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Introduction of Acute Coronary Syndrome PowerPoint Presentation

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  • Slide 1 - Coronary Artery Disease Cardiac Pharmacology Myocardial Infarction Lecture 2 NUR240 Joy Borrero, RN, MSN 9/10 Angina PectorisAcute Coronary Syndrome
  • Slide 2 - Coronary Artery Disease Etiology Risk factors Nonmodifiable vs. modifiable risk factors Clinical manifestations Goals of therapy Medications
  • Slide 3 - ATHEROSCLEROSIS START END
  • Slide 4 - STATINS aka: (COENZYME INHIBITOR) Mevacor, Zocor, Lipitor BLOCKS BIOSYNTHESIS OF CHOLESTEROL HIGH FIRST PASS EFFECT *MONITOR LFT SIDE EFFECTS N/V/D & ABDOMINAL CRAMPS MYALGIA, ARTHRALGIA,Cataracts HEADACHES, DIZZINESS, INSOMNIA Liver and kidney dysfunction
  • Slide 5 - Angina Pectoris Episode of chest pain or pressure due to insufficient artery flow of oxygenated blood. Myocardial 02 demand exceeds 02 supply. CAD is the most common cause. One coronary artery branch becomes completely occluded; therefore, 02 is not perfused to the myocardium, resulting in transient ischemia and subsequent retrosternal pain.
  • Slide 6 - Angina Pectoris Precipitating Factors: Warning Sign for MI Clinical Signs & Symptoms: do not occur until lumen is 75% narrowed. Sternal pain: mild to severe. May be described as heavy, squeezing, pressing, burning, crushing or aching. Onset sudden or gradual. May radiate to L. shoulder and arm. Radiates less commonly to R. shoulder, neck, jaw. Pt may have weakness/numbness of wrist, arm, hands. pain usually short duration and relieved by removal precipitating factors,rest or NTG. Can be gradual (CAD) or sudden(vasospasm) Associated Symptoms: dyspnea, N & V, tachycardia, palpitations, fatigue, diaphoresis, pallor, weakness, syncope, factors
  • Slide 7 - Types of Angina Stable: There is a stable pattern of onset, duration and intensity of sx, pain is triggered by a predictable degree of exertion or emotion. Variant Angina (Prinzmetal's) Cyclical, may occur at rest. Ventricular arrhythmia, brady arrhythmia and conduction disturbances occur. Syncope associated with arrhythmia may occur Nocturnal Angina only at night. Possible associated with REM sleep. Unstable Angina AKA Pre infarction angina Pain is more intense, lasts longer
  • Slide 8 - Assesment 1. Hx 2. Physical Exam 3. EKG 4. Exercise EKG 5. Thallium Scan 6. Coronary Angiography 7. Cardiac Enzymes
  • Slide 9 - Medications for Angina 1. Nitrates decrease myocardial 02 demand via peripheral vasodilation and reverse coronary artery spasm thus increase 02 supply to myocardial tissue. 2. Understanding how Nitrates Work: peripheral vasodilation results in: -decreased 02 demand -decreased venous return to heart -decreased ventricular filling which results in decreased wall tension and thus -decreased 02 demand
  • Slide 10 - NTG Forms: SL (Nitrostat) Lingual Sprays - similar to SL in use (Nitrolingual) Sustained release capsules/tablets (Nitrobid) Ointments 2% (Nitrobid)- wear gloves when applying Transdermal Patch (Nitro-Dur) IV (Tridil) For attacks unresponsive to other tx
  • Slide 11 - Side/Adverse Effects Vascular HA (may be severe) Hypotension (may be marked) Tachycardia Palpitations
  • Slide 12 - Acute Angina Treatment Goal: Enhance 02 supply to myocardium: M- Morphine for pain O- Oxygen 4-6L as ordered N- NTG sublingual, repeat q5 minutes x3 A- Aspirin to prevent platelet aggregation
  • Slide 13 - Angina Treatment The focus is to relieve acute attacks and prevent further attacks. 1. Activity/exercise tolerance - a regular exercise prescription is established after stress testing and/or cardiac cath. Baseline Gradual increase Avoid Alternate ADLS NTG before exercise
  • Slide 14 - Patient education Lifestyle modifications for controllable risk factors. Support groups are helpful, Example: Weight watchers, Smoke-enders, stress workshops, cardiac rehabilitation. Supply patients with information, name of contact person and phone numbers Identify precipitating factors for Anginal pain Medication compliance
  • Slide 15 - Cardiac Pharmacology
  • Slide 16 - Beta-adrenergic Blockers Therapeutic effect - decrease the rate and force of the cardiac contraction (resulting in decreased 02 demand) and decrease vasoconstriction in the myocardium and vasculature. Mechanism of Action - inhibit circulating catecholamines from stimulating beta receptor sites. There are two type of beta receptors (B1 & B2).
  • Slide 17 - Beta-adrenergic Blockers B1 receptor stimulation by catecholamines results in increased HR & myocardial contractility so, blocking the B1 effect results in slowed HR & decreased myocardial contractility. Cardio-selective Excess blockade can result in bradycardia, heart block, heart failure and/or hypotension. atenolol (Tenormin) metoprolol (Lopressor, Toprol)
  • Slide 18 - Beta-adrenergic Blockers B2 receptor stimulation by catecholamines results in dilation of the bronchial tree, the coronary arteries and the peripheral vasculature Blocking the B2 effect results in bronchoconstriction, coronary artery vasoconstriction and peripheral vascular constriction. Drugs that have a B2 blockade effect are used cautiously/contraindicated in clients with COPD. Non-selective Beta Blockers - Block B1 and B2 receptors propanolol (Inderal) carvedilol (Coreg)
  • Slide 19 - Beta-adrenergic Blockers Side Effects - many may be predicted based upon understanding the mechanism of action. Hypotension Bradycardia Heart Failure Weakness/Fatigue Depression Impotence Hypoglycemia Hallucinations Patient Teaching: Use with caution in clients prone to coronary artery spasm due to vasoconstrictive effects. Contraindicated in clients with CHF and second or third degree heart block due to the rate slowing and reduction in contractility. Non-selective beta blockers contraindicated with COPD. Do not abruptly discontinue beta blockers
  • Slide 20 - Calcium Channel Blockers Action - inhibit flow of Ca+ across cell membrane. Ca+ is essential for cardiac stimulation, conduction, contractility and relax vascular smooth muscle which results in decreased 02 demand and increased coronaryblood supply VASODILATION Indications: angina, HTN, arrhythmia Drugs- verapamil (Calan, Isoptin) diltiazem (Cardizem) nifedipine (Procardia) amlodipine (Norvasc)
  • Slide 21 - Calcium Channel Blockers Side Effects of Calcium Channel Blockers Constipation (with Verapamil) Dizziness Facial Flushing HA Edema of ankles/feet Bradycardia Hypotension
  • Slide 22 - Epinenepherine (adrenalin) Vasoconstriction- Increase BP Alpha, Beta 1 and Beta 2 agonist Decrease congestion of nasal mucosa Catacholamine- produced by…… Tx of AV block and cardiac arrest
  • Slide 23 - ACE INHIBITORS –The “prils” Angiotensin Converting Enzymes Inhibitors Action: Blocks production of Angiotensin II in kidneys Indications: HF, HTN, MI, DM neuropathy Causes: Vasodilation (mostly arteriole) Decreased BP Excretion of Na and H2O (but not K) Ex.: captopril (Capoten) enalapril (Vasotec) fosinopril (Monopril) ramapril (Altace) SE : ortho hypotension, dry cough, hyperkalemia
  • Slide 24 - Angiotensin Receptor Blockers- ARBs Action- Block the binding of Angiotensin II to it’s receptor in the vascular and adrenal tissues Examples: candesartan (Atacand) losartan (Cozaar)
  • Slide 25 - Cardiac Glycoside digoxin (Lanoxin) Action :+Inotropic effect Increases force of myocardial contraction - Chronotropic effect- decreases HR Tx: heart failure, afib Nsg: Apical Pulse for 1 full minute, hold for <60, same time daily Monitor Dig levels 0.5-0.8 ng/ml Monitor K levels Monitor for Dig toxicity: anorexia, fatigue, weakness, vision changes (halos)
  • Slide 26 - Myocardial Infarction Leading cause of death in US Thrombosis in atherosclerotic artery causes 90% of MIs. A region of the myocardium is abruptly deprived of blood supply due to restricted coronary blood flow Ischemia results and may lead to necrosis within 6 hours JCAHO Core Measures for AMI (4/10)
  • Slide 27 - Gender Differences in MI Females, when compared to males: -present with MI later in life -have poorer prognosis and high morbidity -are 2x as likely to die in the first weeks -are more likely to die from the first MI -have higher rates of unrecognized MI -NSTEMI MI vs STEMI
  • Slide 28 - EKG changes with MI
  • Slide 29 - Location of MI Depends on which artery is affected LV receives most of the CA supply and so it is the most affected Left Anterior Descending (LAD) Left Circumflex artery (LCA) Right Coronary Artery (RCA)
  • Slide 30 - General Types of MI Transmural-invades full thickness of myocardium Subenedocardial-invades partial thickness
  • Slide 31 - Collateral Circulation A network of blood vessels present at birth that can dilate and become functional a/r/o coronary artery occlusion and ischemia. “collateral circulation” Natural “bypass” mechanism helps decrease the size of the MI
  • Slide 32 - Risk Factors and Etiology CAD and its risk factors Any situation requiring increased O2 in the presence of decreased O2 supply. Non atherosclerotic coronary artery occlusions
  • Slide 33 - Effects of MI Cell death Contractility in the affected areas reduced or absent Electrical instability
  • Slide 34 - Dysrhythmias occur in 90% of patients PVCs V tach V fib Bradycardia
  • Slide 35 - Complications of MI CHF Mitral Valve Insufficiency Dysrhythmias Pericarditis Post Infarction MI Thromboembolic Complications Rupture of Ventricular Wall
  • Slide 36 - MI Precipitating Factors None in most cases Severe exertion and stress 59% occur at rest or while asleep
  • Slide 37 - Clinical Manifestations Angina-Chest Pain Vital Signs Heart and Lung Associated S&S
  • Slide 38 - What’s the difference? Angina Myocardial Infarction
  • Slide 39 - Diagnosis of MI Based on 2 out of 3 criteria Chest pain indicative of ischemic heart disease Characteristic EKG changes (ST elevation) Marked rise and eventual decline in serum markers of cardiac injury
  • Slide 40 - Diagnostic studies EKG Serum Enzymes/Cardiac Biomarkers Cardiac Catheterization Other lab tests Echocardiogram CXR Pulse Ox
  • Slide 41 - Goals Limit size of infarct/prevent further damage Increase O2 supply and decrease O2 demand Prevent and /or recognize complications early Reduce pain
  • Slide 42 - Nursing Diagnosis
  • Slide 43 - Nursing InterventionsRemember: MONA and Oh Batman Obtain EKGs Monitor mentation Assess heart sounds Assess lungs Assess peripheral circulation/skin Assess urinary output Assess GI function Assess pain
  • Slide 44 - OH BATMAN! O H B A T M A N
  • Slide 45 - Nursing Interventions Activity Safety Reduce anxiety Patient Education Nutrition
  • Slide 46 - Pharmacology Therapy for MI Thrombolytic Agents a/k/a Plasminogen Activators (Streptokinase, T-PA,Retavase) -decrease infarct size -improved ventricular function -increased survival rates Glycoprotein IIB and IIIA
  • Slide 47 - Pharmacology Therapy ASA Nitrates Morphine Sulfate Beta blockers Calcium channel blockers ACEs and ARBs
  • Slide 48 - Antiarrhythmics Class IA- Na channel blockers Class IB- Na channel blockers Class II- Beta blockers Class III- Amiodarone Class IV- Ca Channel blockers
  • Slide 49 - Anticoagulants Heparin LMWH- Lovenox, Fragmin
  • Slide 50 - Post MI Cardiac rehab Begins in acute phase and continues indefinitely as outpatient Includes: education activity progression counseling medical management
  • Slide 51 - Non-Pharmacologic Therapy Percutaneous transluminal coronary angioplasty (PTCA) Dilates coronary arteries obstructed by plague. 30% restenosis rate within first 6 months. Patient Criteria Non-calcified lesions less than 2 cm. The ideal candidate would have less than a one year history of angina and be able to undergo coronary artery by-pass grafting if necessary. Patients with calcified lesions or lesions in branch vessels are not considered good candidates
  • Slide 52 - Non-Pharmacologic Therapy Cardiac Catheterization/ Balloon Angioplasty Performed in the cardiac cath lab. A catheter with a balloon tip is passed into the obstructed artery and is alternately inflated and deflated to increase arterial diameter and perfusion. Complications Arterial rupture, spasm, emboli, MI Post-procedure care
  • Slide 53 - Other Procedures Coronary Artery Stents Stainless steel mesh stent is placed in lumen to prevent restenosis after angioplasty. Requires anticoagulation and antiplatelet tx to prevent local-thrombosis. Coronary Laser Surgery Laser can destroy atherosclerotic plaque. Research is being conducted in transluminal laser angioplasty to coronary arteries. Atherectomy - surgical removal of atheroma.
  • Slide 54 - Coronary Artery By-Pass Grafting (CABG) Procedure - Surgical revascularization to increase coronary blood flow. Patients with severe disease may not be candidates. Longevity after surgery still being debated. Surgery does not cure atherosclerosis and patients must still control risk factors
  • Slide 55 - Post-op CABG Post-Operative Nursing Assessments & Care Cardiovascular function Respiratory function - pt may be on mechanical ventilator for short time. Renal Function Neurologic Function Peripheral Vascular Function Fluid & Electrolyte Balance Pain management Psychological Status Safety - Pt may be restrained to present self extubation
  • Slide 56 - Cardiac Tamponade of CABG Etiology - heart is compressed by fluid within the pericardial sac. Ventricular filling is thus impaired resulting in decreased cardiac output and circulatory collapse. Clinical Signs Pulsus Paradoxus Blood Pressure Neck Veins Heart Sounds Respirations Mental Status Pain Treatment Thoracotomy Pericardiocentesis
  • Slide 57 - NCLEX TIME Modifiable risk factors associated with CAD include: age, weight, cholesterol level Smoking, diet, BP Family hx, weight, BP Blood glucose, activity level, family hx
  • Slide 58 - NCLEX TIME A patient has just returned from cardiac cath. Which nursing intervention is most appropriate? Assist pt to ambulate to the BR Restrict fluids Monitor peripheral pulses Insert an indwelling catheter
  • Slide 59 - NCLEX TIME A 63 man is resuscitated successfully after cardiac arrest. Blood studies show that he is acidotic. Why? Decreased tissue perfusion causes lactic acid production The pt typically has an irregular heart beat The pt was treated inappropriately with Na Bicarb Fat forming ketoacids are breaking down
  • Slide 60 - NCLEX TIME Rosie is preparing her client for discharge following his inpatient stay with angina, which is now stable. Rosie is reviewing both modifiable and nonmodifiable risk factors. Select all factors below that are nonmodifiable. A.Age B.Gender C.Obesity D.Family history E.Hypertension
  • Slide 61 - NCLEX TIME Following her inferior wall MI, Mrs. Green is quiet, reserved, and avoiding contact with her family. Understanding the psychosocial aspects of ACS, which intervention would be best for the nurse to do first? A.Have the client’s cardiologist write for a psychiatric referral. B.Provide an atmosphere of acceptance. C.Foster mechanisms to suppress anger and hostility. D.Provide factual information to the client’s family alone.
  • Slide 62 - NCLEX TIME When Rosie is assessing her client with chest pain, she is evaluating whether or not the client is suffering from angina or MI. Which symptom would be indicative of an MI? A.Substernal chest discomfort B.Chest pain brought on by exertion or stress C.Substernal chest discomfort relieved by nitroglycerin or rest D.Substernal chest pressure relieved only by opioids
  • Slide 63 - NCLEX TIME All of the following clients are being cared for on the coronary care “stepdown” unit. When making client assignments, which client will be best for the charge nurse to assign to a new graduate RN who has completed 6 months of orientation to the unit? A.A client who has a new diagnosis of heart failure and needs discharge teaching about medications B.A client who has just returned to the unit after having a coronary arteriogram and has orders for vital signs every 15 minutes C.A client with a history of angina who is requesting nitroglycerin for left anterior chest pain D.A client who has many questions about the electrophysiology studies that are scheduled
  • Slide 64 - NCLEX TIME 4.An RN and an LPN who both have several years of experience in the intensive care unit are caring for a group of clients. Which task will be most appropriate for the RN to delegate to the LPN? A.Obtaining pulmonary artery wedge pressures every hour for a client admitted with pulmonary edema B.Monitoring vital signs and assessing the catheter insertion site for a client who returned from a coronary arteriogram an hour ago C.Teaching the family members of a client who is scheduled for myocardial nuclear perfusion imaging about the procedure D.Completing the admission assessment for a client admitted to the unit with acute coronary syndrome
  • Slide 65 - NCLEX TIME The nurse is caring for a client who has been admitted with chest pain of unknown etiology. All of the following laboratory tests are obtained. Which test results require the most immediate action by the nurse. A.Troponin T is elevated. B.Creatinine kinase is decreased. C.Myoglobin is increased. D.High-density lipoproteins are decreased.
  • Slide 66 - Cardiac Case Study A 57yo male is admitted to your unit c/o dull pain in the left side of his chest and radiating to his neck. There’s no diaphoresis or SOB. Risk factors include hypercholesteremia and a 70 pack year hx of smoking. PE reveals BP 140/86, HR 110, normal heart sounds and clear lungs bilat. Cardiac markers drawn ½ hour after the onset of pain show Myoglobin 45mcg. Troponin I at 0.01ng/mL and CPK-MB of 10u/L. EKG shows nonspecific ST wave changes in the anterior leads.
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