A myocardial infarction (MI or heart attack) occurs when blood flow to part of the heart is blocked, damaging heart muscle cells. This is usually caused by a buildup of fatty deposits in the coronary arteries. An MI can be life-threatening and is characterized by chest pain or discomfort. Diagnosis involves ECG changes, elevated cardiac enzyme levels, and symptoms. Treatment focuses on restoring blood flow, relieving pain, and preventing further damage.

1. •Necrosis ( death ) of
myocardial cells
•A life threatening event
•Heart Attack, Coronary
occlusion (closure)

2. • MI is usually caused by reduced blood flow/
oxygen supply in a coronary artery
• vasospasm (sudden constriction/ narrowing) of a
coronary artery
• and increased demand for oxygen

4. Nonmodifiable Risk Factors
• Family history of coronary heart disease
• Increasing age
• Gender (heart disease occurs more often in
men and in premenopausal women) *men and
premenopausal women have low estrogen = helps in ↑HDL and ↓LDL
• Race : higher incidence of heart disease in
African Americans than in Caucasians
(NHLBI, 2002)

5. Modifiable Risk Factors
• High blood cholesterol level (high blood lipids)
• Cigarette smoking, tobacco use (nicotine causes
vasoconstriction)
• Hypertension (high blood pressure causes vasoconstriction)
• Diabetes mellitus (impaired insulin production- excess glucose-
liver uses glucose to make fatty acids)
• Lack of estrogen in women
• Physical inactivity (fats are not burned, lodges in blood
vessels)
• Obesity (high fat deposits in the body)

6. • Cardiovascular
– Chest pain or discomfort.
• Palliative: not relieved by rest or sublingual
vasodilator therapy, requires opioids.
• Quality: variable, but often diffuse, steady substernal
chest pain. Other sensations include a crushing and
squeezing feeling in the chest.
• Radiation: pain may radiate to the arms (commonly
the left), and to the shoulders, neck, back, or jaw.
• Time: pain continues for more than 15 minutes.
– Increased jugular venous distention may be
seen if the MI has caused ® heart failure.

7. • Respiratory
– Shortness of breath, dyspnea, tachypnea,
and crackles (decreased oxygen supply)
• Genitourinary
– Decreased urinary output (*when there is decreased
blood flow RAAS is activated, aldosterone = water retention)

8. • Skin
– Cool, clammy, diaphoretic, (compensatory
mechanism = Pumping blood through clogged arteries takes more
effort from your heart, so your body will sweat more to try o keep
your body temperature down during the extra exertion. )
and Pale appearance
• Neurologic
– Anxiety, restlessness, light-headedness
(there is a decrease in contractility and cerebral oxygenation.)

9. ECG
•Ischemia causes inversion of T wave because of altered repolarization.
•Cardiac muscle injury causes elevation of the ST segment and tall,
symmetrical T waves.
•With Q-wave infarction, Q or QS waves develop because of the absence of
depolarization current from the necrotic tissue and opposing currents from
other parts of the heart.

10. STEMI: ST-segment Elevation MI
– Significant damage to Myocardium
NSTEM : Non-ST-segment
Elevation MI
– Cardiac biomarkers are high but no
ECG evidence of MI

11. LABORATORY TESTS
• Creatine Kinase and Its Isoenzymes.
• There are three CK isoenzymes:
– CK-MM (skeletal muscle),
– CK-MB (heart muscle), N = 0-3% of total CK
– CK-BB (brain tissue).
• CK-MB is the cardiac-specific isoenzyme;
• CK-MB is found mainly in cardiac cells and therefore
rises only when there has been damage to these cells.
• the most specific index for the diagnosis of acute MI
(Braunwald et al., 2001).
• The level starts to increase within a few hours and peaks
within 24 hours of an MI. If the area is reperfused (eg,
due to thrombolytic therapy or PTCA), it peaks earlier.

12. • Nonspecific enzyme myoglobin may be
elevated
– Myoglobin: a heme protein that helps to
transport oxygen. Like CK-MB enzyme,
myoglobin is found in cardiac and skeletal
muscle.
– The normal ("negative") range is 0 - 85
nanograms per milliliter (ng/mL).

13. • Triponin T and I are myocardial proteins that
increase in the serum about 3 to 4 hours after
an MI, peak in 4 to 24 hours, and are
detectable for up to 2 weeks;
• the test can help diagnose an MI up to 2
weeks earlier, and only unstable angina
causes a false positive.
• N = < 0.2 mcg/L
• N = < 3.1 mcg/L

15. Pharmacologic Intervention:
•Analgesics: Morphine
•Vasodilator : Nitrogylcerine
•ACE Inhibitors
•Thrombolytics: to dissolve
thrombus formation

16. • Anticoagulants or other anti-platelet
medications : Aspirin / Heparin
• Beta-adrenergic blockers, to improve
oxygen supply and demand, decrease
sympathetic stimulation to the heart,
promote blood flow in the small vessels
of the heart, and provide antiarrhythmic
effects.

17. EMERGENT PERCUTANEOUS CORONARY
INTERVENTION (PCI)
• PCI may be used to open the
occluded coronary artery in an acute
MI and promote reperfusion to the
area that has been deprived of
oxygen.
• Angioplasty

18. Nursing Interventions:
• Monitor baseline vital signs before and 10 to 15
minutes after administering drugs. Also monitor
blood pressure continuously when giving
nitroglycerin I.V. (causes vasodilation =
improving blood flow)
• Monitor continuous ECG to watch for life
threatening arrhythmias (common within 24
hours after infarctions) and evolution of the MI
(changes in ST segments and T waves).

19. • Administer O2 at 2-5 L per cannula : Oxygen
therapy may increase the oxygen supply to
the myocardium and other tissues
• pain relief : administer analgesics promptly. Place
the patient in supine position during administration
(to minimize hypotension)
• Promote rest (to decrease cardiac workload) with
early gradual increase in mobilization (to prevent
deconditioning)

20. Cardiac Rehabilitation
• After the MI patient is free of symptoms, an active
rehabilitation program is initiated.
• Targets risk reduction by means of education,
individual and group support, and physical activity.
• Goals are extend and improve the quality of life.
• The immediate objectives
– to limit the effects and progression of atherosclerosis,
– return the patient to work and a pre-illness lifestyle,
– enhance the psychosocial and vocational status of the
patient,
– and prevent another cardiac event.

21. Phase I
• may begin with the diagnosis of atherosclerosis,
which may occur when the patient is admitted to the
hospital for ACS (unstable angina, acute MI).
• It consists of low-level activities and initial education
for the patient and family.
• The amount of activity recommended at discharge
depends on the age of the patient, his or her
condition before the cardiac event, the extent of the
disease, the course of the hospital stay, and the
development of any complications.

22. Phase II
• occurs after the patient has been discharged.
• It usually lasts for 4 to 6 weeks but may last up to 6
months.
• This outpatient program consists of supervised, often
ECG-monitored, exercise training that is
individualized based on the results of an exercise
stress test.
• Support and guidance related to the treatment of
the disease and education and counseling related to
lifestyle modification for risk factor reduction are a
significant part of this phase.

23. Phase III
• focuses on maintaining cardiovascular
stability and long-term conditioning.
• The patient is usually self-directed
during this phase and does not require a
supervised program, although it may be
offered.
• The goals of each phase build on the
accomplishments of the previous phase.