NLE Cardiovascular Nursing — Coronary Artery Disease, Angina and Myocardial InfarctionSummary

Coronary artery disease develops through progressive atherosclerotic narrowing of the coronary arteries. The process begins with endothelial injury (caused by hypertension, smoking, or hyperlipidemia), followed by low-density lipoprotein (LDL) deposition in the arterial intima. Inflammatory cells (macrophages, T lymphocytes) infiltrate the region, forming a lipid core surrounded by a fibrous cap—the atheroma or plaque. Over years, the plaque enlarges, narrowing the arterial lumen and reducing coronary blood flow. When plaque ruptures, its thrombogenic core is exposed to circulating platelets, triggering rapid thrombus formation. A partial thrombus causes acute coronary syndrome (unstable angina, NSTEMI); complete occlusion leads to STEMI. The degree of ischemia depends on the rate of vessel occlusion, presence of collateral circulation, and myocardial oxygen demand.

Myocardial ischemia is a temporary, reversible reduction in blood flow and oxygen supply to the heart muscle. When oxygen supply is restored (by rest, vasodilation, or increased collateral flow), the myocardium recovers without permanent damage. This is the basis of angina. In contrast, myocardial infarction (MI) represents irreversible necrosis of myocardial tissue due to prolonged, complete interruption of blood supply—lasting more than 20 to 30 minutes. Once myocytes die, they are replaced by scar tissue, permanently reducing cardiac contractility. The diagnosis of MI is confirmed by elevated cardiac biomarkers (troponin, CK-MB) that leak from necrotic cells into the bloodstream. This distinction is crucial: angina patients have normal biomarkers; MI patients have elevated ones.

Angina pectoris is reversible myocardial ischemia manifesting as substernal chest pain or pressure, often described as 'heavy,' 'squeezing,' or 'crushing.' Pain may radiate to the left arm, jaw, back, or epigastrium. The three main types are: (1) Stable (exertional) angina—predictable, triggered by exertion or emotional stress, lasts 5 to 15 minutes, relieved by rest and sublingual nitroglycerin, with normal cardiac markers and normal or near-normal coronary arteries with significant stenosis; (2) Unstable angina—a form of ACS occurring at rest or with minimal exertion, more frequent and severe than prior angina, not reliably relieved by rest or nitroglycerin, indicating imminent MI; cardiac markers are normal, but coronary angiography shows severe narrowing and possible plaque rupture; (3) Variant (Prinzmetal's) angina—caused by coronary artery spasm rather than atherosclerotic plaque, often occurring at rest or at night, responsive to calcium channel blockers and nitrates. Associated symptoms include diaphoresis, anxiety, and a sense of impending doom. Importantly, atypical presentations (fatigue, dyspnea, indigestion) are common in women, older adults, and diabetics.

Myocardial infarction presents with classic chest pain—severe, crushing, substernal, radiating to the left arm, jaw, neck, or back, lasting longer than 20 to 30 minutes and unrelieved by rest or nitroglycerin. Autonomic signs include profuse diaphoresis (cold, clammy skin), nausea, vomiting, anxiety, and a sense of impending doom or 'heaviness.' Dyspnea (from pulmonary edema), palpitations, and hemodynamic instability (hypotension, tachycardia) may occur. Importantly, atypical presentations are common: women, older adults, and people with diabetes may present with fatigue, shortness of breath, abdominal pain, or back discomfort without classic chest pain. Silent MIs (no symptoms) occur in diabetics due to autonomic neuropathy, delaying diagnosis and worsening outcomes. MI is classified by ECG findings: (1) STEMI (ST-elevation MI)—indicates transmural (full-thickness) infarction with complete coronary occlusion; (2) NSTEMI (non-ST-elevation MI)—indicates subendocardial (partial-thickness) infarction with partial occlusion, showing ST depression or T-wave inversion; (3) Unstable angina—ischemia without necrosis (normal biomarkers).

The diagnosis of acute coronary syndrome relies on a triad: clinical presentation, ECG changes, and cardiac biomarkers. The 12-lead ECG is obtained within 10 minutes of presentation and shows: (1) In STEMI—ST-segment elevation (≥1 mm in contiguous leads) indicating transmural injury; may also show reciprocal ST depression in non-infarcted regions and, later, pathologic Q waves (>0.04 seconds wide and >25% of QRS height); (2) In NSTEMI or unstable angina—ST-segment depression (<1 mm) and/or T-wave inversion indicating subendocardial ischemia; the ST may be isoelectric or normal in early presentations. Cardiac biomarkers confirm myocardial necrosis. Cardiac troponin I and T are the gold standards: highly specific and sensitive, they begin rising within 2 to 4 hours of symptom onset, peak at 24 to 48 hours, and remain elevated for 7 to 14 days. Serial troponins (drawn at presentation, 3 hours, and 6 hours) improve diagnostic accuracy; a rise and/or fall is diagnostic of MI. Creatine kinase-MB (CK-MB) is less specific (found in skeletal muscle) but rises within 3 to 12 hours and falls by 48 to 72 hours, helping date the infarction. Myoglobin is the earliest biomarker (rises within 1 to 2 hours) but is nonspecific. Myeloperoxidase (MPO) and high-sensitivity troponins are emerging markers but not yet routine in Philippine practice. In unstable angina, cardiac biomarkers are normal despite symptoms.

The traditional MONA mnemonic (Morphine, Oxygen, Nitroglycerin, Aspirin) has been refined by current evidence and is a frequent NLE testing point. Modern application: (1) Aspirin—chewable 160 to 325 mg, given as soon as possible (often first) to inhibit platelet aggregation; chewing speeds absorption. It is one of the most evidence-based interventions, reducing mortality and recurrent events. Contraindicated in aspirin allergy or active bleeding. (2) Nitroglycerin—a rapid-acting vasodilator given sublingually (0.3 to 0.4 mg per tablet) every 5 minutes for up to three doses, checking blood pressure before and after each dose. It relieves ischemic chest pain by reducing preload and afterload, decreasing myocardial oxygen demand. Critical contraindications: hypotension (SBP <90 mm Hg), right ventricular infarction (RV-MI causes right-sided preload dependence—nitroglycerin worsens perfusion), inferior MI (often involves RV), and recent phosphodiesterase-5 inhibitor use (sildenafil, tadalafil) within 24 to 48 hours—the combination causes profound, refractory hypotension. (3) Oxygen—given only if the patient is hypoxic (SpO₂ <90 to 94%). Routine oxygen in normoxic patients is no longer recommended and may increase oxidative stress and worsen outcomes. High-flow oxygen can cause coronary vasoconstriction. (4) Morphine—reserved for pain not relieved by nitroglycerin (after 2 to 3 doses). It is a potent analgesic, reduces anxiety, and decreases myocardial oxygen demand through vasodilation and negative inotropic effects. However, overuse is discouraged as it may mask ongoing ischemia and has been associated with worse outcomes in some trials. Monitor for respiratory depression and hypotension.

The goal of STEMI management is rapid reperfusion—reopening the occluded coronary artery to restore blood flow and limit myocardial necrosis. Two strategies are available: (1) Percutaneous coronary intervention (PCI)—angioplasty ± stent placement—is the preferred, first-line reperfusion when available at a capable center. The target door-to-balloon time is <90 minutes (or <120 minutes for transfers). PCI restores TIMI (Thrombolysis in Myocardial Infarction) flow more rapidly and completely than thrombolytics, with lower rates of reinfarction and recurrent ischemia. (2) Thrombolytic (fibrinolytic) therapy—using agents such as alteplase (tPA), reteplase (rPA), tenecteplase (TNK), or streptokinase—dissolves the thrombus. Used when timely PCI is unavailable (e.g., in rural Philippine settings without catheterization labs), the goal is door-to-needle time <30 minutes, ideally within 6 hours of symptom onset (window extends to 12 hours if symptoms persist). Thrombolytics are contraindicated in NSTEMI (no complete occlusion to lyse). Streptokinase is less expensive and available in Philippine settings but carries higher risk of allergy and resistance if prior exposure. Alteplase and tenecteplase are more fibrin-specific (lower rates of systemic fibrinolysis) and preferred if available. Nursing considerations for thrombolytics include: monitor for bleeding (the major risk, including intracranial hemorrhage), assess neurologic status frequently (headache, confusion, focal deficits may indicate hemorrhagic stroke), obtain baseline PT/INR and aPTT, minimize venipunctures and invasive procedures, hold pressure on venipuncture sites (5 to 10 minutes), avoid intramuscular injections, monitor for reperfusion signs (relief of chest pain, return of ST segment toward baseline, sudden ventricular dysrhythmias indicating restored flow), and educate on bleeding precautions (no NSAIDs, use soft toothbrush, avoid activities with injury risk).

Beyond MONA, ACS management includes several drug classes: (1) Antiplatelets—aspirin (initial loading 160 to 325 mg, then 81 mg daily) plus a P2Y12 inhibitor (clopidogrel [Plavix] 600 mg loading, then 75 mg daily; ticagrelor 180 mg loading, then 90 mg twice daily; prasugrel 60 mg loading, then 5 mg daily if <60 kg). Dual antiplatelet therapy (DAPT) prevents stent thrombosis and reduces recurrent events; duration is typically 12 months. (2) Anticoagulants—unfractionated heparin (bolus 5,000 to 10,000 units IV, then infusion 1,000 units/hour, titrated to aPTT 50 to 70 seconds) or low-molecular-weight enoxaparin (LMWH, 30 mg IV bolus then 1 mg/kg subcutaneously every 12 hours, or weight-based dosing for renal function). These prevent clot propagation and are given for 48 hours to several days depending on strategy. Bivalirudin (a direct thrombin inhibitor) is an alternative in PCI. (3) Beta-blockers—metoprolol (25 to 50 mg orally or 5 mg IV every 5 minutes up to 15 mg, then switch to oral) reduce heart rate, blood pressure, and myocardial oxygen demand; hold if HR <60 or SBP <90 mm Hg. (4) ACE inhibitors—lisinopril, enalapril (started 2.5 to 5 mg daily after hemodynamic stabilization)—reduce afterload, prevent ventricular remodeling, and improve survival; monitor for persistent dry cough, hyperkalemia, and hypotension; contraindicated in hypotension or bilateral renal artery stenosis. (5) Statins—atorvastatin, rosuvastatin (started at high intensity, e.g., 80 mg daily)—lower LDL and stabilize plaque; monitor for muscle pain (myalgia/rhabdomyolysis) and liver enzyme elevation. (6) Other agents: calcium channel blockers (diltiazem, verapamil) if beta-blockers contraindicated; ezetimibe to further lower LDL; inotropic agents (dobutamine) if cardiogenic shock; diuretics and vasodilators for pulmonary edema.

Nursing care in ACS is organized by Maslow's hierarchy and the acuity of ischemia. The first priority is to address physiologic safety needs (restoring oxygenation and perfusion) and prevent death from dysrhythmias. Key interventions: (1) Position the patient upright (semi-Fowler's or high Fowler's) to reduce anxiety, decrease myocardial oxygen demand, and ease breathing; provide reassurance and presence to reduce sympathetic activation. (2) Obtain a 12-lead ECG within 10 minutes of presentation and give a copy to the physician immediately; any ST elevation must be communicated urgently. (3) Establish two large-bore IV lines and draw labs: CBC, comprehensive metabolic panel (to assess renal function for drug dosing, electrolytes, glucose), PT/INR, aPTT, cardiac troponin, CK-MB, myoglobin, lipid panel, and blood glucose. (4) Administer aspirin (chewed, 160 to 325 mg) and nitroglycerin (sublingual) as ordered; give oxygen only if SpO₂ <90%; do not delay other interventions to place oxygen. (5) Establish continuous cardiac monitoring with pulse oximetry; dysrhythmias, especially ventricular fibrillation, are the leading cause of death in the first hours—defibrillator pads must be applied and the defibrillator readily available. (6) Maintain strict bed rest to minimize cardiac workload. (7) Provide pain assessment every 5 to 15 minutes; if nitroglycerin does not relieve pain after 2 to 3 doses, notify the physician for morphine or other analgesics and prepare for urgent reperfusion. (8) Monitor vital signs continuously and assess for hypotension before each nitroglycerin dose; hold if SBP <90 mm Hg. (9) Prepare for emergency procedures: ensure IV access is adequate, draw baseline labs, and have emergency equipment (crash cart, defibrillator, emergency medications) immediately available. (10) Provide brief, clear explanations to reduce anxiety; allow a support person if feasible. (11) Obtain a focused history (time of symptom onset, risk factors, current medications, allergies) to inform reperfusion decisions (thrombolytic contraindications).

Myocardial infarction carries significant risk of life-threatening complications, categorized by timing: (1) Immediate (first hours): Dysrhythmias are the leading cause of death in the acute phase. Ventricular fibrillation (VF) is the most lethal; other common dysrhythmias include ventricular tachycardia (VT), accelerated idioventricular rhythm (AIVR, a reperfusion dysrhythmia), bradycardia (from vagal stimulation in inferior MI), and atrial fibrillation. Continuous monitoring and defibrillator availability are essential. (2) Early (hours to days): Heart failure and acute pulmonary edema result from reduced contractility and elevated filling pressures; managed with diuretics, vasodilators, oxygen, and inotropes if needed. Cardiogenic shock (systolic BP <90 mm Hg despite adequate filling, with evidence of hypoperfusion: altered mental status, oliguria, cool extremities) occurs in 5 to 10% of acute MI and carries high mortality; managed with IV fluids (in RV-MI), vasopressors, and mechanical support (intra-aortic balloon pump, Impella). Right ventricular infarction (complicating 30 to 50% of inferior MIs) causes hypotension and requires careful fluid management (avoid diuretics, give IV fluids cautiously). Pericarditis (inflammation of the pericardium) presents with pleuritic chest pain (worse with inspiration, lying flat) and is distinguished from recurrent ischemia by pain character and ECG (diffuse ST elevation and PR depression); managed with NSAIDs or colchicine. (3) Subacute (days to weeks): Mechanical complications—papillary muscle rupture (causes acute mitral regurgitation and pulmonary edema), ventricular septal defect (VSD, causes left-to-right shunt and acute pulmonary edema), and cardiac rupture (free wall rupture is catastrophic)—occur in <1% but are life-threatening; managed with urgent surgery. Ventricular aneurysm (dyskinetic outpouching of infarcted myocardium) may lead to dysrhythmias, heart failure, or thromboembolism; managed medically or surgically. (4) Late (weeks to months): Dressler's syndrome is a post-MI pericarditis with pleurisy, occurring weeks after MI; managed with NSAIDs or corticosteroids. Left ventricular remodeling and progressive heart failure are long-term consequences of large infarcts.

The distinction between STEMI and NSTEMI is fundamental to management strategy and urgency. STEMI (ST-elevation MI) reflects complete coronary artery occlusion with transmural (full-thickness) myocardial necrosis. ECG shows ST-segment elevation ≥1 mm in two contiguous leads, often with reciprocal ST depression. Troponin is elevated. Management is urgent and revolves around immediate reperfusion: PCI (preferred, door-to-balloon <90 minutes) or thrombolytics (door-to-needle <30 minutes, within 6 to 12 hours). The goal is to restore TIMI 3 flow (normal coronary flow) as rapidly as possible to minimize infarct size. Aspirin, loading dose of P2Y12 inhibitor (clopidogrel, ticagrelor, prasugrel), anticoagulation, beta-blockers, and ACE inhibitors are given. NSTEMI (non-ST-elevation MI) reflects partial coronary occlusion with subendocardial (partial-thickness) necrosis. ECG shows ST-segment depression <1 mm and/or T-wave inversion; ST may be normal early. Troponin is elevated (confirming MI despite no ST elevation). Thrombolytics are not used (there is no complete occlusion to lyse). Management is initially conservative with dual antiplatelets (aspirin + P2Y12 inhibitor), anticoagulation, beta-blockers, and nitrates. The timing of coronary angiography is risk-stratified: high-risk patients (ongoing ischemia, hemodynamic instability, ventricular dysrhythmias, elevated troponin) undergo urgent or early angiography (within 24 hours); lower-risk patients may have delayed angiography. Unstable angina is similar to NSTEMI in ECG findings and management but differs in that troponin is normal (no myocardial necrosis).

Cardiac rehabilitation is a structured, evidence-based program aimed at recovery, risk factor modification, and prevention of recurrent events. It spans phases: (1) In-hospital phase—begins immediately after MI or intervention, including early mobilization (progressing from bed rest to sitting, standing, walking), education on medications and warning signs, and psychological support. (2) Early outpatient phase (weeks 2 to 8 post-MI)—supervised exercise program starting with low-intensity walking (10 to 15 minutes), gradually increasing duration and intensity, plus group education on diet, medications, stress management, and return to activities. (3) Late/maintenance phase—long-term exercise program (at least 150 minutes/week of moderate activity) and ongoing risk factor management. Goals are to restore functional capacity, prevent reinfarction, reduce mortality, and improve quality of life. Key teaching points for patients: (1) Medication adherence—emphasize DAPT (aspirin + clopidogrel/ticagrelor/prasugrel) for 12 months post-PCI or post-MI, not stopping early (risk of stent thrombosis and reinfarction); beta-blockers, ACE inhibitors, statins indefinitely. (2) Nitroglycerin use—sit down, place one tablet under the tongue (not swallowed), and if pain persists after 5 minutes, call emergency services; may repeat every 5 minutes up to three doses total; if three doses do not relieve pain, assume MI and seek urgent care (do not drive self). Store tablets in a dark, airtight, cool container (away from heat and light); discard after 6 months (potency diminishes). (3) Warning signs—chest pain/discomfort, dyspnea, palpitations, syncope, diaphoresis; seek immediate care if pain lasts >5 minutes and is not relieved by rest or nitroglycerin. (4) Lifestyle modification: smoking cessation (zero tolerance, no secondhand smoke exposure), low-sodium diet (Philippine DOH goal <5 g/day), low saturated-fat diet (align with Philippine Dietary Guidelines), regular aerobic exercise (150 min/week moderate or 75 min/week vigorous), stress management (yoga, meditation, counseling if needed), and weight management (BMI 18.5 to 24.9 kg/m²). (5) Psychosocial support—address depression (common post-MI), sexual activity (safe once able to climb two flights of stairs without symptoms; may use phosphodiesterase inhibitors if ejection fraction adequate), and return to work (discuss with provider). (6) Diabetes and hypertension control—tight glycemic control (A1C <7%) and BP <130/80 mm Hg reduce reinfarction risk. (7) Driving restrictions—avoid driving for at least 2 weeks post-MI, longer if arrhythmias, heart failure, or syncope occurred; discuss return-to-work timeline with employer and provider.