Lesson 3 Part 1 Coronary Vascular Disorders

Coronary Artery Disease (CAD)

Atherosclerosis causing narrowing or obstruction of one or more coronary arteries; causes decreased perfusion of myocardial tissue and inadequate myocardial oxygen supply; leads to hypertension (HTN), myocardial infarction (MI), heart failure (HF), and death

Aorta

Main artery emerging from top of heart; origin point for coronary arteries

Right Coronary Artery

Branches from aorta; courses along right side of heart; supplies blood to right ventricle and portions of left ventricle

Left Coronary Artery

Branches from aorta; splits into circumflex artery and left anterior descending artery

Circumflex Artery

Curves around left side of heart; supplies blood to left atrium and lateral/posterior walls of left ventricle

Left Anterior Descending Artery (LAD)

Descends down anterior (front) surface of heart; supplies blood to anterior wall of left ventricle and interventricular septum; often called "widowmaker" due to critical importance

Coronary Atherosclerosis

Accumulation of fatty plaque on artery walls; blocks and narrows coronary vessels; reduces blood flow to myocardium and plaques can rupture; symptoms occur when enough blockage causes ischemia

Coronary Atherosclerosis Ischemia Thresholds

Left main artery ischemia occurs when reduced by 50%; any vessel ischemia occurs when reduced by 75%

Coronary Atherosclerosis Goal

Alter progression of atherosclerosis

CAD Modifiable Risk Factors

BMI greater than 30, diabetes mellitus, hypertension, alcohol use, high LDL and low HDL, smoking

CAD Non-Modifiable Risk Factors

Age 65 and older, family history

CAD Medications Overview

Nitrates (dilate coronary arteries, decrease preload and afterload), calcium channel blockers (dilate coronary arteries, decrease vasospasms), cholesterol-lowering medications (HMG-CoA statins, nicotinic acids, fibric acid, bile acid sequestrants, cholesterol absorption inhibitors, omega-3 fatty acids)

Stable Angina Characteristics

Predictable; occurs with exertion; triggered by exercise or strenuous activity; follows consistent pattern

Unstable Angina Characteristics

Preinfarction angina; occurs at rest and more frequently; more dangerous than stable angina; unpredictable pattern; warning sign of potential heart attack

Prinzmetal's/Variant Angina Characteristics

Coronary artery vasospasm; pain at rest with reversible ST-elevation; caused by coronary artery spasm; typically occurs at rest; shows ST-segment elevation on ECG that reverses when spasm resolves

Angina Pectoris Definition

Chest pain resulting from myocardial ischemia in one major artery; imbalance between oxygen demand and supply

Variant (Prinzmetal) Angina Etiology

Coronary vasospasm with strong association with cocaine and smoking use

Variant (Prinzmetal) Angina Symptoms

Occurs at rest without provocation; triggered by smoking; transient ST segment elevation during pain; associated with AV block or ventricular arrhythmias; with or without presence of CAD

Variant (Prinzmetal) Angina Treatment

Smoking cessation, calcium channel blockers

Stable Angina Etiology

Myocardial atherosclerosis

Stable Angina Symptoms

Exertional, 5-10 minutes; aggravated by exercise, exposure to cold, emotional stress; stable pattern of onset, duration, severity, and relieving factors; relieved by rest

Stable Angina Treatment

Nitrates, beta blockers, calcium channel blockers, aspirin

Unstable Angina (Pre-infarction Angina) Etiology

Ruptured or thickened plaque with platelet and fibrin thrombus

Unstable Angina Symptoms

Angina of increasing intensity, frequency, or duration; occurs at rest or with minimal activity; longer than 15 minutes; pain unresponsive to nitroglycerin (NTG)

Unstable Angina Treatment

Oxygen, pain medication, nitrates, beta blockers, aspirin, statins, tPA

Angina Insufficient Blood Flow

Insufficient blood flow to heart muscle from narrowing of coronary artery may cause chest pain from plaque in coronary artery

Nitrates for Angina

Vasodilators; decrease ischemia resulting in decreased pain

Beta Blockers for Angina

Decrease myocardial oxygen consumption

Calcium Channel Blockers for Angina

Relaxes blood vessels; increases oxygen supply to heart; decreases workload of heart

Antiplatelet Medications for Angina

Prevents platelet aggregation and thrombosis formation

Medications that Reduce Heart Rate

Beta-blockers and calcium channel blockers to address increased myocardial oxygen consumption from increased heart rate

Medications that Reduce Preload

Beta-blockers, nitrates, and calcium channel blockers to address increased myocardial oxygen consumption from increased blood volume (preload)

Medications that Reduce Afterload

Beta-blockers, nitrates, and calcium channel blockers to address increased myocardial oxygen consumption from increased blood pressure (afterload)

Medications that Reduce Contractility

Beta-blockers and calcium channel blockers to address increased myocardial oxygen consumption from increased muscle contractility

Antianginal Nitrates (Nitro-Bid, Nitrostat) Uses

Chest pain associated with angina

Antianginal Nitrates Mechanism

Vasodilation to increase oxygen to veins and large arteries; does not dilate coronary arteries; improves blood delivery to heart muscle and decreases work of heart thereby decreasing oxygen demand; decreases preload and afterload

Antianginal Nitrates Side Effects

CNS effects include headache, dizziness, weakness; cardiovascular effects include hypotension, flushing, pallor, increased perspiration

Antianginal Nitrates Contraindications

Hepatic/renal disease, hypotension, hypovolemia, increased intracranial pressure (ICP)

Antianginal Nitrates Nursing Pearls

Sublingual administration under tongue until dissolved; 1 tablet for pain up to 3 times; store in dark, tightly capped bottle; check blood pressure before and after administering

Myocardial Infarction (MI) Risk Factors

Atherosclerosis, coronary artery disease (CAD), elevated cholesterol levels, smoking, hypertension (HTN), obesity, sedentary lifestyle, stress

Acute Chest Pain Presentation Differential

Atherosclerosis leads to angina leads to MI; myocardial tissue abruptly and severely deprived of oxygen

MI Classic Presentation

Sudden crushing chest pain radiating to shoulder, nausea/vomiting, shortness of breath, sweating

MI Atypical Signs and Symptoms in Women

Shortness of breath, fatigue, indigestion, nausea

MI Atypical Signs and Symptoms in Older Adults

Shortness of breath, pulmonary edema, dizziness, altered mental status, dysrhythmias

Low Density Lipoproteins (LDL)

Bad cholesterol produced by liver; enters circulation as tightly packed cholesterol, triglycerides, and lipids; carried by proteins that enter circulation; broken down for energy or stored for future

High Density Lipoprotein (HDL)

Good cholesterol produced by liver; enters circulation as loosely packed lipids; used for energy; picks up remnants of fats and cholesterol left in periphery by LDL breakdown

Dyslipidemia Types

Hypercholesterolemia, hypertriglyceridemia, hyperlipidemia

Cholesterol Normal and Abnormal Levels

Normal less than 200 mg/dL; borderline 200-239 mg/dL; high greater than 240 mg/dL

LDL Normal and Abnormal Levels

Optimal less than 100 mg/dL; borderline 100-159 mg/dL; high greater than 160 mg/dL; lower is better (bad cholesterol)

HDL Normal and Abnormal Levels

Optimal greater than 60 mg/dL; borderline 41-59 mg/dL; low less than 40 mg/dL; higher is better (good cholesterol)

HMG-CoA Reductase Inhibitor Atorvastatin (Lipitor) Uses

Hyperlipidemia; primary prevention for those at risk for CAD; secondary prevention to stabilize fatty plaques in those with CAD

HMG-CoA Reductase Inhibitor Atorvastatin Mechanism

Blocks enzyme HMG-CoA (rate limiting step for cholesterol synthesis); causes plaque stabilization and reduction in plaque inflammation

HMG-CoA Reductase Inhibitor Atorvastatin Side Effects

GI effects include flatulence, abdominal cramps, constipation; neuro effects include dizziness and headache; liver effects include elevated enzymes, pruritus, muscle cramps and fatigue, hepatotoxicity

HMG-CoA Reductase Inhibitor Atorvastatin Drug Interactions

Grapefruit juice (increases risk for toxicity), fibrates (myopathy)

HMG-CoA Reductase Inhibitor Atorvastatin Nursing Pearls

Monitor liver levels (should lower LDL and increase HDL); report muscle pain immediately; pregnancy Category X

Bile Acid Sequestrant Cholestyramine Uses

Prevention of CAD by decreasing serum cholesterol levels (usually combination with statin); gallstone dissolution; pruritus associated with partial biliary obstruction

Bile Acid Sequestrant Cholestyramine Mechanism

Bile made and secreted in liver, stored in gallbladder; once emulsified, fats and lipids absorbed in intestines; bile acid resins bind to bile acid to form insoluble substance (cannot be absorbed); excreted in feces; decreased bile acid means liver uses cholesterol to make more bile, decreasing cholesterol

Bile Acid Sequestrant Cholestyramine Side Effects

Constipation; increased risk for bleeding related to vitamin K malabsorption; vitamin A and D deficiencies

Bile Acid Sequestrant Cholestyramine Drug Interactions

Malabsorption of fat-soluble vitamins (A, K, E, D), TZD, diuretics, digoxin, warfarin, thyroid hormones, corticosteroids

Bile Acid Sequestrant Cholestyramine Nursing Pearls

Comes in gritty powder; must be dissolved; taken with lots of fluids

Cholesterol Absorption Inhibitor Ezetimibe (Zetia) Uses

Lower serum cholesterol levels; treat familial hypercholesterolemia; treat homozygous sitosterolemia

Cholesterol Absorption Inhibitor Ezetimibe Mechanism

Works in small intestine to inhibit absorption of cholesterol

Cholesterol Absorption Inhibitor Ezetimibe Side Effects

GI effects include abdominal pain and diarrhea; muscle aches and pain

Cholesterol Absorption Inhibitor Ezetimibe Drug Interactions

Caution with combination with statin; cholestyramine, fenofibrate, gemfibrozil, warfarin

Niacin for Lipid Lowering

Vitamin B3; inhibits release of free fatty acids from adipose tissues; increases rate of triglyceride removal from plasma; side effects include GI disturbance, flushing, hepatotoxicity

Fenofibrates for Lipid Lowering

Inhibits triglyceride synthesis in liver to lower LDL; increases uric acid secretion; stimulates triglyceride breakdown

Omega-3 Fatty Acids for Lipid Lowering

Omega 3-acid ethyl esters (Lovaza) inhibits liver enzyme system to decrease synthesis of triglyceride; Omega 3-carboxylic acid (Epanova) is fish oil mixture of free fatty acids approved as adjunct to diet to reduce triglyceride levels with severe hypertriglyceridemiaRetryClaude can make mistakes. Please double-check responses.