Chapter 27- Management of Patients With Coronary Vascular Disorders PDF

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Chapter 27: Management of Patients with Coronary Vascular DisordersCORONARY ARTERY DISEASE (CAD)Coronary Atherosclerosis Abnormal accumulation of lipid, or fatty substances, and fibrous tissue in the lining of arterial blood vessel walls Block and narrow the coronary vessels in a way that reduces bl...

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Chapter 27: Management of Patients with Coronary Vascular Disorders

CORONARY ARTERY DISEASE (CAD) Coronary Atherosclerosis - Abnormal accumulation of lipid, or fatty substances, and fibrous tissue in the lining of arterial blood vessel walls - Block and narrow the coronary vessels in a way that reduces blood flow to the myocardium - Pathophysiology    

Lipids are transported into arterial wall  smooth muscle cells proliferate and form a fibrous cap over a core filled with lipid and inflammatory infiltrate (PLAQUES)  plaques go into the lumen of the vessel, narrow it and obstruct blood flow Fibrous cap over the plaque is thick and the lipid pool remains relatively stable, it can resist the stress of blood flow and vessel movement Fibrous cap is thin and inflammation is ongoing, the lesion becomes vulnerable plaque and the lipid core may grow, causing the fibrous plaque to rupture Ruptured plaque attracts platelets and causes thrombus formation which can obstruct blood flow and lead to acute coronary syndrome or acute myocardial infarction

- Clinical Manifestations     

Myocardial ischemia, and angina pectoris (chest pain) Decreased blood supply – persistently low cardiac output and heart failure Some complain of epigastric distress, and pain that radiates to the jaw or left arm Those who are older or have diabetes or heart failure – shortness of breath Women have atypical symptoms – indigestion, nausea, palpitations, numbness

- Risk Factors 

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Nonmodifiable Risk Factors  Family history of CAD  Increasing age (older than 45 in men; older than 55 in women)  Gender  Race (higher in African Americans) Modifiable Risk Factors  Hyperlipidemia  Cigarette smoking (tobacco use)  Hypertension  Diabetes  Metabolic syndrome  Obesity  Physical inactivity Metabolic Syndrome (diagnosis needs at least three of the following)  Insulin resistance (fasting glucose more than 100 mg/dL or abnormal glucose tolerance test)  Central obesity (waist circumference greater than 35 inches in women, 45 in men)

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Dyslipidemia (triglycerides more than 150 mg/dL, HDL less than 50 mg/dL in females and less than 40 in men) Blood Pressure greater than 130/85 mm Hg Proinflammatory state (high levels of C – reactive protein [CRP]) Prothrombic state (high fibrinogen level)

- Prevention 

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Controlling Cholesterol Abnormalities  Four elements of fat metabolism – total cholesterol, LDL, HDL, and triglycerides (all affect the development of heart disease)  Should have a fasting lipid profile done at least once every 5 years, and more often if the profile is abnormal  High HDL protects against heart disease  High triglycerides can be: genetic, obesity, physical inactivity, excessive alcohol intake, high carbohydrate diets, diabetes, kidney disease, certain medications  Lipid profile  LDL less than 100 mg/dL  Total cholesterol less than 200 mg/dL  HDL cholesterol greater than 40 mg/dL for males and greater than 50 mg/dL in females  Triglycerides less than 150 mg/dL  Dietary Measures  Diet low in saturated fat and high in soluble fiber  Mediterranean diet – promotes vegetables and fish, and restricts red meat  Weight loss, cessation of tobacco use, and increased physical activity  On labels, pay attention to: serving size, total fat per serving, amount of saturated and trans fat, amount of cholesterol and fiber per serving  Physical Activity  Regular moderate physical activity increases HDL and reduces triglyceride level  Engage in moderate – intensity aerobic activity of at least 150 minutes per week, or vigorous – intensity aerobic activity of at least 75 minutes per week, or an equivalent combination  Engage in an activity or variety of activities that interest them to maintain motivation  Exercise to an intensity that doesn’t impair ability to talk  Stop if: chest pain, unusual shortness of breath, dizziness, lightheadedness, nausea occur  Medications  3 – hydroxyl – 3 – methylglutaryl coenzyme A (HMG – CoA) (statins)  lowers LDL, triglycerides, total cholesterol, and increases HDL  Nicotinic Acids  lowers LDL, triglycerides, and increases HDL  Fibric Acids (Fibrates)  increases HDL, and lowers triglycerides  Bile Acid Sequestrates (Resins)  lowers LDL, and slight increase in HDL  Cholesterol absorption inhibitors  lowers LDL  Omega – 3 – acid ethyl esters  lowers triglycerides Promoting Cessation of Tobacco Use

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Nicotine acid in tobacco triggers the release of catecholamine’s, which raise the heart rate and blood pressure. Can also cause coronary arteries to constrict.  Smoking can increase the oxidation of LDL, damaging the vascular endothelium. Increases platelet adhesion and leads to a higher probability of thrombus function.  Inhalation of smoke increases the blood carbon monoxide level and decreases the supply of oxygen to the myocardium. Results in myocardial ischemia, reduced contractility  Medications that help: nicotine patch, varenicline, bupropion Managing Hypertension  Defined as 140/90 mm Hg  May result in increased stiffness of the vessel walls, leading to vessel injury and a resulting inflammatory response within intima  causes: acceleration and aggravation of atherosclerosis  Increases the work of the left ventricle, which needs to pump harder to eject blood into the arteries  Over time the heart enlarges and thicken = heart failure Controlling Diabetes  Diabetes is known to accelerate development of heart disease  Hyperglycemia fosters dyslipidemia, increased platelet aggregation, and altered red blood cell function – leads to thrombus formation and promotes development of atherosclerosis  Treatment with insulin, metformin, or other therapeutic interventions

- Gender    

Cardiovascular events in women occur an average of 10 years later in life than compared to men Women have a higher incidence of complications from cardiovascular disease and a higher mortality, and do not recognize the symptoms of CAD as early as men Hormone therapy – increased incidence of CAD, breast cancer, DVT, stroke, pulmonary embolism Women have poorer outcomes with increased morbidity and mortality after coronary events and interventions, and have poorer results related to symptom relief

Angina Pectoris - Characterized by episodes or paroxysms of pain or pressure in the anterior chest - Caused by insufficient coronary blood flow, resulting in decreased oxygen supply when there is increased myocardial demand for oxygen (NEED FOR OXYGEN EXCEEDS THE SUPPLY) - Pathophysiology       

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Usually caused by atherosclerotic disease Has significant obstruction of at least one major coronary artery Associating factors: physical exertion, exposure to cold, eating a heavy meal, stress Stable angina  predictable and consistent pain that occurs on exertion and is relieved by rest and/or nitroglycerin Unstable angina  symptoms increase in frequency and severity; may not be relieved with rest or nitroglycerin Intractable or refractory angina  severe incapacitating chest pain Variant angina  pain at rest with reversible ST segment elevation

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Silent ischemia  objective evidence of ischemia, but patient reports no pain

- Clinical Manifestations        

Pain Mild indigestion – choking – heavy sensation in upper chest Pain may be accompanied by severe apprehension and a feeling of impending death and is felt deep in the chest Pain or discomfort is poorly localized and may radiate to the neck, jaw, shoulders, and inner aspects of the upper arms, usually left arm Feels tightness or a heavy choking or strangling sensation Diabetic neuropathy can blunt nociceptor transmission and dull perception of pain Feeling of weakness or numbness in the arms, wrists, and hands, as well as shortness of breath, pallor, diaphoresis, dizziness or lightheadedness, and nausea and vomiting Presenting symptoms in older adult is dyspnea, or there might be no symptoms

- Assessment and Diagnostic Findings   

Diagnosis begins with the patient’s history related to the clinical manifestations of ischemia 12 – lead ECG may show changes indicative of ischemia, such as T wave inversion Laboratory studies are performed, and the patient may need to undergo an exercise or pharmacologic stress test

- Medical Management  

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Objective is to: decrease the oxygen demand of the myocardium and to increase the oxygen supply Pharmacologic Therapy  Nitroglycerin  Potent vasodilator that improves blood flow to the heart muscle and relieves pain  Dilation of veins causes venous pooling of blood throughout the body, resulting in less blood return to the heart, and reduced filling pressure (preload)  If patient is hypovolemic, the decrease in filling pressure can cause a significant decrease in cardiac output and blood pressure  Nitrates lower blood pressure and decrease afterload  Can be given by: sublingual tablet or spray, oral capsule, topical agent and IV administration  Usually not administered if systolic pressure is less than 90 mm Hg  Common adverse effect is headache  Beta – Adrenergic Blocking Agents  Reduce myocardial oxygen consumption by blocking beta – adrenergic sympathetic stimulation to the heart  Results in reduced heart rate, slowed conduction of impulses through the conduction system, decreased blood pressure, and reduced myocardial contractility  Reduce the incidence of recurrent angina, infarction, and cardiac mortality  Cardiac side effects and possible contraindications include: hypotension, bradycardia, advanced atrioventricular block, heart failure

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 Side effects if given IV: depressed mood, fatigue, decreased libido, dizziness  Don’t stop taking abruptly; must be titrated  If you have diabetes, it can mask signs of hypoglycemia: monitor glucose Calcium Channel Blocking Agents  Decrease sinoatrial node automaticity and atrioventricular node conduction, resulting in a slower heart rate and a decrease in the strength of myocardial contraction  Increase myocardial oxygen supply, and decrease myocardial oxygen demand  Common ones are amlodipine (Norvasc) and diltiazem (Cardizem)  Used to treat angina and sometimes hypertension  Side effects: hypertension, atrioventricular block, bradycardia, constipation Antiplatelet and Anticoagulant Medications  Administered to prevent platelet aggregation and subsequent thrombosis  Aspirin  Prevents platelet aggregation and reduces the incidence of MI and death in patients with CAD  Patients should be advised to continue aspirin even if they concurrently take other analgesics  Use of histamine – 2 (H2) blockers or proton pump inhibitors should be considered concomitant with continued aspirin therapy  Thienopyridines  Blocks platelet activation  Clopidogrel (Plavix) is commonly prescribed in addition to aspirin in patients at high risk for MI  Heparin  Unfractionated IV heparin prevents the formation of new blood clots  Amount of heparin administered is based on the results of the activated partial thromboplastin time (aPTT)  Therapeutic when aPTT is 2 – 2.5 times the normal value  Low molecular weight heparin provides effective and stable anticoagulation, and possible reduced the risk of rebound ischemic events, and eliminates the need to monitor aPTT results  Unfractionated and low molecular weight heparin increase the risk of bleeding so monitor patient for signs of external/internal bleeding (hypotension, tachycardia, low hemoglobin/hematocrit)  Decrease in platelet count or evidence of thrombosis may indicate heparin – induced thrombocytopenia (HIT)  Glycoprotein IIb/IIIa Agents  Abciximab (ReoPro) or eptifibatide (Integrilin): for those patients with unstable angina and as adjunct therapy for PCI  Prevent platelet aggregation by blocking the GP IIb/IIIa receptors on the platelets, preventing adhesions of fibrinogen and other factors that crosslink platelets to each other and form intracoronary clots

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 Major side effect: BLEEDING Oxygen Administration  Initiated at the onset of chest pain  Therapeutic effectiveness is determined by observing the rate and rhythm of respirations and the color of skin and mucous membranes  Normal oxygen saturation is greater than 90%

Nursing Process: The Patient with Angina Pectoris - Assessment  

Assess for angina pectoris or its equivalent Assess the patient’s risk factors for CAD, patient’s response to angina, the patient’s and family’s understanding of response to the diagnosis, and adherence to the current treatment

- Nursing Diagnosis    

Risk for decreased cardiac tissue perfusion Anxiety related to cardiac symptoms and possible death Deficient knowledge about the underlying disease and methods for avoiding complications Noncompliance, ineffective management of therapeutic regimen related to failure to accept necessary lifestyle changes

- Collaborative Problems/ Potential Complications    

ACS and/or MI Dysrhythmias and cardiac arrest Heart Failure Cardiogenic Shock

- Planning and Goals     

Immediate and appropriate treatment when angina occurs Prevention of angina Reduction of anxiety Awareness of disease process and understanding of the prescribed care Adherence to self-care program and absence of complications

- Nursing Interventions 

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Treating Angina  If the patient reports pain the nurse takes immediate action  Experiencing angina: stop all activities, sit or rest in bed in a semi-fowler position  Assess the patient: monitor vital signs, and observe for signs of respiratory distress  12 – lead ECG  obtain and assess for ST-segment and T-wave changes  administer nitroglycerin sublingually  administer oxygen therapy if the patient’s respiratory rate is increased or if the oxygen saturation level is decreased Reducing Anxiety

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Explore implications that the diagnosis has for the patient and providing information about the illness, its treatment, and methods of preventing its progression  Guided imagery and music therapy help Preventing Pain  Identify level of activity that causes the patient’s pain or prodromal symptoms  Alternate activities with rest Promoting Home and Community Care  Goals of education: reduce the frequency and severity of angina attacks, delay the progress of the underlying disease, prevent complications  Activities should be planned to minimize the occurrence of angina episodes  Any pain unrelieved within 15 minutes by the usual methods, including nitroglycerin should be treated at the closest ED

- Evaluation    

Reports that pain is relieved promptly Reports decreased anxiety Understands ways to avoid complications and is free of complications Adheres to self-care program

Acute Coronary Syndrome and Myocardial Infarctions - Acute coronary syndrome is an emergent situation characterized by an acute onset of myocardial ischemia that results in myocardial death - Spectrum of ACS: unstable angina  NSTEMI  ST – segment elevation myocardial infarction (STEMI) - Pathophysiology      

Unstable angina  reduced blood flow in a coronary artery  clot begins to form on top of the coronary lesion, but artery isn’t completely occluded  chest pain and other symptoms (preinfarction angina) MI  plaque rupture and subsequent thrombus formation  complete occlusion of the artery  ischemia and necrosis of the myocardium supplied by that artery MI can also be caused by: vasospasm of coronary artery, decreased oxygen supply, increased demand for oxygen Area of infarction develops over minutes to hours: as the cells are deprived of oxygen, ischemia develops Identify MI: type, location of injury to the ventricular wall, point in time within process of infarction 12 – lead ECG identifies the type and location of the MI

- Clinical Manifestations     

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chest pain that develops suddenly and continues despite rest Chest pain, shortness of breath, indigestion, nausea, vomiting, anxiety, and pale, moist, cool skin Faster than normal heart rate and respiratory rate, increased jugular vein distention, hypertension, irregular pulse Dyspnea, tachypnea, crackles, pulmonary edema Decreased urinary output

- Assessment and Diagnostic Findings  

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Diagnosis based on: presenting symptoms, the 12-lead ECG and laboratory tests Patient History  Description of presenting symptoms, history of previous cardiac and other illnesses, family history of heart disease, and information about the patient’s risk factors for heart disease Electrocardiogram  Should be obtained within 10 minutes from time patient reports pain or arrives in emergency department  Location, evolution, and resolution of an MI can be identified and measured on ECG  Expected ECG changes: T-wave inversion, ST-segment elevation, and development of an abnormal Q wave  First ECG sign of MI is seen in the T-wave and ST segment  An elevation in the ST segment in two contiguous leads is a key diagnostic indicator for MI  Appearance of abnormal Q waves is another indication of MI  MI may also cause significant decrease in height of R wave  Unstable angina  patient has clinical manifestations of coronary ischemia, but ECG and cardiac biomarkers show no evidence of acute MI  STEMI  The patient has ECG evidence of acute MI with characteristic changes in two contiguous leads on a 12 – lead ECG. Significant damage to myocardium  NSTEMI  The patient has elevated cardiac biomarkers but no definite ECG evidence of acute MI. Less damage to myocardium Echocardiogram  Used to evaluate ventricular function  May be used to assist in diagnosing an MI  Can detect hypokinetic and akinetic wall motion and determine ejection fraction Laboratory Tests  Cardiac enzymes and biomarkers are used to diagnose an acute MI  Troponin  Regulates myocardial contractile process, and there are three isomers: C, I, and T  Troponins I and T are specific for cardiac muscle and are reliable and critical markers of myocardial injury  Increase in troponin can be detected within a few hours of acute MI  Remains elevated for up to 3 weeks  Can be used to detect recent myocardial damage  Creatine Kinase and Its Isoenzymes  Three CK isoenzymes: CK-MM (skeletal muscle), CK-MB (heart muscle), CK-BB (brain tissue)  CK-MB is cardiac specific isoenzyme and it increases when there is damage to these cells  Elevated CK-MB is an indicator of acute MI  Myoglobin  Heme protein that helps transport oxygen  Found in cardiac and skeletal muscle

 Increase in myoglobin is not very specific of a MI, but a negative result can rule out MI - Medical Management  

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Goals: minimize myocardial damage, preserve myocardial function, and prevent complications  May be achieved by interventions that reestablish coronary flow Initial management  Supplemental oxygen, aspirin, nitroglycerin, and morphine  Morphine reduces pain, anxiety, and preload and afterload  Beta – Blocker may be used if dysrhythmia occurs  Unfractionated or LMW heparin and platelet – inhibiting agents may be used to prevent further clot formation Emergent percutaneous coronary intervention  Patient has STEMI – immediate PCI  Used to open the occluded coronary artery and promote reperfusion to the area that has been deprived of oxygen  Treats the underlying atherosclerotic lesion  Time from the patient’s arrival to time PCI is done should be less than 60 minute Thrombolytics (Fibrinolytics)  Initiated when PCI is not available or the transport time to a PCI capable hospital is too long  Administered IV  Alteplase (Activase), reteplase (r-PA), and tenecteplase (TNKase)  Dissolve t...