Myocardial Infarction

Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack, is the
interruption of blood supply to part of the heart, causing some heart cells to die. This is most commonly due to
occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an
unstable collection of lipids (fatty acids) and white blood cells (especially macrophages) in the wall of an artery. The
resulting ischemia (restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time,
can cause damage or death (infarction) of heart muscle tissue (myocardium).

Classical symptoms of acute myocardial infarction include sudden chest pain (typically radiating to the left arm or
left side of the neck), shortness of breath, nausea, vomiting, palpitations, sweating, and anxiety (often described as a
sense of impending doom). Women may experience fewer typical symptoms than men, most commonly shortness of
breath, weakness, a feeling of indigestion, and fatigue.[1] Approximately one quarter of all myocardial infarctions
are silent, without chest pain or other symptoms.

People will receive a number of diagnostic tests, such as an electrocardiogram, a chest X-ray and blood tests to
detect heart muscle damage. The most often used markers are the creatine kinase-MB (CK-MB) fraction and the
troponin levels. On the basis of the ECG, a distinction is made between ST elevation MI (STEMI) or non-ST
elevation MI (non-STEMI). Immediate treatment for suspected acute myocardial infarction includes oxygen, aspirin,
and sublingual nitroglycerin. If further pain relief is needed morphine sulfate is typically used.[2] A 2009 review
about the use of high flow oxygen for treating myocardial infarction found high flow oxygen administration
increased mortality and infarct size, calling into question the recommendation for its routine use.[3] Most cases of
STEMI are treated with thrombolysis or percutaneous coronary intervention (PCI). NSTEMI is managed with
medication, although PCI is often performed during hospital admission. In people who have multiple blockages and
who are relatively stable, or in a few emergency cases, bypass surgery maybe an option.

Heart attacks are the leading cause of death for both men and women worldwide.[4] Important risk factors are
previous cardiovascular disease, older age, tobacco smoking, high blood levels of certain lipids (triglycerides, low-
density lipoprotein) and low levels of high density lipoprotein (HDL), diabetes, high blood pressure, obesity, chronic
kidney disease, heart failure, excessive alcohol consumption, the abuse of certain drugs (such as cocaine and
methamphetamine), and chronic high stress levels

Anatomy and Physiology

The heart is a hollow, muscular organ located in the center of the thorax, where it occupies the space between the
lungs (mediastinum) and rests on the diaphragm. It weighs approximately 300 g (10.6 oz), although heart weight and
size are influenced by age, gender, body weight, extent of physical exercise and conditioning, and heart disease. The
heart pumps blood to the tissues, supplying them with oxygen and other nutrients. The pumping action of the heart is
accomplished by the rhythmic contraction and relaxation of its muscular wall. During systole (contraction of the
muscle), the chambers of the heart become smaller as the blood is ejected. During diastole (relaxation of the
muscle), the heart chambers fill with blood in preparation for the subsequent ejection. A normal resting adult heart
beats approximately
60 to 80 times per minute. Each ventricle ejects approximately 70 mL of blood per beat and has an output of
approximately 5 L per minute.

ANATOMY OF THE HEART

The heart is composed of three layers (Fig. 26-1). The inner layer, or endocardium, consists of endothelial tissue and
lines the inside of the heart and valves. The middle layer, or myocardium, is made

up of muscle fibers and is responsible for the pumping action. The exterior layer of the heart is called the
epicardium. The heart is encased in a thin, fibrous sac called the pericardium, which is composed of two layers.
Adhering to the epicardium is the visceral pericardium. Enveloping the visceral pericardium is the

parietal pericardium, a tough fibrous tissue that attaches to the great vessels, diaphragm, sternum, and vertebral
column and supports the heart in the mediastinum. The space between these two layers (pericardial space) is filled
with about 30 mL of fluid, which lubricates the surface of the heart and reduces friction during systole.

Heart Chambers

The four chambers of the heart constitute the right- and leftsided pumping systems. The right side of the heart, made
up of the right atrium and right ventricle, distributes venous blood (deoxygenated blood) to the lungs via the
pulmonary artery (pulmonary circulation) for oxygenation. The right atrium receives

blood returning from the superior vena cava (head, neck, and upper extremities), inferior vena cava (trunk and lower
extremities), and coronary sinus (coronary circulation). The left side of the heart, composed of the left atrium and
left ventricle, distributes oxygenated blood to the remainder of the body via

the aorta (systemic circulation). The left atrium receives oxygenated blood from the pulmonary circulation via the
pulmonary veins. The varying thicknesses of the atrial and ventricular walls relate to the workload required by each
chamber. The atria are thin-walled because blood returning to these chambers generates low pressures. In contrast,
the ventricular walls are thicker because they generate greater pressures during systole. The right ventricle contracts
against low pulmonary vascular pressure and has thinner walls than the left ventricle. The left ventricle, with walls
two-and-a-half times more muscular than those of the right ventricle, contracts against high systemic pressure.
Because the heart lies in a rotated position within the chest cavity, the right ventricle lies anteriorly (just beneath the
sternum) and the left ventricle is situated posteriorly. The left ventricle is responsible for the apex beat or the point
of maximum impulse (PMI), which is normally palpable in the left midclavicular line of the chest wall at the fifth
intercostal space.

Heart Valves

The four valves in the heart permit blood to flow in only one direction. The valves, which are composed of thin
leaflets of fibrous tissue, open and close in response to the movement of blood and pressure changes within the
chambers. There are two types of valves: atrioventricular and semilunar.

ATRIOVENTRICULAR VALVES
The valves that separate the atria from the ventricles are termed atrioventricular valves. The tricuspid valve, so
named because it is composed of three cusps or leaflets, separates the right atrium

from the right ventricle. The mitral, or bicuspid (two cusps) valve, lies between the left atrium and the left ventricle.
Normally, when the ventricles contract, ventricular pressure rises, closing the atrioventricular valve leaflets. Two
additional structures, the papillary muscles and the chordae tendineae, maintain valve closure. The papillary
muscles, located on the sides of the ventricular walls, are connected to the valve leaflets by thin fibrous bands called
chordae tendineae. During systole, contraction of the papillary muscles causes the chordae tendineae to become taut,
keeping the valve leaflets approximated and closed.

SEMILUNAR VALVES

The two semilunar valves are composed of three half-moon-like leaflets. The valve between the right ventricle and
the pulmonary artery is called the pulmonic valve; the valve between the left ventricle and the aorta is called the
aortic valve.

Coronary Arteries

The left and right coronary arteries and their branches (Fig. 26-2) supply arterial blood to the heart. These arteries
originate from the aorta just above the aortic valve leaflets. The heart has large metabolic requirements, extracting
approximately 70% to 80%of the oxygen delivered (other organs consume, on average, 25%). Unlike other arteries,
the coronary arteries are perfused during diastole. An increase in heart rate shortens diastole and can decrease
myocardial perfusion. Patients, particularly those with

coronary artery disease (CAD), can develop myocardial ischemia (inadequate oxygen supply) when the heart rate
accelerates. The left coronary artery has three branches. The artery from the point of origin to the first major branch
is called the left main coronary artery. Two bifurcations arise off the left main coronary artery. These are the left
anterior descending artery, which courses down the anterior wall of the heart, and the circumflex artery, which
circles around to the lateral left wall of the heart.

The right side of the heart is supplied by the right coronary artery, which progresses around to the bottom or inferior
wall of the heart. The posterior wall of the heart receives its blood supply by an additional branch from the right
coronary artery called the posterior descending artery. Superficial to the coronary arteries are the coronary veins.
Venous blood from these veins returns to the heart primarily

through the coronary sinus, which is located posteriorly in the right atrium.

Cardiac Muscle

The myocardium is composed of specialized muscle tissue. Microscopically, myocardial muscle resembles striated
(skeletal) muscle, which is under conscious control. Functionally, however,

myocardial muscle resembles smooth muscle because its contraction is involuntary. The myocardial muscle fibers
are arranged in an interconnected manner (called a syncytium) that allows for coordinated

myocardial contraction and relaxation. The sequential pattern of contraction and relaxation of individual muscle
fibers ensures the rhythmic behavior of the myocardium as a whole and

enables it to function as an effective pump.

Pathophsyiology
 Precipitating Factors
Predisposing Factors
• Smoking
• Age
• Diabetes
• Family history of heart
• High Blood Pressure
attack
• Sedentary Lifestyle
• Obesity

Artherosclerosis

Narrowing of lumen

Rupture of plaques

Thrombosis

Occlusion of coronary
artery

If Treated
Necrosis of myocardium

Laboratory Tests Diagnostic Test

• Creatine- • ECG (ST-

Kinase (CK-MB) elevation)
and Troponin
• Lactate
Hydrogenase
• LDL

Myocardial Infarction

Prognosis

Medical Management Surgical

If Treated Nsg Mgt If not treated
• Antiplatelet Management • Vs • Arrythmias
Agents • Coronar monitoring • Cardiogenic Shock
• Lidocaine(vaso y artery • LSLF • Myocardial
dilator) bypass Diet Rupture
• Nitroglycerin graft(CABG) • Rest • Congestive Heart
• Morphine • Angiopl (CBR s BRP) Failure
Pathophysiology Narrative

CK-MB

CK catalyses the conversion of creatine and consumes adenosine triphosphate (ATP) to create phosphocreatine and adenosine diphosphate
(ADP). Elevated CK-MB signifies damage to muscle tissue including the heart.

LDH

Damage to heart tissues releases heart LDH, which is rich in LDH-1, into the bloodstream.

Angiography

A catheter is inserted into an artery (usually the femoral artery) and pushed to the vessels supplying the heart to determine narrowing of blood
vessels.

CABG

Arteries or veins from elsewhere in the patient's body are grafted to the coronary arteries to bypass atherosclerotic narrowings and improve the
blood supply to the coronary circulation supplying the myocardium (heart muscle).

Angioplasty

Angioplasty is the technique of mechanically widening a narrowed or obstructed blood vessel; typically as a result of atherosclerosis. An empty
and collapsed balloon on a guide wire, known as a balloon catheter, is passed into the narrowed locations and then inflated

Cardiogenic Shock

Cardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a cardiac output to supply an adequate amount
of oxygenated blood to the tissues of the body.

Myocardial Rupture

Myocardial rupture (or heart rupture) is a laceration or tearing of the walls of the ventricles or atria of the heart

Heart attack risk factors include:

* Age. Men who are 45 or older and women who are 55 or older are more likely to have a heart attack than younger men and women.

* Tobacco. Smoking and long-term exposure to secondhand smoke damage the interior walls of arteries — including arteries to your heart —
allowing deposits of cholesterol and other substances to collect and slow blood flow. Smoking also increases the risk of deadly blood clots
forming and causing a heart attack.
 * Diabetes. Diabetes is the inability of your body to adequately produce or respond to insulin properly. Insulin, a hormone secreted by your
pancreas, allows your body to use glucose, which is a form of sugar from foods. Diabetes can occur in childhood, but it appears more often in
middle age and among overweight people. Diabetes greatly increases your risk of a heart attack.

* High blood pressure. Over time, high blood pressure can damage arteries that feed your heart by accelerating atherosclerosis. The risk of
high blood pressure increases as you age, but the main culprits for most people are eating a diet too high in salt and being overweight. High blood
pressure can also be an inherited problem.

* High blood cholesterol or triglyceride levels. Cholesterol is a major part of the deposits that can narrow arteries throughout your body,
including those that supply your heart. A high level of the wrong kind of cholesterol in your blood increases your risk of a heart attack. Low-
density lipoprotein (LDL) cholesterol (the "bad" cholesterol) is most likely to narrow arteries. A high LDL level is undesirable and is often a
result of a diet high in saturated fats and cholesterol. A high level of triglycerides, a type of blood fat related to your diet, also is undesirable.
However, a high level of high-density lipoprotein (HDL) cholesterol (the "good" cholesterol), which helps the body clean up excess cholesterol,
is desirable and lowers your risk of heart attack.

* Family history of heart attack. If your siblings, parents or grandparents have had heart attacks, you may be at risk, too. Your family may
have a genetic condition that raises unwanted blood cholesterol levels. High blood pressure also can run in families.

* Lack of physical activity. An inactive lifestyle contributes to high blood cholesterol levels and obesity. People who get regular aerobic
exercise have better cardiovascular fitness, which decreases their overall risk of heart attack. Exercise is also beneficial in lowering high blood
pressure.

* Obesity. Obese people have a high proportion of body fat (a body mass index of 30 or higher). Obesity raises the risk of heart disease
because it's associated with high blood cholesterol levels, high blood pressure and diabetes.