Focus on Coronary Artery Disease and Acute Coronary Syndrome

1. Focus onCoronary Artery Disease and Acute Coronary Syndrome (Relates to Chapter 34, “Nursing Management: Coronary Artery Disease and Acute Coronary Syndrome,” in the textbook)

2. Coronary Artery Disease and Acute Coronary Syndrome • A type of blood vessel disorder that is included in the general category of atherosclerosis • Begins as soft deposits of fat that harden with age • Referred to as “hardening of arteries”

3. 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. Coronary Artery Disease and Acute Coronary Syndrome • Cardiovascular diseases are the major cause of death in the United States • Heart attacks are still the leading cause of all cardiovascular disease deaths and deaths in general

5. Progression of Atherosclerosis Fig. 34-2

6. Coronary Artery Disease Etiology and Pathophysiology Fatty streaks Fibrous plaque • Result = narrowing of vessel lumen Complicated lesion • Continued inflammation can result in plaque instability, ulceration, and rupture • Platelets accumulate and thrombus forms • Increased narrowing or total occlusion of lumen

7. Development of Collateral Circulation Fig. 34-3

8. Risk Factors for CAD • Risk factors can be categorized as • Nonmodifiable risk factors • Age • Gender • Ethnicity • Family history • Genetic predisposition

9. Modifiable risk factors Elevated serum lipids Hypertension Tobacco use Physical inactivity Obesity Diabetes Metabolic syndrome Psychologic states Homocysteine level Risk Factors for CAD • Risk factors can be categorized as

10. 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 • Values and beliefs about health and illness

11. Risk Factors for CADHealth Promotion • Health-promoting behaviors • Physical fitness 30 minutes >5 days/week • Regular physical activity contributes to: • Weight reduction • Reduction of BP • increase in HDL cholesterol

12. Risk Factors for CADHealth Promotion • Health-promoting behaviors • Nutritional therapy • Therapeutic Lifestyle Changes • Omega-3 fatty acids

13. 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)

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

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

16. Clinical Manifestations of CAD Chronic Stable Angina • Etiology and Pathophysiology • Primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis • For ischemia to occur, the artery is usually 75% or more stenosed

17. 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

18. Clinical Manifestations of CAD Chronic Stable Angina • Pain usually lasts minutes • Subsides when the precipitating factor is relieved • Pain at rest is unusual • ECG may reveal ST segment depression

19. Location of Chest Pain (Angina) Fig. 34-7

20. 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

21. 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

22. Chronic Stable Angina Nursing and Collaborative Management • Drug therapy: Goal: O2 demand and/or O2 supply • Short-acting nitrates: Sublingual • Long-acting nitrates • Nitroglycerin ointment • Transdermal controlled-release nitroglycerin

23. 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 anginal symptoms • Used to manage Prinzmetal’s angina • Angiotensin-converting enzyme inhibitors

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

25. Chronic Stable AnginaNursing and Collaborative Management • Diagnostic Studies • Cardiac catheterization • Diagnostic • Coronary revascularization: Percutaneous coronary intervention • Balloon angioplasty • Stent

26. Placement of aCoronary Artery Stent Fig. 34-9

27. Pre- and Post-PCIwith Stent Placement Fig. 34-10

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

29. Relationship Between CAD, Chronic Stable Angina, and ACS Fig. 34-11

30. Acute Coronary Syndrome Etiology and Pathophysiology • Deterioration of a once stable plaque rupture platelet aggregation thrombus • Result • Partial occlusion of coronary artery: UA or NSTEMI • Total occlusion of coronary artery: STEMI

31. Coronary Thrombogenesis Secondary to Plaque Deterioration

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

33. 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

34. Acute Myocardial Infarction Fig. 34-13

35. Clinical Manifestations of ACS Myocardial Infarction • The degree of altered function depends on the area of the heart involved and the size of the infarct • Contractile function of the heart is disrupted in areas of myocardial necrosis)

36. Occlusion of the Left Anterior Descending Coronary Artery, Resulting in MI Fig. 34-12

37. Clinical Manifestations of ACS Myocardial Infarction • Pain • Total occlusion → anaerobic metabolism and lactic acid accumulation

38. Clinical Manifestations of ACS Myocardial Infarction • Pain • Described as heaviness, constriction, tightness, burning, pressure, or crushing • Common locations: substernal, retrosternal, or epigastric areas; pain may radiate

39. Clinical Manifestations of ACS Myocardial Infarction • Sympathetic nervous system stimulation results in • Release of glycogen • Diaphoresis • Vasoconstriction of peripheral blood vessels • Skin: ashen, clammy, and/or cool to touch

40. Clinical Manifestations of ACS Myocardial Infarction • Cardiovascular • Initially, ↑ HR and BP, then ↓ BP (secondary to ↓ in CO) • Crackles • Jugular venous distention • Abnormal heart sounds • S3 or S 4 • New murmur

41. Clinical Manifestations of ACS Myocardial Infarction • Nausea and vomiting • Can result from reflex stimulation of the vomiting center by the severe pain • Fever • Systemic manifestation of the inflammatory process caused by cell death

42. Myocardial InfarctionHealing Process • Development of collateral circulation improves areas of poor perfusion • Necrotic zone identifiable by ECG changes and nuclear scanning • 10 to 14 days after MI, scar tissue is still weak and vulnerable to stress

43. Complications of Myocardial Infarction • Dysrhythmias • Most common complication • Present in 80% of MI patients • Life-threatening dysrhythmias seen most often with anterior MI, heart failure, or shock

44. Complications of Myocardial Infarction • Heart failure • A complication that occurs when the pumping power of the heart has diminished

45. Complications of Myocardial Infarction • Cardiogenic shock • Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failure • Requires aggressive management

46. Complications of Myocardial Infarction • Papillary muscle dysfunction • Causes mitral valve regurgitation • Condition aggravates an already compromised LV • Ventricular aneurysm • Results when the infarcted myocardial wall becomes thinned and bulges out during contraction

47. Complications of Myocardial Infarction • Acute pericarditis • An inflammation of visceral and/or parietal pericardium • May result in cardiac compression, ↓ LV filling and emptying, heart failure • Pericardial friction rub may be heard on auscultation

48. Diagnostic Studies Unstable Angina and Myocardial Infarction • Detailed health history and physical • 12-lead ECG: Changes in QRS complex, ST segment, and T wave can rule out or confirm UA or MI • Serum cardiac markers • Coronary angiography • Others: Exercise stress testing, echocardiogram

49. Serum Cardiac Markers After MI Fig. 34-15

50. Collaborative CareAcute Coronary Syndrome • Emergency management • Initial interventions • Ongoing monitoring • Emergent PCI • Treatment of choice for confirmed MI • Balloon angioplasty + drug-eluting stent(s) • Ambulatory 24 hours after the procedure