The classic symptom of coronary artery disease (CAD) is angina—pain caused by loss of oxygen and nutrients to the myocardial tissue because of inadequate coronary blood flow. In most but not all patients presenting with angina, CAD symptoms are caused by significant atherosclerosis. Unstable angina is sometimes grouped with MI under the diagnosis of acute coronary syndrome. Angina has three major forms: (1) stable (precipitated by effort, of short duration, and easily relieved), (2) unstable (longer lasting, more severe, may not be relieved by rest/nitroglycerin; may also be new onset of pain with exertion or recent acceleration in severity of pain), and (3) variant (chest pain at rest with ECG changes due to coronary artery spasm). The AHCPR guidelines of May 1994 state that unstable angina is a transitory syndrome that causes significant disability and death in the United States.
Patients judged to be at intermediate or high likelihood of significant CAD are often hospitalized for further evaluation and therapeutic intervention. Classification of angina (provided by Canadian Cardiovascular Society Classification [CCSC]) aids in determining the risk of adverse outcomes for patients with unstable angina and, therefore, level of treatment needs. Class III angina is identified as occurring if the patient walks less than two blocks and normal activity is markedly limited, and class IV angina occurs at rest or with minimal activity and level of activity is severely limited. These two classes may require inpatient evaluation/therapeutic adjustments.
1. Relieve/control pain.
2. Prevent/minimize development of myocardial complications.
3. Provide information about disease process/prognosis and treatment.
4. Support patient/SO in initiating necessary lifestyle/behavioral changes.
1. Achieves desired activity level; meets self-care needs with minimal or no pain.
2. Free of complications.
3. Disease process/prognosis and therapeutic regimen understood.
4. Participating in treatment program, behavioral changes.
5. Plan in place to meet needs after discharge.
Nursing diagnosis for Angina Pectoris: Risk for Decreased Cardiac Output may be related to Inotropic changes (transient/prolonged myocardial ischemia, effects of edications); and Alterations in rate/rhythm and electrical conduction.
1. Report/display decreased episodes of dyspnea, angina, and dysrhythmias.
2. Demonstrate increased activity tolerance.
3. Participate in behaviors/activities that reduce the workload of the heart.
Nursing intervention with rationale:
1.Maintain bed/chair rest in position of comfort during acute episodes.
Rationale: Decreases oxygen consumption/demand, reducing myocardial workload and risk of decompensation.
2. Monitor vital signs (e.g., heart rate, BP) and cardiac rhythm.
Rationale: Tachycardia may be present because of pain, anxiety, hypoxemia, and reduced cardiac output. Changes may also occur in BP (hypertension or hypotension) because of cardiac response. ECG changes reflecting ischemia/dysrhythmias indicate need for additional evaluation and therapeutic intervention.
3. Auscultate breath sounds and heart sounds. Listen for murmurs.
Rationale: S3, S4, or crackles can occur with cardiac decompensation or some medications (especially beta-blockers). Development of murmurs may reveal a valvular cause for chest pain (e.g., aortic stenosis, mitral stenosis) or papillary muscle rupture.
4. Provide for adequate rest periods. Assist with/perform self-care activities, as indicated.
Rationale: Conserves energy, reduces cardiac workload.
5. Stress importance of avoiding straining/ bearing down, especially during defecation.
Rationale: Valsalva maneuver causes vagal stimulation, reducing heart rate (bradycardia), which may be followed by rebound tachycardia, both of which may impair cardiac output.
6. Encourage immediate reporting of pain for prompt administration of medications as indicated.
Rationale: Timely interventions can reduce oxygen consumption and myocardial workload and may prevent/minimize cardiac complications.
7. Monitor for and document effects of/adverse response to medications, noting BP, heart rate, and rhythm (especially when giving combination of calcium antagonists, betablockers, and nitrates).
Rationale: Desired effect is to decrease myocardial oxygen demand by decreasing ventricular stress. Drugs with negative inotropic properties can decrease perfusion to an already ischemic myocardium. Combination of nitrates and betablockers may have cumulative effect on cardiac output.
8. Assess for signs and symptoms of heart failure.
Rationale: Angina is only a symptom of underlying pathology causing myocardial ischemia. Disease may compromise cardiac function to point of decompensation.
9. Administer supplemental oxygen as needed.
Rationale: Increases oxygen available for myocardial uptake to improve contractility, reduce ischemia, and reduce lactic acid levels.
10. Administer medications as indicated: Calcium channel blockers, e.g., diltiazem (Cardizem), nifedipine (Procardia), verapamil (Calan), bepridil (Vascor), amlodipine (Norvasc), felodipine (Plendil), isradipine (DynaCirc).
Rationale: Although differing in mode of action, calcium channel blockers play a major role in preventing and terminating ischemia induced by coronary artery spasm and in reducing vascular resistance, thereby decreasing BP and cardiac workload.
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