Imbalances in fluid and electrolytes may be due to changes in the total quantity of either substance (deficit or excess), protein deficiencies, or extracellular fluid volume shifts. Clients who are older and very young are particularly susceptible.

1. FLUID VOLUME DEFICIT (dehydration): mechanism that influences fluid balance and sodium levels; decreased quantities of fluid and electrolytes may be caused by deficient intake (poor dietary habits, anorexia, and nausea), excessive output (vomiting, nasogastric suction, and prolonged diarrhea), or failure of regulatory mechanism that influences fluid balance and sodium levels.
1. Pathophysiology: water moves out of the cells to replace a significant water loss; cells eventually become unable to compensate for the lost fluid, and cellular dehydration begins, leading to circulatory collapse.
2. Risk factors:
1. No fluids available.
2. Available fluids not drinkable.
3. Inability to take fluids independently.
4. No response to thirst; does not recognize the need for fluids.
5. Inability to communicate need; does not speak same language.
6. Aphasia.
7. Weakness, comatose.
8. Inability to swallow.
9. Psychological alterations.
10. Overuse of diuretics.
11. Increased vomiting.
12. Fever.
13. Wounds, burns.
14. Blood loss.
15. Endocrine abnormalities (e.g., diabetes insipidus).
16. Diarrhea.
3. Assessment:
1. Subjective data:
1. Thirst.
2. Behavioral changes: apprehension, apathy, lethargy, confusion, restlessness.
3. Dizziness.
4. Numbness and tingling of hands and feet.
5. Anorexia and nausea.
6. Abdominal cramps.
2. Objective data:
1. Sudden weight loss of 5%.
2. Vital signs:
1. Decreased BP; postural changes.
2. Increased temperature.
3. Irregular, weak, rapid pulse.
4. Increased rate and depth of respirations.
3. Skin: cool and pale in absence of infection; decreased turgor.
4. Urine: oliguria to anuria, high specific gravity.
5. Eyes: soft, sunken.
6. Tongue: furrows.
7. Laboratory data:
1. Blood—increased hematocrit and blood urea nitrogen (BUN).
2. Urine—decreased 17-ketosteroids; increased specific gravity, dark-colored urine.
4. Analysis/nursing diagnosis:
1. Fluid volume deficit related to inadequate fluid intake.
5. Nursing care plan/implementation:
1. Goal: restore fluid and electrolyte balance—increase fluid intake to hydrate client.
1. IVs and blood products as ordered; small, frequent drinks by mouth.
2. Daily weights (same time of day) to monitor progress of fluid replacement.
3. I&O, hourly outputs (when in acute state).
4. Avoid hypertonic solutions (may cause fluid shift when compensatory mechanisms begin to function).
2. Goal: promote comfort.
1. Frequent skin care (lack of hydration causes dry skin, which may increase risk for skin breakdown).
2. Position: change every hour to relieve pressure.
3. Medications as ordered: antiemetics, antidiarrheal.
3. Goal: prevent physical injury.
1. Frequent mouth care (mucous membrane dries due to dehydration; therefore, client is at risk for breaks in mucous membrane, halitosis).
2. Monitor IV flow rate—observe for circulatory overload, pulmonary edema related to potential fluid shift when compensatory mechanisms begin or client is unable to tolerate rate of fluid replacement.
3. Monitor vitals, including level of consciousness ( decreasing BP and level of consciousness indicate continuation of fluid loss).
4. Prepare for surgery if hemorrhage present (internal bleeding can only be relieved by surgical intervention).
6. Evaluation/outcome criteria:
1. Mentally alert.
2. Moist, intact mucous membranes.
3. Urinary output approximately equal to intake.
4. No further weight loss.
5. Gradual weight gain.
2. FLUID VOLUME EXCESS (fluid overload): most common cause is an increase in sodium; excessive quantities of fluid and electrolytes may be due to increased ingestion, tube feedings, intravenous infusions, multiple tap-water enemas, or a failure of regulatory systems, resulting in inability to excrete excesses.
1. Pathophysiology: hypo-osmolar water excess in extracellular compartment leads to intracellular water excess because the concentration of solutes in the intracellular fluid is greater than that in the extracellular fluid. Water moves to equalize concentration, causing swelling of the cells. The most common cause is an increase in sodium.
2. Risk factors:
1. Excessive intake of electrolyte-free fluids.
2. Increased secretion of antidiuretic hormone (ADH) in response to stress, drugs, anesthetics (Table 6.4. Diabetes Insipidus (DI) Versus Syndrome of Inappropriate Antidiuretic Hormone (SIADH)).
3. Decreased or inadequate output of urine.
4. Psychogenic polydipsia.
5. Certain medical conditions: tuberculosis; encephalitis; meningitis; endocrine disturbances; tumors of lung, pancreas, duodenum; heart failure.
6. Inadequate kidney function or kidney failure.
3. Assessment:
1. Subjective data:
1. Behavioral changes: irritability, apathy, confusion, disorientation.
2. Headache.
3. Anorexia, nausea, cramping.
4. Fatigue.
5. Dyspnea.
2. Objective data:
1. Vital signs: elevated blood pressure.
2. Skin: warm, moist; edema—eyelids, facial, dependent, pitting.
3. Sudden weight gain of 5 lb.
4. Pink, frothy sputum; productive.
5. Constant, irritating cough.
6. Crackles in lungs.
7. Pulse: bounding.
8. Engorgement of neck veins in sitting position.
9. Urine: polyuria, nocturia, pale color.
10. Laboratory data:
1. Blood—decreasing hematocrit, BUN.
2. Urine—decreasing specific gravity.
4. Analysis/nursing diagnosis:
1. Fluid volume excess related to excessive fluid intake or decreased fluid output.
5. Nursing care plan/implementation:
1. Goal: maintain oxygen to all cells.
1. Position: semi-Fowler's or Fowler's to facilitate improved gas exchange.
2. Vital signs: prn, minimum q4h.
3. Fluid restriction.
2. Goal: promote excretion of excess fluid.
1. Medications as ordered: diuretics.
2. Monitor electrolytes, especially Mg⁺⁺, K⁺.
3. If in kidney failure: may need dialysis; explain procedure.
4. Assist client during paracentesis, thoracentesis, phlebotomy.
1. Monitor vital signs to detect shock.
2. Prevent injury by monitoring sterile technique.
3. Prevent falling by stabilizing appropriate position during procedure.
4. Support client psychologically.
3. Goal: obtain/maintain fluid balance.
1. Daily weights; 1 kg = 1,000 mL fluid.
2. Measure: all edematous parts, abdominal girth, I&O.
3. Limit: fluids by mouth, IVs, sodium.
4. Strict monitoring of IV fluids.
4. Goal: prevent tissue injury.
1. Skin and mouth care as needed.
2. Evaluate feet for edema and discoloration when client is out of bed.
3. Observe suture line on surgical clients (potential for evisceration due to excess fluid retention).
4. IV route preferred for parenteral medications; Z track if medications are to be given IM (otherwise injected liquid will escape through injection site).
5. Goal: health teaching.
1. Improve nutritional status with low-sodium diet.
2. Identify cause that put client at risk for imbalance, methods to avoid this situation in the future.
3. Desired and side effects of diuretics and other prescribed medications.
4. Monitor urinary output, ankle edema; report to health-care manager when fluid retention is noticed.
5. Limit fluid intake when kidney/cardiac function impaired.
6. Evaluation/outcome criteria:
1. Fluid balance obtained.
2. No respiratory, cardiac complications.
3. Vital signs within normal limits.
4. Urinary output improved, no evidence of edema.
3. COMMON ELECTROLYTE IMBALANCES: Electrolytes are taken into the body in foods and fluids; normally lost through sweat and urine. May also be lost through hemorrhage, vomiting, and diarrhea. Electrolytes have major influences on: body water regulation and osmolality, acid-base regulation, enzyme reactions, and neuromuscular activity. Clinically important electrolytes are:
1. Sodium (Na⁺): normal 135 to 145 mEq/L. Most prevalent cation in extracellular fluid. Controls osmotic pressure; essential for neuromuscular functioning and intracellular chemical reactions. Aids in maintenance of acid-base balance. Necessary for glucose to be transported into cells.
1. Hyponatremia—sodium deficit, resulting from either a sodium loss or water excess. Serum sodium level below 135 mEq/L; symptoms usually do not occur until below 120 mEq/L unless rapid drop.
2. Hypernatremia—excess sodium in the blood, resulting from either high sodium intake, water loss, or low water intake. Serum sodium level above 145 mEq/L.
2. Potassium(K⁺): normal 3.5 to 5.0 mEq/L.
   Direct effect on excitability of nerves and muscles. Contributes to intracellular osmotic pressure and influences acid-base balance. Major cation of the cell. Required for storage of nitrogen as muscle protein.
1. Hypokalemia—potassium deficit related to dehydration, starvation, vomiting, diarrhea, diuretics. Serum potassium level below 3.5 mEq/L; symptoms may not occur until below 2.5 mEq/L.
2. Hyperkalemia—potassium excess related to severe tissue damage, renal disease, excess administration of oral or IV potassium. Serum potassium level above 5 mEq/L; symptoms usually occur when above 6.5 mEq/L.
3. Calcium(Ca⁺⁺): normal 4.5 to 5.5 mEq/L. Essential to muscle metabolism, cardiac function, and bone health. Controlled by parathyroid hormone; reciprocal relationship between calcium and phosphorus.
1. Hypocalcemia—loss of calcium related to inadequate intake, vitamin D deficiency, hypoparathyroidism, damage to the parathyroid gland, decreased absorption in the GI tract, excess loss through kidneys. Serum calcium level below 4.5 mEq/L.
2. Hypercalcemia—calcium excess related to hyperparathyroidism, immobility, bone tumors, renal failure, excess intake of Ca⁺⁺ or vitamin D. Serum calcium level above 5.5 mEq/L.
4. Magnesium(Mg⁺⁺): normal 1.5 to 2.5 mEq/L. Essential to cellular metabolism of carbohydrates and proteins.
1. Hypomagnesemia—magnesium deficit related to impaired absorption from GI tract, excessive loss through kidneys, and prolonged periods of poor nutritional intake. Hypomagnesemia leads to neuromuscular irritability. Serum magnesium level below 1.5 mEq/L.
2. Hypermagnesemia—magnesium excess related to renal insufficiency, overdose during replacement therapy, severe dehydration, repeated enemas with Mg⁺⁺ sulfate (epsom salts). Serum magnesium level above 2.5 mEq/L.
5. Table 6-5. Electrolyte Imbalances provides assessment, analysis/nursing diagnosis, nursing care plan/implementation, and evaluation/outcome criteria of the various electrolyte imbalances.
4. ACID-BASE BALANCE: Concentration of hydrogen ions in extracellular fluid is determined by the ratio of bicarbonate to carbonic acid. The normal ratio is 20:1. Even when arterial blood gases are abnormal, if the ratio remains at 20:1, no imbalance will occur. Table 6-6. Blood Gas Variations with Acid-Base Imbalances shows blood gas variations with acid-base imbalances.
1. Causes of blood gas abnormalities: see Table 6-7. Blood Gas Abnormalities: Causes .
2. Types of acid-base imbalance:
1. Acidosis: hydrogen ion concentration increases and pH decreases.
2. Alkalosis: hydrogen ion concentration decreases and pH increases.
3. Metabolic imbalances: bicarbonate is the problem. In primary conditions, the level of bicarbonate is directly proportional to pH.
1. Metabolic acidosis: excessive acid is produced or added to the body, bicarbonate is lost, or acid is retained due to poorly functioning kidneys. Deficit of bicarbonate.
2. Metabolic alkalosis: excessive acid is lost or bicarbonate or alkali is retained. Excess of bicarbonate.
3. As compensatory mechanism, PCO₂ will be low in metabolic acidosis, as the body attempts to eliminate excess carbonic acid and elevate pH. PCO₂ will become elevated in metabolic alkalosis.
4. Respiratory imbalances: carbonic acid is the problem. In primary conditions, PCO₂ is inversely proportional to the pH.
1. Respiratory acidosis: pulmonary ventilation decreases, causing an elevation in the level of carbon dioxide or carbonic acid. Excess of PCO₂.
2. Respiratory alkalosis: pulmonary ventilation increases, causing a decrease in the level of carbon dioxide or carbonic acid. Deficit of PCO₂.
3. As a compensatory mechanism, the level of bicarbonate will increase in respiratory acidosis and decrease in respiratory alkalosis.
3. Assessment: see Table 6-8. Acid-Base Imbalances .
4. Analysis/nursing diagnosis:
1. Impaired gas exchange related to hyperventilation.
2. Ineffective breathing pattern related to decreased thoracic movements.
3. Ineffective airway clearance related to retained secretions.
4. Risk for injury related to poorly functioning kidneys.
5. Altered renal tissue perfusion related to dehydration.
6. Altered urinary elimination related to renal failure.
7. Fluid volume excess related to altered kidney function.
8. Fluid volume deficit related to diarrhea or dehydration.
9. Knowledge deficit (learning need) related to self-administration of antacid medications.
5. Nursing care plan/implementation: see Table 6-8. Acid-Base Imbalances .
6. Evaluation/outcome criteria: see Table 6-8. Acid-Base Imbalances .