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Focus on Coronary Artery Disease and Acute Coronary Syndrome

Focus on Coronary Artery Disease and Acute Coronary Syndrome. Leading Causes of Death. eFig. 34-1. Leading causes of death for all men and women. CVD , Cardiovascular disease. . 2. Coronary Artery Disease and Acute Coronary Syndrome. Atherosclerosis: Type of blood vessel disorder

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Focus on Coronary Artery Disease and Acute Coronary Syndrome

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  1. Focus onCoronary Artery Disease and Acute Coronary Syndrome

  2. Leading Causes of Death eFig. 34-1. Leading causes of death for all men and women. CVD, Cardiovascular disease. 2

  3. Coronary Artery Disease and Acute Coronary Syndrome • Atherosclerosis: Type of blood vessel disorder • Begins as soft deposits of fat that harden with age • Referred to as “hardening of arteries” 3

  4. Coronary Artery Disease and Acute Coronary Syndrome • Atherosclerosis (cont’d) • Can occur in any artery in the body • Atheromas (fatty deposits) • Preference for the coronary arteries 4

  5. Coronary Artery Disease and Acute Coronary Syndrome • Atherosclerosis (cont’d) • Terms to describe the disease process • Arteriosclerotic heart disease • Cardiovascular heart disease • Coronary artery disease (CAD) 5

  6. Coronary Artery Disease Etiology and Pathophysiology • Atherosclerosis is the major cause of CAD. • Characterized by a focal deposit of cholesterol and lipid, primarily within the intimal wall of the artery • Endothelial lining altered as a result of inflammation and injury 6

  7. Pathogenesis of Atherosclerosis Fig. 34-1. Pathogenesis of atherosclerosis. A, Damaged endothelium. B, Diagram of fatty streak and lipid core formation. C, Diagram of fibrous plaque. Raised plaques are visible: some are yellow, others are white. D, Diagram of complicated lesion: thrombus is red, collagen is blue. Plaque is complicated by red thrombus deposition. 7

  8. Coronary Artery Disease Etiology and Pathophysiology • C-reactive protein (CRP) • Nonspecific marker of inflammation • Increased in many patients with CAD • Chronic exposure to CRP associated with unstable plaques and oxidation of LDL cholesterol 8

  9. Coronary Artery Disease Etiology and Pathophysiology • Developmental stages: Fatty streaks • Earliest lesions • Characterized by lipid-filled smooth muscle cells • Potentially reversible 9

  10. Coronary Artery Disease Etiology and Pathophysiology • Developmental stages: Fibrous plaque • Beginning of progressive changes in the arterial wall • Lipoproteins transport cholesterol and other lipids into the arterial intima. • Fatty streak is covered by collagen, forming a fibrous plaque that appears grayish or whitish. • Result = Narrowing of vessel lumen 10

  11. Coronary Artery Disease Etiology and Pathophysiology • Developmental stages: Complicated lesion • Continued inflammation can result in plaque instability, ulceration, and rupture. • Platelets accumulate and thrombus forms. • Increased narrowing or total occlusion of lumen 11

  12. Coronary Artery Disease Etiology and Pathophysiology • Collateral circulation • Normally, some arterial anastomoses (or connections) exist within the coronary circulation. 12

  13. Coronary Artery Disease Etiology and Pathophysiology • Growth and extent of collateral circulation are attributed to two factors. • Inherited predisposition to develop new vessels (angiogenesis) • Presence of chronic ischemia 13

  14. Coronary Artery Disease Etiology and Pathophysiology • When occlusion of the coronary arteries occurs slowly over a long period, the chance that adequate collateral circulation will develop is greater. 14

  15. Vessel Occlusion With Collateral Circulation Fig. 34-2. Vessel occlusion with collateral circulation. A, Open, functioning coronary artery. B, Partial coronary artery closure with collateral circulation being established. C, Total coronary artery occlusion with collateral circulation bypassing the occlusion to supply blood to the myocardium. 15

  16. Risk Factors for CAD • Nonmodifiable risk factors • Age • Gender • Ethnicity • Family history • Genetic predisposition 16

  17. Risk Factors for CAD • Modifiable risk factors • Elevated serum lipids • Hypertension • Tobacco use • Physical inactivity 17

  18. Risk Factors for CAD • Modifiable risk factors • Obesity • Diabetes • Metabolic syndrome • Psychologic states • Homocysteine level 18

  19. Risk Factors for CADHealth Promotion • Identification of people at high risk • Health history, including use of prescription/nonprescription medications • Presence of cardiovascular symptoms • Environmental patterns: Diet, activity • Psychosocial history • Values and beliefs about health and illness 19

  20. Risk Factors for CADHealth Promotion • Health-promoting behaviors • Physical fitness • FITT formula: 30 minutes >5 days/week • Regular physical activity contributes to • Weight reduction • Reduction of >10% in systolic BP • In some men more than women, increase in HDL cholesterol 20

  21. Risk Factors for CADHealth Promotion • Health-promoting behaviors • Nutritional therapy • Therapeutic lifestyle changes • Omega-3 fatty acids 21

  22. Risk Factors for CADHealth Promotion • Health-promoting behaviors • Cholesterol-lowering drug therapy • Drugs that restrict lipoprotein production: Statins, niacin • Drugs that increase lipoprotein removal: Bile acid sequestrants • Drugs that decrease cholesterol absorption: Ezetimibe (Zetia) 22

  23. Risk Factors for CADHealth Promotion • Health-promoting behaviors • Antiplatelet therapy • ASA • Clopidogrel (Plavix) 23

  24. Question Two risk factors for coronary artery disease that increase the workload of the heart and increase myocardial oxygen demand are: 1. Hypertension and cigarette smoking. 2. Obesity and smokeless tobacco use. 3. Elevated serum lipids and diabetes mellitus. 4. Physical inactivity and elevated homocysteine levels. 24

  25. Question The nurse determines that teaching about implementing dietary changes to decrease the risk of CAD has been effective when the patient says, 1. “I should not eat any red meat such as beef, pork, or lamb.” 2. “I should have some type of fish at least 3 times a week.” 3. “Most of my fat intake should be from olive oil or the oils in nuts.” 4. “If I reduce the fat in my diet to about 5% of my calories, I will be much healthier.” 25

  26. Gerontologic Considerations • Strategies to reduce risk factors are effective but often underprescribed. • Necessary to modify guidelines for physical activity • Two points when elderly may consider lifestyle change(s): • When hospitalized • When symptoms result from CAD and not from normal aging 26

  27. Clinical Manifestations of CAD Chronic Stable Angina • Etiology and pathophysiology • Reversible (temporary) myocardial ischemia = Angina (chest pain) • O2 demand > O2 supply 27

  28. Clinical Manifestations of CAD Chronic Stable Angina • Etiology and pathophysiology • Primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis. • Referred pain in left shoulder and arm is from transmission of the pain message to the cardiac nerve roots. 28

  29. Clinical Manifestations of CAD Chronic Stable Angina • Intermittent chest pain that occurs over a long period with the same pattern of onset, duration, and intensity of symptoms 29

  30. Location of Pain During Angina Fig. 34-4. Location of pain during angina or myocardial infarction. 30

  31. Clinical Manifestations of CAD Chronic Stable Angina • Pain usually lasts 3 to 5 minutes. • Subsides when the precipitating factor is relieved • Pain at rest is unusual. • ECG reveals ST-segment depression and/or T-wave inversion. 31

  32. Chronic Stable Angina Types of Angina • Silent ischemia • Ischemia that occurs in the absence of any subjective symptoms • Associated with diabetic neuropathy • Confirmed by ECG changes 32

  33. Chronic Stable Angina Types of Angina • Nocturnal angina • Occurs only at night but not necessarily during sleep • Angina decubitus • Chest pain that occurs only while lying down • Relieved by standing or sitting 33

  34. Chronic Stable AnginaTypes of Angina • Prinzmetal’s (variant) angina • Occurs at rest usually in response to spasm of major coronary artery • Seen in patients with a history of migraine headaches and Raynaud’s phenomenon • Spasm may occur in the absence of CAD. 34

  35. Chronic Stable Angina Types of Angina • Prinzmetal’s (variant) angina • When spasm occurs • Chest pain • Marked, transient ST-segment elevation • May occur during REM sleep • May be relieved by moderate exercise or may disappear spontaneously 35

  36. Chronic Stable Angina Types of Angina • Microvascular angina • May occur in the absence of significant coronary atherosclerosis or coronary spasm • Pain is related to myocardial ischemia associated with abnormalities of the coronary microcirculation. • Coronary microvascular disease 36

  37. Chronic Stable Angina Nursing and Collaborative Management • Drug therapy: Goal: ↓ O2 demand and/or ↑ O2 supply • Short-acting nitrates: Sublingual • Long-acting nitrates • Nitroglycerin (NTG) ointment • Transdermal controlled-release NTG 37

  38. Chronic Stable Angina Nursing and Collaborative Management • Drug therapy: Goal: ↓ O2 demand and/or ↑ O2 supply • β-Adrenergic blockers • Calcium channel blockers • If β-adrenergic blockers are poorly tolerated, contraindicated, or do not control angina • Used to manage Prinzmetal’s angina • Angiotensin-converting enzyme inhibitors 38

  39. Chronic Stable AnginaNursing and Collaborative Management • Diagnostic studies • Health history/physical examination • Laboratory studies • 12-lead ECG • Chest x-ray • Echocardiogram • Exercise stress test 39

  40. Chronic Stable AnginaNursing and Collaborative Management • Diagnostic studies • Cardiac catheterization/coronary angiography • Diagnostic • Coronary revascularization: Percutaneous coronary intervention (PCI) • Balloon angioplasty • Stent 40

  41. Placement of a Coronary Artery Stent Fig. 34-6. Placement of a coronary artery stent. A, The stent is positioned at the site of the lesion. B, The balloon is inflated, expanding the stent. The balloon is then deflated and removed. C, The implanted stent is left in place. 41

  42. Pre- and Post-PCI With Stent Placement Fig. 34-7. A, A thrombotic occlusion of the right coronary artery is noted (arrows).B, Right coronary artery is opened and blood flow restored following angioplasty and placement of a 4-mm stent. 42

  43. Acute Coronary Syndrome • When ischemia is prolonged and is not immediately reversible, acute coronary syndrome (ACS) develops. • ACS encompasses • Unstable angina (UA) • Non–ST-segment-elevation myocardial infarction (NSTEMI) • ST-segment-elevation MI (STEMI) 43

  44. Relationship Between CAD, Chronic Stable Angina, and ACS Fig. 34-8. Relationships among coronary artery disease, chronic stable angina, and acute coronary syndrome. Ml, Myocardial infarction. 44

  45. Acute Coronary Syndrome Etiology and Pathophysiology • Result • Partial occlusion of coronary artery: UA or NSTEMI • Total occlusion of coronary artery: STEMI 45

  46. Clinical Manifestations of ACS Unstable Angina • Unstable angina • Change in usual pattern • New in onset • Occurs at rest • Has a worsening pattern • UA is unpredictable and represents a medical emergency. 46

  47. Clinical Manifestations of ACS Myocardial Infarction (MI) • Result of sustained ischemia (>20 minutes), causing irreversible myocardial cell death (necrosis) • Necrosis of entire thickness of myocardium takes 4 to 6 hours. 47

  48. Myocardial Infarction From Occlusion Fig. 34-9. Occlusion of the left anterior descending coronary artery, resulting in a myocardial infarction. 48

  49. Acute Myocardial Infarction Fig. 34-10. Acute myocardial infarction in the posterolateral wall of the left ventricle. This is demonstrated by the absence of staining in the areas of necrosis (white arrow). Note the scarring from a previous anterior wall myocardial infarction (black arrow). 49

  50. Full-Thickness MI Fig. 34-11. Myocardial infarction involving the full thickness of the left ventricular wall. 50

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