1. MYOCARDIAL INFARCTION PRESENTED BY- SAM MATHEW STAFF NURSE
DH ED
2. Objectives Define and understand the epidemiology of MIs and
how they are classified Will be able to identify the risk factors
associated with MIs Will be able to recognize signs and symptoms of
MI and what the appropriate interventions are. Understand the
treatment options available to treat MI. Nursing responsibilities
Follow up care
3. DEFINITION . Myocardial infarction is a disease condition
which is caused by reduced blood flow in a coronary artery due to
atherosclerosis and occlusion of an artery by an embolus or
thrombus .
4. Epidemiology MIs 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.
5. MI Classifications MIs can be subcategorized by anatomy and
clinical diagnostic information. Anatomic Transmural -
atherosclerosis involving a major coronary artery, it is usually as
a result of complete occlusion of the artery in addition on ECG ST
elevation and q waves are seen(STEMI)(epicardium,myo,endocardium)
Subendocardial - small area in the subendocardial wall of the left
ventricle, ventricular septum, or papillary muscles. It is
particularly susceptible to ischemia,in addition to ST depression
is seen on ecg(NSTEMI) Diagnostic ST elevations (STEMI)-ECG must
show new ST elevation in two or more adjacent ECG leads or new LBBB
, it must be greater than 2 mm in leads V2 and V3 or greater than 1
mm in all other leads. non ST elevations (NSTEMI)-ST segment
depression 0.5mm or dynamic T- wave inversion with pain or
discomfort , and cardio specific proteinstroponin are rises in
blood in NSTEMI.
6. CORONARY ARTERIES OF HEART
7. Tunica Intima T. Adventitia Tunica media plaques Thrombus
Atherosclerosis is a narrowing of the arteries caused by a buildup
of plaque
10. NON-MODIFIABLE RISK FACTORS FACTOR AGE SEX FAMILY
HISTORY
11. AGE: More than 40 years. FAMILY HISTORY: Myocardial
infarction can be inherited from parents to children. GENDER:
Myocardial infarction is 3 times more in men than women.
13. HIGH BLOOD CHOLESTROL LEVEL LOW DENSITY LIPOPROTEIN (LDL)
DANGEROUS HIGH DENSITY LIPOPROTEIN (HDL) LIPIDS (LIPOPROTIENS)
14. HYPERTENSION High blood pressure our arteries are designed
to pump blood at a certain pressure. If that pressure is exceeded,
the walls of the arteries will be damaged . injury to endothelial
lining , atherosclerosis narrowed & thickened arterial walls
risk of M.I.
15. SMOKING Smoking can damage the walls of your arteries.(
toxic substances in cigarette) Atherosclerosis narrowed &
thickened arterial walls Risk of M.I.
16. PHYSICAL INACTIVITY Improper lipid metabolism LDL level
increases Starts accumulating in blood vessels Risk of M.I.
17. OBESITY More lipids are produced LDL level increases
Atherosclerosis Risk of M.I.
18. DIABETES MELLITUS Diabetes increases the risk of MI because
it increases the rate of atherosclerotic progression and adversely
affects the lipid profile Risk of having M.I.
19. STRESS Release stress hormones like adrenaline,
noradrenaline, and cortisol increase in heart rate, and elevated
blood pressure its causing damage over time to all your blood
vessel That damage increases the risk of plaque buildup in coronary
arteries or can even cause a rupture of plaque MI The way you
handle stress also matters. If you respond to it in unhealthy ways
-- such as smoking, overeating,or not exercising - that makes
matters worse.
20. PATHOPHYSIOLOGY
21. How a Heart Attack Happens
22. Cholesterol deposition within the wall of the main artery
This deposited cholesterol ultimately forms a plaque in the wall of
the artery called atherosclerotic plaque. Atherosclerotic plaque
formation is a long term process, required many years to establish.
Sometimes this plaque may rupture or erode,it leads to activate
clotting mechanism so platelet aggregation and fibrin deposition,
which lead to formation of an occlusive thrombus in a coronary
artery. This occlusive thrombus completely block a coronary artery
and interrupts blood supply to part of the myocardium (heart
muscle), It lead to irreversible changes and death of myocardial
cells, and ultimately ST-segment elevation myocardial infarction
develops. PATHOPHYSIOLOGY
23. CLINICAL MANIFESTATIONS Chest pain due to a lack of blood
and oxygen supply of the heart muscle Characteristics: Severe,
immobilizing chest pain. Usually prescribed as heaviness, pressure,
tightness, burning. Location: Substernal, Retrosternal or
Epigastric. Radiation: It may radiate to neck, jaw, arm or back.
Duration: Lasts for 20 minutes or more. PAIN
24. Cardiovascular- Initially the BP and pulse may be elevated.
Later, BP will drop due to decreased cardiac output. palpitation.
Jugular veins may become distended and have obvious
pulsations.
25. CONTD.. Respiratory- Respiratory symptoms occur when the
damaged the heart muscle limits the pumping action of the left
ventricle, causing acute left heart failure and consequent lung
congestion. Shortness of breath Dyspnea/Tachypnea Crackles
Pulmonary edema
26. Gastrointestinal- Nausea Vomiting Stimulation of vomiting
center by severe pain causes nausea & vomiting FEVER It is due
to inflammatory process caused by Myocardial cell death.
27. In response to pain and the blood flow abnormalities that
result from dysfunction of the heart muscle SYMPATHETIC NERVOUS
SYSTEM STIMULATION Increased catecholamine releases.(adrenal
medulla) Diaphoresis (perfuse sweating Cold & clammy skin (cold
sweat). Integumentary system (Skin) cool, clammy skin Diaphoresis
Pallor, Cyanosis Coolness of extremities
28. Genitourinary- Hypoperfusion to the kidneys leads to
decrease renal perfusion pressure which is required to maintain
glomerular filteration rate in the kidney Decrease GFR leads to
decrease urinary output Urine output (Oliguria): 30ml/HR or