ANGINA DEFINITION Angina is a temporary chest pain that results from inadequate oxygen flow to the myocardium.

Its usually described as burning, squeezing, or a tight feeling in the substernal or precordial chest. This pain may radiate to the left arm, neck, jaw, or shoulder blade. Typically, the patient clenches his fist over his chest or rubs his left arm when describing the pain, which may also be accompanied by nausea, vomiting, fainting, sweating, and cool extremities.

Angina commonly occurs after physical exertion, but may also follow emotional excitement, exposure to cold, or a large meal. It may also develop during sleep, and symptoms may awaken the patient. Types of Angina y Variant angina is a rare form of angina that is caused by coronary spasms (vasospasm). y Microvascular angina is a recently discovered type of angina.

ANATOMY AND PHYSIOLOGY

ANGINA is characterized by the accumulation of plaque within coronary arteries, which progressively enlarge, thicken and calcify. This causes critical narrowing of the coronary artery lumen (75% occlusion), resulting in a decrease in coronary blood flow and an inadequate supply of oxygen to the heart muscle.
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Ischemia may be silent (asymptomatic but evidenced by ST depression of 1 mm or more on electrocardiogram (ECG) or may be manifested by angina pectoris (chest pain).

Risk factor for Coronary Artery Disease include dyslipidemia, smoking, hypertension, male gender (women are protected until menopause), aging, nonwhite race, family history, obesity, sedimentary lifestyle, diabetes mellitus, metabolic syndrome, elevated homocysteine, and stress.

Acute coronary syndrome is a complication of CAD due to lack of oxygen to the myocardium. Manifestations include unstable angina, non ST-segment elevation infarction, and ST-segment elevation infarction.

Other causes of angina include coronary artery spasm, aortic stenosis, cardiomyopathy, severe anemia, and thyrotoxicosis.

PATHOPHYSIOLOGY The normal heart muscle s or myocardium are supplied by healthy blood vessels like coronary arteries, the blood supply caries the much need oxygen and nutrition for the cardiac muscles. With genetics and lifestyle playing major roles in the development of this disease, an abnormal amount of fats, platelets, and blood clots start to deposit on the walls of the coronary arteries, this cause the blood vessels diameter to shrink and in effect, reduces the amount of blood that is able to pass through it. As time goes by, more and more debris accumulate on the walls of the blood vessels and make the passage way of blood even tighter, when a person with this condition starts to do an activity that makes the heart go through an extra load, the oxygen and blood supply requirements of the heart muscles also increase, only this time, the adequate amount of blood can no longer pass through the narrowed blood vessels leading to an ischemia, this is where the chest pain comes in.

SYNTHESIS OF THE DISEASE: Symptoms: The most common symptoms of angina are:
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Increased heart rate. Increased blood pressure. Chest pain described as a feeling of tightness, pressure, heaviness, squeezing, or burning. This pain is usually on the left side and radiates to the lower jaw, neck, shoulder, back, arm, or hand.

Other symptoms of angina include burning in throat, feelings of indigestion and Risk factors: All of us have fatty deposits in our arteries to some degree. Atherosclerosis can start as early as our 20s and increases with age. But there are risk factors that are

known to increase the development of fatty deposits that can cause your arteries to narrow.
y a family history of atherosclerosis y high levels of LDL cholesterol in the blood y high blood pressure y smoking y being male y diabetes y Obesity. y Stress.

MANAGEMENTS Diagnostic Evaluation: 1. Resting ECG may show left ventricular hypertrophy, ST-T changes, arrhythmias, and possible Q waves. 2. Exercise stress testing with or without perfusion studies shows ischemia. 3. Cardiac catheterization shows blocked vessels. 4. Position emission tomography may show small perfusion defects. 5. Radionuclide ventriculography shows wall motion abnormalities and ejection fraction. 6. Fasting blood levels of cholesterol, low density lipoprotein, high density lipoprotein, lipoprotein A, homocysteine, and triglycerides may be abnormal. 7. Coagulation studies, hemoglobin level, fasting blood sugar as baseline studies. Pharmacologic Interventions: 1. Antianginal medications (nitrates, beta-adrenergic blockers, calcium channel blockers, and angiotensin converting enzyme inhibitors) to promote a favorable balance of oxygen supply and demand. 2. Antilipid medications to decrease blood cholesterol and tricglyceride levels in

patients with elevated levels. 3. Antiplatelet agents to inhibit thrombus formation. 4. Folic acid and B complex vitamins to reduce homocysteine levels. Surgical Interventions: 1. Percutaneous transluminal coronary angioplasty or intracoronary atherectomy, or placement of intracoronarystent. 2. Coronary artery bypass grafting. 3. Transmyocardial revascularization. Nursing Interventions: 1. Monitor blood pressure, apical heart rate, and respirations every 5 minutes during an anginal attack. 2. Maintain continuous ECG monitoring or obtain a 12-lead ECG, as directed, monitor for arrhythmias and ST elevation. 3. Place patient in comfortable position and administer oxygen, if prescribed, to enhance myocardial oxygen supply. 4. Identify specific activities patient may engage in that are below the level at which anginal pain occurs. 5. Reinforce the importance of notifying nursing staff whenever angina pain is experienced. 6. Encourage supine position for dizziness caused by antianginals. 7. Be alert to adverse reaction related to abrupt discontinuation of beta-adrenergic blocker and calcium channel blocker therapy. These drug must be tapered to prevent a rebound phenomenon; tachycardia, increase in chest pain, and hypertension. 8. Explain to the patient the importance of anxiety reduction to assist to control angina. 9. Teach the patient relaxation techniques.

MYOCARDIAL INFARCTION

DEFINITION

Myocardial infarction (MI or AMI for acute myocardial infarction), commonly known as a heart attack, occurs when the blood supply to part of the heart is interrupted causing some heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (like cholesterol) and white blood cells (especially macrophages) in the wall of an artery. The resulting ischemia (restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time, it can cause damage and/or death (infarction) of heart muscle tissue (myocardium).

ANATOMY AND PHYSIOLOGY

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. The affected muscle tissue subsequently becomes necrotic.

Onset of Myocardial Infarction may be sudden or gradual, and the process takes 3 to 6 hours to run its course.

It is the most serious manifestation of acute coronary syndrome, a complication of coronary artery disease (CAD).

Approximately 90% of Myocardial Infarction are precipitated by acute coronary thrombosis (partial or total) secondary to severe CAD (greater than 70% narrowing of the artery).

Other causative factors include coronary artery spasm, coronary artery embolism, infectious diseases causing arterial inflammation, hypoxia, anemia, and severe exertion or stress on the heart in the presence of significant coronary artery disease.

PATHOPHYSIOLOGY

In Myocardial Infarction, inadequate coronary blood flow rapidly results in myocardial ischemia in the affected area. The location and extent of the infarct determine the effects on cardiac function. Ischemia depresses cardiac function and triggers autonomic nervous system responses that exacerbate the imbalance between myocardial oxygen supply and demand. Persistent ischemia results in tissue necrosis and scar tissue formation, with permanent loss of myocardial contractility in the affected area. Cardiogenic shock may develop because of inadequate CO from decreased myocardial contractility and pumping capacity.

SYNTHESIS OF THE DISEASE

Signs and Symptoms:

Although chest pain or pressure is the most common symptom of a heart attack, heart attack victims may experience a variety of symptoms including: y Pain, fullness, and/or squeezing sensation of the chest y Jaw pain, toothache, headache y Shortness of breath y Nausea, vomiting, and/or general epigastric (upper middle abdomen) discomfort y Sweating y Heartburn and/or indigestion y Arm pain (more commonly the left arm, but may be either arm) y Upper back pain y General malaise (vague feeling of illness) y No symptoms (Approximately one quarter of all heart attacks are silent, without chest pain or new symptoms. Silent heart attacks are especially common among patients with diabetes mellitus.)

Manifestations: y anxiety y diaphoresis y facial pallor y hypertension or hypotension y bradycardia or tachycardia y palpitations y dyspnea y disorientation y nausea y vomiting

Risk factors: y male gender y age over 45 for men y smoking y high blood cholesterol levels y hypertension y family history of premature CAD y diabetes y obesity MANAGEMENTS

Diagnostic Evaluation: 1. Serial 12-lead electrocardiograms (ECGs) detect changes that usually occur within 2 to 12 hours, but may take 72 to 96 hours
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ST-segment depression and T-wave inversion indicate a pattern of ischemia; ST elevation indicates an injury pattern.

Q waves indicate tissue necrosis and are permanent

2. Nonspecific enzymes including aspartate transaminase, lactate dehydrogenase, and myoglobulin may be elevated 3. More specific creatinine phosphokinase isoenzyme CK-MB will be elevated. 4. Triponin T and I are myocardial proteins that increase in the serum about 3 to 4 hours after an MI, peak in 4 to 24 hours, and are detectable for upto 2 weeks; the test is easy to run, can help diagnose an MI up to 2 weeks earlier, and only unstable angina causes a false positive. 5. White blood cell count and sedimentation rate may be elevated. 6. Radionuclide imaging, positron emission tomography, and echocardiography may be done to evaluate heart muscle.

Pharmacologic Intervention: 1. Pain control drugs to reduce catecholamine-induced oxygen demand to injured heart muscle.
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Opiate analgesics: Morphine Vasodilators: Nitroglycerin Anxiolytics: Benzodiazepines

2. Thrombolytic therapy by I.V. or intracoronary route, to dissolve thrombus formation and reduce the size of the infarction. 3. Anticoagulants or other anti-platelet medications such as adjunct to thrombolytic therapy. 4. Reperfusion arrhythmias may follow successful therapy. 5. Beta-adrenergic blockers, to improve oxygen supply and demand, decrease sympathetic stimulation to the heart, promote blood flow in the small vessels of the heart, and provide antiarrhythmic effects. 6. Calcium channel blockers, to improve oxygen supply and demand.

Nursing Interventions: 1. Monitor continuous ECG to watch for life threatening arrhythmias (common within 24 hours after infarctions) and evolution of the MI (changes in ST segments and T waves). Be alert for any type of premature ventricular beats- these may herald ventricular fibrillation or ventricular tachycardia. 2. Monitor baseline vital signs before and 10 to 15 minutes after administering drugs. Also monitor blood pressure continuously when giving nitroglycerin I.V. 3. Handle the patient carefully while providing care, starting I.V. infusion, obtaining baseline vital signs, and attaching electrodes for continuous ECG monitoring. 4. Reassure the patient that pain relief is a priority, and administer analgesics promptly. Place the patient in supine position during administration to minimize hypotension. 5. Emphasize the importance of reporting any chest pain, discomfort, or epigastric

distress without delay. 6. Explain equipment, procedures, and need for frequent assessment to the patient and significant others to reduce anxiety associated with facility environment. 7. Promote rest with early gradual increase in mobilization to prevent deconditioning, which occurs during bed rest. 8. Take measures to prevent bleeding if patient is thrombolitic therapy 9. Be alert to signs and symptoms of sleep deprivation such as irritability, disorientation, hallucinations, diminished pain tolerance, and aggressiveness. 10. Tell the patient that sexual relations may be resumed on advise of health

care provider, usually after exercise tolerance is assessed.