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 syndromeI. ASSESSMENTa. 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 self-treatments 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 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 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.
ST-segment 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 AbstractMI 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 pressureIn myocardial infarction (MI), blood supply
to the myocardium is interrupted. Heres what happens:
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 residentmacrophages, 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.
Lacking oxygen, the myocardial cells die. This decreases
contractility, stroke volume, and blood pressure.
Hypotension stimulates baroreceptors, which in turn stimulate
theadrenal glands to release epinephrine and norepinephrine. This
cycle is shown above. These catecholamines increase heart rate and
cause peripheralvasoconstriction, 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), CK-MB, aspartateaminotransferase, and lactate
dehydrogenase.
INJURY SITEAll 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.
Thrombolytic therapy Glycoprotein IIB/IIIA receptor
antagonistsDiagram (Pathophysiology with treatment &clinical
manifestations
Change in the condition of plaque in the coronary artery
Aspirin antiplatelet aggregatesElevated ST segment Q
waveappearsActivations of platelets
Formation of thrombus
NitratesAltered repolarization of the myocardiumElevated CPK-MB
Elevated myoglobin Troponin T & Troponin ISchemia of tissue in
the region supplied by the artery
Release of lysosomal enzymes
Coronary blood supply less than demand
Beta-blockersLactic acid productionAnaerobic glycolysis
OxygenMyocardial cell death
Myocardial irritabilityNitro-glycerin
Angina
Stimulation of the sympathetic nervous sysytem
Decreased contractilityDys-rhytmiasAnti-dysrhythmics
Increased Heart needs
Angiotensin-Converting EnzymeinhibitorsDecreased left
ventricular function
Increased O2 needsIncreased afterload
Increased preloadNItratesDecreased cardiac output
CVP PCWPDecreased LV ejection fractionVaso-contrictionFluid
restriction
III. A. FORMULATION OF NURSING DIAGNOSIS # 1 Priority Nursing
diagnosis # 1 Ineffective Cardiopulmonary tissue perfusion r/t
reduced coronary blood flowIV. A. FORMULATION OF NURSING PLAN
#1After 8 hours of Nursing Intervention, client will be relief of
chest pain or any discomfortV. A. NURSING INTERVENTIONS #1
DependentNursing interventionsRationale
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 fatigueb.)
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)
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.
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 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.2. Physical rest reduces myocardial oxygen consumption.
Fear and anxiety precipitate the stress response ; this results in
increased levels of endogenous catecholamines, which increases
myocardial oxygen consumption. Also with increased epinephrine, the
pain threshold id decreased, and pain increases myocardial oxygen
consumption.
DependentNursing interventionRationale
1. administer oxygen as prescribed1. oxygen therapy may increase
the oxygen supply to the myocardium if actual oxygen saturation is
less than normal
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.
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.
CollaborativeNursing interventionRationale
Obtain a 12-lead ECG recording during the sympatomatic event as
prescribed, to determine extension of infarction.An ECG during
symptoms may be useful in the diagnosis of an extension of MI
VI. A. FORMULATION OF EVALUATION #1After 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
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 PLANAfter 8 hours of nursing intervention,
client will not experience any respiratory difficulties. V. B.
NURSING INTERVENTIONS # 2 IndependentNursing
interventionRationale
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.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.
2. Teach patient :a.) to adhere to the diet prescribed(for
example, explain low sodium, low calorie diet)
b.) To adhere to activity prescription 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 the heart rate
and blood pressure within safe limits.
3. Watch for signs and symptoms of fluid retention(crackles,
cough, tachypnea, and edema. Carefully monitordaily weight, intake
and output, respirations, serumenzyme levels, and blood pressure.
Auscultate foradventitious breath sounds periodically (patients
onbed rest commonly have atelectaticcrackles) and forS3 or S4
gallops.
3. Fluid retention mayindicate impending heart failure.
DependentNursing interventionsRationale
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 toxicityTo anticipate possible effects of
the drugs.
CollaborativeNursing interventionRationale
1. Ask the dietary department to provide a clear liquid diet
until nausea subsides1. A low-cholesterol, low-sodium diet may be
ordered.
2.Counsel the patient about lifestylechanges. Review dietary
restrictions. Ifthe patient must follow a low-sodium orlow-fat and
low-cholesterol diet, provide a list of undesirable foods. Ask the
dietician to speak to the patient and his family2. to learn more on
appropriate diet.
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 #2After 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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