Module 3B - Coronary Artery Disease And Acute Coronary Syndrome PDF
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This document provides an overview of coronary artery disease and acute coronary syndrome. It covers the pathophysiology, clinical manifestations, and treatments associated with these conditions. The text is a learning resource likely from a nursing course.
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UA-CONP: C-NCM112 aidè à vivrè Care of Clients with Problems in Oxygenation, Fluid and Electrolytes, Infectious, Inflammatory,...
UA-CONP: C-NCM112 aidè à vivrè Care of Clients with Problems in Oxygenation, Fluid and Electrolytes, Infectious, Inflammatory, #HelpLive Immunologic Response, and Cellular Aberration (Acute and Chronic) Lecture [TRANS] UNIT XX: CORONARY ARTERY DISEASE AND ACUTE CORONARY SYNDROME The injury may be initiated by: Module 3B Smoking Coronary Artery Disease and Acute Coronary Syndrome Hypertension Hyperlipidemia, and other factors Outline 1. Describe the pathophysiology, clinical manifestations, The endothelium undergoes changes and stops producing the and treatment of coronary atherosclerosis. normal antithrombotic (to prevent the formation of clot that 2. Describe the pathophysiology, clinical manifestations, causes obstruction) and vasodilating agents. and treatment of angina pectoris. ↓ 3. Use the nursing process as a framework for care of The presence of inflammation attracts inflammatory cells, such patients with angina pectoris. 4. Describe the pathophysiology, clinical manifestations, as monocytes (macrophages) which ingest lipids, becoming and treatment of myocardial infarction. “foam cells” that transport the lipids into the arterial wall. 5. Use the nursing process as a framework for care of a ↓ patient with acute coronary syndrome. Some of the lipid is deposited on the arterial wall, forming fatty streaks. Unhealthy lifestyle brings about deposition of fats and ↓ smoking contributes to vasoconstriction. Activated macrophages also release biochemical substances So many people suffer or die from cardiovascular that can further damage the endothelium by contributing to the disorders. oxidation of low-density lipoprotein (LDL). Common in males before but now it is common to both ↓ because of a sedentary lifestyle. The oxidized LDL is toxic to the endothelial cells and fuels These cardio diseases can affect all ethnic races, but it is progression of the atherosclerotic process. more common in people who engage in a lifestyle that is not ↓ healthy which promotes deposition of fats in the blood Following the transport of lipid into the arterial wall, smooth vessels. muscle cells proliferate and form a fibrous cap over a core filled with lipid and inflammatory infiltrate. These cardiovascular disorders are more common among ↓ people who are adults until such time it will manifest tissue These deposits, called atheromas, or plaques, which protrude necrosis depending on what tissue will affect. into the lumen of the vessel causing. Coronary Atherosclerosis ↓ An abnormal accumulation of lipid, or fatty substances, and Narrowing it and obstruction of blood flow. fibrous tissue in the lining of arterial blood vessel walls. ↓ Sclerosis is the narrowing and hardening of blood vessels. Plaque may be stable or unstable, depending on the degree of inflammation and thickness of the fibrous cap. Causes reduced perfusion because of the obstruction or ↓ constriction of the arteries. If the fibrous cap over the plaque is thick and the lipid pool Coronary Artery Disease remains relatively stable, it can resist the stress of blood flow and vessel movement. ↓ If the cap is thin and inflammation is ongoing, the lesion becomes what is called vulnerable plaque. ↓ Lipid core may grow, causing the fibrous plaque to rupture. ↓ A ruptured plaque attracts platelets and causes thrombus formation. ↓ Thrombus may then obstruct blood flow, leading to: ↓ Acute coronary syndrome ↓ Acute myocardial infarction (MI) → portion of the heart becomes necrotic. Clinical Manifestations CAD produces symptoms and complications according to CTTO: https://www.phlbi.org the location and degree of narrowing of the arterial lumen, thrombus formation, and obstruction of blood flow to the Pathophysiology myocardium leading to deficient blood supply. The inflammatory response involved with the development The condition is known as ischemia – low blood supply and of atherosclerosis begins with injury to the vascular oxygen. endothelium and progresses. Jopar Jose C. Ramos | Bachelor of Science in Nursing 3-A 1 UA-CONP: C-NCM112 aidè à vivrè Care of Clients with Problems in Oxygenation, Fluid and Electrolytes, Infectious, Inflammatory, #HelpLive Immunologic Response, and Cellular Aberration (Acute and Chronic) Lecture o Chest pain - most common manifestation “angina Blood pressure persistently greater than 130/85 mmHg pectoris” Pro-inflammatory state (high levels of C-reactive protein) o Epigastric distress and pain that radiates to the jaw or Prothrombic state (high fibrinogen level) left arm (even the left shoulder). o Shortness of breath Includes Three of the Following Conditions o Many women have been found to have atypical Insulin resistance symptoms, including indigestion, nausea, palpitations, Central obesity and numbness. Dyslipidemia Prodromal symptoms may occur (i.e., angina a few hours Blood pressure persistently greater than 130/85 mm Hg to days before the acute episode), or a major cardiac event Pro-inflammatory state may be the first indication of coronary atherosclerosis. Prothrombotic state Risk Factors Prevention Controlling cholesterol abnormalities: Non-Modifiable o Dietary measures Family history of CAD o Physical activity Increasing age o Medications Gender (males are more prone for CAD) Promoting cessation of tobacco use Race Managing hypertension Controlling diabetes Modifiable Hyperlipidemia - increase of fats in the blood (measured thru lipid profile) Angina Pectoris 10-hr fasting prior to lipid testing Cigarette smoking, tobacco use A clinical syndrome usually characterized by episodes or Hypertension – poor perfusion to different organs paroxysms of pain or pressure in the anterior chest. o Blood pressure that is persistently elevated to greater The cause is insufficient coronary blood flow. than 130/85 mmHg is a risk factor for CAD. A decreased oxygen supply when there is increased Diabetes – lesser flow due to viscosity causing injury to myocardial demand for oxygen in response to physical blood vessels exertion or emotional stress. o People do not die from diabetes, they die because of complication of diabetes (hypertension, stroke, or heart attack). Metabolic syndrome – includes three conditions: o Insulin resistance ▪ Fasting blood sugar – to check the level of sugar in the blood done routinely. 6-8 hours NPO. Normal range: 70-100 mg/dL ▪ HbA1c (glycosylated hemoglobin) – it is a reflection of three-month sugar level. This is more accurate. There is no need for fasting. Normal: less than 6% o C-reactive protein ▪ Protein that has a connection with inflammation. ▪ Indicator of an inflammatory process in the body. ▪ Any inflammation in the body causes an increase CRP in the blood, not only specific for the inflammation of blood vessels. ▪ The liver produces CRP in response to a stimulus such as tissue injury. ▪ Normal range: 0.8-1 mg /dL > 3 mg/dL – indication of heart disease o High fibrinogen levels in the blood Obesity Physical inactivity Metabolic Syndrome CTTO: https://medizzy.com Has emerged as a major risk factor for cardiovascular disease. Increases demand for oxygen. The heart will feel that there Insulin resistance is insufficient blood supply that triggers chest pain. Central obesity Too much physical activity will require a higher demand of Dyslipidemia blood supply to the coronary arteries. Jopar Jose C. Ramos | Bachelor of Science in Nursing 3-A 2 UA-CONP: C-NCM112 aidè à vivrè Care of Clients with Problems in Oxygenation, Fluid and Electrolytes, Infectious, Inflammatory, #HelpLive Immunologic Response, and Cellular Aberration (Acute and Chronic) Lecture A person with fever has increase metabolic demand. breath, pallor, diaphoresis, dizziness or lightheadedness, and nausea and vomiting, may accompany the pain. Risk Factors An important characteristic of angina is that it subsides with Atherosclerosis rest or administering nitroglycerin. o Sublingual nitroglycerin is the most commonly used Pathophysiology nitrate; not swallowed since it undergoes first-pass Angina is usually caused by atherosclerotic disease. metabolism by the liver; readily absorbed into the Angina is associated with a significant obstruction of at circulation through the SL vessels. least one major coronary artery. o Instruct the client to take no more than 3 nitroglycerin When demand increases, flow through the coronary SL tablets (1 tablet every 5 minutes); if pain persists arteries needs to be increased. after a total of 3 tablets, the patient should immediately ↓ call for medical assistance. When there is blockage in a coronary artery, there is ▪ If the patient experience chest pain, he or she will deficiency in blood flow. take 1 tablet of nitroglycerin SL and after 5 ↓ minutes, he or she will take again, and after 5 Ischemia minutes, he or she will take again. A total of 3 only. ▪ If in the 3rd time, the pain is still present, you need Factors are Associated with Typical Anginal Pain to call now a doctor because it can be already a Physical exertion myocardial infarction. Exposure to cold ▪ Patients taking nitroglycerin should be in a safe Eating a heavy meal environment since this cause vasodilation that Stress or any emotion can lead to hypotension. o Nitroglycerin SL tablet decompose when exposed to Types of Angina heat and light, so they must be kept in their original, airtight glass containers. 1. Stable Angina ▪ It should be placed in an amber colored bottle. Predictable and consistent pain that occurs on exertion Unstable angina is characterized by attacks that increase and is relieved by rest and/or nitroglycerin (given SL). in frequency and severity and are not relieved by rest and Class: Vasodilator administering nitroglycerin and require medical 2. Unstable Angina intervention. Also called preinfarction angina or crescendo angina. Symptoms increase in frequency and severity; may not be Assessment and Diagnostic Findings relieved with rest or nitroglycerin. History related to the clinical manifestations of ischemia 12-lead electrocardiogram (ECG) 3. Intractable / Refractory Angina Exercise or pharmacologic stress test Severe incapacitating chest pain. Nuclear scan or invasive procedure (such as cardiac catheterization and coronary angiography) checks inner lining of blood 4. Variant / Prinzmetal’s Angina vessels Pain at rest with reversible ST segment elevation; Medical Management thought to be caused by coronary artery vasospasm. Pharmacologic therapy, preventive measures, and control of risk factors. 5. Silent Ischemia Reperfusion procedure to restore the blood supply to the Objective evidence of ischemia to the heart muscle (such myocardium. as electrocardiographic changes with a stress test), but o Oxygen administration should be initiated at the onset patient reports no pain. of the chest pain in order to increase the amount of oxygen delivered to the heart muscle (adjunct). Clinical Manifestations ▪ The effectiveness of this oxygen therapy is Pain or other symptoms, varying from mild indigestion to a determined by checking or monitoring the rate and choking or heavy sensation in the upper chest. Pain or rhythm of the respiration, the color of the skin as discomfort is poorly localized and may radiate to the neck, well as of the mucous membrane. Also, O2 sat is jaw, shoulders, and inner aspects of the upper arms, checked using the pulse oximetry. >90% indicates usually the left arm. that the oxygen administration as a supplement for Feels tightness or a heavy choking or strangling the patient’s oxygenation is being effective. sensation. o Percutaneous procedures (e.g., percutaneous Severe apprehension and a feeling of impending death. transluminal coronary angioplasty and intracoronary o Anxiety increases stents and coronary artery bypass graft). Patient with diabetes may not have severe pain with angina PCI - Percutaneous coronary intervention because diabetic neuropathy. Nursing Management o Sensation is diminished. It is hard to assess if they Direct to stop all activities and sit or rest in bed in a semi- are already experiencing chest pain. Fowler’s position to reduce the oxygen requirements of the Women may have a feeling of weakness or numbness in ischemic myocardium. the arms, wrists, and hands, as well as shortness of Assess the patient, measuring vital signs and observing for signs of respiratory distress. Jopar Jose C. Ramos | Bachelor of Science in Nursing 3-A 3 UA-CONP: C-NCM112 aidè à vivrè Care of Clients with Problems in Oxygenation, Fluid and Electrolytes, Infectious, Inflammatory, #HelpLive Immunologic Response, and Cellular Aberration (Acute and Chronic) Lecture Obtain a 12-lead ECG and assess for ST-segment and T- Ischemia and necrosis of the myocardium supplied by that wave changes. artery. Cardiac monitoring with continuous ST-segment. Nitroglycerin is administered sublingually, and the Clinical Manifestations patient’s response is assessed. Chest pain that occurs suddenly and continues despite rest Administers oxygen therapy. and medication is the presenting symptom in most patients Ask: with ACS. o Where is the pain? Using the COLDSPA o In heart attack, the chest is dull and heavy. o Based on the client’s complain, you will be able to Shortness of breath establish nursing diagnosis. Indigestion ▪ Risk for decreased cardiac tissue perfusion Nausea ▪ Risk for decreased tissue perfusion (cardiac Anxiety muscles) Cool, pale, and moist skin ▪ Anxiety Heart rate and respiratory rate may be faster than normal o If these problems are not addressed, it will result to complications such as hear attack, heart failure, or Assessment and Diagnostic Findings dysthymias. Presenting symptoms 12-lead ECG Echocardiogram Laboratory tests (e.g., serial cardiac biomarkers) are performed to clarify whether the patient has unstable angina, NSTEMI, or STEMI NSTEMI - ▪ Serial cardiac biomarkers are isoenzymes that partial are present in the cardiac muscle. blockage of coronary artery ▪ When death occurs in the cardiac muscle, the STEMI - total isoenzymes are released in the blood. or near total ▪ If the value is elevated, it means that means the blockage of coronary cardiac muscle is dead. artery that supplies blood o Troponin to the heart ▪ There are three isomers of troponin: C, I, and T. muscle ▪ Troponins I and T are specific for cardiac muscle. ▪ An increase in the level of troponin in the serum can be detected within a few hours during acute MI and remains elevated for a long period, often as long as 3 weeks → indicative of myocardial damage. CTTO: https://www.pinterest.ph o Creatine kinase and its isoenzymes ▪ There are three CK isoenzymes: Acute Coronary Syndrome (ACS) CK-MM (skeletal muscle) An emergent situation characterized by an acute onset CK-MB (heart muscle) of myocardial ischemia that results in myocardial death CK-BB (brain tissue) (MI) if definitive interventions do not occur promptly. ▪ CK-MB is the cardiac-specific isoenzyme. The spectrum of ACS includes unstable angina, NSTEMI, ▪ Elevated CK-MB is an indicator of acute MI; the and ST-segment elevation myocardial infarction (STEMI). level begins to increase within a few hours and peaks within 24 hours of an infarct. Pathophysiology o Myoglobin In unstable angina, there is reduced blood flow in a coronary ▪ Hemeprotein that helps transport oxygen. artery, often due to rupture of an atherosclerotic plaque. ▪ Like the CK-MB enzyme, myoglobin is found in ↓ cardiac and skeletal muscle. A clot begins to form on top of the coronary lesion, but the ▪ When MI occurs, the myoglobin level starts to artery is not completely occluded. increase within 1 to 3 hours and peaks within 12 ↓ hours after the onset of symptoms. An acute situation that can result in chest pain and other symptoms that may be referred to as preinfarction angina. Unstable Angina ↓ Patient has clinical manifestations of coronary ischemia, but The patient will likely have an MI if prompt interventions do not ECG and cardiac biomarkers show no evidence of acute occur. MI. ↓ In an MI, plaque rupture and subsequent thrombus formation. ST-Elevation Myocardial Infarction ↓ Patient has ECG evidence of acute MI with characteristic Complete occlusion of the artery. changes in two contiguous leads on a 12-lead ECG. In this ↓ type of MI, there is significant damage to the myocardium. Jopar Jose C. Ramos | Bachelor of Science in Nursing 3-A 4 UA-CONP: C-NCM112 aidè à vivrè Care of Clients with Problems in Oxygenation, Fluid and Electrolytes, Infectious, Inflammatory, #HelpLive Immunologic Response, and Cellular Aberration (Acute and Chronic) Lecture o There is possible total occlusion of the artery leading Relieving Pain and Other Signs and Symptoms of to a loss of blood supply to the heat. Ischemia Oxygen should be administered along with medication Non-ST-Elevation Myocardial Infarction therapy to assist with relief of symptoms. Patient has elevated cardiac biomarkers (e.g., troponin) but Vital signs are assessed frequently as long as the patient is no definite ECG evidence of acute MI. In this type of MI, experiencing pain and other signs or symptoms of acute there may be less damage to the myocardium. ischemia. o Partial reduction in blood flow to the heart. o Attachment to a cardiac monitor. Medical Management Promote physical rest in bed with the head of the bed The goals of medical management are to minimize elevated or in a supportive chair helps decrease chest myocardial damage, preserve myocardial function, and discomfort and dyspnea. prevent complications. Improving Respiratory Function Initial Management Monitors fluid volume status to prevent fluid overload. Immediately receive supplemental oxygen, aspirin, Encourage the patient to breathe deeply and change nitroglycerin, and morphine. position frequently to maintain effective ventilation Morphine is the drug of choice to reduce pain and anxiety. throughout the lungs. It also reduces preload and afterload, decreasing the work Use pulse oximetry to guide in the use of oxygen therapy of the heart. Promoting Adequate Tissue Perfusion Beta-blocker may also be used if dysrhythmias occur. Bed or chair rest during the initial phase of treatment helps If a beta-blocker is not needed in the initial management reduce myocardial oxygen consumption. period, it should be introduced within 24 hours of Skin temperature and peripheral pulses must be checked admission, once hemodynamics has stabilized and it is frequently to monitor tissue perfusion. confirmed that the patient has no contraindications. Unfractionated heparin (anticoagulant) or LMWH Reducing Anxiety o Together with medication (platelet inhibiting medication Provide information to the patient and family. such as Clopidogrel) to inhibit platelet aggregation in Ensure a quiet environment. order to prevent progression of clot formation. Prevent interruptions that disturb sleep. Emergent percutaneous coronary intervention -surgical Provide spiritual support consistent with the patient’s procedure wherein cardiac catheterization will be beliefs. performed especially to client who are diagnosed to have Provides frequent opportunities for the patient to privately STEMI. This is done immediately. share concerns and fears. The patient with STEMI is taken directly to the cardiac catheterization laboratory for an immediate PCI. Monitoring and Managing Potential Complications Monitors the patient closely for changes in cardiac rate and Inpatient Management rhythm, heart sounds, blood pressure, chest pain, Following PCI or thrombolytic therapy, continuous cardiac respiratory status, urinary output, skin color and monitoring is indicated, preferably in a cardiac intensive temperature, mental status, ECG changes, and laboratory care unit (ICU). values. Instruct client to immediately report changes (chest pain, palpitations) Continuing pharmacologic management includes aspirin, a beta-blocker, and an ACE inhibitor If an ACE inhibitor is Educating Patients About Self-Care not suitable, an ARB should be prescribed. Identify the patient’s priorities, provide adequate education Blood pressure, urine output, and serum sodium, about heart-healthy living, and facilitate the patient’s potassium, and creatinine levels monitored closely. involvement in a cardiac rehabilitation program. Monitor chest pain of patient Cardiac Rehabilitation Take Time to Watch Targets risk reduction by providing patient and family https://www.youtube.com/watch?v=EATkbpqlxvc education, offering individual and group support, and encouraging physical activity and physical conditioning. The goals of rehabilitation for the patient who has had an MI are to extend life and improve the quality of life. Physical conditioning is achieved gradually over time. Patients are observed for chest pain, dyspnea, weakness, fatigue, and palpitations and are instructed to stop exercise if any of these occur. The amount and type of activity recommended at discharge depends on the patient’s age, his or her condition before the cardiac event, the extent of the disease, the course of the hospital stay, and the development of any complications. Nursing Management Jopar Jose C. Ramos | Bachelor of Science in Nursing 3-A 5