NLE Cardiovascular Nursing — Coronary Artery Disease, Angina and Myocardial InfarctionCheat Sheet

Important facts

• CAD is the #1 cause of death in the Philippines (DOH data); prevention is a pillar of the DOH NCD program.
• Non-modifiable risk factors: age, male sex, family history, ethnicity.
• Modifiable risk factors: hypertension, dyslipidemia (high LDL, low HDL), diabetes mellitus, cigarette smoking, obesity, physical inactivity, stress.
• Plaque rupture triggers platelet aggregation and thrombus formation → acute coronary syndrome (ACS).
• Endothelial injury is the first step in atherosclerotic plaque development.
• Women's cardiovascular risk increases significantly after menopause due to loss of estrogen-mediated cardioprotection.
• Diabetes increases risk regardless of LDL levels and is associated with silent MIs due to autonomic neuropathy.

Key definitions

Diagrams to know

• Cross-section of a coronary artery showing normal lumen, endothelial injury, plaque formation, and lumen narrowing.
• Cascade of atherosclerosis: endothelial injury → LDL infiltration → macrophage activation → foam cell formation → fibrous cap.

Important facts

• Stable angina = reversible ischemia with normal cardiac biomarkers (troponin, CK-MB).
• Unstable angina is a form of ACS and signals impending MI; requires urgent hospitalization and ECG within 10 minutes.
• Unstable angina has elevated risk of progression to NSTEMI or STEMI; troponins remain negative but ECG may show ST depression or T-wave inversion.
• Anginal pain is classically described as substernal pressure, heaviness, tightness, or squeezing (not sharp, pleuritic, or positional).
• Atypical presentations in women: fatigue, dyspnea, indigestion, nausea, weakness—not always classic chest pain.
• Variant angina responds to calcium channel blockers and nitrates (not beta-blockers alone).
• Nocturnal angina at rest is a red flag for unstable angina or vasospastic angina.

Key definitions

Diagrams to know

• Spectrum of angina: stable → unstable → MI with increasing severity, frequency, and myocardial damage.

Common values

Important facts

• MI = irreversible myocardial necrosis; angina = reversible ischemia. The key differentiator is cardiac biomarkers (troponin, CK-MB).
• Troponin is the most specific and sensitive marker for myocardial necrosis; elevated within 2–3 hours, peaks at 24–48 hours, remains elevated for 7–14 days.
• CK-MB (creatine kinase-MB isoenzyme) rises within 4–6 hours, peaks at 24–36 hours, useful early in MI but less specific than troponin.
• Myoglobin rises earliest (within 1–2 hours) but is non-specific (from skeletal muscle too); rarely used.
• Serial troponins are drawn (typically at 0, 3, and 6 hours) to detect the rise and fall pattern diagnostic of MI.
• ECG changes in STEMI: ST elevation (full-thickness injury), pathologic Q waves (late marker of transmural necrosis), T-wave inversion.
• STEMI demands immediate reperfusion (PCI or thrombolytics) within 90 minutes; NSTEMI is managed with medical therapy plus risk-stratified angiography.
• Atypical MI presentations (especially in women, elderly, and diabetics): fatigue, dyspnea, indigestion, nausea, diaphoresis, syncope—NOT always chest pain.
• Silent MI occurs in diabetics due to autonomic neuropathy; patient has no pain but biomarkers and ECG confirm infarction.

Key definitions

Diagrams to know

• Schematic of MI development: plaque rupture → thrombus formation → complete coronary occlusion → myocardial necrosis.
• Evolution of ECG changes in MI over time: hours (hyperacute T-wave peaking) → hours to days (ST elevation, T-wave inversion) → days to weeks (Q waves, resolution).
• Cardiac biomarker timeline: myoglobin (1–2 h) → troponin (2–3 h, peaks 24–48 h) → CK-MB (4–6 h, peaks 24–36 h).

Common values

Important facts

• ASPIRIN (160–325 mg, chewed) is a TOP-PRIORITY first drug; reduces mortality by inhibiting platelet aggregation; give ASAP in any suspected ACS.
• Chewing aspirin speeds absorption and onset (versus swallowing) — critical in the first minutes of ACS.
• NITROGLYCERIN (sublingual, 0.3–0.4 mg) relieves ischemic chest pain and reduces preload; give up to 3 tablets, 5 minutes apart, checking blood pressure between doses.
• Nitroglycerin contraindications: hypotension (SBP < 90 mmHg), right ventricular/inferior MI (can cause severe hypotension), recent use of phosphodiesterase inhibitors (sildenafil, tadalafil) within 24–48 hours (profound vasodilation and hypotension).
• OXYGEN — ONLY if hypoxic (SpO₂ < 90–94%); routine oxygen in normoxic patients is NOT recommended (may be harmful by increasing oxidative stress).
• MORPHINE — reserved for pain NOT relieved by nitroglycerin; may mask ongoing ischemia and has been linked to worse outcomes if overused; monitor for respiratory depression and hypotension.
• Modern MONA prioritizes: Aspirin → Nitroglycerin (if not contraindicated and BP adequate) → Oxygen (only for hypoxia) → Morphine (only for refractory pain).
• Reperfusion (PCI or thrombolytics) is the definitive therapy for STEMI and must be initiated urgently in parallel with MONA.
• Obtain 12-lead ECG within 10 minutes of presentation; this determines STEMI vs NSTEMI vs unstable angina and drives reperfusion decisions.

Key definitions

Diagrams to know

• MONA decision tree: suspicion of ACS → aspirin → ECG within 10 minutes → if STEMI, activate reperfusion → nitroglycerin (check contraindications) → oxygen (only if SpO₂ low) → morphine (if pain unrelieved).

Common values

Important facts

• PCI is the preferred reperfusion for STEMI when available; goal is door-to-balloon (D2B) time < 90 minutes.
• If PCI unavailable within 120 minutes of first medical contact, thrombolytics should be given.
• Thrombolytic drugs: alteplase (tPA), reteplase (rPA), tenecteplase (TNK), streptokinase (SK); all dissolve fibrin in thrombus.
• Thrombolytic door-to-needle time: < 30 minutes (earlier = better myocardial salvage).
• Thrombolytic window: ideally < 6 hours from symptom onset; can extend to 12 hours for posterior MI or if symptoms ongoing.
• #1 risk of thrombolytics: BLEEDING — including intracranial hemorrhage (ICH), GI bleeding, retroperitoneal bleeding.
• Absolute contraindications to thrombolytics: active internal bleeding, history of hemorrhagic stroke, ischemic stroke within 3 months, intracranial neoplasm, recent major surgery or trauma (within 3 weeks).
• Relative contraindications: uncontrolled hypertension, recent invasive procedure, severe liver disease, pregnancy.
• Monitor thrombolytic patient for: bleeding signs, reperfusion dysrhythmias (PVCs, bradycardia, transient ST normalization), relief of chest pain, hemodynamic changes.
• Minimize invasive procedures and venipunctures in thrombolytic patient; use one IV line only if possible.
• Assess neurologic status frequently post-thrombolytic (monitor for signs of intracranial hemorrhage: headache, altered mental status, focal neurologic deficit).

Key definitions

Diagrams to know

• Reperfusion decision algorithm: STEMI diagnosis → PCI available within 120 min? → YES: PCI within 90 min D2B. NO: Thrombolytic within 30 min D2N.
• Timeline of fibrinolytic window: symptom onset → ideal < 6 hours → acceptable to 12 hours (for posterior MI or ongoing symptoms).

Common values

Important facts

• Antiplatelets: Aspirin + P2Y12 inhibitor (clopidogrel, ticagrelor, prasugrel); ticagrelor and prasugrel are faster-acting, preferred in ACS.
• Clopidogrel loading dose: 600 mg (or 300 mg if elderly); maintenance 75 mg daily.
• Ticagrelor loading dose: 180 mg; maintenance 60 mg twice daily (faster onset, more potent than clopidogrel).
• Prasugrel loading dose: 60 mg; maintenance 5–10 mg daily (avoid in weight < 60 kg or age ≥ 75).
• Anticoagulants: Unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH, e.g., enoxaparin); monitor aPTT for UFH; prevent clot propagation.
• Unfractionated heparin: initial bolus 60–70 units/kg IV, then infusion; target aPTT 1.5–2.5 times control.
• Enoxaparin: 1 mg/kg SC twice daily or 1.5 mg/kg daily; no aPTT monitoring needed.
• Beta-blockers (metoprolol, atenolol): reduce heart rate, BP, and myocardial oxygen demand; hold if bradycardic or hypotensive.
• ACE inhibitors (lisinopril, enalapril): reduce afterload, prevent ventricular remodeling; monitor for cough, hyperkalemia, hypotension.
• Statins (atorvastatin, rosuvastatin): reduce LDL, stabilize plaque; monitor for myalgia (rhabdomyolysis) and elevated transaminases.
• Calcium channel blockers (diltiazem, verapamil): use cautiously in ACS; contraindicated if heart failure or reduced ejection fraction; useful for variant angina.
• Start dual antiplatelets, anticoagulation, beta-blockers, and ACE inhibitors early in ACS; add statins routinely.

Key definitions

Diagrams to know

• ACS medication timeline: aspirin (stat) → nitroglycerin (stat if not contraindicated) → anticoagulant (UFH or LMWH) → beta-blocker, ACE-I, statin (early) → P2Y12 inhibitor (at PCI or in hospital).

Common values

Important facts

• 12-lead ECG within 10 minutes of arrival is mandatory in suspected ACS — drives diagnosis and reperfusion decisions.
• STEMI = ST elevation ≥ 1 mm (0.1 mV) in ≥ 2 contiguous leads (or new LBBB); mandates immediate reperfusion.
• NSTEMI / unstable angina = NO ST elevation; may have ST depression, T-wave inversion, or normal ECG.
• ST elevation criteria by location:
• • Anterior: leads V1–V4 (LAD territory)
• • Inferior: leads II, III, aVF (RCA or LCx territory)
• • Lateral: leads I, aVL, V5–V6 (LCx territory)
• • Posterior: ST depression in V1–V3 (reciprocal changes; true posterior elevation in V7–V9)
• Inferior STEMI → check for RIGHT VENTRICULAR (RV) involvement (ST elevation in V4R); if present, avoid nitroglycerin and give fluids.
• Hyperacute T-wave (peaked, tall, symmetric) appears within minutes of STEMI — earliest ECG sign.
• Pathologic Q waves develop over hours to days after transmural MI; presence indicates prior infarction.
• LBBB (left bundle branch block) can mask ST elevation; new LBBB in ACS context is treated as STEMI equivalent.
• Posterior wall MI often has subtle findings on anterior leads (ST depression V1–V3); use posterior leads (V7–V9) for confirmation.
• Serial ECGs (repeat every 5–10 minutes in acute phase) help detect evolving changes and confirm diagnosis.

Key definitions

Diagrams to know

• 12-lead ECG territories: LAD (anterior, anterolateral) → V1–V4, I, aVL; LCx (lateral) → I, aVL, V5–V6; RCA (inferior) → II, III, aVF.
• Evolution of ECG in STEMI: hyperacute T (minutes) → ST elevation (hours) → T-wave inversion (hours–days) → pathologic Q waves (days–weeks) → resolution.

Important facts

• Dysrhythmias are the #1 cause of death in the first hours of MI; ventricular fibrillation (VF) is the deadliest.
• Common dysrhythmias in MI: premature ventricular contractions (PVCs), ventricular tachycardia (VT), VF, bradycardia (from vagal stimulation in inferior MI), AV block.
• Continuous cardiac monitoring is essential in acute MI to detect and treat dysrhythmias immediately.
• Cardiogenic shock indicates massive myocardial damage and carries high mortality; may require inotropic support, IABP, or mechanical circulatory support.
• Acute heart failure / pulmonary edema: LV dysfunction → elevated LVEDP → pulmonary congestion (crackles, orthopnea, PND); treat with diuretics, vasodilators, ACE-I.
• Pericarditis (post-MI): pleuritic chest pain, friction rub, ST elevation diffuse (NOT localized); use NSAIDs or colchicine; avoid anticoagulation if possible.
• Dressler's syndrome: occurs weeks to months post-MI; autoimmune; treat with NSAIDs, steroids if severe.
• Papillary muscle rupture: acute, severe mitral regurgitation from rupture of PM or chordae tendineae; presents with acute pulmonary edema and murmur; surgical emergency.
• Ventricular free wall rupture: catastrophic complication within first week; sudden, severe drop in BP and loss of pulse; almost uniformly fatal.
• Ventricular aneurysm: paradoxical wall motion (bulging outward during systole) developing weeks post-MI; risk factor for dysrhythmias and thrombus; detected on echo.
• Mural thrombus: clot in LV cavity post-MI (especially anterior wall infarcts); risk of systemic embolism; treated with anticoagulation.
• Right ventricular infarction (from RCA occlusion): hypotension, elevated JVP, clear lungs; avoid nitroglycerin and diuretics; give IV fluids.

Key definitions

Diagrams to know

• Timeline of MI complications: first hours (dysrhythmias, VF) → first 24–48 h (cardiogenic shock, heart failure) → first week (free wall rupture, papillary muscle rupture) → weeks (Dressler's, ventricular aneurysm, thrombus).

Important facts

• Nursing Priority (Maslow / NANDA): Acute coronary syndrome is a physiologic emergency (Maslow Level 1 — safety/physiologic).
• Primary nursing diagnoses:
• • Acute pain related to myocardial ischemia/infarction (NANDA 00132)
• • Decreased cardiac output related to myocardial dysfunction or dysrhythmia (NANDA 00029)
• • Anxiety related to fear of death or uncertain prognosis (NANDA 00146)
• • Ineffective tissue perfusion (cardiac, cerebral, peripheral) related to reduced coronary flow (NANDA 00200)
• • Risk for dysrhythmia / sudden cardiac death (NANDA 00126)
• Immediate nursing interventions:
• 1. Position: upright, semi-Fowler's (reduces work of breathing, decreases anxiety).
• 2. IV access: establish 2 large-bore IVs for medications and fluid.
• 3. ECG: 12-lead within 10 minutes; continuous cardiac monitoring (detect dysrhythmias).
• 4. Medications: aspirin, nitroglycerin (check BP), O₂ (if hypoxic), morphine (if pain unrelieved).
• 5. Rest: enforce bed rest to reduce myocardial workload.
• 6. Monitoring: vital signs, cardiac rhythm, chest pain (location, quality, radiation, relieving factors), urine output.
• 7. Reassurance: calm, supportive presence; explain procedures; involve family.
• Cardiac monitoring: watch for dysrhythmias (PVCs, VT, VF, bradycardia, AV block) and ST segment changes.
• Pain assessment: use pain scale (0–10); assess pain characteristics and response to intervention.
• Fluid and electrolyte management: monitor I&O; maintain adequate hydration without overload; monitor serum K+ (hypokalemia increases dysrhythmia risk).
• Avoid: vigorous coughing, straining at stool (increased myocardial workload); rectal thermometers (stimulate vagal response in inferior MI).
• Health teaching (post-acute phase): recognize angina warning signs, nitroglycerin use, medication compliance, risk factor modification, cardiac rehabilitation, return-to-activity guidelines.
• RA 9173 (Philippine Nursing Practice Law): Nurses conduct assessment, nursing diagnosis, planning, implementation, and evaluation within their scope; coordinate with physician for medication administration and reperfusion decisions.

Key definitions

Diagrams to know

• Acute MI nursing care workflow: assessment → ECG within 10 min → IV access + meds → continuous monitoring → pain/vitals monitoring → reassurance → coordination with physician for reperfusion.

Common values

Important facts

• Cardiac rehabilitation reduces mortality by 25–30% and improves quality of life post-MI.
• Phase 1 (In-hospital): bedside ECG monitoring, gentle mobilization, education, discharge planning.
• Phase 2 (Early outpatient, weeks 3–12): supervised exercise (monitored treadmill, cycling), education on risk factors, psychosocial support.
• Phase 3 (Maintenance, 3+ months): unsupervised or group-based exercise, ongoing education, reinforcement of lifestyle change.
• Risk factor modification (NANDA: ineffective health maintenance):
• • Smoking cessation: absolute priority; use nicotine replacement, counseling, behavioral therapy.
• • Hypertension control: target BP < 130/80 mmHg; antihypertensives (ACE-I, ARB, beta-blockers, diuretics).
• • Dyslipidemia: target LDL < 70 mg/dL (or even < 55 in very high risk); statins, ezetimibe, PCSK9 inhibitors.
• • Diabetes control: target HbA1c < 7%; metformin, SGLT2 inhibitors, GLP-1 agonists.
• • Physical activity: 150 minutes moderate aerobic activity per week (or 75 minutes vigorous) after clearance.
• • Diet: Mediterranean or DASH diet; low saturated fat (< 7% of calories), low sodium (< 2.3 g/day), high fiber.
• • Stress management: cognitive-behavioral therapy, mindfulness, yoga, counseling.
• • Medication adherence: educate on why each drug is needed; use pill organizer; simplify regimen if possible.
• Nitroglycerin education for long-term use:
• • Carry nitroglycerin at all times; refresh supply every 3 months (tablets lose potency).
• • Sit down before taking nitroglycerin; place one tablet under tongue.
• • If pain persists after 5 minutes, may repeat up to 2 more doses (total 3) at 5-minute intervals.
• • If pain not relieved after 3 doses, call emergency services immediately (do NOT drive).
• • Store in dark, airtight container away from heat and moisture.
• Return to work/activity: typically cleared 4–6 weeks post-MI if uncomplicated; always per provider clearance.
• Sexual activity: generally safe to resume 4–6 weeks post-MI; if erectile dysfunction develops, PDE5 inhibitors (sildenafil) are contraindicated with nitrates.
• Philippine context (DOH NCD program): community health workers, barangay health stations, and primary care clinics support cardiac rehab and risk factor screening in underserved areas.

Key definitions

Diagrams to know

• Cardiac rehabilitation phases: Phase 1 (in-hospital, days 1–3) → Phase 2 (early outpatient, weeks 3–12, supervised exercise) → Phase 3 (maintenance, 3+ months, ongoing lifestyle).