NLE Cardiovascular Nursing — Coronary Artery Disease, Angina and Myocardial InfarctionStudy Notes

Coronary artery disease is the progressive narrowing of the coronary arteries, most commonly caused by atherosclerosis—the buildup of fatty, fibrous plaque (atheroma) within the arterial intima. This process occurs over years and involves multiple pathophysiologic stages: endothelial injury (from hypertension, hyperlipidemia, smoking, and inflammation), lipid deposition (particularly low-density lipoprotein [LDL]), inflammatory cell infiltration, and fibrous cap formation. As plaque accumulates, the arterial lumen narrows, reducing blood flow to the myocardium. When myocardial oxygen demand exceeds oxygen supply—such as during exertion or stress—reversible myocardial ischemia develops, manifesting as angina. The critical transition to acute coronary syndrome (ACS) occurs when an atherosclerotic plaque ruptures, exposing thrombogenic material and triggering platelet aggregation and thrombus formation. This thrombus may partially or completely occlude the coronary artery, leading to myocardial infarction if the occlusion is sustained and collateral circulation is inadequate. The duration and completeness of the occlusion determine whether myocardial necrosis (death) occurs, making 'time is muscle' a central principle in ACS management. In the Philippine context, where many patients present late to healthcare facilities, understanding these pathophysiologic mechanisms underscores the urgency of rapid assessment, ECG interpretation, and reperfusion decision-making.

Understanding CAD risk factors is essential for conducting nursing assessments and patient education aligned with the DOH PhilPEN (Philippine Health Equity Network) screening priorities. Non-modifiable risk factors—age, male sex, family history, and ethnicity—provide context but cannot be changed; however, their presence elevates the urgency of controlling modifiable risk factors. Modifiable risk factors are the primary targets of nursing intervention and patient teaching: hypertension (the leading modifiable risk factor in the Philippines), dyslipidemia (high LDL, low HDL), diabetes mellitus (increasingly prevalent in Filipino populations), cigarette smoking, obesity, physical inactivity, stress, and poor dietary habits. The presence of multiple risk factors has a synergistic (multiplicative, not additive) effect on CAD risk. For example, a 50-year-old male with hypertension, smoking, and prediabetes has significantly greater risk than the sum of individual risks. Filipino nurses must incorporate culturally appropriate patient teaching—addressing dietary patterns (high sodium intake, coconut-based foods high in saturated fat), physical activity barriers (urbanization, long work hours), and stress management specific to Filipino communities. According to RA 9173, nurses are responsible for health promotion and disease prevention; therefore, identifying modifiable risk factors during every patient encounter and providing tailored teaching is a core professional duty.

Angina pectoris is chest pain or discomfort caused by transient reversible myocardial ischemia—the heart muscle is not permanently damaged, and cardiac biomarkers remain normal. Patients typically describe substernal pressure, tightness, squeezing, heaviness, or burning that may radiate to the left arm, jaw, neck, shoulders, or back. Associated symptoms often include dyspnea, nausea, diaphoresis, and anxiety. The key feature distinguishing angina from MI is that myocardial necrosis does not occur; therefore, troponin and creatine kinase-MB (CK-MB) remain within normal limits. Angina is classified into three main types, each with distinct clinical features and management implications. (1) Stable (exertional) angina is predictable, triggered by physical exertion (climbing stairs, walking uphill), emotional stress, or cold exposure. Pain typically lasts 5–15 minutes and is reliably relieved by rest and sublingual nitroglycerin. It signals significant stenosis (usually >70%) of a major coronary artery but reflects a chronic, compensated state. (2) Unstable angina is a form of acute coronary syndrome characterized by new-onset chest pain, pain at rest, or pain that is more frequent, severe, and prolonged than the patient's usual stable pattern. Unstable angina is not reliably relieved by rest or nitroglycerin. It reflects plaque rupture with partial thrombosis or microembolization, signaling imminent MI risk. Cardiac biomarkers are negative (distinguishing it from NSTEMI), but the ECG may show ST-segment depression or T-wave inversion. Unstable angina requires urgent hospitalization, intensive monitoring, and aggressive medical therapy. (3) Variant (Prinzmetal's) angina is caused by coronary artery vasospasm, often occurring at rest or during sleep and typically at night. Patients may have normal coronary arteries on angiography; the underlying pathology is abnormal endothelial vasoreactivity. Variant angina is often responsive to calcium channel blockers and long-acting nitrates. Understanding these distinctions is critical for NLE success because examination items test the ability to differentiate clinical presentations and appropriate management priorities. In Filipino nursing practice, many patients present late with unstable symptoms, requiring rapid triage, ECG, and risk stratification.

Myocardial infarction is the irreversible death (necrosis) of myocardial tissue resulting from prolonged, complete interruption of coronary blood flow, usually due to thrombotic occlusion. Unlike angina, where ischemia is reversible, MI involves permanent myocardial damage. The underlying mechanism is typically plaque rupture with superimposed thrombus that completely or near-completely blocks a coronary artery. The extent and location of infarction depend on the vessel occluded (left anterior descending, left circumflex, or right coronary artery), the presence and degree of collateral circulation, and the duration of occlusion before reperfusion. Myocardial necrosis begins within minutes of complete occlusion and progresses from the subendocardium (innermost layer) to the subepicardium (outermost layer). This process is why early reperfusion within the first few hours can salvage myocardium and reduce the extent of infarction—hence the crucial concept 'time is muscle.' MI is classified as (1) STEMI (ST-elevation MI), indicating transmural (full-thickness) infarction with complete coronary occlusion, or (2) NSTEMI (non-ST-elevation MI), indicating subendocardial or partial-thickness infarction, usually from partial coronary occlusion or transient occlusion with reflow. Clinical presentation of MI classically includes severe, crushing, substernal chest pain lasting longer than 20 minutes and not relieved by rest or nitroglycerin. The pain often radiates to the left arm, jaw, neck, shoulders, or back. Associated autonomic symptoms are prominent: diaphoresis (cold, clammy skin), nausea and vomiting, palpitations, dyspnea, and a sense of impending doom or severe anxiety. However, atypical presentations are extremely common and often underrecognized, particularly in vulnerable populations. Women, older adults, and patients with diabetes frequently present with fatigue, weakness, shortness of breath, epigastric discomfort (mistaken for indigestion), back pain, or jaw pain rather than classic chest pain. Diabetic patients may experience 'silent MI'—infarction without significant pain—due to diabetic neuropathy affecting pain perception. These atypical presentations delay diagnosis and treatment, making nurse awareness critical for timely triage. In the Philippine context, where many patients present after a significant delay from symptom onset, recognizing atypical presentations is essential. Diagnosis of MI requires integration of clinical presentation, ECG findings, and cardiac biomarkers. The 12-lead ECG is obtained immediately (target within 10 minutes of presentation) and provides crucial information: in STEMI, the ECG shows ST-segment elevation (≥1 mm in two contiguous leads) in the distribution of the occluded artery; in NSTEMI, the ECG may show ST-segment depression, T-wave inversion, or may be nondiagnostic. Pathologic Q waves (deep, wide waves) develop over hours to days following MI and indicate transmural infarction. Cardiac biomarkers confirm myocardial necrosis. Troponin (cardiac troponin I or T) is the most specific and sensitive marker for myocardial injury; it begins to rise 3–4 hours after infarction, peaks at 24–48 hours, and remains elevated for 7–14 days. Serial troponin measurements (typically at 0, 3, and 6 hours) improve diagnostic sensitivity. CK-MB (creatine kinase-myocardial band) is less specific than troponin but rises earlier (1–3 hours), peaks at 24–48 hours, and clears by 72 hours; it is useful for detecting reinfarction. Myoglobin rises earliest (within 1 hour) but lacks specificity for cardiac muscle. The diagnosis of MI requires both ECG evidence of ischemia (ST elevation, ST depression, or T-wave changes) and elevated cardiac biomarkers.

Acute coronary syndrome (ACS) is an umbrella term encompassing unstable angina, NSTEMI, and STEMI. The unifying feature is acute myocardial ischemia, usually from plaque rupture and thrombosis. Immediate management prioritizes pain relief, restoration of myocardial perfusion, prevention of clot propagation, and monitoring for life-threatening complications. The traditional mnemonic 'MONA' (Morphine, Oxygen, Nitroglycerin, Aspirin) has been refined by contemporary evidence, and understanding the modern nuance is essential for NLE success. Current best practice emphasizes aspirin and reperfusion as the primary early priorities, with oxygen reserved for hypoxic patients and morphine reserved for pain unrelieved by nitroglycerin. (1) ASPIRIN: Administer chewable aspirin 160–325 mg (typically 325 mg) as soon as possible—this is often the first priority drug in ACS. Chewing accelerates absorption compared to swallowing. Aspirin irreversibly inhibits platelet cyclooxygenase, preventing thromboxane A2 synthesis and blocking platelet aggregation. Aspirin reduces mortality by approximately 20–30% in ACS and is a cornerstone of acute and long-term management. There are no absolute contraindications to a single dose of aspirin in the acute setting except true anaphylactic allergy. (2) NITROGLYCERIN: Sublingual nitroglycerin (0.3–0.6 mg per tablet) is a vasodilator that relieves ischemic chest pain by reducing preload and myocardial oxygen demand and by dilating epicardial coronary arteries. Give one tablet sublingually and repeat every 5 minutes for up to 3 doses, checking blood pressure before each dose. Nitroglycerin requires systolic BP ≥90 mmHg to be given safely. CRITICAL CONTRAINDICATIONS include: hypotension (SBP <90 mmHg), right ventricular infarction (usually inferior MI), and recent use of phosphodiesterase-5 inhibitors (sildenafil [Viagra], tadalafil [Cialis]). Sildenafil combined with nitrates causes profound vasodilation and severe hypotension—a potentially fatal interaction. Always ask about recent use of ED medications. In right ventricular infarction (recognized by ST elevation in right-sided ECG leads V4R-V6R), the right ventricle is dependent on preload; nitrates reduce preload and can cause cardiogenic shock. Nitroglycerin may also be given as an IV infusion for ongoing ischemia and hypertension. (3) OXYGEN: Modern evidence no longer routinely recommends oxygen for all ACS patients. Oxygen is given ONLY if the patient is hypoxic—oxygen saturation below approximately 90–94%. Routine oxygen in normoxic patients may increase myocardial oxygen demand paradoxically and is associated with worse outcomes in some studies. Therefore, check oxygen saturation first; if SpO₂ ≥94%, withhold supplemental oxygen. If hypoxic, deliver oxygen via nasal cannula (2–4 L/min) to target SpO₂ 94–98%. This represents a significant shift from older 'give O₂ to all MI patients' teaching. (4) MORPHINE: Morphine is a powerful opioid that relieves pain, reduces anxiety, and decreases myocardial oxygen demand through vasodilation and reduced preload. However, modern guidelines reserve morphine for pain unrelieved by nitroglycerin (e.g., pain persisting after 2–3 nitroglycerin doses). Morphine may mask ongoing ischemia and has been associated with worse outcomes in some analyses when used early or excessively. Typical dose is 2–4 mg IV, repeated every 5–15 minutes as needed, titrated to pain relief. Monitor for respiratory depression, hypotension, and bradycardia. In the Philippine setting, where morphine availability and nursing comfort with opioid administration may vary by facility, understanding the indications and safety profile is important. The practical sequence in modern ACS management generally prioritizes: (1) Aspirin (chewed) and IV access/ECG, (2) Assessment for reperfusion eligibility and rapid referral for PCI or thrombolytics, (3) Nitroglycerin for pain and hypertension (with caution regarding contraindications), (4) Oxygen only if hypoxic, and (5) Morphine if pain persists despite nitroglycerin.

The primary goal in acute STEMI is rapid reperfusion—reopening the occluded coronary artery as quickly as possible to restore blood flow and salvage myocardium. 'Door-to-balloon time' (time from first medical contact to opening the vessel via PCI) should be ≤90 minutes; 'door-to-needle time' (time to initiate thrombolytic therapy) should be ≤30 minutes. These metrics are critical because myocardial necrosis progresses from moment zero, and every minute counts. Two main reperfusion strategies are available: percutaneous coronary intervention (PCI) and thrombolytic (fibrinolytic) therapy. PCI is the preferred, gold-standard reperfusion strategy when available at a capable center with 24/7 interventional cardiology services. PCI involves coronary angiography to identify the occluded vessel, followed by percutaneous transluminal angioplasty (PTCA) to mechanically open the artery, and placement of an intracoronary stent (bare-metal or drug-eluting) to maintain vessel patency. PCI has higher success rates (>90% vessel patency), lower rates of reinfarction and recurrent ischemia, and lower bleeding risk compared to thrombolytics. The target door-to-balloon time is <90 minutes from first medical contact. In the Philippines, PCI capability is concentrated in major tertiary centers (e.g., Philippine Heart Center, major private hospitals in Metro Manila and key regional centers). For patients presenting to hospitals without PCI capability, transfer to a PCI center is arranged if door-to-balloon time can be achieved within 120 minutes from first medical contact; otherwise, thrombolytics are given at the presenting facility. Thrombolytic therapy involves IV administration of fibrinolytic agents that dissolve the thrombus by converting plasminogen to plasmin, which degrades fibrin. Common agents include alteplase (rt-PA, Activase), reteplase (Retavase), tenecteplase (TNKase), and streptokinase (used less commonly now). Thrombolytics are administered when PCI is not available or when transfer time exceeds the recommended window. The goal door-to-needle time is ≤30 minutes, and thrombolytics are effective if administered within 6–12 hours of symptom onset (ideally within the first 3 hours). Success rates are 50–80%, with higher rates of reinfarction and recurrent ischemia compared to PCI. The major risk of thrombolytic therapy is bleeding, including life-threatening intracranial hemorrhage (ICH). Absolute contraindications to thrombolytics include: (1) Active internal bleeding, (2) History of hemorrhagic stroke or intracranial hemorrhage, (3) Recent (within 3 months) ischemic stroke, (4) Intracranial neoplasm or structural abnormalities, (5) Recent major surgery, trauma, or head injury (within 2–4 weeks), (6) Severe uncontrolled hypertension (SBP >180 mmHg or DBP >110 mmHg), and (7) Known bleeding disorder or anticoagulation that cannot be reversed. Relative contraindications (requiring risk-benefit analysis) include: prolonged CPR, recent minor surgery, diabetic retinopathy, and aortic dissection. Nursing assessment and documentation of contraindications is critical; nurses often are the first to identify historical red flags. Following thrombolytic administration, monitor closely for reperfusion signs (relief of chest pain, normalization of ST segments on repeat ECG, return of reperfusion dysrhythmias such as accelerated idioventricular rhythm [AIVR]) and bleeding complications (oozing from IV sites, hematuria, hemoptysis, sudden severe headache suggesting ICH, abdominal pain suggesting intra-abdominal hemorrhage). Minimize invasive procedures; consolidate venipunctures; avoid intramuscular injections; monitor CBC for anemia. If bleeding occurs, alert the physician immediately; reversal agents or blood products may be needed. In the Philippine healthcare context, where PCI availability is limited outside major urban centers and many patients present late, understanding thrombolytic protocols, screening for contraindications, and nursing monitoring for complications are essential competencies.

Beyond the initial 'MONA' framework, ACS management involves multiple adjunct medications that reduce thrombosis, prevent clot propagation, reduce myocardial oxygen demand, stabilize ischemic myocardium, and modify underlying atherosclerotic disease. Understanding the indications, doses, mechanisms, and nursing monitoring for these drugs is essential for NLE preparation and clinical practice. DUAL ANTIPLATELET THERAPY (DAPT): Aspirin is combined with a P2Y12 inhibitor to provide dual antiplatelet effects. P2Y12 inhibitors include clopidogrel (Plavix), ticagrelor (Brilinta), and prasugrel (Effient). These drugs irreversibly inhibit adenosine diphosphate (ADP)-mediated platelet activation. Loading doses are given acutely (e.g., clopidogrel 600 mg or ticagrelor 180 mg), followed by maintenance doses (clopidogrel 75 mg daily, ticagrelor 60 mg BID). DAPT significantly reduces stent thrombosis and recurrent ischemic events. Nursing consideration: assess for bleeding risk; counsel patients on medication adherence (premature discontinuation increases stent thrombosis risk). ANTICOAGULATION: Unfractionated heparin (UFH) is given as an IV bolus (60–70 units/kg, typically 5,000–7,000 units) followed by continuous infusion (15 units/kg/hour, typically 1,000–1,200 units/hour), with aPTT monitoring targeting 1.5–2.5 times control (typically 50–70 seconds). UFH prevents thrombus propagation and is used during and after PCI. Alternatively, enoxaparin (low-molecular-weight heparin [LMWH]) is given as an IV bolus (30 mg) followed by subcutaneous injections (1 mg/kg Q12H). LMWH has more predictable pharmacokinetics and does not require aPTT monitoring. Nursing considerations: monitor for bleeding; maintain IV patency; check aPTT for UFH; assess for heparin-induced thrombocytopenia (HIT) if platelet count drops >50% or thrombotic events occur. BETA-BLOCKERS: Metoprolol, atenolol, and carvedilol reduce heart rate, blood pressure, and myocardial oxygen demand, thereby reducing infarct size and mortality. Beta-blockers are initiated early in ACS (IV metoprolol 5 mg every 2–5 minutes × 3 doses, then oral) and continued long-term. Contraindications include bradycardia (HR <50), hypotension (SBP <90), and decompensated heart failure. Nursing consideration: assess HR and BP before each dose; educate patients on adherence and not stopping abruptly. ACE INHIBITORS: Lisinopril, enalapril, and ramipril reduce afterload, decrease ventricular remodeling, and improve survival post-MI, especially in anterior MI with reduced ejection fraction. ACE inhibitors are initiated after hemodynamic stability is achieved and are continued long-term. Nursing considerations: monitor for hypotension, hyperkalemia (check K+ regularly), and persistent cough (common side effect). Contraindicated in bilateral renal artery stenosis and pregnancy. STATINS: High-intensity statins (atorvastatin 80 mg daily, rosuvastatin 20–40 mg daily) lower LDL cholesterol, stabilize atherosclerotic plaques, reduce inflammation, and improve outcomes. Statins are initiated immediately in ACS and continued indefinitely. Nursing considerations: monitor for muscle pain (myopathy/rhabdomyolysis); check liver enzymes and CK if symptoms occur; educate on adherence. In the Philippines, statin affordability and availability vary; nurses should advocate for access to generic statins where available. CALCIUM CHANNEL BLOCKERS: Diltiazem and verapamil reduce heart rate and blood pressure; they are used particularly in variant angina (vasospasm) and when beta-blockers are contraindicated. They should not be used in the immediate post-MI period if left ventricular dysfunction is present. NITRATES: Long-acting nitrates (isosorbide mononitrate, isosorbide dinitrate) are used for angina prevention and symptom relief. Sublingual nitroglycerin is for acute relief. Nursing consideration: educate on nitrate tolerance (develops with continuous exposure; mitigated by a nitrate-free interval daily). Additional agents used in ACS include glycoprotein IIb/IIIa inhibitors (abciximab, eptifibatide, tirofiban) for high-risk PCI patients and newer anticoagulants such as apixaban (Eliquat) in select post-MI patients. The specific medication regimen depends on clinical presentation (STEMI vs. NSTEMI), reperfusion strategy, and comorbidities.

In acute coronary syndrome, nursing management is guided by Maslow's hierarchy of needs and the nursing process, prioritizing patient safety, pain relief, and hemodynamic stability. The immediate priorities upon arrival are airway, breathing, circulation (ABCs); pain assessment and relief; and rapid diagnostic workup. Using NANDA-I nursing diagnosis frameworks, common diagnoses in ACS include: (1) Acute pain related to myocardial ischemia, (2) Ineffective tissue perfusion (cardiac) related to coronary artery occlusion, (3) Risk for decreased cardiac output related to myocardial necrosis and dysrhythmias, (4) Anxiety related to threat of death and pain, and (5) Deficient knowledge related to disease process and lifestyle modifications. ASSESSMENT: Upon presentation, rapidly assess the patient for: chest pain (location, quality, radiation, onset, duration, severity using 0–10 pain scale, and aggravating/relieving factors); vital signs (heart rate, blood pressure, respiratory rate, temperature, oxygen saturation); cardiac rhythm via continuous monitoring; peripheral perfusion (skin temperature, color, capillary refill, peripheral pulses); signs of heart failure (rales, JVD, edema); and psychological state (anxiety, fear, sense of impending doom). Document the time of symptom onset, as this is critical for reperfusion decisions. Obtain a comprehensive history including prior cardiac history, medications (especially ED drugs), allergies, and comorbidities. POSITION AND ENVIRONMENT: Position the patient upright or semi-Fowler's (if hemodynamically stable) to optimize respiratory effort and reduce preload, thereby decreasing dyspnea and myocardial oxygen demand. Provide a calm, quiet environment to reduce anxiety and sympathetic stimulation. Family presence (if available and patient consents) often provides psychological support. AIRWAY AND OXYGENATION: Assess airway patency. Deliver oxygen only if SpO₂ <90–94%; target SpO₂ 94–98% (not >98%, as hyperoxia may increase myocardial oxygen demand). Apply pulse oximetry and monitor continuously. Be ready for airway management if respiratory status deteriorates. VASCULAR ACCESS AND BASELINE LABS: Establish two large-bore IV lines for medication and fluid administration. Draw labs immediately: troponin (high-sensitivity if available), CK-MB, CBC, PT/INR, aPTT, electrolytes (especially potassium and creatinine), glucose, lipid panel, and blood cultures if fever is present. Blood cultures may be drawn if sepsis is suspected, though infection is not the usual cause of MI. In the Philippines, where some rural facilities have limited lab capability, consider transfer requirements if labs cannot be processed on-site. 12-LEAD ECG: Obtain a 12-lead ECG within 10 minutes of presentation. This is often done by paramedics during transport or by nurses at triage in the emergency department. The ECG is placed on the patient's chart and interpreted by the physician to determine STEMI vs. NSTEMI. Serial ECGs (e.g., every 5–10 minutes if presentation is within 30 minutes) may reveal evolving infarction. PAIN MANAGEMENT: Assess pain on a 0–10 scale and reassess after each intervention. Administer medications as ordered (nitroglycerin, morphine) and document response. Non-pharmacologic measures (positioning, reassurance, guided breathing, family presence) complement medication. Monitor for adequate pain control; unrelieved pain suggests ongoing ischemia and worsening prognosis. CONTINUOUS CARDIAC MONITORING: Place the patient on cardiac monitoring immediately and maintain throughout hospitalization. Dysrhythmias, especially ventricular fibrillation (VF), are the leading cause of death in the first hours of MI. Assess rhythm continuously; recognize and respond to: (1) Ventricular fibrillation (VF) — immediately initiate ACLS (CPR and defibrillation), (2) Pulseless ventricular tachycardia (pVT) — initiate ACLS, (3) Accelerated idioventricular rhythm (AIVR) — a benign reperfusion dysrhythmia; do not treat unless symptomatic, (4) Bradycardia and heart blocks — may require atropine or pacing in inferior MI, and (5) Atrial fibrillation — common in first 24 hours; may require rate control or anticoagulation. Maintain defibrillator at bedside and ensure staff can respond within 1–2 minutes. FLUID AND HEMODYNAMIC MANAGEMENT: Monitor blood pressure and urine output. In uncomplicated MI, cautious fluid restriction may be appropriate to prevent pulmonary edema; however, in right ventricular infarction or cardiogenic shock, IV fluids may be needed. Insert a Foley catheter to monitor urine output (target ≥0.5 mL/kg/hour) and to assess kidney perfusion. In some cases, invasive monitoring (pulmonary artery catheter or non-invasive hemodynamic monitoring) may guide fluid and medication titration. BED REST: Initially, strict bed rest reduces myocardial workload. As the patient stabilizes (usually after 24–48 hours without complications), gradual mobilization is encouraged. Progressive activity (bedside sitting, standing, walking) is guided by patient tolerance and physician orders. This is a key component of cardiac rehabilitation. ANXIETY AND PSYCHOLOGICAL SUPPORT: Anxiety increases sympathetic stimulation and myocardial oxygen demand, worsening ischemia. Provide reassurance, explain procedures clearly, answer questions honestly, and maintain a calm demeanor. Involve the patient's family or support persons. Some facilities offer chaplain or psychosocial services. Anxiolytics (lorazepam) may be prescribed; ensure they do not mask pain or hemodynamic deterioration. COMPLICATIONS MONITORING: Continuously assess for complications: (1) Cardiogenic shock (hypotension, cool extremities, altered mental status, oliguria) — requires aggressive management with medications (inotropes, vasopressors) and possibly mechanical support, (2) Acute heart failure/pulmonary edema (rales, JVD, orthopnea) — managed with diuretics, nitrates, oxygen, and fluid restriction, (3) Papillary muscle rupture — causes acute severe mitral regurgitation with pulmonary edema and new holosystolic murmur; may require emergency surgery, (4) Ventricular free wall rupture — causes acute hemopericardium, pericardial tamponade, and cardiovascular collapse; requires emergency surgical repair, (5) Pericarditis (pleuritic chest pain, pericardial friction rub) — may develop days post-MI; managed with NSAIDs or colchicine, (6) Ventricular aneurysm — a weakened, aneurysmal segment of infarcted myocardium; increases thrombosis risk; managed anticoagulation, and (7) Dressler's syndrome (post-MI pericarditis with fever, pleuritis, and pericardial effusion, weeks to months post-MI) — autoimmune phenomenon managed with NSAIDs or corticosteroids. Early recognition and communication of complications are critical nursing responsibilities. DOCUMENTATION: Document comprehensively: time of arrival, symptom onset (critical for reperfusion decisions), vital signs at regular intervals, ECG findings, lab results, medications given (times and doses), patient responses (pain, vital sign changes), and any complications observed. In the Philippine context, where nursing documentation standards may vary by facility, ensure charting is clear, timely, and legible, supporting continuity of care and legal protection.

Cardiac rehabilitation is a comprehensive, evidence-based program of structured exercise, patient education, and risk factor modification designed to restore the patient's physical and psychological functioning post-MI and prevent recurrent cardiac events. In the Philippines, cardiac rehabilitation is increasingly recognized as a standard of care, though access varies by facility and socioeconomic status. RA 9173 emphasizes nurses' role in health promotion and patient teaching; therefore, initiating rehabilitation education early and providing culturally relevant guidance is a core nursing responsibility. PHASES OF CARDIAC REHABILITATION: Phase I (Inpatient, 2–7 days post-MI): Begins during hospitalization. Goals are to stabilize the patient, relieve pain, prevent complications, and initiate early mobilization and education. Nursing activities include: (1) Bedside counseling on disease process and expected recovery timeline, (2) Introduction to risk factors and lifestyle changes needed, (3) Gradual mobilization (sitting, standing, walking at slow pace), (4) Teaching on medication adherence, (5) Psychological support for anxiety and depression (which commonly develop post-MI), and (6) Involving family/caregivers in education. Phase II (Early Outpatient, weeks 1–8 post-discharge): The patient attends supervised exercise sessions (usually 2–3 times per week) in a cardiac rehabilitation center under medical supervision. Exercises are graded, beginning with low intensity and progressing as tolerated (determined by symptom-limited exercise stress testing). Nurses and cardiac specialists monitor exercise response (heart rate, blood pressure, ECG, symptoms). Educational sessions cover cardiac medications, dietary modifications (low-sodium, heart-healthy, low saturated fat), smoking cessation, stress management, and return to work/activity. Phase III (Late Outpatient/Maintenance, 8–12 weeks and beyond): The patient transitions to independent or community-based exercise maintenance. Goals are sustained adherence to medications, continued exercise, risk factor control, and long-term prevention of recurrent MI. Some facilities offer maintenance programs; many rely on patient self-management with periodic physician follow-up. PATIENT EDUCATION: Comprehensive education is central to rehabilitation. Topics include: (1) Cardiac disease process and the patient's specific type/location of MI, (2) Medications: name, dose, frequency, indication, side effects, and importance of adherence (especially antiplatelets—stress not to stop clopidogrel without physician approval); (3) Activity progression: when to resume work, driving, sexual activity, and household tasks. General guideline: sexual activity can resume when the patient can climb one flight of stairs without dyspnea or chest pain; driving can resume after 2–4 weeks if reaction time is normal and symptoms controlled; (4) Dietary modifications: low sodium (<2,300 mg/day, ideally <1,500 mg/day), low saturated fat and trans fat, heart-healthy diet rich in vegetables, fruits, whole grains, lean proteins, and low-fat dairy. In the Philippines, nurses should provide culturally tailored dietary guidance—e.g., reducing salt in Filipino cooking (soy sauce, fish sauce), choosing lean protein sources (fish more than fatty red meat), incorporating Filipino vegetables (malunggay, pechay), and limiting high-fat coconut-based dishes. (5) Exercise: gradual return to aerobic activity (walking, swimming, cycling), typically targeting 150 minutes of moderate-intensity aerobic activity per week. Encourage warm-up and cool-down periods. Avoid strenuous activity or isometric exercises (e.g., heavy lifting) for several weeks. (6) Risk factor modification: smoking cessation (essential; refer to cessation programs), blood pressure control (target <130/80 mmHg), lipid management (target LDL <70 mg/dL post-MI per guidelines), diabetes control (HbA1c <7%), and weight management (BMI 18.5–24.9). (7) Stress management: relaxation techniques (deep breathing, progressive muscle relaxation), mindfulness, hobbies, social support, and formal counseling if depression or anxiety develops. (8) Warning signs: Teach the patient to recognize signs of recurrent ischemia or heart failure and to seek immediate care: chest pain or pressure lasting >5 minutes, shortness of breath at rest or with minimal exertion, palpitations, syncope, and unusual fatigue. Advise: 'If you experience chest pain, sit down immediately, chew one aspirin tablet (unless allergic), and call for emergency help or have someone drive you to the hospital. Do not wait.' (9) Medication storage and compliance: sublingual nitroglycerin should be stored in a dark, airtight glass container; it degrades in light and when exposed to heat and humidity. Replace the bottle every 3 months, even if unused. SEXUAL ACTIVITY COUNSELING: Many post-MI patients have concerns about resuming sexual activity. Nurses should provide frank, supportive counseling: (1) Sexual activity is generally safe once the patient can perform exertion equivalent to climbing one flight of stairs (i.e., about 3–4 metabolic equivalents [METs]) without dyspnea or chest pain. (2) Recommend positions that minimize workload (e.g., patient on back or side). (3) Avoid sexual activity immediately after large meals, alcohol consumption, or in extremes of temperature. (4) Discuss use of medications: sildenafil (Viagra) and other phosphodiesterase-5 inhibitors are contraindicated with nitrates due to profound hypotension risk. (5) Address psychosocial concerns: erectile dysfunction may develop from psychological factors or medications; reassurance and counseling can help. RETURN TO WORK AND DRIVING: (1) Driving: Patient should not drive for 2–4 weeks post-MI and only after physician approval. Reaction time must be assessed; psychotropic medications (sedatives) that impair cognition should be minimized. (2) Work: Return to work depends on job demands. Light-duty work may be resumed at 2–4 weeks post-MI if uncomplicated; return to strenuous work may take 8–12 weeks. Physicians often issue work restrictions (e.g., 'no lifting >10 pounds for 4 weeks'). DEPRESSION AND PSYCHOLOGICAL ADJUSTMENT: Post-MI depression is common (occurring in 15–25% of patients) and is associated with worse outcomes if untreated. Nurses should screen for symptoms (depressed mood, anhedonia, fatigue, sleep disturbance, hopelessness) and refer for formal psychological assessment and treatment if indicated. Antidepressants (SSRIs like sertraline) are safe and effective. Counseling and support groups are valuable. LONG-TERM FOLLOW-UP: Patients require periodic physician follow-up (typically at 2–4 weeks post-discharge, then at 3 months, 6 months, and annually). Labs include lipid panel, fasting glucose, renal function, and electrolytes. Repeat exercise stress testing or advanced imaging may be done to assess for residual ischemia. Medications are adjusted based on tolerance and disease response. In the Philippine healthcare context, where barriers to follow-up care (distance, cost, facility availability) may be significant, nurses play a crucial role in motivating adherence and connecting patients to available resources (e.g., primary health centers, community health workers, medication assistance programs).

While many patients recover uneventfully from MI, serious complications can develop in the acute phase (first hours to days) or subacute phase (days to weeks). Nurses must recognize these complications early and communicate findings promptly to the physician, as some require urgent intervention. DYSRHYTHMIAS: The most common complication, occurring in 80–90% of MI patients. Dysrhythmias range from benign (sinus bradycardia, sinus tachycardia) to life-threatening (ventricular fibrillation [VF], pulseless ventricular tachycardia [pVT]). (1) VF and pVT are the leading causes of sudden cardiac death in the first hours; they require immediate ACLS (CPR and defibrillation). All staff must be trained in ACLS and defibrillators must be immediately available at bedside. (2) Accelerated idioventricular rhythm (AIVR) is a benign reperfusion dysrhythmia (120–140 bpm, wide QRS) that occurs when thrombolytic therapy or PCI successfully reperfuses the infarct vessel. AIVR is not treated unless it causes hemodynamic compromise. (3) Bradycardia and heart blocks are common in inferior MI (due to right coronary artery occlusion causing SA and AV node ischemia). Atropine (0.5–1 mg IV, repeat every 3–5 minutes up to 3 mg) is given for symptomatic bradycardia. Temporary pacing may be needed for high-degree heart block. (4) Atrial fibrillation occurs in 10–15% of patients, especially with large infarcts or heart failure. Rate control with beta-blockers or calcium channel blockers is the priority; anticoagulation is considered if duration >48 hours due to stroke risk. (5) Premature ventricular contractions (PVCs) are common and generally benign unless they are frequent (>5 per minute), occur in couples, or show an 'R-on-T' pattern (landing on the T wave of the preceding beat), which increases VF risk. IV beta-blockers or amiodarone may be given for dangerous patterns. CARDIOGENIC SHOCK: A state of inadequate tissue perfusion resulting from severe left ventricular dysfunction. It occurs in about 5–7% of MI patients and carries high mortality (40–50%) if not aggressively managed. Manifestations include: hypotension (SBP <90 mmHg), cool extremities, oliguria (<0.5 mL/kg/hour), altered mental status, and metabolic acidosis. Management includes: aggressive IV fluid administration (especially in RV MI), inotropic agents (dobutamine, milrinone) to improve contractility, vasopressors (norepinephrine) if fluid and inotropes fail to restore blood pressure, diuretics if pulmonary edema develops, and consideration of mechanical circulatory support (intra-aortic balloon pump [IABP], extracorporeal membrane oxygenation [ECMO]) or urgent revascularization (PCI, CABG) if feasible. Nursing care includes continuous hemodynamic monitoring (blood pressure, heart rate, urine output, mental status), careful fluid balance, medication titration, and psychological support for the critically ill patient. ACUTE HEART FAILURE AND PULMONARY EDEMA: Occurs in 25–50% of MI patients, depending on infarct size and location. Left ventricular dysfunction from myocardial necrosis impairs cardiac output and causes pulmonary vascular congestion. Manifestations include: dyspnea (at rest or with exertion), orthopnea, paroxysmal nocturnal dyspnea (PND), rales on lung auscultation, elevated JVD, peripheral edema, fatigue, and in severe cases, frothy sputum (pink froth indicates pulmonary edema). Chest X-ray shows pulmonary infiltrates or 'bat wing' appearance in severe pulmonary edema. Management includes: oxygen (target SpO₂ 94–98%), diuretics (furosemide IV, titrated to urine output and symptom relief), nitrates (IV nitroglycerin or isosorbide dinitrate infusion) for preload and afterload reduction, bed rest and elevation of head of bed to 45 degrees to ease breathing, fluid restriction, afterload reduction with ACE inhibitors, and possibly inotropes if hypotensive. Some patients progress to acute decompensated heart failure requiring ICU care and mechanical ventilation. MECHANICAL COMPLICATIONS: Severe and often fatal, these complications result from rupture or dysfunction of cardiac structures. (1) Papillary muscle rupture (posteromedial papillary muscle most common in inferior MI) causes acute severe mitral regurgitation. Presentation: acute dyspnea, pulmonary edema, new holosystolic murmur, and possible cardiogenic shock. The murmur may be subtle or absent if the atrium is already volume-overloaded. Diagnosis: echocardiography shows severe mitral regurgitation and ruptured papillary muscle. Management: emergency mitral valve replacement (surgical) is the definitive treatment, but mortality remains high (30–50% even with surgery). (2) Ventricular free wall rupture causes acute hemopericardium and pericardial tamponade. Presentation: sudden cardiovascular collapse, elevated JVD, muffled heart sounds, hypotension, and loss of consciousness. This is nearly always fatal unless the patient undergoes emergency surgery immediately; most patients die before reaching the OR. (3) Ventricular septal rupture (VSR) causes a left-to-right shunt and acute heart failure/cardiogenic shock. Presentation: new holosystolic murmur best heard at the left lower sternal border, accompanied by dyspnea, hypoxemia, and signs of low cardiac output. Diagnosis: echocardiography or right heart catheterization. Early surgical repair is needed; medical management (inotropes, vasodilators, IABP) bridges to surgery but is temporary. PERICARDITIS: Inflammation of the pericardium occurring days to weeks post-MI. Post-MI pericarditis (early pericarditis) is caused by transmural infarction and necrotic myocardial inflammation; Dressler's syndrome (delayed pericarditis) is an autoimmune phenomenon occurring weeks to months post-MI. Presentation: pleuritic chest pain (worse with deep breathing and lying flat), pericardial friction rub on auscultation, and possibly pericardial effusion or tamponade. ECG may show diffuse ST elevation and PR depression. Management: NSAIDs (indomethacin, ibuprofen) for pain and inflammation; colchicine may be added; if pericardial effusion causes tamponade, pericardiocentesis is performed. Avoid aggressive anticoagulation if large effusion present due to risk of hemorrhagic tamponade. VENTRICULAR ANEURYSM: A weakened, aneurysmal segment of infarcted myocardium (usually anterior wall post-anterior MI). The aneurysm paradoxically bulges outward during systole rather than contracting, reducing ejection fraction and increasing thrombosis risk. Diagnosis: echocardiography shows the akinetic or dyskinetic segment; ECG shows persistent ST elevation weeks to months post-MI. Complications include thromboembolism and refractory heart failure. Management: anticoagulation (warfarin or newer anticoagulants) to prevent thrombus; surgical resection if refractory heart failure or recurrent thromboembolic events occur. RUPTURE OF INTRAVENTRICULAR SEPTUM (VSR): As noted above, VSR is a mechanical complication requiring urgent recognition and management. RIGHT VENTRICULAR INFARCTION (RVI): Occurs in 40–50% of inferior MI cases. Manifests as RV dysfunction with hypotension, elevated JVD, bradycardia, and AV block. The key difference from other complications: nitroglycerin is CONTRAINDICATED in RVI because the RV is preload-dependent (relies on ventricular filling to maintain output); nitrates reduce preload and cause cardiovascular collapse. Management: IV fluid administration (aggressive), avoid diuretics and nitrates, and treat bradycardia/blocks with atropine or pacing. Right-sided ECG leads (V4R-V6R) confirm RVI. THROMBOEMBOLISM: Mural thrombus can form on the endocardium overlying the infarct, especially if the infarct is large, anterior, or associated with reduced ejection fraction. The thrombus may embolize to the brain, causing stroke, or to other organs. Echocardiography detects mural thrombus. Anticoagulation (UFH, LMWH, or warfarin) prevents thromboembolism; anticoagulation is typically continued for 3 months or longer if the patient has a large anterior MI, severely reduced ejection fraction, or detected thrombus.

The Philippine Nursing Licensure Examination (NLE) administered by the PRC Board of Nursing heavily tests knowledge of CAD, angina, and MI. Success requires mastery of key distinctions and evidence-based management. Here are the high-yield points most likely to appear on the NLE: (1) ANGINA VS. MI: The fundamental distinction is that angina involves reversible ischemia with NORMAL cardiac biomarkers, while MI involves irreversible myocardial necrosis with ELEVATED troponin and CK-MB. Stable angina is relieved by rest and nitroglycerin; unstable angina (a form of ACS) is not reliably relieved and signals impending MI. (2) ASPIRIN DOSING AND TIMING: Aspirin 160–325 mg CHEWED (not swallowed) is the first-priority drug in ACS. It inhibits platelet aggregation and reduces mortality. Give ASAP; no absolute contraindication except true anaphylaxis. (3) NITROGLYCERIN CONTRAINDICATIONS: Never give nitroglycerin if: (a) hypotension (SBP <90), (b) right ventricular/inferior MI (preload-dependent), or (c) recent phosphodiesterase-5 inhibitor use (sildenafil, tadalafil—causes fatal hypotension). Always ask about ED medications before giving nitrates. (4) OXYGEN: Give ONLY for hypoxia (SpO₂ <90–94%). Do NOT give routine oxygen to normoxic patients; it may harm outcomes. (5) MORPHINE: Reserve for pain UNRELIEVED by nitroglycerin. It masks ischemia and has been associated with worse outcomes when overused early. (6) PCI VS. THROMBOLYTICS: PCI is preferred (higher success, lower reinfarction, lower bleeding). Door-to-balloon time ≤90 minutes. Thrombolytics used when PCI unavailable; door-to-needle ≤30 minutes, effective within 6–12 hours of onset. (7) THROMBOLYTIC CONTRAINDICATIONS: Screen for active bleeding, hemorrhagic stroke, recent (3 months) ischemic stroke, intracranial neoplasm, recent major surgery/trauma, severe uncontrolled HTN, and bleeding disorders. This is a nursing responsibility. (8) TROPONIN: Most specific and sensitive marker for MI; begins to rise 3–4 hours, peaks 24–48 hours, remains elevated 7–14 days. Serial troponins improve sensitivity. (9) ECG: STEMI shows ST elevation; NSTEMI shows ST depression or T inversion. Obtain within 10 minutes. (10) ATYPICAL MI PRESENTATIONS: Common in women, older adults, diabetics—fatigue, dyspnea, epigastric pain, silent MI. High index of suspicion is critical. (11) DUAL ANTIPLATELET THERAPY (DAPT): Aspirin + P2Y12 inhibitor (clopidogrel, ticagrelor, prasugrel). Loading doses acutely (e.g., clopidogrel 600 mg), maintenance long-term. Do not stop prematurely—increases stent thrombosis risk. (12) BETA-BLOCKERS: Reduce myocardial oxygen demand, infarct size, mortality. Contraindicated if bradycardic or hypotensive. (13) ACE INHIBITORS: Prevent ventricular remodeling, reduce mortality, especially anterior MI with reduced EF. Monitor for hypotension, hyperkalemia, cough. (14) STATINS: High-intensity (atorvastatin 80 mg). Reduce LDL, stabilize plaque, improve outcomes. Monitor for myopathy (muscle pain, elevated CK). (15) CONTINUOUS CARDIAC MONITORING: Essential; dysrhythmias (especially VF) are the leading early cause of death. ACLS must be immediately available. (16) REPERFUSION SIGNS: With successful PCI or thrombolytics: pain relief, ST normalization, AIVR dysrhythmia (benign), return of perfusion. (17) COMPLICATIONS: VF/pVT (require ACLS), cardiogenic shock, acute heart failure, mechanical complications (papillary muscle rupture, free wall rupture, VSR—require emergency surgery), pericarditis, ventricular aneurysm, RVI (avoid nitrates). (18) SECONDARY PREVENTION: Medications (DAPT, beta-blocker, ACE inhibitor, statin), smoking cessation, low-sodium low-saturated-fat diet, 150 min/week moderate aerobic exercise, stress management, diabetes/hypertension/lipid control. (19) RETURN TO ACTIVITY: Driving 2–4 weeks post-MI (with physician approval), sexual activity when able to climb one flight of stairs without dyspnea, work return light-duty 2–4 weeks, strenuous 8–12 weeks. (20) PATIENT TEACHING: Nitroglycerin storage (dark airtight glass container, replace Q3 months), medication adherence (especially antiplatelets), warning signs (chest pain >5 minutes, dyspnea, syncope—call 911), diet (low-sodium, heart-healthy), exercise, smoking cessation, stress management.