ENGLISH TASK

NURSING CARE PLAN FOR MYOCARD INFARCTION

Lecturer : BAHARUDDIN k. s.pd., m.pd

Disusun Oleh :
GROUP 8

- Anggi Anggoro Kasih Anwar (PO713201221008)

- Asdar (PO713201221009)
- Musdalifah Muslimin (PO713201221022)
- Nadya Latifah (PO713201221023)
- Wilanda Dwimaras (PO713201221042)
- Sulastri (PO713201221041)

KEMENTERIAN KESEHATAN REPUBLIK INDONESIA

POLTEKKES KEMENKES MAKASSAR
JURUSAN KEPERAWATAN MAKASSAR
PRODI D III KEPERAWATAN
2023/2024
 1. Definitions

Myocardial infarction (MI) is commonly referred to as a “heart attack”. Myocardial

ischemia is inadequate perfusion to the myocardium that occurs from a partial or
complete blockage of blood and oxygen to the heart. The major cause of a heart attack
is coronary artery disease.

2. Etiology
 Atherosclerosis:
− Primary cause of myocardial infarction.
− Gradual buildup of fatty deposits (plaques) within coronary arteries.
− Plaques may rupture or erode, leading to thrombus formation and subsequent
occlusion of blood vessels.
 Coronary Artery Disease (CAD):
− CAD is a major contributing factor.
− Conditions such as hypertension, hyperlipidemia, and diabetes mellitus increase the
risk of atherosclerosis and coronary artery narrowing.
 Thrombosis:
− Formation of blood clots (thrombi) within coronary arteries.
− Thrombosis can result from plaque rupture, endothelial injury, or conditions that
promote abnormal blood clotting.
 Coronary Vasospasm:
− Sudden, intense contraction of coronary arteries.
− Can occur spontaneously or be triggered by drug use, stress, or other factors.
− Vasospasm leads to temporary or prolonged reduction of blood flow to the
myocardium, causing ischemia and potential infarction.
 Risk Factors:
− Smoking: Increases atherosclerosis and promotes clot formation.
− Hypertension: Raises the workload on the heart and contributes to arterial damage.
− Diabetes: Accelerates atherosclerosis and impairs blood vessel function.
− Hyperlipidemia: Elevated levels of cholesterol contribute to plaque formation.
− Family History: Genetic predisposition may increase susceptibility to CAD and myocardial
infarction.

3. Pathophysiology
Myocardial infarction is defined as sudden ischemic death of myocardial tissue. In the
clinical context, myocardial infarction is usually due to thrombotic occlusion of a coronary
vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and
ionic perturbations in the affected myocardium and causes rapid depression of systolic
function. Prolonged myocardial ischemia activates a "wavefront" of cardiomyocyte death that
extends from the subendocardium to the subepicardium. Mitochondrial alterations are
prominently involved in apoptosis and necrosis of cardiomyocytes in the infarcted heart. The
adult mammalian heart has negligible regenerative capacity, thus the infarcted myocardium
heals through formation of a scar. Infarct healing is dependent on an inflammatory cascade,
triggered by alarmins released by dying cells. Clearance of dead cells and matrix debris by
infiltrating phagocytes activates anti-inflammatory pathways leading to suppression of
cytokine and chemokine signaling. Activation of the renin-angiotensin-aldosterone system and
release of transforming growth factor-β induce conversion of fibroblasts into myofibroblasts,
promoting deposition of extracellular matrix proteins. Infarct healing is intertwined with
geometric remodeling of the chamber, characterized by dilation, hypertrophy of viable
segments, and progressive dysfunction. This review manuscript describes the molecular
signals and cellular effectors implicated in injury, repair, and remodeling of the infarcted
heart, the mechanistic basis of the most common complications associated with myocardial
infarction, and the pathophysiologic effects of established treatment strategies. Moreover, we
discuss the implications of pathophysiological insights in design and implementation of new
promising therapeutic approaches for patients with myocardial infarction.

4. A s s e s s m e n t

a. Subjective Data
 Chest Pain
 Chest Pressure/Squeezing
 PQRST pain assessment
− P- provoke, precipitate, palliate
− Q- quality
− R- radiate
− S- severity, symptoms
 − T- time
 Patient may report a feeling of impending doom
 Shortness of Breath

b. Objective Data
 ST elevation on the ECG- Called an STEMI
 Decreased oxygenation
 Signs of left ventricular failure such as crackles in the lungs or S3 heart sound
 Tachycardia (Bradycardia can be seen if patient is having an inferior MI)
 Elevated Cardiac Enzymes

5. Nursing Diagnosis
Once the nurse identifies nursing diagnoses for myocardial infarction, nursing care
plans help prioritize assessments and interventions for both short and long-term goals of
care. In the following section you will find nursing care plan examples for myocardial
infarction.
1. Acute Pain

2. Anxiety

3. Decreased Cardiac Output

4. Ineffective Tissue Perfusion
5. Risk for Unstable Blood Pressure

6. Nursing Care Plan

1. Nursing Diagnosis: Acute Pain

Acute pain associated with myocardial infarction is caused by chest pain/discomfort from
inadequate blood flow to the heart.

Related to:

 Blockage of coronary arteries

 Low or no oxygen-rich blood flowing to the heart
 As evidenced by:

Verbal reports of chest pain, pressure, or tightness


Clutching the chest

Restlessness

Labored breathing and dyspnea

Diaphoresis

Changes in vital signs

Expected outcomes:

Patient will verbalize pain relief or control.


Patient will rate the chest pain lower than the baseline pain scale.

Patient will appear relaxed and able to sleep or rest appropriately.

Patient will be able to perform daily activities without assistance.

Assessment:

1) Determine if the chest pain is angina or myocardial infarction.

Chest pain in myocardial infarction is characterized by the following:

 Occurs without warning (usually in the early morning)

 Crushing pain in the substernum
 May radiate to the jaw, back, and left arm
 Lasts for 30 minutes or longer
 Unrelieved by rest or nitroglycerin
2) Assess pain characteristics.
Have the patient explain when the symptoms started, if they were precipitated activity or
emotion, and if they took any measures to relieve the pain.
3) Obtain ECG during chest pain symptoms.
Expressions of chest pain should always be investigated using an ECG for quick results.

Interventions:

1) Administer nitroglycerin.
When chest pain initially appears in an adult, one tablet of nitroglycerin should be placed
under the tongue or in the space between the cheek and gum. Nitroglycerin dilates blood
vessels.
2) Administer oxygen as ordered.
Chest pain can happen when the demand for oxygen is not being met. Supplemental
oxygen administration will improve the oxygenation for the heart to function effectively.
3)Administer morphine.
Morphine may decrease the oxygen demand of the heart. It can also reduce blood pressure
and slow the heart rate. Morphine will relax the patient and relieve anxiety.
4) Evaluate the effectiveness of pain control measures.
Frequently assess administered pain control measures for effectiveness.
2. Nursing Diagnosis: Anxiety

Anxiety associated with myocardial infarction can be caused by the stimulation of the
sympathetic nervous system (fight or flight response). Anxiety can also be a cause of MI.

Related to:

 Threat of death
 Threat to health status
 Change to role functioning
 Lifestyle modification
As evidenced by:

Increased tension

Fearful attitude

Apprehension

Expressed concerns or uncertainty

Restlessness

Dyspnea

Expected outcomes:

Patient will be able to verbalize the cause of their anxiety.

Patient will verbalize an understanding of the necessary changes following myocardial
infarction.
 Patient will implement individual coping mechanisms.
 Patient will display signs of reduced anxiety such as vital signs within normal limits
and a calm demeanor.
Assessment:

1) Observe anxiety during myocardial infarction.

Anxiety is the most common psychological symptom which is linked to a poor
prognosis following MI.
2) Examine the subjective and objective cues of anxiety.
Subjective and objective cues may reflect signs of anxiety in MI patients. Patients
may not complain of chest pain yet they are holding their chest. Remain aware of
symptoms to intervene.
3) Assess the patient’s coping mechanisms.
Recovery following MI is a long-term process of adapting to changes in all aspects of
life. Help the patient recognize and develop coping behaviors to utilize later.

Interventions:

1) Recognize that the patient’s anxieties are valid.

Encourage them to verbalize their feelings and assure them that they will not be
 judged because of it. With support, the patient is more likely to overcome this threat
to their health.
2) Offer information and answer questions.
The nurse should provide thorough explanations of tests, procedures, and
interventions to alleviate the patient’s anxiety. Allow time for patients and families to
ask questions and answer honestly.
3) Include the patient in the care planning process.
Involve the patient in the care plan by allowing them to take time to prepare for
scheduled treatments. Patient involvement may restore a patient’s sense of autonomy
when coping with the treatment and recovery from MI.
4) Manage stress.
Stress management will lower the risk of posttraumatic stress disorder
(PTSD) following MI. PTSD is linked to decreased quality of life and increased risk
of recurring MI.
5) Teach ways to reduce anxiety.
In conjunction with the patient, uncover ways the patient can reduce anxiety such as
through exercise, journaling, breathing, music, and medications.

3. Nursing Diagnosis: Decreased Cardiac Output

Decreased cardiac output associated with myocardial infarction can be caused by the
loss of viable heart muscle. This can result in decreased cardiac output and, in severe cases,
cardiogenic shock and death.

Related to:

 Changes in heart rate and electrical conduction

 Reduced preload
 Reduced cardiovascular blood flow
 Rupture of atherosclerotic plaque
 Occluded artery
 Altered muscle contractility
As evidenced by:

 Sudden and continuous chest pain unrelieved by rest and medication

 Shortness of breath
 Nausea
 Vomiting
 Anxiety
 Cool, pale, and moist skin
 Tachycardia
 Tachypnea
 Fatigue
 Dizziness
  Confusion
 Dysrhythmia
Expected outcomes:

 Patient will maintain blood pressure within acceptable limits set by the provider.
 Patient will be able to demonstrate decreased or absent dyspnea, angina, and
dysrhythmias.
 Patient will be able to verbalize an understanding of myocardial infarction and its
management.
 Patient will be able to participate in activities that decrease the workload of the heart.
Assessment:

1) Determine the patient’s risk and causative factors for decreased cardiac output.
Assess the patient’s medical history for atherosclerosis, blood clots, heart failure, and
other conditions that place them at risk for decreased cardiac output and MI.
2) Determine if the condition is angina or myocardial infarction.
Stable angina is chest pain or discomfort that occurs with activity or stress but is
relieved with rest or medications. MI occurs without regard to activity, lasts longer than
stable angina, and is not relieved by rest or medications.
3) Closely monitor the blood pressure.
Immediately inform the provider when systolic blood pressure is less than 100 mmHg
or 25 mmHg lower than the previous reading as it can lead to a cardiogenic shock. This
is a complication that develops when the heart muscle deteriorates if oxygen-rich blood
is not flowing to the heart.
4) Obtain ECG.
The most convenient and efficient approach for an early diagnosis of acute myocardial
infarction is a 12-lead ECG. STEMI, NSTEMI, and other dysrhythmias can be detected.
5) Assess for signs of poor cardiac output.

 Cool, diaphoretic skin

 Weak or absent pulses
 Decreased urine output
 Altered mental status
 Peripheral vasoconstriction

6) Assess cardiac enzymes.

Myoglobin, troponin, and creatine kinase are cardiac enzymes, also known as
cardiac biomarkers. Cardiac troponin I or cardiac troponin T are both extremely
sensitive and specific for MI.

Interventions:

1) Administer oxygen as ordered.

Administer oxygen to increase perfusion to the heart and other tissues.
 2) Administer thrombolytic therapy as ordered.
If cardiac catheterization is not required immediately, administer thrombolytic therapy
within the first 6 hours following the first symptom. Monitor for signs of bleeding.
3) Administer beta blockers as ordered.
Beta-blockers are used to lower myocardial contraction force, promote myocardial
perfusion, and slow the heart rate.
4) . Establish IV access.
IV access is used for the immediate administration of medication, IV fluids, and blood
products.
5) Prepare for possible cardiac catheterization.
Urgent cardiac catheterization evaluates the degree and location of coronary artery
blockages. A stent may be placed to restore blood flow to myocardial tissue.
6) . Encourage bed rest and activity restrictions.
Bed rest lessens the workload, preventing inadequate perfusion and potential harm to
the heart. Following a cardiac catheterization, the patient should be advised not to lift
over 10 lbs or partake in strenuous activity.
7) . Encourage cardiac rehabilitation.
Cardiac rehabilitation teaches the patient about diet modifications, exercise, and
recovery following MI to improve outcomes and prevent further cardiac complications.

4.Nursing Diagnosis: Ineffective Tissue Perfusion

Ineffective tissue perfusion associated with myocardial infarction can be caused by

inadequate or blocked oxygenated blood flow to the tissues and organs.

Related to:

 Formation of plaque
 Narrowed arteries
 Obstructed arteries
 Rupture of unstable plaque
 Vasospasm of coronary arteries
 Ineffective cardiac muscle contraction
 Conditions that compromise the blood supply
 Difficulty of the heart muscle to contract
 Increased exertion in workload
 Inadequate blood supply to the heart
As evidenced by:

 Diminished peripheral pulses

 Increased central venous pressure (CVP)
 Tachycardia
 Dysrhythmias
 Decreased oxygen saturation
 Angina
  Dyspnea
 Change in the level of consciousness
 Restlessness
 Fatigue
 Exertional dyspnea or chest pain during activities
 Cold and clammy skin
 Prolonged capillary refill time
 Pallor
 Edema
 Reports of claudication
 Numbness
 Change in sensation
 Pain in the lower extremities
 Poor wound healing
Expected outcomes:

 Patient will achieve pulses and capillary refill time within normal limits.
 Patient will display warm skin without pallor or cyanosis.
 Patient will present an alert and coherent level of consciousness.
Assessment:

1) Obtain ECG.
An electrocardiogram (ECG) is a crucial test for a suspected heart attack. Upon admission to
the hospital, obtain ECG within 10 minutes to capture the heart’s electrical activity. An ECG
can reveal signs of a present heart attack or one that has already occurred. The patterns on
the ECG can identify the severity of the damage to the heart and the specific affected area.
2) Assess the cardiovascular status.
Myocardial infarction may result from the blockage of one or more coronary arteries for
longer than 20 to 40 minutes. The blockage is often thrombotic and brought on by a plaque
that has ruptured in the coronary arteries. The obstruction causes ischemia resulting in
inadequate cardiac output and ineffective cardiac tissue perfusion.
3) Assess the patient’s color, capillary refill, and pulses.
A cardiac blockage causes symptoms such as numbness, altered sensations, reduced
capillary refill time, poor peripheral pulses, and a change in skin color (pallor, cyanosis, or
mottled skin color) and temperature.

Interventions:

1)Start CPR.
If myocardial infarction is suspected, call emergency help and begin CPR if a pulse is
not detected.
2)Initiate reperfusion treatment.
All patients with prolonged ST-segment elevation and symptoms of ischemia lasting less
than 12 hours should receive reperfusion treatment.
 3)Consider surgical procedures.
Percutaneous coronary intervention (PCI) can be completed within 120 minutes after an
ECG diagnosis.
4) Immediately administer fibrinolytics.
Fibrinolytics should be initiated within 10 minutes following STEMI when urgent PCI is
impossible (>120 minutes). Fibrinolytics bust blood clots and can salvage tissue by
prompt blood flow restoration, improving short- and long-term survival.
5) Administer aspirin.
PO aspirin is often given immediately when MI is suspected. It aids in maintaining blood
flow through a constricted artery while clot-busting medications (thrombolytics or
fibrinolytics) aid in dissolving any blood clots obstructing blood flow.
6) Refer the patient to cardiac rehab.
After discharge, the cardiac rehabilitation program usually lasts for a few weeks or
months. After a heart attack, those participating in cardiac rehab live longer and are less
likely to experience another heart attack.

5. Nursing Diagnosis: Risk for Unstable Blood Pressure

Risk for unstable blood pressure (BP) associated with myocardial infarction can be
caused by blood pressure instability leading to insufficient blood flow and poorly oxygenated
blood to the heart.

Related to:

 Ineffective heart muscle contraction

 Ischemia
 Constricted arteries
 Obstructed arteries
 Rupture of unstable plaque
 Coronary artery spasm
 Underlying cardiac conditions
 Increased workload exertion
As evidenced by:

A risk diagnosis is not evidenced by signs and symptoms as the problem has not yet occurred
and the goal of nursing interventions is aimed at prevention.

Expected outcomes:

 Patient will manifest blood pressure within normal limits.

 Patient will perform activities without blood pressure fluctuations.
 Patient will adhere to their medication regimen to control blood pressure.
Assessment:

1)Monitor the patient’s blood pressure.

The heart muscle is deprived of oxygen and blood flow during myocardial infarction.
Blood pressure may become unstable (increase or decrease) depending on the body’s
compensation.
2)Assess the cardiovascular status.
Cardiac muscle injury is frequently the cause of heart attack complications. Arrhythmias,
cardiogenic shock, heart failure, pericarditis, and cardiac arrest are possible myocardial
infarction complications.
3)Assess for signs and symptoms.
In myocardial infarction, changes in blood pressure can cause headaches, chest pain,
mental status changes, diaphoresis, and dizziness.
4)Determine the patient’s risk factors.
Combining several risk factors (such as uncontrolled blood pressure and other conditions
that can cause vasoconstriction) makes myocardial infarction more likely.
5)Assess the chest pain.
Myocardial infarction-related chest pain is accompanied by sympathetic stimulation,
increasing vasoconstriction, and the ischemic heart’s workload. Hence, it causes unstable
blood pressure.

Interventions:

1) Stabilize blood pressure in myocardial infarction.

Beta-blockers lessen the amount of oxygen the myocardium uses by reducing heart rate,
blood pressure, and myocardial contractility. ACE inhibitors and calcium channel
blockers relax blood vessels to lower blood pressure.
2) Administer vasodilators as prescribed.
Blood pressure goals of less than 140/90 mm Hg can be achieved with antihypertensive
medication. Patients with systolic left ventricular dysfunction, heart failure, hypertension,
or diabetes should take ACE inhibitors and beta-blockers. Patients with left ventricular
ejection fraction (LVEF) lower than 40% should take beta-blockers if there are no other
contraindications.
3) Relieve fluid overload.
Diuretics can be administered to reduce the circulating volume if heart failure or fluid
overload is a potential cause of hypertension.

Provide education.
The majority of the time, elevated blood pressure has no symptoms. The only method to check
blood pressure is to monitor it, which makes high blood pressure a “silent killer” in some cases.