Bedside Clinic MI
-
Upload
pinksapphire929 -
Category
Documents
-
view
225 -
download
0
Transcript of Bedside Clinic MI
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 1/19
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
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 2/19
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.
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 3/19
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
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 4/19
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
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 5/19
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
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 6/19
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.
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 7/19
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
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 8/19
(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
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 9/19
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
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 10/19
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
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 11/19
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.
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 12/19
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
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 13/19
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.
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 14/19
- 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
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 15/19
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.
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 16/19
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
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 17/19
- 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
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 18/19
- 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
8/9/2019 Bedside Clinic MI
http://slidepdf.com/reader/full/bedside-clinic-mi 19/19
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.