Download Running head: Acute Myocardial Infarction Acute Myocardial

Running head: ACUTE MYOCARDIAL INFARCTION
Acute Myocardial Infarction
Student Number
Columbia Basin College
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ACUTE MYOCARDIAL INFARCTION
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Acute Myocardial Infarction
An acute myocardial infarction (AMI) is also known as a heart attack. A heart attack
occurs when the blood supply to part of the heart muscle itself, the myocardium, is severely
reduced or stopped. The reduction or stoppage happens when one or more of the coronary
arteries supplying blood to the heart muscle are blocked. This is usually caused by the buildup of
plaque, a process called atherosclerosis. The plaque can eventually tear or rupture, creating a
place where a blood clot forms and blocks the artery. This leads to a heart attack. If the blood
supply is cut off for more than a few minutes, muscle cells suffer permanent injury and die. This
can ultimately lead to death of the patient, depending on how much heart muscle is damaged.
(Erdogan, 2010).
Statistics
Heart disease remains the leading cause of death in the United States (LeMone & Burke,
2008).
The following statistics are from the American Heart Association:

About every 34 seconds, an American will suffer a heart attack.

The estimated annual incidence of a heart attack in the United States is 610,000 new
attacks and 325,000 recurrent attacks.

The estimated average number of years of life lost due to a heart attack is 15.

Depending on gender and clinical outcome, people who survive the acute phase of a
heart attack have a chance of illness and death that’s 1.5 – 15 times higher than the
general population.

The estimated direct and indirect 2010 cost of heart disease is $177.1 billion.
ACUTE MYOCARDIAL INFARCTION
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The average age of a person having a first heart attack is 64 for men and 70 for
women.

Within five years following a first heart attack:
-at age 40 or older, 33% of men and 43% of women will die.
- at ages 40-69, 15 % of white men, 22% of white women, 27% of black men, and
32% of black women will die.
- at age 70 and older, 50% of white men, 56% of white women, 56% of black men,
and 62% of black women will die.
Predisposing Factors
Certain factors contribute to the unwanted buildup of fatty deposits (atherosclerosis) that
narrow arteries throughout the body, including arteries to the heart. Improving or eliminating
many of these risk factors can reduce the chances of having a first or second heart attack.
(Lackey, 2006).
Heart attack risk factors include:

Age.

Tobacco

Diabetes Mellitus.

High blood pressure.

High blood cholesterol or triglyceride levels.

Family history of heart attack.

Lack of physical activity.

Obesity.

Stress.
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ACUTE MYOCARDIAL INFARCTION
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Illegal drug use.
Onset/Duration
All people experience heart attacks in different ways and to different degrees. Some can
occur without any previous signs or symptoms. Others can show signs such as angina over the
last few weeks, and the person may not realize it’s a risk factor. In any case, prompt medical
attention is key because the longer the blood flow is restricted the higher the incidence of cellular
death. “Cellular injury occurs when the cells are denied adequate oxygen and nutrients. When
ischemia is prolonged, lasting longer than 20 to 45 minutes, irreversible hypoxemic damage
causes cellular death and tissue necrosis” (LeMone & Burke., 2008). Therefore, a person having
a heart attack must seek medical attention immediately and have a full cardiac workup done
within 45 minutes to reduce permanent damage.
Decreased blood flow through the coronary arteries causes symptoms of myocardial
distress. Patients commonly describe the discomfort as crushing, oppressive, or constricting or as
pressure that may radiate to the left arm, neck, jaw, intrascapular area, or epigastric region.
Transient symptoms that disappear with rest are classified as angina. The discomfort associated
with AMI typically lasts more than 30 minutes, isn’t relieved by rest or nitroglycerin, and may or
may not be severe (Lackey, 2006).
Usual Signs, Symptoms, and Complications
Behavior: anxiety, distress, confusion, feelings of impending doom
Skin: pale, cool, and clammy
Respirations: productive cough with pink frothy or blood-tinged sputum, crackles in
lower fields, tachypnea
Heart: S3 gallop, arrhythmias, murmur
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Kidneys: oliguria
Vital signs: fever in first 24-48 hours, bradycardia or tachycardia, hypotension or
hypertension
With right ventricular infarct: jugular vein distension, peripheral edema, lung fields
usually clear
Other signs and symptoms of AMI include nausea, vomiting, diaphoresis, palpitations,
and dyspnea. The patient may have cool, clammy skin due to vasoconstriction and a low-grade
fever caused by the systemic response to inflammation. Some patients, especially those with
diabetes or over age 75, may not experience the classic signs and symptoms of AMI. For
example, they may have dyspnea or palpitations rather than chest discomfort. In women, fatigue,
jaw pain, back pain, nausea, vomiting, and dyspnea should raise a red flag (Lackey, 2006).
Complications include: sudden cardiac death, arrhythmias, right ventricular failure, left
ventricular failure, acute pulmonary edema, angina, cardiogenic shock, pericarditis, Dressler’s
syndrome (late pericarditis), pulmonary embolism, and cardiac tamponade. (Found in Joanie’s
lecture handouts).
Diagnostics
The gold standard of diagnosing an AMI is having a 12-lead ECG taken and reviewed by
a physician within 10 minutes of arrival at the emergency department. Classic ECG changes seen
in AMI include T-wave inversion, ST-segment elevation, and formation of a Q-wave. Ischemic
changes in the heart are seen as a depressed ST-segment or inversion of the T-wave. With
myocardial injury, elevation of the ST-segment occurs. Significant Q-wave development
indicates a full thickness infarction. Myocardial damage can be localized with the 12-lead ECG.
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If the patient has a new left bundle branch block (LBBB) and other signs and symptoms of AMI,
he should be evaluated immediately for reperfusion therapy (Lackey, 2006).
Serum cardiac markers: Within 10 minutes of arrival at the ED, the patient should have
blood drawn to measure substances released when myocardial inflammation, injury, and necrosis
are present (Lackey, 2006). Creatine Kinase is an important enzyme for cellular function found
principally in skeletal and cardiac muscle and the brain. CK levels rise rapidly with damage to
these tissues, appearing in the serum 4-6 hours after AMI, peak at 12-24 hours, and decline 4872 hours. The greater the CK level, the greater the amount of infarcted tissue. CK-MB is specific
to cardiac muscle and is the most sensitive indicator of AMI. Serum CK-MB levels increase
within 2 to 6 hours, peak at 18 hours, and return to normal within 24 hours. A level elevated
greater than 5 percent is considered a positive indicator of AMI. Troponin I, a muscle protein, is
the most accurate marker of myocardial injury, when skeletal muscle damage has taken place
and distorted the CK level. Troponin I appears in the bloodstream 4 to 12 hours after the onset of
injury to cardiac muscle, peaks at 12 hours, and remains elevated for 10 to 14 days, making it the
best test for AMI if treatment was delayed. Myoglobin, a protein found in cardiac and skeletal
muscle, can aid in the diagnosis of AMI but isn’t cardiac-specific. Serum myoglobin levels can
rise above normal within 2 to 4 hours, so an elevation may be the earliest indicator of a coronary
event. The levels return to normal in less than 24 hours. Serum levels of cardiac markers are
ordered upon arrival to the emergency department and routinely ordered for 3 consecutive days
following AMI; having a flow sheet of cardiac markers help with diagnosis and to see the extent
of damage. (LeMone & Burke, 2008).
CBC shows an elevated WBC count due to inflammation of the injured myocardium. The
ESR also rises because of inflammation. ABGs may be ordered to assess acid-base balance and
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blood-oxygen levels. The electrocardiogram reflects changes in conduction due to myocardial
ischemia and necrosis. Echocardiography is done to evaluate cardiac wall motion and left
ventricular function. Infarcted tissue doesn’t contract effectively, if at all, as a healthy
myocardium would. “If the patient has a new left bundle branch block (LBBB) and other signs
and symptoms of AMI, he should be evaluated immediately for reperfusion therapy” (Lackey,
2006). Radionuclide imaging may be done to evaluate myocardial perfusion. These studies
cannot differentiate between AMI and old scar tissue, but do help identify the area of myocardial
ischemia and damage. Hemodynamic monitoring may be initiated when AMI significantly
affects cardiac output and hemodynamic status. (LeMone & Burke, 2008).
Usual Treatment
Therapies
Many patients with AMI are treated with prompt percutaneous coronary revascularization
(PCR) such as angioplasty and stent placement. PCR is used to restore blood flow to ischemic
myocardium. Nursing care after a PCR includes assess for bleeding at the insertion site,
infection, vascular compromise on the extremity used, and hematoma formation. Coronary
Artery Bypass Graft (CABG) surgery may be performed based on patient’s age and immediate
condition; the time elapsed from the onset of manifestations and the extent of disease and
damage to the myocardium. Nursing responsibilities following a CABG include monitoring
cardiovascular status, assessing arterial pressure every 15 minutes until stable, auscultate heart
sounds and determine rhythms, assess peripheral pulses, hemodynamic and ECG monitoring,
assess cardiac enzymes, monitor urinary output, observe for persistent bleeding, and auscultate
chest for breath sounds. For patients who have suffered a large MI, and have evidence of pump
failure, invasive devices may be used to take over the function of the heart allowing the injured
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myocardium to heal. The intra-aortic balloon pump temporarily supports cardiac function
allowing the heart to heal by decreasing workload and oxygen demands and increasing perfusion.
Nursing responsibilities include monitoring vital signs and urine output closely, monitoring for
dysrhythmias, daily chest x-ray to monitor balloon placement, using log rolls to turn, monitor
peripheral pulses, and elevate head of bed 45 degrees. Ventricular assistive devices (VAD) are
often used for patients who need more or longer term artificial support than the intra-aortic
balloon pump provides. Ventricular assistive devices are used as temporary or complete assist in
AMI and cardiogenic shock when there is a chance for recovery of normal heart function after a
period of cardiac rest. Nursing care for a client with a VAD includes strict sterile technique,
monitoring for signs and symptoms of a stroke, pulmonary embolism, or another AMI, and
constant hemodynamic monitoring. (LeMone, & M., 2008).
Other treatment includes cardiac rehabilitation, which is a long-term treatment program
that focuses on education, counseling, risk factor modification, medical evaluation and exercise.
It is used to limit physical and psychological effects of cardiac illness and improve the cardiac
patient’s quality of life. “Cardiac rehabilitation can reduce mortality by 20 to 27 percent” (Tod,
2008).
Cardiac rehab has three phases:

Phase I: Inpatient phase- begins with admission for a cardiac event. Nursing
responsibilities include bed rest for the first 24 hours, then allow patient to sit in
bedside chair for 15 to 20 minutes. Increase activity according to patient’s tolerance
and endurance. Start taking patient for walks in the hall with supervision. Assess for
signs of dyspnea, chest pain, tachycardia, and sense of exhaustion.
ACUTE MYOCARDIAL INFARCTION
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Phase II: Outpatient phase- begins 3 weeks of cardiac event. Nursing responsibilities
include increasing levels of exercise in a supervised setting. Holter monitoring or
telemetry during exercise. Educate patient about smoking cessation, diet, exercise,
weight loss and develop and individualized plan of care.

Phase III: Maintenance Phase- begins 12 weeks after cardiac event. The patient is
now doing exercises independently and is to return every 3 months for a check-up.
Nursing responsibilities include patient teaching about medications, diet, monitoring
cholesterol levels, exercise routine, avoiding stress, and maintaining a heart healthy
lifestyle. (Tod, 2008).
Pharmacological Treatment
The standard of care when a patient comes into the emergency department presenting
with AMI is to get IV access and initiate MONA protocol. MONA stands for Morphine, Oxygen,
Nitroglycerin, and Aspirin. Aspirin is a platelet inhibitor and is essentially the most important in
decreasing the changes of developing a STEMI because it decreases oxygen demand which
decreases the incidence of a full thickness infarct. Nursing responsibilities when giving aspirin is
to give 160 to 325 mg tablets initially, followed by a daily dose of the same mg. Instruct the
patient to chew the tablet to increase absorption. Closely monitor patients with active ulcer
disease or asthma when giving aspirin. Nitroglycerin is given sublingual as 0.4 mg tablets, one
every 5 minutes, with a maximum of three tablets, to relieve chest pain and decrease cardiac
workload. It can also be given IV for the first 24 to 48 hours to decrease cardiac workload. It is a
vasodilator that not only relieves pain but decreases oxygen demand, therefore increasing the
supply of oxygen to the myocardium. Nursing responsibilities include making sure systolic blood
pressure is above 100 mmHg before administering the first dose and rechecking the blood
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pressure before any additional doses are given. Have patient sit or lie down during administration
and watch for headache, drop in blood pressure, syncope, and tachycardia. Morphine sulfate is
the drug of choice for pain unrelieved by nitro. Initial dosing is 4 to 8 mg IV, followed by 2-4 mg
IV every 5 minutes until pain is relieved or sedation occurs. Nursing responsibilities include
monitoring blood pressure, making sure it stays above 100 systolic, respiratory rate, making sure
it doesn’t fall below 12, and level of sedation. Monitor for anaphylactic reactions: rise in
temperature, rash, SOB, and significant changes in vital signs. Oxygen is used to saturate
hemoglobin and increase the oxygen capacity of the blood, closely monitor pulse oximetry as
well as the client. Other medications include: fibrinolytic therapy, which are drugs that break up
clots and restore blood flow to the obstructed artery. Antidysrhythmics are used as needed and
prophylactically to reduce dysrhythmias. Beta blockers are used to reduce pain, limit infarct size,
and decrease incidence of serious dysrhythmias. ACE inhibitors are used to reduce ventricular
remodeling following AMI, reducing the risk of heart failure. Anticoagulants and antiplatelets
are used to maintain coronary artery patency by preventing clots from forming or increasing in
size. Dopamine, a vasopressor, may also be given to improve blood flow to the kidneys,
preventing renal ischemia. (Overbaugh, 2009).
Prognosis
Many factors influence the recovery phase of AMI. Factors that influence the short-term
prognosis are the time in which treatment was received, the amount of tissue that was damaged,
the hospitals ability to correct the infarct and the patient’s response and understanding of the
event. Factors that influence long term recovery are the compliance with cardiac rehabilitation,
making serious lifestyle modifications, and coping with the diagnosis of a heart attack.
Modifiable risk factors that should be addressed to increase prognosis and prevent future attacks
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are: don't smoke, avoid secondhand smoke, routinely check cholesterol levels, get regular
medical checkups, control blood pressure, exercise regularly, maintain a healthy weight, eat a
heart-healthy diet, manage stress, and drink alcohol in moderation.
Conclusion
I chose to write this paper because of the incidence of this condition. It has been the
leading cause of death in the United States for over 100 years. AMI can happen suddenly and has
a considerably high mortality rate. During my research I found numerous ways to prevent the
incidence of a heart attack. I can use the information I have learned in my personal life, and
make some serious changes at a young age, which will significantly increase my chances of
preventing a heart attack. Also, in knowing the modifiable risk factors I can educate and improve
the lives of my patients as well as friends and family members.
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References
Erdogan, D., Ozaydin, M., Türker, Y., Karabacak, M., Varol, E., & Dogan, A. (2010). Influence
of statin therapy on circadian variation of acute myocardial infarction. Anatolian Journal
of Cardiology / Anadolu Kardiyoloji Dergisi, 10(5), 429-433. doi:10.5152/akd.2010.141
Lackey, S. (2006). Suppressing the scourge of AMI: Learn the seven key steps for improving
survival and your role in implementing them. Nursing, 36(5), 37-42. Retrieved from
Academic Search Premier database.
LeMone, P., & Burke, K. M. (2008). Medical-surgical nursing: Critical thinking in client care.
Upper Saddle River, N.J: Pearson/Prentice Hall.
Overbaugh, K. J. (2009). Acute Coronary Syndrome. American Journal of Nursing, 109(5), 4252. Retrieved from Academic Search Premier database.
Tod, A. (2008). Exploring the meaning of recovery following myocardial infarction. Nursing
Standard, 23(3), 35-42. Retrieved from Academic Search Premier database.