I.

DEFINITION

Myocardial Infarction is defined by the demonstration of myocardial cell necrosis due to

significant and sustained ischaemia. It is usually, but not always, an acute manifestation of
atherosclerosis-related coronary heart disease. MI results from either coronary heart disease,
which implies obstruction to blood flow due to plaques in the coronary arteries or, much less
frequently, to other obstructing mechanisms (e.g. spasm of plaque-free arteries).
Locally, cardiovascular diseases (CVD), including heart attack (MI) and stroke, are among
the top 5 causes of death in the Philippines according to the Department of Health. Dr. Shelbay
Blanco of DOH Center for Health Development said that five years ago CVDs only placed 7th as
the leading cause of morbidities and mortalities but today it is among the top. Internationally,
Cardiovascular disease (CVD), including heart attack remains the leading cause of death in the
United States, responsible for 840,768 deaths (635,260 cardiac) in 2016. From 2006 to 2016, the
US death rate from CVD decreased by 18.6% and from coronary heart disease by 31.8%.
The risk factors for MI are the same as those for stroke (cerebrovascular disease)
or peripheral vascular disease. These risk factors include:a family history or heredity,
cigarette smoking, high blood pressure, high cholesterol, and diabetes.While heredity is beyond
a person's control, all the other risk factors can be minimized to try to prevent coronary artery
disease from developing. If atherosclerosis (atheroma=fatty plaque + sclerosis=hardening) is
already present, minimizing these risk factors can decrease further narrowing. While the classic
symptoms of a heart attack are chest pain and shortness of breath, the symptoms can be quite
varied. The most common symptoms of a heart attack include: pressure or tightness in the chest,
pain in the chest, back, jaw, and other areas of the upper body that lasts more than a few
minutes or that goes away and comes back, shortness of breath, sweating, nausea, vomiting,
anxiety, a cough, dizziness, and a fast heart rate.
The prevention of myocardial infarction (MI) is based on some well designed strategies
aimed at treating both asymptomatic high-risk patients (primary prevention) and patients with
established CHD (secondary prevention). A positive impact from primary prevention can be
basically achieved trough a reduction in high blood pressure and by correcting dyslipidemia. The
benefit can be substantially increased by smoking cessation, increasing physical exercise,
reduction of body weight, use of post-menopausal oestrogen, moderate alcohol consumption
and use of high doses of vitamin E in those patients who are compliant with the specific
strategies. Secondary prevention of MI can be again obtained by controlling blood pressure and
reducing serum cholesterol in patients surviving acute MI who can also benefit from the
administration of beta-blockers, aspirin and probably ace-inhibitors particularly in presence of left
ventricular dysfunction
The goals of medical management are to minimize myocardial damage, preserve
myocardial function, and prevent complications. Emergent Percutaneous Coronary Intervention
is the procedure used to open the occluded coronary artery and promote reperfusion to the area
that has been deprived of oxygen. PCI may also be indicated in patients with unstable angina
and NSTEMI for patients who are at high risk due to persistent ischemia. Pharmacological
management includes: Morphin-administered in IV boluses is used for MI to

reduce pain and anxiety. ACE Inhibitors which prevent the conversion of angiotensin I to
angiotensin II to decrease blood pressure and for the kidneys to secrete sodium and fluid,
decreasing the oxygen demand of the heart. Thrombolytics-dissolve the thrombus in the
coronary artery,allowing blood to flow through the coronary artery again, minimizing the size of
the infarction and preserving ventricular function.
Complications of MI include arrhythmic, mechanical, and inflammatory (early pericarditis and
post-MI syndrome) sequelae, as well as left ventricular mural thrombus (LVMT). In addition to
these broad categories, right ventricular (RV) infarction and cardiogenic shock are other possible
complications of acute MI.

II. PATHOPHYSIOLOGY

Causes:
Myocardial Decreased
-Coronary Atherosclerotic Heart Disease
Ischemia Myocardial
-Coronary Thrombosis/Embolism Oxygen Supply

-Decreased Blood Flow with Shock and/or

Hemorrhage

Decreased
Cardiac Decreased Altered Cell Increased
Output Myocardial Membrane Cellular
Contractility Hypoxia
 Decreased Stimulation of Stimulation of Sympathetic
Arterial Baroreceptors receptors
Pressure

Increased
Increased Myocardial
Pheripheral Contractility
Vasoconstriction

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Increased Increased
Afterload Heart Rate
 Myocardial Decreased
Oxygen Demand Diastoic Filling

Myocardial
Ischemia