INTRODUCTION

The heart requires a balance between oxygen supply and oxygen demand in order to function
properly. The integrity of coronary artery is an important determinant of oxygen supply to the
heart muscle. Any disorder that reduces the lumen of one of the coronary arteries may cause a
decrease in blood flow and oxygen delivery to the area of myocardium supplied by the
vessels and lead to acute coronary syndrome of angina, myocardial infarction and sudden
cardiac death. MI refers to the process by which areas of myocardial cells in the heart are
permanently destroyed. Like unstable angina, MI is usually caused by reduced blood flow in
a coronary artery due to atherosclerosis and occlusion of an artery by an embolus or
thrombus.
The incidence of myocardial infarction in the world varies greatly. According to Spanish
study the incidence rate of coronary heart disease in world is 300.6/1000 persons years for
men and 47.9/100,000 persons years for women. The incidence of MI in India is 64.37/1000
people. In men aged 29-69 years, alcohol intake led to 30% lower CHD incidence.

ACUTE CORONARY SYNDROME

The term acute coronary syndrome (ACS) is used to encompass the continuum of coronary
artery disease such as unstable angina pectoris and myocardial infarction.

UNSTABLE ANGINA
Unstable angina occurs in patients with worsening CAD and is noted by its changing or
unpredictable pattern. Rest does not decrease the chest pain of unstable angina. This pain may
even occur when the patient is at rest. The episode of chest pain with unstable angina increase
in frequency and severity, placing the patient at risk for myocardial damage or sudden death.
Symptoms of angina usually occur when an artery is narrowed by at least 60% to 70%.

DEFINITION OF MYOCARDIAL INFARCTION

Myocardial infarction is also known as heart attack. It is life threatening condition
characterised by the formation of localized necrotic area within the myocardium. Acute
myocardial infarction follows the sudden occlusion of the coronary artery and abrupt
cessation of blood and oxygen flow to the heart muscle.

ANATOMY AND PHYSIOLOGY OF HEART

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 approxi-mately 70 mL of blood per beat and has an output of
approximately 5 L per minute.
 The heart is composed of three layers. 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.

ETIOLOGY AND RISK FACTORS OF MYOCARDIAL INFARCTION

Modifiable Risk factors of myocardial infarction are as follows;

 1. Obesity
2. Smoking
3. A high fat diet
4. Hypertension
5. Family history
6. Male gender
7. Diabetes mellitus
8. Sedentary lifestyle
9. Excessive stress
Other etiological factors include

1. The most common cause of AMI is complete or nearly complete occlusion of a

coronary artery, usually precipitate by rupture of a vulnerable atherosclerosis plaque
and subsequent thrombus formation. Plaque rupture by both internal and external
factors.

INTERNAL FACTORS

 Plaque characteristics, such as the size and consistency of the lipid core and the thickness
of fibrous cap, as well as condition to which it is exposed, such as coagulation status and
degree of arterial vasoconstriction.
 Vulnerable plaque most frequently occur in areas with less than 70% stenosis and are
characterised by an eccentric shape with an irregular border, a large thin lipid core; and a
thin fibrous cap.

EXTERNAL FACTOR

External factors result from action of the client or from external conditions that affect the
client.

1. Strenuous physical activity and severe emotional stress, such as anger, increase
nervous system responses, that may lead to plaque rupture. At the same time,
sympathetic nervous system responses increase myocardial oxygen demand.
2. Scientist have reported that external factor, such as exposure to cold and time of day,
also affect plaque rupture.
3. Acute coronary events occur more frequently with exposure to cold and during the
morning hours.
4. Researches hypothesize that the sudden increase in sympathetic nervous system
responses associated with this factors may contribute to plaque rupture. The role of
inflammation in triggering plaque rupture is currently being studied.
5. Regardless of cause rupture of the atherosclerotic plaque results in
 Exposure of the plaque’s lipid-rich core to flowing blood
 Seepage of blood into the plaque
  Triggering of thrombus formation
 Partial or incomplete occlusion of the coronary artery that last more than 1
hour.

PATHOPHYSIOLOGY

Due to etiological factors

Changes in the condition of the plaque in the coronary artery

 Formation of a thrombus

Ischemia of the tissue in the region supplied by the artery

Coronary blood supply less than demand

Myocardial cell death

Altered repolarization of the myocardium

Release of liposomal enzymes

Anaerobic glycosis which leads to lactic acid production

Myocardial irritability

Decrease contractility

Stimulation of sympathetic nervous system leads to Increase 02 needs

Decrease left ventricular function

Increase preload and decrease cardiac output

CLINICAL MANIFESTATIONS
The clinical manifestation occurs with AMI result from ischemia of the heart muscle and the
decrease in function and acidosis associated with it. The major manifestation of AMI is chest
pain.

1. Cardiovascular
 Chest pain or discomfort; Chest pain that occurs suddenly and continues despite rest
and medication is the presenting symptom in most patients with an MI. One study
showed that 2% of patients who eventually were diagnosed with an acute MI were
incorrectly discharged and sent home from the emergency department
 Palpitations.
 Heart sounds may include S3, S4, and new onset of a murmur.
 Increased jugular venous distention may be seen if the MI has caused heart failure.
 Blood pressure may be elevated because of sympathetic stimulation or decreased
because of decreased contractility, impending cardiogenic shock, or medications.
Pulse deficit may indicate atrial fibrillation.
 In addition to ST-segment and T-wave changes, ECG may show tachycardia,
bradycardia, and dysrhythmias.

Pain areas

In the area between shoulder blades, arm chest, jaw, left arm, or upper abdomen.

Pain types
Can be burning in the chest, crushing like a clenched fist in the chest, radiating from the
chest, sudden in the chest or mild.

Pain circumstances
Can occur during rest.

2. Respiratory
Shortness of breath, dyspnea, tachypnea, and crackles if MI has caused pulmonary
congestion. Pulmonary edema may be present.

3. Gastrointestinal
Nausea and vomiting.

4. Genitourinary
Decreased urinary output may indicate cardiogenic shock.

5. Skin
Cool, clammy, diaphoretic, and pale appearance due to sympathetic stimulation from loss of
contractility may indicate cardiogenic shock. Dependent edema may also be present due to
poor contractility.
6. Neurologic
Anxiety, restlessness, light-headedness may indicate increased sympathetic stimulation or a
decrease in contractility and cerebral oxygenation. The same symptoms may also herald
cardiogenic shock.
Headache, visual disturbances, altered speech, altered motor function, and further changes in
level of consciousness may indicate cerebral bleeding if patient is receiving thrombolytics.

7. Psychological
Fear with feeling of impending doom, or patient may deny that anything is wrong.

ASSESSMENT AND DIAGNOSTIC FINDINGS

Diagnosis of MI is generally based on the presenting symptoms, the ECG, and laboratory test
results (eg, serial serum enzyme values). The prognosis depends on the severity of coronary
artery obstruction and the extent of myocardial damage. Physical examination is always
conducted, but the examination alone is insufficient to confirm the diagnosis.

1. PATIENT HISTORY

The patient history has two parts: the description of the presenting symptom (eg, pain) and
the history of previous illnesses and family health history, particularly of heart disease.
Previous
history should also include information about the patient’s risk factors for heart disease.

2. PHYSICAL EXAMINATION
In inspection general appearance of patients
Patient may according to the experience symptoms, the patient may be comfortable, or
restless and in severe distress with an increase respiratory rate.

Skin condition
A cool and pale skin is common point to vasoconstriction. Some patient have low grade fever
(38-390c.)

Blood pressure
Blood pressure may be elevated or decreased, and the pulse can become irregular. If the heart
failure ensure, elevated jugular venous pressure, or swelling of the legs due to peripheral
edema may be found on inspection.

Auscultation
Various abnormalities found on auscultation, such as third and fourth heart sound, systolic
murmer, a pericardial friction rub and rales over the lung.

3. ELECTROCARDIOGRAM

The ECG provides information that assists in diagnosing acute MI. It should be obtained
within 10 minutes from the time a patient reports pain or arrives in the emergency
department. By monitoring the ECG over time, the location, evolution, and resolution of
an MI can be identified and monitored. The ECG changes that occur with an MI are seen
in the leads that view the involved surface of the heart.
 The classic ECG changes are T-wave inversion, ST-segment elevation, and
development of an abnormal Q wave. Because infarction evolves over time, the ECG
also changes over time.
 The first ECG signs of an acute MI are from myocardial ischemia and injury.
 Myocardial injury causes the T wave to become enlarged and symmetric. As the area
of injury becomes ischemic, myocardial repolarization is altered and delayed, causing
the T wave to invert.
 The ischemic region may remain depolarized while adjacent areas of the myocardium
return to the resting state. Myocardial injury also causes ST-segment changes.
 The injured myocardial cells depolarize normally but repolarize more rapidly than
normal cells, causing the ST segment to rise at least 1 mm above the isoelectric line
(area between the T wave and the next P wave is used as the reference for the
isoelectric line) when measured 0.08 seconds after the end of the QRS.
 If the myocardial injury is on the endocardial surface, the ST segment is depressed 1
mm or more for at least 0.08 seconds. The ST-segment depression is usually
horizontal or has a downward slope. MI is classified as a Q-wave or non-Q-wave
infarction.
 With Q-wave infarction, abnormal Q waves develop within 1 to 3 days because there
is no depolarization current conducted from necrotic tissue.
 The lead system then views the flow of current from other parts of the heart. An
abnormal Q wave is 0.04 seconds or longer, 25% of the R-wave depth (provided the R
wave exceeds a depth of 5 mm), or one that did not exist before the event (Wagner,
2001).
 An acute MI may cause a significant decrease in the height of the R wave. During an
acute MI, injury and ischemic changes are also present.
 An abnormal Q wave may be present without ST-segment and T-wave changes,
which indicates an old, not acute, MI.
 Patients with non-Q-wave MIs do not develop a Q wave on the ECG after the ST-
segment and T-wave changes, but symptoms and cardiac enzyme analysis confirm the
diagnosis of an MI. During recovery from an MI, the ST segment often is the first to
return to normal (1 to 6 weeks). The T wave becomes large and symmetric for 24
hours, and it then inverts within 1 to 3 days for 1 to 2 weeks. Q-wave alterations are
usually permanent.
  An old Q wave MI is usually indicated by an abnormal Q wave or decreased height of
the R wave without ST-segment and T-wave changes.

4. ECHOCARDIOGRAM
The echocardiogram is used to evaluate ventricular function. It may be used to assist in
diagnosing an MI, especially when the ECG is nondiagnostic. The echocardiogram can detect
hypokinetic and akinetic wall motion and can determine the ejection fraction.

LABORATORY TESTS

Historically, laboratory tests used to diagnose an MI included creatine kinase (CK), with
evaluation of isoenzymes and lactic dehydrogenase (LDH) levels. Newer laboratory tests
with faster results, resulting in earlier diagnosis, include myoglobin and troponin analysis.
These tests are based on the release of cellular contents into the circulation when myocardial
cells die. An LDH test is now infrequently ordered because it is not useful in identifying
cardiac events.

1. Creatine Kinase and Its Isoenzymes.

There are three CK isoenzymes: CK-MM (skeletal muscle), CK-MB (heart muscle), and 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. CK-MB
assessed by mass assay is the most specific index for the diagnosis of acute MI. The level
starts to increase within a few hours and peaks within 24 hours of an MI. If the area is
perfused (eg, due to thrombolytic therapy or PTCA), it peaks earlier

2. Myoglobin.
Myoglobin is a heme protein that helps to transport oxygen. Like CK-MB enzyme,
myoglobin is found in cardiac and skeletal muscle. The myoglobin level starts to increase
within 1 to 3 hours and peaks within 12 hours after the onset of symptoms. The test takes
only a few minutes to run. An increase in myoglobin is not very specific in indicating an
acute cardiac event; however, negative results are an excellent parameter for ruling out an
acute MI. If the first myoglobin test results are negative, the test may be repeated 3 hours
later. Another negative test result confirms that the patient did not have an MI.

3. TROPONIN.
Troponin, a protein found in the myocardium, regulates the myocardial contractile process.
There are three isomers of troponin (C, I, and T). Because of the smaller size of this protein
and the increased specificity of the troponins I and T for cardiac muscle, these tests are used
more frequently to identify myocardial injury (unstable angina or acute MI). The increase in
the level of troponin in the serum starts and peaks at approximately the same time as CK-MB.
However, it remains elevated for a longer period, often up to 3 weeks, and it therefore cannot
be used to identify subsequent extension or expansion of an MI.

Cardiac troponin T is similar to CK-MB with regard to sensitivity, and levels within
increases within 3-6 hours after pain has started. Levels remain elevated for 14-21
days. This is useful (and more accurate than LDH) in conformation of distant MI.
Cardiac troponin I levels increase 7-14 hours after AMI. This is a very specific and
sensitive indicator of AMI and is not affected by any other disease or injury to any
other muscle except cardiac muscle. Elevation persist for 5-7 days.

4. LDH (lactate dehydrogenase)

The LDH1 subunit is plentiful in heart muscle and release into the serum when myocardial
damage occurs. Serum level of LDH elevate14-24 hour after onset of myocardial damage,
peak within 48-72 hours and slowly return to normal over the next 7-14 days.
5. AST (aspartate transaminase)
Serum levels of AST increase within several hours after the onset of chest pain, peak within
12 to 18 hours, and return to normal within 3 -4 days.

6. Leucocytosis
Leucocytosis (10,000/mm3) appears on the second day after AMI and disappears in 1 week.
Myeloperoxidase, a leukocyte enzyme, was recently shown to be predictive of AMI even in
clients without elevations in troponin T level
IMAGING STUDIES
Radionuclide imaging studies provide information on the presence of coronary artery disease
as well as the location of the ischemic and infarcted tissue. Cardiac imaging studies have
been used to provide information for management decisions of client who present to the
emergency department with acute chest pain.
1. Positron Emission Tomography
Positron Emission Tomography (PET) is used to evaluate cardiac metabolism and to
assess tissue perfusion. It can also be used to detect CHD, assess coronary artery flow
reserve, measure absolute myocardial blood flow, detect AMI and differentiate ischemic
from no ischemic cardiomyopathy. It may also be used to assess myocardial viability to
determine which client can benefit from CABG.

2. Magnetic resonance imaging (MRI)

Magnetic resonance imaging (MRI) helps identify the sites and extent of an MI, assess the
effect of reperfusion therapy, and differentiate reversible and irreversible tissue injury. Its use
as a diagnostic tool for coronary artery disease in increasing, although MRI cannot be used in
client with implanted metallic device, such as pacemaker or defibrillator.
3. Transesophageal echocardiography
Transesophageal echocardiography (TEE) is an imaging technique in which the transducer is
placed against the wall of the esophagus. The image of the myocardium is clearer when the
esophageal site is used because no air and no ribs are between the transducer and the heart.
This technique is particularly useful for viewing the posterior wall of the heart.
 PROGNOSIS OF MYOCARDIAL INFACRCTION
Since the advent of coronary care units and device that aid in promptly recognizing and
treating life threatening dysrhythmias, 70% to 80% of people experiencing an AMI survive
the initial attack. Chances for survival greatly diminish with the presence of the following.
1. Older age (clients 80 years or older have q 60% death rate)
2. Manifestation of heart failure.
3. ST- segment elevation
4. Elevation of cardiac marker
5. Hypotension (systolic blood pressure less than 55mmhg on admission has a 60%
death rate)
6. More than three coronary risk factors
7. More than two angina events within 24 hours.
Death generally result from severe dysrhythmias, cardiogenic shock, heart failure, rupture of
the heart and recurrent AMI. Client who avoid complication after AMI still require 6 to 12
weeks for complete recovery. However, 25% of men and 38% of female die within 1 year
after having AMI and 22% of men and 46% of women are disabled with heart failure within
6 years of an AMI.
 MANAGEMENT OF MYOCARDIAL INFARCTION
Medical management
Major goals of care for clients with AMI include the following
I. Initiating prompt care
II. Determining the type of AMI (STEMI vs. NSTMI).
III. Reducing pain
IV. Delivering successful treatment for the acute pain and reperfusion of the myocardium
V. Preventing complication
VI. Preventing remodelling and heart failure
VII. Rehabilitating and educating the client and significant others.

1. TREAT THE ACUTE ATTACK IMMEDIATELY

Client with manifestation of AMI must receive immediate treatment. Delay may increase
damage to the heart & reduce the chance of survival. The goal for treatment of AMI is “door
to needle” is less than 30 minutes, or specifically from onset of pain till thrombolytic therapy
within 30 minutes of percutaneous angioplasty within 1 hour.
 Most communities have an emergency medical system (EMS) that responds quickly (call
911). Until EMS personnel arrives, keep the client quiet and calm. It is recommended
that, if conscious, a client chew an aspirin at the onset of manifestation because mortality
is reduced 23% with this action alone.
 Clients who become unconscious before reaching the emergency department may require
defibrillation or cardiopulmonary ressucitation (CPR).

2. DETERMINING THE TYPE OF AMI

For purposes of determining appropriate treatment, AMI is viewed as part of a spectrum of
coronary syndrome, which include
i. ST- segment elevation MI
ii. Non ST- segment elevation MI
iii. Unstable angina

 Clients with persist ants elevation should be considered for reperfusion therapy.
 Those without ST elevation will be diagnosed either with NSTEMI if cardiac markers are
elevated or with unstable angina if serum cardiac markers provides no evidence of injury.
 Clients with no ST segment elevation are not candidate for immediate thrombolytic but
should receive anti ischemic therapy and may be candidate for PCI urgently or during
admission.

3. REDUCE PAIN
 Upon admission, the clients who complaints of chest pain is admitted to the emergency
department, given oxygen therapy, and placed on ECG monitoring.
 An IV line is placed, serum cardiac markers are drown, and a 12 lead ECG is undertaken
within 10 minutes.
 Pain control is priority, and pain is usually treated with IV morphine.
 Continued pain is manifestation of myocardial ischemia. Pain also stimulates the
autonomic nervous system and increase preload, which in turn increases myocardial
oxygen demand. Oxygen is used to treat tissue hypoxia.

4. MONITOR HEART RHYTHM

Because dysrhythmias are common, ECG monitoring is essential and antidysrhytymic
medication should be on hand. A two dimensional echocardiogram and test may be
performed in the emergency department to aid in ruling out MI.
5. IMPROVE PERFUSION
In general principles of pharmacological treatment of AMI consist of anti-ischemic therapy
and antithrombotic therapies.

6. DETERMINE THE LOCATION OF THE MYOCARDIAL INFARCTION

Determine the exact coronary vessels that has infarcted is done through analysis of the 12
lead ECG and is validated with coronary angiography to determine the degree of conclusion.
Determine the exact artery that is involved is important so potential complication can be
assessed and minimize.
7. MONITOR FOR COMPLICATION
The possibility of death from complications always accompanies an AMI. Thus prime
collaborative goals include the prevention of life-threateing complications or atleat
recognition of them.
PHARMACOLOGIC THERAPY FOR MYOCARDIAL INFARCTION

The patient with an acute MI receives the same medications as the patient with unstable
angina, with the possible additions of thrombolytics, analgesics, and angiotensin-converting
enzyme (ACE) inhibitors. Patients should receive a beta-blocker initially, throughout the
hospitalization, and a prescription to continue its use after hospital discharge. Thrombolytics.
Thrombolytics are medications that are usually administered intravenously, although some
may also be given directly into the coronary artery in the cardiac catheterization laboratory.
The purpose of thrombolytics is to dissolve and lyse the thrombus in a coronary artery
(thrombolysis), allowing blood to flow through the coronary artery again (reperfusion),
minimizing the size of the infarction, and preserving ventricular function. Even though
thrombolytics may dissolve the thrombus, they do not affect the underlying atherosclerotic
lesion. The patient may be referred for a cardiac catheterization and other invasive
interventions.

A. THROMBOLYTIC THERAPY

 Thrombolytics dissolve all clots, not just the one in the coronary artery. They should
not be used if the patient has formed a protective clot, such as after major surgery or
hemorrhagic stroke. Because thrombolytics reduce the patient’s ability to form a
stabilizing clot, the patient is at risk for bleeding.
 Thrombolytics should not be used if the patient is bleeding or has a bleeding disorder.
All patients who receive thrombolytic therapy are placed on bleeding precautions to
minimize the risk for bleeding. This means minimizing the number of punctures for
inserting intravenous lines, avoiding intramuscular injections, preventing tissue
trauma, and applying pressure for longer than usual after any puncture.
 To be effective, thrombolytics must be administered as early as possible after the
onset of symptoms that indicate an acute MI. They are not given to patients with
unstable angina.
 Hospitals monitor their ability to administer these medications within 30 minutes
from the time the patient arrives in the emergency department. This is called door-to-
needle time (Ryan et al., 1999).
 The thrombolytic agents used most often are streptokinase (Kabikinase, Streptase),
alteplase (Activase), and reteplase (r-PA, TNKase). Anistreplase (Eminase) is another
thrombolytic agent that may be used.
 Streptokinase increases the amount of plasminogen activator, which then increases the
amount of circulating and clot-bound plasmin. Because streptokinase is made from a
bacterium, its use also entails a risk of an allergic reaction.
 Vasculitis has occurred up to 9 days after administration. Streptokinase is not used if
the patient has been exposed to a recent Streptococcus infection or has received
streptokinase in the past 6 to 12 months.
 Alteplase is a type of tissue plasminogen activator (t-PA). In contrast to streptokinase,
alteplase activates the plasminogen on the clot more than the circulating plasminogen.
Because it does not decrease the clotting factors as much as streptokinase,
unfractionated or low molecular weight heparin is used with t-PA to prevent another
clot from forming at the same lesion site. Because t-PA is a naturally occurring
 enzyme, allergic reactions are minimized, but t-PA costs considerably more than
streptokinase.
 Reteplase is structurally very similar to alteplase and has similar effects. Anistreplase
is similar to streptokinase and has similar effects.

THROMBOLYTIC THERAPY

Indications
• Chest pain for longer than 20 minutes, unrelieved by nitroglycerin
• ST-segment elevation in at least two leads that face the same
area of the heart
• Less than 24 hours from onset of pain

Absolute Contraindications
• Active bleeding
• Known bleeding disorder
• History of hemorrhagic stroke
• History of intracranial vessel malformation
• Recent major surgery or trauma
• Uncontrolled hypertension
• Pregnancy

Nursing Considerations
• Minimize the number of times the patient’s skin is punctured.
• Avoid intramuscular injections.
• Draw blood for laboratory tests when starting the IV line.
• Start IV lines before thrombolytic therapy; designate one line to use for blood draws.
• Avoid continual use of noninvasive blood pressure cuff.
• Monitor for acute dysrhythmias, hypotension, and allergic reaction.
• Monitor for reperfusion: resolution of angina or acute ST-segment changes.
• Check for signs and symptoms of bleeding: decrease in haematocrit and hemoglobin values,
decrease in blood pressure, increase in heart rate, oozing or bulging at invasive procedure
sites, back pain, muscle weakness, changes in level of consciousness, complaints of
headache
• Treat major bleeding by discontinuing thrombolytic therapy and any anticoagulants; apply
direct pressure and notify the physician immediately.
• Treat minor bleeding by applying direct pressure if accessible and appropriate; continue to
monitor.
B. ANALGESICS.

 The analgesic of choice for acute MI is morphine sulfate (Duramorph, Astramorph)

administered in intravenous boluses.
 Morphine reduces pain and anxiety. It reduces preload, which decreases the workload
of the heart. Morphine also relaxes bronchioles to enhance oxygenation. The
cardiovascular response to morphine is monitored carefully, particularly the blood
pressure, which can be lowered, and the respiratory rate, which can be depressed.
Because morphine decreases sensation of pain, STsegment monitoring may be a better
indicator of subsequent ischemia than assessment of pain.

C. ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE-I).

 ANGIOTENSIN I is formed when the kidneys release renin in response to decreased

blood flow. Angiotensin I is converted to angiotensin II by ACE, a substance found in
the lumen of all blood vessels, especially the pulmonary vasculature.
 Angiotensin II causes the blood vessels to constrict and the kidneys to retain sodium
and fluid while excreting potassium. These actions increase circulating fluid and raise
the pressure against which the heart must pump, resulting in significantly increased
cardiac workload.
 ACE inhibitors (ACE-I) prevent the conversion of angiotensin from I to II. In the
absence of angiotensin II, the blood pressure decreases and the kidneys excrete
sodium and fluid (diuresis), decreasing the oxygen demand of the heart. Use of ACE
inhibitors in patients after MI decreases the mortality rate and prevents the onset of
heart failure.
 It is important to ensure that the patient is not hypotensive, hyponatremic,
hypovolemic, or hyperkalemic before ACE-I administration. Blood pressure, urine
output, and serum sodium, potassium, and creatinine levels need to be monitored
closely.
 COMPLICATIONS OF MYOCARDIAL INFARCTION
1) DYSRHYTHMIAS
 Dysrhythmias are the cause of 40% to 50% of deaths after AMI. Ectopic rhythm
arises in or near the borders of intensely ischemic and damaged myocardial tissues.
Damaged myocardium may also interfere with the conduction system, causing
dissociation of the atria and ventricles (heart block).
 Supraventricular tachycardia (SVT) sometimes occurs as a result of heart failure.
Spontaneous or pharmacologic reperfusion of a previously ischemic area may also
precipitate ventricular dysrhythmias.
Management
 Provide continues cardiac monitoring and frequent counts of PVCs. Notify the
physicians if more than six PVCs occurs per minute and the client is symptomatic. Eg.
Hypotension, chest pain.
 For dysrhythmias, provide prompt intervention per protocol or orders.

2) CARDIOGENIC SHOCK
 Cardiogenic shock accounts for only 9% of death from AMI, but more than 70% of
client in shock die of it.
 Cause include,
- Decrease myocardial contraction with diminish cardiac output
- Undetected dysrhythmias
- Sepsis clinical manifestation include systolic blood pressure significantly below the
client’s normal range, diaphoresis, rapid pulse, restlessness, cold and clammy skin
colour.
- Shock can be prevented with sufficient IV fluids to prevent circulatory collapse and
the identification of dysrhythmias.
Management
 Vasopressor are administered (dopamine, dobutamine) or raise blood pressure by
increasing peripheral resistance.
 Vasodilators (nitripruside, nitroglycerine) promote better blood flow in the
microcirculation and reduce afterload.

3) HEART FAILURE AND PULMONARY EDEMA

 The most common cause of in- hospital death in client with cardiac disorders in heart
failure.
 Heart failure disables 22% of male client and 46% of female client who experience an
AMI and is responsible for one third of death after an AMI.
 Heart failure may develop at the onset of the infarction or may occur weeks later.
 Clinical manifestation include dyspnoea, orthopnoea, weight gain, and edema, enlarge
tender liver, distended neck vein and crackles.
 It is manage by correcting the underlying cause, relieving clinical manifestation and
enhancing cardiac performance.

4) PULMOPNARY EMBOLISM
 PE may develop secondary to phlebitis of the leg or pelvic veins or from atrial
flutter or fibrillation.
 PE occurs in 10% to 20% of clients at some point, during either the acute attack
or convalescence.

5) RECURRENT MYOCARDIAL INFARCTION

 Within 6 years after an AMI, 18% of men and 35% of women may experience
recurrent MI.
 Possible cause include overexertion, embolization and further thrombotic occlusion of
a coronary artery by atheroma.

6) COMPLICATION CAUSE BY MYOCARDIAL NECROSIS

 Complications that are due to necrosis of the myocardium include ventricular
aneurysm rupture of the heart, ventricular septal defect, and ruptured papillary
muscle.
 These complications are infrequent but serious, usually occurring about 5 to 7 days
after MI.
 Week friable necrotic myocardial tissue increases vulnerability to these
complications.

7) PERICARDITIS
 In up to 28% of client with an acute Trans mural MI, early pericarditis develop
(within 2to 4 days).
 The inflame area of the infarction rub against the pericardial surface and causes it to
loss its lubricating fluid.
 A pericardial friction rub can be auscultated across the precordium.
 The client’s complaints that chest pain is worst with movement, deep inspiration and
cough. The pain of pericarditis is relieve is sitting up and leaning forward.
 Frequent assessment may lead to early identification and intervention.

8) DRESSLER’S SYNDROME
 DS, a form of pericarditis, can occur as late as 6 week to month after AMI. Although
the etiologic agent is unknown, and autoimmune cause is suggested the client usually
present with a fever lasting one week or longer, pericardial chest pain, pericardial
friction rub, and occasionally pleuritis with pleural effusions
 NURSING MANAGENT OF THE MYOCARDIAL INFARCTION

The goals of the nursing management after AMI are as follows,

1) Recognise and treat cardiac ischemia.
2) Administer thrombolytic therapy as ordered, or ready client for PTCA and observe
for complications.
3) Recognise and treat potentially life threatening dysrhythmias.
4) Monitor for complications of reduce cardiac output.
5) Maintain a therapeutic critical care environment.
6) Identify the psychosocial impact of AMI on the client and family.
7) Educate the client in lifestyle changes the rehabilitation.
8) A care plan on care of the client with AMI list specific nursing diagnosis,
intervention, rationale and eveluauons outcomes.

NURSING PROCESS:

ASSESSMENT
One of the most important aspects of care of the patient with an MI is the assessment. It
establishes the baseline for the patient so that any deviations may be identified, systematically
identifies the patient’s needs, and helps determine the priority of those needs. Systematic
assessment includes a careful history, particularly as it relates to symptoms: chest pain or
discomfort, difficulty breathing (dyspnea), palpitations, unusual fatigue, faintness (syncope),
or sweating (diaphoresis). Each symptom must be evaluated with regard to time, duration, the
factors that precipitate the symptom and relieve it, and comparison with previous symptoms.
A precise and complete physical assessment is critical to detect complications
and any change in patient status.

NURSING DIAGNOSES
Based on the clinical manifestations, history, and diagnostic assessment data, the patient’s
major nursing diagnoses may include:

• Ineffective cardiopulmonary tissue perfusion related to reduced coronary blood flow from
coronary thrombus and atherosclerotic plaque
• Potential impaired gas exchange related to fluid overload from left ventricular dysfunction
• Potential altered peripheral tissue perfusion related to decreased cardiac output from left
ventricular dysfunction.
• Anxiety related to fear of death
• Deficient knowledge about post-MI self-care
PLANNING AND GOALS
The major goals of the patient include relief of pain or ischemic signs and symptoms (eg, ST-
segment changes), prevention of further myocardial damage, absence of respiratory
dysfunction, maintenance or attainment of adequate tissue perfusion by decreasing the heart’s
workload, reduced anxiety, adherence to the self-care program, and absence or early
recognition of complications.

NURSING INTERVENTIONS

I. RELIEVING PAIN AND OTHER SIGNS AND SYMPTOMS OF ISCHEMIA

Balancing the cardiac oxygen supply with its oxygen demand (eg, as evidenced by the
relief of chest pain) is the top priority for the patient with an acute MI. Although
medication therapy is required to accomplish this goal, nursing interventions are also
important.
Collaboration among the patient, nurse, and physician is critical in assessing the
patient’s response to therapy and in altering the interventions accordingly.
The accepted method for relieving symptoms associated with MI is revascularization
with thrombolytic therapy or emergent PCI for patients who present to the health care
facility immediately and who have no major contraindications.
These therapies are important because, in addition to relieving symptoms, they aid in
minimizing or avoiding permanent injury to the myocardium.
With or without revascularization, administration of aspirin, intravenous beta-blocker,
and nitroglycerin is indicated.
Use of heparin may also be indicated.
The nurse administers morphine for relief of pain and other symptoms, anxiety, and
reduction of preload.
 Oxygen should be administered along with medication therapy to assist with relief of
symptoms. Administration of oxygen even in low doses raises the circulating level of
oxygen to reduce pain associated with low levels of myocardial oxygen.
The route of administration, usually by nasal cannula, and the oxygen flow rate are
documented. A flow rate of 2 to 4 L/min is usually adequate to maintain oxygen
saturation levels of 96% to 100% if no other disease is present.
Vital signs are assessed frequently as long as the patient is experiencing pain and
other signs or symptoms of acute ischemia. Physical rest in bed with the backrest
elevated or in a cardiac chair helps to decrease chest discomfort and dyspnea.
Elevation of the head is beneficial for the following reasons:
• Tidal volume improves because of reduced pressure from abdominal contents on the
diaphragm and better lung expansion and gas exchange.
• Drainage of the upper lung lobes improves.
• Venous return to the heart (preload) decreases, which reduces the work of the heart.

II. IMPROVING RESPIRATORY FUNCTION

Regular and careful assessment of respiratory function can help the nurse detect early
signs of pulmonary complications. Scrupulous attention to fluid volume status
prevents overloading the heart and lungs.
Encouraging the patient to breathe deeply and change position frequently helps keep
fluid from pooling in the bases of the lungs.

III. PROMOTING ADEQUATE TISSUE PERFUSION

Limiting the patient to bed or chair rest during the initial phase of treatment is
particularly helpful in reducing myocardial oxygen consumption (mV_O2). This
limitation should remain until the patient is pain-free and hemodynamically stable.
Checking skin temperature and peripheral pulses frequently is important to ensure
adequate tissue perfusion. Oxygen may be administered to enrich the supply of
circulating oxygen.

IV. REDUCING ANXIETY

Alleviating anxiety and fears is an important nursing function to reduce the

sympathetic stress response. Decreased sympathetic stimulation decreases the
workload of the heart, which may relieve pain and other signs and symptoms of
ischemia.
Developing a trusting and caring relationship with the patient is critical in reducing
anxiety. Providing information to the patient and family in an honest and supportive
manner invites the patient to be a partner in care and greatly assists in developing a
positive relationship.
 Ensuring a quiet environment, preventing interruptions that disturb sleep, using a
caring and appropriate touch, teaching the patient the relaxation response, using
humor and assisting the patient to laugh, and providing the appropriate prayer book
and assisting the patient to pray if consistent with the patient’s beliefs are other
nursing interventions that can be used to reduce anxiety.
Frequent opportunities are provided for the patient to privately share concerns and
fears. An atmosphere of acceptance helps the patient to know that these concerns and
fears are both realistic and normal.
Music therapy, in which the patient listens to selected music for a predetermined
duration and at a set time, has been found to be an effective method for reducing
anxiety and managing stress.
Pet therapy, in which animals are brought to the patient, appears to provide emotional
support and reduce anxiety. Administrative and infectious control practitioners are
usually involved in developing standards for the animals, animal handlers, and
patients who are eligible for pet therapy.

V. MONITORING AND MANAGING POTENTIAL COMPLICATIONS

Complications that can occur after acute MI are caused by the damage that occurs to
the myocardium and to the conduction system as a result of the reduced coronary
blood flow. Because these complications can be lethal, close monitoring for and early
identification of the signs and symptoms is critical
The nurse monitors the patient closely for changes in cardiac rate and rhythm, heart
sounds, blood pressure, chest pain, respiratory status, urinary output, skin color and
temperature, sensorium, ECG changes, and laboratory values.
Any changes in the patient’s condition are reported promptly to the physician, and
emergency measures are instituted when necessary.

PROMOTING HOME AND COMMUNITY-BASED CARE

Teaching Patients Self-Care

The most effective way to increase the probability the patient will implement a self-
care regimen after discharge is to identify the priorities as perceived by the patient,
provide adequate education about heart-healthy living, and facilitate the patient’s
involvement in a cardiac rehabilitation program.
Working with patients in developing plans to meet their specific needs further
enhances
the potential for an effective treatment plan.

EVALUATION
EXPECTED PATIENT OUTCOMES
Expected patient outcomes may include the following:
1. Relief of angina
2. No signs of respiratory difficulties
3. Adequate tissue perfusion
4. Decreased anxiety
5. Adherence to a self-care program
6. Absence of complications.

CARDIAC REHABILITATION
After the MI patient is free of symptoms, an active rehabilitation program is initiated.
Cardiac rehabilitation is a program that targets risk reduction by means of education,
individual and group support, and physical activity.
Most insurance programs, including Medicare, cover the cost of a cardiac
rehabilitation program. However, some studies indicate that only 8% to 39% of
patients who are candidates for cardiac rehabilitation services typically participate in
these programs.
The goals of rehabilitation for the patient with an MI are to extend and improve the
quality of life. The immediate objectives are 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.
These objectives are accomplished by encouraging physical activity and physical
conditioning, educating patient and family, and providing counseling and behavioral
interventions.