Pharmacotherapy of Myocardial infraction
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Transcript of Pharmacotherapy of Myocardial infraction
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