NURSING DIAGNOSIS: Fluid Volume excess
- Compromised regulatory mechanism (e.g., syndrome of inappropriate antidiuretic hormone [SIADH], decreased plasma proteins, malnutrition)
- Excess sodium/fluid intake
- Edema, anasarca, weight gain
- Intake greater than output, oliguria, changes in urine specific gravity
- Dyspnea, adventitious breath sounds, pleural effusion
- BP changes, altered CVP
- JVD, positive hepatojugular reflex
- Altered electrolyte levels
- Change in mental status
- Demonstrate stabilized fluid volume, with balanced I&O, stable weight, vital signs within patient’s normal range, and absence of edema.
Nursing Interventions & Rationale
|Measure I&O, noting positive balance (intake in excess of output). Weigh daily, and note gain more than 0.5 kg/day.||Reflects circulating volume status, developing/resolution of fluid shifts, and response to therapy. Positive balance/weight gain often reflects continuing fluid retention. Note: Decreased circulating volume (fluid shifts) may directly affect renal function/urine output, resulting in hepatorenal syndrome.|
|Monitor BP (and CVP if available). Note JVD/abdominal vein distension.||BP elevations are usually associated with fluid volume excess but may not occur because of fluid shifts out of the vascular space. Distension of external jugular and abdominal veins is associated with vascular congestion.|
|Assess respiratory status, noting increased respiratory rate, dyspnea.||Indicative of pulmonary congestion/edema.|
|Auscultate lungs, noting diminished/absent breath sounds and developing adventitious sounds (e.g., crackles).||Increasing pulmonary congestion may result in consolidation, impaired gas exchange, and complications, e.g., pulmonary edema.|
|Monitor for cardiac dysrhythmias. Auscultate heart sounds, noting development of S3/S4 gallop rhythm.||May be caused by HF, decreased coronary arterial perfusion, and electrolyte imbalance.|
|Assess degree of peripheral/dependent edema.||Fluids shift into tissues as a result of sodium and water retention, decreased albumin, and increased antidiuretic hormone (ADH).|
|Measure abdominal girth.||Reflects accumulation of fluid (ascites) resulting from loss of plasma proteins/fluid into peritoneal space. Note:Excessive fluid accumulation can reduce circulating volume, creating a deficit (signs of dehydration).|
|Encourage bedrest when ascites is present.||May promote recumbency-induced diuresis.|
|Provide frequent mouth care; occasional ice chips (if NPO).||Decreases sensation of thirst.|
|Monitor serum albumin and electrolytes (particularly potassium and sodium).||Decreased serum albumin affects plasma colloid osmotic pressure, resulting in edema formation. Reduced renal blood flow accompanied by elevated ADH and aldosterone levels and the use of diuretics (to reduce total body water) may cause various electrolyte shifts/imbalances.|
|Monitor serial chest x-rays.||Vascular congestion, pulmonary edema, and pleural effusions frequently occur.|
|Restrict sodium and fluids as indicated.||Sodium may be restricted to minimize fluid retention in extravascular spaces. Fluid restriction may be necessary to correct/prevent dilutional hyponatremia.|
|Administer salt-free albumin/plasma expanders as indicated.||Albumin may be used to increase the colloid osmotic pressure in the vascular compartment (pulling fluid into vascular space), thereby increasing effective circulating volume and decreasing formation of ascites.|
|Administer medications as indicated:
Diuretics, e.g., spironolactone (Aldactone),furosemide (Lasix);
Positive inotropic drugs and arterial vasodilators.
|Used with caution to control edema and ascites, block effect of aldosterone, and increase water excretion while sparing potassium when conservative therapy with bedrest and sodium restriction does not alleviate problem.
Serum and cellular potassium are usually depleted because of liver disease and urinary losses.
Given to increase cardiac output/improve renal blood flow and function, thereby reducing excess fluid.