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

Angina is the heart telling you it is starving. Blood flow through a narrowed coronary artery cannot keep up with demand, the myocardium runs short on oxygen, and the patient feels it as chest pain or pressure. Your job at the bedside is to recognize the pattern, relieve the ischemia fast, and know when stable angina has crossed into something that kills.

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 of paroxysmal pain or pressure in the anterior chest. The cause is insufficient coronary blood flow: oxygen supply falls short when myocardial oxygen demand climbs in response to physical exertion or emotional stress.

Classification

There are 5 types of angina.

• Stable angina. Predictable, consistent pain on exertion, relieved by rest and/or nitroglycerin.
• Unstable angina. Symptoms increase in frequency and severity and may not be relieved by rest or nitroglycerin.
• Intractable or refractory angina. Severe, incapacitating chest pain.
• Variant angina. Pain at rest with reversible ST-segment elevation, thought to be caused by coronary artery vasospasm.
• Silent ischemia. Objective evidence of ischemia, but the patient reports no pain.

Pathophysiology

Angina is usually caused by atherosclerotic disease and is almost invariably associated with significant obstruction of at least one major coronary artery. The myocardium normally extracts a large amount of oxygen from the coronary circulation to meet its continuous demands. When demand rises, coronary flow has to rise with it. When a coronary artery is blocked, flow cannot increase, and ischemia results, which may progress to necrosis or myocardial infarction.

Causes

• Physical exertion. Precipitates an attack by increasing myocardial oxygen demand.
• Exposure to cold. Causes vasoconstriction and elevated blood pressure, raising oxygen demand.
• Eating a heavy meal. Blood shunts to the mesenteric area for digestion, reducing supply to the heart muscle; in a severely compromised heart that shunting alone can trigger anginal pain.
• Stress. Releases catecholamines, which raise blood pressure, heart rate, and myocardial workload.

Clinical Manifestations

Symptom severity tracks with the precipitating activity and its effect on daily living.

• Chest pain. Often felt deep behind the sternum, may radiate to the neck, jaw, and shoulders.
• Numbness. Weakness or numbness in the arms, wrists, and hands.
• Shortness of breath. Rising oxygen demand drives dyspnea.
• Pallor. Inadequate supply to peripheral tissues.

Gerontologic Considerations

The elderly patient with angina often does not show the typical pain profile, because neurotransmitter responses diminish with aging. The presenting symptom is frequently dyspnea, and sometimes there are no symptoms at all ("silent" CAD), which makes recognition and diagnosis a real challenge. Teach elderly patients to read their chest-pain equivalent (for example, weakness) as the cue to rest or take prescribed medications.

Complications

• Myocardial infarction. The end result of angina pectoris left untreated.
• Cardiac arrest. The heart pumps harder to compensate for falling oxygen supply until the cardiac muscle fails.
• Cardiogenic shock. MI also predisposes the patient to cardiogenic shock.

Assessment and Diagnostic Findings

• ECG. Often normal at rest or pain-free; ST-segment depression or T-wave inversion signifies ischemia. Dysrhythmias and heart block may be present. Significant Q waves are consistent with a prior MI.
• 24-hour ECG monitoring (Holter). Shows whether pain episodes correlate with exercise or activity. ST depression without pain is highly indicative of ischemia.
• Exercise or pharmacologic stress electrocardiography. Adds diagnostic detail such as the duration and level of activity reached before angina onset. A markedly positive test indicates severe CAD. Stress echo has been shown to be more accurate than exercise stress testing alone in some groups.
• Cardiac enzymes (AST, CPK, CK, and CK-MB; LDH and isoenzymes LD1, LD2). Usually within normal limits; elevation indicates myocardial damage.
• Chest x-ray. Usually normal; infiltrates may reflect cardiac decompensation or pulmonary complications.
• Pco2, potassium, and myocardial lactate. May be elevated during the anginal attack, and all play a role in myocardial ischemia and may perpetuate it.
• Serum lipids (total lipids, lipoprotein electrophoresis, and isoenzyme cholesterols [HDL, LDL, VLDL]; triglycerides; phospholipids). May be elevated, a 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. The definitive test for CAD: indicated in known ischemic disease with angina or incapacitating chest pain, in patients with cholesterolemia and familial heart disease who have chest pain, and in patients with abnormal resting ECGs. Abnormal results occur in valvular disease, altered contractility, ventricular failure, and circulatory abnormalities. Ten percent of patients with unstable angina have normal-appearing coronary arteries.
• Ergonovine (Ergotrate) injection. Occasionally used in patients with angina at rest to demonstrate hyperspastic coronary vessels. These patients usually experience chest pain, ST elevation or depression, and/or a pronounced rise in left ventricular end-diastolic pressure (LVEDP), a fall in systemic systolic pressure, and/or high-grade coronary artery narrowing. Some may also have severe ventricular dysrhythmias.

Medical Management

The objectives are to reduce myocardial oxygen demand and increase oxygen supply.

• Oxygen therapy. Started at the onset of chest pain to increase oxygen delivered to the myocardium and reduce pain.

Pharmacologic Therapy

• Nitroglycerin gives long- and short-term reduction of myocardial oxygen consumption through selective vasodilation within 3 minutes.
• Beta-blockers reduce 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

Pain control comes first: stop activity, give oxygen, and treat with nitroglycerin per protocol while you reassess. Monitor the ECG for evolving ischemia, track pain character and response to nitroglycerin, and escalate the moment a stable pattern starts behaving like unstable angina.