NURSING DIAGNOSIS: Decreased cardiac output

related to alterations in preload, afterload, and myocardial contractility associated with:
  1. the cardiac condition causing the heart failure (e.g. ischemia of the myocardium, valve malfunction, cardiomyopathy);
  2. the effects of sympathetic nervous system and renin-angiotensin-aldosterone stimulation that occur in response to decreased cardiac output;
  3. structural changes in the heart (e.g. dilation, hypertrophy, spherical shape) that occur with prolonged activation of neurohormonal adaptive responses.
Desired Outcome
The client will have improved cardiac output as evidenced by:
  1. B/P within normal range for client
  2. apical pulse between 60 - 100 beats/minute and regular
  3. resolution of gallop rhythm
  4. verbalization of feeling less fatigued and weak
  5. unlabored respirations at 12 - 20/minute
  6. improved breath sounds
  7. usual mental status
  8. absence of dizziness and syncope
  9. palpable peripheral pulses
  10. skin warm and usual color
  11. capillary refill time less than 3 seconds
  12. urine output at least 30 ml/hour
  13. decrease in edema and jugular vein distention
  14. central venous pressure (CVP) within normal range.
Nursing Actions and Selected Purposes/Rationales
  1. Assess for signs and symptoms of heart failure and decreased cardiac output:
    1. variations in B/P (may be increased because of compensatory vasoconstriction; may be decreased when compensatory mechanisms and pump fail)
    2. tachycardia
    3. pulsus alternans (alternating strong and weak pulse)
    4. presence of an S3 heart sound
    5. fatigue and weakness
    6. dyspnea, orthopnea, tachypnea
    7. dry, hacking cough or cough productive of frothy or blood-tinged sputum
    8. abnormal breath sounds (e.g. crackles [rales], wheezes, diminished sounds)
    9. restlessness, change in mental status
    10. dizziness, syncope
    11. diminished or absent peripheral pulses
    12. cool extremities
    13. pallor or cyanosis of skin
    14. capillary refill time greater than 3 seconds
    15. decreased urine output during day, nocturia
    16. edema
    17. jugular vein distention (JVD)
    18. increased CVP (use internal jugular vein pulsation method to estimate CVP if monitoring device not present)
    19. chest x-ray results showing pulmonary vascular congestion, pleural effusion, or pulmonary edema.
  2. Implement measures to improve cardiac output:
    1. perform actions to reduce cardiac workload:
      1. place client in a semi- to high Fowler's position
      2. instruct client to avoid activities that create a Valsalva response (e.g. straining to have a bowel movement, holding breath while moving up in bed)
      3. implement measures to promote emotional and physical rest (e.g. maintain a calm, quiet environment; limit the number of visitors; maintain activity restrictions)
      4. implement measures to improve respiratory status (see Diagnosis 2, action b) in order to improve alveolar gas exchange and promote adequate tissue oxygenation
      5. discourage smoking (nicotine has a cardiostimulatory effect and causes vasoconstriction; the carbon monoxide in smoke reduces oxygen availability)
      6. provide small meals rather than large ones (large meals can increase cardiac workload because they require a greater increase in blood supply to gastrointestinal tract for digestion)
      7. discourage excessive intake of beverages high in caffeine such as coffee, tea, and colas (caffeine is a myocardial stimulant and can increase myocardial oxygen consumption)
      8. increase activity gradually as allowed and tolerated
      9. implement measures to reduce fluid volume excess (see Diagnosis 3, action D.1)
    2. administer the following medications if ordered:
      1. diuretics (e.g. furosemide, torsemide, bumetanide, spironalactone, metolazone) to reduce sodium and water retention and subsequently reduce cardiac workload
      2. angiotensin-converting enzyme (ACE) inhibitors (e.g. captopril, ramipril, enalapril, lisinopril) to reduce vascular resistance and subsequently decrease cardiac workload; they also alter the course of cardiac remodeling and slow disease progression
      3. positive inotropic agents (e.g. digoxin, dopamine, dobutamine) to improve myocardial contractility
      4. beta-adrenergic blocking agents (e.g. carvedilol) to blunt the effects of the sympathetic nervous system stimulation that occurs and subsequently improve the clinical status and course of the disease.
  3. Consult physician if signs and symptoms of decreased cardiac output persist or worsen.