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MYOCARDIAL INFARCTION

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.

Defined by Current diagnosis and treatment in Cardiology - 2013


The degree of altered function depends on the
area of heart involved and the size of infarction
In acute MI cardiac cells can withstand
ischemic conditions for approximately 20
minutes before cellular death begins
It takes 4-6 hours for the entire thickness of
the heart to become necrosed
CLASSIFICATION
CLASSIFICATION
AWMI
IWMI
PWMI
LWMI
RVMI
ETIOLOGY AND PATHOPHYSIOLOGY
CLINICAL MANIFESTATIONS

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)

PCI may be used to open the occluded


coronary artery in an acute MI and promote
reperfusion to the area that has been deprived
of oxygen.
PCI is performed should be less than 90
minutes.
Usually PCI with the placement of stent will be
performed
Complications- dissection of ccoronary artery
Cardiac tamponade
Restenosis
Hematoma formation at the site
Thrombolytic therapy/fibrinolytic
therapy
The purpose of thrombolytics is to dissolve and
lyse the thrombus in a coronary artery
(thrombolysis), allowing blood to flow through the
coronary artery again (reperfusion), minimizing the
size of the infarction, and preserving ventricular
function
Indications
Chest pain for longer than 20 minutes,
unrelieved by nitroglycerin
ST-segment elevation in at least two leads that
face the same area of the heart
Less than 24 hours from onset of pain
Absolute Contraindications
Active bleeding
Known bleeding disorder
History of hemorrhagic stroke
History of intracranial vessel malformation
Recent major surgery or trauma
Relative contraindications
Active peptic ulcer disease
Pregnancy
Stroke more than 3 months back
Uncontrolled hypertension
Start within 30 minutes( door-to-needle time)
Common thrombolytics
1st generation
Streptokinase
Urokinase
2nd generation
alteplase ( tPA)
reteplase
Anistreplase
Nursing considerations
Minimize the number of times the patients skin is
punctured.
Avoid intramuscular injections.
Draw blood for laboratory tests when starting the
IV line.
Monitor for acute dysrhythmias, hypotension, and
allergic reaction.
Monitor for reperfusion: resolution of angina or
acute ST-segment changes.
Check for signs and symptoms of bleeding:
Pharmacologic management
Analgesics
morphine sulphate
decreases preload and afterload
reduce anxitey
Nitrates
IV nitroglycerin
ACE inhibitors
increases the left ventricular function
prevent ventricular remodelling
Beta-adrenergic blockers
decreases the contractility and myocardial
oxygen demand
Cholesterol lowering agents
Stool softeners
SURGICAL MANAGEMENT
CORONARY ARTERY BYPASS GRAFT(CABG)
Construction of new conduits between aorta
or other major arteries with help of CPB machine
Indications
Triple vessel disease
60% occlusion of LAD
Fails medical management
Grafts used
Internal mammary artery
Great saphenous vein
Inferior epigastric artery
Radial artery
Nursing Management
Assessment
subjective data
objective data
Diagnosis
Ineffective cardiopulmonary tissue perfusion
related to reduced coronary blood flow from
coronary thrombus and atherosclerotic plaque
Acute pain related to myocardial ischemia as
evidenced by severe chest pain and tightness,
radiation of pain to the neck and arms
Anxiety related to perceived threat of death,
possible lifestyle changes as evidenced by
fearful attitudes, frequent questioning
Cardiac rehabilitation
phase 1- hospital
pahse 11- early recovery- 2-12 wk
phase 111- late recovery- long term
maintanece programme

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