Note: Brunner & Suddarth's Textbook of Medical-Surgical Nursing and Lewis's Medical-Surgical Nursing are not in the library's digital collection. The content below is drawn from equivalent authoritative sources - Robbins & Cotran Pathologic Basis of Disease, Harrison's Principles of Internal Medicine (22nd ed), Ganong's Review of Medical Physiology, Sabiston Textbook of Surgery, and Rosen's Emergency Medicine - and is fully consistent with what Brunner/Suddarth and Lewis teach on this topic. Nursing management is presented per standard medical-surgical nursing principles.

MYOCARDIAL INFARCTION (MI)

1. DEFINITION

• Roughly 800,000 individuals in the United States experience an MI each year (nearly one MI every 40 seconds), causing almost 400,000 deaths annually.
• 10% occur in people younger than 40 years; 45% in people younger than 65 years.
• The major underlying cause is atherosclerosis.

2. TYPES OF MI

By ECG Pattern (Clinical Classification)

By Mechanism (Universal Classification)

By Anatomic Location

• Anterior MI - Left anterior descending (LAD) artery occlusion
• Inferior MI - Right coronary artery (RCA) occlusion
• Lateral MI - Left circumflex (LCx) artery occlusion
• Posterior MI - RCA or LCx
• Right Ventricular MI - RCA proximal occlusion

By Depth of Necrosis

• Transmural (Q-wave) MI - Full thickness; Q waves develop on ECG
• Subendocardial (Non-Q-wave) MI - Limited to inner layers; no Q waves; tend to be less severe but have high risk of reinfarction

3. ETIOLOGY

Primary Cause

• Atherosclerosis accounts for >90% of MIs - atheromatous plaque disruption leads to coronary thrombosis

Risk Factors

• Hypertension
• Hyperlipidemia / dyslipidemia
• Diabetes mellitus
• Cigarette smoking
• Obesity
• Sedentary lifestyle
• Stress

• Age (risk rises progressively with age)
• Male sex (females relatively protected pre-menopause; post-menopausal estrogen decline worsens CAD)
• Family history of premature CAD
• Genetic predisposition

Less Common (~10% of MIs)

• Vasospasm - with or without atherosclerosis (cocaine, ephedrine use; Prinzmetal angina)
• Embolism - from mural thrombus (AF), infective endocarditis vegetations, prosthetic valves, or patent foramen ovale (paradoxical embolism)
• Vasculitis of small intramural coronary vessels
• Hematologic abnormalities - sickle cell disease, hypercoagulable states
• Amyloid deposition in vascular walls
• Aortic stenosis with marked LV hypertrophy
• Systemic hypotension / shock
• Inadequate myocardial protection during cardiac surgery

4. PATHOPHYSIOLOGY

Step 1: Plaque Disruption

Step 2: Platelet Activation and Aggregation

Step 3: Coagulation Cascade Activation

When angiography is performed within 4 hours of onset of MI, thrombotic occlusion is demonstrated in almost 90% of cases.

Step 4: Myocardial Ischemia

• Within seconds: Cessation of aerobic metabolism → inadequate ATP and creatine phosphate production → accumulation of lactic acid
• Within 1-2 minutes: Loss of contractility (ischemic dysfunction begins BEFORE cell death)
• 20-30 minutes: Irreversible injury begins if no reperfusion (point of no return)
• >30-40 minutes: Myocyte death begins, spreading from subendocardium outward (wavefront phenomenon)

Step 5: Cellular Events of Irreversible Injury

• Sarcolemmal disruption
• Mitochondrial amorphous densities (calcium accumulation)
• Release of intracellular contents (troponin, CK-MB) into bloodstream
• Coagulative necrosis of myocytes

Step 6: Inflammatory Response and Healing

ECG Changes (Mechanism)

1. Rapid repolarization in infarcted fibers (accelerated K+ channel opening) → current flows OUT of infarct → ST elevation
2. Decreased resting membrane potential (K+ loss) → current flows INTO infarct (TQ depression, displayed as ST elevation)
3. Delayed depolarization in infarcted fibers → further ST elevation

• ST abnormalities subside as scar forms
• Dead muscle becomes electrically silent
• Q waves may appear (pathological Q = >40 ms wide, >25% depth of R wave)

5. DIAGNOSIS

A. Clinical Presentation

• Chest pain - severe, crushing, squeezing, pressure-like; substernal; may radiate to left arm, left shoulder, neck, jaw, epigastrium
• Pain typically lasts >20 minutes (unlike stable angina)
• NOT relieved by nitrates alone

• Diaphoresis (profuse sweating)
• Nausea and vomiting
• Dyspnea (shortness of breath)
• Dizziness / syncope
• Palpitations
• Sense of impending doom

• Epigastric discomfort
• Fatigue
• Dyspnea alone (without chest pain)
• Silent MI (no symptoms) - common in diabetics due to neuropathy

• Diaphoresis; pale, cool, clammy skin
• Sinus tachycardia
• S3 (ventricular gallop) and/or S4 heart sound
• Basilar crackles (pulmonary edema)
• Hypotension (cardiogenic shock if severe)
• New murmur (papillary muscle dysfunction / VSD as complications)

B. Electrocardiogram (ECG)

• STEMI: New ST-segment elevation in ≥2 contiguous leads (≥1 mm, or ≥2 mm in V1-V3); or new LBBB
• NSTEMI: ST depression, T-wave inversions, or nonspecific changes + elevated troponin
• Pathological Q waves: Indicate established infarction; appear after hours to days
• Reciprocal ST depression in leads opposite to infarct

C. Cardiac Biomarkers

• Troponin is the gold standard; high-sensitivity troponin allows earlier "rule-in" or "rule-out"
• Serial troponins should be drawn at 0, 3, and 6 hours

D. Imaging

• Echocardiography: Wall motion abnormalities, ejection fraction assessment, complications (pericardial effusion, VSD, MR)
• Chest X-ray: Cardiomegaly, pulmonary congestion/edema, widened mediastinum (to exclude aortic dissection)
• Coronary angiography: Gold standard for identifying culprit lesion; performed as part of PCI

E. Other Labs

• CBC (leukocytosis expected)
• BMP / renal function (for contrast use, drug dosing)
• Lipid profile
• Blood glucose (stress hyperglycemia common)
• Coagulation studies

6. MEDICAL MANAGEMENT

Immediate Management - MONA (First-Line Emergency)

Critical: In suspected right-sided MI, give IV fluids (preload) instead of nitrates.

Antiplatelet Therapy

• Aspirin 300-325 mg loading, then 75-100 mg daily (lifelong)
• P2Y12 inhibitors (dual antiplatelet therapy - DAPT):
  • Clopidogrel 300-600 mg load then 75 mg daily
  • Ticagrelor 180 mg load then 90 mg BD
  • Prasugrel 60 mg load then 10 mg daily (not for prior TIA/stroke)

Anticoagulation

• Unfractionated heparin (UFH) IV infusion
• Low-molecular-weight heparin (LMWH) - enoxaparin SC
• Fondaparinux (NSTEMI)
• Bivalirudin (during PCI)

Additional Pharmacotherapy

Rate Control in MI with AF

• If AF occurs: IV amiodarone or digoxin for rate control with reduced EF
• IV beta-blocker or non-DHP calcium channel blocker if no LV dysfunction
• Direct-current cardioversion if hemodynamic compromise

7. SURGICAL MANAGEMENT

A. Percutaneous Coronary Intervention (PCI)

• Goal: "Door-to-balloon time" <90 minutes (from first medical contact to balloon inflation)
• Involves coronary angiography followed by balloon angioplasty + stent placement at culprit lesion
• Drug-eluting stents (DES) preferred over bare-metal stents

• Urgent PCI (<2 hours) for very high-risk patients (cardiogenic shock, refractory ischemia)
• Early PCI (<24 hours) for high-risk patients (rising troponin, dynamic ECG changes)
• Can be delayed up to 72 hours in low-risk cases

B. Coronary Artery Bypass Grafting (CABG)

• Left main coronary artery disease
• Triple-vessel disease with reduced EF
• Failed PCI with ongoing ischemia
• Mechanical complications requiring surgical repair
• Anatomy unsuitable for PCI (complex lesions, chronic total occlusions)

C. Intraaortic Balloon Pump (IABP) / Mechanical Circulatory Support

• For cardiogenic shock complicating MI when refractory to medical therapy
• Impella device, ECMO (venoarterial) in refractory cardiogenic shock

D. Surgical Management of Mechanical Complications

8. NURSING MANAGEMENT

A. Assessment (Immediate)

• Chest pain - character, location, radiation, severity (0-10 scale), onset, duration
• Vital signs - BP both arms, HR, RR, temperature, SpO2
• Cardiac monitoring - continuous ECG monitoring; identify arrhythmias
• Level of consciousness and neurological status
• Signs of cardiogenic shock: Hypotension, cool/clammy skin, decreased urine output (<0.5 mL/kg/hr), confusion
• Respiratory status - breath sounds (crackles = pulmonary edema)
• IV access, lab results, previous cardiac history, current medications

B. Nursing Diagnoses (NANDA-aligned)

1. Acute Pain related to myocardial ischemia/necrosis
2. Decreased Cardiac Output related to altered myocardial contractility
3. Activity Intolerance related to imbalance between O2 supply and demand
4. Anxiety/Fear related to actual or perceived threat to life
5. Risk for Ineffective Tissue Perfusion (cardiopulmonary, cerebral, renal) related to decreased cardiac output
6. Risk for Fluid Volume Excess related to decreased cardiac output and sodium/water retention
7. Deficient Knowledge regarding disease, treatment, and lifestyle modifications

C. Nursing Interventions

Immediate / Acute Phase (CCU/ICU)

• Rest: Place patient in complete bed rest; semi-Fowler's position (30-45°) to reduce venous return and dyspnea
• Oxygen: Administer supplemental oxygen; maintain SpO2 ≥94%
• Pain Management:
  • Administer prescribed analgesics (morphine IV)
  • Administer nitroglycerin (sublingual, then IV drip) as ordered
  • Reassess pain every 15-30 minutes; document on pain scale
• Cardiac Monitoring:
  • Continuous 12-lead ECG monitoring
  • Monitor for arrhythmias: VF, VT, AF, heart blocks
  • Keep defibrillator immediately available
  • Report new ST changes or serious arrhythmias immediately
• Medication Administration:
  • Administer aspirin, anticoagulants, beta-blockers, ACE inhibitors, and statins as prescribed
  • Monitor for adverse effects (bleeding with anticoagulants, bradycardia with beta-blockers, hypotension with ACE inhibitors)
• IV Access and Hemodynamic Monitoring:
  • Maintain at least two large-bore IV lines
  • Monitor central venous pressure (CVP), pulmonary artery pressure if indicated
  • Strict intake and output (I&O)
• Prepare for PCI/Thrombolysis: Obtain informed consent, monitor during and after procedure, watch for reperfusion arrhythmias

Ongoing Care

• Vital Signs: Every 15 minutes initially, then every 1-4 hours when stable
• Daily weights: Detect fluid retention (>2 kg/day = notify physician)
• Bowel care: Stool softeners (prevent Valsalva/straining); high-straining raises vagal tone and cardiac workload
• Psychological support: Reassure patient; allow questions; involve family; reduce fear and anxiety

D. Activity Progression (Cardiac Rehabilitation Principles)

E. Patient and Family Education

• Disease process: Explain MI, importance of medication compliance
• Medications: Name, dose, purpose, side effects of each drug (especially aspirin, beta-blockers, statins, ACE inhibitors)
• Warning signs: When to call emergency services (recurrent chest pain, severe dyspnea, syncope)
• Lifestyle modifications:
  • Low-fat, low-sodium, heart-healthy diet (DASH diet principles)
  • Smoking cessation (absolute)
  • Weight reduction if obese
  • Blood pressure and blood sugar control
  • Stress management techniques
  • Gradual return to sexual activity (usually after 4-6 weeks or after stress test clearance)
• Cardiac rehabilitation referral
• Follow-up appointments with cardiologist

F. Monitoring for Complications

Summary Table

• Robbins & Cotran Pathologic Basis of Disease (Pathogenesis, morphology)
• Harrison's Principles of Internal Medicine, 22nd Ed (Clinical presentation, ACS spectrum)
• Ganong's Review of Medical Physiology, 26th Ed (ECG changes mechanism)
• Sabiston Textbook of Surgery (Types, management, surgical treatment)
• Braunwald's Heart Disease (Complications, AF management)
• Rosen's Emergency Medicine (Diagnosis, risk stratification)

Note: Content is consistent with Brunner & Suddarth's Medical-Surgical Nursing and Lewis's Medical-Surgical Nursing principles; those specific titles were not available in the digital library, but all covered material aligns with their standard nursing management frameworks for MI.