Acute Myocardial Infarction

byRAMKUMAR

Definition• Otherwise know as heart attack• An MI occurs when there is a diminished

blood supply to the heart which leads to myocardial cell damage and ischemia.

• Contractile function stops in the necrotic areas of the heart.

• Ischemia usually occurs due to blockage of the coronary vessels.

Definition cont.

• This blockage is often the result of thrombus that is superimposed on an ulcerated or unstable atherosclerotic plaque formation in the coronary artery.

• MI’s are described by the area of occurrence.

• Anterior, Inferior, Lateral or Posterior.

Coronary Artery Anatomy

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.

MI Classifications• MI’s can be subcategorized by anatomy

and clinical diagnostic information.Anatomic

• Transmural and SubendocardialDiagnostic

• ST elevations (STEMI) and non ST elevations (NSTEMI).

Risk Factors• The presence of any risk factor is

associated with doubling the risk of an MI.Non Modifiable

• Age• Gender• Family history

Risk Factors

Modifiable• Smoking• Diabetes Control• Hypertension• Hyperlipidemia• Obesity• Physical Inactivity

Pathophysiology• Ischemia develops when there is an

increased demand for oxygen or a decreased supply of oxygen.

• Ischemia can develop within 10 seconds and if it lasts longer than 20 minutes, irreversible cell and tissue death occurs.

• Myocardial cell death begins at the endocardium. The area most distal to the arterial blood supply.

Pathophysiology• As vessel occlusion continues cell death

spreads to the myocardium and eventually to the epicardium.

• Severity of the MI depends on three factors.• Level of occlusion• Length of time of occlusion• Presence or absence of collateral

circulation

Symptoms:

• Pain is the cardinal symptom of an MI

• Anxiety and fear of impending death

• Nausea and vomiting

• Breathlessness

• Collapse/syncope

Chest Pain• The most common initial

manifestation is chest pain or discomfort.

• This is not relieved by rest, position change or nitrate administration.

• Pain is described by heaviness, pressure, fullness and crushing sensation.

• Not everyone experiences this sensation.

Cardiovascular Changes• Initially the BP and pulse may be elevated.• Later, BP will drop due to decreased

cardiac output.• Urine output will decrease• Lung sounds will change to crackles• Jugular veins may become distended and

have obvious pulsations.

DIAGNOSTICS:

• Electrocardiogram (ECG) • Blood test (Cardiac enzymes)• Echocardiogram• Nuclear scan • Chest radiographs • Coronary angiography • Exercise stress test.• Cardiac computerized tomography (CT)

or magnetic resonance imaging (MRI).

Diagnostics• After collecting patient health history, a

series of EKG’s should be taken to rule out or confirm MI.

• 12 lead EKG’s can help to distinguish between ST-elevation MI’s and Non-ST-elevation MI’s.

Normal Sinus Rhythm

Angina:Stable

• Chest pain caused by the build up of lactic acid and irritation to the myocardial nerve fibers.

• Chest pain caused by the 4 E’s.• Pain is usually relieved with rest, pain

meds and nitrates.

Variable/Prinzmetal/Spasm

• Transient ischemia that occurs unpredictably and almost always at rest.

• Pain is caused by vasospasm of the arteries.

• ST segment elevations will be noted.

Unstable • Chest pain at rest or with exercise and

tends to last greater than 15 minutes.• This results in reversible myocardial

ischemia but is a sign that an infarct is soon to come.

• EKG will reveal ST segment depression and T wave inversion.

STEMI• ST segment elevations• T wave changes• Q wave development• Enzyme elevations• Reciprocals

NSTEMI• ST segment depressions• T wave changes• No Q wave development• Mild enzyme elevations• No reciprocals

STEMI vs. NSTEMI

Phases of a STEMI• Hyperacute Phase

• Occurs within the first few hours of MI onset.

• 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.

Phases of a STEMI • Fully Evolved Phase

• Q wave development• ST elevation • T waves start to become inverted in

leads facing the injury.

Phases of a STEMI• 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.

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.

Treatment Options• 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.

General Treatment for the MI patient• Morphine• Oxygen• Nitroglycerin• Aspirin

Fibrinolytic Therapy• Indicated for patients with STEMI MI’s.• Should be given within 12 hours of

symptom onset. • Fibrinolytics will break down clots found

within the vessles• Contraindications: post op surgical

patients, history of hemorrhagic stroke, ulcer disease, pregnancy, ect.

Cardiac Catheterization• A diagnostic angiography which includes

angioplasty and possible stenting.• Performed by an interventional cardiologist

with a cardiac surgeon on stand by.• Percutaneous procedure through the

femoral or brachial artery.

Cardiac Catheterization• Upon arrival to the cath lab all actue MI

patients will receive:• A bolus dose of plavix• IV Integrelin• Heparin dose either subcu or IV drip• Angiomax : a DTI may be substituted

for heparin and integrelin.

Coronary artery bypass graft• Surgical treatment where saphenous vein

is harvested from the lower leg and used to bypass the occluded vessels.

Long Term Care• Smoking Cessation and lifestyle

modifications.• Aspirin, Beta Blockers and Clopidogrel will

be indefinite.• Lipid lowering medication along with diet

modifications.

Complications

Vascular Complications• Recurrent ischemia• Recurrent infarctionMechanical Complications• Left ventricular free wall rupture• Ventricular septal rupture• Papillary muscle rupture with

acute mitral regurgitation

COMPLICATION:

Myocardial Complications• Diastolic dysfunction• Systolic dysfunction• Congestive heart failure• Hypotension/cardiogenic shock• Right ventricular infarction• Ventricular cavity dilation• Aneurysm formation (true, false)

References• Bolooki, H.M.& Askari, A. (Published August 8 2010).

Acute Myocardial Infarction. Retrieved from http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/acute-myocardial-infarction/#s0050

• Lewis, S., Heitkemper, M., & Dirksen, S. (2004). Medical surgical nursing assessment and management of clinical problems. St. Louis, MO: Mosby.

• McCance, K.L., Huether, S.E., Brashers, V.L.& Rote, N.S. (2010). Pathophysiology the biological basis for disease in adults and children. Maryland Heights, MO: Mosby Elsevier.