8 Myocardial Infarction (Heart Attack) Nursing Care Plans

An MI is heart muscle dying for lack of oxygen, and the clock is the enemy. Almost half of sudden deaths from MI happen before the patient ever reaches the hospital, within the first hour of symptoms. Your job at the bedside is to read the pain fast, cut myocardial oxygen demand, restore flow, and catch the complication (a lethal dysrhythmia, pump failure, shock) before it kills. Treat fast and the prognosis improves sharply.

What Is Myocardial Infarction

Myocardial infarction (MI), or acute myocardial infarction (AMI), is irreversible necrosis of heart muscle from prolonged ischemia. Oxygen supply no longer meets demand, usually because plaque ruptures and a thrombus forms in a coronary vessel, cutting blood supply to part of the myocardium.

MI sits inside the broader category of acute coronary syndrome (ACS), the continuum of ongoing myocardial ischemia or injury that runs from unstable angina, to non-ST-segment elevation MI (NSTEMI), to ST-segment elevation MI (STEMI). Cardiovascular disease remains the leading cause of death in the United States and Western Europe, and much of that mortality traces to MI damage or its complications.

MI is also classified by mechanism. Type 1 MI is atherothrombotic, precipitated by atherosclerotic plaque disruption. Type 2 MI is ischemic injury from a mismatch between oxygen supply and demand. Type 3 MI is presumed when the clinical picture is a classic MI and the patient dies before cardiac biomarkers can be drawn.

Nursing Care Plan and Management

The goals in acute MI are to limit myocardial damage, preserve cardiac function, and prevent complications by restoring coronary flow. You reduce oxygen demand and raise oxygen supply through medications, oxygen therapy, and rest. Pain relief and improving ECG findings signal a rebalanced supply and demand and possible reperfusion. Confirmed flow through an open vessel in the cath lab confirms it.

Nursing Problem Priorities

1. Manage pain and ischemia.
2. Monitor for complications.
3. Promote adequate tissue perfusion.
4. Reduce anxiety.

Nursing Assessment

Patients with MI typically present with acute, continuous chest pain, often with dyspnea, indigestion, nausea, and anxiety. Skin is frequently cool, pale, and moist, with elevated heart and respiratory rates from sympathetic activation. Symptoms alone do not reliably separate MI from unstable angina, which is why the umbrella term ACS exists.

Assess for the following subjective and objective data:

• Chest pain with or without radiation
• Facial grimacing
• Restlessness, changes in level of consciousness
• Changes in pulse and BP
• Heart rate and BP changes with activity
• Development of dysrhythmias
• Changes in skin color and moisture
• Exertional angina
• Generalized weakness

Assess for factors related to the cause:

• Tissue ischemia (coronary artery occlusion)
• Imbalance between myocardial oxygen supply and demand
• Ischemic or necrotic myocardial tissue
• Cardiac depressant effects of certain drugs (beta-blockers, antiarrhythmics)

Nursing Diagnosis

Formulate the diagnosis from your assessment and clinical judgment of the patient's condition. The label is a framework. Your judgment shapes the plan around the patient's actual priorities.

Nursing Goals

• The patient will report relief or control of chest pain within the time frame appropriate for the medications given, show reduced tension and a relaxed manner, and use relaxation techniques.
• The patient will recognize and verbalize feelings, identify causes and contributing factors, report reduced anxiety, and use resources appropriately.
• The patient will maintain stable hemodynamics (normal BP, adequate cardiac output), report reduced dyspnea and angina, and demonstrate improved activity tolerance.

Nursing Interventions and Actions

1. Relieving Pain and Ischemia, Improving Respiratory Function
2. Monitoring Laboratory and Diagnostic Tests
3. Administering Medications and Pharmacologic Support
4. Improving Cardiac Output and Monitoring for Complications
5. Improving Tissue Perfusion and Starting Cardiac Rehabilitation
6. Reducing Anxiety and Fear
7. Improving Activity Tolerance
8. Health Education and Teaching

1. Relieving Pain and Ischemia, Improving Respiratory Function

Pain is the classic event in an MI, and you have to separate it from the many syndromes that mimic a coronary event, including pericarditis, aortic aneurysm, and dissection.

Monitor and document the characteristics of pain, including verbal reports and nonverbal cues (moaning, crying, grimacing, restlessness, diaphoresis, clutching the chest). Most patients with an acute MI look ill, distracted, and focused on the pain. Hold the deeper history of precipitating factors until the pain is relieved. Pain and anxiety drive up respirations, and stress catecholamines raise heart rate and BP. Some patients present with abdominal discomfort or jaw pain as their anginal equivalent, and women present with atypical symptoms more often than men.

Get a full description of the pain: location, intensity (0 to 10 scale), duration, character (dull, crushing, "like an elephant on my chest"), and radiation. Pain is subjective and must be described by the patient. This sets a baseline for judging whether therapy is working. Discomfort is commonly crushing, oppressive, or constricting pressure that may radiate to the left arm, neck, jaw, infrascapular area, or epigastrium. Transient symptoms lasting less than 15 minutes that ease at rest point to angina. MI discomfort typically lasts more than 30 minutes, is not relieved by rest or nitroglycerin, and may or may not be severe.

Review any history of prior angina, anginal equivalent, or MI pain, and a pertinent family history. Delayed reporting hinders relief and may require higher doses. Severe pain can stimulate the sympathetic nervous system enough to induce shock, causing further damage. 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 had an MI.

Check vital signs before and after narcotic medication. Morphine sulfate is the analgesic of choice for anginal pain in STEMI and for unstable angina and NSTEMI, barring contraindications. Hypotension and respiratory depression can follow narcotic administration and may worsen myocardial damage when ventricular function is already impaired.

Monitor vital signs closely. Hypertension may precipitate MI or reflect elevated catecholamines from anxiety or pain. Hypotension may signal ventricular dysfunction from ischemia. Impaired left ventricular diastolic function produces pulmonary congestion with dyspnea and tachypnea and, eventually, pulmonary edema with orthopnea.

Monitor respirations and note the work of breathing. Pump failure or ischemic pain can precipitate respiratory distress, but sudden or continued dyspnea may signal thromboembolic pulmonary complications. Careful, repeated respiratory assessment catches pulmonary complications early.

Administer supplemental oxygen by nasal cannula or face mask as indicated. Oxygen is given by nasal prongs at 2 to 5 L/minute to improve myocardial and tissue oxygenation. Limit oxygen therapy to hypoxic patients, since it raises coronary vascular resistance and may increase mortality in non-hypoxic patients. A flow rate of 2 to 4 L/minute by nasal cannula is often enough to keep oxygen saturation above 95% unless there is underlying chronic pulmonary disease. In non-hypoxic STEMI patients, supplemental oxygen can increase the risk of myocardial injury, recurrent MI, and major arrhythmias.

Instruct the patient to report pain immediately. Atypical presentations are common and frequently misdiagnosed, especially in older patients and patients with diabetes. Morbidity and mortality drop significantly when symptoms are recognized early, EMS is activated, and time to definitive treatment is shortened.

Provide a quiet environment, calm activity, and a position of comfort. Approach the patient calmly and confidently. This lowers external stimuli that aggravate anxiety and cardiac strain. Physical rest in bed with the backrest elevated, or in a cardiac chair, eases chest discomfort and dyspnea.

Teach relaxation techniques such as slow deep breathing, distraction, visualization, and guided imagery. Assist as needed. These reduce pain perception, give the patient a sense of control, and support a positive attitude.

Administer medications for pain relief as indicated. See pharmacologic interventions.

2. Monitoring Laboratory and Diagnostic Tests

Cardiac biomarkers (troponin, creatine kinase, and myoglobin) are the core tools for diagnosing acute MI. They detect cellular components released into the blood when heart muscle cells are damaged, and their time courses allow a prompt, accurate diagnosis.

Monitor cardiac enzymes, ABGs, and electrolytes. Enzymes track the resolution or extension of the infarct. Remeasuring cardiac enzymes at regular intervals over the first 24 hours improves the sensitivity of detection, and the degree of elevation aids prognosis. Hypoxemia signals a need for supplemental oxygen. Electrolyte imbalances such as hypokalemia or hyperkalemia adversely affect cardiac rhythm and contractility.

Troponin. Troponin regulates myocardial contraction, and troponin I and troponin T are specific to cardiac muscle, making them reliable markers of myocardial damage. Levels rise within a few hours of an acute MI and stay elevated for up to 2 weeks. Troponin can also rise in inflammation, sepsis, heart failure, and respiratory failure.

Creatine kinase. CK 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 with cardiac damage, starting within hours and peaking within 24 hours of the infarct.

Myoglobin. Myoglobin is present in cardiac and skeletal muscle and carries oxygen. Levels begin to rise within 1 to 3 hours and peak within 12 hours of symptom onset. A rise is not specific for a cardiac event, but a negative result helps rule out an acute MI.

3. Administering Medications and Pharmacologic Support

The patient with suspected MI should promptly receive supplemental oxygen, aspirin, nitroglycerin, and morphine to relieve pain and anxiety. Watch closely for hypotension and respiratory depression during morphine administration. Beta-blockers may manage dysrhythmias, and unfractionated heparin or LMWH plus platelet inhibitors prevent further clot formation.

Antianginals: nitroglycerin, isosorbide dinitrate, and mononitrate. Nitrates control pain by dilating the coronaries, increasing coronary blood flow and myocardial perfusion. Peripheral vasodilation drops preload, lowering myocardial workload and oxygen demand. Systolic BP below 90 mm Hg, HR below 60 or above 100, and right ventricular infarction contraindicate nitrate use.

Beta-blockers: atenolol, pindolol, propranolol, nadolol, and metoprolol. Beta-blockers are important second-line agents for pain control. By blocking sympathetic stimulation, they cut heart rate, systolic BP, and myocardial oxygen demand. Metoprolol is the standard of care, a selective beta-1 blocker that decreases automaticity. Contraindications include signs of heart failure, low-output state, increased risk for cardiogenic shock, a PR interval greater than 0.24 seconds, and active asthma.

Analgesics: morphine and meperidine. IV morphine is the usual choice, but other injectable narcotics may be used in acute or recurrent chest pain unrelieved by nitroglycerin, to reduce severe pain, provide sedation, and decrease myocardial workload. Avoid IM injections when possible, since they can alter the CPK diagnostic indicator and are poorly absorbed in under-perfused tissue.

Antiplatelet agents: aspirin, abciximab (ReoPro), clopidogrel (Plavix). These reduce mortality in MI and are taken daily. Aspirin also reduces coronary occlusion after percutaneous transluminal coronary angioplasty (PTCA). ReoPro is an IV adjunct to PTCA that prevents acute ischemic complications. There is increased bleeding risk if emergency coronary artery bypass graft (CABG) becomes necessary.

Anticoagulants: heparin or enoxaparin (Lovenox). Low-dose heparin is given during PTCA and may be given prophylactically in high-risk patients (atrial fibrillation, obesity, ventricular aneurysm, history of thrombophlebitis) to reduce thrombophlebitis or mural thrombus. LMWH is favored for convenient dosing, reliable therapeutic levels, and lower rates of HIT, especially when use is expected to exceed 2 to 3 days.

Thrombolytics: streptokinase, urokinase, and reteplase. Thrombolytic therapy improves survival in STEMI but is not indicated in NSTEMI. Door-to-drug time should be no more than 30 minutes. The aim is to restore flow through the occluded vessel by rapidly removing the thrombus the body's own fibrinolytic system could not.

Administer antidysrhythmics as indicated. Dysrhythmias are usually treated symptomatically, except PVCs, which are often treated prophylactically. Start ACE inhibitors as soon as possible when the patient is stable and has no contraindications, especially with a large anterior MI, ventricular aneurysm, or heart failure. ACE inhibitors help most in patients with ventricular dysfunction, improving output and survival and slowing heart failure progression.

Administer beta-blockers as indicated. In myocardial ischemia, beta-blockers have antiarrhythmic effects and reduce myocardial oxygen demand. They also lower the inotropic state of the left ventricle, decrease diastolic dysfunction, and increase LV compliance.

Administer diuretics: furosemide (Lasix), spironolactone with hydrochlorothiazide (Aldactazide), hydralazine (Apresoline). Diuretics correct fluid overload by lowering plasma volume and peripheral edema. The drop in extracellular fluid may initially reduce cardiac output and BP, but with continued therapy plasma volume and peripheral vascular resistance usually return to pretreatment values.

Administer vasodilators such as dopamine and fenoldopam. In small doses, dopamine selectively dilates the renal vasculature and enhances renal perfusion. Fenoldopam maintains or increases renal perfusion while lowering BP, useful mainly in patients with renal insufficiency presenting in hypertensive crisis.

Administer anti-anxiety agents and hypnotics as indicated: alprazolam (Xanax), diazepam (Valium), lorazepam (Ativan), flurazepam (Dalmane). These promote rest and reduce anxiety that can block recovery. Always evaluate the effectiveness of anxiolytics, since combining them with pain medications such as morphine can have serious consequences.

4. Improving Cardiac Output and Monitoring for Complications

MI reduces the heart's ability to pump, dropping cardiac output, which can cascade into heart failure, arrhythmia, and shock. A left coronary artery MI tends to produce extensive injury because it covers more territory than the right system, with greater risk of pulmonary congestion and low output.

Auscultate BP. Compare both arms and obtain lying, sitting, and standing pressures when able. Hypotension may stem from ventricular dysfunction, myocardial hypoperfusion, and vagal stimulation. Hypertension is also common, related to pain, anxiety, catecholamine release, or preexisting vascular disease. Orthostatic hypotension may accompany complications such as heart failure.

Evaluate the quality of pulses at both pulse points. Decreased cardiac output produces weak, thready pulses. Irregularities suggest dysrhythmias needing further evaluation. Falling output reduces the strength and amplitude of peripheral pulses and can slow or destabilize the rate.

Auscultate heart sounds. Note S3, S4, murmurs, or friction rubs. S3 is usually associated with heart failure but also appears with mitral regurgitation and LV overload from severe infarction. S4 is associated with myocardial ischemia, ventricular stiffening, and hypertension. Murmurs or friction rubs indicate disturbed flow (incompetent valve, septal defect, papillary muscle or chordae tendineae problems), and a rub also points to inflammation, pericardial effusion, and pericarditis.

Auscultate breath sounds. Crackles reflect pulmonary congestion from depressed myocardial function. Rales or wheezes can occur secondary to pulmonary venous hypertension from extensive ventricular infarction, and pleural effusions may produce egophony at the lung bases.

Monitor heart rate and rhythm. Document dysrhythmias via telemetry. Rate and rhythm respond to medication, activity, and developing complications. PVCs and progressive heart blocks can compromise cardiac function or worsen ischemic damage.

Note the response to activity and promote rest appropriately. Overexertion raises oxygen consumption and demand and can compromise myocardial function. Damaged heart muscle needs time to heal, and rest improves blood flow to the myocardium.

Monitor vital signs. Even non-lethal dysrhythmias may need immediate treatment when cardiac output and tissue perfusion are altered. Heart rate often rises from sympathoadrenal discharge. With right ventricular infarction or severe LV dysfunction, expect hypotension. Respiratory rate may climb with pulmonary congestion.

Review serial ECGs. The ECG tracks the progression or resolution of infarction, ventricular function, electrolyte balance, and drug effects. It is the most important tool in the initial evaluation and triage of suspected ACS and is confirmatory in roughly 80% of cases. Obtain daily serial ECGs for the first 2 to 3 days, and more as needed.

Review chest x-ray and echocardiography. These can reveal pulmonary edema from ventricular dysfunction. On chest radiographs, pleural effusion shows as blunted costophrenic angles; on echocardiography, as echo-lucent zones next to the heart.

Measure cardiac output and other functional parameters as appropriate. Cardiac index, preload, afterload, contractility, and cardiac work can be measured noninvasively with thoracic electrical bioimpedance (TEB). One key TEB parameter, thoracic fluid conductivity, reflects total thoracic fluid and relates to circulation and myocardial contractility. This helps evaluate response to therapy and the need for more aggressive care.

Provide small, easily digested meals. Limit caffeine and caffeine-containing products. Large meals raise myocardial workload and cause vagal stimulation, leading to bradycardia or ectopic beats. Caffeine is a direct cardiac stimulant. Current guidelines do not require restricting caffeine in regular coffee drinkers, but caffeine can raise BP and the risk of type 2 diabetes mellitus, so use caution with daily intake.

Provide a calm, quiet environment. Review the reasons for activity limits during the acute phase. This reduces stress catecholamines that cause or worsen dysrhythmia and vasoconstriction. Limiting the patient to bed or chair rest early on reduces myocardial oxygen consumption and should continue until the patient is pain-free and hemodynamically stable.

Encourage stress management behaviors such as relaxation techniques, guided imagery, and slow deep breathing. These give the patient some control in a stressful situation. Techniques such as progressive muscle relaxation and meditation calm the mind and lower stress.

Keep emergency equipment and medications available. Sudden coronary occlusion, lethal dysrhythmias, infarct extension, and unrelenting pain can precipitate cardiac arrest and require immediate life-saving therapy or transfer to the CCU. Give all suspected MI patients chewable aspirin unless they have a documented aspirin allergy. For severe pain, give IV morphine, and reverse toxicity with naloxone if needed.

Maintain IV or Hep-Lock access as indicated. A patent line is essential for emergency drugs during persistent lethal dysrhythmias or chest pain. Treat refractory or severe pain with IV morphine, meperidine, or pentazocine. Treat relative hypotension with fluids, and atropine may raise BP.

Assist with insertion and maintenance of a pacemaker when used. Pacing may be temporary support during the acute phase, or permanent if the infarct severely damages the conduction system. Implantable cardioverter defibrillators (ICDs) may be unnecessary in select post-MI patients with severe LV dysfunction and a negative electrophysiology study, who show no inducible ventricular tachycardia and low long-term rates of arrhythmia or death without one.

5. Improving Tissue Perfusion and Starting Cardiac Rehabilitation

Decreased systolic performance impairs perfusion of vital organs and triggers compensatory responses: restlessness, impaired mentation, pallor, peripheral vasoconstriction, sweating, tachycardia, and prerenal failure. With extensive injury, coronary flow falls further as output drops and heart rate climbs, and ischemia at a distance from the infarct can drive a vicious cycle ending in profound LV failure, hypotension, and cardiogenic shock.

Investigate sudden or continued changes in mentation (changes in LOC, stupor). Cerebral perfusion tracks cardiac output and is influenced by electrolyte and acid-base shifts, hypoxia, and systemic emboli. Ineffective perfusion starves the brain of oxygen and nutrients, altering cognition.

Inspect for pallor, cyanosis, mottling, and cool, clammy skin. Note the strength of peripheral pulses. Systemic vasoconstriction from low output shows as decreased skin perfusion and diminished pulses. Peripheral cyanosis, edema, pallor, low pulse volume, and delayed capillary refill point to vasoconstriction, low output, and right ventricular dysfunction.

Monitor intake and note changes in urine output. Record urine specific gravity as indicated. Low intake or persistent nausea reduces circulating volume and perfusion. Specific gravity reflects hydration and renal function. When perfusion to the kidneys drops, they cannot filter waste or make urine effectively.

Assess GI function: anorexia, decreased or absent bowel sounds, nausea, vomiting, abdominal distension, constipation. Reduced mesenteric flow produces GI dysfunction such as loss of peristalsis, worsened by analgesics, decreased activity, and dietary changes.

Assess for Homans' sign (calf pain on dorsiflexion), erythema, and edema. These suggest deep vein thrombosis (DVT), though DVT can be present without a positive Homans' sign. Grade dependent edema 0 to 4 by the depth of persistent pitting after thumb pressure to the inner shin for more than 10 seconds.

Monitor CBC, ABGs, BUN, creatinine, electrolytes, and coagulation studies (PT, aPTT, clotting times). These reflect organ perfusion and function, and coagulation abnormalities can follow therapy. Obtain a CBC to rule out anemia as a cause of low oxygen supply and before giving thrombolytics. Platelets can fall dangerously after heparin from heparin-induced thrombocytopenia (HIT).

Elevate the head of the bed as appropriate. This improves tidal volume by reducing abdominal pressure on the diaphragm, improves drainage of the upper lobes, and increases venous return, lowering cardiac workload.

Encourage active or passive leg exercises and avoid isometric exercises. Leg exercises enhance venous return, reduce stasis, and lower DVT risk, while isometric work raises myocardial workload and oxygen consumption. Flex, extend, and rotate the feet periodically, and assist with gradual ambulation as tolerated.

Apply or periodically remove anti-embolic hose or graduated compression stockings as used. Apply and regulate intermittent pneumatic compression as indicated. These limit venous stasis, improve venous return, and reduce thrombophlebitis risk in the patient on limited activity. Sequential compression devices act as an artificial muscle pump.

Apply warm, moist compresses or a heat cradle to an affected extremity if indicated. These promote vasodilation and venous return to resolve local edema. Use caution, since heat is contraindicated in arterial insufficiency, where it raises cellular oxygen demand and worsens the supply-demand imbalance.

Assist with reperfusion therapy. Percutaneous coronary intervention is the preferred reperfusion method when it can be done in a timely way. It places a small mesh stent into the narrowed or infarcted artery via cardiac catheterization, using a balloon-tipped catheter to open the vessel.

Prepare for PTCA (balloon angioplasty), with or without intracoronary stents. Stents provide structural support and improve long-term patency. Rapidly available primary PTCA by skilled operators gives long-term outcomes similar to IV thrombolysis.

Transfer to critical care or a specialty center. More intensive monitoring and aggressive intervention improve outcomes. Transfer to an invasive-treatment center for primary PCI is superior to onsite fibrinolysis as long as it can be done within 2 hours, and should be considered for patients likely to benefit from PCI or cardiac surgery where access is not immediate.

Auscultate breath sounds for crackles. Crackles may indicate pulmonary edema from cardiac decompensation. A Killip classification above II or III carries a poor prognosis.

Perform risk stratification with the Killip classification. Killip class I is no clinical signs of heart failure; class II is rales or crackles, an S3 gallop, and elevated jugular venous pressure; class III is frank acute pulmonary edema; class IV is cardiogenic shock or hypotension with evidence of low cardiac output.

Note jugular vein distention and dependent edema. These suggest developing heart failure or fluid volume excess. In acute inferior-wall MI with right ventricular involvement, neck vein distention is a common sign of right ventricular failure.

Measure I&O, noting decreased and concentrated output. Calculate fluid balance. Low output impairs kidney perfusion, causing sodium and water retention and reduced urine output. Heart failure with reduced ejection fraction is a risk factor for kidney disease.

Weigh daily. Sudden weight changes reflect fluid shifts. Edema adds body weight, limits mobility, and can further raise cardiac workload.

Monitor potassium as indicated. Hypokalemia limits therapy and can occur with potassium-depleting diuretics. All diuretics except potassium-sparing agents (which cause hyperkalemia) can cause hypokalemia.

Monitor urine specific gravity. This measures the kidney's ability to concentrate urine. In intrarenal failure, specific gravity is usually 1.010 or less, showing lost concentrating ability.

Maintain total fluid intake at 2000 mL/24 hours within cardiovascular tolerance. This meets normal adult fluid needs but may require restriction with cardiac decompensation. Cardiologists commonly use ice chips to relieve thirst in heart failure.

Encourage moderate sodium intake in diet and beverages. Moderate salt intake is associated with the best outcomes for mortality and morbidity compared with high or low intake.

Refer to a cardiac rehabilitation program. Cardiac rehab is a long-term program of medical evaluation, exercise, risk-factor modification, education, and counseling that limits the physical and psychological effects of cardiac illness and improves quality of life.

6. Reducing Anxiety and Fear

Reducing anxiety and fear lowers the sympathetic stress response, which decreases cardiac workload and can relieve pain and other ischemic signs. Managing anxiety helps preserve myocardium and reduce further deterioration.

Acknowledge the patient's perception of the threat. Encourage expression of anger, grief, sadness, and fear without denying those feelings. The emotional trauma of an MI is hard. Patients may fear death or be anxious about the environment, and ongoing anxiety about lifestyle, unfinished matters, and the illness's effect on family can persist and surface as depression.

Note hostility, withdrawal, or denial (inappropriate affect, refusal to comply). Studies show some correlation between the degree of anger or hostility and increased MI risk, and denial contributes to delayed adherence to effective treatment.

Observe verbal and nonverbal signs of anxiety (restlessness, vital sign changes) and stay with the patient. Intervene if behavior turns destructive. Patients may not voice concern directly, but words and actions can convey agitation and hostility. Intervention helps the patient regain control.

Assess the patient's and caregiver's anxiety level and coping mechanisms. Causes of anxiety vary: acute illness, hospitalization, pain, disrupted daily life, role and self-image changes, and financial worry. Anxious family members transmit anxiety to the patient, so address the family's fear too.

Maintain a confident manner but avoid false reassurance. The patient and caregiver pick up on team anxiety. Honest, supportive explanations ease anxiety and make the patient a partner in care.

Accept but do not reinforce denial. Avoid confrontation. Denial can ease anxiety but postpones dealing with reality. Confrontation breeds anger and more denial, reducing cooperation. Acceptance signals that the patient's fears are realistic and normal.

Orient the patient and caregiver to routine procedures and expected activities. Promote participation when possible. Predictability decreases anxiety and improves the patient's ability to absorb new information about the diagnosis and procedures.

Answer questions factually. Provide consistent information and repeat as needed. Accurate information reduces fear and strengthens the nurse-patient relationship. Attention spans are short, so repetition aids retention.

Encourage the patient and caregiver to communicate, share concerns, and provide privacy. Sharing elicits support and comfort and relieves the tension of unspoken worry. Privacy lets partners share feelings and build effective coping.

Provide rest periods, uninterrupted sleep, and quiet surroundings, with the patient controlling external stimuli. This conserves energy and supports coping. Offering control over simple activities such as visitor timing, bathing, and eating lowers anxiety.

Promote relaxation and stress management. Bedside relaxation, imagery, meditation, and music therapy promote relaxation, while breathing exercises and massage reduce tension and enhance coping.

Encourage independence, self-care, and decision-making within the treatment plan. Independence builds confidence and reduces feelings of abandonment after transfer or discharge. Identify the patient's own priorities, teach heart-healthy living, and involve them in cardiac rehab.

Encourage discussion about post-discharge expectations. This helps set realistic goals and reduces discouragement when limits or a slow recovery become apparent.

Administer anti-anxiety agents and hypnotics as indicated. See pharmacologic interventions.

Provide timely, effective pain relief. Relieving pain is the most effective way to reduce anxiety. When nitroglycerin or fibrinolytics do not relieve ischemic pain, morphine sulfate usually does.

Provide referrals for spiritual counseling or social services. Spiritual counseling can ease anxiety for patients who find support in religion, and social services can help with post-hospital care and financial concerns.

7. Improving Activity Tolerance

ACS comes from inadequate oxygen flow to the heart muscle through occluded coronaries. The drop in oxygen supply limits everything from light to heavy activity and can cause ventricular contraction failure, falling cardiac output, and hemodynamic instability.

Assess and document heart rate, rhythm, and BP before, during, and after activity. Correlate with chest pain or dyspnea. Trends show the patient's response and may flag myocardial oxygen deprivation that calls for less activity, a return to bedrest, medication changes, or supplemental oxygen. Older patients and patients with diabetes may have subtle presentations and complain of weakness, fatigue, or syncope.

Review signs and symptoms of intolerance that require notifying a nurse or provider. Palpitations, pulse irregularities, chest pain, or dyspnea may mean the exercise plan or medications need changing.

Encourage rest initially, then limit activity based on pain and cardiac response. Provide non-stress diversional activity. This reduces myocardial workload and oxygen consumption. Keep the patient on bed rest to minimize oxygen consumption until reperfusion and initial therapy are complete, usually about 24 to 48 hours, then advance activity slowly as tolerated.

Instruct the patient to avoid increasing abdominal pressure (straining during defecation). The Valsalva maneuver can cause bradycardia and rebound tachycardia with elevated BP and may be contraindicated in MI, where it can trigger sudden cardiac death.

Provide a quiet environment and limit visitors. Encourage stress management and diversional activity. This reduces stress and excess stimulation and promotes rest, giving the patient a sense of control.

Explain the graded activity plan: getting up to the commode or sitting in a chair, progressive ambulation, and resting after meals. Graded activity provides a controlled demand that builds strength while preventing overexertion. The bedside commode is generally allowed and is less stressful than a bedpan. If the patient is stable, sitting in a bedside chair is permitted after 12 hours, then activity advances gradually.

Promote tolerable, light physical exercise as indicated. Exercise shifts blood supply from inactive to active organs, lengthens inspiration, and clears more metabolic waste. Muscles need adequate oxygen during activity so energy distribution stays smooth and stable.

Assist with insertion of ventricular assist devices. Ventricular assist devices (VADs) support the failing heart and take partial or complete control of cardiac function. They may serve as temporary or complete assist in AMI and cardiogenic shock when there is a chance of recovery after a period of cardiac rest.

8. Health Education and Teaching

To improve adherence to a self-care regimen after discharge, identify the patient's priorities, teach heart-healthy living thoroughly, and support enrollment in cardiac rehab. Involving the patient in building the program makes the plan more effective.

Assess the patient's or family member's knowledge, ability, and desire to learn. This shapes an individualized teaching plan. Patients on an LVAD need intensive education, family support, and frequent direction from LVAD nurses or coordinators to self-manage home care.

Watch for signs of avoidance (changing the subject, extremes of behavior). This reinforces that this is a learning experience and lets you clarify misunderstandings. After discharge, LVAD patients are often highly dependent on caregivers for weeks to months while adhering to the home care regimen.

Encourage enrollment in smoking cessation classes. Educate every patient on the central role of smoking in coronary artery disease and offer cessation classes to help them avoid smoking after their MI.

Promote moderate consumption of alcohol. Mild alcohol consumption has been associated with decreased risk of stroke and MI. Discuss alcohol use case by case.

Warn against isometric activity, the Valsalva maneuver, and activities with the arms above the head. These directly stress cardiovascular function and can impede recovery. A single session of isometric exercise does not provide the vascular and hemodynamic benefits of aerobic exercise after primary PCI.

Present information in varied formats: programmed books, audiovisual material, question-and-answer, and group activities. Anger or denial can block learning, so a less formal style may work better until the patient and caregiver are ready to engage.

Reinforce risk factors, dietary and activity restrictions, medications, and symptoms requiring immediate attention. Multiple learning methods improve retention. Keep a high index of suspicion for MI in women, patients with diabetes, older patients, patients with dementia, those with heart failure or hypercholesterolemia, cocaine users, and those with a family history of early coronary disease.

Review graded increases in activity. Teach gradual resumption of walking, work, recreation, and sexual activity, plus target heart rate and pulse taking. These activities greatly raise cardiac workload and myocardial oxygen consumption. Aerobic interval training has been shown to raise peak oxygen uptake more than usual-care rehabilitation after MI.

Identify alternative activities for bad-weather days, such as walking around the house or a shopping mall. Gradual increases build strength, prevent overexertion, may enhance collateral circulation, and support a return to normal life. Sexual activity can be safely resumed once the patient can manage activity equal to climbing 2 flights of stairs without adverse cardiac effects.

Review signs and symptoms requiring reduced activity and provider notification. Pulse elevations beyond set limits, chest pain, or dyspnea may require exercise and medication changes. Patients often overdo it trying to reach goals too fast. Watch for chest pain, dyspnea, weakness, fatigue, and palpitations, and instruct the patient to stop exercising if any occur.

Differentiate the normal heart rate rise during activity from worsening cardiac stress (chest pain, dyspnea, palpitations, heart rate elevated more than 15 minutes after stopping, or excessive next-day fatigue). Also watch for a systolic or diastolic BP rise of more than 20 mm Hg, a drop in systolic BP, new or worsening dysrhythmias, or ST-segment changes.

Stress the importance of followup care, community resources, and support groups. This is an ongoing health problem with support available after discharge. A home care nurse can help with scheduling and keeping followup appointments and with adherence to cardiac rehab, diet, and medications.

Emphasize contacting the provider if chest pain, a change in anginal pattern, or other symptoms recur. Timely evaluation can prevent complications. Call 911 if chest pressure or pain is not relieved in 15 minutes by 3 nitroglycerin tablets taken at 5-minute intervals. Also contact the provider for dyspnea, fainting, slow or rapid heartbeat, or swelling of the feet and ankles.

Stress reporting fever with diffuse, atypical chest pain (pleural, pericardial) and joint pain. This points to Dressler's syndrome, a post-MI pericardial inflammation needing evaluation. Before the reperfusion era, post-MI syndrome occurred in 1 to 5% of acute MIs, a rate that has fallen sharply with thrombolysis and angioplasty.

Encourage the patient and family to share concerns and feelings. Discuss pathological depression versus transient feelings, and recommend professional help if depression persists. Depressed patients have a greater risk of dying within 6 to 18 months after a heart attack, so timely intervention matters. SSRIs such as paroxetine (Paxil) are as effective as tricyclics with significantly fewer adverse cardiac effects.

Stress proper dietary intake. Diet plays a major role in coronary artery disease. Teach post-MI patients about a low-cholesterol, moderate-salt diet and the American Heart Association dietary guidelines, and have a dietitian evaluate every post-MI patient before discharge.