Atherosclerosis & Coronary Heart Disease – Comprehensive Study Notes
Page 1 – Course & Lecture Identification
Course: NURSING 200
Topic: Care of the Client with Atherosclerosis and Coronary Heart Disease
Instructor: Caroline Patanovich, RN, MSN
Page 2 – Learning Outcomes (1–3)
Discuss the pathophysiology of atherosclerosis & coronary heart/artery disease (CAD/CHD).
Explain core nutritional concepts for clients with atherosclerosis.
Identify medications used in atherosclerosis management.
Page 3 – Learning Outcomes (4–6)
Discuss clinical manifestations of coronary heart/artery disease.
Differentiate the various diagnostic tests used for CHD.
Utilize the Nursing Process when caring for a client with CHD.
Page 4 – Anatomy of an Artery
Three tunics (layers):
Intima (tunica interna) – endothelial layer + basement membrane
Media (tunica media) – smooth muscle & elastic fibers
Adventitia/Externa (tunica externa) – connective tissue
Lumen = central opening through which blood flows.
Page 5 – Disease Continuum & Terminology
Atherosclerosis → Coronary Artery/Heart Disease → Angina Pectoris → Acute Coronary Syndromes (ACS).
Angina sub-types: Stable, Variant (Prinzmetal’s), Unstable.
ACS outcomes: NSTEMI, STEMI, MI.
Page 6 – CAD vs. CHD
CAD (Coronary Artery Disease): narrowing/obstruction in coronary arteries.
CHD (Coronary Heart Disease): broader term including resulting myocardial damage (ischemia, infarction, HF, etc.).
Page 7 – Less-Common Etiologies of CAD
Embolus
Inflammation of vascular lumen
Vasospasm
Page 8 – Atherosclerosis: Definition & Etymology
Greek roots: “Athero” = paste/gruel, “sclerosis” = hard.
Begins as soft fatty deposits; hardens with age (→ arteriosclerosis).
Page 9 – Atherosclerosis: Distribution & Synonyms
Can occur in any artery; coronary arteries are preferential.
Alternate terms: Atherosclerotic Heart Disease, Cardiovascular Heart Disease, Ischemic Heart Disease.
Page 10 – Visual Progression
Normal → Mild atherosclerosis → Severe atherosclerosis (progressive lumen narrowing).
Page 11 – Nutrition: Cholesterol Basics
Endogenous production: liver manufactures; rate ≈ genetics + diet.
Roles: fat absorption, nerve conduction.
Body needs only intrinsic cholesterol; extrinsic sources = animal products.
Page 12 – Cholesterol Transport & Desirable Levels
Carried by lipoproteins (protein + fat complexes).
Desirable total cholesterol: <200\,\text{mg/dL}.
Page 13 – Lipoprotein Classes
HDL = High-Density Lipoprotein
LDL = Low-Density Lipoprotein
Page 14 – HDL Details
Composition: more protein, less lipid.
Function: returns cholesterol to liver for excretion.
Values:
Desirable: >60\,\text{mg/dL}.
Acceptable: 40–60\,\text{mg/dL}.
Lower HDL ⇒ ↑ CAD risk.
Page 15 – LDL Details
Delivers cholesterol to tissues; promotes atheroma formation.
↑ with dietary saturated fats.
Reference ranges:
Optimal: <100\,\text{mg/dL}.
Near-optimal: 100–129\,\text{mg/dL}.
Borderline-high: 130–159\,\text{mg/dL}.
Higher LDL ⇒ ↑ CAD risk.
Page 16 – Triglycerides (TG)
Formed in liver from glycerol + fatty acids.
High TG strongly linked to CAD (esp. in diabetics).
Normal: <150\,\text{mg/dL}; Borderline high: 150–199\,\text{mg/dL}.
Page 17 – Other Laboratory Markers
Lipoprotein Lp(a) – familial risk screening.
C-Reactive Protein (CRP) – systemic inflammation predictor.
Homocysteine – elevated levels correlate with CHD risk.
Page 18 – Client Teaching: Lipid Profile Testing
Frequency: q 4–6 yrs starting age 20 (earlier if FHx).
Pre-test prep: 8–12 hr fast, no alcohol 24 hr, verify meds that affect lipids.
Page 19 – Dietary Modification Targets
Total fat: 20 – 35 % total kcal.
Saturated fat: <10\,\% of kcal.
Dietary cholesterol: <200\,\text{mg/day}.
Page 20 – Practical Nutrition Teaching
Prefer olive / canola oil.
Track calories; aim for healthy weight.
≥ 5 servings fruits & vegetables daily.
Choose skinless poultry & fish.
≥ 6 servings whole grains.
Limit salt & alcohol.
Page 21 – Humor Slide
Cartoon: “Why does bad cholesterol taste so much better than good cholesterol?” – reinforces challenge of dietary change.
Page 22 – AHA Resources
Directs to American Heart Association Diet & Lifestyle Recommendations (URL provided).
Page 23 – Lifestyle Modifications Summary
Smoking cessation
Weight reduction
Regular exercise (≥ 30 min/day)
Control comorbidities: HTN, Diabetes
Page 24 – Epidemiology (Textbook p.593)
CAD affects ≈ 18.2 million Americans; > 400,000 deaths/year.
Can be asymptomatic or progress to angina, ACS, MI, dysrhythmias, HF, or sudden death.
Page 25 – Coronary Artery Anatomy
Major branches: Right Coronary Artery (RCA), Left Coronary Artery (LCA) → Circumflex & Left Anterior Descending (LAD).
Page 26 – “Widowmaker” MI
LAD occlusion → large anterior wall infarct; high mortality.
Pathology: plaque + clot → blocked flow → “dying heart muscle”.
Page 27 – CAD Pathophysiology Overview
Progressive; early fatty streak may appear in teens.
Progression influenced by genetics + environment.
Page 28 – Fatty Streak Characteristics
Accumulation of foam cells in subendothelial space – earliest visible lesion.
Page 29–31 – Fibrous Plaque & Complicated Lesion
LDLs + platelet growth factors → smooth muscle proliferation (media) & intimal thickening.
Atheroma: lipid core + fibrous cap.
Continued inflammation → plaque instability, ulceration, rupture → thrombosis – most dangerous stage.
Page 32 – Injury–Inflammation Cascade Diagram
Endothelial injury (HTN, smoking, diabetes, etc.) → monocyte/macrophage infiltration → lipid pool → fibrous cap → fissure → thrombus.
Page 33 – Effect on Blood Flow
Normal vs. narrowed artery: turbulent flow, decreased perfusion.
Page 34 – Non-Modifiable Risk Factors
Age, Gender, Ethnicity, Family History/Genetics, Type I DM, Post-menopause.
Page 35 – Modifiable Risk Factors
Hyperlipidemia, Smoking, Sedentary lifestyle, Poor diet/Obesity, Stress, Excess alcohol, Type II DM.
Page 36 – Special Risk Issues in Women
Premature menopause, Oral contraceptive use.
Page 37 – Health Promotion Prompt
(Interactive question) – anticipate teaching on diet, exercise, screening, smoking cessation, stress management.
Page 38–39 – Gerontologic Considerations
High CAD incidence; emphasize lifestyle measures.
Older adults need: longer warm-up, low-level activity with rests, caution in temperature extremes.
Page 40 – NCLEX Question (Modifiable Risks)
Correct answers: A & E (“stop smoking”; “obesity is modifiable”).
Page 41 – Angina Pectoris Terminology
Latin: Angina = pain, Pectoris = chest.
Page 42 – Angina Pathophysiology Core
Pain occurs when O₂ demand > supply to myocardium.
Page 43 – Angina / ACS Spectrum
Stable → Variant (Prinzmetal) → Unstable → NSTEMI → STEMI → ACS.
Page 44 – Normal Resting Heart
Balance: O₂ Supply = O₂ Demand.
Page 45 – CAD Heart
Supply < Demand → ischemia.
Page 46 – Cellular Consequences of Ischemia
↓O₂ → shift to anaerobic metabolism → ↑ lactic acid → pain.
Diseased coronaries cannot dilate appropriately.
Page 47 – Factors Affecting Supply & Demand
Decreased supply: coronary occlusion.
Increased demand triggers: physical exertion, emotions, heavy meals, stimulants, smoking, temperature extremes.
Page 48 – Table 30-1 Highlights
Coronary Perfusion issues: atherosclerosis, thrombosis, vasospasm.
Myocardial Workload ↑: rapid HR, ↑ preload/afterload/contractility, metabolic disease (e.g., hyperthyroidism).
Blood O₂ Content ↓: altitude, respiratory disease, anemia, hypotension.
Page 49 – Chest Pain Descriptors
Substernal, radiates to arms; squeezing/fullness; brief duration.
Page 50 – Common Pain Radiation Sites (Diagram)
Neck, jaw, left arm, shoulders, epigastrium, back (intrascapular).
Page 51 – Stable (Chronic) Angina Characteristics
Long-term, predictable onset/duration/intensity.
Triggered by exertion; feels like pressure/ache.
Relieved by rest.
Page 52 – Unstable Angina Characteristics
Type of ACS; new or worsening pattern.
Occurs at rest, pain more intense.
Medical emergency – high MI risk.
Page 53 – Progression Graphic
Stable plaque → rupture → thrombus → MI (occlusive).
Page 54 – Variant (Prinzmetal) Angina
Occurs at rest due to coronary spasm.
Rare; may occur with/without CAD.
Thought mechanism: ↑ intracellular Ca²⁺.
Page 55 – NCLEX (Highest CAD Risk)
Correct: D. 65-yr-old obese female with LDL 188.
Page 56 – NCLEX (Stable Angina Assessment)
Correct: C. Correlation between activity level & pain.
Page 57 – Assessment Overview
History & physical, ECG, labs/diagnostics, invasive procedures.
Page 58 – Pain History Mnemonic OPQRST
O Onset, P Provoking factors, Q Quality, R Radiation, S Severity, T Timing.
Page 59 – Focused Physical Exam
Systems: Cardiovascular & Respiratory.
Page 60 – ECG Utility
Assesses conduction; detects ischemia, injury, necrosis; extent evaluation (p.595).
Page 61–64 – Cardiac Biomarkers
Troponin I/T: appear ≈ 3 hr, stay up to 10 days – most specific.
CK-MB: appear ≈ 4 hr, return to normal ≈ 36 hr – quantifies muscle damage.
Page 65 – Simple Exercise Stress Test
Treadmill; monitor ECG & vitals; stop upon symptoms/changes.
Page 67 – Nuclear Exercise Stress Test
Treadmill + radioisotope injection; scan at peak & 2–4 hr later for perfusion mapping.
Page 68 – Pharmacologic Nuclear Stress Test
For non-ambulatory clients; IV vasodilator mimics exercise → isotope imaging.
Page 69 – Nursing Considerations for Testing
Explain procedures; wear comfy shoes/clothes; report symptoms.
Scans: possible NPO, no caffeine, clarify med holds.
Page 70 – Coronary Angiography (Cardiac Cath)
Visualizes arteries, % occlusion, valve function, CO.
May incorporate angioplasty or stent; in- or outpatient.
Page 71–72 – Cath Access Sites
Femoral (groin), Radial, Ulnar arteries.
Page 73–75 – Angioplasty & Stenting Graphics
Balloon inflates → plaque compressed → stent expands → maintains lumen.
Page 76 – Pre-Cath Nursing Responsibilities
Verify informed consent.
Check iodine/shellfish allergy & med hx.
Draw labs: renal function.
Ensure IV access.
Administer pre-sedation if ordered.
Page 77 – Post-Cath Nursing Responsibilities
Frequent vital signs.
Inspect insertion site (bleeding/hematoma).
Assess distal pulses.
Encourage fluids to flush dye.
Immobilize limb if femoral.
Document all assessments.
Page 78 – Coronary Artery Bypass Grafting (CABG)
Uses saphenous vein or internal mammary artery to bypass occlusions.
Page 79 – Pharmacotherapy Categories (detailed in pharmacology lecture)
Nitrovasodilators (e.g., Nitroglycerin)
Antiplatelet agents (e.g., Aspirin, Clopidogrel)
Beta-Blockers
Calcium Channel Blockers
Page 80 – Nursing Process Framework
Assessment/Recognize cues
Analyze cues/Prioritize hypotheses
Plan/Generate solutions
Implement/Take action
Evaluate outcomes
Page 81 – Priority Client Problems
Impaired tissue perfusion
Acute pain
Activity intolerance
Anxiety
Risk for decreased cardiac output
Deficient knowledge
Page 82 – Goals / Expected Outcomes
Improved perfusion & pain control
↑ activity tolerance; ↓ anxiety
Demonstrate knowledge of disease & self-management.
Page 83 – Immediate Nursing Actions for Chest Pain
Stop activity
Apply O₂ 2 L/min nasal cannula
Check vitals + obtain ECG
Notify HCP
Administer nitrates/morphine as ordered
Prep for possible ICU transfer.
Page 84 – Evaluation Benchmarks
Client remains pain-free, ↑ activity tolerance.
Able to verbalize medication regimen & lifestyle changes.
Page 85-88 – Review Questions (NCLEX Style)
Pathologic change in CAD = Accumulation of lipid + fibrous tissue within coronary arteries (Answer C).
Stable angina: Relieved by stopping physical activity (Answer A).
Page 89-90 – Post-Angiogram Nursing Priorities (Order)
A Assess vital signs
E Assess catheter site
D Assess peripheral circulation
C Encourage PO fluids
F Document findings
B Perform discharge teaching
Page 91-92 – Simvastatin Discharge Teaching
Take in the evening (statins work best at night; answer choices list morning so not correct).
Possible GI upset – monitor (Correct answer = C).
Teach about myopathy/rhabdo warning signs & periodic liver/kidney tests.
End of comprehensive, page-by-page study notes on Atherosclerosis & Coronary Heart Disease.