I.

INTRODUCTION

Myocardial Infarction (MI) is a medical emergency in which some of the

heart’s blood supply is suddenly and severely reduced or cut-off, causing the heart

muscle (myocardium) to die because it is deprived of its oxygen supply.

In the United States, more than 1.1 million people have a heart attack each

year; about two-thirds of them are men. Almost all of them have underlying coronary

artery disease.

Myocardial Infarction (MI) usually occurs when a blockage in a coronary

artery greatly reduces or cuts off the blood supply in the area of the heart. If the

supply is greatly reduced or cut off for more than a few minutes, heart tissue dies.

A blood clot is the most common cause of blocked coronary artery. Usually,

the artery is partially narrowed by atheromas. An atheroma may rupture or tear,

narrowing the artery further and making blockage by a clot more likely. The ruptured

atheroma not only reduces the flow of the blood through an artery but also releases

substances that make platelets stickier, further encouraging clots to form.

Uncommonly, a heart attack results when a clot forms in the heart itself, breaks

away, and lodges in a coronary artery. Another uncommon cause is a spasm of a

coronary artery that stops blood flow. Spasms may be caused by drugs. Sometimes

the cause is unknown.

About two of three people who have heart attacks experience intermittent

chest pain, shortness of breath or fatigue a few days or weeks beforehand. The

episodes of pain may become more frequent and occur after less and less physical
exertion. Such a change in the pattern of chest pain (unstable angina) may

culminate in a heart attack.

Usually, the most recognizable symptom of heart attack is pain in the middle

of the chest that may spread to the back, jaw, or left arm. Less often, the pain

spreads to the right arm. The pin may occur in one or more of these places and not

in the chest at all. The pain of a heart attack is similar to the pain of angina but is

generally more severe, lasts longer and is not relieved by rest or nitroglycerin. Less

often, pain is felt in the abdomen, where it may be mistaken for indigestion,

especially because belching may bring partial or temporary relief.

About one third of people who have a heart attack have a chest pain. Such

people are likely to be women, people who are not white, those who are older than

75, those who have heart failure or diabetes, or those who have had a stroke.

Other symptoms include a feeling of faintness, sudden heavy sweating,

nausea, shortness of breath and a heavy pounding of the heart.

Abnormal heart rhythms (arrhythmias) occur in more than 90% of people who

have had a heart attack. Immediately and up to a few days after a heart attack,

abnormal heart rhythms are a common reason that the heart cannot pump

adequately. Abnormal heart rhythms originating in the ventricles may greatly

interfere with the heart’s pumping ability or may cause the heart to stop pumping

effectively (cardiac arrest). A loss of consciousness or death can result. Sometimes

loss of consciousness is the first symptom of a heart attack.

 During a heart attack, a person may become restless, sweaty, and anxious

and may experience a sense of impending doom. The feet, hands, or lips may turn

slightly blue.

Older people may have unusual symptoms. In many, the most obvious

symptom is breathlessness. Symptoms may resemble those of a stomach upset or a

stroke. Older people may become disoriented. Nonetheless, about two-thirds of

older people have chest pain as do younger people. Older people, especially

women, often take longer than younger people to admit they are ill or to seek

medical help.

Despite all the possible symptoms, as many as one of the five people who

have a heart attack have only mild symptoms or none at all. Such a silent heart

attack may be recognized only when electrocardiography is routinely performed

sometime afterward. During the early hours of a heart attack, heart murmurs and

other abnormal heart sounds may be heard through a stethoscope.

Risk Factors

 Occur primarily in men; lower incidence in women, rises in women after

menopause

 Increased blood cholesterol

 High blood pressure

 Smoking

 Diabetes milletus

 Family history
 The general objectives of this study is for us to be familiar of the disease and

know the causes, symptoms, complications, diagnosis, treatment, prognosis and

prevention of the disease.

Our specific objectives for this study is for us to 1) know the pathophysiology

of the disease, 2) formulate nursing diagnosis according to the problem, 3) formulate

goals or objectives directed to the needs of the patient, 4) implement nursing

interventions and know its rationale and 5) evaluate the outcome of our Nursing

Care Plan.

II. ANATOMY AND PHYSIOLOGY

ANATOMY OF THE HEART

The relative size and weight of the heart give few hints of its incredible

strength. Approximately the size of a person’s fist, the hollow, cone-shaped heart

weighs less than a pound. Snugly enclosed within the inferior mediastinum, the

middle cavity of the thorax, the heart is flanked on each side of the lungs. Its

more pointed apex is directed toward the left hip and rests on the diaphragm,

approximately at the level of the fifth intercostal space. It’s broader

posterosuperior aspect, or base, from which the great vessels of the body

emerge, points toward the right shoulder and lies beneath the second rib.

The heart is the organ that helps supply blood and oxygen to all parts of

the body. It is divided by a partition or septum into two halves, and the halves are

in turn divided into four chambers. The heart is situated within the chest cavity

and surrounded by a fluid filled sac called the pericardium. This amazing muscle
produces electrical impulses that cause the heart to contract, pumping blood

throughout the body.

The heart has four hollow chambers or cavities—two atria and two

ventricles. The lower two chambers of the heart are called ventricles. They are

separated by a septum into the left ventricle and the right ventricle. The upper

two heart chambers are called atria. Atria receive blood returning to the heart

from the body and ventricles pump blood from the heart to the body. Due to the

force needed to pump blood to the body, ventricles have thicker walls than do

atria.

The wall of the heart has three layers and these are epicardium,

myocardium and endocarium. The epicardium is the outer layer of the wall of the

heart. It is composed of connective tissue covered by epithelium. The epicardium

is also known as the visceral pericardium and provides an outer protective layer

for the heart. Myocardium is the muscular middle layer of the wall of the heart. It

is composed of spontaneously contracting cardiac muscle fibers which allow the

heart to contract and it stimulates heart contractions to pump blood from

the ventricles and relaxes the heart to allow the artria to receive blood. The

endocardium is the inner layer of the heart. It consists of epithelial tissue

andconnective tissue. It lines the inner cavities of the heart, covers

heart valves and is continuous with the inner lining of blood vessels and they

participate in the contraction of the heart muscle.

Cardiac conduction is the rate at which the heart conducts electrical

impulses. The following structures play an important role in causing the heart to

contract. The structures are Atrioventricular bundle which are bundle of fibers
that carry cardiac impulses, atrioventricular node that is a section of nodal tissue

that delays and relays cardiac impulses, purkinje fibers branches that extend

from the atrioventricular bundle and lastly is the sinoatrial node that is a section

of nodal tissue that sets the rate of contraction for the heart.

The Cardiac Cycle is the sequence of events that occurs when the heart

beats. Below are the two phases of the cardiac cycle: Diastole Phase where the

heart ventricles are relaxed and the heart fills with blood and Systole Phase in

which the ventricles contract and pump blood to the arteries.

Heart valves are flap-like structures that allow blood to flow in one

direction. The four valves of the heart are Aortic Valve which prevents the back

flow of blood as it is pumped from the left ventricle to the aorta., Mitral Valve that

prevents the back flow of blood as it is pumped from the left atrium to the left

ventricle, Pulmonary Valve that prevents the back flow of blood as it is pumped

from the right ventricle to the pulmonary artery and Tricuspid Valve that prevents

the back flow of blood as it is pumped from the right atrium to the right ventricle.

PHYSIOLOGY OF THE HEART

As the heart beats or contracts, the blood makes continuous round trips—

into and out of the heart, through the rest of the body, and then back to the heart

—only to be sent out again. The amount of work that the heart does is almost too

incredible to believe. In one day it pushes the body’s supply of 6liters or so of

blood through the blood vessels over 1000miles, meaning that it can actually

pumps about 6000 quarts of blood in a single day.

 CONDUCTION SYSTEM

The specialized heart cells of the cardiac conduction system methodically

generate and coordinate the transmission of electrical impulses to the myocardial

cells. The result is sequential atrioventricular contraction, which provides for the

most effective flow of blood, thereby optimizing the cardiac output. Three

physiologic characteristics of the cardiac conduction cells account for this

coordination:

 Automaticity: ability to initiate an electrical impulse.

 Excitability: ability to respond to an electrical impulse

 Conductivity: ability to transmit an electrical impulse from

one cell to another.

The pump action performed by the heart is achieved by a sequence of

alternating contraction and relaxation of the heart muscle (illustrated above).

In this context the term "systole" refers to the contraction part of the sequence

and the term "diastole" to the relaxation part of the sequence. Hence, the

"systolic" and "diastolic" pressures may be measured and recorded separately

when monitoring blood pressure.

This process is directed by the nervous system, nerve impulses initiating

each sequence. The whole series of actions that cause alternating contractions

and relaxations may be summarized in five stages:

1) The vagus nerve stimulates the sinoatrial node (SAN), the pacemaker

of the heart. The sinoatrial node (SAN) is a tiny area of specialised cardiac
(meaning "heart") muscle in the upper wall of the right atrium, near the vena cava

- as shown above. The fibres of the SAN contract rhythmically approx. 70 times

each minute. After each of these contractions, the impluse is dispersed across

the atrial cardiac muscle, leading to ...

2) ... simultaneous contraction of both the right and left atria. This

movement of the cardiac muscle pushes blood from the atria into the ventricles

(via the tricuspid and bicuspid valves).

3) The contractions of the atria send impulses down the Purkinje fibers,

which in turn stimulate the atrioventricular node (AVN). The atrioventricular node

is a mass of modified cardiac muscle located in the lower/central part of the right

atrium of the heart. The Purkinje fibres are referred to by various names in

different textbooks, so are also known as "Purkyne Fibres", "Purkynje Fibres",

and as the "Bundle of His". This/these are a bundle of modified cardiac muscle

fibers that transmit impulses from the atra, via the AVN, to the ventricles.

4) The action potential from the impulse transmitted down the Purkinje

fibers reaches the right and left branches of the Purkinje fibres - as shown in the

diagram on the right. This causes the ...

5) ... ventricles to contract, which pushes blood upwards into the arteries that

take the blood away from the heart (the pulmonary artery taking blood to the

lungs, and the aorta taking blood to the body).

Acute myocardial infarction refers to two subtypes of acute coronary

syndrome, namely non-ST-elevated myocardial infarction and ST-elevated

myocardial infarction, which are most frequently (but not always) a manifestation

of coronary artery disease. The most common triggering event is the disruption of

an atherosclerotic plaque in an epicardial coronary artery, which leads to a

clotting cascade, sometimes resulting in total occlusion of the artery.

Atherosclerosis is the gradual buildup of cholesterol and fibrous tissue in plaques

in the wall of arteries (in this case, the coronary arteries), typically over decades.

Blood stream column irregularities visible on angiography reflect artery lumen

narrowing as a result of decades of advancing atherosclerosis. Plaques can

become unstable, rupture, and additionally promote a thrombus (blood clot) that

occludes the artery; this can occur in minutes. When a severe enough plaque

rupture occurs in the coronary vasculature, it leads to myocardial infarction

(necrosis of downstream myocardium).

If impaired blood flow to the heart lasts long enough, it triggers a process

called the ischemic cascade; the heart cells in the territory of the occluded

coronary artery die (chiefly through necrosis) and do not grow back. A collagen

scar forms in its place. Recent studies indicate that another form of cell death

called apoptosis also plays a role in the process of tissue damage subsequent to

myocardial infarction. As a result, the patient's heart will be permanently

damaged. This Myocardial scarring also puts the patient at risk for potentially life

threatening arrhythmias, and may result in the formation of a ventricular

aneurysm that can rupture with catastrophic consequences.

Injured heart tissue conducts electrical impulses more slowly than normal

heart tissue. The difference in conduction velocity between injured and uninjured

tissue can trigger re-entry or a feedback loop that is believed to be the cause of
 many lethal arrhythmias. The most serious of these arrhythmias is ventricular

fibrillation (V-Fib/VF), an extremely fast and chaotic heart rhythm that is the

leading cause of sudden cardiac death. Another life threatening arrhythmia is

ventricular tachycardia (V-Tach/VT), which may or may not cause sudden

cardiac death. However, ventricular tachycardia usually results in rapid heart

rates that prevent the heart from pumping blood effectively. Cardiac output and

blood pressure may fall to dangerous levels, which can lead to further coronary

ischemia and extension of the infarct.

The cardiac defibrillator is a device that was specifically designed to

terminate these potentially fatal arrhythmias. The device works by delivering an

electrical shock to the patient in order to depolarize a critical mass of the heart

muscle, in effect "rebooting" the heart. This therapy is time dependent, and the

odds of successful defibrillation decline rapidly after the onset of cardiopulmonary

arrest.

III. PATHOPHYSIOLOGY

Myocardial infarction ("heart attack") is the irreversible damage of

myocardial tissue caused by prolonged ischemia and hypoxia. This most

commonly occurs when a coronary artery becomes occluded following the

rupture of an atherosclerotic plaque, which then leads to the formation of a blood

clot (coronary thrombosis). This event can also trigger coronary vasospasm. If a

vessel becomes completely occluded, the myocardium normally supplied by that

vessel will become ischemic and hypoxic. Without sufficient oxygen, the tissue

dies. The damaged tissue is initially comprised of a necrotic core surrounded by

a marginal (or border) zone that can either recover normal function or become

irreversibly damaged. The hypoxic tissue within the border zone may become a

site for generating arrhythmias. Collateral blood flow is an important determinant

of infarct size and whether or not the border zone becomes irreversibly damaged.

Infarcted tissue does not contribute to tension generation during systole, and

therefore can alter ventricular systolic and diastolic function and disrupt electrical

activity within the heart. After several weeks, the infarcted tissue forms a fibrotic

scar. Long-term consequences include ventricular remodeling of the remaining

myocardium (e.g., development of compensatory hypertrophy or dilation),

ventricular failure, arrhythmias and sudden death.

Myocardial infarctions produce clinical symptoms that include intense

chest pain that may radiate into the neck, jaw or arms (i.e., referred pain), a

sense of substernal heaviness, squeezing or pressure, shortness of breath

(dyspnea), fatigue, fainting (syncope), nausea, sweating (diaphoresis), anxiety,

sleeplessness, hypertension or hypotension (depending in part on the extent of

cardiac damage), tachycardia and arrhythmias. Recent clinical research indicates

that the symptoms may be very different between men and women. Chest pain is

less common in women. Instead, their most common symptoms are weakness,

fatigue and dyspnea.

The pathophysiology of acute myocardial infarction is complex. Loss of

viable myocardium impairs global cardiac function, which can lead to reduced

cardiac output, and if damage is severe, to cardiogenic shock. Systolic and

diastolic dysfunction are associated with ischemic myocardium. If left ventricular

function is significantly impaired, pulmonary congestion and edema can occur.

 Ischemia can also precipitate abnormal cardiac rhythms and conduction blocks

that can further impair function and become life-threatening in some cases.

Reduced cardiac output and arterial pressure can elicit baroreceptor reflexes that

lead to activation of neurohumoral compensatory mechanisms (e.g., activation of

sympathetic nerves and the renin-angiotensin-aldosterone system) similar to

what occurs during heart failure. The pain and anxiety associated with

myocardial infarction further activates the sympathetic nervous system, which

causes systemic vasoconstriction and cardiac stimulation (this explains why

some patients become hypertensive and have tachycardia). While sympathetic

activation helps to maintain arterial pressure, it also leads to a large increase in

myocardial oxygen demand that can lead to greater myocardial hypoxia, enlarge

the infarcted region, precipitate arrhythmias, and further impair cardiac function.

Sympathetic activation is responsible for the diaphoresis (sweating) experienced

by the patient. Renal hypoperfusion and sympathetic activation stimulate renin

release, which leads to increased plasma levels of angiotensin II and aldosterone

that enhance renal retention of sodium and water.

NURSING DIAGNOSIS

Acute Pain related to ischemia of myocardial tissue

Decreased Cardiac Output related to changes in rate and electrical conduction of the

Heart
Activity Intolerance r/t cardiac dysfunction, changes in oxygen supply and consumption

AEB shortness of breath

Deficient knowledge r/t new diagnosis and lack of understanding of medical conditions

Anxiety related to threat of death, change of health status or role functioning and

lifestyle

MEDICAL MANAGEMENT

Goal: minimize myocardial damage, preserve myocardial function, and prevent

complications.

PHARMACOLOGIC THERAPY:

THROMBOLYTICS

- medications that are usually administered intravenously, to

dissolve and lyse the thrombus in a coronary artery, allowing blood

to flow through the coronary artery again.

ANALGESICS

- Morphine Sulfate (Duramorph, Astramorph) administered in

intravenous boluses to reduce pain and anxiety, also relaxes

bronchioles to enhance oxygenation. Binds with opiate receptors in

the CNS, altering both perception and emotional response to pain.

Reassess pt. level of pain at least 15-30 minutes after parenteral

administration and 30 mins after oral administration.

 - Keep opioid antagonist (naloxone) and resuscitation available.

Oral solutions of various concentrations and an intensified solution

are available. Carefully note strength given. Don’t crush or break or

chew extended release tablets or sustained release capsule.

ANGIOTENSIN-CONVERTING ENZYME INHIBITOR

- Prevents the conversion of angiotensin from I to II, the

absence of Angiotensin II, the blood pressure decreases and the

kidneys excrete sodium and fluid, decreasing the oxygen demand

of the heart.

EMERGENT PERCUTANEOUS CORONARY INTERVENTION (PCI)

- Used to open occluded coronary artery in an acute MI and

promote repurfusion to the area that has been deprived of oxygen.

- Treats the underlying atherosclerotic lesion.

ANTI-ANGINAL

- Nitroglycerine (Nitrolingual spray), a nitrate that reduces cardiac

oxygen demand by decreasing left ventricular end diastolic

pressure (preload) and to a lesser extent, systemic vascular

resistance (afterload). Also increases blood flow through the

 collateral coronary blood vessels. Closely monitor vital signs, during

infusion, particularly blood pressure, especially in a patient with

MI.Drug may cause headaches, especially at the beginning of

therapy.

ANTICOAGULANT

- Warfarin is a prophylaxis & treatment of venous thrombosis, atrial

fibrillation w/ embolization, pulmonary embolism, adjunct in

prophylaxis of systemic embolism after MI. Inhibits Vitamin K-

dependent activation of clotting factors II, VII, IX, and X formed in

the liver. Draw blood to establish baseline coagulation parameters

before therapy. PT and INR determinations are essential for proper

control.Give warfarin at same time daily. IM administration isn’t

recommended. Check for unexpected bleeding.

NURSING MANAGEMENT

Assessment

Obtain baseline data on current status of patient for comparison with

ongoing status. Include history of chest pain or discomfort, dsypnea, palpitations,

faintness or sweating. Perform a complete physical assessment, which is crucial

for detecting complications and any change in status. The examination should

include the following.

  Assess level of consciousness.

 Evaluate chest pain (most important clinical finding)

 Assess heart rate and rhythm; dysrrythmias may indicate not

enough oxygen to the myocardium.

 Assess heart sounds; S3 can be an early sign of impending left

ventricular failure.

 Measure blood pressure to determine response to pain and

treatment; note pulse pressure, which may be narrowed after an MI,

suggesting ineffective ventricular contraction.

 Assess peripheral pulses: rate rhythm, and vulome.

 Evaluate skin color and temperature.

 Auscultate lung fields at frequent intervals for signs of ventricular

failure (crackles in lung bases).

 Assess bowel motility; mesenteric artery thrombosis is a potentially

fatal complication.

 Observe urine output and check for edema; an early sign of

cardiogenic shock is hypotension with oliguria.

NURSING INTERVENTION

 Relieving pain and other signs and symptoms of ischemia

 - Balancing the cardiac oxygen supply with its oxygen

demand.

- Administer morphine for relief of pain according to

physician’s order

 Improving respiratory function

- Careful assessment of respiratory function to detect early

signs of pulmonary complications.

- Encourage patient to breathe deeply and change position

frequently to help keep fluid to pooling in the base of the lungs.

 Promoting adequate tissue perfusion

- Limiting the patient to bed or chair rest during the initial

phase of treatment to reduce myocardial oxygen consumption. This

limitation should remain until the patient is pain-free and

hemodynamically stable.

- Oxygen may be administered to enrich the supply of

circulating oxygen.

 Reducing anxiety

- Develop a trusting and caring relationship with the patient.

- Ensure a quiet environment.

 Monitoring and managing potential complications

 - Monitor changes in cardiac rate and rhythm, heart sounds,

blood pressure, chest pain, respiratory status, urinary output, skin

color and temperature, sensorium, ECG changes, and lab results.

 Promoting home and community based care

- Provide adequate education about heart-healthy living

- Facilitate the patient’s involvement in a cardiac rehabilitation

program.

DISCHARGE PLAN

Patient is encouraged/ advised to visit his Attending Physician regularly to

monitor his condition after discharging from the hospital. He needs to follow his

medication regimen and keep a list of the dose, timing and reason why he needs

to take them. Instruct client not to take any over the counter drugs, herbs, food

supplements and vitamins without consulting his physician. He may need to take

aspirin a day to help prevent heart problems. Report any signs of bleeding.

Encourage client to use soft washcloth on skin for bathing and a soft

toothbrush to brush teeth to help prevent bleeding, not to shave but use an

electric shaver. Advise client not to play any contact sports because he may
bleed or bruise easily. Wear a medic alert bracelet or necklace that says he’s

taking a blood thinner.

Try a cardiac rehabilitation to help patient return to an active lifestyle.

Instruct patient not to drive and not to lift anything more than 10pounds or any

hard activity and be sure to take a rest whenever possible.

Diet should be low fat, low salt and low cholesterol. Quit smoking and

avoid stress which may slow healing and cause illness later. Contact a caregiver

if 1) your skin is itchy or you get a rash. Your medicine may be causing these

symptoms. This may mean you are allergic to your medicine. 2) You have angina

that is happening more frequently, lasting longer, or causing worse pain. 3) You

are dizzy or nauseated (upset stomach) after taking your medicine. 4) You have

trouble breathing while resting. 5) You have new or worsening swelling in your

feet or ankles. 6) You are bleeding from your gums or nose, or have blood in

your urine or BMs. 7) You have any questions or concerns about your illness or

medicine.