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Definition
Acute myocardial infarction (MI) is a clinical
syndrome that results from occlusion of a
coronary artery, with resultant death of cardiac
myocytes in the region supplied by that artery.
CHEST PAIN
SYMPATHETIC NERVOUS SYSTEM
STIMULATION
CATECHOLAMINE RELEASE
DIAPHORESIS
COOL AND CLAMMY EXTRIMITIES DUE TO
VASOCONSTRICTION
CARDIOVASCULAR
MANIFESTATIONS
TACHYCARDIA
ELEVATED BP INITIALLY
CRACKLES ON AUSCULTATION
NAUSEA
VOMITING AS A RESULT OF VASOVAGAL
REFLEX BY SEVERE PAIN
FEVER- 100.4 F AS A RESULT OF INFLAMATION
Diagnostics
History collection, physical exmn
After collecting patient health history, a series
of EKGs should be taken to rule out or confirm
MI.
12 lead EKGs can help to distinguish between
ST-elevation MIs and Non-ST-elevation MIs.
NORMAL SINUS RHYTHM
STEMI
ST segment elevations
T wave changes
Q wave development
Enzyme elevations
Reciprocals
Coronary artery events
Ischemia Outer most area, source of
arrhythmias, viable if no further infarction.
Injury Viable tissue found between ischemic
and infarcted areas.
Infarction/necrosis Center area, dead not
viable tissue that turn into scar.
NSTEMI
ST segment depressions
T wave changes
No Q wave development
Mild enzyme elevations
No reciprocals
STEMI vs. NSTEMI
Serum Cardiac Markers
Myocardial cells produce certain proteins and
enzymes associated with cellular functions.
When cell death occurs, these cellular enzymes
are released into the blood stream.
CPK and troponin
CPK
Creatine Phosphokinase
Begin to rise 3 to 12 hours after acute MI.
Peak in 24 hours
Return to normal in 2 to 3 days
Troponin
Myocardial muscle protein released into
circulation after injury.
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.
Cardiac catheterization
echocardiography
COMPLICATIONS
DYSRHYTHMIAS
Most common present 80% patients
HEART FAILURE
occur when the pumping power of heart
diminished
CARDIOGENIC SHOCK
Inadequate oxygen and nutrients are
supplied to the tissues because of severe LV
dysfunction
PAPILLARY MUSCLE DYSFUNCTION
valvular dysfuction, causes- MR,TR
VENTRICULAR ANEURYSM
Myocardial wall thinned and bulges out
during contraction
PERICARDITIS
DRESSLER SYNDROME
pericarditis with effusion and fever develops
4-6 weeks after MI
MANAGEMENT
preserve cardiac muscle fibers
Vital signs
Iv assess
ECG
Biomarkers
MANAGEMENT
INITIAL MANAGEMENT
M- Morphine
O- oxygen
N-Nitrates
A- Antiplatelets
EMERGENT PERCUTANEOUS CORONARY
INTERVENTION (PCI)