Drugs Used to Treat Angina Pectoris
Objectives
1 Define angina pectoris and identify assessment data needed to evaluate an anginal attack.
2 Define ischemic heart disease.
4 Identify medication therapy health teaching used for an anginal patient in the clinical setting.
Key Terms
angina pectoris () (p. 404)
ischemia () (p. 404)
chronic stable angina () (p. 404)
unstable angina () (p. 404)
variant angina () (p. 404)
Angina Pectoris
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Coronary artery disease (CAD) is the leading cause of disability, socioeconomic loss, and death in the United States, and angina pectoris is the first clinical indication of underlying coronary artery disease in many patients. Angina pectoris is the name given to a feeling of chest discomfort arising from the heart because of lack of oxygen getting to the heart cells. It is a symptom of coronary artery disease, and is also called ischemic heart disease. Ischemia develops when the supply of oxygen needed by the heart cells is inadequate. The lack of oxygen occurs when blood flow through the coronary arteries is reduced by atherosclerosis or spasm of the arteries. Atherosclerosis can develop as localized plaques or as a generalized narrowing of the coronary arteries. Patients are usually asymptomatic until there is at least 50% narrowing of the artery. Coronary artery disease caused by atherosclerosis is a progressive disease; however, progression can be slowed with diet control and with the use of cholesterol-lowering agents (see Chapter 22).
The presentation of angina pectoris is highly variable. The sensation of discomfort is often described variously as squeezing, tightness, choking, pressure, burning, or heaviness. This discomfort may radiate to the neck, lower jaw, shoulder, and arm. The usual anginal attack begins gradually, reaches its peak intensity over the next several minutes, and then gradually subsides after the person stops activity and rests. Attacks can last from 30 seconds to 30 minutes. Anginal episodes are usually precipitated by factors that require an increased oxygen supply (e.g., physical activity, such as climbing a flight of stairs or lifting). Other precipitating factors include exposure to cold temperatures, emotional stress, sexual intercourse, and eating a large meal.
Angina pectoris is classified as chronic stable, unstable, or variant angina. Chronic stable angina is precipitated by physical exertion or stress, lasts only a few minutes, and is relieved by rest or nitroglycerin. It is usually caused by fixed atherosclerotic obstruction in the coronary arteries. Unstable angina is unpredictable; it changes in ease of onset, frequency, duration, and intensity. It is probably caused by a combination of atherosclerotic narrowing, vasospasm, and thrombus formation. Variant angina occurs while the patient is at rest; it is characterized by specific electrocardiographic changes, and it is caused by vasospasm of a coronary artery reducing blood flow. The type of angina pectoris is diagnosed by a combination of history, electrocardiographic changes during an anginal attack, and exercise tolerance testing with or without thallium-201 scintigraphy.
Treatment of Angina Pectoris
The goals for the treatment of angina pectoris are to prevent myocardial infarction and death (thereby prolonging life), and to relieve anginal pain symptoms, thereby improving the quality of life. In many cases, coronary angioplasty or coronary artery bypass surgery will be considered first, because these treatments have been proven to save lives over time. The choice of therapy often depends on the patient’s clinical response to initial medical therapy.
All patients should receive extensive patient education to help them reduce their risks related to coronary artery disease. The avoidance of activities that can precipitate attacks (e.g., strenuous exercise, exposure to cold weather, drinking caffeine-containing beverages, cigarette smoking, eating heavy meals, emotional stress) should be attempted. Risk factors (e.g., diabetes mellitus, hypertension, dyslipidemia) must also be treated. A structured exercise program designed for each patient can be successful for weight reduction among overweight patients, and it can also improve cardiovascular health. Healthy muscle tissue requires less oxygen. Medications, in combination with risk reduction and exercise, are effective in preventing ischemic attacks and myocardial infarction.
Drug Therapy for Angina Pectoris
Actions
The underlying pathophysiology of ischemic heart disease is an imbalance between the oxygen demands of the heart and the ability of coronary arteries to deliver the needed oxygen, the spasticity of the coronary arteries, platelet aggregation, and thrombus formation. The oxygen demand of the heart is determined by the heart rate, contractility, and ventricular volume. Therefore, the pharmacologic treatment of angina is aimed at decreasing oxygen demand by decreasing heart rate, myocardial contractility, and ventricular volume without inducing heart failure. Because platelet aggregation, blood flow turbulence, and blood viscosity also play certain roles—especially with unstable angina—platelet inhibitors are also prescribed to prevent anginal attacks (see Chapter 27). Because atherosclerosis causes narrowing and closure of the coronary arteries, inducing angina and myocardial infarction, the use of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (i.e., the statins) has also become standard therapy in treating angina pectoris (see Chapter 22).
Uses
Seven groups of drugs may be used to treat angina pectoris: nitrates, beta-adrenergic blockers, angiotensin-converting enzyme (ACE) inhibitors, calcium channel blockers, statins, platelet-active agents, and fatty oxidase enzyme inhibitors. Combination therapy is beneficial for many patients. Beta blockers, calcium channel blockers, long-acting nitrates, and ranolazine can prevent anginal episodes. Risk factor management, healthy lifestyle changes, antiplatelet agents, and ACE inhibitors can prevent disease progression and myocardial infarction or death.
Drug therapy for patients with angina must be individualized. Most patients will be given prescriptions for medication (e.g., nitroglycerin in the form of sublingual tablets or translingual spray) to treat acute attacks and prescriptions for therapy to prevent further ischemia and myocardial infarction (and possible death). Therapy to prevent myocardial infarction consists of statins to lower low-density lipoprotein (LDL) cholesterol levels and to reduce inflammation; platelet inhibitors to prevent platelet aggregation and thrombus formation; and ACE inhibitors to help dilate coronary blood vessels and to reduce the potential for thrombus formation.
The most effective agents for relieving ischemia and angina are beta blockers, calcium channel blockers, and nitrates. The drug ranolazine, which is a fatty oxidase enzyme inhibitor, modifies metabolism in the myocardial cells to reduce the oxygen demand of the contracting heart muscles, thereby reducing symptoms of angina.
Deciding which medicine to use depends on other conditions that the patient may have and the expected adverse effects of therapy. Aspirin, clopidogrel, or ticlopidine (see Chapter 27), which are platelet-active agents, may also be considered to slow platelet aggregation. Many patients will have revascularization procedures (e.g., stent placement, coronary artery bypass grafting) to restore blood flow and to reduce symptomatology. Even after revascularization, patients will still require antianginal drug therapy.
Nursing Implications for Anginal Therapy
Assessment
History of Anginal Attacks.
Ask the patient specific questions to identify the onset, duration, and intensity of the pain. Ask the patient to describe the chest sensation and the pattern of occurrence (e.g., under the sternum; in the jaw, neck, and shoulder; radiation down the left arm, the right arm, or both; into the wrist, hand, and fingers). What activities precipitate an attack? Does the pain occur with or without exertion? Is the pain relieved by rest? Does the chest pain occur shortly after eating? Does the individual experience fatigue, shortness of breath, indigestion, or nausea in relation to the anginal attack? Work with the patient to plan interventions that will minimize the factors that trigger attacks. Mutually establish goals with the patient to alter risk factors that are modifiable.
Medication History
Central Nervous System
Cardiovascular System
Nutritional History
Implementation
Obtain the patient’s vital signs, and include an assessment of the individual’s pain rating.
For information about medication administration, see the individual drug monographs.
Patient Education and Health Promotion
Medications
• Teach specific administration techniques to the patient for the type of medication prescribed (e.g., sublingual or transmucosal tablets, translingual spray, topical ointment, transdermal disks). Refer to Figure 8-2 and Figure 8-3 for further description of percutaneous administration of nitroglycerin.
Lifestyle Modifications
Lifestyle modifications are essential for many individuals with angina. Teach the patient about appropriate behavioral changes, such as stress management (e.g., relaxation techniques, meditation, three-part breathing).
Fostering Health Maintenance
Written Record.
Enlist the patient’s help with developing and maintaining a written record of monitoring parameters (e.g., blood pressure, pulse, degree of pain relief, exercise tolerance, adverse effects experienced)(see Patient Self-Assessment Form for Cardiovascular Agents on the Evolve website). Complete the Premedication Data column for use as a baseline to track the patient’s response to drug therapy. Ensure that the patient understands how to use the form, and instruct the patient to bring the completed form to follow-up visits. During follow-up visits, focus on issues that will foster the patient’s adherence with the therapeutic interventions prescribed.
Drug Class: Nitrates
Actions
The nitrates are the oldest effective therapy for angina pectoris. Although they have also been called coronary vasodilators, these agents do not increase total coronary blood flow. First, nitrates relieve angina pectoris by inducing the relaxation of the peripheral vascular smooth muscles, which results in the dilation of the arteries and veins. This reduces venous blood return (i.e., reduced preload) to the heart, which in turn leads to decreased oxygen demands on the heart. Second, nitrates increase the myocardial oxygen supply by dilating the large coronary arteries and redistributing blood flow, thereby enhancing oxygen supply to ischemic areas.
Uses
Nitroglycerin is the drug of choice for the treatment of angina pectoris. It is available in different dosages so that it can be adjusted to patient needs. Sublingual tablets dissolve quite rapidly and are used primarily for acute attacks of angina. The sustained-release tablets and capsules, ointments, and transdermal patches are used prophylactically to prevent anginal attacks. All long-acting nitrates, including isosorbide dinitrate and mononitrate, appear to be equally effective when a sufficient nitrate-free interval (as discussed later in this chapter) is incorporated into the medicine regimen. The translingual spray may be used for both the prophylaxis and acute treatment of anginal attacks.
Amyl nitrite is a volatile liquid available in small glass ampules encased in a loosely woven material so that they can be crushed easily under the patient’s nostrils for inhalation. The onset of action is less than 1 minute, but the duration is about 10 minutes.
Continued use of transdermal nitroglycerin patches and frequent doses of oral nitrates and sustained-release nitrates causes tolerance and the loss of the antianginal response to develop. The best way to avoid tolerance is to have periodic 8- to 12-hour nitrate-free periods. Depending on the type of angina, patients will be told when not to use nitrates (e.g., bedtime), unless they have an acute attack. When used with beta blockers or calcium antagonists, nitrates produce greater antianginal and anti-ischemic effects than when they are used alone. These agents also help provide prophylaxis against attacks during nitrate-free periods.
Therapeutic Outcomes
The primary therapeutic outcomes from nitrate therapy are as follows:
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