Question

Nursing Diagnosis (Must have 3)	Goals (Measurable, specific, time line)	Interventions (include 3 for each diagnosis: Assess, monitor, teach).	Rationale (Reason for this intervention)	Evaluation (Met, partially met, not met and explain progress)
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Please Complete the care plan by using NANDA nursing diagnosis as a concept FLUID & ELECTROLYTE with the focus being on fluid and electrolyte.

Answer 1

#. Nursing care plan for fluid and electrolyte imbalance :-

1. Excess Fluid Volume: Increased isotonic fluid retention

May be related to :-

Excess fluid or sodium intake.

Compromised regulatory mechanism.

Possibly evidenced by :-

Ascites.

Aphasia, muscle twitching, tremors, seizures.

Bounding pulses.

Changes in the level of consciousness (lethargy, disorientation, confusion to coma).

Crackles.

Distended neck and peripheral veins.

Edema variable from dependent

Elevated central venous pressure.

Extra heart sounds S3.

Hypertension.

Productive cough.

Shortness of breath.

Sudden weight gain, often in excess of 5% of total body weight.

Tachypnea with or without dyspnea, orthopnea.

Desired Outcomes :-

Client will verbalize understanding of individual dietary and fluid restrictions.

Client will demonstrate behaviors to monitor fluid status and prevent or limit recurrence.

Client will demonstrate stable fluid volume as evidenced by stable vital signs, balanced intake and output, stable weight, and absence of signs of edema.

Nursing Interventions and Rationale :-

Monitor vital signs as well as central venous pressure, if available.Tachycardia and hypertension are common manifestations. Tachypnea usually present with or without dyspnea. Elevated CVP may be noted before dyspnea and adventitious breath sounds occur. Hypertension may be a primary disorder or occur secondary to other associated conditions such as heart failure.

Weigh client daily. Observe for sudden weight gain.One liter of fluid retention equals a weight gain of 1 kilogram (2.2 pounds).

Note presence of neck and peripheral vein distention, along with pitting edema, and dyspnea.Signs of cardiac decompensation and heart failure.

Auscultate lung and heart sounds. Adventitious sounds (crackles) and extra heart sounds (S3) are indicative of fluid excess, possibly returning in the rapid development of pulmonary edema.

Monitor intake and output. Note decreased urinary output and positive fluid balance on 24-hour calculations.Decreased renal perfusion, cardiac insufficiency, and fluid shifts may cause decreased urinary output and edema formation.

Assess for presence and location of edema formation.Edema can be either a cause or a result of various pathological conditions reflecting four competing forces: blood hydrostatic and osmotic pressures and interstitial fluid hydrostatic and osmotic pressures. The dynamic interaction of these four forces allows fluid to shift from one body compartment to another. Edema may be generalized or localized in dependent areas. Elderly clients may develop dependent edema with relatively little excess fluid.

Monitor infusion rate of parenteral fluids closely; May use infusion pump, as necessary.Rapid fluid bolus or prolonged excessive administration potentiates volume overload and risk of cardiac decompensation.

Administer oral fluids with caution. Do a 24-hour schedule fluid intake if fluids are restricted.Fluid restrictions, as well as extracellular shifts, can aggravate drying of mucous membranes, and the client may desire more fluids that are prudent.

Encourage adequate bed rest.Limited cardiac reserves result in fatigue and activity intolerance. Rest, particularly lying down, favors diuresis and reduction of edema.

Encourage deep breathing and coughing exercises.Pumonary fluid shifts potentiate respiratory complications.

Turn or reposition, and provide skin care at regular intervals. Decreases pressure and friction on edematous tissue, which is more prone to breakdown than normal tissue.

Maintain semi-Fowler’s position if dyspnea or ascites is present.Gravity improves lung expansion by lowering diaphragm and shifting fluid to the lower abdominal cavity.

Provide safety measures as indicated:

Bed in a low position.

Frequent observation.

Soft restraints.

Use of side rails.

Fluid shifts may cause cerebral edema and changes in mentation, especially in the geriatric population.

Monitor laboratory studies, such as sodium, potassium, and arterial blood gasses (ABGs), as indicated.Extracellular fluid shifts, sodium and water restriction, and renal function all affect serum sodium levels. Potassium deficit may occur with kidney dysfunction or diuretic therapy. BUN may be increased as a result of renal dysfunction. ABGs may reflect metabolic acidosis.

Replace potassium losses, as indicated.Potassium deficit may occur, especially if the client is receiving potassium-wasting diuretic. This can cause lethal cardiac dysrhythmias if untreated.

Provide a balanced protein, low-sodium diet. Restrict fluids, as indicated.If serum proteins are low because of malnutrition or gastrointestinal (GI) losses, intake of dietary proteins can enhance colloidal osmotic gradients and promote a return of fluid to the vascular space. Restriction of sodium or water decreases extracellular fluid retention.

Administer diuretics as indicated:

Loop diuretics such as furosemide (Lasix).

Potassium-sparing diuretics such as spironolactone (Aldactone).

Thiazide diuretics such as hydrochlorothiazide (Microzide).

To achieve excretion of excess fluid, either a single thiazide diuretic or a combination of agents may be selected, such as thiazide and spironolactone. The combination can be particularly helpful when two drugs have different sites of action, allowing more effective control of fluid excess.

Prepare for and assist with dialysis or ultrafiltration, if indicated. May be done to rapidly reduce fluid overload, especially in the presence of severe cardiac or renal failure.

2. Deficient Fluid Volume: Decreased intravascular, interstitial, and intracellular fluid.

May be related to :-

Active fluid loss-burns, diarrhea, fistulas, gastric intubation, hemorrhage, wounds.

Regulatory failure- diabetes insipidus, diabetic ketoacidosis (DKA), adrenal disease, systemic infections, recovery phase of acute renal failure.

Possibly evidenced by :-

Abdominal distention.

Confusion, restlessness.

Dark concentrated urine.

Decreased urine volume.

Decreased central venous pressure.

Flattened neck veins.

Hypotension.

Pale, moist, clammy skin.

Tachycardia.

Tachypnea.

Weak pulses.

Desired Outcomes :-

Client will verbalize understanding of causative factors and purpose of therapeutic interventions.

Client will demonstrate behaviors to monitor and correct deficit, as appropriate.

Client will maintain fluid volume at a functional level as evidenced by stable vital signs, good skin turgor, good capillary refill, moist mucous membranes and adequate urinary output with normal specific gravity.

Nursing Interventions and Rationale :-

Weigh client daily and compare with 24-hour intake and output.Although fluid intake and weight gain greater than output may not accurately reflect intravascular volume, these measurements provide useful data for comparison.

Monitor vital signs and CVP. Observe for temperature elevation and orthostatic hypotension. Tachycardia is present along with a varying degree of hypotension, depending on the degree of fluid deficit. CVP measurements are helpful in determining the degree of fluid deficit and response to replacement therapy. Fever increases metabolism and exacerbates fluid loss

Monitor urine output. Measure or estimate fluid losses from all sources such as diaphoresis, wound drainage, and gastric losses.Fluid replacement needs are based on the correction of current deficits and ongoing losses. A decreased urinary output may indicate hypovolemia, insufficient renal perfusion or polyuria can be present, requiring more aggressive fluid replacement.

Investigate reports of sudden or sharp chest pain, cyanosis, restlessness, increased anxiety, and dyspnea.Hemoconcentration and increased platelet aggregation may result in systemic emboli formation.

Palpate peripheral pulses; Observe for skin color, temperature, and capillary refill.Conditions that contribute to extracellular fluid deficit can result in inadequate organ perfusion to all areas and may cause circulatory collapse and shock.

Monitor for a sudden or marked elevation of blood pressure, dyspnea, basilar crackles, frothy sputum, moist cough, and restlessness. Too rapid correction of fluid deficit may compromise the cardiopulmonary system, especially if colloids are used in general fluid replacement.

Evaluate client’s ability to manage own hydration.Impaired gag and swallow reflexes, anorexia, oral discomfort, nausea, and changes in mentation are among factors that affect client’s ability to replace fluids orally.

Provide skin and mouth care. Bathe every other day using mild soap. Apply lotion, as indicated. Skin and mucous membranes are dry with decreased elasticity because of vasoconstriction and reduced intracellular water. Daily bathing may increase dryness.

Ascertain client’s beverage preferences, and set up a 24-hour schedule for fluid intake. Encourage foods with high fluid content.Relieves thirst and discomfort of dry mucous membranes and augments parenteral replacement.

Provide safety precautions, as indicated, such as the use of side rails when appropriate, bed in low position, frequent observation, and soft restraints if required.Decreased cerebral perfusion frequently results in changes in mentation or altered thought process, requiring protective measures to prevent client injury.

Turn frequently, gently massage skin, and protect bony prominence.Tissues are susceptible to breakdown because of vasoconstriction and increased cellular fragility.

Monitor laboratory studies, as indicated. Depending on the degree of fluid loss, differing electrolyte and metabolic imbalances may be present and require correction.

Provide tube feedings, including free water, as appropriate. Enteral replacement can provide proteins and other needed elements in addition to meeting general fluid replacements when swallowing is not intact.

3. Risk For Electrolyte Imbalance (Hypokalemia)

May be related to :-

Diarrhea, vomiting.

Diabetic acidosis, renal failure.

High-sodium diet, starvation.

Profuse sweating.

Treatment-related side effects such as diuretics, TPN, some antibiotic

Desired Outcomes :-

Client will display heart rhythm and laboratory results within the normal limit for client and absence of paresthesias, muscle weakness, and cognitive impairment.

Nursing Interventions and Rationale :-

Monitor respiratory rate, depth, and effort. Encourage deep breathing and coughing exercise. Encouraged frequent re-positions.Respiratory muscle weakness may progress to paralysis leading to respiratory arrest.

Monitor heart rate and rhythm. Abnormalities in heart conduction and contractility are associated with hypokalemia. Tachycardia may develop as well as potentially life-threatening atrial and ventricular dysrhythmias–AV blocks, AV dissociation, ventricular tachycardia and PVCs.

Note for signs of metabolic alkalosis such as tachycardia, dysrhythmias, hypoventilation, tetany, and changes in mentation.These are usually associated with hypokalemia.

Monitor level of consciousness and neuromuscular function, noting movement, strength, and sensation.Tetany, paresthesia, apathy, drowsiness, irritability, and coma may occur.

Monitor gastric, urinary, and wound losses accurately.Guide for calculating fluid and potassium replacement needs.

Observe for absence or changes in bowel sounds. Paralytic ileus commonly follows gastric losses through vomiting, gastric suction, or protracted diarrhea.

Discuss preventable causes of the condition such as nutritional choices and the proper use of laxatives.Provides an opportunity for the client to prevent a recurrence. In addition, dietary control is more palatable than oral replacement medications.

Encourage high potassium diet such as oranges, bananas, tomatoes, coffee, red meat, and dried fruits. Discuss the use of potassium chloride salt substitutes for a client receiving long-term diuretics.Potassium may be replaced and level maintained through the diet when the client is allowed oral food and fluids. Dietary replacement of 40 to 60 mEq/L/day is usually sufficient if no abnormal losses are happening.

Monitor rate of IV potassium administration using micro drop set or infusion pump. Observe for side effects, provide ice pack, as indicated.Ensures controlled delivery of medication to prevent bolus effect and reduce associated discomfort such as burning sensation at IV site. When a solution cannot be administered via central vein and slowing of rate is not possible or effective, applying an ice pack to the infusion site may help relieve discomfort.

Review medication regimen for potassium-wasting drugs such as:

Amphotericin B (Fungizone).

Catecholamines IV.

Carbenicillin (Geocillin).

Furosemide (Lasix).

Gentamicin (Garamycin).

Hydrochlorothiazide (Diamox)

If alternative drugs such as potassium-sparing diuretics (e.g., Aldactone, Midamor) cannot be administered or when high-dose sodium drugs are administered (e.g., carbenicillin), close monitoring and replacement of potassium are important.

Observe for signs of digoxin toxicity when used: reports if blurred vision, vomiting, nausea, increasing atrial dysrhythmias, and heart block.Hypokalemia enhances the effect of digoxin, slowing cardiac conduction.

Monitor laboratory results as indicated.

Arterial blood gasses (ABGs).

Correction of metabolic alkalosis raises serum potassium level and decreased replacement needs. Correction of acidosis drives potassium back into the cells, resulting in reduced serum levels and increased replacement needs.

Serum potassium.

Frequent regular checking of serum potassium should be done during replacement therapy especially in the presence of insufficient renal function.

Administer potassium orally or intravenously.May be required to correct deficiencies when changes in medication, therapy, and dietary intake are inadequate