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

Exam Tips

• NLE TRICK: If a question asks 'what is the PRIMARY cause of CAD?' — the answer is atherosclerosis.
• Remember the sequence: endothelial injury → LDL deposit → inflammation → plaque → rupture → thrombus → ACS. Knowing this chain helps answer pathophysiology questions logically.
• Modifiable vs. non-modifiable risk factors are a classic NLE question format. Non-modifiable = age, sex, family history. Modifiable = HTN, smoking, dyslipidemia, DM, obesity, inactivity, stress.
• The concept of 'Time is muscle' is frequently referenced in NLE items about reperfusion goals — link it to door-to-balloon time (under 90 min for PCI) and door-to-needle time (under 30 min for thrombolytics).

Key Points

• CAD is the progressive narrowing of coronary arteries, most commonly caused by atherosclerosis — the buildup of fatty, fibrous plaque (atheroma) in the arterial intima (inner lining).
• The atherosclerotic process involves four key steps: (1) endothelial injury from hypertension, smoking, or hyperglycemia; (2) LDL (bad cholesterol) deposits into the damaged intima; (3) inflammatory response with macrophage infiltration forming foam cells; (4) fibrous cap formation over the lipid core, creating a plaque.
• When the plaque narrows the coronary artery lumen by more than 70%, blood flow is significantly reduced, causing ischemia when demand increases (e.g., during exercise).
• Plaque rupture is the critical event in acute coronary syndrome (ACS) — a ruptured plaque triggers platelet aggregation and thrombus (clot) formation, which can partially or completely block the artery.
• Ischemia = reversible oxygen deprivation (cell function impaired but cells alive). Infarction = irreversible necrosis (cell death) due to prolonged, complete oxygen deprivation.
• The phrase 'Time is muscle' means every minute of coronary artery occlusion results in more myocardial cell death — this is the justification for the door-to-balloon time goal of under 90 minutes.
• In the Philippine context, the DOH NCD (Non-Communicable Disease) program and PhilPEN (Philippine Package of Essential NCD Interventions) target modifiable CAD risk factors at the community level.

Definitions

Section Title

Pathophysiology of Coronary Artery Disease (CAD)

Common Mistakes

• Confusing ischemia (reversible) with infarction (irreversible) — ischemia is what happens in angina; infarction is what happens in MI. This distinction is the most-tested concept in this topic.
• Thinking atherosclerosis causes sudden heart attacks — it is a slow, decades-long process. The acute event is plaque RUPTURE leading to thrombus formation.
• Forgetting that the endothelium can be damaged by factors other than cholesterol — hypertension, cigarette smoking, and hyperglycemia also injure the endothelium and initiate atherosclerosis.
• Neglecting the Philippine DOH context — NLE questions may reference PhilPEN screening or community-based risk factor modification as part of primary prevention.

Exam Tips

• NLE frequently asks which risk factor is the MOST COMMON or MOST IMPORTANT modifiable risk factor — hypertension is the most prevalent in the Philippines; smoking is often cited as most potent globally.
• For health teaching questions, always frame modifiable risk factor modification as the nursing action — stop smoking, control BP and blood sugar, heart-healthy diet, regular moderate exercise.
• If an NLE question describes a post-menopausal woman with fatigue and indigestion — think atypical MI presentation, not just gastrointestinal disease.

Key Points

• Non-modifiable risk factors CANNOT be changed: age (risk increases with age), male sex (women's risk equalizes after menopause due to loss of estrogen protection), family history of premature CAD, and ethnicity.
• Modifiable risk factors CAN be changed through lifestyle and medical management: hypertension (the single most prevalent modifiable risk factor in the Philippines), dyslipidemia (high LDL, low HDL), cigarette smoking, diabetes mellitus, obesity, physical inactivity, and chronic psychological stress.
• Hypertension directly damages the arterial endothelium, accelerating atherosclerosis — this is why BP control is a priority nursing teaching point.
• Cigarette smoking causes endothelial injury, increases platelet aggregation, lowers HDL, and causes coronary artery spasm — it is one of the most potent modifiable risk factors.
• Diabetes mellitus accelerates atherosclerosis through advanced glycation end-products (AGEs) that damage endothelium, and through dyslipidemia.
• In primary and secondary prevention, the DOH PhilPEN program equips rural health units (RHUs) and barangay health centers (BHCs) to screen for hypertension, diabetes, and dyslipidemia — conditions nurses routinely manage in community health settings under RA 9173.
• Women, older adults, and people with diabetes frequently present with atypical symptoms of CAD (fatigue, indigestion, dyspnea, jaw pain) rather than classic chest pain — nurses must maintain a high index of suspicion.

Definitions

Section Title

Risk Factors for CAD

Common Mistakes

• Stating that family history is modifiable — it is NOT. Family history is a classic non-modifiable risk factor.
• Assuming women are protected from CAD at all ages — women's risk equalizes and may even surpass men's risk AFTER menopause. Post-menopausal women are high-risk.
• Forgetting that diabetes is both a risk factor and a reason for atypical (silent) MI presentations due to autonomic neuropathy affecting pain perception.
• Overlooking stress and sedentary lifestyle as modifiable risk factors — these are increasingly included in NLE health teaching scenarios.

Exam Tips

• HIGHEST-YIELD NLE DISTINCTION: Stable angina = relieved by rest + NTG + NORMAL biomarkers. Unstable angina = NOT relieved by rest/NTG + NORMAL biomarkers. MI = NOT relieved by rest/NTG + ELEVATED biomarkers (troponin, CK-MB).
• For NTG administration NLE questions: the correct sequence is sit/lie down → check BP → give 1 tablet SL → wait 5 minutes → check BP → if pain persists, call emergency + give 2nd tablet → wait 5 minutes → if still persists, give 3rd tablet. Maximum 3 tablets.
• NTG contraindications are heavily tested: HYPOTENSION (SBP below 90 mmHg), RIGHT VENTRICULAR/INFERIOR MI, and recent use of PHOSPHODIESTERASE INHIBITORS (sildenafil/Viagra, tadalafil). The combination can cause profound life-threatening hypotension.
• For Prinzmetal's angina questions: calcium channel blockers (amlodipine, diltiazem) and nitrates are used; beta-blockers are generally AVOIDED because they can worsen spasm.

Key Points

• Angina pectoris is chest pain caused by transient, REVERSIBLE myocardial ischemia. The heart muscle is temporarily deprived of oxygen but is NOT permanently damaged — no necrosis, no elevated cardiac biomarkers.
• Classic angina is described as substernal pressure, tightness, squeezing, or heaviness — patients often place a clenched fist over the sternum (Levine's sign). Pain may radiate to the left arm, jaw, neck, shoulder, or back.
• STABLE (EXERTIONAL) ANGINA: Predictable, triggered by physical exertion, emotional stress, cold weather, or heavy meals. Duration less than 5–15 minutes. RELIEVED by rest and sublingual nitroglycerin (NTG). Cardiac biomarkers are NORMAL. This is NOT a medical emergency but requires prompt evaluation.
• UNSTABLE ANGINA: A form of ACS. Occurs at rest OR with minimal exertion. More frequent, more severe, and LONGER than usual. NOT reliably relieved by rest or NTG alone. Cardiac biomarkers are NEGATIVE (no necrosis yet). This IS a medical emergency — it signals impending MI.
• VARIANT (PRINZMETAL'S) ANGINA: Caused by coronary artery SPASM (not plaque). Occurs at rest, often at night or early morning. Responds to calcium channel blockers and nitrates. ECG shows transient ST elevation during the episode that resolves when spasm ends.
• Nitroglycerin (NTG) works by dilating coronary arteries and systemic veins, reducing preload and myocardial oxygen demand. It relieves ischemic pain within 1–3 minutes when given sublingually.
• For stable angina: instruct patient to sit or lie down, place ONE NTG tablet (0.3–0.4 mg) under the tongue, check BP before each dose, repeat every 5 minutes for up to 3 doses total. If pain persists after the first dose (5 minutes), call emergency services (911 or nearest DOH facility).
• Patient teaching for NTG storage: keep tablets in original dark-colored glass container, away from heat, light, and moisture. Do NOT store in the bathroom medicine cabinet or car glove compartment. Tablets lose potency if exposed to air or light.

Definitions

Section Title

Angina Pectoris — Types, Features, and Nursing Management

Common Mistakes

• Confusing unstable angina with stable angina — the KEY differentiator is that unstable angina occurs AT REST and is NOT relieved by rest or NTG. If a patient takes NTG and the pain goes away with rest, it suggests stable angina.
• Forgetting that cardiac biomarkers are NEGATIVE in both stable and unstable angina — elevated troponin means MI, not angina.
• Giving all three NTG doses before calling for help — the correct teaching is: take the FIRST tablet, and if pain is NOT gone in 5 minutes, call emergency services AND take the second tablet. Do not wait for all three tablets before seeking help.
• Omitting BP assessment before each NTG dose — nitroglycerin drops blood pressure and is dangerous in hypotensive patients.
• Advising patients to store NTG in a shirt pocket next to the body — body heat degrades nitroglycerin. Store in a cool, dark place.

Exam Tips

• BIOMARKER MEMORY AID: 'Troponin is the GOLD STANDARD — most specific, most sensitive, stays longest (7–14 days). CK-MB normalizes fastest — use it to catch REINFARCTION.'
• ECG CHANGES MEMORY AID: STEMI = ST Elevation (think: the S in STEMI = Segment Elevated). NSTEMI = No ST elevation but biomarkers UP.
• NLE TIP: A patient has chest pain for 25 minutes, diaphoresis, and NTG gave no relief — this is MI until proven otherwise. The FIRST nursing action is to obtain a 12-lead ECG (within 10 minutes) and notify the physician.
• LOCATION-BASED MI MEMORY: Right coronary artery occlusion causes INFERIOR MI (leads II, III, aVF) — this is the MI where NTG and morphine must be used with extreme caution due to right ventricular involvement and risk of hypotension.
• ATYPICAL PRESENTATIONS mnemonic: 'DEJA' — Diabetics, Elderly, JAw pain, atypical symptoms. Always think cardiac if these patients present with unusual fatigue, indigestion, or dyspnea.

Key Points

• Myocardial Infarction (MI) is the IRREVERSIBLE DEATH (necrosis) of myocardial tissue due to prolonged, complete interruption of blood supply, usually from thrombotic occlusion following plaque rupture.
• CLASSIC SYMPTOMS: Severe, crushing, substernal chest pain radiating to the left arm, jaw, neck, or back. Pain lasts MORE THAN 20–30 minutes and is NOT relieved by rest or nitroglycerin.
• ASSOCIATED SYMPTOMS: Diaphoresis (cold, clammy sweating), nausea and vomiting, severe anxiety and a sense of impending doom, dyspnea, palpitations, and possible hypotension.
• ATYPICAL PRESENTATIONS — critically important for NLE: Women, older adults, and people with diabetes mellitus may present WITHOUT classic chest pain. Instead they may report: unusual fatigue, indigestion, epigastric pain, shortness of breath, back or jaw pain, or nausea alone. Diabetics may have SILENT MI due to autonomic neuropathy that blunts pain sensation.
• STEMI (ST-Elevation MI): Complete occlusion of coronary artery causing full-thickness (transmural) myocardial injury. ECG shows ST-segment elevation in leads corresponding to the affected artery. Requires IMMEDIATE reperfusion.
• NSTEMI (Non-ST-Elevation MI): Partial occlusion causing subendocardial injury. ECG shows ST depression or T-wave inversion (NO ST elevation). Cardiac biomarkers ARE elevated (unlike unstable angina). Managed with aggressive medical therapy; thrombolytics are NOT used.
• PATHOLOGIC Q WAVES develop hours to days after MI on ECG, representing areas of dead tissue that cannot depolarize. They are permanent evidence of past MI.
• TROPONIN is the MOST SENSITIVE AND SPECIFIC cardiac biomarker. Troponin I and Troponin T begin to rise 3–6 hours after MI onset, peak at 12–24 hours, and remain elevated for 7–14 days. Serial troponins (at 0, 3, and 6 hours) are drawn to confirm diagnosis.
• CK-MB (Creatine Kinase-MB) rises earlier (3–6 hours), peaks at 12–24 hours, and returns to normal within 48–72 hours. Because it normalizes faster, it can be used to DETECT REINFARCTION (a new peak of CK-MB after it had normalized).
• Obtain a 12-LEAD ECG within 10 MINUTES of patient presentation — this is a core time-sensitive nursing priority and is heavily tested.

Definitions

Section Title

Myocardial Infarction — Manifestations, Diagnostics, and Classification

Common Mistakes

• Thinking elevated troponin occurs in angina — WRONG. Troponin is only elevated in MI (when myocardial cells are actually dying). Normal troponin = no necrosis = angina (not MI).
• Assuming NSTEMI can be treated with thrombolytics — NEVER. Thrombolytics are contraindicated in NSTEMI because there is no complete occlusion to dissolve. Using thrombolytics in NSTEMI risks bleeding without benefit.
• Forgetting atypical MI presentations in women, elderly, and diabetics — a classic NLE distractor scenario. Do not dismiss a female patient's fatigue and jaw pain as non-cardiac.
• Mixing up CK-MB and troponin kinetics — remember troponin stays elevated LONGER (7–14 days, useful for diagnosing recent MI) while CK-MB normalizes faster (useful for detecting reinfarction).
• Stating that pathologic Q waves are an early sign — they develop LATER (hours to days after MI). The earliest ECG change in MI is ST elevation (in STEMI) or hyperacute T-wave changes.

Exam Tips

• MODERN MONA PRIORITY FOR NLE: A = Aspirin FIRST (chewable). N = Nitroglycerin second (if not contraindicated). O = Oxygen ONLY if hypoxic. M = Morphine LAST if NTG fails. Remember: 'ANO-M' or the modern sequence is A → N → O (conditional) → M (last resort).
• THROMBOLYTIC CONTRAINDICATIONS MEMORY AID: 'BASH' — Bleeding (active internal), Any hemorrhagic stroke (ever), Surgery or head trauma (recent), Hypertensive crisis. These are absolute contraindications.
• For STEMI management priority NLE questions: the correct hierarchy is (1) Call for help / activate code, (2) 12-lead ECG within 10 min, (3) IV access + draw labs (cardiac markers), (4) Aspirin chewable, (5) Nitroglycerin (if not contraindicated), (6) Notify cardiologist for reperfusion decision.
• REPERFUSION GOAL MEMORY: 'PCI = 90 minutes (P has 9 letters if you add an O, or think door-to-BAlloon = 90); Thrombolytics = 30 minutes (door-to-Needle = 30)'.
• Beta-blocker CONTRAINDICATIONS (when to HOLD): HARB — Hypotension, Acute heart failure/decompensated HF, Rate below 60 (bradycardia), Block (heart block).

Key Points

• The traditional mnemonic MONA (Morphine, Oxygen, Nitroglycerin, Aspirin) organizes initial ACS management, but current evidence has significantly refined the sequence and indications for each component. NLE items increasingly reflect these updates.
• ASPIRIN — FIRST PRIORITY DRUG: Give chewable (not swallowed whole) aspirin 160–325 mg as soon as ACS is suspected. Chewing speeds absorption. Aspirin inhibits platelet aggregation via COX-1 inhibition, reducing further clot formation and significantly reducing mortality. This is often the FIRST pharmacologic action.
• NITROGLYCERIN — SECOND: Sublingual NTG 0.3–0.4 mg every 5 minutes for up to 3 doses. Relieves ischemic chest pain by vasodilation. CHECK BLOOD PRESSURE BEFORE EACH DOSE. CONTRAINDICATED in: systolic BP below 90 mmHg, right ventricular or inferior MI (leads II, III, aVF ST elevation), and within 24–48 hours of phosphodiesterase inhibitor use (sildenafil, tadalafil, vardenafil).
• OXYGEN — CONDITIONAL: Give supplemental oxygen ONLY if SpO₂ is below 90–94% (hypoxic). Routine oxygen in normoxic (normal oxygen saturation) patients is NO LONGER recommended and may actually be harmful by causing coronary vasoconstriction and oxidative stress. This is a modern evidence-based update heavily reflected in current NLE questions.
• MORPHINE — RESERVED/LAST RESORT: IV morphine sulfate 2–4 mg is reserved for pain NOT relieved by nitroglycerin. Morphine reduces pain, anxiety, and myocardial oxygen demand but can mask ongoing ischemia, cause hypotension and bradycardia, and has been associated with worse outcomes when used routinely. Monitor for respiratory depression; have naloxone (Narcan) available.
• REPERFUSION is the ULTIMATE GOAL for STEMI. Two main options: (1) PCI (Percutaneous Coronary Intervention) — preferred; (2) Thrombolytic therapy — alternative when PCI is unavailable.
• PCI (PERCUTANEOUS CORONARY INTERVENTION): Angioplasty with balloon dilation and coronary stent placement to physically reopen the occluded artery. This is the GOLD STANDARD and PREFERRED reperfusion strategy for STEMI. GOAL: DOOR-TO-BALLOON TIME UNDER 90 MINUTES.
• THROMBOLYTIC (FIBRINOLYTIC) THERAPY: Drugs that dissolve the blood clot chemically. Agents include alteplase (tPA), reteplase (rPA), tenecteplase (TNK-tPA), and streptokinase. Used when timely PCI is unavailable (e.g., in rural Philippine settings without catheterization laboratory). GOAL: DOOR-TO-NEEDLE TIME UNDER 30 MINUTES, ideally within 6 hours of symptom onset (up to 12 hours).
• THROMBOLYTICS — ABSOLUTE CONTRAINDICATIONS (HIGH-YIELD NLE): (1) Active internal bleeding (not menstruation), (2) History of hemorrhagic stroke at any time, (3) Recent ischemic stroke within 3 months, (4) Intracranial neoplasm or arteriovenous malformation, (5) Significant closed-head trauma within 3 months, (6) Aortic dissection (suspected).
• THROMBOLYTICS — NURSING RESPONSIBILITIES: Monitor continuously for bleeding (neurological, GI, urinary, IV sites); assess neurologic status hourly (watch for signs of intracranial hemorrhage — sudden headache, altered consciousness, slurred speech, unequal pupils); minimize invasive procedures and venipunctures; apply manual pressure to all puncture sites for at least 10 minutes; monitor for REPERFUSION signs — relief of chest pain, return of ST segment toward baseline on ECG, and reperfusion dysrhythmias (accelerated idioventricular rhythm is a common benign reperfusion dysrhythmia).
• DUAL ANTIPLATELET THERAPY (DAPT): Aspirin PLUS a P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel). DAPT reduces risk of stent thrombosis after PCI and recurrent ACS. Patients post-stent should NOT stop DAPT without physician consultation — a critical patient teaching point.
• ANTICOAGULATION: Heparin (unfractionated IV or low-molecular-weight subcutaneous enoxaparin) is given to prevent clot propagation. For unfractionated heparin, monitor aPTT (target: 1.5–2.5 times normal). LMWH (enoxaparin) does not require aPTT monitoring.
• BETA-BLOCKERS (metoprolol, carvedilol): Reduce heart rate, blood pressure, and myocardial oxygen demand. Started within 24 hours if no contraindications. HOLD if: heart rate below 60 bpm, SBP below 100 mmHg, signs of acute heart failure, or heart block.
• ACE INHIBITORS (lisinopril, enalapril, captopril): Reduce afterload and prevent ventricular remodeling post-MI, especially important in patients with reduced ejection fraction. Monitor for: DRY COUGH (most common side effect), hyperkalemia, and hypotension. Start within 24 hours if stable.
• STATINS (atorvastatin 40–80 mg, rosuvastatin): High-intensity statin therapy started early regardless of baseline LDL. Stabilize plaque, reduce inflammation, and lower LDL. Monitor for: myalgia and myopathy (muscle pain), rhabdomyolysis (severe muscle breakdown with elevated CK), and elevated liver enzymes (AST, ALT).

Definitions

Section Title

ACS Management — MONA Framework with Modern Nuance and Reperfusion Therapy

Common Mistakes

• Giving oxygen routinely to ALL ACS patients — WRONG per current evidence. Oxygen is given ONLY if SpO₂ is below 90–94%. This is one of the most frequently updated concepts in current NLE examination items.
• Using morphine as the FIRST drug in ACS — WRONG. Aspirin is the first priority drug. Morphine is LAST RESORT, reserved for pain unrelieved by nitroglycerin.
• Administering thrombolytics to a patient with NSTEMI — NEVER. Thrombolytics are contraindicated in NSTEMI. They are ONLY for STEMI.
• Forgetting to ask about sildenafil (Viagra) use before giving nitroglycerin — the combination causes severe hypotension and can be fatal. Always ask the patient when they last took any ED medications.
• Not monitoring neurological status during thrombolytic therapy — intracranial hemorrhage is the most feared complication. Any sudden change in consciousness, severe headache, or neurologic deficit during or after thrombolytics is an emergency.
• Stopping clopidogrel or aspirin after PCI without consulting the cardiologist — abrupt cessation of DAPT risks stent thrombosis and is a serious patient safety issue.

Exam Tips

• NLE PRIORITY QUESTION TIP: When asked 'what is the FIRST/PRIORITY nursing action for acute MI?' — the answer is usually obtaining a 12-lead ECG within 10 minutes OR giving chewable aspirin, depending on the specific question context. Know both.
• NANDA PRIORITY: Acute Pain is the highest-priority nursing diagnosis because it directly relates to the ischemic event driving all other complications. Under Maslow, it is a physiological safety need.
• For NLE documentation questions: note that under RA 9173 and the Philippine NLE scope of practice, nurses must document all assessments, interventions, and patient responses accurately and in a timely manner — this includes rhythm strips, vital signs, medication administration, and patient teaching.
• Remember the 4 Ps of MI nursing management: Position (semi-Fowler's), Pain management, Prevention of complications (monitoring, bed rest), Patient teaching (discharge planning).

Key Points

• PRIORITY NURSING DIAGNOSIS (Maslow-based): The highest priority NANDA nursing diagnosis is Acute Pain related to myocardial ischemia/necrosis, evidenced by reports of severe crushing chest pain — this addresses a physiological safety need and the pain drives other complications (↑HR, ↑BP, ↑oxygen demand).
• Second priority: Decreased Cardiac Output related to impaired myocardial contractility, evidenced by hypotension, tachycardia, and poor peripheral perfusion. This is a life-threatening circulatory problem under Maslow's physiological safety tier.
• Third priority: Anxiety related to perceived threat of death, evidenced by restlessness and verbalization of fear — emotional support and clear communication reduce catecholamine release and oxygen demand.
• Additional relevant NANDA diagnoses: Activity Intolerance, Risk for Decreased Cardiac Tissue Perfusion, Ineffective Tissue Perfusion (cardiac), and Deficient Knowledge regarding the condition and treatment regimen.
• FIRST 10 MINUTES PRIORITIES — a classic NLE scenario question: (1) Position patient in semi-Fowler's or upright position to ease breathing and reduce preload; (2) Establish IV access; (3) Obtain 12-lead ECG WITHIN 10 MINUTES; (4) Attach continuous cardiac monitor and pulse oximetry; (5) Draw cardiac biomarkers and CBC; (6) Administer CHEWABLE ASPIRIN 160–325 mg; (7) Give supplemental oxygen ONLY if SpO₂ below 90–94%; (8) Administer sublingual NTG as ordered (if not contraindicated); (9) Notify physician immediately; (10) Prepare for reperfusion decision (PCI vs. thrombolytics).
• CONTINUOUS CARDIAC MONITORING is mandatory — ventricular fibrillation (VF) is the LEADING CAUSE OF DEATH in the first hours of MI and can occur without warning. The defibrillator must be at bedside and functional.
• MAINTAIN BED REST in the acute phase to minimize myocardial oxygen demand. Assist with all activities of daily living. Avoid straining at stool (use stool softeners — docusate sodium to prevent Valsalva maneuver which increases cardiac workload).
• REASSURE THE PATIENT calmly and continuously — anxiety activates the sympathetic nervous system, increasing heart rate and BP, which raises myocardial oxygen demand. A calm environment is a therapeutic nursing intervention.
• MONITOR VITAL SIGNS frequently in the acute phase (every 15–30 minutes initially) — watch for hypotension (cardiogenic shock), hypertension, arrhythmias, tachycardia, bradycardia, and respiratory distress.
• INTAKE AND OUTPUT MONITORING — fluid balance is critical. Oliguria may indicate cardiogenic shock. Excessive IV fluids can worsen pulmonary edema in a compromised heart.
• NPO or clear liquid diet initially until stable — nausea/vomiting is common; small frequent meals reduce cardiac workload. Avoid caffeine, large meals, and cold drinks.

Definitions

Section Title

Priority Nursing Management of Acute MI

Common Mistakes

• Positioning the MI patient flat (supine) — INCORRECT. The patient should be in semi-Fowler's (30–45 degrees) or high Fowler's to reduce respiratory effort and preload.
• Prioritizing pain relief over establishing IV access and ECG — while pain management is important, obtaining a 12-lead ECG within 10 minutes and establishing IV access are time-critical life-saving actions that may take priority in actual sequencing.
• Forgetting the defibrillator at bedside — VF can occur suddenly in the first hours of MI. The defibrillator must be immediately accessible.
• Allowing the patient to ambulate early without physician clearance — in the acute phase, bed rest is mandatory to minimize myocardial oxygen demand.
• Omitting the stool softener or Valsalva precautions — straining at stool causes the Valsalva maneuver, which increases intrathoracic pressure, reduces venous return, and can trigger dysrhythmias.

Exam Tips

• COMPLICATION TIMELINE MEMORY: HOURS = Dysrhythmias (most common early), Days 1–3 = Pericarditis, Weeks–Months = Dressler's Syndrome, Ventricular Aneurysm.
• For pericarditis vs. MI pain NLE questions: 'SHARP and worse with INSPIRATION and LEANING BACK, better LEANING FORWARD = pericarditis.' The patient may even sit and lean forward on a bedside table.
• Beck's Triad mnemonic: '3 Hs' — Hypotension, Hyposounds (muffled), and High JVD (distended neck veins) = cardiac tamponade.
• Ventricular fibrillation NLE tip: ANY patient in acute MI who suddenly becomes pulseless and unresponsive — start CPR and defibrillate. Do not delay for an ECG rhythm check in a witnessed, pulseless patient.

Key Points

• DYSRHYTHMIAS: The MOST COMMON early complication of MI. Ventricular fibrillation is the most LETHAL and is the leading cause of pre-hospital and early in-hospital death. Ventricular tachycardia, premature ventricular contractions (PVCs), and heart block also occur. Continuous cardiac monitoring is the cornerstone of early detection.
• CARDIOGENIC SHOCK: Most serious hemodynamic complication, occurring when a large portion (more than 40%) of the left ventricle is infarcted and cardiac output falls critically. Signs: profound hypotension, tachycardia, cold clammy extremities, oliguria (urine output below 30 mL/hour), and altered mental status. Requires vasopressors and urgent reperfusion.
• HEART FAILURE AND PULMONARY EDEMA: Left ventricular failure leads to fluid backflow into pulmonary circulation. Signs: dyspnea, orthopnea, crackles (rales) at lung bases, pink frothy sputum (severe pulmonary edema), elevated JVD. Treatment: diuretics (furosemide), oxygen, positioning (high Fowler's), and afterload reduction.
• PERICARDITIS: Inflammation of the pericardium overlying the infarcted area. Presents 24–72 hours post-MI with SHARP, pleuritic chest pain (worse on inspiration and leaning forward, better leaning forward or sitting up) — distinct from ischemic chest pain. Treatment: NSAIDs, colchicine.
• DRESSLER'S SYNDROME (Post-Cardiac Injury Syndrome): An autoimmune-mediated pericarditis occurring 2 weeks to several months after MI. Characterized by fever, pericarditis, and pleuritis. Treated with NSAIDs or corticosteroids.
• PAPILLARY MUSCLE RUPTURE: Rupture of the papillary muscle supporting the mitral valve leaflets, causing acute severe mitral regurgitation. Presents with sudden onset of pulmonary edema and hemodynamic deterioration. Requires emergency surgical repair.
• VENTRICULAR ANEURYSM: A weakened, bulging area of the ventricular wall that develops after transmural MI. Paradoxical wall motion on echocardiogram. Can harbor clots (risk of embolism) and contribute to dysrhythmias.
• CARDIAC TAMPONADE (rare): Rupture of the ventricular wall with blood accumulating in the pericardial sac. Beck's Triad: hypotension, muffled heart sounds, distended neck veins. Medical emergency requiring pericardiocentesis.
• REINFARCTION and EXTENSION: Reocclusion of the coronary artery or extension of the area of necrosis, presenting with recurrence of chest pain and new ECG changes. CK-MB is useful to detect reinfarction (new rise after normalization).

Definitions

Section Title

Complications of Myocardial Infarction

Common Mistakes

• Confusing pericarditis chest pain with reinfarction chest pain — pericarditis pain is SHARP, PLEURITIC (worse with inspiration), POSITIONAL (better leaning forward). MI pain is crushing, pressure-like, not positional.
• Forgetting that Dressler's syndrome is DELAYED (weeks to months post-MI), not an acute complication — it will not present on day 1.
• Not recognizing cardiogenic shock early — falling urine output (below 30 mL/hour) and deteriorating mental status are early signs that precede profound hypotension.
• Missing the significance of PVCs post-MI — frequent PVCs (more than 6 per minute), couplets, or R-on-T phenomenon are warning dysrhythmias that may precede ventricular fibrillation and require immediate reporting.

Exam Tips

• NLE TEACHING SCENARIO TIP: If a question asks what to teach a patient about NTG at home, remember the 5 Ss: Sit down, Sublingual (not swallowed), 5-minute intervals, maximum 3 doses, Store properly (dark glass, cool place).
• For NLE cardiac rehabilitation questions: Phase I = inpatient (hospital), Phase II = supervised outpatient, Phase III = independent maintenance. These are classic NLE recall items.
• DIET MNEMONIC for heart-healthy eating: 'LESS FAT, MORE FISH' — less saturated fat and sodium, more omega-3 rich fish (abundant in Philippines), fruits, vegetables, and fiber.
• RA 9173 CONNECTION: Patient teaching is a core independent nursing function under Section 28 (Scope of Nursing Practice). Documenting discharge teaching for MI patients and assessing readiness to learn are professional nursing responsibilities examined in NLE items.

Key Points

• CARDIAC REHABILITATION is a structured, evidence-based program of exercise, education, counseling, and risk-factor modification. It reduces mortality, prevents reinfarction, and improves quality of life. It is recommended for all post-MI and post-PCI patients.
• PHASES OF CARDIAC REHABILITATION: Phase I (Inpatient) — begins during hospitalization; focuses on gradual mobilization, self-care activities, and education. Phase II (Outpatient supervised) — begins 1–3 weeks post-discharge; supervised exercise, lifestyle coaching, and psychological support. Phase III (Maintenance/Lifelong) — independent, community-based maintenance of lifestyle changes and exercise.
• NITROGLYCERIN PATIENT TEACHING (high-yield): (1) Sit or lie down BEFORE taking NTG to prevent orthostatic hypotension and syncope. (2) Place 1 tablet under the tongue — do NOT swallow. (3) If pain not gone in 5 minutes: CALL EMERGENCY (911 or nearest emergency room) AND take a second tablet. (4) May take up to 3 tablets total, 5 minutes apart. (5) The medication often causes a tingling sensation under the tongue and headache — this is NORMAL. (6) Store in original DARK GLASS BOTTLE, tightly capped, away from heat, light, and moisture. Do NOT store in the bathroom, car, or shirt pocket. Replace every 6 months or per expiry. (7) Do NOT take sildenafil (Viagra) or similar medications within 24–48 hours of NTG use.
• RETURN TO ACTIVITY: Most patients can resume light household activities within 1–2 weeks, driving within 1–4 weeks per physician guidance, sexual activity within 3–6 weeks (if they can climb 2 flights of stairs without symptoms), and return to work within 4–8 weeks depending on job demands.
• DIET TEACHING: Heart-healthy diet — low in saturated fats, trans fats, cholesterol, and sodium (low-salt diet consistent with Philippine community health education). Increase fruits, vegetables, whole grains, and lean protein (fish, particularly common in the Philippine diet). Avoid excessive red meat and processed foods.
• SMOKING CESSATION: The MOST IMPORTANT modifiable risk factor change post-MI. Every cigarette smoked increases the risk of reinfarction. Offer pharmacotherapy (nicotine replacement, varenicline) and referral to cessation programs.
• MEDICATION ADHERENCE: Emphasize that aspirin and antiplatelet therapy (clopidogrel) must NEVER be stopped without cardiologist approval, especially after PCI with stent placement. Stopping DAPT prematurely can cause life-threatening stent thrombosis.
• PSYCHOLOGICAL SUPPORT: Depression occurs in up to 30% of post-MI patients and significantly worsens prognosis. Screen for depression, provide emotional support, encourage family involvement, and refer for counseling as needed.
• WARNING SIGNS TO REPORT IMMEDIATELY: Chest pain or pressure lasting more than 5 minutes; dyspnea at rest; palpitations; syncope or near-syncope; sudden severe headache; or any new neurological symptom (especially if on anticoagulants or thrombolytics).

Definitions

Section Title

Cardiac Rehabilitation and Patient Teaching

Common Mistakes

• Advising the patient to swallow NTG — it must be placed SUBLINGUALLY (under the tongue) for rapid absorption through the sublingual mucosa. Swallowing it greatly reduces its effectiveness.
• Forgetting to teach the patient to SIT DOWN before taking NTG — the vasodilatory effect causes hypotension that can lead to syncope if the patient is standing.
• Teaching patients that the lack of tingling or headache means NTG is not working or is expired — while loss of tingling MAY indicate expired NTG, the absence of tingling alone does not confirm inefficacy. Efficacy is measured by relief of pain and a significant decrease in BP.
• Clearing patients for all activities immediately — sexual activity and strenuous physical exertion should only be resumed after physician clearance, typically using the 2-flight stair test as a functional benchmark.
• Neglecting the psychological component — depression post-MI is clinically significant and undertreated. The nurse must assess mood and coping and not dismiss it as expected sadness.