Coronary Artery Diseases (CAD)

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Coronary Artery Diseases (CAD)

  1. 1. Management of Patients with Coronary Vascular DisordersMa. Tosca Cybil A. Torres, RN
  2. 2. Coronary Artery Disease (CAD) • Coronary artery disease (CAD) (or atherosclerotic heart disease) is the end result of the accumulation of atheromatous plaques within the walls of the coronary arteries that supply the myocardium with oxygen and nutrients. It is sometimes also called coronary heart disease (CHD), but although CAD is the most common cause of CHD, it is not the only cause.
  3. 3. ATHEROSCLEROSIS (AS) • is a disease of large and medium-sized muscular arteries (e.g., coronary, carotid, arteries of the lower extremities) and the elastic arteries such as the aorta and iliac vessels (supplying blood to the lower trunk and lower limbs arising from the bifurcations of aorta). • it is a slowly progressive disease that begins in childhood, but does not manifest until middle age or later, when the arterial lesions precipitate clinical manifestations by virtue of organ injury.
  4. 4. • the basic lesion – the atheroma (fibrinofatty plaque) – consists of a raised focal plaque within the intima, having a core of lipid (mainly cholesterol) and a covering fibrous cap. • atheromas compromise arterial blood flow and weaken affected arteries. Many eventually undergo a variety of complications (e.g., calcification, ulceration, thrombus formation, and aneurysmal dilation)
  5. 5. Atheroma
  6. 6. Atherothrombosis (1)
  7. 7. Atherothrombosis (2)
  8. 8. Athérothrombosis (3) a b c d e
  9. 9. Athérothrombosis (4) a b c d e
  10. 10. Thrombus position and consequences Infarct
  11. 11. Many risk factors have been associated with CAD. Nonmodifiable risk factors Age Gender Ethnicity Family history and genetic inheritance.
  12. 12. Modifiable risk factors include elevated serum lipids, hypertension, tobacco use, physical inactivity, obesity, diabetes, metabolic syndrome, psychologic states, and homocysteine level. • Elevated serum lipid levels are one of the four most firmly established risk factors for CAD. • Lipids combine with proteins to form lipoproteins and are vehicles for fat mobilization and transport. The different types of lipoproteins are classified as high-density lipoproteins (HDLs), low-density lipoproteins (LDLs), and very-low-density lipoproteins (VLDLs). – HDLs carry lipids away from arteries and to the liver for metabolism. High serum HDL levels are desirable. – HDL levels are increased by physical activity, moderate alcohol consumption, and estrogen administration. – Elevated LDL levels correlate most closely with an increased incidence of atherosclerosis and CAD.
  13. 13. • Hypertension, defined as a BP greater than or equal to 140/90 mm Hg, is a major risk factor in CAD. • Tobacco use is also a major risk factor in CAD. The risk of developing CAD is two to six times higher in those who smoke tobacco than in those who do not. • Obesity is defined as a body mass index (BMI) of less than 30 kg/m2. The increased risk for CAD is proportional to the degree of obesity. – Diabetes, metabolic syndrome, and certain behavioral states (i.e., stress) have also been found to be contributing risk factors for CAD. •
  14. 14. ARTERIAL OCCLUSIVE DISORDERS The most common cause is arteriosclerosis obliterans (ASO). The lower extremities are more commonly affected. The aorta may also be affected. Atheromatous plaque develops at the points of branching, bifurcations, or vessel narrowing. More prevalent among men, 50-70 years old.
  15. 15. Clinical manifestations: • Pain – intermittent claudication is an aching, persistent, cramp-like, squeezing pain that occurs after a certain amount of exercise of the affected extremities. It is relieved by rest. • Coldness or cold sensitivity – coldness in the feet with exposure to a cold environment, associated with blanching or cyanosis due to tissue ischemia. • Impaired arterial pulsations – impaired or absent pulse indicates decrease blood flow due to arterial spasm.
  16. 16. • Color changes – cyanosis or rubor may be observed when the extremities are placed in dependent position. • Ulceration and gangrene – may be due to ischemia or trauma. Impaired tissue perfusion inhibits healing process. • Edema – results from severe obstruction. • Sexual dysfunction - occlusive disease of the terminal aorta decreases the blood supply to the vascular tree supplying penile circulation. Unsustained erection may be experienced by the client
  17. 17. Prevention: Primary Prevention – Provide information on the effects of : • a. cigarette smoking- nicotine causes vasoconstriction, spasms of the arteries, reduced circulation to the extremities. The carbon monoxide inhaled in cigarette smoking reduces O2 transport to the tissues. • b. hypertension – causes elastic tissue in the arteries to be replaced by fibrous collagen tissue. This reduces arterial elasticity and increases resistance to blood flow. • c. hyperlipidemia – cholesterol and triglycerides contribute to the development of atherosclerotic plaque in the vessels. • d. obesity – places an added burden on the heart and blood vessels. It enhances propensity to DM, hypertension, and hyperlipidemia. • e. physical inactivity – compresses circulation • f. emotional stress – stimulates the sympathetic response which results to vasoconstriction. Stress may also cause increase cholesterol and platelet levels and hypertension. • g. DM – changes in glucose and fat metabolism enhance atherosclerotic process.
  18. 18. Secondary Prevention • Encourage client with early symptoms to seek medical care. This is to prevent complications like infection, injury, thrombosis and amputation. Tertiary Prevention • Rehabilitation is an important aspect of management of clients with arterial occlusive disorder. Exercises develop collateral circulation will be beneficial.
  19. 19. Management: • Quit smoking • Control of serum lipid levels • Skin and foot care • Diet- low fat, low cholesterol • Activity – daily walking program
  20. 20. If levels remain elevated despite modifiable changes, drug therapy is considered – Statin drugs work by inhibiting the synthesis of cholesterol in the liver. Liver enzymes must be regularly monitored. (ex. Simvastatin) – Niacin, a water-soluble B vitamin, is highly effective in lowering LDL and triglyceride levels by interfering with their synthesis. Niacin also increases HDL levels better than many other lipid-lowering drugs.(Ex. Niacin SR) – Fibric acid derivatives work by accelerating the elimination of VLDLs and increasing the production of apoproteins A-I and A-II. (ex. Lipofen, Tricor) – Bile-acid sequestrants increase conversion of cholesterol to bile acids and decrease hepatic cholesterol content. The primary effect is a decrease in total cholesterol and LDLs. (ex. Questran)
  21. 21. Angina Pectoris Definition: Angina: Choking or suffocation. Pectoris: Chest. Angina pectoris, is the medical term used to describe acute chest pain or discomfort. Angina occurs when the heart’s need for oxygen increases beyond the level of oxygen available from the blood nourishing the heart. It has 3 types • Stable Angina • Un stable angina & • Variant Angina (Prinzmetal’s or resting angina) :
  22. 22. Types of Angina • Stable angina: – People with stable angina have episodes of chest discomfort that are usually predictable. That occur on exertion or under mental or emotional stress. Normally the chest discomfort is relieved with rest, nitroglycerin (GTN) or both. – It has a stable pattern of onset, duration and intensity of symptoms.
  23. 23. • Unstable angina: – It is triggered by an un predictable degree of exertion or emotion. – (progressive), more severe than stable. Characterized by increasing frequency & severity. Provoked by less than usual effort, occurring at rest & – interferes with pt lifestyle.
  24. 24. • Variant Angina (Prinzmetal’s or resting angina) : occur spontaneously with no relationship to activity. Occurs at rest due to spasm. Pt discomfort that occurs rest usually of longer duration. Appears to by cyclic & often occurs at about the same time each day (usually at night). Thought to be caused by coronary artery spasm
  25. 25. CHRONIC STABLE ANGINA • Chronic stable angina refers to chest pain that occurs intermittently over a long period with the same pattern of onset, duration, and intensity of symptoms. – Angina is rarely sharp or stabbing, and it usually does not change with position or breathing. Many people with angina complain of indigestion or a burning sensation in the epigastric region. – Anginal pain usually lasts for only a few minutes (3 to 5 minutes) and commonly subsides when the precipitating factor is relieved. Pain at rest is unusual.
  26. 26. • The treatment of chronic stable angina is aimed at decreasing oxygen demand and/or increasing oxygen supply and reducing CAD risk factors. – In addition to antiplatelet and cholesterol-lowering drug therapy, the most common drugs used to manage chronic stable angina are nitrates. • Short-acting nitrates are first-line therapy for the treatment of angina. Nitrates produce their principal effects by dilating peripheral blood vessels, coronary arteries, and collateral vessels. (Isordil) • Long acting nitrates are also used to reduce the incidence of anginal attacks. (Imdur) • -Adrenergic blockers are the preferred drugs for the management of chronic stable angina. (Inderal) • Calcium channel blockers are used if -adrenergic blockers are contraindicated, are poorly tolerated, or do not control anginal symptoms. The primary effects of calcium channel blockers are (1) systemic vasodilation with decreased SVR, (2) decreased myocardial contractility, and (3) coronary vasodilation. (Norvasc, Plendil) • Certain high-risk patients (e.g., patients with diabetes) with chronic stable angina may benefit from the addition of an angiotensin-converting enzyme (ACE) inhibitor. (Capoten)
  27. 27. Diagnostic tests  chest x-ray  12-lead ECG  laboratory tests (e.g., lipid profile)  nuclear imaging  exercise stress testing  coronary angiography
  28. 28. ACUTE CORONARY SYNDROME • Acute coronary syndrome (ACS) develops when ischemia is prolonged and not immediately reversible. ACS encompasses the spectrum of unstable angina, non–ST- segment-elevation myocardial infarction (NSTEMI), and ST- segment-elevation myocardial infarction (STEMI). • ACS is associated with deterioration of a once stable atherosclerotic plaque. This unstable lesion may be partially occluded by a thrombus (manifesting as UA or NSTEMI) or totally occluded by a thrombus (manifesting as STEMI). • Unstable angina (UA) is chest pain that is new in onset, occurs at rest, or has a worsening pattern. UA is unpredictable and represents an emergency.
  29. 29. ISCHEMIA VS INFARCTION ISCHEMIA INFARCTION PAIN SUBSTERNAL PRESSURE/ HEAVINESS SQUEEZING SUBSTERNAL CONSTRICTIVE (+ SX OF SHOCK) DURATION 3-5 MIN > 5 MIN PRECIPITANTS STRESS/ EXERTION NO REST NITROGLYCERINE RELIEVED NOT RELIEVED CARDIAC TISSUE DAMAGE NOT PERMANENT PERMANENT
  30. 30. Myocardial infarction (MI) • Myocardial infarction (MI) Myo means muscle, “Cardiac” heart, infarction means “death of tissues due to lack of blood supply”. • occurs as a result of sustained ischemia, causing irreversible myocardial cell death. Eighty percent to 90% of all MIs are due to the development of a thrombus that halts perfusion to the myocardium distal to the occlusion. Contractile function of the heart stops in the infracted area(s). – Cardiac cells can withstand ischemic conditions for approximately 20 minutes. It takes approximately 4 to 6 hours for the entire thickness of the heart muscle to infarct. – Infarctions are described based on the location of damage (e.g., anterior, inferior, lateral, or posterior wall infarction). – Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration is the hallmark of an MI. The pain is usually described as a heaviness, pressure, tightness, burning, constriction, or crushing.
  31. 31. Myocardial infarction (MI)
  32. 32. PATHOPHYSIOLOGY Coronary artery cannot supply enough blood to the heart in response to the demand due to CAD Within 10 seconds myocardial cells experience ischemia Ischemic cells cannot get enough oxygen or glucose Ischemic myocardial cells may have decreased electrical & muscular function Cells convert to anaerobic metabolism. Cells produce lactic acid as waste Pain develops from lactic acid accumulation Pt feels anginal symptoms until receiving demand increase 02 requirements of myocardial cells
  33. 33. MYOCARDIAL INFARCTION IRREVERSIBLE CARDIAC DAMAGE FROM OCCLUSION OF 1 OR MORE CORONARY ARTERY E.C.G. Recent M.I. – ST elevation (injury) T wave inversion (ischemia) Previous M.I. – Q wave (necrosis / old infarct) BLOOD STUDIES Troponin T & I LDH CPK MB
  34. 34. P Q R S T E.C.G.
  35. 35. P Q R S T E.C.G. ST SEGMENT ELEVATION
  36. 36. P Q R S T E.C.G. INVERTED T - WAVE
  37. 37. P Q R S T E.C.G. Q wave
  38. 38. Signs and Symptoms • Classic symptom of heart attack are chest pain radiating to neck, jaws, back of shoulder, or left arm  The pain can be felt like:  Squeezing or heavy pressure  A tight band on the chest  An elephant sitting on the chest
  39. 39. ContOther symptoms include: • Shortness of breath (SOB) • Weakness and tiredness • Anxiety • Lightheadedness • Dizziness • Nausea vomiting • Sweating, which may be profuse
  40. 40. MYOCARDIAL INFARCTION NURSING CARE 1. Pain relief – Morphine ( + preload & afterload) Demerol causes vomiting 2. Oxygen 3. Inotropics 4. Beta Blockers 5. Antiarrhythmics 6. No ice or very hot drinks 7. Anticoagulants 8. ECG and CVP monitoring 9. Laxatives – Lactulose 10. PTCA 11. Thrombolytic Therapy BEFORE CELLULAR DEATH, US. 6 HRS AFTER THE ATTACK
  41. 41. Collaborative Management • Assessment: • History • Clinical manifestation • Cardiovascular assessment • Laboratory assessment • Troponin T & I • CK-MB
  42. 42. Radiographic Assessment  ECG  Stress Test  Myocardial perfusion imaging  MRI  Cardiac Catheterization
  43. 43. IMMEDIATE MANAGEMENT OF MI: GOALS: • To prolong life. • Minimize infarct size. • Reverse ischemia. • Reduce cardiac work. • Prevent and treat complications. A) INITIAL TREATMENT: • Rapid triage. • OMI (oxygen, monitor and I/V line). • Check vital signs and O2 saturation. • ECG within 10 minutes and repeat ECG. • Blood samples for enymes, CBC, lytes, and lipid profile.
  44. 44. Drug therapy Analgesic – for relief of pain, this is a priority. Pain may cause shock. Examples, morphine sulfate, lidocaine, Nitroglycerine IV Thrombolytic Therapy – to disintegrate blood clot by activating the fibrinolytic processes. • Ex. Streptokinase, urokinase and tissue plasminogen activator (TPA).  Administration is most crucial between 3-6 hours after the initial infarction has occurred.  Detect for occult bleeding during and after thrombolytic therapy.  Assess neurologic status changes which may indicate GI bleeding or cardiac tamponade. Anticoagulant and antiplatelet medications – are administered after thrombolytic therapy to maintain arterial patency. Other Medications: • Beta-adrenergic blocking agents • Diazepam
  45. 45. Coronary revascularization with coronary artery bypass graft (CABG) surgery is recommended for patients who (1) fail medical management, (2) have left main coronary artery or three-vessel disease Surgical Therapy
  46. 46. The off-pump coronary artery bypass (OPCAB) procedure uses full or partial sternotomy to enable access to all coronary vessels. OPCAB is also performed on a beating heart using mechanical stabilizers and without cardiopulmonary bypass (CPB). Surgical Therapy
  47. 47. Transmyocardial laser revascularization (TMR) is an indirect revascularization procedure used for patients with advanced CAD who are not candidates for traditional bypass surgery and who have persistent angina after maximum medical therapy. Surgical Therapy
  48. 48. Surgical management • PTCA (Percutaneous Transluminal Coronary Angioplasty
  49. 49. Balloon Angioplasty – involves insertion of a special catheter through fluoroscopy into the site of occlusion. The balloon tip of the catheter is inflated to compress and rupture the atheromatous plaque.
  50. 50. Stent – involves use of rigid but flexible structure that maintains the integrity of the vascular wall and patency of the artery.
  51. 51. Nursing Diagnoses • Acute pain R/T imbalance between myocardial oxygen supply and demand • Ineffective tissue perfusion R/T interruption of arterial blood flow • Ineffective coping R/T effects of acute illness and major changes in life style • Impaired gas exchange related to ineffective breathing pattern and decreased systemic tissue perfusion. • Anxiety related to present status and unknown future, possible lifestyle changes, pain, and perceived threat of death. • Activity intolerance related to fatigue
  52. 52. Nursing Management: Chronic Stable Angina and Acute Coronary Syndrome The following nursing measures should be instituted for a patient experiencing angina: (1) administration of supplemental oxygen, (2) determination of vital signs (3)12-lead ECG (4) prompt pain relief first with a nitrate followed by an opioid analgesic if needed, (5) auscultation of heart sounds (6) comfortable positioning of the patient.
  53. 53. • Initial treatment of a patient with ACS includes pain assessment and relief, physiologic monitoring, promotion of rest and comfort, alleviation of stress and anxiety, and understanding of the patient’s emotional and behavioral reactions. – Nitroglycerin, morphine sulfate, and supplemental oxygen should be provided as needed to eliminate or reduce chest pain. – Continuous ECG monitoring is initiated and maintained throughout the hospitalization. – Frequent vital signs, intake and output (at least once a shift), and physical assessment should be done to detect deviations from the patient’s baseline parameters. Included is an assessment of lung sounds and heart sounds and inspection for evidence of early HF (e.g., dyspnea, tachycardia, pulmonary congestion, distended neck veins).
  54. 54. Nursing Management 1. Promoting oxygenation and tissue perfusion • instruct the patient to avoid over fatigue; stop activity immediately in the presence of chest pain, dyspnea, lightheadedness and faintness. • O2 therapy by cannula for the first 24-48 hours or longer if pain, hypotension, dyspnea or dysrhythmias persist. Monitor VS changes, indicative of complication. • Position the client in semi-fowler’s position to allow greater diaphragm expansion thereby lung expansion and better CO2 - O2 exchange. 2. Promoting adequate CO • Monitor the following parameters: dysrhhythmias on ECG tracings, VS, effects of daily activities on cardiac status, rate and rhythm of pulse. • Administer pharmacotherapy as prescribed • Promote rest and minimize unnecessary disturbances. 3. Promoting comfort: • relieve pain; administer Morphine SO4 as ordered. This is to reduce sympathetic • stimulation, which increases myocardial O2 demand. In addition, this will prevent • shock which may result from severe pain.
  55. 55. 4. Providing rest: • place patient in bed rest with commode privileges for 24 – 48 hours. • administer diazepam(Valium) as ordered. • provide psychosocial support to the client and his family. Calmness and competency are extremely reassuring. 5. Promoting Activity • gradual increase in activity is encouraged after the first 24-48 hours. May be allowed to sit on a chair for increasing periods of time and begins ambulation on the 4th or 5th day. • monitor for signs of dysrhythmias, chest pain, and changes in VS during activity.
  56. 56. 6. Promoting nutrition and elimination a. provide small, frequent feedings b. provide low – calorie, low-cholesterol, low Na diet c. avoid stimulants d. avoid taking very hot or very cold beverages and gas forming foods. Vasovagal stimulation may occur, thereby bradycardia. e. use of bedpan and straining at stool should be avoided. Valsalva maneuver changes BP and HR which may trigger ischemia; dysrhythmias, pulmonary embolism or cardiac arrest. f. use of bedside commode g. administer stool softener as ordered (ex. Lactulose) 7. Promoting relief of anxiety and feeling of well-being:  provide an opportunity for the client and family to explore their concerns and to identify alternative methods of coping as necessary. 8. Facilitating learning • teaching is started once the client is free of pain and excessive anxiety • promote a positive attitude and active participation of the client and the family.
  57. 57. CARDIAC REHABILITATION: Cardiac rehabilitation provides a venue for continued education, re-enforcement of lifestyle modification, and adherence to a comprehensive prescription of therapies for recovery from MI, which includes exercise training Goals of Rehabilitation program: •Develop a program for progressive physical activity •Lives as full, vital and productive life •Remain within the limits of the heart’s ability to respond to increases in activity and stress.
  58. 58. FOLLOW UP

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