Pharmacotherapy of Myocardial infraction

Myocardial infarction pathophysiology and its pharmacotherapy

1. Acute Myocardial
Infarction
RVS Chaitanya koppala

2. 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.
Cont……

3. •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.

6. 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.

8. MI Classifications
MI’s can be subcategorized by anatomy and
clinical diagnostic information.
Anatomic
Transmural
Subendocardial
Diagnostic
ST elevations (STEMI) and
Non ST elevations (NSTEMI).

9. 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.
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.

10. Risk Factors
The presence of any risk factor is associated with
doubling the risk of an MI.
Non Modifiable
Age
Gender
Family history

11. Risk Factors
Modifiable
•Smoking
•Diabetes Control
•Hypertension
•Hyperlipidemia
•Obesity
•Physical Inactivity

12. 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.

13. 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.

14. 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.

15. 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.

16. 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.

17. 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

18. 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.

19. Chest Pain
PQRST assessment for chest pain
P- Precipitating events
Q- Quality of pain
R- Radiation of pain
S- Severity of pain
T- Timing

20. Nausea and Vomiting
Not everyone will experience this.
Vomiting results as a reflex from severe pain.
Vasovagal reflexes initiated from area of
ischemia.

21. 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.

22. 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.

23. 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

24. 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.

25. Normal Sinus Rhythm