Chapter 28 Management of Patients With Coronary Vascular Disorders

1. Chapter 28Management of Patients With Coronary Vascular Disorders

2. Coronary Atherosclerosis • CAD, coronary artery disease, is the most prevalent cardiovascular disease in adults. • Atherosclerosis is the abnormal accumulation of lipid or fibrous tissue in the lining of arterial walls. • In coronary atherosclerosis, blockages and narrowing of the coronary vessels reduce blood flow to the myocardium.

3. deposit fatty streaks of lipids in the intima of the arterial wall - fatty streaks advanced into lesions (Genetics and environmental factors)  injury to the vascular endothelium - inflammatory response - attract inflammatory cells  macrophages ingest lipids, becoming “foam cells” that transport the lipids into the arterial wall. Pathophysiology of Atherosclerosis

4. Activated macrophages release biochemical substances -- damage the endothelium, attracting platelets and initiating clotting - Smooth muscle cells within the vessel wall subsequently proliferate  form a fibrous cap over a core filled with lipid and inflammatory infiltrate. - atherosclerosis

5. Plaques (inflammation and thickness of the fibrous cap): • Stable: • cap over the plaque is thick • the lipid pool remains relatively stable • it can resist the stress of blood flow and vessel movement.

6. Unstable: (vulnerable plaque.) • cap is thin • inflammation is ongoing, • the lipid core may grow  rupture and hemorrhage into the plaque  thrombus formation  obstruct blood flow  leading to acute coronary syndrome (ACS)  acute myocardial infarction (MI)  a portion of the heart muscle becomes necrotic.

7. Other causes of heart disease • vasospasm (sudden constriction or narrowing) of a coronary artery, • myocardial trauma from internal or external forces, • structural disease, • congenital anomalies, • decreased oxygen supply (eg, from acute blood loss, anemia, or low blood pressure), • and increased oxygen demand (eg, from rapid heart rate, thyrotoxicosis, or use of cocaine).

8. Coronary Arteries

9. Clinical Manifestations • Symptoms are due to myocardial ischemia • Symptoms and complications: • the location and degree of narrowing of the arterial lumen, • thrombus formation, • and obstruction of blood flow to the myocardium. • Angina pectoris • Myocardial infarction • Heart failure • Sudden cardiac death

10. The most common manifestation of myocardial ischemia is the onset of chest pain. • some individuals may be asymptomatic or have atypical symptoms such as weakness, dyspnea, and nausea. • Atypical symptoms are more common in women and in persons who are older, or who have a history of heart failure or diabetes. (shortness of breath) • Prodromal symptoms may occur (ie, angina a few hours to days before the acute episode) • a major cardiac event may be the first indication of coronary atherosclerosis.

11. Risk factors • Nonmodifiable Risk Factors: • Family history of CAD (first-degree relative with cardiovascular disease at 55 years of age or younger for men and at 65 years of age or younger for women) • Increasing age (more than 45 years for men; more than 55 years for women) • Gender (men develop CAD at an earlier age than women) • Race (higher incidence of heart disease in African Americans than in Caucasians)

12. Modifiable Risk Factors • Hyperlipidemia • Cigarette smoking, tobacco use • Hypertension • Diabetes mellitus • Metabolic syndrome • Obesity • Physical inactivity

13. Metabolic syndrome • Insulin resistance (fasting plasma glucose more than100 mg/dL or abnormal glucose tolerance test) • Central obesity (waist circumference more than 35 inches in women, more than 40 inches in men) • Dyslipidemia (triglycerides more than 150 mg/dL, HDL less than 50 mg/dL in women, less than 40 mg/dL in men) • Blood pressure persistently greater than 130/85 mmHg

14. Angina Pectoris • A syndrome characterized by episodes or paroxysms pain or pressure in the anterior chest caused by insufficient coronary blood flow. • Physical exertion or emotional stress increases myocardial oxygen demand and the coronary vessels are unable to supply sufficient blood flow to meet the oxygen demand. (need for oxygen exceeds the supply.)

15. Types of angina • Stable angina: predictable and consistent pain that occurs on exertion and is relieved by rest and/or nitroglycerin • Unstable angina (also called preinfarction angina or crescendo 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 (also called Prinzmetal’s angina): pain at rest with reversible ST-segment elevation; thought to be caused by coronary artery vasospasm • Silent ischemia: objective evidence of ischemia (such as electrocardiographic changes with a stress test), but patient reports no pain

16. factors associate with typical anginal pain: • Physical exertion: increasing myocardial oxygen demand • Exposure to cold: vasoconstriction and elevated blood pressure, with increased oxygen demand • Eating a heavy meal: increases the blood flow to the mesenteric area for digestion, thereby reducing the blood supply available to the heart muscle • Stress or any emotion-provoking situation, causing the release of catecholamines, which increases blood pressure, heart rate, and myocardial workload

17. Angina pain varies from mild to severe • pain is often felt deep in the chest behind the sternum (retrosternal area). • Pain may radiate to the neck, jaw, shoulders, and inner aspects of the upper arms, usually the left arm. • Patients may feel tightness, choking, strangling sensation or a heavy sensation. • A 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 • Anxiety frequently accompanies the pain. • Pain may Subsides with rest or administering nitroglycerin

18. Unstable angina is characterized by attacks that increase in frequency and severity and are not relieved by rest and administering nitroglycerin.

19. Assessment and Diagnostic Findings • patient’s history related to the clinical manifestations of ischemia. • 12 lead ECG • Exercise stress • Cardiac catheterization • CRP (reactive protein)

20. Treatment • Treatment seeks to decrease myocardial oxygen demand and increase oxygen supply • Medications • Oxygen • Reduce and control risk factors • Reperfusion therapy may also be done (These include PCI procedures (eg, percutaneous transluminal coronary angioplasty [PTCA], intracoronary stents, and atherectomy)and CABG.

21. Medications • Nitroglycerin (Short-term and long-term reduction of myocardial oxygen consumption through selective vasodilation)  balance between supply and demand (which decreases ischemia and relieves pain) as a result: • less blood returns to the heart, and filling pressure (preload) is reduced. • decrease in cardiac output and blood pressure - decreasing afterload.

22. Beta-Adrenergic Blocking Agents (beta-blockers) • Reduction of myocardial oxygen consumption by blocking beta-adrenergic stimulation of the heart, Atenolol (Tenormin), (reduce the incidence of recurrent angina, infarction, and cardiac mortality.) as a result: • Reduction in heart rate, • Slowed conduction of impulses through the conduction system, • Decreased blood pressure, and • Reduced myocardial contractility

23. Calcium Channel Blocking Agents • Indicated in patients not responsive to beta-blockers; used as primary treatment for vasospasm, Diltiazem (Cardizem, Tiazac) • These agents decrease sinoatrial node automaticity and atrioventricular node conduction, resulting in: • A slower heart rate and • A decrease in the strength of myocardial contraction • relax the blood vessels, causing a decrease in blood pressure and an increase in coronary artery perfusion.

24. Antiplatelet Medications: Aspirin, Clopidogrel (Plavix), Aggrastat • Prevention of platelet aggregation • Anticoagulants: Heparin, Low-molecular-weight heparins (LMWHs): • Prevention of thrombus formation • Oxygen Administration

25. Nursing Process: The Care of the Patient with Angina Pectoris—Assessment • Symptoms and activities, especially those that precede and precipitate attacks • Risk factors, lifestyle, and health promotion activities • Patient and family knowledge • Adherence to the plan of care

26. Nursing Process: The Care of the Patient with Angina Pectoris—Diagnoses • Ineffective cardiac tissue perfusion secondary to CAD as evidenced by chest pain • Death anxiety related to cardiac symptoms • Deficient knowledge • Noncompliance, ineffective management of therapeutic regimen related to failure to accept necessary lifestyle changes

27. Collaborative Problems • Acute pulmonary edema • Heart failure • Cardiogenic shock • Dysrhythmias and cardiac arrest • Myocardial infarction

28. Nursing Process: The Care of the Patient with Angina Pectoris—Planning • Goals include the immediate and appropriate treatment of angina, prevention of angina, reduction of anxiety, awareness of the disease process, understanding of prescribed care, adherence to the self-care program, and absence of complications.

29. Treatment of Angina Pain • Treatment of angina pain is a priority nursing concern. • Patient is to stop all activity and sit or rest in bed (semi-Fowler’s position). • assesses the patient’s angina • Assess the patient while performing other necessary interventions. Assessment includes VS, and observation for respiratory distress, and assessment of pain. In the hospital setting, the ECG is assessed or obtained. • Administer oxygen. • Administer medications as ordered or by protocol, usually NTG.

30. Anxiety • Use a calm manner • Stress-reduction techniques • Patient teaching • Addressing patient spiritual needs may assist in allaying anxieties • Address both patient and family needs

31. Patient Teaching • To Reduce the frequency and severity of anginal attacks, to delay the progress of the underlying disease if possible, and to prevent complications. • Lifestyle changes and reduction of risk factors • Explore, recognize, and adapt behaviors to avoid to reduce the incidence of episodes of ischemia • Teaching regarding disease process • Medications • Stress reduction • When to seek emergency care

32. Myocardial Infarction • ACS is an emergent situation characterized by an acute onset of myocardial ischemia that results in myocardial death (ie, MI) if definitive interventions do not occur promptly. • The spectrum of ACS includes unstable angina, non–St-segment elevation MI (NSTEMI), and ST-segment elevation MI (STEMI).

33. Myocardial Infarction • In unstable angina, there is reduced blood flow in a coronary artery, often due to rupture of an atherosclerotic plaque, but the artery is not completely occluded. • This is an acute situation that is sometimes referred to as preinfarctionangina because the patient will likely have an MI if prompt interventions do not occur.

34. Myocardial Infarction • An area of the myocardium is permanently destroyed. Usually caused by reduced blood flow in a coronary artery due to rupture of an atherosclerotic plaque and subsequent occlusion of the artery by a thrombus. • Vasospasm (sudden constriction or narrowing) of a coronary artery, decreased oxygen supply (eg, from acute blood loss, anemia, or low blood pressure), and increased demand for oxygen (eg, from a rapid heart rate, thyrotoxicosis, or ingestion of cocaine) are other causes of MI.

35. Myocardial Infarction • Various descriptions are used to identify an MI: • the type (NSTEMI, STEMI), • the location of the injury to • the ventricular wall (anterior, inferior, posterior, or lateral wall), • and the point in time within the process of infarction (acute, evolving, or old).

36. Descriptions of an MI • The differences between NSTEMI and STEMI are diagnostic • The ECG usually identifies the type and location of the MI • ECG indicators such as a Q wave and patient history identify the timing. • Regardless of the location, the goals of medical therapy are to prevent or minimize myocardial tissue death and prevent complications.

37. Effects of Ischemia, Injury, and Infarction on ECG

38. Clinical Manifestations and Diagnosis • Chest pain, • other symptoms (shortness of breath, indigestion, nausea, and anxiety.) • (tachycardia, cool, pale, and moist skin)

39. Diagnosis • Clinical Manifestations, the history of previous cardiac and other illnesses, the family history of heart disease, and patient’s risk factors for heart disease. • ECG • Unstable angina: The 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. In this type of MI, there is significant damage to the myocardium. • NSTEMI: The patient has elevated cardiac biomarkers but no definite ECG evidence of acute MI.

40. Diagnosis • Laboratory tests—biomarkers • CK-MB: the level begins to increase within a few hours and peaks within 24 hours • Myoglobin: level starts to increase within 1 to 3 hours and peaks within 12 hours • Troponin T or I: detected within a few hours during acute MI.

41. The echocardiogram can detect hypokinetic and akinetic wall motion and can determine the ejection fraction

42. Medical Management The goals of medical management are to: • Minimize myocardial damage, • Preserve myocardial function, and • Prevent complications.

43. These goals may be achieved by reperfusion the area with the emergency use of thrombolytic medications or by PCI. • Reducing myocardial oxygen demand and • Increasing oxygen supply with medications, • oxygen administration, and • Bed rest. • The resolution of pain and ECG changes indicate that demand and supply are in equilibrium; indicate reperfusion.

44. Treatment of Acute MI • Obtain diagnostic tests including ECG within 10 minutes of admission to the ED • Oxygen, Aspirin, nitroglycerin, morphine, beta-blockers • Angiotensin-converting enzyme inhibitor within 24 hours • Evaluate for percutaneous coronary intervention • open the occluded coronary artery and promote reperfusion to the area • Treats the underlying atherosclerotic • arrival in the emergency department to the time PCI is performed should be less than 60 minutes or thrombolytic therapy

45. Thrombolytics • dissolve (ie, lyse) the thrombus • allowing blood to flow • minimizing the size of the infarction • and preserving ventricular function. • IV heparin or LMWH

47. Treatment of Acute MI • Cardiac Rehabilitation: (continuing care program) The goals of rehabilitation for the patient who has had an MI are to: • extend life and improve the quality of life. • limit the effects and progression of atherosclerosis, • return the patient to work and preillness lifestyle, • enhance the psychosocial and vocational status of the patient, and • prevent another cardiac event.

48. Nursing Process: The Care of the Patient with ACS—Assessment • A vital component of nursing care! • establishes the baseline for the patient so that any deviations may be identified, • systematically identifies the patient’s needs, • and helps determine the priority of those needs. • Take medical history of symptoms and complete physical assessment • time, duration, and the factors that precipitate the symptom and relieve it and in comparison with previous symptoms. • Two IV lines are typically placed • Monitoring ECG

49. Nursing Process: The Care of the Patient with ACS—Diagnoses • Ineffective cardiac tissue perfusion related to reduced coronary blood flow • Risk for fluid imbalance • Risk for ineffective peripheral tissue perfusion related to decreased cardiac output from left ventricular dysfunction • Death anxiety • Deficient knowledge

50. Collaborative Problems • Acute pulmonary edema • Heart failure • Cardiogenic shock • Dysrhythmias and cardiac arrest • Pericardial effusion and cardiac tamponade