8 Myocardial Infarction (Heart Attack) Nursing Care Plans

Nurses play a critical role in assessing, monitoring, and caring for patients who are experiencing a heart attack. This comprehensive care plan guide focuses on the essential nursing assessment, interventions, nursing care plans and nursing diagnoses for effectively managing patients with myocardial infarction.

What is Myocardial Infarction?

Myocardial infarction (MI) or acute myocardial infarction (AMI) commonly known as heart attack, is the irreversible necrosis of heart muscle secondary to prolonged ischemia. This usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium (Zafari, 2015).

Myocardial infarction is a part of a broader category of a disease known as acute coronary syndrome (ACS), resulting from prolonged myocardial ischemia due to reduced blood flow through one of the coronary arteries. The ACS continuum representing ongoing myocardial ischemia or injury consists of unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).

Cardiovascular diseases, the leading cause of death in the United States and Western Europe usually result from cardiac damage or complications of MI. Mortality is high when treatment is delayed and almost one-half of sudden deaths due to an MI occur before hospitalization, within one hour of the onset of symptoms. The prognosis improves if vigorous treatment begins immediately.

MI may be classified into various types based on pathological, clinical, and prognostic differences, along with different treatment strategies. MI caused by atherothrombotic coronary artery disease and usually precipitated by atherosclerotic plaque disruption is designated as a type 1 MI. The pathophysiological mechanism leading to ischemic myocardial injury in the context of a mismatch between oxygen supply and demand has been classified as type 2 MI. Type 3 MI is suspected when an acute myocardial ischemic event is high, even when cardiac biomarker evidence of MI is lacking. This includes clients who manifest a typical presentation of MI and die before it is possible to obtain blood for cardiac biomarker determination. (Thygesen et al., 2018)

Nursing Care Plans and Management

The primary goals of managing acute myocardial infarction (MI) are to limit myocardial damage, preserve cardiac function, and prevent complications. This is achieved by interventions that restore blood flow in the coronary arteries. To minimize damage, strategies focus on reducing oxygen demand and increasing oxygen supply through medications, oxygen therapy, and rest. Relief of pain and improvement in ECG findings indicate a balanced oxygen demand and supply, as well as potential reperfusion. Confirmation of blood flow through an open vessel in the catheterization laboratory provides evidence of successful reperfusion.

Nursing Problem Priorities

The following are the nursing priorities for patients with myocardial infarction:

1. Managing pain and ischemia.
2. Monitoring for potential complications.
3. Promoting adequate tissue perfusion.
4. Reducing anxiety.

Nursing Assessment

Patients with MI commonly present with acute and continuous chest pain, often accompanied by symptoms like shortness of breath, indigestion, nausea, and anxiety. They may exhibit cool, pale, and moist skin, along with an increased heart and respiratory rate. These signs and symptoms, caused by sympathetic nervous system activation, can be brief or persistent. Distinguishing between MI and unstable angina based on symptoms alone can be challenging, leading to the broader term acute coronary syndrome.

Assess for the following subjective and objective data:

• Reports of chest pain with/without radiation
• Facial grimacing
• Restlessness, changes in the level of consciousness
• Changes in pulse, BP
• Alterations in heart rate and BP with activity
• Development of dysrhythmias
• Changes in skin color/moisture
• Exertional angina
• Generalized weakness

Assess for factors related to the cause of myocardial infarction:

• Tissue ischemia (coronary artery occlusion)
• An imbalance between myocardial oxygen supply and demand
• Presence of ischemic/necrotic myocardial tissues
• Cardiac depressant effects of certain drugs (beta-blockers, antiarrhythmics)

Nursing Diagnosis

Following a thorough assessment, it is essential to formulate a nursing diagnosis that specifically addresses the problems associated with myocardial infarction (heart attack). This diagnosis reflects your clinical judgment regarding the patient’s health conditions and needs.

Nursing Goals

The main goals for patients with acute coronary syndrome (ACS) include pain relief, prevention of myocardial damage, respiratory function maintenance, adequate tissue perfusion, anxiety reduction, adherence to self-care, and early recognition of complications. Goals and expected outcomes may include:

• The client will verbalize relief/control of chest pain within the appropriate time frame for administered medications, display reduced tension, a relaxed manner, and ease of movement, and demonstrate the use of relaxation techniques.
• The client will recognize and verbalize feelings, identify causes and contributing factors, verbalize the reduction of anxiety, demonstrate positive problem-solving skills, and identify and use resources appropriately.
• The client will maintain stable hemodynamics (e.g., normal blood pressure, cardiac output) and report reduced dyspnea and angina, while demonstrating improved activity tolerance.

Nursing Interventions and Actions

Therapeutic interventions and nursing actions for patients with myocardial infarction may include:

• 1. Initiating Pain Relief and Ischemia & Improving Respiratory Function
• 2. Monitor Laboratory and Diagnostic Tests
• 3. Administering Medication and Pharmacologic Support
• 4. Improving Cardiac Output & Monitoring Potential Complications
• 5. Improving Tissue Perfusion & Initiating Cardiac Rehabilitation
• 6. Reducing Anxiety and Fear
• 7. Improving Tolerance to Activity
• 8. Initiating Health Education & Teaching

1. Initiating Pain Relief and Ischemia & Improving Respiratory Function

The classic symptom a client experience during a cardiac event is pain. It is important for the nurse to differentiate the pain of an MI or angina attack from a multitude of other pain syndromes that can mimic a coronary event. Non-cardiac chest pain may be caused by other cardiovascular issues including pericarditis, aortic aneurysm, or dissection. 

Monitor and document characteristics of pain, noting verbal reports, and nonverbal cues (moaning, crying, grimacing, restlessness, diaphoresis, and clutching of the chest).
Variations in the appearance and behavior of clients in pain may present a challenge in assessment. Most clients with an acute MI appear ill, distracted, and focused on pain. Verbal history and deeper investigation of precipitating factors should be postponed until the pain is relieved. Respirations may be increased as a result of pain and associated anxiety; the release of stress-induced catecholamines increases heart rate and BP. The client may present with abdominal discomfort or jaw pain as their anginal equivalent. Women tend to present more commonly with atypical symptoms than men (Zafari, 2015).

Obtain a full description of pain from the client including location, intensity (using a scale of 0–10), duration, characteristics (dull, crushing, described as “like an elephant in my chest”), and radiation. Assist the client to quantify pain by comparing it to other experiences.
Pain is a subjective experience and must be described by the client. This also provides a baseline for comparison to aid in determining the effectiveness of therapy, resolution, and progression of the problem. Clients commonly describe the discomfort as crushing, oppressive, or constricting or as a pressure that may radiate to the left arm, neck, jaw, infrascapular area, or epigastric region. Transient symptoms that last less than 15 minutes and disappear at rest are classified as angina. The discomfort associated with MI typically lasts more than 30 minutes, is not relieved by rest or nitroglycerin, and may or may not be severe.

Review the history of previous angina, anginal equivalent, or MI pain. Discuss family history if pertinent.
A delay in reporting pain hinders pain relief and may require an increased dosage of medication to achieve relief. In addition, severe pain may induce shock by stimulating the sympathetic nervous system, thereby creating further damage and interfering with diagnostics and relief of pain. A positive family history includes any first-degree male relative aged 45 years or younger or any first-degree female relative aged 55 years or younger who experienced MI (Zafari, 2015).

Check vital signs before and after narcotic medication.
Morphine sulfate is the analgesic of choice for anginal pain relief in STEMI and for unstable angina and NSTEMI barring contraindications (Zafari, 2015). Hypotension and respiratory depression can occur as a result of narcotic administration. These problems may increase myocardial damage in presence of ventricular insufficiency.

Monitor the client’s vital signs closely.
Hypertension may precipitate myocardial infarction, or it may reflect elevated catecholamine levels due to anxiety, pain, or exogenous sympathomimetics. Hypotension may indicate ventricular dysfunction due to ischemia. Impaired left ventricular diastolic function leads to pulmonary vascular congestion with shortness of breath and tachypnea and, eventually, pulmonary edema with orthopnea. Shortness of breath may be the client’s anginal equivalent or a symptom of heart failure (Zafari, 2015).

Monitor respirations and note the work of breathing.
Cardiac pump failure and/or ischemic pain may precipitate respiratory distress; however, sudden or continued dyspnea may indicate thromboembolic pulmonary complications. Impaired left ventricular diastolic function leads to pulmonary vascular congestion with shortness of breath and tachypnea and, eventually, pulmonary edema with orthopnea (Zafari, 2015). Regular and careful assessment of respiratory functions detects early signs of pulmonary complications.

Administer supplemental oxygen by means of a nasal cannula or face mask, as indicated.
Oxygen is administered via nasal prongs at a flow rate of 2 to 5 L/minute to improve myocardial and tissue oxygenation. It can alleviate discomfort associated with tissue ischemia by increasing the available oxygen for myocardial uptake. However, the use of oxygen therapy should be limited to hypoxic patients, as it may increase coronary vascular resistance and potentially lead to higher mortality rates in non-hypoxic patients (Shah et al., 2019). Alongside medication therapy, oxygen supplementation is recommended to relieve symptoms and reduce pain related to inadequate myocardial oxygen. The administration route, typically using nasal cannula, and flow rate should be documented, with a range of 2 to 4 L/min often sufficient to maintain oxygen saturation levels above 95%, unless there is underlying chronic pulmonary disease. It’s important to note that supplemental oxygen may have adverse effects on non-hypoxic patients with ST-elevation myocardial infarction (STEMI), increasing the risk of myocardial injury, recurrent myocardial infarction, and major cardiac arrhythmias (Zafari, 2015).

Instruct the client to report pain immediately.
Atypical presentations are common and frequently lead to misdiagnosis. Moreover, any client may present with atypical symptoms, which are considered the anginal equivalent for that client. Atypical chest pain is common, especially in older clients and clients diagnosed with diabetes. Morbidity and mortality from MI are significantly reduced if clients and bystanders recognize symptoms early, activate the emergency medical service system, and thereby shorten the time to definitive treatment (Zafari, 2015).

Provide a quiet environment, and calm activities, and place the client in a position of comfort. Approach the client calmly and confidently.
This decreases external stimuli, which may aggravate anxiety and cardiac strain, limiting coping abilities and adjustment to the current situation. Physical rest in bed with the backrest elevated or in a cardiac chair helps to decrease chest discomfort and dyspnea.

Instruct the client to do relaxation techniques such as deep and slow breathing, distraction behaviors, visualization, and guided imagery. Assist as needed.
This is helpful in decreasing perception and response to pain, provides a sense of having some control over the situation, and increases a positive attitude. Alternative therapies such as pet therapy can also help certain clients relax and reduce anxiety, therefore reducing chest pain.

Administer medications for pain relief as indicated. 
See pharmacological interventions

2. Monitor Laboratory and Diagnostic Tests

Cardiac enzymes and biomarkers, including troponin, creatine kinase (CK), and myoglobin, are essential diagnostic tools for identifying acute myocardial infarction (MI). These tests detect the release of cellular components into the bloodstream when heart muscle cells are damaged. Analyzing the time courses of these biomarkers allows for a prompt and accurate diagnosis.

Monitor laboratory data such as cardiac enzymes, ABGs, and electrolytes.
Enzymes monitor the resolution or extension of infarction. Remeasuring cardiac enzyme levels at regular intervals for the first 24 hours is a reasonable approach to improving the sensitivity of detection of myocardial necrosis, and the degree of positivity can be important for prognostication. The presence of hypoxemia indicates the need for supplemental oxygen. Hypoxemia may result from pulmonary congestion, atelectasis, or ventilatory impairment secondary to complications of MI or excessive sedation or analgesia (Zafari, 2015). Electrolyte imbalances such as hypokalemia or hyperkalemia adversely affect cardiac rhythm and contractility.

Troponin
Troponin, a protein that regulates myocardial contraction, is a critical biomarker for detecting myocardial injury. Troponin I and troponin T, which are specific to cardiac muscle, are reliable indicators of myocardial damage. The level of troponin in the blood increases within a few hours of an acute myocardial infarction (MI) and remains elevated for up to 2 weeks. However, it’s important to note that troponin levels can also rise in conditions such as inflammation, sepsis, heart failure, and respiratory failure.

Creatine Kinase
CK (creatine kinase) has three isoenzymes: CK-MM (skeletal muscle), CK-MB (heart muscle), and CK-BB (brain tissue). CK-MB is specific to the heart and rises when there is cardiac damage. Increased levels of CK-MB indicate an acute myocardial infarction (MI), with levels starting to rise within hours and peaking within 24 hours of the infarct.

Myoglobin
Myoglobin, present in cardiac and skeletal muscle, plays a role in oxygen transport. Its levels begin to rise within 1 to 3 hours and peak within 12 hours after symptom onset. While an increase in myoglobin is not highly specific to indicate an acute cardiac event, negative results can help rule out an acute myocardial infarction (MI).

3. Administering Medication and Pharmacologic Support

The patient with suspected MI should promptly receive supplemental oxygen, aspirin, nitroglycerin, and morphine to alleviate pain and anxiety. Careful monitoring for adverse effects, such as hypotension or respiratory depression, is essential during morphine administration. Beta-blockers may be utilized to manage dysrhythmias, and unfractionated heparin or LMWH can be prescribed, along with platelet-inhibiting agents, to prevent additional clot formation.

Antianginals such as nitroglycerin, isosorbide dinitrate, and mononitrate
Nitrates are useful for pain control by coronary vasodilating effects, which increase coronary blood flow and myocardial perfusion. Peripheral vasodilation effects reduce the volume of blood returning to the heart (preload), thereby decreasing myocardial workload and oxygen demand. Systolic BP <90 mm Hg, HR <60 or >100, and right ventricular infarction are contraindications to nitrate use (Zafari, 2015).

Beta-blockers such as atenolol, pindolol, propranolol, nadolol, and metoprolol
Beta-blockers are important second-line agents for pain control through the effect of blocking sympathetic stimulation, thereby reducing heart rate, systolic BP, and myocardial oxygen demand. These may be given alone or with nitrates. Metoprolol is the standard of care and is a selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions. Specific contraindications to the usage of this therapy include signs of heart failure, low output state, increased risk for cardiogenic shock, pulse rate interval greater than 0.24 seconds, and active asthma (Zafari, 2015).

Analgesics such as morphine and meperidine
Although intravenous (IV) morphine is the usual drug of choice, other injectable narcotics may be used in acute-phase and/or recurrent chest pain unrelieved by nitroglycerin to reduce severe pain, provide sedation, and decrease myocardial workload. IM injections should be avoided, if possible because they can alter the CPK diagnostic indicator and are not well absorbed in under-perfused tissue.

Antiplatelet agents: aspirin, abciximab (ReoPro), clopidogrel (Plavix).
These agents reduce mortality in MI clients and are taken daily. Aspirin also reduces coronary occlusion after percutaneous transluminal coronary angioplasty (PTCA). ReoPro is an IV drug used as an adjunct to PTCA for the prevention of acute ischemic complications. Antiplatelet agents have a strong mortality benefit. There is an increased risk of bleeding in cases of emergency coronary artery bypass graft (CABG) (Zafari, 2015).

Anticoagulants: heparin or enoxaparin (Lovenox).
Low-dose heparin is given during PTCA and may be given prophylactically in high-risk clients (e.g., atrial fibrillation, obesity, a ventricular aneurysm, or history of thrombophlebitis) to reduce the risk of thrombophlebitis or mural thrombus formation. LMWH is commonly used because of convenient dosing, reliable therapeutic levels, and decreased incidence of HIT, especially if anticipated use is greater than 2 to 3 days (Zafari, 2015).

Thrombolytic therapy such as streptokinase, urokinase, and reteplase.
Thrombolytic therapy has been shown to improve survival rates in ST-segment elevation MI but is not indicated in the treatment for non-ST-segment elevation MI. Door-to-door drug time should be no more than 30 minutes. The main objective of thrombolysis is to restore circulation through a previously occluded vessel by the rapid and complete removal of a pathologic intraluminal thrombus or embolus that has not been dissolved by the endogenous fibrinolytic system.

Administer antidysrhythmic drugs as indicated.
Dysrhythmias are usually treated symptomatically, except for PVCs, which are often treated prophylactically. Early inclusion of ACE inhibitor therapy (especially in presence of large anterior MI, ventricular aneurysm, or HF) enhances ventricular output, increases survival, and may slow the progression of HF. Administer ACE inhibitors as soon as possible as long as the client has no contraindications and remains in stable condition. ACE inhibitors have the greatest benefit in clients with ventricular dysfunction (Zafari, 2015).

Administer beta-blockers as indicated.
In the setting of myocardial ischemia, beta-blockers have antiarrhythmic properties and reduce myocardial oxygen demand secondary to elevations in heart rate and inotropy. Beta-blockers also reduce the inotropic state of the left ventricle, decrease diastolic dysfunction, and increase LV compliance (Zafari, 2015).

Administer diuretics:  furosemide (Lasix), spironolactone with hydrochlorothiazide (Aldactazide), hydralazine (Apresoline).
Diuretics may be necessary to correct fluid overload. Drug choice is usually dependent on the acute or chronic nature of symptoms. Diuretics are used to decrease plasma volume and peripheral edema. The reduction in extracellular fluid and plasma volume associated with diuresis may initially decrease cardiac output, and, consequently, blood pressure. With continuing diuretic therapy, the plasma volume and peripheral vascular resistance usually return to pretreatment values (Ren, 2019).

Administer vasodilators such as dopamine and fenoldopam.
Given in small doses, dopamine causes selective dilation of the renal vasculature, therefore enhancing renal perfusion. Fenoldopam maintains or increases renal perfusion while it lowers BP, however, this may be particularly beneficial only to clients with renal insufficiency who present in hypertensive crisis.

Administer anti-anxiety and hypnotics as indicated:  alprazolam (Xanax), diazepam (Valium), lorazepam (Ativan), and flurazepam (Dalmane).
This promotes relaxation and rest and reduces feelings of anxiety, which may act as barriers to health restoration. However, in a study, only 15 subjects (15%) had documented that the efficacy of this therapy had been evaluated, although evaluation of the efficacy of an administered drug is standard nursing care. The effectiveness of anxiolytic therapy must always be evaluated because pain medication such as morphine may create serious consequences when taken with anxiolytics at the same time (Frazier et al., 2002).

4. Improving Cardiac Output & Monitoring Potential Complications

Myocardial infarction occurs when there is a loss of blood supply to part of the heart muscle, causing damage or death to the heart cells. This damage reduces the heart’s ability to pump effectively, leading to decreased cardiac output. The decrease in cardiac output can also cause further complications such as heart failure, arrhythmia, and even shock. MI at the left coronary artery system is most likely to produce extensive injury because it covers more territory than the right system; with impairment of function, pulmonary congestion, and low output (Zafari, 2015).

Auscultate BP. Compare both arms and obtain lying, sitting, and standing pressures when able.
Hypotension may occur related to ventricular dysfunction, hypoperfusion of the myocardium, and vagal stimulation. However, hypertension is also a common phenomenon, possibly related to pain, anxiety, catecholamine release, and/or preexisting vascular problems. Orthostatic (postural) hypotension may be associated with complications of infarction (heart failure) (Zafari, 2015)

Evaluate the quality of pulses on both pulse points.
Decreased cardiac output results in diminished weak or thready pulses. Irregularities suggest dysrhythmias, which may require further evaluation and monitoring. A decrease in the cardiac output causes a reduction in the strength and amplitude of peripheral pulses, such as the radial pulse in the wrist or the femoral pulse in the groin. It can also result in decreased pulse rate and variability, reflecting a slowing or instability in the heart rate.

Auscultate heart sounds. Note the development of S3, S4, and the presence of murmurs or friction rubs.
S3 is usually associated with HF, but it may also be noted with mitral insufficiency (regurgitation) and left ventricular overload that can accompany severe infarction. S4 may be associated with myocardial ischemia, ventricular stiffening, and pulmonary or systemic hypertension. The presence of murmurs or friction rubs Indicates disturbances of normal blood flow within the heart: incompetent valve, septal defect, or vibration of papillary muscle and/or chordae tendineae (a complication of MI). The presence of rub with infarction is also associated with inflammation, pericardial effusion, and pericarditis.

Auscultate breath sounds.
Crackles reflecting pulmonary congestion may develop because of depressed myocardial function. Rales or wheezes may be auscultated; these occur secondary to pulmonary venous hypertension, which is associated with extensive acute ventricular myocardial infarction. Unilateral or bilateral pleural effusions may produce egophony at the lung bases (Zafari, 2015).

Monitor heart rate and rhythm. Document dysrhythmias via telemetry.
Heart rate and rhythm respond to medication, activity, and developing complications. Dysrhythmias (especially premature ventricular contractions or progressive heart blocks) can compromise cardiac function or increase ischemic damage. Acute or chronic atrial flutter may be seen with coronary artery or valvular involvement and may or may not be pathological.

Note the response to the activity and promote rest appropriately.
Overexertion increases oxygen consumption and demand and can compromise myocardial function. The heart muscle is damaged in MI, therefore it needs time to heal. Additionally, stress from overexertion can also have a negative impact on the heart. Resting helps improve blood flow to the heart muscles and promotes the healing process. 

Monitor vital signs.
Although not all dysrhythmias are life-threatening, immediate treatment may be required to terminate dysrhythmia in the presence of alterations in cardiac output and tissue perfusion. The client’s heart rate is often increased secondary to sympathoadrenal discharge. With right ventricular myocardial infarction or severe left ventricular dysfunction, hypotension is seen. The respiratory rate may be increased in response to pulmonary congestion (Zafari, 2015).

Review serial ECGs.
ECG provides information regarding the progression or resolution of infarction, the status of ventricular function, electrolyte balance, and the effects of drug therapies. The ECG is the most important tool in the initial evaluation and triage of clients for whom an ACS is suspected. It is confirmatory of the diagnosis in approximately 80% of cases. Obtain daily serial ECGs for the first 2 to 3 days and additionally as needed (Zafari, 2015).

Review chest x-ray and echocardiography.
This may reflect pulmonary edema related to ventricular dysfunction. On chest radiographs, pleural effusion is evidenced by blunted costophrenic angles; on echocardiography, they are evidenced by echo lucent zones adjacent to the heart (Zafari, 2015).

Measure cardiac output and other functional parameters as appropriate.
Cardiac index, preload, afterload, contractility, and cardiac work can be measured noninvasively with the thoracic electrical bioimpedance (TEB) technique. An important parameter obtained by the TEB technique is thoracic fluid conductivity (TFC), which represents the whole fluid component in the thorax and is related to the blood circulation state and myocardial contractility (Meng et al., 2021). This is useful in evaluating responses to therapeutic interventions and identifying the need for more aggressive and emergency care.

Provide small and easily digested meals. Limit caffeine intake and caffeine-containing products.
Large meals may increase myocardial workload and cause vagal stimulation, resulting in bradycardia or ectopic beats. Caffeine is a direct cardiac stimulant that can increase heart rate. Note: New guidelines suggest no need to restrict caffeine in regular coffee drinkers. However, studies have reported a rapid increase in the risk of stroke and MI right after coffee ingestion was observed. The main components of caffeine can increase the risk of hypertension, serum concentrations of cholesterol and homocysteine, and the incidence of type 2 diabetes mellitus. Therefore, caution still should be applied with regard to the amount of coffee consumed daily (Mo et al., 2018).

Provide a calm and quiet environment. Review reasons for the limitation of activities during the acute phase.
This reduces stimulation and release of stress-related catecholamines, which can cause or aggravate dysrhythmia, and vasoconstriction, increasing myocardial workload. Limiting the client to bed or chair rest during the initial phase of treatment is particularly helpful in reducing myocardial oxygen consumption. This limitation should remain until the client is pain-free and hemodynamically stable.

Encourage the use of stress management behaviors such as relaxation techniques, guided imagery, and slow, deep breathing.
This promotes client participation in exerting some sense of control in a stressful situation. Gentle physical activity, such as walking or yoga, can help reduce stress and improve cardiovascular circulation. Techniques such as deep breathing, progressive muscle relaxation, and meditation, can help calm the mind and reduce stress levels.

Have emergency equipment and/or medications available.
Sudden coronary occlusion, lethal dysrhythmias, an extension of infarct, and unrelenting pain are situations that may precipitate cardiac arrest, requiring immediate life-saving therapies and/or transfer to CCU. All clients with suspected MI should be given chewable aspirin unless they have a documented allergy to aspirin. When severe pain is present, the client may be given IV morphine. Should toxicity occur, naloxone should be given to reverse it (Zafari, 2015).

Maintain IV or Hep-Lock access as indicated.
A patent intravenous line is important for the administration of emergency drugs in presence of persistent lethal dysrhythmias or chest pain. Refractory or severe pain should be treated symptomatically with IV morphine, meperidine, or pentazocine. Relative hypotension may be treated by giving fluids. Atropine, in doses similar to those given in the prehospital phase, may increase blood pressure (Zafari, 2015).

Assist with insertion and maintenance of pacemaker, when used.
Pacing may be a temporary support measure during the acute phase or may be needed permanently if infarction severely damages the conduction system, impairing systolic function. Evaluation is based on echocardiography or radionuclide ventriculography. However, implantable cardioverter defibrillators (ICD) may be unnecessary in select post-MI clients with severe LV dysfunction and negative electrophysiology study (EPS). Clients with severe LV dysfunction and negative EPS show no inducible ventricular tachycardia and have low long-term rates of arrhythmia or death without receiving an ICD (Zafari, 2015).

5. Improving Tissue Perfusion & Initiating Cardiac Rehabilitation

Decreased systolic ventricular performance may lead to impaired perfusion of vital organs and reflex-mediated compensatory responses, such as restlessness, impaired mentation, pallor, peripheral vasoconstriction and sweating, tachycardia, and prerenal failure. In clients with extensive myocardial injury, coronary blood flow diminishes as cardiac output declines and heart rate accelerates. Because coronary artery disease is usually generalized or diffuse, ischemia occurs at a distance from the infarcted segment and may result in a vicious cycle in which stuttering and expanding myocardial infarction ultimately leads to profound LV failure, hypotension, and cardiogenic shock (Zafari, 2015).

Investigate sudden or continued alterations in mentation (changes in LOC, mentation, stupor).
Cerebral perfusion is directly related to cardiac output and is influenced by electrolyte and/or acid-base variations, hypoxia, and systemic emboli. Ineffective peripheral tissue perfusion can cause a lack of oxygen and nutrients in the brain, which can affect cognitive function and lead to changes in mental status.

Inspect for pallor, cyanosis, mottling, and cool and clammy skin. Note the strength of peripheral pulses.
Systemic vasoconstriction resulting from diminished cardiac output may be evidenced by decreased skin perfusion and diminished pulses. Peripheral cyanosis, edema, pallor, diminished pulse volume, delayed rise, and delayed capillary refill may indicate vasoconstriction, diminished cardiac output, and right ventricular dysfunction or failure (Zafari, 2015). 

Monitor intake, and note changes in urine output. Record urine specific gravity as indicated.
Decreased intake or persistent nausea may result in reduced circulating volume, which negatively affects perfusion and organ function. Specific gravity measurements reflect hydration status and renal function. The kidneys receive a significant portion of their blood supply from the renal arteries. When peripheral tissue perfusion is ineffective, it can reduce the blood flow to the kidneys, impairing their ability to filter waste products and produce urine.

Assess GI function, noting anorexia, decreased or absent bowel sounds, nausea, and vomiting, abdominal distension, and constipation.
Reduced blood flow to mesentery can produce GI dysfunction, e.g., loss of peristalsis. Problems may be aggravated by the use of analgesics, decreased activity, and dietary changes. Clients frequently develop tricuspid incompetence; hepatojugular reflux may be elicited even when hepatomegaly is not marked (Zafari, 2015).

Assess for Homans’ sign (pain in calf on dorsiflexion), erythema, and edema.
Indicators of deep vein thrombosis (DVT), although DVT can be present without a positive Homans’ sign. Dependent edema may be graded 0 to 4 by assessing the depth of persistent pitting after thumb pressure is applied to the client’s inner shin for more than 10 seconds or by evaluating the lower back if the client has had their legs elevated (Zafari, 2015).

Monitor laboratory data: CBC, ABGs, BUN, creatinine, electrolytes, and coagulation studies (PT, aPTT, clotting times).
These are indicators of organ perfusion and function. Abnormalities in coagulation may occur as a result of therapeutic measures. Obtain a CBC if MI is suspected in order to rule out anemia as a cause of decreased oxygen supply and prior to giving thrombolytic agents. The platelet count may become dangerously low after the use of heparin because of heparin-induced thrombocytopenia (HIT) (Zafari, 2015).

Elevate the client’s head of the bed as appropriate.
Elevation of the head of the bed is beneficial because it improves tidal volume due to reduced pressure from abdominal contents on the diaphragm and better lung expansion and gas exchange. This position also improves the drainage of the upper lung lobes and increases venous return to the heart, resulting in a decrease in the workload of the heart (Zafari, 2015).

Encourage active or passive leg exercises and avoidance of isometric exercises.
This enhances venous return, reduces venous stasis, and decreases the risk of thrombophlebitis; however, isometric exercises can adversely affect cardiac output by increasing myocardial work and oxygen consumption. Flex, extend, or rotate the feet periodically Assist the client with ambulation as tolerated gradually to promote organ function and enhance general well-being.

Instruct the client in the application or periodic removal of the anti-embolic hose, elastic support hose, or graduated compression stockings, when used. Apply and regulate intermittent pneumatic compression as indicated
This limits venous stasis improves venous return and reduces the risk of thrombophlebitis in the client who is limited in activity. Sequential compression devices may be used to improve blood flow velocity and empty vessels by providing artificial muscle-pumping action.

Apply warm, moist compresses or heat cradle to the affected extremity if indicated.
This may be prescribed to promote vasodilation and venous return for resolution of local edema and to enhance comfort. However, caution must be given in applying warm compresses because this may be contraindicated in arterial insufficiency, in which heat can increase cellular oxygen consumption and nutritional needs, aggravating the imbalance between supply and demand.

Assist with reperfusion therapy.
Percutaneous transluminal coronary intervention (PTCI) is a recommended method of reperfusion when it can be performed in a timely manner. PTCI is the placement of a small mesh tube called a stent into an infarcted or narrowed coronary artery. The procedure consists of cardiac catheterization and the insertion of a catheter with a balloon tip that is inflated to open the artery.

Prepare for PTCA (balloon angioplasty), with or without intracoronary stents.
Intracoronary stents may be placed at the time of PTCA to provide structural support within the coronary artery and improve the odds of long-term patency. Several randomized trials have demonstrated that rapidly available primary PTCA, performed by skilled operators, for acute MI is associated with long-term outcomes similar to those achieved with IV thrombolysis (Zafari, 2015).

Transfer to critical care or a specialty center.
More intensive monitoring and aggressive interventions are necessary to promote optimum outcomes. A study showed that the transfer of clients to an invasive-treatment center for primary PCI is superior to on-site fibrinolysis provided that the transfer can be accomplished within two hours. The transfer should be considered for those clients who are likely to benefit from PCI or cardiac surgery but who are in an institution where access to such interventions is not immediate (Zafari, 2015).

Auscultate breath sounds for the presence of crackles.
This may indicate pulmonary edema secondary to cardiac decompensation. Poor prognosis is associated with evidence of congestive heart failure or frank pulmonary edema by Killip classification of >II or >III (Zafari, 2015). 

Perform a risk stratification using the Killip classification.
The Killip classification is widely used in clients presenting with acute MI for the purpose of risk stratification. Killip class I includes individuals with no clinical signs of heart failure; Killip class II includes individuals with rales or crackles in the lungs, an S3 gallop, and elevated jugular venous pressure; Killip class III describes individuals with frank acute pulmonary edema; and Killip class IV describes individuals in cardiogenic shock or hypotension, and evidence of low cardiac output (Zafari, 2015).

Note jugular vein distention (JVD) and development of dependent edema.
This suggests developing congestive heart failure or fluid volume excess. In clients with acute inferior-wall myocardial infarction with right ventricular involvement, distention of neck veins is commonly described as a sign of failure of the right ventricle (Zafari, 2015).

Measure I&O, noting a decrease in output, and concentrated appearance. Calculate fluid balance.
Decreased cardiac output results in impaired kidney perfusion, sodium and water retention, and reduced urine output. Heart failure with reduced ejection fraction is a risk factor for kidney disease. When the heart is unable to pump forcefully, the amount of blood it ejects with each contraction decreases. This reduces the amount of blood that reaches the kidneys, causing urine and waste output to drop (Cleveland Clinic, 2020).

Weigh daily.
Sudden changes in weight reflect alterations in fluid balance. Edema that occurs in a client with MI can increase the body weight, which can result in the client being unable to move around freely and become active. This can further increase the workload of the heart and potentially worsen cardiovascular function.

Monitor potassium as indicated.
Hypokalemia can limit the effectiveness of therapy and can occur with the use of potassium-depleting diuretics. Electrolyte abnormalities are commonly associated with all diuretic agents, and their mechanisms of such effect are well-established. Hypokalemia, for example, is caused by all diuretics except potassium-sparing diuretics, which cause hyperkalemia (Arumugham & Shahin, 2022).

Monitor urine-specific gravity.
This measures the kidney’s ability to concentrate urine. In intrarenal failure, specific gravity is usually equal to or less than 1.010, indicating loss of ability to concentrate the urine.

Maintain total fluid intake at 2000 mL/24 hours within cardiovascular tolerance.
This meets normal adult body fluid requirements but may require alteration or restriction in presence of cardiac decompensation. A study showed that frequently drinking small volumes exerted benefits for CHF rats, which may be partially mediated through the water diuresis mechanism. Cardiologists commonly use ice chips to relieve thirst in clients diagnosed with CHF (Zheng et al., 2017).

Encourage moderate consumption of sodium in the diet and beverages.
A study showed that those who use salt more liberally while preparing meals are less likely to have a history of MI. Overall, the average amount of salt consumed per day by the general public in the US would be considered moderate, according to most studies. An emerging number of studies have found an association between increased mortality and low sodium intake. Moderate salt intake seems to have the best outcomes in terms of mortality and morbidity compared to high or low salt intakes (Mohan, 2021).

Refer to a cardiac rehabilitation program.
This provides continued support and/or additional supervision and participation in the recovery and wellness process. Cardiac rehabilitation is a long-term program of medical evaluation, exercise, risk factor modification, education, and counseling designed to limit the physical and psychological effects of cardiac illness and improve the client’s quality of life.

6. Reducing Anxiety and Fear

Alleviating anxiety and fear is an important nursing function to reduce the sympathetic stress response. Decreased sympathetic stimulation decreases the workload of the heart, which may relieve pain and other signs and symptoms of ischemia. It is critical to optimize anxiety management in order to preserve myocardial muscle and minimize the risk of further deterioration.

Identify and acknowledge the client’s perception of the threat and situation. Encourage expressions of, and do not deny feelings of, anger, grief, sadness, and fear.
Coping with the pain and emotional trauma of an MI is difficult. The client may fear death and/or be anxious about the immediate environment. Ongoing anxiety (related to concerns about the impact of a heart attack on future lifestyle, matters left unattended or unresolved, and effects of illness on family) may be present in varying degrees for some time and may be manifested by symptoms of depression.

Note the presence of hostility, withdrawal, and/or denial (inappropriate affect or refusal to comply with medical regimen).
Research into survival rates between type A and type B individuals and the impact of denial has been ambiguous; however, studies show some correlation between the degree or expression of anger or hostility and an increased risk for MI. Some exploratory studies provided preliminary evidence that denial contributes to delayed adherence to effective cardiac treatment by disavowing the diagnosis and minimizing the perceived symptom burden and symptom severity (Fang et al., 2016).

Observe verbal and nonverbal signs of anxiety (restlessness, changes in vital signs), and stay with the client. Intervene if the client displays destructive behavior.
The client may not express concern directly, but words and actions may convey a sense of agitation, aggression, and hostility. Intervention can help the client regain control of their own behavior.

Assess the client’s and caregiver’s level of anxiety and coping mechanisms.
These data provide information about psychological well-being. Causes of anxiety are variable and individual and may include acute illness, hospitalization, pain, disruption of activities of daily living at home and at work, changes in role and self-image due to illness, and financial concerns. Because anxious family members can transmit anxiety to the client, the nurse must also identify strategies to reduce the family’s fear and anxiety.

Maintain a confident manner but avoid giving false reassurances.
The client and caregiver can be affected by the anxiety/uneasiness displayed by health team members. Honest explanations can alleviate anxiety. Providing information to the client and family in an honest and supportive manner encourages the client to be a partner in care and greatly assists in creating a positive relationship.

Accept but do not reinforce the use of denial. Avoid confrontations.
Denial can be beneficial in decreasing anxiety but can postpone dealing with the reality of the current situation. Conflict can promote anger and increase the use of denial, reducing cooperation and possibly impeding recovery. An atmosphere of acceptance helps the client know that their concerns and fears are realistic and normal.

Orient the client and caregiver to routine procedures and expected activities. Promote participation when possible.
Predictability and information can decrease anxiety for the client. Decreasing anxiety may also increase the client’s ability to process new information regarding their diagnoses, and to better understand instructions for tests or procedures that will be done.

Answer all questions factually. Provide consistent information; repeat as indicated.
Accurate information about the situation reduces fear, strengthens the nurse-client relationship, and assists the client and caregiver to deal realistically with the situation. Attention span may be short, and repetition of information helps with retention.

Encourage the client and caregiver to communicate with one another, share questions and concerns, and provide privacy.
Sharing information elicits support and comfort and can relieve the tension of unexpressed worries. Privacy provides an opportunity for the client and their partner to share their feelings and fear, offer support and encouragement to one another, relieve anxiety, and establish effective coping methods.

Provide rest periods and/or uninterrupted sleep time, and quiet surroundings, with the client controlling type and amount of external stimuli.
This conserves energy and enhances coping abilities. Anxiety can also be decreased by offering the client opportunities for control in the acute setting. Examples include the timing of simple activities such as visitor presence, bathing, and eating.

Promote the use of relaxation and stress management techniques.
A number of interventions may be done at the bedside to promote relaxation, including specific relaxation and imagery techniques, meditation, music therapy, and the use of relaxation tapes. Stress management techniques such as breathing exercises and massage can help reduce tension and anxiety, provide a sense of control, and enhance coping skills.

Encourage independence, self-care, and decision-making within the accepted treatment plan.
Increased independence from staff promotes self-confidence and reduces feelings of abandonment that can accompany transfer from the coronary unit or discharge from the hospital. The most effective way to increase the probability the client will implement a self-care regimen after discharge is to identify the priorities as perceived by the client, provide adequate education about heart-healthy living, and facilitate the client’s involvement in a cardiac rehabilitation program. Client’s participation in developing plans to meet their specific needs further enhances the potential for an effective treatment plan.

Encourage discussion about post-discharge expectations.
This helps the client and/or caregiver identify realistic goals, thereby reducing the risk of discouragement in the face of the reality of the limitations of the condition and/or pace of recovery.

Administer anti-anxiety and hypnotics as indicated.
See pharmacological interventions.

Administer timely and effective pain relief.
Relief of pain is most effective in reducing client anxiety. In the event that pain is not relieved with nitroglycerin, or fibrinolytic in the initial treatment of ischemia, pain relievers such as morphine sulfate are usually effective.

Provide referrals for spiritual counseling or social services.
If the client finds support in religion, spiritual counseling may assist in reducing anxiety and fear. Social services can also assist with posthospital care and financial concerns, somehow relieving the sense of anxiety about hospital bills if the financial situation is tight.

7. Improving Tolerance to Activity

Acute coronary syndrome (ACS) occurs due to inadequate oxygen flow to the heart muscle due to occlusion of the coronary arteries. The decrease in oxygen supply will have an impact on daily activities from light to heavy activities. Additionally, it also causes ventricular contraction failure and continues to decrease cardiac output which is characterized by hemodynamic instability (Andriani et al., 2022).

Assess and document heart rate and rhythm and changes in BP before, during, and after activity. Correlate with reports of chest pain or shortness of breath.
Trends determine the client’s response to activity and may indicate myocardial oxygen deprivation that may require a decrease in activity level and/or return to bedrest, changes in medication regimen, or use of supplemental oxygen. Older adult clients and those diagnosed with diabetes may have particularly subtle presentations and may complain of weakness, fatigue, or syncope (Zafari, 2015).

Review signs and symptoms reflecting intolerance of present activity level or requiring notification of a nurse or healthcare provider.
Palpitations, pulse irregularities, development of chest pain, or dyspnea may indicate a need for changes in an exercise regimen or medications. The client may also appear weak and have disturbances in carrying out activities from mild to severe levels (Andriani et al., 2022).

Encourage rest initially. Thereafter, limit activity on the basis of pain and/or adverse cardiac response. Provide non-stress diversional activities.
This reduces myocardial workload and oxygen consumption, reducing the risk of complications. Confine the client to bed rest to minimize oxygen consumption until reperfusion and initial therapy are complete. This usually lasts about 24 to 48 hours; after that, the client’s activity may be accelerated slowly as tolerated (Zafari, 2015).

Instruct the client to avoid increasing abdominal pressure (straining during defecation).
Activities that require holding the breath and bearing down (Valsalva maneuver) can result in bradycardia (temporarily reduced cardiac output) and rebound tachycardia with elevated BP. Due to cardiovascular effects produced during the Valsalva maneuver, it may be contraindicated in certain medical conditions such as myocardial infarction and could be a trigger of sudden cardiac death (O Fisher-Hubbard et al., 2016).

Provide a quiet environment and limit visitors. Encourage stress management and diversional activities as appropriate.
This reduces stress and excess stimulation, therefore promoting rest. Stress management techniques can help reduce tension and anxiety, providing the client with a sense of control and enhancing their coping skills.

Explain the pattern of graded increase of activity level: getting up to commode or sitting in a chair, progressive ambulation, and resting after meals.
The progressive activity provides a controlled demand on the heart, increasing strength, and preventing overexertion. The bedside commode generally is allowed; studies have shown this to be less stressful than using a bedpan. If the client’s condition is stable, sitting in a chair at the bedside is permitted after 12 hours. Activities are increased gradually as tolerated.

Promote tolerable, light physical exercise as indicated.
Physical exercises have an impact on changes in cardiac output and redistribution of blood supply from inactive organs to active organs. Physical exercise provides the client the ability to inspire longer and it is also able to remove more metabolic waste through expiration. During physical activity, muscles need adequate oxygen as fuel so that energy distribution is smooth and stable (Andriani et al., 2022).

Assist in procedures for inserting ventricular assist devices.
The use of ventricular assist devices (VAD) to aid the failing heart is becoming more common with advances in technology. These devices temporarily take partial or complete control of cardiac function, depending on the type of device used. VADs may be used as a 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.

8. Initiating Health Education & Teaching

To enhance patient adherence to a self-care regimen post-discharge, it is crucial to identify their priorities, provide comprehensive education on heart-healthy living, and support their engagement in a cardiac rehabilitation program. Involving the patient in the development of an individualized program promotes the effectiveness of the treatment plan.

Assess the client or family member’s level of knowledge and ability and desire to learn.
This is necessary for the creation of individual instruction plans. The client requires intensive education, support from family members, and frequent direction from left-ventricular assistive device (LVAD) nurses or coordinators to self-management of the LVAD home care regimen (Casida et al., 2016).

Be alert to signs of avoidance (changing the subject away from information being presented or extremes of behavior).
This reinforces the expectation that this will be a “learning experience.” Verbalization identifies misunderstandings and allows for clarification. Clients and caregivers are generally prepared for the self-management of LVAD home care regimen before discharge during the first implant hospitalization. However, during the first few weeks to several months after hospital discharge, clients are completely or highly dependent on their caregivers in regard to implementing and adhering to the LVAD home care regimen (Casida et al., 2016).

Encourage the client to enroll in smoking cessation classes.
This provides the opportunity for the client to retain information and assume control and participate in the rehabilitation program. Following MI, educate all clients regarding the critical role of smoking in the development of coronary artery disease. Smoking cessation classes should be offered to help clients avoid smoking after their MI (Zafari, 2015).

Promote a moderate consumption of alcoholic beverages.
Mild alcohol consumption has been associated with a decreased risk of stroke and myocardial infarction. Cautiously consider recommending and discussing alcohol use on a case-by-case basis (Zafari, 2015).

Warn against the isometric activity, Valsalva maneuver, and activities requiring arms positioned above the head.
These behaviors and chemicals have direct adverse effects on cardiovascular function and may impede recovery, and increase complications. When compared with a single bout of aerobic exercise, one session of isometric exercise apparently does not have vascular and hemodynamic benefits in clients undergoing primary PCI after MI (Kollet et al., 2021).

Present information in varied learning formats: programmed books, audiovisual tapes, question and answer sessions, and group activities.
Natural defense mechanisms, such as anger or denial of the significance of the situation, can block learning, affecting the client’s response and ability to assimilate information. Changing to a less formal or structured style may be more effective until the client and caregiver are ready to accept or deal with the current situation.

Reinforce explanations of risk factors, dietary and/or activity restrictions, medications, and symptoms requiring immediate medical attention.
Using multiple learning methods enhances the retention of material. A high index of suspicion should be maintained for MI, especially when evaluating women, clients with diabetes, older adult clients, clients with dementia, clients with a history of heart failure, cocaine users, clients with hypercholesterolemia, and clients with a positive family history for early coronary disease (Zafari, 2015).

Review programmed increases in levels of activity. Educate the client regarding the gradual resumption of activities, e.g., walking, work, recreational and sexual activity. Provide guidelines for gradually increasing activity and instruction regarding target heart rate and pulse taking, as appropriate.
These activities greatly increase cardiac workload and myocardial oxygen consumption and may adversely affect myocardial contractility and output. A Norwegian randomized trial found that aerobic interval training (treadmill) increased peak oxygen uptake more than the usual care rehabilitation (aerobic exercise training) after myocardial infarction (Zafari, 2015).

Identify alternative activities for “bad weather” days, such as measured walking around the house or shopping mall.
Gradual increase in activity increases strength and prevents overexertion, may enhance collateral circulation, and allows a return to a normal lifestyle. Note: Sexual activity can be safely resumed once the client can accomplish activity equivalent to climbing two flights of stairs without adverse cardiac effects.

Review signs and symptoms requiring a reduction in activity and notification of healthcare provider.
Pulse elevations beyond established limits, development of chest pain, or dyspnea may require changes in exercise and medication regimen. Physical conditioning is achieved gradually over time. Many times, clients will overdo it in an attempt to achieve their goals too rapidly. Clients are observed for chest pain, dyspnea, weakness, fatigue, and palpitations and are instructed to stop the exercise if any of these occur.

Differentiate between increased heart rate that normally occurs during various activities and worsening signs of cardiac stress (chest pain, dyspnea, palpitations, increased heart rate lasting more than 15 minutes after cessation of activity, and excessive fatigue the following day).
Pulse elevations beyond established limits, development of chest pain, or dyspnea may require changes in exercise and medication regimen. Clients may be monitored for an increase in heart rate above the target heart rate, an increase in systolic or diastolic blood pressure of more than 20 mm Hg, a decrease in systolic blood pressure, onset or worsening of dysrhythmias, or ST-segment changes in the ECG.

Stress the importance of follow-up care, and identify community resources and support groups.
This reinforces that this is an ongoing and continuing health problem for which support and assistance are available after discharge. After discharge, clients encounter limitations in physical functioning and often incur difficulty with emotional, social, and role functioning requiring ongoing support. The nurse making a home visit can assist the client with scheduling and keeping follow-up appointments and with adhering to the prescribed cardiac rehabilitation regimen. In addition, the home care nurse monitors the client’s adherence to dietary restrictions and to prescribed medications.

Emphasize the importance of contacting the healthcare provider if chest pain, change in anginal pattern, or other symptoms recur.
Timely evaluation and intervention may prevent complications. The client must learn to recognize and take appropriate action for recurrent symptoms. A call must be placed to 911 if chest pressure or pain (or prodromal symptoms) is not relieved in 15 minutes by taking 3 nitroglycerin tablets at 5-minute intervals. The HCP should also be contacted if shortness of breath, fainting, slow or rapid heartbeat, or swelling of the feet and ankles occur.

Stress the importance of reporting the development of fever in association with diffuse and atypical chest pain (pleural, pericardial) and joint pain.
A post-MI complication of pericardial inflammation (Dressler’s syndrome) requires further medical evaluation and intervention. Before the era of reperfusion, the incidence of post-myocardial infarction syndrome ranged from 1 to 5% after acute MI, but this rate has dramatically declined with the advent of thrombolysis and coronary angioplasty (Zafari, 2015).

Encourage the client and family members to share concerns and feelings. Discuss signs of pathological depression versus transient feelings frequently associated with major life events. Recommend seeking professional help if depressed feelings persist.
Depressed clients have a greater risk of dying in 6 to 18 months following a heart attack. Timely intervention may be beneficial. Note: Selective serotonin reuptake inhibitors (SSRIs), paroxetine (Paxil), have been found to be as effective as tricyclic antidepressants but with significantly fewer adverse cardiac complications.

Stress the importance of proper dietary intake.
Diet plays an important role in the development of CAD. Educate post-MI clients about the role of a low-cholesterol and moderate-salt diet. Educate clients about the American Heart Association (AHA) dietary guidelines. A dietitian should see and evaluate all clients post-MI prior to their discharge (Zafari, 2015).

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