Acute Myocardial Infarction

Sarah Priore RN BSN

Objectives

– Define and understand the epidemiology of MI’s and how they are classified

– Will be able to identify the risk factors associated with MI’s

– Will be able to recognize signs and symptoms of acute MI and what the appropriate interventions are.

– Understand the treatment options available to treat acute MI.

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 Subendocardial

Diagnostic

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

Epidemiology

• MI’s are the leading cause of death in the United States, affecting one in five men and one in six women.

• 450,000 people in the US die from coronary disease each year.

• Incidence rates increase with age as do mortality rates due to infarction.

Epidemiology

• The survival rate for those hospitalized due to MI has reached approximately 95%.

• This is the result of the advancements made in modern medical technology.

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

Smoking

• Tobacco use increases the risk of coronary artery disease two to six times more than non smokers.

• Nicotine increases platelet thrombus adhesion and vessel

inflammation.

Diabetes & Hypertension

• Diabetes not only increases the rate of atherosclerotic formation in vascular vessels but also at an earlier age.

• The constant stress of high blood pressure has been associated with the increased rate of plaque formation.

• Shearing Stress and inflammation of endothelial lining begins the process.

Hyperlipidemia

• Elevated levels of cholesterol, LDL’s or triglycerides are associated with the increased risk of coronary plaque formation and MI.

• Almost 50% of the U.S.

population has some

form of dyslipidemia.

Obesity and Physical Inactivity

• Mortality rate from CAD is higher in those who are obese.

• Some evidence shows that those who carry their weight in their abdomen have a higher incidence of CAD

• Physically inactive people have lower HDL levels with higher LDL levels and an increase in clot formation.

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

Signs and Symptoms

• Signs and symptoms are unique to each individual patient.

• Ranging from no symptoms to sudden cardiac arrest.

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.

Chest Pain

• PQRST assessment for chest pain

• P- Precipitating events

• Q- Quality of pain

• R- Radiation of pain

• S- Severity of pain

• T- Timing

Nausea and Vomiting

• Not everyone will experience this.

• Vomiting results as a reflex from severe pain.

• Vasovagal reflexes initiated from area of ischemia.

Sympathetic Nervous System Stimulation

• During an MI increased catecholamines are released.

• This results in diaphoresis and vasoconstriction of peripheral blood vessels.

• “Cool Sweat” with a temperature increase during the first 24 hours.

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.

Video

• Watch your own heart attack…This is a little graphic!

http://www.youtube.com/watch?v=LUt1xXASm_s

Within the first 10 minutes upon arrival to the hospital:

• Check vital signs and evaluate oxygen saturation

• Establish IV access• Obtain and review 12-lead ECG• Take a brief focused history and perform a

physical exam• Obtain blood samples to evaluate initial cardiac

markers, electrolytes and coagulation

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

AnginaStable

• 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.

Serum Cardiac Markers

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 patientMONA

• 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.

Cardiac Catheterization while undergoing an MI

• http://www.youtube.com/watch?v=TS0Je1m9Q8A&feature=related

Angioplasty and Stenting

http://www.youtube.com/watch?v=9FPapBbbS4o&feature=related

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.

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.