Angina Pectoris (Stable Angina) Nursing Care Management: Study Guide

Learn about the nursing care management of patients with angina pectoris in this nursing study guide.

What is Angina Pectoris?
Classification
Pathophysiology
Causes
Clinical Manifestations
Gerontologic Considerations
Complications
Assessment and Diagnostic Findings
Medical Management
- Pharmacologic Therapy
Nursing Management
Practice Quiz: Angina Pectoris
See Also

What is Angina Pectoris?

Cardiovascular disease is the leading cause of death in the United States for men and women of all racial and ethnic groups.

Angina pectoris is a clinical syndrome usually characterized by episodes of paroxysms of pain or pressure in the anterior chest.
The cause is insufficient coronary blood flow, resulting in a decreased oxygen supply when there is increased myocardial demand for oxygen in response to physical exertion or emotional stress.

Classification

There are five (5) classifications or types of angina.

Stable angina. There is predictable and consistent pain that occurs on exertion and is relieved by rest and/or nitroglycerin.
Unstable angina. The symptoms increase in frequency and severity and may not be relieved with rest or nitroglycerin.
Intractable or refractory angina. There is severe incapacitating chest pain.
Variant angina. There is pain at rest, with reversible ST-segment elevation and thought to be caused by coronary artery vasospasm.
Silent ischemia. There is objective evidence of ischemia but the patient reports no pain.

Pathophysiology

Angina is usually caused by atherosclerotic disease.

Almost invariably, angina is associated with significant obstruction of at least one major coronary artery.
Oxygen demands not met. Normally, the myocardium extracts a large amount of oxygen from the coronary circulation to meet its continuous demands.
Increased demand. When there is an increase in demand, flow through the coronary arteries needs to be increased.
Ischemia. When there is blockage in a coronary artery, flow cannot be increased, and ischemia results which may lead to necrosis or myocardial infarction.
Schematic Diagram for Angina Pectoris via Scribd.

Causes

Several factors are associated with angina.

Physical exertion. This can precipitate an attack by increasing myocardial oxygen demand.
Exposure to cold. This can cause vasoconstriction and elevated blood pressure, with increased oxygen demand.
Eating a heavy meal. A heavy meal increases the blood flow to the mesenteric area for digestion, thereby reducing the blood supply available to the heart muscle; in a severely compromised heart, shunting of the blood for digestion can be sufficient to induce anginal pain.
Stress. Stress causes the release of catecholamines, which increased blood pressure, heart rate, and myocardial workload.

Clinical Manifestations

The severity of symptoms of angina is based on the magnitude of the precipitating activity and its effect on activities of daily living.

Chest pain. The pain is often felt deep in the chest behind the sternum and may radiate to the neck, jaw, and shoulders.
Numbness. A feeling of weakness or numbness in the arms, wrists and hands.
Shortness of breath. An increase in oxygen demand could cause shortness of breath.
Pallor. Inadequate blood supply to peripheral tissues cause pallor.

Gerontologic Considerations

Here’s what you need to know when caring for geriatric patients with angina pectoris:

The elderly person with angina may not exhibit the typical pain profile because of the diminished responses of neurotransmitters that occur with aging.
Often, the presenting symptom in the elderly is dyspnea.
Sometimes, there are no symptoms (“silent” CAD), making recognition and diagnosis a clinical challenge.
Elderly patients should be encouraged to recognize their chest pain–like symptom (eg, weakness) as an indication that they should rest or take prescribed medications.

Complications

Here are the common complications for patients with angina pectoris.

Myocardial infarction. Myocardial infarction is the end result of angina pectoris if left untreated.
Cardiac arrest. The heart pumps more and more blood to compensate the decreased oxygen supply, and.the cardiac muscle would ultimately fail leading to cardiac arrest.
Cardiogenic shock. MI also predisposes the patient to cardiogenic shock.

Assessment and Diagnostic Findings

The diagnosis of angina pectoris is determined through:

ECG: Often normal when a patient at rest or when pain-free; depression of the ST segment or T wave inversion signifies ischemia. Dysrhythmias and heart block may also be present. Significant Q waves are consistent with a prior MI.
24-hour ECG monitoring (Holter): Done to see whether pain episodes correlate with or change during exercise or activity. ST depression without pain is highly indicative of ischemia.
Exercise or pharmacological stress electrocardiography: Provides more diagnostic information, such as duration and level of activity attained before the onset of angina. A markedly positive test is indicative of severe CAD. Note: Studies have shown stress echo studies to be more accurate in some groups than exercise stress testing alone.
Cardiac enzymes (AST, CPK, CK, and CK-MB; LDH and isoenzymes LD1, LD2): Usually within normal limits (WNL); elevation indicates myocardial damage.
Chest x-ray: Usually normal; however, infiltrates may be present, reflecting cardiac decompensation or pulmonary complications.
Pco2, potassium, and myocardial lactate: May be elevated during the anginal attack (all play a role in myocardial ischemia and may perpetuate it).
Serum lipids (total lipids, lipoprotein electrophoresis, and isoenzymes cholesterols [HDL, LDL, VLDL]; triglycerides; phospholipids): May be elevated (CAD risk factor).
Echocardiogram: May reveal abnormal valvular action as the cause of chest pain.
Nuclear imaging studies (rest or stress scan): Thallium-201: Ischemic regions appear as areas of decreased thallium uptake.
MUGA: Evaluates specific and general ventricle performance, regional wall motion, and ejection fraction.
Cardiac catheterization with angiography: Definitive test for CAD in patients with known ischemic disease with angina or incapacitating chest pain, in patients with cholesterolemia and familial heart disease who are experiencing chest pain, and in patients with abnormal resting ECGs. Abnormal results are present in valvular disease, altered contractility, ventricular failure, and circulatory abnormalities. Note: Ten percent of patients with unstable angina have normal-appearing coronary arteries.
Ergonovine (Ergotrate) injection: On occasion, may be used for patients who have angina at rest to demonstrate hyper spastic coronary vessels. (Patients with resting angina usually experience chest pain, ST elevation, or depression and/or pronounced rise in left ventricular end-diastolic pressure [LVEDP], fall in systemic systolic pressure, and/or high-grade coronary artery narrowing. Some patients may also have severe ventricular dysrhythmias.)

Medical Management

The objectives of the medical management of angina are to increase the oxygen demand of the myocardium and to increase the oxygen supply.

Oxygen therapy. Oxygen therapy is usually initiated at the onset of chest pain in an attempt to increase the amount of oxygen delivered to the myocardium and reduce pain.

Pharmacologic Therapy

Nitroglycerin gives long-term and short-term reduction of myocardial oxygen consumption through selective vasodilation within three (3) minutes.
Beta-blockers reduces myocardial oxygen consumption by blocking beta-adrenergic stimulation of the heart.
Calcium channel blockers have negative inotropic effects.
Antiplatelet medications prevent platelet aggregation, and anticoagulants prevent thrombus formation.

Nursing Management

For the detailed nursing care plan, assessment, nursing diagnosis, interventions, and management of patients with chest pain (angina pectoris), please visit: Chest Pain (Angina Pectoris) Nursing Care Plan & Management

Practice Quiz: Angina Pectoris

Here’s a 5-item quiz about the study guide. Please visit our nursing test bank for more NCLEX practice questions.

1. The pain of angina pectoris is produced primarily by:

A. Vasoconstriction.
B. Movement of thromboemboli.
C. Myocardial ischemia.
D. The presence of atheromas.

2. The nurse advises a patient that sublingual nitroglycerin should alleviate angina pain within:

A. 3 to 4 minutes.
B. 10 to 15 minutes.
C. 30 minutes.
D. 60 minutes.

3. The scientific rationale supporting the administration of beta-blockers is the drug’s ability to:

A. Block sympathetic impulses to the heart.
B. Elevate blood pressure.
C. Increase myocardial contractility.
D. Induce bradycardia.

4. Calcium channel blockers act by:

A. Decreasing SA node automaticity.
B. Increasing AV node conduction.
C. Increasing the heart rate.
D. Creating a positive inotropic effect.

5. All of the following are type of angina except for:

A. Stable angina.
B. Unstable angina.
C. Refractory angina.
D. Direct angina.

Answers and Rationale

1. Answer: C. Myocardial ischemia.

Ischemia causes lactic acid production that triggers the pain.

2. Answer: A. 3 to 4 minutes.

Nitroglycerin given sublingually alleviates angina pain within 3 minutes.

3. Answer: A. Block sympathetic impulses to the heart.

Beta-blockers reduces myocardial oxygen consumption by blocking beta-adrenergic stimulation of the heart.

4. Answer: A. Decreasing SA node automaticity.

Calcium channel blockers decrease sinoatrial node automaticity.

5. Answer: D. Direct angina.

Direct angina is not a type of angina.

Chest Pain (Angina Pectoris)

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