UNSTABLE ANGINA AND NON-ST SEGMENT ELEVATION MYOCARDIAL INFARCTION, THE 12-
LEAD ECG WILL SHOW SIGNIFICANT ST SEGMENT ELEVATION DURING STEMI — AS THE NAME IMPLIES.
*THE TERMS “TRANSMURAL,” “NON-TRANSMURAL,” “Q WAVE MI” AND “NON-Q WAVE MI”
ARE NO LONGER RECOMMENDED.

53. THE KILLIP CLASSIFICATION IS FREQUENTLY USED TO PREDICT MORTALITY DURING STEMI. THIS SYSTEM FOCUSES ON
PHYSICAL EXAMINATION AND THE DEVELOPMENT OF HEART FAILURE TO PREDICT RISK, AS DESCRIBED BELOW.
 CLASS I: NO EVIDENCE OF HF (MORTALITY 6%)
 CLASS II: FINDINGS OF MILD TO MODERATE HF (S3 GALLOP, RALES < HALFWAY UP LUNG FIELDS OR ELEVATED
JUGULAR VENOUS PRESSURE (MORTALITY 17%)
 CLASS III: PULMONARY EDEMA (MORTALITY 38%)
 CLASS IV: CARDIOGENIC SHOCK DEFINED AS SYSTOLIC BLOOD PRESSURE < 90 MM HG AND SIGNS OF
HYPOPERFUSION SUCH AS OLIGURIA, CYANOSIS AND SWEATING (MORTALITY 67%).
NOTE: THE ORIGINAL DATA FROM 1967 SHOWED THE ABOVE MORTALITY RATES IN EACH CLASS. THIS WAS BEFORE
REPERFUSION THERAPY (THROMBOLYTIC AND/OR PERCUTANEOUS CORONARY INTERVENTION). WITH ADVANCES IN
THERAPY, THE MORTALITY RATES HAVE DECLINED ABOUT 30% TO 50% IN EACH CLASS.
THE PHYSICAL EXAMINATION FINDINGS DURING STEMI ARE RELATIVELY NON-SPECIFIC & ARE SIMILAR TO THOSE OF
STABLE ANGINA, UNSTABLE ANGINA AND NON-STEMI, BUT THEY ARE FREQUENTLY MORE SEVERE DUE TO THE
LARGER AMOUNT OF MYOCARDIUM EXPERIENCING ISCHEMIA.

54. ECG CRITERIA IN STEMI:
 THE OVERALL ST VECTOR IS DIRECTED TOWARD THE EPICARDIAL SURFACE OVER THE INJURY
ZONE RESULTING IN:
 ST SEGMENT ELEVATIONS: LOCALIZED ST ELEVATION IN THE LEADS OVERLYING THE AFFECTED
AREA.
 T WAVE CHANGES
 Q WAVE DEVELOPMENT
 ENZYME ELEVATIONS
 RECIPROCALS: RECIPROCAL ST DEPRESSION IN THE LEADS DIRECTED TOWARD THE
CONTRALATERAL SURFACE OF THE AFFECTED AREA.

55. DIAGNOSIS IN STEMI:
THE DIAGNOSIS OF STEMI IS MADE PREDOMINANTLY USING THE 12-LEAD ECG AND CARDIAC ENZYMES.
THERE IS SIGNIFICANT MYOCARDIAL NECROSIS OCCURRING IN THE SETTING OF STEMI, RESULTING IN
ELEVATION OF THE CARDIAC ENZYMES.
ST SEGMENT ELEVATION, UNLIKE DEPRESSION, WILL LOCALIZE TO THE ECG LEAD OF THE AFFECTED
MYOCARDIUM. NOTE THAT 1 MILLIMETER OF ST SEGMENT ELEVATION IN TWO CONTIGUOUS LEADS IS
REQUIRED TO DIAGNOSE STEMI, BUT THERE ARE TWO MAJOR EXCEPTIONS.
ANTERIOR STEMI REQUIRES 2 MM OF ST SEGMENT ELEVATION IN V2 AND V3 IN MEN, OR 1.5 MM IN
WOMEN, AGED OLDER THAN 40 YEARS, ACCORDING TO THE AMERICAN COLLEGE OF
CARDIOLOGY/AMERICAN HEART ASSOCIATION DEFINITION.
POSTERIOR STEMI FREQUENTLY HAS ST SEGMENT DEPRESSION IN V1 TO V3 INSTEAD OF ELEVATION, AS
THE VECTORS ARE COMPLETELY REVERSED.

56. THERE ARE FOUR MAJOR SITUATIONS WHERE ST SEGMENT ELEVATION CAN BE SEEN ON AN ECG WHEN
THERE IS NO STEMI PRESENT, BUT MANY OTHER CAUSES OF ST SEGMENT ELEVATION ON THE ECG EXIST. A
GOOD MNEMONIC TO REMEMBER ALL THE CAUSES OF ST SEGMENT ELEVATION ON THE ECG IS
“ELEVATION.”
ELECTROLYTE ABNORMALITIES
LEFT BUNDLE BRANCH BLOCK
ANEURYSM OF LEFT VENTRICLE
VENTRICULAR HYPERTROPHY
ARRHYTHMIA DISEASE (BRUGADA SYNDROME, VENTRICULAR TACHYCARDIA)
TAKOTSUBO/TREATMENT (IATROGENIC PERICARDITIS)
INJURY (MI OR CARDIAC CONTUSION)
OSBORNE WAVES (HYPOTHERMIA OR HYPOCALCEMIA)
NON-ATHEROSCLEROTIC (VASOSPASM OR PRINZMETAL’S ANGINA)

57. NSTEMI
ANGINAL SYMPTOMS AT REST THAT RESULT IN MYOCARDIAL NECROSIS AS IDENTIFIED BY ELEVATED CARDIAC
BIOMARKERS WITH NO ST SEGMENT ELEVATION ON THE 12-LEAD ECG.
THE DIAGNOSIS OF UNSTABLE ANGINA AND NON-STEMI IS PREDOMINANTLY BASED ON THE ECG AND
CARDIAC ENZYMES. PHYSICAL EXAMINATION, AS PREVIOUSLY DESCRIBED, IS NON-SPECIFIC. NSTEMI HAPPENS
WITH SUBENDOCARDIAL. A NON-STEMI IS USUALLY CAUSED BY A SEVERELY NARROWED ARTERY.
• 12 LEAD EKG’S CAN HELP TO DISTINGUISH BETWEEN ST-ELEVATION MI’S (STEMI) AND NON-ST-
ELEVATION MI’S (NSTEMI).

58. ECG CRITERIA IN NSTEMI:
• THERE IS NO ST SEGMENT ELEVATION. THE MOST COMMON FINDING IS ST SEGMENT DEPRESSION
[HORIZONTAL OR DOWN-SLOPING IN SHAPE].
• T WAVE CHANGES: THE T WAVES MAY BE INVERTED, USUALLY SYMMETRICALLY.
• NO Q WAVE DEVELOPMENT
• MILD ENZYME ELEVATIONS
• NO RECIPROCALS
• AFTER COLLECTING PATIENT HEALTH HISTORY, A SERIES OF EKG’S SHOULD BE TAKEN TO RULE OUT OR
CONFIRM MI.

59. DIAGNOSIS IN NSTEMI:
SURPRISINGLY, UNSTABLE ANGINA AND NON-STEMI CAN BOTH OCCUR, EVEN WITH A COMPLETELY
NORMAL ECG; THIS MAKES DIAGNOSIS QUITE A CHALLENGE. OBSERVATION IN THE HOSPITAL FOR
CARDIAC ENZYMES IN CONTEXT OF SERIAL ECGS (USUALLY 6-8 HOURS APART) IS REQUIRED TO
COMPLETELY EXCLUDE UNSTABLE ANGINA AND NON-STEMI, AS THE ECG CHANGES CAN BE DYNAMIC
(COME AND GO) AND THE FINDINGS NORMAL INITIALLY. ALSO, CARDIAC ENZYMES (TROPONIN AND
CREATINE KINASE) REQUIRE 3 TO 4 HOURS AFTER THE INJURY BEFORE SHOWING SIGNIFICANT ELEVATION.
 DURING NON-STEMI, THERE WILL BE ELEVATION OF THE CARDIAC ENZYMES, INDICATIVE OF
MYOCARDIAL NECROSIS.
 DURING UNSTABLE ANGINA, HOWEVER, THERE IS NO — OR ONLY VERY MINIMAL — ELEVATION. THIS
IS THE MAIN DISTINGUISHING FEATURE BETWEEN THE TWO DIAGNOSES.

60. NOTE:
• MI MAY BE ST ELEVATED MI OR NON ST ELEVATED MI.
• FULLY EVOLVED PHASE IS USUALLY SEEN AFTER 24 HOURS.
• ST ELEVATION MAY NOT OCCUR BEFORE 6 HOURS.
• PATHOLOGICAL Q WAVE: - BROAD >1MM &
• DEEP >2MM IS SUGGESTIVE OF MI.
• Q WAVE MAY APPEAR AFTER 8-16 HOURS, THAT’S WHY THERE’S NO Q WAVE IN HYPERACUTE PHASE.
• ST SEGMENT RETURNS TO NORMAL AFTER FEW DAYS.
• ACUTE MI MAY BE MASKED IN PRESENCE OF LBBB, WPW
• T WAVE MAY REMAIN UPRIGHT FOR WEEKS TO MONTH.

61. UNSTABLE ANGINA NSTEMI STEMI
- Myocardial necrosis is present
but is less severe than STEMI.
- Myocardial ischemia is
present.
- Complete Myocardial
necrosis is present.
- Non-occlusive thrombus. - Occluding thrombus sufficient
to cause tissue damage & mild
myocardial necrosis.
- Complete thrombus
occlusion
- Normal level of biomarkers seen
in unstable angina.
- Elevation in the level of cardiac
biomarkers like troponin 1 or T,
Creatine- phosphokinase-
myocardial band (CPK-MB)
- Elevated cardiac
enzymes.
- Non-specific ECG - ST depression +/- T wave
inversion on ECG
- ST elevation on ECG or
new LBBB.
DIFF. BETWEEN UNSTABLE ANGINA & NSTEMI AND STEMI:

62. STEMI NSTEMI
INCIDENCE  >5% all STEMI  Common (upto 30% Unstable angina)
CLINICAL PRESENTATION  Victims of primary VF may not reach the hospital.  Severe rest angina
MYOCARDIAL JEOPARDY  100%,  At risk, but no true necrosis
ECG  STEMI has an elevated ST segment.
 Reciprocal ST depression in the leads directed toward
the contralateral surface of the affected area.
 NSTEMI has a depressed ST segment.
 no reciprocals observed
DAMAGE  More extensive myocardial damage occur  Smaller, less extensive myocardial damage occur
Q WAVE  Q wave present  Q wave absent
CARDIAC ENZYMES  Markers elevated consistently  Troponins can be positive
 CPK-MB typically normal (Creatine Phosphokinase-
myocardial band)
OCCLUSION  Complete occlusion: STEMI happens when the whole
artery is blocked causing a part of the heart to die off.
 Non- occlusive: as there is partial dynamic block to
coronary artery.
CARDIOGENIC SHOCK  CS almost always expected  True CS rare.
MANAGEMENT  Probably no role for medical.
 Still thrombolysis should be tried if PCI is not available.
 Medical stabilization possible.
 Thrombolysis not indicated as no myocardial
salvage is attempted
 Will require early CAG to confirm and proceed.
NSTEMI & STEMI are of two different types of MI.
NSTEMI & STEMI can be both traced by chemical markers to determine whether it is angina pectoris or a MI.
DIFF. BETWEEN STEMI AND NSTEMI:

63. DIAGNOSIS BY SERUM CARDIAC
MARKERS

64. CARDIAC ENZYMES — ALSO KNOWN AS CARDIAC BIOMARKERS — INCLUDE MYOGLOBIN, TROPONIN AND
CREATINE KINASE. HISTORICALLY, LACTATE DEHYDROGENASE, OR LDH, WAS ALSO USED BUT IS NONSPECIFIC.
CARDIAC ENZYMES ARE RELEASED INTO THE CIRCULATION WHEN MYOCARDIAL NECROSIS OCCURS, AS SEEN IN
MI.
WHEN CELL DEATH OCCURS, THESE CELLULAR ENZYMES ARE RELEASED INTO THE BLOOD STREAM.
MYOGLOBIN:
MYOGLOBIN IS RELEASED INTO CIRCULATION WITH ANY DAMAGE TO MUSCLE TISSUE, INCLUDING
MYOCARDIAL NECROSIS. BECAUSE SKELETAL MUSCLE CONTAINS MYOGLOBIN, THIS MEASUREMENT IS QUITE
NONSPECIFIC FOR MIS. THE BENEFIT IS IN THE FACT THAT A DETECTABLE INCREASE IS SEEN ONLY 30
MINUTES AFTER INJURY OCCURS, UNLIKE TROPONIN AND CREATINE KINASE, WHICH CAN TAKE 3 TO 4 HOURS.

65. TROPONIN:
 THESE ARE HIGHLY SPECIFIC INDICATORS OF MI.
 TROPONIN RISES QUICKLY LIKE CK BUT WILL CONTINUE TO STAY ELEVATED FOR 2 WEEKS.
 MYOGLOBIN-LACKS CARDIAC SPECIFICITY.
 THE LONG HALF-LIFE ALLOWS FOR THE LATE DIAGNOSIS OF MI BUT MAKES IT DIFFICULT TO DETECT RE-
INFARCTION AS CAN OCCUR IN ACUTE STENT THROMBOSIS AFTER PCI. ALTHOUGH, THERE ARE A NUMBER
CAUSES FOR TROPONIN ELEVATION UNRELATED TO MI, TROPONIN ELEVATION IS MUCH MORE SENSITIVE
AND SPECIFIC THAN MYOGLOBIN AND EVEN CK.

66. CREATINE KINASE:
• CREATINE KINASE — ALSO KNOWN AS CREATINE
PHOSPHOKINASE, OR CPK — IS A MUSCLE ENZYME THAT
EXISTS AS ISOENZYMES.
• BEGIN TO RISE IN APPROXIMATELY 3 TO 4 HOURS AFTER
ACUTE MI.
• PEAK IN 24 HOURS
• RETURN TO NORMAL IN 2 TO 3 DAYS
• THIS MAKES IT USEFUL FOR THE DETECTION OF RE-
INFARCTION IN THE 4- TO 10-DAY WINDOW OF TIME
AFTER THE INITIAL INSULT COMPARED WITH TROPONIN,
WHICH REMAINS ELEVATED FOR 10 DAYS AND IS LESS
USEFUL FOR THIS PURPOSE.

67. COMPLICATIONS OF
MYOCARDIAL INFARCTION

69. EARLY:
 ARRHYTHMIA:
 VENTRICULAR ECTOPY’S (COMMON)
 VF
 VT
 SINUS BRADYCARDIA
 COMMON IN INFERIOR MI
 CARDIAC FAILURE:
 ACUTE PERICARDITIS, COMMON IN 2ND OR 3RD DAY.
 THROMBOEMBOLISM:
 RUPTURE OF THE VENTRICULAR WALL LEADING TO CARDIAC TAMPONADE.

70. LATE:
 VENTRICULAR ANEURYSM.
 POST MI SYNDROME:
 IT IS LATE COMPLICATION OF MI THAT OCCURS USUALLY A FEW WEEKS OR EVEN MONTHS I.E.,
2-10 WEEKS AFTER ACUTE MI.
 IT IS CHARACTERIZED BY 5 PS:
• PAIN (CHEST PAIN)
• PYREXIA (FEVER)
• PLEURISY (INFLAMMATION OF THE PLEURA, ALSO CALLED PLEURITIS)
• PERICARDITIS (OR PERICARDIAL EFFUSION)
• PNEUMONITIS (OR PULMONARY INFILTRATE)

71. MANAGEMENT OF
MYOCARDIAL INFARCTION

72. • THE IMMEDIATE GOAL FOR ANY ACUTE MI IS TO RESTORE NORMAL CORONARY BLOOD FLOW TO VESSELS
AND SALVAGE MYOCARDIUM.
• THERE ARE A VARIETY OF MEDICAL AND MEDICINAL THERAPIES TO TREAT AN MI.
• THE TREATMENT OF STEMI INCLUDES PROMPT REVASCULARIZATION AND MEDICAL THERAPY.
REVASCULARIZATION CAN BE PERFORMED BY EITHER PRIMARY PCI (PERCUTANEOUS CORONARY
INTERVENTION), FIBRINOLYTIC THERAPY (THROMBOLYTIC THERAPY) OR SURGICALLY. PRIMARY PCI IS
PREFERRED IF AVAILABLE WITHIN A REASONABLE TIME-FRAME — THAT IS, A DOOR-TO-BALLOON TIME OF
LESS THAN 90 MINUTES.

73. MEDICAL THERAPY
INITIAL MEDICAL THERAPY DURING STEMI CONSISTS OF:
 OXYGEN ADMINISTRATION
 ANTIPLATELET THERAPY (ASPIRIN, THIENOPYRIDINES AND GLYCOPROTEIN IIB/IIIA INHIBITORS)
 ANTICOAGULATION (HEPARIN OR BIVALIRUDIN)
 ANGINAL PAIN RELIEF WITH NITRATES AND MORPHINE AND BETA-BLOCKADE.
MEDICAL THERAPY UPON HOSPITAL DISCHARGE MAY INCLUDE ACE INHIBITORS, ARBS, ALDOSTERONE
ANTAGONISTS AND HMG-COA REDUCTASE INHIBITORS.

74. REVASCULARIZATION
REVASCULARIZATION IS THE RESTORATION OF PERFUSION TO A BODY PART OR ORGAN THAT HAS SUFFERED ISCHEMIA.
 PRIMARY PCI (PERCUTANEOUS CORONARY INTERVENTION):
IN CERTAIN SITUATIONS, PRIMARY PCI IS STRONGLY PREFERRED OVER THROMBOLYTIC THERAPY.
 THERE ARE NO SITUATIONS IN WHICH FIBRINOLYTIC THERAPY IS PREFERRED OVER PRIMARY PCI, UNLESS THE
PATIENT REFUSES INVASIVE PROCEDURES.
 FIBRINOLYTIC THERAPY WORKS BEST WHEN SYMPTOM ONSET IS LESS THAN 3 HOURS, AS FRESH THROMBOLYSIS
IS MORE READILY TREATED THAN MORE ORGANIZED, SUBACUTE THROMBUS.
 IF SYMPTOMS HAVE BEEN PRESENT FOR MORE THAN 3 HOURS, THEN PRIMARY PCI IS PREFERRED.
THE BEST OUTCOMES OCCUR WHEN PRIMARY PCI IS PERFORMED IN A TIME OF LESS THAN 90 MINUTES AND
WHEN SYMPTOMS ONSET WAS LESS THAN 12 HOURS. PRIMARY PCI IS NOT RECOMMENDED WHEN SYMPTOM
ONSET IS MORE THAN 12 HOURS AND THE PATIENT IS ASYMPTOMATIC.

75.  FIBRINOLYTIC THERAPY:
FIBRINOLYTIC THERAPY MUST BE INSTITUTED WITHIN 24 HOURS OF SYMPTOM ONSET. AFTER THIS TIME FRAME,
FIBRINOLYTIC THERAPY IS CONTRAINDICATED AND LIKELY TO BE INEFFECTIVE.
CONTRAINDICATIONS: POST OP SURGICAL PATIENTS, HISTORY OF HEMORRHAGIC STROKE, ULCER DISEASE,
PREGNANCY, ETC.
FACILITATED PCI REFERS TO USING FIBRINOLYTIC THERAPY TO STABILIZE THE PATIENT WHILE TRANSPORT TO A
PRIMARY PCI FACILITY IS BEING ARRANGED. THIS STRATEGY RECEIVES A CLASS IIB INDICATION FOR HIGH-RISK
PATIENTS WITH A LOW BLEEDING RISK WHEN PRIMARY PCI IS NOT READILY AVAILABLE.
RESCUE PCI REFERS TO THE USE OF PCI WHEN FIBRINOLYTIC THERAPY FAILS. THIS IS INDICATED AFTER
FIBRINOLYTIC THERAPY, WHEN CARDIOGENIC SHOCK OR SEVERE CONGESTIVE HF DEVELOPS (KILLIP CLASS III),
OR WHEN ELECTRICAL INSTABILITY (VENTRICULAR TACHYCARDIA OR FIBRILLATION) OR PERSISTENT ISCHEMIC
SYMPTOMS ARE PRESENT.

76.  CORONARY ARTERY BYPASS GRAFTING (CABG):
SURGICAL TREATMENT WHERE SAPHENOUS VEIN IS HARVESTED FROM THE LOWER LEG AND USED TO BYPASS
THE OCCLUDED VESSELS.
CORONARY ARTERY BYPASS GRAFTING AS A MEANS OF CORONARY REVASCULARIZATION DURING STEMI IS
INDICATED IN THE FOLLOWING SITUATIONS:
 WHEN PCI FAILS, AND PERSISTENT SYMPTOMS OR HEMODYNAMIC INSTABILITY ARE PRESENT
 WHEN A PATIENT IS NOT A CANDIDATE FOR PCI AND HAS CONTINUED SYMPTOMS WITH A
SIGNIFICANT AREA OF MYOCARDIUM AT RISK
 DURING THE TIME OF VSD OR MITRAL VALVE REPAIR
 WHEN LEFT MAIN CORONARY DISEASE OR THREE-VESSEL CORONARY DISEASE IS PRESENT WITH
CARDIOGENIC SHOCK OR VENTRICULAR ARRHYTHMIAS (VENTRICULAR TACHYCARDIA OR FIBRILLATION)
CABG IS NOT INDICATED WHEN THERE IS A SMALL AREA OF MYOCARDIUM IN JEOPARDY AND THE PATIENT IS
STABLE.

77.  CARDIAC CATHETERIZATION:
• A DIAGNOSTIC ANGIOGRAPHY WHICH INCLUDES ANGIOPLASTY AND POSSIBLE STENTING.
• PERFORMED BY AN INTERVENTIONAL CARDIOLOGIST WITH A CARDIAC SURGEON ON STANDBY.
• PERCUTANEOUS PROCEDURE THROUGH THE FEMORAL OR BRACHIAL ARTERY.
• UPON ARRIVAL TO THE CATH. LAB ALL ACUTE MI PATIENTS WILL RECEIVE:
• A BOLUS DOSE OF PLAVIX
• IV INTEGRELIN
• HEPARIN DOSE EITHER SUBCUTANEOUS OR IV DRIP
• ANGIOMAX: A DTI MAY BE SUBSTITUTED FOR HEPARIN AND INTEGRELIN.

78. PREVENTION OF
MYOCARDIAL INFARCTION

79. PRIMARY PREVENTION
PRIMARY PREVENTION CONSISTS PREDOMINANTLY OF CONTROLLING CVD RISK FACTORS SUCH AS:
 LDL CHOLESTEROL
 TOBACCO USE
 HYPERTENSION
 OBESITY
 DIETARY AND LIFESTYLE MODIFICATIONS
 MEDICAL THERAPY WITH HMG-COA REDUCTASE INHIBITORS.

80. SECONDARY PREVENTION
MANAGEMENT OF CORONARY RISK EQUIVALENTS (10-YEAR RISK FOR CARDIAC EVENT > 20%) INCLUDE THE
FOLLOWING:
 NON-CORONARY ATHEROSCLEROTIC DISEASE:
o PERIPHERAL ARTERIAL DISEASE OR PAD
o CAROTID ARTERY DISEASE
o RENAL ARTERY DISEASE
o ABDOMINAL AORTIC ANEURYSM
 TYPE 2 DIABETES
 MULTIPLE RISK FACTORS: USING THE FRAMINGHAM RISK SCORE, A 10-YEAR RISK FOR A CARDIAC EVENT IS
GREATER THAN 20%
 CHRONIC KIDNEY DISEASE