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Antilipemic Drugs CAD/ Cholesterol What is Coronary Artery Disease? Damage or disease in heart’s major blood vessels Usual cause is buildup of plaque Causes coronary arteries to narrow limiting blood flow to the heart Coronary Atherosclerosisa Atherosclerosis is the abnormal accumu...
Antilipemic Drugs CAD/ Cholesterol What is Coronary Artery Disease? Damage or disease in heart’s major blood vessels Usual cause is buildup of plaque Causes coronary arteries to narrow limiting blood flow to the heart Coronary Atherosclerosisa Atherosclerosis is the abnormal accumulation of lipid deposits and fibrous tissue within arterial walls and lumen In coronary atherosclerosis, blockages and narrowing of the coronary vessels reduce blood flow to the myocardium Cardiovascular disease is the leading cause of death in the United States for men and women of all racial and ethnic groups Coronary artery disease (CAD) is the most prevalent cardiovascular disease in adults Cholesterol and physiologic roles Component of all cell membranes Required for synthesis of certain hormones (estrogen, progesterone, and testosterone) Synthesis of bile salts needed to absorb and digest dietary fats Some of cholesterol comes from dietary sources (exogenous) and some manufactured by cells in the liver (endogenous) Copyright © 2017, Elsevier Inc. All rights reserved. 4 Structure of Lipoprotein Copyright © 2017, Elsevier Inc. All rights reserved. 5 HDL vs LDL Copyright © 2017, Elsevier Inc. All rights reserved. 6 Classes of lipoproteins Distinctions among classes are based on size, density, apolipoprotein content, transport function, and primary core lipids (cholesterol or TG) Various classes of lipoproteins differ in density. Protein is denser than lipid, lipoproteins that have a higher percentage of protein, and low percentage of lipid have a relatively high density. Lipoproteins that have lower percentage of protein have a lower density. Copyright © 2017, Elsevier Inc. All rights reserved. 7 Lipoproteins and development of atherosclerosis Dietary cholesterol and saturated fat are processed by the GI tract, chylomicrons enter the blood. They are broken down into Chylomicron remnants in the capillaries. Liver processes them into lipoproteins. When released into the circulation, excess lowdensity lipoproteins (LDLs) adhere to receptors on intimal wall Macrophages ingest LDLs and transport them into the vessel wall beginning plaque formation. Copyright © 2017, Elsevier Inc. All rights reserved. 8 continued Macrophages are inflammatory cells Play an important role in the initiation and progression of atherosclerotic plaque Within a lesion, macrophages take up large amounts of cholesterol rendering them macrophage foam cells. These foam cells can be highly inflammatory and exacerbate lesion formation. Copyright © 2017, Elsevier Inc. All rights reserved. 9 Copyright © 2017, Elsevier Inc. All rights reserved. 10 Lipoproteins High-density (HDL) – Transports cholesterol for destruction and removes it from the body. “Good cholesterol” Low-density (LDL)- Carries the highest amount of cholesterol. LDL transports cholesterol from the liver to the tissues and organs. Storage of cholesterol in lining of blood vessels leads to “plaque” buildup and atherosclerosis. “Bad cholesterol” Very low-density lipoproteins (VLDL)- Primary carrier of triglycerides in blood. VLDL reduces in size and becomes LDL. Reducing LDL levels in the blood has shown to decrease the incidence of Coronary Artery Disease. Risk Factors for Coronary Artery Disease (CAD) Four modifiable risk factors cited as major (cholesterol abnormalities, tobacco use, HTN, and diabetes) Elevated LDL: primary target for cholesterol-lowering medication Metabolic syndrome hs-CRP (high-sensitivity C-reactive protein) AAP Guidelines for cholesterol screening Lipid screening for ALL children between 9 and 11 years, followed by another screen between 18-21 years. If family history of high cholesterol or heart disease screening should be sooner between 2 and 8 years Cholesterol for Children and Adolescents acceptable level is less than 170 Adult Screening All adults over 20 years old should be screened every 5 years for total cholesterol, LDL cholesterol, HDL cholesterol, and TGs. In absence of risk factors, middle aged adult should be screened for dyslipidemia at least every 1 to 2 years. See table 10.1 Plasma cholesterol and triglyceride levels Controlling Lipid Levels through Lifestyle Changes Monitor blood lipid levels regularly Maintain weight at optimal level Implement a medically supervised exercise plan Reduce dietary saturated fats and cholesterol (Cholesterol intake is not to exceed 300mg/day) Increase soluble fiber in diet ( oat bran, apples, beans, broccoli) Eliminate tobacco * Pharmacotherapy should only be initiated after lifestyle changes fail. Question #1 The nurse is caring for a patient with hypercholesterolemia who has been prescribed atorvastatin (Lipitor). What serum levels should be monitored in this patient? A. Complete blood count (CBC) B. Blood cultures C. Na and K levels D. Liver enzymes Antilipemics: Statins Hydroxymethylglutaryl–coenzyme A (HMG– CoA) reductase inhibitors (HMGs, or statins) Atovastatin-(Lipitor) Most common statin used Simvastatin (Zocor) One of the first statins to become generic. Lovastain (Mevacor)* Copyright © 2017, Elsevier Inc. All rights reserved. 17 Statins Therapeutic classification: Antihyperlipidemic Pharmacologic class: HMG-CoA reductase inhibitor, statin Statins are drugs of choice for reducing lipid levels Mechanism of Action: Inhibits HMG-CoA reductase which is essential to hepatic production of cholesterol. This increase LDL receptors in the liver, which results in removal of LDL from the blood. LDL and triglyceride levels are reduced and HDL is increased. *It takes approximately 2 weeks for effects to be seen. Primary goal: Reduce the risk of MI (Heart Attack) and CVA (Stroke).] Hypercholesterolemia Uses:Primary and Secondary Prevention of CV events Statin continued: Contraindicated in patients with history of liver disease, Rhabdomyolysis, seizures, pregnancy (Category X) Cholesterol biosynthesis in the liver is greater at night, and should be taken in the evening. Generally, statins preferred taken in evening or bedtime, Atorvastatin has a long half life, and can be given without regard to time of day. HMG-CoA Reductase Inhibitors: Adverse Effects Mild, transient gastrointestinal (GI) disturbances Rash Headache Myopathy (muscle pain), possibly leading to the serious condition rhabdomyolysis Elevations in liver enzymes or liver disease Copyright © 2017, Elsevier Inc. All rights reserved. 20 Continued: Small percentage experience liver damage; but frequent monitoring of hepatic function is essential Most serious adverse effect: Rhabdomyolysis. Nursing implications: CK should be measured at baseline before start of drug and whenever symptoms of myositis. Monitor client for muscle pain, tenderness, or weakness. If present report to Dr. and check CK Creatine KinaseDISCONTINUE DRUG IF LEVELS ARE ELEVATED OR MYOPATHY is suspected. Monitor glucose levels especially in diabetics. Monitor LFTs (Liver function tests) Monitor lipid and cholesterol levels Rhabdomyolysis Breakdown of muscle fibers usually due to muscle trauma or ischemia. Contents of muscle cells spill into the systemic circulation causing fatal acute renal failure. Mechanism why statins cause this is unknown Client Teaching Statins Tell client to report muscle pain, tenderness, weakness, yellowing of skin, eyes, stomach pain, nausea/vomiting, or loss of appetite. Do not take if pregnant! Minimize alcohol intake with this drug Avoid grapefruit juice Bile-Acid SequestrantsCholestyramine Bile contains bile acids which are critical for digestion, and absorption of fats and fatsoluble vitamins in the small intestine. Many waste products including bilirubin are eliminated from the body by secretion into bile and elimination in feces. MOA: Reduce LDL levels by increasing LDL receptors on hepatocytes. Bile acids secreted in the intestine are normally reabsorbed and reused. These drugs prevent the reabsorption. Used primarily as adjuncts to statins Copyright © 2017, Elsevier Inc. All rights reserved. 24 Adverse Effects Mainly GI- Abd. Fullness, flatulence, diarrhea, constipation Mainly constipation Contraindications: Patients with complete biliary obstruction Drugs binds with Vitamin K so caution with any coagulopathy problems Decreases absorption of many meds: Digoxin, folic acid, glipizide, propranolol, tetracycline, thiazide diuretics, thyroid hormones, fat soluble vitamins and warfarin Herbs and food high in fiber can increase effects Administration: Mix powder with water, other fluids, soups, applesauce and follow with more fluids. Do not take with other meds. Should take drugs 1 hour before or 4-6 hours after cholestryramine Copyright © 2017, Elsevier Inc. All rights reserved. 25 Ezetimibe (Zeitia) Blocks cholesterol absorption in small intestine Can be used alone or with statin drugs Contraindicated in pregnancy and lactation Copyright © 2017, Elsevier Inc. All rights reserved. 26 Gender HRT Cardiovascular events in women tend to occur 10 years later in life than men. Women tend not to recognize symptoms of CAD as early as men They wait longer to report symptoms and seek treatment Menopause and HRT HRT: decreases symptoms of osteoporosis fractures but has been associated with increased risk for CAD, Breast cancer, DVT, CVA, and PE HRT is not promoted as primary or secondary prevention of CAD (AHA,2015) Copyright © 2017, Elsevier Inc. All rights reserved. 27 Matching Atherosclerosis a. Damaged cells/tissues Angina inadequate oxygen supply Ischemia b. Plaques in arterial walls Myocardial Infarction (MI) attack c. Necrosis of myocardium; heart d. Chest pain when unable to heart Copyright © 2017, Elsevier Inc. All rights reserved. heart’s oxygen meet demands of the 28 Angina Pectoris Acute chest pain caused by insufficient oxygen to a portion of the myocardium. Pharmacology is aimed at lowering the myocardial oxygen demand. Angina Pectoris (Chest Pain) When the supply of oxygen and nutrients in the blood is insufficient to meet the demands of the heart, the heart muscle “aches.” The heart requires a large supply of oxygen to meet the demands placed on it. Copyright © 2017, Elsevier Inc. All rights reserved. 30 Benefit of drug therapy for angina through increasing oxygen supply and decreasing oxygen demand Copyright © 2017, Elsevier Inc. All rights reserved. 31 Treatment Treatment seeks to decrease myocardial oxygen demand and increase oxygen supply Medications Oxygen Reduce and control risk factors Reperfusion therapy may also be done Audience Response System Question A patient is mowing his lawn on a hot Saturday afternoon. He begins to notice chest pain. What should his first action be? A. Take his nitroglycerin tablet B. Stop mowing and sit or lie down C. Go inside the house to cool off and get a drink of water D. Call 911 Copyright © 2017, Elsevier Inc. All rights reserved. 33 Drugs for Angina Nitrates or nitrites Beta blockers (Ex: Atenolol/Tenormin)Beta Adrenergic Antagonists Calcium channel blockers (CCBs) *Nifedipine (Amlodipine/Norvasc) Copyright © 2017, Elsevier Inc. All rights reserved. 34 Nitrates and Nitrites Available forms Transdermal Sublingual* Chewable Oral tablets capsules/tablets Intravenous (IV) patches* Ointments* Translingual sprays* solutions* *Bypass the liver and the first-pass effect. Copyright © 2017, Elsevier Inc. All rights reserved. 35 If the chest pain goes away after sitting down what type of angina is it? Questions ? What is the underlying cause of exertional angina? If blood flow is only partially blocked in an artery what type of pain is this? If complete blockage occurs, blood flow will stop and what will occur? Copyright © 2017, Elsevier Inc. All rights reserved. 36 Questions? What type of angina is caused by coronary artery spasm, which constricts blood flow to the myocardium? How is it different than stable angina? Copyright © 2017, Elsevier Inc. All rights reserved. 37 Angina: Organic Nitrates: Nitroglycerin (Nitro-Bid) Oldest and most widely used Antianginal drug Action: Potent vasodilator, relaxes vascular smooth muscle. Dilation of both venous and arterial blood vessels. SL, PO , IV, Transdermal (Leave on for 12 hours and then off for 10-12 hours), Topical, Extended Release form Kinetics: SL FORM 0nset: 1-3 minutes, Peak: 4-8 minutes, Duration: 30-60 minutes Storage: Dark sealed glass bottle at room temperature Use gloves when applying paste or ointment Dose: 0.4 mg SL every 5 minutes X 3 maximum doses. (Max. 3 doses in 15 minutes) Nitroglycerin Adverse Effects Dilates cerebral vessels: HEADACHE is common and can be severe. (Seldom lasts longer than 20 minutes) Postural hypotension- Teach patient Occasionally the venous dilation can occur too rapidly, the cardiovascular system overcompensates and causes a REFLUX TACHYCARDIA MONITOR B/P Prior to administering and in between doses. What are the parameters? Contraindicated in clients with Head trauma, ICP(Intracranial pressure) Avoid alcohol Beta Blockers Propranolol and Metoprolol Prevents pain of stable angina by decreasing the heart rate and contractability of the heart, which decreases cardiac oxygen demand. What does beta 1 and beta 2 do? What should the nurse assess when patient is taking a beta blocker? Do not stop abruptly or can precipitate MI Asthma patients and beta blockers? Beta blockers can also mask the signs of ____ and used with caution with diabetics. Copyright © 2017, Elsevier Inc. All rights reserved. 40 amlodipine Calcium Channel Blockers for Chronic Stable Angina Copyright © 2017, Elsevier Inc. All rights reserved. diltiazem nicardipine nifedipine verapamil 41 Calcium Channel Blockers: Prototype: Nifedipine Contraction of muscle is regulated by amount of Calcium ion inside the cell Selectively blocks calcium channels in the myocardial and vascular smooth muscle, including those in the coronary arteries. Decreases muscle contraction, and relaxes arterial smooth muscle, lowering peripheral resistance and decreases B/P. Results in less oxygen utilization of the heart, an increase in cardiac output, and a fall in B/P. Uses: HTN, Angina Do not give within the first 1-2 weeks following a MI Grapefruit juice can may enhance absorption of nifedipine. Place the following nursing intervention s in order for a client experiencin g chest pain Administer Nitroglycerin SL Assess Heart Rate and B/P Assess the location, quality, and intensity of pain Document interventions and outcomes Evaluate the location, quality, and intensity of pain ED drugs such as sildenafil/ Viagra are contraindicated in client’s taking Nitrates because: A. They contain nitrates, resulting in overdose B. They decrease B/P and may result in prolonged and severe hypotension when combined with nitrates. C. They will adequately treat the patient’s angina as well as ED D. They will increase the possibility of nitrate tolerance developing and should be avoided unless other drugs can be used. Nursing Intervention— Treat Angina Priority Patient is to stop all activity and sit or rest in bed (semiFowler positioning) Assess the patient while performing other necessary interventions. Assessment includes VS, observation for respiratory distress, and assessment of pain. In the hospital setting, the ECG is assessed or obtained Administer medications as ordered or by protocol, usually NTG. Reassess pain and administer NTG up to three doses Teach patient to carry NTG at all times. Administer oxygen 2 L/min by nasal cannula- See QSEN EBP Page 573 Ranolazine Anti-ischemic modulator Approved first-line treatment for chronic angina NOT approved for acute angina symptoms Increases energy production of the heart to preserve cardiac function without decreasing blood pressure or heart rate. Reserved for patients: 1. Haven’t had adequate response to beta blockers 2) Combination with beta blockers when initial treatment with BB has not been successful. Copyright © 2017, Elsevier Inc. All rights reserved. 47 Use a calm manner Nursing Interventio n: Reduce Anxiety Stress-reduction techniques Patient teaching Addressing needs may anxieties patient’s spiritual assist in allaying Address both patient and family needs Myocardial Infarction Acute Coronary Syndrome Relationships among coronary artery disease, chronic stable angina, and acute coronary syndrome. Copyright © 2017, Elsevier Inc. All Rights Reserved. Assessment and Findings May be described as tightness, choking, or a heavy sensation Frequently retrosternal and may radiate to neck, jaw, shoulders, back or arms (usually left) Anxiety frequently accompanies the pain Other symptoms may occur: dyspnea or shortness of breath, dizziness, nausea, and vomiting The pain of typical angina subsides with rest or NTG Unstable angina is characterized by increased frequency and severity and is not relieved by rest and NTG. Requires medical intervention! Clinical Manifestations of ACS Myocardial Infarction (MI) ST-elevation and non-ST-elevation Result of abrupt stoppage of blood flow through a coronary artery, causing irreversible myocardial cell death (necrosis) Most MIs occur in the presence of preexisting CAD STEMI - occlusive thrombus NSTEMI - non-occlusive thrombus Copyright © 2017, Elsevier Inc. All Rights Reserved. Each small box is 0.04 sec Copyright © 2017, Elsevier Inc. All rights reserved. 55 ECG Patho Changes with MI 12 lead ECG –Perform within 10 minutes-CRUCIAL Expected ECG changes with a MI includes: T wave inversion ST-segment elevation Abnormal Q wave As area of injury becomes ischemic, myocardial repolarization is altered and delayed causing T wave to invert. Myocardial injury also causes ST changes. ST is normally flat. The injured myocardial cells depolarize normally but repolarize more rapidly than normal cells, causing the ST to elevate Abnormal Q waves is another indication of MI, usually will develop within 1-3 days. It is 0.04 sec longer and 25% of the R wave depth. An acute MI can cause a significant decrease in the height of the R wave. Effects of Ischemia, Injury, and Infarction on ECG Myocardial Infarction From Occlusion Copyright © 2017, Elsevier Inc. All Rights Reserved. Copyright © 2017, Elsevier Inc. All rights reserved. 61 Acute Myocardial Infarction Copyright © 2017, Elsevier Inc. All Rights Reserved. Locations and Patterns of Angina and MI Copyright © 2017, Elsevier Inc. All Rights Reserved. Acute Coronary Syndrome: MI WR. a 48-year-old male complaining of chest pain is brought to the emergency room by ambulance. The pain began six hours ago and has become more severe over the past hour prompting him to call emergency services. He describes the pain as retrosternal, pressure-like, and non-radiating. He says it feels like “bad indigestion.” He endorses some dyspnea and nausea accompanying the pain. He has also noted intermittent palpitations since last evening. VS 160/90, HR 110, RR 26, Temp 99 Questions? Using the PQRST and assessing him for pain. What did the nurse miss? Evaluate Top vital signs priority problems (Physical and psychological) Continued… He has a past medical history of hypertension and tobacco use of one pack per day of cigarettes for the past 36 years. He has significant male-pattern obesity (beer belly). Hx of eating high fat diet. He was put on O2 2 L NC to keep sat greater than 93%. He was started on a Nitroglycerin infusion. He was given 325 mg ASA to chew. He reports no allergies and no medication use. He says he is just “fine” in a loud angry voice and demands a cigarette. Copyright © 2017, Elsevier Inc. All rights reserved. 66 Question What are WR’s risk factors? Question? What first actions should the nurse take after the patient has arrived in the emergency department? Copyright © 2017, Elsevier Inc. All rights reserved. 68 Question? Before starting the Nitroglycerin drip what is an important question the nurse should ask the patient? Question You monitor W.R. for side effects of the NTG infusion. Side effects of NTG include which of the following? Select all that apply A. Constipation B. Headache C. Tachycardia D. Postural hypotension E. Decreased respirations Which lab is Appropriate or Inappropriate for WR? CBC EEG in am Basic metabolic panel Prothrombin time PT and Partial Thromboplastin time (PTT) Bilirubin UA STAT 12 lead ECG Type and crossmatch for 2 units PRBCs CXR on admission and in am Question What significant labs are missing? How are you going to respond to his angry demands for smoking? He is also requesting something for his “heartburn.” How will you respond? His wife is present and asks, “Why can’t you give him one of those nicotine patches? How should the nurse respond? What about use of Morphine? Special precautions, Considerations, New Research Continued… ECG reveals an anterior wall STelevation myocardial infarction Copyright © 2017, Elsevier Inc. All rights reserved. 73 Results: CPK 350 u/L (39-308 u/L) CPK-MB 75 u/L (5-25 u/L) Troponin 10 (0-0.4 ng/ml Myoglobin 95 ng/ml (0-85 ng/ml CXR reveals cardiomegaly BNP 150 CBC, CMP, Coagulation labs Normal results Question What is the priority and plan for the patient now? Results Cardiac catherization 80% LAD was blocked and a cardiac stent was placed. Ejection fraction 35% Left ventricular systolic dysfunction Stent Discharge teaching What would the nurse expect to teach the patient based on WR’s medical management, life-style modification, and post-procedure? The patient asks the nurse why each of these medications are needed and what should the nurse teach the patient about these meds? Clopidogrel 75 mg daily Aspirin 81 mg daily Metoprolol 50 mg daily Atrorvastatin 80 mg daily What medication is missing on the discharge instructions? JC Core Measures :AMI AMI-1 Aspirin at Arrival (Type of oral? And dose?) AMI-2 Aspirin Prescribed at Discharge (Dose?) AMI-3 ACEI or ARB for LVSD AMI-4 Adult Smoking Cessation Advice/Counseling* AMI- 5 Beta Blocker Prescribed at discharge AMI-7 Median Time to Fibrinolysis (alteplase) AMI-7a Fibrinolytic Therapy Received Within 30 Minutes of Hospital Arrival AMI-8 Median Time to Primary PCI AMI-8a Primary PCI Received Within 90 Minutes of Hospital Arrival Antiplatelet Drugs- Aspirin If a client is taking ASA 81 mg by mouth daily. is the reason for this? What Usually low dose 80-325mg mg/day. MOA: Inhibits thromboxane A2 which causes platelet aggregation U.S. Preventative Services Task Force updated guidelines on the use of aspirin for primary prevention of MI. Recommends ASA for men ages 45 to 79 years and women ages 55 to 79 when the potential benefit of a reduction in MI outweighs the potential harm of GI Bleed. Adding a PPI may be helpful to decrease gastric acid. Clopidogrel (Plavix) Antiplatelet drug Pharmacological class: ADP Receptor blocker Inhibits Platelet aggregation (clumping) by preventing the binding of adenosine diphosphate to its platelet receptor. Uses: Secondary Prevention of MI, Stroke, and vascular death Prevention of clot formation post stent placement Monitor for GI bleeding and bleeding. Monitor Platelet count- may decrease PLT Countthrombocytopenia. Teach patient to avoid ASA, NSAID unless approved by health care provider. Fibrinolytic System Initiates the breakdown of clots and serves to balance the clotting process Fibrinolysis: mechanism by which formed thrombi are lysed to prevent excessive clot formation and blood vessel blockage Copyright © 2017, Elsevier Inc. All rights reserved. 82 Fibrinolytic System (Cont.) Fibrin in the clot binds to a circulating protein known as plasminogen. This binding converts plasminogen to plasmin. Plasmin is the enzymatic protein that eventually breaks down the fibrin thrombus into fibrin degradation products. This keeps the thrombus localized to prevent it from becoming an embolus. Copyright © 2017, Elsevier Inc. All rights reserved. 83 ALTEPLASE (tpa) Known It as tissue plasminogen activator is identical to natural occurring human tPA Binds with plasminogen Alteplase-plasminogen complex then catalyzes the conversion of other plasminogen molecules into plasmin, an enzyme that digests the fibrin meshwork of clots. Copyright © 2017, Elsevier Inc. All rights reserved. 84 Uses: Alteplase Major indications: Acute MI- What type of MI? Acute ischemic stroke Acute massive PE The For sooner it is administered better the outcome. Acute MI within 4-6 hours or sooner! Always Very given by IV infusion short ½ life (5 minutes) Adverse effects: BLEEDING/ Intracranial bleeding Copyright © 2017, Elsevier Inc. All rights reserved. 85
