Nursing Diagnosis: Decreased cardiac output related to inotropic changes, such as transient or prolonged myocardial ischemia and effects of medications; alterations in rate, rhythm, and electrical conduction.
Possibly evidenced by
(Not applicable; presence of signs and symptoms establishes an actual diagnosis)
Desired Outcomes/Evaluation Criteria—Client Will
Cardiac Pump Effectiveness
Demonstrate increased activity tolerance.
Report or display decreased episodes of dyspnea, angina, and dysrhythmias.
Participate in behaviors and activities that reduce the workload of the heart.
Nursing care plan intervention with rationale:
1. Maintain bedrest or chair rest in position of comfort during acute episodes.
Rationale: Decreases oxygen consumption and demand, reducing myocardial workload and risk of decompensation.
2. Monitor vital signs and cardiac rhythm.
Rationale: Tachycardia and changes in blood pressure (hypotension or hypertension) may be present because of pain, anxiety, hypoxemia, and reduced cardiac output. ECG changes reflecting ischemia and dysrhythmias indicate need for additional evaluation and therapeutic intervention.
3. Auscultate breath sounds and heart sounds. Listen for murmurs.
Rationale: S3, S4, or crackles may occur with cardiac decompensation or some medications, especially beta blockers. Development of murmurs may reveal a valvular cause for chest pain,
such as aortic or mitral stenosis or papillary muscle rupture.
4. Provide for adequate rest periods. Assist with or perform self-care activities, as indicated.
Rationale: Conserves energy and reduces cardiac workload.
5. Stress importance of avoiding straining and bearing down, especially during defecation.
Rationale: Valsalva’s maneuver causes 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 or minimize cardiac complications.
7. Monitor for and document effects of and adverse response to medications, noting BP, heart rate, and rhythm (especially when giving combination of calcium antagonists, beta blockers, 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 beta blockers 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. Evaluate mental status, noting development of confusion and disorientation.
Rationale: Reduced perfusion of the brain can produce observable changes in sensorium.
10. Note skin color and presence and quality of pulses.
Rationale: Peripheral circulation is reduced when cardiac output falls, giving the skin a pale or gray color depending on level of hypoxia and diminishing the strength of peripheral pulses.
11. Assess lung for adventitious sounds, such as crackles.
Rationale: Respiratory system may become decompensated with anginal attack.
Collaborative Intervention:
1. Administer supplemental oxygen as needed.
Rationale: Increases oxygen available for myocardial uptake to improve contractility, reduce ischemia, and reduce lactic acid levels.
2. Monitor pulse oximetry or arterial blood gases (ABGs), as indicated.
Rationale: Oxygen saturation may decrease as oxygen demands increase for heart muscle and systemic circulation. Monitoring determines adequacy of respiratory function and O2 therapy.
3. Measure cardiac output and other functional parameters, as indicated.
Rationale: Cardiac index, preload and afterload, contractility, and cardiac work may be measured noninvasively through various means, including TEB technique, and is useful in evaluating response to therapeutic interventions and identifying need for more aggressive emergency care. Note: Evaluation of changes in heart rate, BP, and cardiac output requires consideration of client’s circadian hemodynamic variability. These measurements are normally expected to be lower at night in clients who are active during the day.
4. Administer medications, as indicated, for example: Calcium channel blockers, such as diltiazem (Cardizem), nifedipine (Procardia), verapamil (Calan), bepridil (Vascor), amlodipine (Norvasc), felodipine (Plendil), and 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.
5. Beta blockers, such as atenolol (Tenormin), nadolol (Corgard), propranolol (Inderal), and esmolol (Brevibloc).
Rationale: These medications decrease cardiac workload by reducing heart rate and systolic BP. Note: Overdose produces cardiac decompensation.
6. Antiplatelets, such as aspirin (ASA), clopidogrel (Plavix), ticlopidine (Ticlid), tirofiban (Aggrastat), and eptifibatide (Integrilin).
Rationale: Aspirin is proven beneficial in primary and secondary prevention of coronary artery disease. For clients with major gastrointestinal intolerance, alternative drugs may be indicated. Newer antiplatelets, especially Plavix, are frequently used in conjunction with angioplasty and stent placement for relief of angina.
7. IV heparin.
Rationale: Bolus followed by continuous infusion is recommended to help reduce risk of subsequent MI by reducing the thrombotic complications of plaque rupture for clients diagnosed with intermediate or high-risk unstable angina. Note: Use of low-molecular-weight heparin is increasing because it is more efficacious and predictable and has fewer adverse effects, such as less risk of bleeding and longer half-life. It also does not require anticoagulation monitoring.
8. Monitor laboratory studies, such as PTT and aPTT.
Rationale: Evaluates anticoagulation therapy needs and effectiveness.
9. Discuss purpose and prepare for stress testing and cardiac catheterization when indicated.
Rationale: Stress testing provides information about the health or strength of the ventricles.
10. Prepare for surgical interventions such as angioplasty with or without intracoronary stent placement, valve replacement, and coronary artery bypass grafting (CABG), if indicated.
Rationale: Angioplasty, also called percutaneous transluminal coronary angioplasty (PTCA), increases coronary blood flow by compression of atheromatous lesions and dilation of the vessel lumen in an occluded coronary artery. Intracoronary stints may be placed at the time of PTCA to provide structural support within the coronary artery and improve the odds of long term patency. This procedure is preferred over the more invasive CABG surgery. Drug-coated stents may be considered for clients at high risk for thrombosis, acute closure, and for diabetics.
Several different drugs are available to help decrease restenosis after insertion of stents or
angioplasty. Stent placement may also be effective for the variant form of angina where periodic vasospasms impair arterial flow. Note: A recent innovation in thrombolytic therapy associated with angioplasty and use of stents is the Anjiojet (a device approved for removing blood clots from coronary arteries), which can reduce risk of heart attack or death. CABG is the recommended treatment when testing confirms myocardial ischemia due to left main coronary artery disease or symptomatic three-vessel disease, especially in those with left ventricular dysfunction.
11. Prepare for transfer to critical care unit if condition warrants.
Rationale: Profound or prolonged chest pain with decreased cardiac output reflects development of complications requiring more intense or emergency interventions.
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