Acute Myocardial Infarction

RVS Chaitanya koppala

DefinitionOtherwise know as heart attackAn 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.

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 eventsIschemia – 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.AnatomicTransmural SubendocardialDiagnosticST elevations (STEMI) and Non ST elevations (NSTEMI).

EpidemiologyMI’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.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 FactorsThe presence of any risk factor is associated with doubling the risk of an MI.

Non Modifiable AgeGenderFamily history

Risk FactorsModifiable

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

SmokingTobacco 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 & HypertensionDiabetes 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.

HyperlipidemiaElevated 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 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.

PathophysiologyAs vessel occlusion continues cell death

spreads to the myocardium and eventually to the epicardium.

Severity of the MI depends on three factors.Level of occlusionLength of time of occlusionPresence or absence of collateral circulation

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 PainPQRST assessment for chest painP- Precipitating eventsQ- Quality of pain R- Radiation of painS- Severity of painT- Timing

Nausea and VomitingNot 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.

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