Acute Myocardial Infarction

Myocardial Infarction if the rapid development of

myocardial necrosis by a critical imbalance between
oxygen supply and demand to the myocardium

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 Classification
2
 Acute coronary syndromes include
ST-elevation MI (STEMI)
Non ST-elevation MI ( NSTEMI)
Unstable Angina
 Cardiac markers in circulation indicates
myocardial infarction and help categorize MI
and is a useful adjunct to diagnosis

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 History
 Chest Pain- anterior precordium
3
tightness
 Pain may radiate to jaw, neck and epigastrium
 Dyspnea- angina equivalent, poor LV function
 Nausea/abdominal pain with posterior MI
 Anxiety

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 History
4

 Nausea with and without vomiting

 Diaphoresis or sweating
 Syncope or near syncope
 Elderly present with MS changes, fatigue, syncope or
weakness
 As many as half of MI are clinically silent

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 Physical
5

 The physical exam can often be unremarkable

 Hypertension
 Hypotension
 Acute valvular dysfunction may be present
 Rales
 Neck vein distention

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 Physical

 Third heart sound may be present

 A fourth heart sound poor LV compliance
 Dysrhythmias
 Low grade fever

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 Causes
7

 Most frequent cause is rupture of an atherosclerotic

lesion within coronary wall with subsequent spasm
and thrombus formation
 Coronary artery vasospasm
 Ventricular hypertrophy
 Hypoxia
 Coronary artery emboli

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 Causes
8

 Cocaine
 Arteries
 Coronary anomalies
 Aortic dissection
 Pediatrics Kawasaki disease, Takayasu arteritis
 Increased afterload which increases myocardial
demand

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 Risk factors for atherosclerosis
9

 Age
 Male gender
 Smoking
 Hypercholesterolemia and triglyceridemia
 Diabetes Mellitus
 Poorly controlled hypertension
 Type A personality

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 Risk factors for atherosclerosis
10

 Family History
 Sedentary lifestyle

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 Differentials
11

 Acute coronary syndrome

 Anxiety
 Aortic stenosis
 Asthma
 Cholecystitis and biliary colic
 Cholethiasis
 COPD

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 Differentials
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 Aortic Dissection
 Endocarditis
 Esophagitis
 Shock
 Myocarditis
 Pericarditis
 Pulmonary embolism

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 Mechanisms of Myocardial damage
13

The severity of an MI is dependent of three factors

 The level of the occlusion in the coronary
 The length of time of the occlusion
 The presence or absence of collateral circulation

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 Cardiac Biomarkers
14

 Cardiac biomarkers are protein molecules released

into the blood stream from damaged heart muscle
 Since ECG can be inconclusive , biomarkers are
frequently used to evaluate for myocardial injury
 These biomarkers have a characteristic rise and fall
pattern

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 Troponin T and I
15

 These isoforms are very specific for cardiac injury

 Preferred markers for detecting myocardial cell
injury
 Rise 2-6 hours after injury
Peak in 12-16 hours
Stay elevated for 5-14 days

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 Creatinine Kinase ( CK-MB)
16

 Creatinine Kinase is found in heart muscle (MB),

skeletal muscle (MM), and brain (BB)
 Increased in over 90% of myocardial infraction
 However, it can be increased in muscle trauma,
physical exertion, post-op, convulsions, and other
conditions

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 Creatine Kinase (MB)
17

 Time sequence after myocardial infarction

Begins to rise 4-6 hours
Peaks 24 hours
returns to normal in 2 days
 MB2 released from heart muscle and converted
to MB1.
 A level of MB2 > or = 1 and a ratio of MB2/MB1
> 1.5 indicates myocardial injury

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 Myoglobin
18
 Damage to skeletal or cardiac muscle release
myoglobin into circulation
 Time sequence after infarction
Rises fast 2hours
Peaks at 6-8 hours
Returns to normal in 20-36 hours
 Have false positives with skeletal muscle injury
and renal failure

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 CBC
19

 CBC is indicated if anemia is suspected as

precipitant

 Leukocytosis may be observed within several

hours after myocardial injury and returns
returns to levels within the reference range
within one week

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 Chemistry Profile
20

 Potassium and magnesium levels should be

monitored and corrected

 Creatinine levels must be considered before

using contrast dye for coronary angiography
and percutanous revascularization

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 C-reactive Protein (CRP)
21

 C- reactive protein is a marker of acute

inflammation

 Patients without evidence of myocardial

necrosis but with elevated CRP are at increased
risk of an event

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 Chest X-Ray
22

 Chest radiography may provide clues to an

alternative diagnosis ( aortic dissection or
pneumothorax)

 Chest radiography also reveals complications of

myocardial infarction such as heart failure

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 Echocardiography
23

 Use 2-dimentional and M mode echocardiography

when evaluating overall ventricular function and
wall motion abnormalities
 Echocardiography can also identify complications of
MI ( eg. Valvular or pericardial effusion, VSD)

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 Electrocardiogram
24

 A normal ECG does not exclude ACS

 High probability include ST segment elevation in two
contiguous leads or presence of q waves
 Intermediate probability ST depression
 T wave inversions are less specific

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 Localization of MI
25

 ST elevation only
 Inferior wall- II, III, aVF
 Lateral wall_ I, aVL, V4-V6
 Anteroseptal- V1-V3
 Anterolateral- V1-V6
 Right ventricular- RV4, RV5
 Posterior- R/S ratio >1 in V1 and T wave inversion

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 Ischemia & Infarction
• Indications of an acute infarction
• Usually no ECG changes are seen in the first few minutes after occlusion
• Appearance of tall narrow T-waves or ST-segment elevation
• 5 to 30 minutes post occlusion
• A few hours later, the T-waves invert (ischemia)
• in an MI, the T-wave inversion is symmetrical an may persist for years
• inverted T-waves without other indications are not diagnostic of an MI
• ST-segment elevation – indication of injury (although it may be reversible)
• ST-elevation may also indicate transmural ischemia
• usually the first definite sign of an infarction
• may or may not be accompanied by T-wave inversion
• 1mm or more in limb leads or 2mm or more in precordial leads
• differentiate between early repolarization or “J-point elevation”
• the larger the ischemic area, the greater the ST displacement
• ST elevation persisting for more than a few hours may indicate ventricular aneurysm
• ST depression may be seen in reciprocal leads.

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 Ischemia & Infarction
Acute anteriolateral MI

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 Ischemia & Infarction
• Biomarkers in an MI:

50
Myoglobin

20 Cardiac Troponin
Multiples of the AMI cutoff Limit

CK-MB
10
Cardiac Troponin after unstable angina

1
AMI decision limit
Upper normal limit
0
0 1 2 3 4 5 6 7 8
Days after MI Onset
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 Ischemia & Infarction
Old Inferior MI

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 Therapy
30

The goals of therapy in AMI are

the expedient restoration of
normal coronary flow and the
maximum salvage of functional
myocardium

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 Antiplatelet Agents
 Aspirin at lease 160mg31immediately
 Interferes with function of cyclooxygenase and
inhibits the formation of thromboxane
 ASA alone has one of the greatest impact on the
reduction of MI mortality.
 Clopidogrel, ticlopidine, have not been shown in
any large scal trail to be superior to Aspirin in
acute MI

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 Supplemental
32
Oxygen

 Because MI impairs the circulatory function of

the heart, oxygen extraction by the heart and
other tissues may be diminished
 Supplemental oxygen should be administered to
patient with symptoms and or signs of
pulmonary edema or pulse oximetry readings
less than 90%.

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 Nitrates
 IV nitrates to all patients with MI and
33
congestive heart failure, persistent ischemia,
hypertension, or large anterior wall MI
 Primary benefit vasodilator effect
 Metabolized to nitric oxide in the vascular
endothelium, relaxes endothelium
 Vasodilatation reduces myocardial oxygen
demand and preload and afterload

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 Beta-blockers
34

 Recommended within 12 hours of MI symptoms and

continued indefinitely
 Reduces Myocardial mortality by decreasing
arrythmogenic death
 Decrease the rate and force of myocardial
contraction and decreases overall oxygen demand

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 Unfractionated heparin
35

 Forms a chemical complex with antithrombin III

inactivates both free thrombin and factor Xa
 Recommended in patients with MI who undergo
PTCA or fibrinolytic therapy with alteplase

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 Low-molecular weight heparin
36
 Direct activity against factors Xa and IIa
 Proven to be effective in treating ACS that are
characterized by unstable angina or non ST-
elevation MI
 Their fixed doses are easy to administer and
laboratory testing to measure their therapeutic
effect is not necessary makes them attractive
alternative of un-fractionated heparin

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 Thrombolytics
37

 Indicated with MI and ST segment elevation

greater than 0.1mV in 2 contiguous ECG leads,
or new onset LBBB, who present less than 12
hours but not more than 24 hours after
symptom onset
 The most critical variable in achieving
successful fibrinolysis is time form symptom
onset to drug administration

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 Thrombolytics
38
 As a class the plasminogen activators have
been shown to restore coronary blood flow in
50-80% of patients
 Contraindication active intracranial bleeding,
CVA 2months, CNS neoplasm, HTN,
coagulopathy
 Retaplase slightly higher angiographic
patency but did not translate into survival
benefit
 Intracranial bleed risk major drawback

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 Glycoprotein IIb/IIIa Antagonists
39

 Potent inhibitors of platelet aggregation

 Use during PCI and in patients with high risk
features ACS have been shown to reduce the
composite end points of death, reinfraction and the
need for target lesion

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 Surgical Revascularization
40
 Emergent or surgical revascularization in
setting of failed PTCA in patients with
hemodynamic instability and coronary anatomy
amendable to surgical grafting
 Also indicated of mechanical complications of
MI including VSD, free wall rupture, or acute
MR
 Carries a higher risk of perioperative mortality
than elective CABG

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 Lipid Management
41
 All post MI patients should be on AMA step II
diet ( < 7% of calories from saturated fats)
 Post MI patients with LDL > 100 mg/dl are
recommended to be on drug therapy to try to
lower levels to <100 mg/dl
 Recent data indicate that all MI patients should
be on statin therapy, regardless of lipid levels or
diet

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 Long term Medications
42

 Most oral medications instituted in the hospital at

the time of MI are continued long term
 Aspirin, beta blockers and statin are continued
indefinitely
 ACEI indefinitely in patients with CHF, ejection
fraction <.40, hypertension, or diabetes

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