Coronary Heart Disease

Angina Pectoris Myocardial Infarction

Coronary Arteries

Angina Pectoris
A syndrome characterized by episodes of paroxysmal 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.

Types of Angina Pectoris

Stable (effort) Angina Pectoris -chest pain precipitated by physical exertion or emotional stress -rest and nitroglycerin relieve the pain 1. Character: -substernal chest pain, pressure, heaviness or discomfort -squeezing, aching, burining, choking or cramping pain -may produce numbness or weakness in arms or hands - associated symptoms include diaphoresis, nausea, indigestion, dyspnea, tachycardia and increased in blood pressure

2. Location: -behind middle or upper third of sternum -the patient generally make a fist over the site of pain (Levine sign: diffuse deep visceral pain) 3. Radiation: -usually radiates to neck, jaw, shoulders, arms, hands and posterior intrascapular area -pain occurs more commonly on the left
4. Duration: -usually lasts 1 to 5 minutes after stopping activity, NTG relieves pain within 1 minute 5. Other precipitating factors: -exposure to hot or cold weather, eating heavy meal, sexual intercourse

 Unstable (Preinfarction) Angina Pectoris -chest pain occurring at rest; no increase oxygen demand is placed on the heart muscle 1. Character: -a change in frequency, duration, and intensity of stable angina symptoms is indicative of progression to unstable angina 2. Duration: -lasts longer than 10 minutes, is unrelieved by rest or sublingual by rest or sublingual nitroglycerin, and mimic signs and symptoms of impending myocardial infarction

Diagnostic Evaluation
Physical assessment -assess for clinical manifestations and clinical history Nitroglycerin test -relief of pain with Nitroglycerin ECG stress testing -progressive increases of speed and elevation of walking on a treadmill increase the workload of the heart. -ST and T wave changes occur if myocardial ischemia is induced Cardiac catheterization -determines the presence, location and extent of coronary lesions

Effects of Ischemia, Injury, and Infarction on ECG

Management
Drug Therapy 1. Nitrates: cause generalized vasodilation 2. Beta blockers: inhibit sympathetic stimulation of receptors that are located in the conduction system of the heart and in heart muscle 3. Calcium channel blockers: inhibit movement of calcium within the heart muscle and coronary vessels; promote vasodilation and prevent or control coronary artery spasm 4. Antilipid agents: decrease cholesterol and triglyceride

 Percutaneous Transluminal Angioplasty

-a balloon-tipped catheter is placed in a coronary vessel narrowed by a plaque -the balloon is inflated and deflated to stretch the vessel wall and flatten -blood flows freely through the unclogged vessel to the heart

Percutaneous Coronary Intervention

 Intracoronary Atherectomy -a blade-tipped catheter is guided into a coronary vessel to the site of the plaque -the plaque is either cut, shaved or pulverized and then removed -requires a larger catheter introduction sheath so its use is limited larger vessels
Intracoronary Stent -a diamond mesh tubular device is placed in the coronary vessel -prevents restenosis by providing a skeletal support

 Coronary Artery Bypass Graft -a graft is surgically attached to the aorta, and the other end of the graft is attached to the distal portion of the coronary vessel -bypasses obstructive lesions in the vessel and returns adequate blood flow to the heart muscle supplied by the artery

Coronary Artery Bypass Grafts

Greater and lesser saphenous veins are commonly used for bypass graft procedures.

Cardiopulmonary Bypass System

 Lifestyle Modification -cessation of smoking -control of high blood pressure -lowering of blood cholesterol level -dietary modifications

Complications
-Sudden death due to lethal dysrhythmias -congestive heart failure -myocardial infarction

Nursing Responsibilities
-assess for the characteristics of pain and ask patient to describe anginal attacks *Relieving Pain -assess vital signs -place patient in comfortable position -administer oxygen as prescribed -administer anti-anginal medication as prescribed -monitor for relief of pain, and note for duration of anginal episode -take vital signs every 5 to 15 minutes until anginal pain subsides

*Maintaining Cardiac Output -take blood pressure and a sitting and lying position on initiation of therapy -note changes in blood pressure more than 10mmHg and changes in heart rate of more than 10 beats per minute. -evaluate for heart failure (beta blockers and calcium channel blockers decrease contractility, thus increasing risk for heart failure) -be sure to remove previous nitrate patch before applying new patch

*Decreasing Anxiety -explain to the patient and family reasons for hospitalization, diagnostic tests and therapies administered -answer the patients questions with concise explanation -explain to patient the importance of anxiety reduction in control of angina -teach relaxation techniques

*Health Education -Advise the patient on the following: :participate in activities that do not produce chest discomfort, shortness of breath and undue fatigue. :begin regular but moderate exercise :avoid activities known to trigger angina attacks, sudden exertion, extremes of temperature, high altitudes, emotionally stressful situations; these may accelerate heart rate, raise blood pressure and increase cardiac work. :refrain from engaging in physical activity for 2 hours after meals :avoid excessive caffeine intake which can increase the heart rate :avoid alcohol or drink only in moderation as alcohol can increase the hypotensive side effects of drug)

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. -refers to a dynamic process by which one or more regions of the heart muscle experience a severe and prolonged decrease in oxygen supply because of insufficient coronary blood flow; subsequently, necrosis or death to the myocardial tissue occurs. -the onset may be sudden or gradual, and the progression of the event to completion takes approximately 3 to 6 hours.

Pathophysiology and Etiology

-acute coronary thrombosis (partial or total); associated with 90% of Myocardial infarction due to severe coronary artery disease -other etiologic factors include: :coronary artery spasm :coronary artery embolism :hypoxia :anemia :severe exertion in the presence of coronary artery disease

 Different degrees of damage may occur to the heart muscle a. zone of necrosis -death to the heart muscle caused by extensive and complete oxygen deprivation, irreversible damage b. zone of injury -region of the heart muscle surrounding the area of necrosis; inflamed and injured, but still viable if adequate oxygenation can be restored c. zone of ischemia -region of the heart muscle surrounding the area of injury, which is ischemic and viable; not endangered unless extension of the infarction occurs

Clinical Manifestations
1. Chest pain a. Severe, diffuse steady substernal pain of a crushing and squeezing nature b. Not relieved by rest or sublingual vasodilator therapy, but requires narcotics c. May radiate to the arms (commonly the left), shoulders, neck, back and jaw d. Continues for more than 15 minutes e. May produce anxiety and fear, resulting in an increase in heart rate, blood pressure and respiratory rate. 2. Diaphoresis, cool and clammy skin, facial pallor 3. Bradycardia or Tachycardia

4. 5. 6. 7. 8.

Palpitations, severe anxiety, dyspnea Disorientation, confusion, restlessness Fainting, weakness Nausea and vomiting Atypical symptoms: :epigastric or abdominal distress, dull aching or tingling sensations, shortness of breath, extreme fatigue

Diagnostic Evaluation
Electrocardiography -necrotic, injured and ischemic tissue alters ventricular depolarization and repolarization *ST segment depression and T wave inversion indicate a pattern of ischemia *ST elevation indicates an injury pattern

 Laboratory Tests *Serum Enzymes and Isoenzymes -enzymes are correlated to the extent of heart muscle damage -enzymes commonly evaluated include Creatinine Phospokinase (CPK) or Creatinine Kinase (CK); and Lactic Dehydrogenase (LDH) -Creatinine Kinase-MB is specific to heart muscle and thus the most sensitive enzyme for determining heart muscle damage

*Hematology -White blood cell count and sedimentation rate are elevated due to inflammatory process associated with damaged heart muscle. Echocardiography - notes cardiac muscle dysfunction

Management
-therapy is aimed at the protection of ischemic and injured heart tissue to preserve muscle function, reduce the infarct size, and prevent death. -innovative modalities include: :early restoration of coronary blood flow :use of pharmacologic agents to improve oxygen supply and inhibits progression of coronary artery disease

 Oxygen therapy -improves oxygenation to ischemic heart muscle

Pain Control a. Opiate Analgesic therapy -Morphine is used to relieve pain, to improve cardiac hemodynamics by reducing preload and afterload, and to provide anxiety relief -Meperidine (Demerol) is useful for pain management in those patients allergic to morphine or sensitive to respiratory depression

b. Vasodilator therapy -Nitroglycerin promote relaxation of coronary vessels and prevents coronary artery spasm

c. Anxiolytic therapy -Benzodiazepines are used with analgesics when anxiety complicates chest pain and its relief

 Other Pharmacologic therapy *Anticoagulation therapy -useful as adjunct to thrombolytic therapy

*Beta-adrenergic blocking agents -improve oxygen supply and demand, decrease sympathetic stimulation to the heart, promote blood flow in the small vessels of the heart and have antidysrhytmic effects

*Antidysrhytmic therapy -Lidocaine (Xylocaine) decrease ventricular irritability, which commonly occurs after Myocardial Infarction

*Calcium Channel blockers -improve the balance between oxygen supply and demand by decreasing heart rate, blood pressure and dilating coronary vessels. -Diltiazem the drug commonly used to decrease the incidence of reinfarction and is currently the only calcium channel blocker proven to be beneficial for Myocardial Infarction

 Percutaneous Transluminal Coronary Angioplasty -mechanical opening of the coronary vessel which can be performed during an evolving infarction Surgical Revascularization -coronary artery bypass surgery can be performed within 6 hours of evolving infraction -definite treatment of the stenosis and less scar formation on the heat are the benefits of this therapy

Complications
Cardiac Failure a. Infract expansion (thinning and dilation of the necrotic zone) b. Congestive Heart failure (with 20% to 35%left ventricle damage) c. Cardiogenic Shock: occurs when the heart muscle loses its contractile power. Cardiac Rupture Thromboembolism Pericarditis (2 to 3 days after Myocardial Infarction)

Nursing Responsibilities

Assessment -gather information regarding the patients chest pain -observe patient for diaphoresis, facial pallor, dyspnea, guarding behaviors, extreme weakness and confusion Interventions *Reducing Pain -administer oxygen and encourage patient to take deep breaths -administer Nitroglycerin as ordered; recheck blood pressure, heart rate and respiratory rate before administering nitrate and 10 to 15 minutes after dose

-administer Morphine or Meperidine: decreases sympathetic activity and reduces heart rate, respirations, blood pressure, muscle tension and anxiety -reassess patient frequently of chest pain.
*Alleviating Anxiety -explain to the family reasons for hospitalization, diagnostic tests and therapies administered -administer anti-anxiety agents as prescribed; explain reason for sedation, anxiety can make the heart more irritable and require more oxygen

*Maintaining Hemodynamic Stability -monitor blood pressure every 2 hours -monitor respirations and lung fields -note for presence of jugular vein distention and liver engorgement -assess for apical heart rate and compare with radial pulse noting for the pulse deficit -evaluate urine output (30ml per hour)

*Increasing Activity Intolerance -promote rest with gradual increase in mobilization -assist patient to rise slowly from a supine position to minimize orthostatic hypotension -encourage passive and active range of motion exercises as directed while on bed -implement a step by step program for progressive activity as directed

*Maintaining Tissue Perfusion -observe for persistent and recurrence of ischemia -administer oxygen as directed -prepare patient for possible emergency procedure
*Health Education -instruct patient to move from one activity to another after the heart has been able to manage the previous workload as determined by signs and symptoms and pulse rate -avoid activities that tense muscle such as weight lifting, pushing or pulling heavy loads -avoid extremes in temperature

-instruct patient not to rush, avoid tension -advise at least 7 hours of sleep each night and take 20 to 30 minute rest periods twice a day -advise limiting caffeine -instruct that sexual relations may resume usually after exercise is tolerated: :if patient can walk briskly or climb two flights of stairs; resumption of sexual activity parallels resumption of usual activities :sexual activity should be avoided after eating a heavy meal, after drinking alcohol, or when tired -advise to eat three to four small meals per day -instruct to immediately report recurrence of signs and symptoms

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Hypertension