Electrolytes
Unit 10: Electrolytes
Sodium (Na+)
Normal Range: 135–145 mEq/L
Function:
Responsible for resting membrane potential.
Essential in depolarization.
Principal cation of the extracellular fluid (ECF).
Sodium-Potassium (Na-K) pump is an important mechanism.
Homeostasis:
Moves out of the cell by the Na-K pump.
Regulated by aldosterone and Atrial Natriuretic Peptide (ANP).
Dietary Sources:
Breads, cereals, chips, cheese, processed meats (e.g., lunch meats, hot dogs, bacon, ham).
Commercially canned foods.
Table salt.
Electrolyte Imbalances: Sodium
Hyponatremia <135 mEq/L
Causes:
Hypovolemic hyponatremia.
Diuretics.
GI fluid loss (vomiting, diarrhea).
Profuse sweating (diaphoresis).
Water intoxication.
Prolonged use of hypotonic IV solutions.
Syndrome of inappropriate antidiuretic hormone secretion (SIADH).
Clinical Manifestations:
Lethargy, confusion, weakness.
Muscle cramping.
Seizures.
Anorexia, nausea, vomiting.
Serum osmolality <285 mOsm/kg.
Hypernatremia >145 mEq/L
Causes:
Excess sodium due to:
Excessive sodium intake.
Hypertonic IV solutions.
Hypertonic enteral feedings without adequate water.
Excess loss of water due to:
Diarrhea.
Inadequate intake of water.
Insensible loss due to fever.
Clinical Manifestations:
Thirst, dry and sticky mucous membranes, weakness, elevated temperature.
Severe cases: confusion, irritability, decreased levels of consciousness, hallucinations, and seizures.
Serum osmolality >290 mOsm/kg.
Hyponatremia Interventions:
Monitor Vital Signs (V/S), Intake & Output (I&O).
Monitor laboratory results (serum sodium and serum osmolality).
Ensure Na+ levels increase by only 4 to 6 mEq/L in any 24-hour period.
Encourage foods high in sodium.
Restrict water intake.
Administer hypertonic IV saline solutions.
Hypernatremia Interventions:
Monitor V/S, I&O, laboratory results (serum sodium and serum osmolality).
Monitor the level of consciousness.
Limit salt intake and foods high in sodium.
Increase water intake.
Administer hypotonic IV solutions.
Potassium (K+)
Normal Range: 3.5–5 mEq/L
Function:
Works with Na+ to produce resting membrane potential.
Essential in depolarization.
Principal cation of the intracellular fluid (ICF).
Essential component of Na-K pump.
Involved in protein synthesis.
Homeostasis:
Moves into the cell via Na-K pump.
Regulated by the kidneys.
Dietary Sources:
Fish (excluding shellfish), whole grains, nuts, broccoli, cabbage, carrots, celery, cucumbers, potatoes with skins, spinach, tomatoes, apricots, bananas, cantaloupe, nectarines, oranges, tangerines.
Electrolyte Imbalances: Potassium
Hypokalemia <3.5 mEq/L
Causes:
Loss of potassium due to:
Vomiting, gastric suction, diarrhea.
Laxative abuse, frequent enemas.
Use of potassium-wasting diuretics.
Inadequate intake.
Hyperaldosteronism.
Clinical Manifestations:
Weak, irregular pulse.
Fatigue, lethargy.
Anorexia, nausea, vomiting.
Muscle weakness and cramping.
Decreased peristalsis, hypoactive bowel sounds.
Paresthesia.
Cardiac dysrhythmias; increased risk for digitalis toxicity.
Hyperkalemia >5 mEq/L
Causes:
Renal failure.
Massive trauma, crushing injuries, burns.
Hemolysis.
IV potassium administration.
Potassium-sparing diuretics.
Acidosis, especially diabetic ketoacidosis.
Clinical Manifestations:
Anxiety, irritability, confusion.
Dysrhythmias (including bradycardia and heart block).
Muscle weakness, flaccid paralysis.
Paresthesia.
Abdominal cramping.
Hypokalemia Interventions:
Monitor V/S, especially heart rate (HR).
Monitor ECG.
Monitor laboratory results (serum potassium).
Assess for signs of digitalis toxicity.
Encourage foods high in potassium.
Administer potassium supplements.
IV potassium:
Must be diluted and administered slowly, usually by infusion.
NEVER administer potassium as an IV bolus or IV push.
Hyperkalemia Interventions:
Monitor V/S, especially HR.
Monitor ECG.
Monitor laboratory results (serum potassium).
Limit potassium-rich foods.
Administer cation-exchange resins (e.g., Kayexalate).
Administer glucose and insulin as needed.
Calcium (Ca2+)
Normal Range: 9–10.5 mg/dL
Function:
Primary component of bones and teeth.
Role in:
Blood clotting.
Nerve impulse transmission.
Cardiac conduction.
Muscle contraction.
Homeostasis:
Deficit regulated by parathyroid hormone (PTH) and calcitriol.
Excess regulated by calcitonin.
Dietary Sources:
Cheese, ice cream, milk, yogurt, rhubarb, spinach, tofu.
Electrolyte Imbalances: Calcium
Hypocalcemia <9 mg/dL
Causes:
Hypoparathyroidism.
Pancreatitis.
Vitamin D deficiency.
Inadequate intake of calcium-rich foods.
Hyperphosphatemia.
Chronic alcoholism.
Clinical Manifestations:
Confusion, anxiety.
Numbness and tingling of extremities.
Muscle cramps that progress to tetany and seizures.
Hyperactive reflexes.
Cardiac dysrhythmias.
Positive Chvostek and Trousseau signs.
Hypercalcemia >10.5 mg/dL
Causes:
Prolonged bed rest.
Hyperparathyroidism.
Bone malignancy.
Paget disease.
Osteoporosis.
Clinical Manifestations:
Lethargy, stupor, coma.
Decreased muscle strength and tone.
Anorexia, nausea, vomiting.
Constipation.
Pathologic fractures.
Dysrhythmias.
Renal calculi.
Hypocalcemia Interventions:
Monitor V/S, especially HR.
Monitor ECG.
Institute fall and seizure precautions.
Administer oral and/or IV calcium supplements as ordered.
Encourage calcium-rich foods.
Hypercalcemia Interventions:
Monitor V/S, especially HR.
Monitor ECG.
Encourage increased fluid intake.
Increase patient activity, including active range of motion.
Magnesium (Mg2+)
Normal Range: 1.5–2.5 mEq/L
Function:
Found primarily inside cells.
Key role in:
Production and use of ATP.
Regulation of intracellular metabolism by activation of enzymes.
Integral part of Na-K pump.
Required for synthesis of nucleic acids and proteins.
Helps maintain Ca2+ levels.
Homeostasis:
Reabsorption or excretion by the kidneys.
Also absorbed by the intestine.
Dietary Sources:
Cashews, halibut, Swiss chard and other green leafy vegetables, tofu, wheat germ, dried fruit.
Electrolyte Imbalances: Magnesium
Hypomagnesemia <1.5 mEq/L
Causes:
Decreased intake.
Total Parenteral Nutrition (TPN) without magnesium.
Decreased absorption due to:
Nasogastric suction.
Draining fistulas.
Prolonged diarrhea.
Laxative abuse.
Malabsorption syndrome.
Ulcerative colitis.
Crohn’s disease.
Increased renal excretion:
Diuresis.
Loop and thiazide diuretics.
Hypermagnesemia >2.5 mEq/L
Causes:
Excessive intake of magnesium-containing antacids or cathartics.
TPN with excessive magnesium.
Prolonged use of intravenous magnesium sulfate.
Renal failure.
Severe dehydration.
Adrenal insufficiency.
Leukemia.
Hypomagnesemia Clinical Manifestations:
Irritable nerves and muscles.
Hyperactive deep tendon reflexes.
Seizures.
Dysrhythmias (especially tachyarrhythmias).
ECG changes.
Altered level of consciousness.
Mood swings, delusions, hallucinations.
Dysphagia, nausea, vomiting.
Hypermagnesemia Clinical Manifestations:
Warm, flushed appearance.
Nausea, vomiting.
Drowsiness, lethargy.
Decreased muscle strength; generalized weakness.
Decreased deep tendon reflexes.
Hypotension.
Dysrhythmias (especially bradycardia and heart block).
Slow, shallow respirations; respiratory arrest.
Hypomagnesemia Interventions:
Assess V/S, especially HR.
Monitor ECG.
Assess mental status, level of consciousness.
Monitor laboratory results (potassium and calcium levels).
Assess swallowing before administering medications, food, or fluid.
Institute seizure precautions.
Administer oral or IV supplements as ordered.
Hypermagnesemia Interventions:
Assess V/S, especially HR.
Monitor ECG.
Assess mental status, changes in level of consciousness.
Assess neuromuscular strength and activity.
Encourage increased oral intake, increased IV fluids.
Administer loop diuretics as ordered.
Provide respiratory support (supplemental oxygen or mechanical ventilation) as needed.
Chloride (Cl−)
Normal Range: 98–106 mEq/L
Function:
Most abundant anion in the extracellular fluid (ECF).
Key role in maintaining serum osmolarity.
Required for the formation of stomach acid.
Plays a buffering role in acid-base balance.
Homeostasis:
"Where sodium goes, chloride also goes."
Dietary Sources:
Seaweed, rye, tomatoes, lettuce, celery, olives.
Table salt, salt substitutes.
Electrolyte Imbalances: Chloride
Hypochloremia <98 mEq/L
Causes:
Overhydration.
Heart failure.
Syndrome of inappropriate antidiuretic hormone secretion (SIADH).
Vomiting or gastric suction.
Addison’s disease.
Burns.
Metabolic alkalosis.
Certain medications (aldosterone, bicarbonates, steroids, loop and thiazide diuretics).
Clinical Manifestations:
Irritable nerves and muscles.
Tetany.
Hypotension.
Shallow breathing.
Hyperchloremia >106 mEq/L
Causes:
Dehydration.
Anemia.
Excessive normal saline infusion.
Cushing syndrome.
Clinical Manifestations:
Weakness.
Lethargy.
Deep breathing.
Hypochloremia Interventions:
Monitor V/S, I&O, laboratory results.
Restrict water intake.
Administer hypertonic IV saline.
Hyperchloremia Interventions:
Monitor V/S, level of consciousness (LOC), I&O, laboratory results.
Limit salt intake.
Increase water intake.
Administer hypotonic IV solutions.
Phosphate (PO43−)
Normal Range: 2–4.5 mg/dL
Function:
Most abundant anion in the intracellular fluid (ICF).
Helps maintain bone and teeth structure.
Plays a key role in cellular metabolism and ATP production.
Essential for carbohydrate metabolism.
Homeostasis:
Inverse relationship with Ca2+ (↑ Ca2+ →↓ PO43−).
PTH increases excretion by the kidneys.
Dietary Sources:
Milk, meat, nuts, legumes, grains.
Electrolyte Imbalances: Phosphate
Hypophosphatemia <2 mg/dL
Causes:
Abnormal shift into the cell.
Hyperventilation.
Respiratory alkalosis.
Hyperglycemia.
Absorption issues from the GI tract (phosphorus-binding antacids).
Starvation, malabsorption syndrome.
Inadequate vitamin D.
Chronic diarrhea, laxative abuse.
Increased excretion by kidneys (thiazides and loop diuretics, diabetic ketoacidosis).
Hyperparathyroidism, hypocalcemia.
Hyperphosphatemia >4.5 mg/dL
Causes:
Impaired renal function.
Hypoparathyroidism.
Acid-base imbalances.
Cellular injury.
Hypophosphatemia Clinical Manifestations:
Weak pulse.
Shallow respirations.
Hypotension, Decreased Cardiac Output (CO).
Hemolytic anemia.
Bleeding, increased bruising.
Muscle weakness.
Decreased deep tendon reflexes.
Tremors.
Bone pain.
Anorexia.
Increased risk for infection.
Hyperphosphatemia Clinical Manifestations:
Signs of hypocalcemia (muscle spasms, tetany).
Hyperreflexia.
Muscle spasms, weakness.
Tachycardia.
Nausea, diarrhea, cramping.
Hypophosphatemia Interventions:
Assess V/S, especially respiratory rate (RR), oxygen saturation (SpO2), and blood pressure (BP).
Assess muscle strength and neuromuscular function.
Assess for signs of heart failure.
Encourage phosphate-rich foods.
Instruct patient to avoid phosphorus-binding antacids.
Administer oral and IV phosphorus.
Administer pain medications.
Monitor for signs of infection.
Hyperphosphatemia Interventions:
Monitor V/S, I&O.
Monitor Laboratories:
Serum phosphorus.
Serum calcium.
Blood Urea Nitrogen (BUN).
Creatinine levels.
Assess signs of hypocalcemia.
Teach patient to avoid phosphorus-rich foods.
Summary Questions
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References
Yoost, B. L., & Crawford, L. R. (2023). Fundamentals of nursing: Active learning for collaborative practice (3rd ed.). Elsevier.
Zerwekh, J. (2024). Mosby’s® fluid & electrolytes memory notecards (3rd ed.). Elsevier.