Risk for Decreased Cardiac Output | Nursing Diagnosis for Chronic Renal Failure

Nursing diagnosis: risk for decreased Cardiac Output

Risk factors may include
Fluid imbalances affecting circulating volume, myocardial workload, and systemic vascular resistance (SVR)
Alterations in rate, rhythm, cardiac conduction (electrolyte imbalances, hypoxia)
Accumulation of toxins (urea), soft tissue calcification (deposition of calcium phosphate)

Possibly evidenced by
(Not applicable; presence of signs and symptoms establishes an actual diagnosis)

Desired Outcomes/Evaluation Criteria—Client Will
Circulation Status
Maintain cardiac output as evidenced by blood pressure (BP) and heart rate within client’s normal range; peripheral pulses strong and equal with prompt capillary refill time.

Nursing intervention with rationale:
1. Auscultate heart and lung sounds. Evaluate presence of peripheral edema, vascular congestion, and reports of dyspnea.
Rationale: S3/S4 heart sounds with muffled tones, tachycardia, irregular heart rate, tachypnea, dyspnea, crackles, wheezes, and edema or jugular distention suggest heart failure (HF).

2. Assess presence and degree of hypertension: Monitor BP and note postural changes, such as sitting, lying, and standing.
Rationale: Significant hypertension can occur because of disturbances in the renin-angiotensin-aldosterone system caused by renal dysfunction. Although hypertension is common, orthostatic hypotension may occur because of intravascular fluid deficit, response to effects of antihypertensive medications, or uremic pericardial tamponade.

3. Investigate reports of chest pain, noting location, radiation, severity (0 to 10 scale), and whether or not it is intensified by deep inspiration and supine position.
Rationale: Although hypertension and chronic HF may cause myocardial infarction (MI), approximately half of CRF clients on dialysis develop pericarditis, potentiating risk of pericardial effusion and tamponade.

4. Evaluate heart sounds for friction rub, BP, peripheral pulses, JVD, capillary refill, and mentation.
Rationale: Presence of sudden hypotension with paradoxical pulse, narrow pulse pressure, diminished or absent peripheral pulses, marked JVD, pallor, and a rapid mental deterioration indicate tamponade, which is a medical emergency.

5. Assess activity level and response to activity.
Rationale: Weakness can be attributed to heart failure and anemia.

6. Monitor laboratory and diagnostic studies, such as the following: Electrolytes—potassium, sodium, calcium, magnesium; BUN/Cr
Rationale: Imbalances can alter electrical conduction and cardiac function.

7. Collaborate in treatment of underlying disease or conditions, where possible.
Rationale: Delaying or halting progression of CRF in early stages can be aided by interventions, such as controlling BP, managing diabetes, treating hyperlipidemia, and avoiding toxins such as NSAIDs, intravenous (IV) contrast dye, aminoglycosides, and so on.

8. Administer medications, as indicated, for example: Antihypertensive drugs, such as prazosin (Minipress), captopril (Capoten), clonidine (Catapres), and hydralazine (Apresoline)
Rationale: Aggressive treatment of hypertension is needed to reduce SVR or renin release to decrease myocardial workload and aid in prevention of HF and MI.

9. Administer oxygen, as indicated.
Rationale: Cardiac function can be improved with use of oxygen if client is severely anemic or metabolic acidosis and electrolyte abnormalities are causing dysrhythmias.

10. Prepare for renal replacement therapy, such as hemodialysis.
Rationale: Reduction of uremic toxins and correction of electrolyte imbalances and fluid overload may limit or prevent cardiac manifestations, including hypertension and pericardial effusion.