Nursing Diagnosis for Myocardial Infarction | Decreased Cardiac Output

Nursing diagnosis: risk for decreased Cardiac Output.

Risk factors may include

Changes in rate, rhythm, electrical conduction

Reduced preload and increased systemic vascular resistance (SVR)

Infarcted or dyskinetic muscle, structural defects—ventricular aneurysm, septal defects

Possibly evidenced by

(Not applicable; presence of signs and symptoms establishes actual diagnosis)

Desired Outcomes/Evaluation Criteria—Client Will

Cardiac Pump Effectiveness

Maintain hemodynamic stability, such as BP, cardiac output within normal range, adequate urinary output, decreased frequency or absence of dysrhythmias.

Report decreased episodes of dyspnea and angina.

Nursing intervention with rationale:

1. Obtain BP readings. Compare both arms and obtain lying, sitting, and standing pressures when able.

Rationale: Hypotension may occur related to ventricular dysfunction, hypoperfusion of the myocardium, and vagal stimulation. However, hypertension is also a common phenomenon, possibly related to pain, anxiety, catecholamine release, and preexisting vascular problems. Orthostatic (postural) hypotension may be associated with complications of infarct, such as heart failure.

2. Evaluate quality and equality of pulses, as indicated.

Rationale: Decreased cardiac output results in diminished, weak, or thready pulses. Irregularities suggest dysrhythmias, which may require further evaluation and monitoring.

3. Auscultate heart sounds: Note development of S3 and S.

Rationale: S3 is usually associated with heart failure, but it may also be noted with the mitral insufficiency (regurgitation) and left ventricular overload that can accompany severe infarction. S4 may be associated with myocardial ischemia, ventricular stiffening, and pulmonary or systemic hypertension.

4. Note presence of murmurs and rubs.

Rationale: Indicates disturbances of normal blood flow within the heart, such as incompetent valve, septal defect, or vibration of papillary muscle and chordae tendineae (complication of MI). Presence of rub with an infarction is also associated with inflammation, such as pericardial effusion and pericarditis.

5. Auscultate breath sounds.

Rationale: Crackles reflect pulmonary congestion; may develop because of depressed myocardial function.

6. Monitor heart rate and rhythm. Document dysrhythmias via telemetry.

Rationale: Heart rate and rhythm respond to medication, activity, and developing complications. Dysrhythmias, especially premature ventricular contractions or progressive heart blocks, can compromise cardiac function or increase ischemic damage. Acute or chronic atrial flutter or fibrillation may be seen with coronary artery or valvular involvement and may or may not be pathological.

7. Note response to activity and promote rest appropriately.

Rationale: Overexertion increases oxygen consumption and demand and can compromise myocardial function.

8. Provide small, easily digested meals. Limit caffeine intake, such as coffee, chocolate, and cola, as indicated.

Rationale: Large meals may increase myocardial workload and cause vagal stimulation, resulting in bradycardia or ectopic beats. Caffeine is a direct cardiac stimulant that can increase heart rate, but may not be a problem for everyone, such as for some clients with regular daily caffeine intake.

9. Have emergency equipment and medications available.

Rationale: Sudden coronary occlusion, lethal dysrhythmias, extension of infarct, and unrelenting pain are situations that may precipitate cardiac arrest, requiring immediate life-saving therapies or transfer to CCU.

Collaborative Management:

1. Administer supplemental oxygen, as indicated.

Rationale: Increases amount of oxygen available for myocardial uptake, reducing ischemia and resultant cellular irritation and dysrhythmias.

2. Measure cardiac output and other functional parameters as appropriate.

Rationale: Cardiac index, preload and afterload, contractility, and cardiac work can be measured noninvasively with thoracic electrical bioimpedance (TEB) technique. Useful in evaluating response to therapeutic interventions and identifying need for more aggressive or emergency care.

3. Maintain IV and saline-lock access, as indicated.

Rationale: Patent line is important for administration of emergency drugs in presence of persistent lethal dysrhythmias or chest pain.

4. Review serial ECGs.

Rationale: Provides information regarding progression or resolution of infarction, status of ventricular function, electrolyte balance, and effect of drug therapies.

5. Review chest x-ray.

Rationale: May reflect pulmonary edema related to ventricular dysfunction.

6. Monitor laboratory data, such as cardiac enzymes, arterial blood gases (ABGs), and electrolytes.

Rationale: Enzymes monitor resolution or extension of infarction. Presence of hypoxia indicates need for supplemental oxygen. Electrolyte imbalances, such as hypo- or hyperkalemia, adversely affect cardiac rhythm and contractility.

7. Administer medications, as indicated: Antidysrhythmic drugs.

Rationale: Dysrhythmias are usually treated symptomatically. Early inclusion of ACE inhibitor therapy, especially in presence of large anterior MI, ventricular aneurysm, or heart failure, enhances ventricular output, increases survival, and may slow progression of heart failure.

8. Antiemetics and stool softener

Rationale: Vomiting (vasovagal reflex) or bearing down to pass stool (Valsalva’s maneuver) can result in bradycardia, temporarily reducing cardiac output followed by rebound tachycardia.

9. Assist with insertion and maintain pacemaker or automatic internal cardiac defibrillator (AICD) when used.

Rationale: Pacing may be a temporary support measure during acute phase or may be needed permanently if infarction severely damages conduction system, impairing systolic function. Use of AICD is currently advocated in client who has had ventricular fibrillation or tachycardia resulting in arrest. Strong supporting data document the benefits of ICDs for the primary prevention of sudden cardiac death.