33.

MYOCARDIAL INFARCTION
MI refers to the process by which areas of myocardial cells in the heart
are permanently destroyed.
An occlusion of a coronary artery, MI leads to oxygen deprivation,
myocardial ischemia, and eventual necrosis. Its one component of
acute coronary syndrome
I. ASSESSMENT
a. Subjective data:
a.1 Important health information

Past Health history

Previous history of illness and family health history particularly of
heart disease

History of present illness

Description of events r/t current illness, including any selftreatments and response
General
The patient experiences severe, persistent chest pain thats
unrelieved by rest or nitroglycerin. He may describe the pain as
crushing or squeezing. Usually substernal, pain may radiate to
the left arm, jaw, neck, or shoulder blades.
b.1 Functional Health Patterns

Health perception-health management

Family History of heart disease
Sedentary lifestyle
Tobacco use
Nutritional-Metabolic
Indigestion
Heartburn
Nausea
Belching
Vomiting
Elimination
Sweating (diaphoresis)
Straining at stool
Activity exercise
Palpitations
Dyspnea

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Dizziness
Weakness
Cognitive-perceptual
Chest pain or discomfort, palpitations.

b. Objective data

Neurologic
Anxiety, restlessness, light-headedness may indicate
sympathetic stimulation or a in contractility and cerebral
oxygenation
Integumentary
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.
Cardiovascular
Heart sounds may include S3, S4, and a new set of a murmur
jugular venous distention may be seen if the Mi has caused
heart failure.
Elevated BP because of symphatetic stimulation or because of
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 dysrhythmia
Gastrointestinal
urinary output may indicate cardiogenic shock
Respirations
Shortness of breath
Dyspnea, tachypnea
Crackles if MI has caused pulmonary congestion
Pulmonary edema may be present
Psychological
Fear with feeling of impending doom, or patient may deny that
anything is wrong.

c. Possible Diagnostic findings

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 Serial 12-lead ECG may show no abnormalities or may

proveinconclusive during the first few hours after MI. When
present,characteristic abnormalities on the ECG can help
pinpoint thelocation of the MI.
ST-segment monitoring tracks the hearts response to MI.
Continuousmonitoring can immediately detect ischemic
episodes.During an MI, monitoring can help differentiate between
an STsegment elevated MI (STEMI) and a non ST-segment
elevated MI (NSTEMI); differentiating between a STEMI and
NSTEMI helps the practitioner better guide treatment. STsegment monitoring can also identify patients at high risk for
reocclusion after PTCA or MI and permits prompt intervention if
reocclusion occurs. After MI, monitoring may reduce or eliminate
the need for angiography in patients receiving thrombolytic
drugs by gaugingthe efficacy of the drugs.
Serial serum cardiac marker measurements show elevated CK,
especially the CK-MB isoenzyme (the cardiac muscle fractionof
CK), troponin I and T, and myoglobin.
Echocardiography shows ventricular wall dyskinesia (with
transmural MI).
II. PSCHO/PATHOPHYSIOLOGY

Abstract
MI results from prolonged ischemia to the myocardium with irreversible
cell damage and muscle death. Functionally, MI causes:
reduced contractility with abnormal wall motion
altered left ventricular compliance
reduced stroke volume
reduced ejection fraction
elevated left ventricular end-diastolic pressure

In myocardial infarction (MI), blood supply to the myocardium is interrupted.

Heres what happens:

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Injury to the endothelial lining of the coronary arteries causes platelets,

white blood cells, fibrin, and lipids to gather at the injured site. Foam cells, or
resident
macrophages, gather beneath the damaged lining and absorb oxidized
cholesterol, forming a fatty streak that narrows the arterial lumen.

As the arterial lumen narrows gradually, collateral circulation develops,which

helps to maintain myocardial perfusion distal to the obstructed vessel lumen.
The illustration above shows collateral circulation.

When myocardial demand for oxygen is more than the collateralcirculation

can supply, myocardialmetabolism shifts from aerobic toanaerobic,
producing lactic acid (A),which stimulates nerve endings.

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Lacking oxygen, the myocardial cells die. This decreases contractility, stroke
volume, and blood pressure.

Hypotension stimulates baroreceptors, which in turn stimulate the

adrenal glands to release epinephrine and norepinephrine. This cycle is
shown above. These catecholamines increase heart rate and cause
peripheral
vasoconstriction, further increasing myocardial oxygen demand.

Damaged cell membrane in the infarcted area allow intracellular contents

into the vascular circulation,asshownabove.. Ventricular arrhythmias then
develop with elevated serum levels of potassium, creatine kinase (CK), CKMB, aspartate
aminotransferase, and lactate dehydrogenase.

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INJURY SITE

All myocardial cells are capable of spontaneous depolarization and

repolarization, so the electrical conduction system may be affected by
infarct, injury, or ischemia.The illustration above shows an injury site.

Extensive damage to the left ventricle may impair its ability to pump,
allowing blood to back up into the left atrium and, eventually, into the
pulmonary veins and capillaries, as shown in the illustration above. Crackles
may be heard in the lungs on auscultation. Pulmonary artery wedge pressure
is increased.

As back pressure rises, fluid crosses the alveolar-capillary membrane,

impeding diffusion of oxygen (O2) and carbon dioxide (CO2). Arterial blood
gas measurements may show decreased partial pressureof arterial oxygen
and arterial pH and increased partial pressure of arterial carbon dioxide.

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Diagram (Pathophysiology

with treatment

&clinical manifestations
Thrombolytic
therapy
Glycoprotein
IIB/IIIA receptor
antagonists

Change in the
condition of plaque in
the coronary artery
Activations of
platelets

Aspirin
antiplatelet
aggregates

Elevated ST segment
Q waveappears

Formation of
thrombus
Nitrates

Elevated CPK-MB Elevated

Schemia of tissue in the

region supplied by the
artery

Altered repolarization
myoglobin Troponin T &
of the myocardium
Troponin I
Release of
lysosomal
enzymes

Coronary blood
supply less than
demand

Beta-blockers
Oxygen

Lactic
acid
producti

Anaerob
ic
glycolys

Myocardi
al cell
death

Nitroglycerin

Myocardial
irritability
Angina

Stimulation of
the sympathetic
nervous
sysytem
Increased
Heart needs

Decreased
contractilit
y

Dys-rhytmias
Antidysrhythmic
s

Decreased left
ventricular function
Increas
ed O2
needs
NItrates

Increas
ed
afterloa

Vaso-contriction

Increased
preload
Fluid
restriction

CVP

PCWP

AngiotensinConverting
Enzyme
inhibitors

Decreased
cardiac
output

Decreased LV ejection

fraction

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III. A. FORMULATION OF NURSING DIAGNOSIS # 1

Priority Nursing diagnosis # 1

Ineffective Cardiopulmonary tissue perfusion r/t reduced
coronary blood flow

IV. A. FORMULATION OF NURSING PLAN #1

After 8 hours of Nursing Intervention, client will be relief of chest pain or any
discomfort
V. A. NURSING INTERVENTIONS #1

Dependent

Nursing interventions
1. Initially assess, document and
report to the physician the ff;

a.) The patients description,

including location, intensity,
radiation, duration, and factors that
affect it. Other symptoms such as
nausea, diaphoresis, or complaints of
unusual fatigue
b.) The effect of chest discomfort on
cardiovascular perfusion to the
heart (e.g. change in blood pressure,
heart sounds) to the brain (e.g
changes in LOC), to the kidneys (e.g.
in urine output) and to the skin
(e.g. color, temperature)

Ensure physical rest ; use of the

bedside commode with assistance ;
backrest elevated to promote
comfort ; diet as tolerated ; arms
supported during upper extremity
activity ; use of stool softener to

Rationale
1. These data assist in determining
the cause and affect of the
discomfort and provide a baseline
data with which post-theraphy
symptoms can be compared.
a.) There are many conditions
associated with discomfort. There are
characteristic clinical findings of
ischemic pain and symptoms.
b.) MI decreases myocardial
contractility and ventricular
compliance and may produce
dysrhythmias. Cardiac output is
reduced, resulting in reduced blood
pressure and decreased oragn
perfusion. The heart rate may
increase as compensatory
mechanism to maintain cardiac
output.
2. Physical rest reduces myocardial
oxygen consumption. Fear and
anxiety precipitate the stress
response ; this results in increased
levels of endogenous
catecholamines, which increases

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prevent straining at stool. Provide a

restful environment, and allay fears
and anxiety by being supportive,
calm and competent. Individualized
visitation based on patients
response.

Dependent

Nursing intervention
1. administer oxygen as prescribed

2. administer medication therapy as

prescribed and evaluate the patients
response continuously.

3. Check the patients blood pressure

after giving nitroglycerin, especially
the first dose.

myocardial oxygen consumption. Also

with increased epinephrine, the pain
threshold id decreased, and pain
increases myocardial oxygen
consumption.

Rationale
1. oxygen therapy may increase the
oxygen supply to the myocardium if
actual oxygen saturation is less than
normal
2. Medication therapy is the first line
of defense in preserving myocardial
tissue. The side effcts of these
medications can be hazardous and
the patients status must be
assessed.

Collaborative

Nursing intervention
Obtain a 12-lead ECG recording
during the sympatomatic event as
prescribed, to determine extension of
infarction.

Rationale
An ECG during symptoms may be
useful in the diagnosis of an
extension of MI

VI. A. FORMULATION OF EVALUATION #1

After 8 hours of nursing intervention patient is able to report of beginning
relief of chest discomfort and symptoms at once as seen by appears
comfortable and pain or symptom free, are rested; respiratory rate, cardiac
rate, and blood pressure return to prediscomfort level, has an adequate

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cardiac output as evidenced by normal heart rate and rhythm, blood

pressure of within normal level, has adequate urine output.
III. B. FORMULATION OF NURSING DIAGNOSIS # 2

Nursing Diagnosis # 2
Potential Ineffective air exchange r/t fluid overload

IV. B. FORMULATION OF NURSING PLAN

After 8 hours of nursing intervention, client will not experience any
respiratory difficulties.
V. B. NURSING INTERVENTIONS # 2

Independent

Nursing intervention
1. Initially, every 4 hours, and with
chest discomfort, or symptoms,
assess, document, and report to the
physician abnormal heart sounds
(particularly S3 and S4 gallops and the
holosystolic murmur of left
ventricular papillary muscle
dysfunction), abnormal breath
sounds (particularly crackles) , and
patient intolerance to specific
activities.

2. Teach patient :
a.) to adhere to the diet
prescribed(for example, explain low
sodium, low calorie diet)
b.) To adhere to activity prescription

Rationale
1.These data are useful in diagnosing
left ventricular failure. Diastolic filling
sounds (S3 and S4) results form the
decreased left ventricular compliance
associated with MI. Papillary muscle
dysfunctiona(from infarction of the
papillary muscle) can result in mitral
regurgitation and a reduction in
storke volume, leading to ventricular
failure. The presence of
crackles(usually at the lung bases)
may indicate pulmonary congestion
from increased left heart pressure.
The association of symptoms and
activity can be used as the guide for
activity prescription and a basis for
patient teaching.
a.) Low sodium diet may reduce
extracellular volume thus reducing
preload and afterload, and thus
myocardial oxygen oxygen
consumption.
b.) The activity prescription is
determined individually to maintain

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3. Watch for signs and symptoms of

fluid retention
(crackles, cough, tachypnea, and
edema. Carefully monitor
daily weight, intake and output,
respirations, serum
enzyme levels, and blood pressure.
Auscultate for
adventitious breath sounds
periodically (patients on
bed rest commonly have
atelectaticcrackles) and for
S3 or S4 gallops.

Dependent

Nursing interventions
To promote compliance with the
prescribed medication regimen and
othertreatment measures, thoroughly
explain dosages and therapy. Warn
about drug adverse effects, and
advise the patient to watch for and
report signs of toxicity

the heart rate and blood pressure

within safe limits.
3. Fluid retention may
indicate impending heart failure.

Rationale
To anticipate possible effects of the
drugs.

Collaborative

Nursing intervention
1. Ask the dietary department to
provide a clear liquid diet until
nausea subsides
2.Counsel the patient about lifestyle
changes. Review dietary restrictions.
If
the patient must follow a low-sodium
or
low-fat and low-cholesterol diet,

Rationale
1. A low-cholesterol, low-sodium diet
may be ordered.
2. to learn more on appropriate diet.

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provide a list of undesirable foods.

Ask the dietician to speak to the
patient and his family
3. Recommend his participation in a
cardiac rehabilitation program for
exercise, education, symptom
management, and support with risk
modification.

3. that will help manage the disease

VI. B. FORMULATION OF NURSING EVALUATION #2

After 8 hours of nursing intervention, patient experiences no shortness of
breath, dyspnea on exertion, orthopnea, or paroxysmal nocturnal dyspnea
and a total relief of chest discomfort, appears comfortable and rested as
evidenced by
respiratory rate of less than 20 breaths/min with physical activity and 16
breaths/min with rest, skin color is normal, PaO2 and PaCO2 within normal
range,heart rate is less than 100 beats/min and greater than 60 beats/min,
with blood pressure within patients normal limits.

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