10 Chronic Renal Failure Nursing Care Plans

Risk for Decreased Cardiac Output

Extracellular volume expansion and total body volume overload result from the failure of sodium and free-water excretion. This generally becomes clinically manifested when the GFR falls to less than 10 to 15 mL/min/1.73 m² when compensatory mechanisms have become exhausted. As kidney function declines further, sodium retention and extracellular volume expansion lead to peripheral edema and, not uncommonly, pulmonary edema and hypertension (Arora & Batuman, 2023). Due to the essential role of the kidney, the human body possesses extensive mechanisms to preserve GFR. An important decrease in cardiac output will lead to a redistribution of blood volume within the body to preserve kidney perfusion (Mullens & Nijst, 2016).

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, and cardiac conduction (electrolyte imbalances, hypoxia)
• Accumulation of toxins (urea), soft-tissue calcification (deposition of calcium phosphate)

Possibly evidenced by

• Not applicable for risk diagnosis. A risk diagnosis is not evidenced by signs and symptoms, as the problem has not occurred and nursing interventions are directed at prevention.

Desired Outcomes

• The client will maintain cardiac output as evidenced by BP and heart rate within the client’s normal range; peripheral pulses are strong and equal with prompt capillary refill time.

Nursing Assessment and Rationales

1. Auscultate heart and lung sounds. Evaluate the presence of peripheral edema, vascular congestion, and reports of dyspnea.
S₃ and S₄ heart sounds with muffled tones, tachycardia, irregular heart rate, tachypnea, dyspnea, crackles, wheezes, edema, and jugular distension suggest heart failure. Progressive renal dysfunction is often attributed to hypoperfusion of the kidney due to progressive impairment of cardiac output. However, a drop in systemic blood pressure, venous congestion, and intra-abdominal pressure are hemodynamic parameters that are strongly associated with worsening renal function in heterogenous populations with heart failure (Mullens & Nijst, 2016).

2. Assess presence and degree of hypertension: monitor BP; note postural changes (sitting, lying, standing).
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. Hypertension is a frequent sign of CKD but should not by itself be considered a marker of it because elevated blood pressure is also common among people without CKD (Arora & Batuman, 2023).

3. Investigate reports of chest pain, noting location, radiation, severity (0–10 scale), and whether or not it is intensified by deep inspiration and supine position.
Although hypertension and chronic heart failure may cause MI, approximately half of CRF clients on dialysis develop pericarditis, potentiating the risk of pericardial effusion or tamponade. A significant key finding in uremic pericarditis is the presence of chest pain in a client with a history of CKD or ESRD. Most clients will present with pleuritic chest pain that improves when leaning forward (Nesheiwat & Lee, 2022). 

4. Evaluate heart sounds (note friction rub), BP, peripheral pulses, capillary refill, vascular congestion, temperature, and sensorium or mentation.
The presence of sudden hypotension, paradoxical pulse, narrow pulse pressure, diminished or absent peripheral pulses, marked jugular distension, pallor, and rapid mental deterioration indicate tamponade, which is a medical emergency. Physical examination reveals a pericardial friction rub which is usually scratchy and squeaky and is best appreciated on the left sternal border with the client leaning forward and holding their breath (Nesheiwat & Lee, 2022).

5. Assess activity level and response to activity.
Weakness can be attributed to heart failure and anemia. Normochromic normocytic anemia principally develops from the decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell production. The anemia starts early in the course of the disease and becomes more severe as viable renal mass shrinks and the GFR progressively decreases (Arora & Batuman, 2023).

6. Monitor electrocardiogram results.
Electrocardiogram findings of pericarditis include diffuse ST and T-wave elevations. To distinguish these findings from an ST-segment elevation myocardial infarction (STEMI), the ST and T-wave findings in pericarditis are typically diffuse and not localized to coronary artery territory. Normalization of the ST segment and diffuse T-wave inversions are seen in later stages (Nesheiwat & Lee, 2022).

7. Monitor laboratory and diagnostic studies.

• 7.1. Electrolytes (potassium, sodium, calcium, magnesium), BUN, and creatinine
  Imbalances can alter electrical conduction and cardiac function. The BUN and serum creatinine levels will be elevated in clients with CKD. Hyperkalemia or low bicarbonate levels may be present. Hyperkalemia usually does not develop until the GFR falls to less than 20 to 25 mL/min/1.73 m², at which point the kidneys have decreased ability to excrete potassium (Arora & Batuman, 2023). 
  
• 7.2. Chest x-rays and echocardiogram
  This is useful in identifying developing cardiac failure or soft-tissue calcification. A chest x-ray can reveal an increased cardiac silhouette, which may represent an effusion. An echocardiogram is also very important to confirm or further evaluate the severity of uremic pericarditis. In up to 50% of uremic pericarditis, pericardial effusion is noticeable on the echocardiogram (Nesheiwat & Lee, 2022).

Nursing Interventions and Rationales

1. Promote sodium restriction and adequate nutritional intake.
Reduction in salt intake may slow the progression of diabetic CKD, at least in part by lowering blood pressure. A meta-analysis found that dietary salt reduction significantly reduced blood pressure in type 1 and type 2 diabetes, with results comparable to those of single-drug therapy. This finding is consistent with other evidence relating salt intake to blood pressure and albuminuria in hypertensive and normotensive clients (Arora & Batuman, 2023).

2. Administer medications as indicated. 

• 2.1. Antihypertensive drugs such as prazosin, captopril, clonidine, and hydralazine
  These agents reduce systemic vascular resistance and renin release to decrease myocardial workload and aid in the prevention of heart failure and MI. aggressive blood pressure control can help to delay the decline in kidney function in clients with CKD. The Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII) and American College of Cardiology (ACC), and American Heart Association guidelines suggest a target blood pressure of less than 130/80 mm Hg (Arora & Batuman, 2023).
  
• 2.2. Serelaxin
  This drug is a recombinant human relaxin-2 that significantly reduces rehospitalization and short-term mortality in acute heart failure and preserves renal function, increases renal blood flow (RBF), and reduces filtration fraction, but does not significantly affect GFR. The increase in RBF is probably related to a reduction in venous congestion and vasodilation of afferent and efferent arteriole unloading the glomerulus (Mullens & Nijst, 2016).
  
• 2.3. Beta-blockers
  At the stage of symptomatically reduced ejection fraction (EF), therapy with beta-blockers is recommended as first-line therapy. On the basis of large randomized studies showing a reduction in total mortality, beta-blockers are also recommended as first-line therapy in parallel to renin-angiotensin-aldosterone inhibitors to counteract sudden cardiac death and progression of heart failure in clients with HFrEF (Jankowski et al., 2021).

3. Prepare for dialysis.
Reduction of uremic toxins and correction of electrolyte imbalances and fluid overload may limit and prevent cardiac manifestations, including hypertension and pericardial effusion. The preferred method is to institute dialysis or intensify dialysis for clients who have been on dialysis already. Uremic pericarditis has been shown to respond rapidly to dialysis, leading to the resolution of chest pain and pericardial effusion in most cases. Effective dialysis therapy has been observed to be helpful in over 50% of cases (Nesheiwat & Lee, 2022).

4. Assist with pericardiocentesis as indicated.
Accumulation of fluid within the pericardial sac can compromise cardiac filling and myocardial contractility, impairing cardiac output and potentiating the risk of cardiac arrest. If there is treatment failure with dialysis, the recommendation is to perform pericardiocentesis in clients with uremic pericarditis with effusion within 7 to 14 days. In clients with severe uremic pericarditis and effusion leading to cardiac tamponade, emergent pericardiocentesis is recommended (Nesheiwat & Lee, 2022).

5. Prepare the client for pericardiectomy.
A pericardiectomy, the surgical removal of the pericardium, is typically not the first-line management option and is only utilized for recurrent pericarditis with pericardial effusions. Recommendations are to pursue an echocardiogram every 3 to 5 days during an acute event to monitor pericarditis and effusion resolution (Nesheiwat & Lee, 2022).