What is the normal serum sodium range?
Answer: 135–145 mEq/L
Explanation
Sodium is the primary extracellular cation and the main determinant of serum osmolality; it governs water distribution between compartments.
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NCLEX-RN: Fluids, Electrolytes and Acid-Base Balance (University)
SodiumPotassiumCalciumMagnesiumFluid Volume ImbalancesIV Fluid TypesABG InterpretationAcid-Base Disorders
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Sodium
Hyponatremia: definition and major causes
Answer: Serum Na+ <135 mEq/L. Causes: excess water intake, SIADH, thiazide diuretics, vomiting/diarrhea, adrenal insufficiency, dilutional states (heart failure, cirrhosis).
Explanation
Low extracellular sodium causes water to shift into cells, producing cellular swelling (important in the brain).
Signs/symptoms of hyponatremia
Answer: Headache, confusion/lethargy, muscle weakness and cramps, nausea, and in severe cases seizures or coma (from cerebral edema).
Explanation
Symptoms reflect cerebral cell swelling from water shifting into neurons.
Treatment of hyponatremia
Answer: Mild/dilutional: fluid restriction. Severe/symptomatic: slow IV 3% hypertonic saline, treat underlying cause.
Explanation
Correct sodium slowly (no more than 8–12 mEq/L in 24h) to avoid osmotic demyelination syndrome (central pontine myelinolysis).
Hypernatremia: definition and major causes
Answer: Serum Na+ >145 mEq/L. Causes: water loss (diabetes insipidus, fever, diarrhea), excess sodium intake, Cushing's syndrome, hypertonic IV fluids.
Explanation
Excess extracellular sodium pulls water out of cells, causing cellular dehydration.
Signs/symptoms of hypernatremia
Answer: Thirst, dry mucous membranes, restlessness and irritability progressing to confusion and seizures, flushed skin, low-grade fever.
Explanation
Reflects cellular (especially neuronal) dehydration.
Treatment of hypernatremia
Answer: Hypotonic IV fluids (0.45% NS or D5W) given slowly, restrict sodium intake, treat the underlying cause.
Explanation
Correct slowly to avoid cerebral edema from rapid fluid shift back into cells.
Potassium
What is the normal serum potassium range?
Answer: 3.5–5.0 mEq/L
Explanation
Potassium is the primary intracellular cation and critical for cardiac and neuromuscular function; even small changes affect the heart.
Hypokalemia: major causes
Answer: Loop/thiazide diuretics, vomiting/diarrhea/NG suction, insulin administration, alkalosis, poor dietary intake, hyperaldosteronism.
Explanation
Insulin and alkalosis drive K+ into cells, lowering serum levels without a true total-body deficit.
ECG changes and symptoms of hypokalemia
Answer: Flattened or inverted T waves, presence of a U wave, ST depression; muscle weakness, leg cramps, fatigue, decreased GI motility/ileus, risk of dysrhythmias.
Explanation
Low extracellular K+ increases the resting membrane potential gap, slowing repolarization.
Treatment of hypokalemia
Answer: Oral or IV potassium replacement (never IV push — dilute and infuse via pump, max rate per policy, e.g., ~10 mEq/hr peripheral), monitor ECG and renal function, encourage high-K foods (bananas, oranges, potatoes).
Explanation
IV potassium bolus can cause fatal cardiac arrest, so it must always be diluted and infused slowly with cardiac monitoring.
Hyperkalemia: major causes
Answer: Renal failure, potassium-sparing diuretics, ACE inhibitors/ARBs, tissue trauma or burns, metabolic acidosis, excessive K+ intake/supplements, Addison's disease.
Explanation
Acidosis shifts K+ out of cells into the serum as H+ moves in.
ECG changes and symptoms of hyperkalemia
Answer: Tall, peaked T waves, widened QRS, prolonged PR interval, flattened/absent P waves; muscle weakness, paresthesia, abdominal cramping, risk of ventricular fibrillation or asystole.
Explanation
High extracellular K+ partially depolarizes cardiac cells, slowing conduction — a true medical emergency.
Emergency treatment of hyperkalemia
Answer: IV calcium gluconate (stabilizes cardiac membrane, does not lower K+), insulin + dextrose and beta-2 agonists (shift K+ into cells), sodium bicarbonate if acidotic, sodium polystyrene sulfonate (Kayexalate) or dialysis to remove K+, loop diuretics, restrict dietary K+.
Explanation
Calcium gluconate is given first to protect the heart while other measures lower the actual serum potassium.
Calcium
What is the normal total serum calcium range?
Answer: 9.0–10.5 mg/dL
Explanation
Calcium is vital for neuromuscular transmission, muscle contraction, bone strength, and blood clotting.
Hypocalcemia: major causes
Answer: Hypoparathyroidism, vitamin D deficiency, renal failure, acute pancreatitis, massive blood transfusion (citrate binds calcium), alkalosis.
Explanation
Low ionized calcium increases neuromuscular excitability.
What is Chvostek's sign and what does it indicate?
Answer: Tapping the facial nerve just anterior to the ear causes facial muscle twitching; a positive sign indicates hypocalcemia (neuromuscular irritability).
Explanation
Reflects increased excitability of peripheral nerves from low ionized calcium.
What is Trousseau's sign and what does it indicate?
Answer: Inflating a BP cuff above systolic pressure for several minutes induces carpal spasm (wrist/hand flexion); a positive sign indicates hypocalcemia.
Explanation
Often considered more specific for hypocalcemia than Chvostek's sign.
Treatment of hypocalcemia
Answer: Oral or IV calcium supplementation (IV calcium gluconate for severe symptoms/tetany), vitamin D therapy, seizure precautions, monitor airway for laryngospasm.
Explanation
Severe hypocalcemia can cause tetany, laryngospasm, and seizures — treat emergently with IV calcium.
Hypercalcemia: causes and classic symptom pattern
Answer: Causes: hyperparathyroidism, malignancy/bone metastasis, prolonged immobilization, excess vitamin D/calcium intake, thiazide diuretics. Symptoms ("bones, stones, groans, psychiatric overtones"): bone pain, kidney stones, constipation/abdominal pain, confusion/lethargy, decreased reflexes, shortened QT interval.
Explanation
High calcium decreases neuromuscular excitability, opposite of hypocalcemia.
Treatment of hypercalcemia
Answer: IV isotonic saline to dilute and promote renal excretion, loop diuretics (furosemide, not thiazides), calcitonin, bisphosphonates, encourage mobility, treat underlying cause.
Explanation
Thiazide diuretics are avoided because they increase calcium reabsorption and would worsen hypercalcemia.
Magnesium
What is the normal serum magnesium range?
Answer: 1.3–2.1 mEq/L (approximately 1.8–2.6 mg/dL)
Explanation
Magnesium affects neuromuscular function and cardiac conduction; its effects parallel calcium in many ways.
Hypomagnesemia: causes and signs
Answer: Causes: alcoholism, malnutrition, malabsorption, chronic diarrhea, diuretics, proton pump inhibitors. Signs: tremors, tetany, positive Chvostek's/Trousseau's signs, hyperreflexia, dysrhythmias (including torsades de pointes), seizures.
Explanation
Low magnesium mimics hypocalcemia signs because it causes neuromuscular and cardiac irritability.
Treatment of hypomagnesemia
Answer: Oral or IV magnesium sulfate replacement; during IV infusion monitor deep tendon reflexes and respiratory rate; implement seizure precautions.
Explanation
Over-replacement can cause hypermagnesemia, so close monitoring is essential.
Hypermagnesemia: causes and signs
Answer: Causes: renal failure, excessive magnesium-containing antacids/laxatives, overcorrection during treatment (e.g., preeclampsia magnesium sulfate therapy). Signs: lethargy, loss of deep tendon reflexes (early warning sign), hypotension, bradycardia, respiratory depression, cardiac arrest.
Explanation
Loss of patellar reflex is a key nursing assessment finding before magnesium sulfate toxicity worsens.
Treatment of hypermagnesemia
Answer: Discontinue magnesium intake/infusion, administer IV calcium gluconate (antidote), give loop diuretics, dialysis if severe; monitor respiratory rate and deep tendon reflexes.
Explanation
Calcium gluconate directly antagonizes magnesium's effect at the neuromuscular junction.
Fluid Volume Imbalances
Fluid volume deficit (hypovolemia): causes and signs
Answer: Causes: vomiting, diarrhea, hemorrhage, excessive diuresis, fever/diaphoresis, insufficient intake. Signs: tachycardia, orthostatic hypotension, weak thready pulse, poor skin turgor, dry mucous membranes, decreased concentrated urine output, weight loss, elevated hematocrit/BUN.
Explanation
Treat with isotonic IV fluids and correct the underlying cause; monitor daily weights and intake/output.
Fluid volume excess (hypervolemia): causes and signs
Answer: Causes: heart failure, renal failure, excessive IV fluids or sodium intake, liver cirrhosis/SIADH. Signs: edema, jugular vein distention, pulmonary crackles, dyspnea/orthopnea, bounding pulse, hypertension, weight gain, S3 heart sound.
Explanation
Treat with fluid/sodium restriction, diuretics, semi-Fowler's positioning, and monitor respiratory status and daily weights.
IV Fluid Types
Isotonic IV fluids: definition, examples, and uses
Answer: Same osmolality as plasma (~275–295 mOsm/L); stays in the intravascular space and expands ECF volume without fluid shifting. Examples: 0.9% NaCl (Normal Saline), Lactated Ringer's. Used for: fluid volume deficit, hypotension, shock, surgery, blood transfusions.
Explanation
Caution: can cause fluid overload in patients with heart failure or renal failure.
Hypotonic IV fluids: definition, examples, and uses
Answer: Lower osmolality than plasma (<250 mOsm/L); fluid shifts from the vascular space into cells, rehydrating them. Examples: 0.45% NaCl (half-normal saline), 0.33% NaCl. Used for: cellular dehydration, hypernatremia, maintenance fluids after initial resuscitation (e.g., DKA).
Explanation
Caution: contraindicated in increased intracranial pressure and burns/trauma because it can worsen cerebral edema or hypotension.
Hypertonic IV fluids: definition, examples, and uses
Answer: Higher osmolality than plasma (>375 mOsm/L); pulls fluid out of cells into the vascular space. Examples: 3% NaCl, 5% NaCl, D5NS, D5LR, D10W. Used for: severe symptomatic hyponatremia, cerebral edema.
Explanation
Caution: administer slowly, often via central line, with close monitoring for fluid overload and osmotic demyelination syndrome.
Compare the osmolality of common IV fluids
Answer: 0.45% NS (~154 mOsm/L, hypotonic), D5W-in-bag (~252 mOsm/L, acts hypotonic once dextrose metabolized), Lactated Ringer's (~275 mOsm/L, isotonic), 0.9% NS (~308 mOsm/L, isotonic), 3% NS (~1026 mOsm/L, hypertonic).
Explanation
Plasma osmolality is about 275–295 mOsm/L; fluids below this range are hypotonic, within range are isotonic, and above are hypertonic.
ABG Interpretation
What are the normal ABG values?
Answer: pH 7.35–7.45, PaCO2 35–45 mmHg, HCO3 22–26 mEq/L, PaO2 80–100 mmHg, SaO2 95–100%.
Explanation
These are the baseline values used to classify a blood gas as acidotic, alkalotic, respiratory, or metabolic.
What does the ROME mnemonic stand for in ABG interpretation?
Answer: ROME = Respiratory Opposite, Metabolic Equal.
Explanation
In respiratory disorders, pH and PaCO2 move in opposite directions (e.g., pH down, CO2 up = respiratory acidosis). In metabolic disorders, pH and HCO3 move in the same direction (e.g., pH down, HCO3 down = metabolic acidosis).
What are the steps for systematically interpreting an ABG?
Answer: 1) Check pH (acidosis <7.35, alkalosis >7.45). 2) Check PaCO2 — if it explains the pH shift, it's respiratory. 3) Check HCO3 — if it explains the pH shift, it's metabolic. 4) Check the other value for compensation: if it moved to normalize pH, compensation is occurring (partial if pH still abnormal, full if pH normal).
Explanation
Example: pH 7.30, PaCO2 50, HCO3 24 → respiratory acidosis, uncompensated (HCO3 normal).
Acid-Base Disorders
Respiratory acidosis: causes, compensation, and nursing care
Answer: Causes: hypoventilation from COPD, respiratory depression (opioids/sedatives), pneumonia, airway obstruction, neuromuscular disease (pH <7.35, PaCO2 >45). Compensation: kidneys retain HCO3 (slow, over hours to days). Nursing care: improve ventilation (deep breathing, bronchodilators, positioning, oxygen), reverse respiratory depressants (e.g., naloxone), mechanical ventilation if severe.
Explanation
CO2 accumulates when the lungs cannot eliminate it, directly lowering pH.
Respiratory alkalosis: causes, compensation, and nursing care
Answer: Causes: hyperventilation from anxiety, pain, fever, hypoxia, mechanical overventilation, high altitude (pH >7.45, PaCO2 <35). Compensation: kidneys excrete HCO3 (slow). Nursing care: treat underlying cause, calm the patient, have them breathe into a paper bag/rebreather, treat pain or fever.
Explanation
Excess CO2 is blown off by rapid breathing, raising pH.
Metabolic acidosis: causes, compensation, and nursing care
Answer: Causes: diabetic ketoacidosis, renal failure, diarrhea (bicarbonate loss), lactic acidosis, sepsis (pH <7.35, HCO3 <22). Compensation: lungs increase rate/depth of breathing (Kussmaul respirations) to blow off CO2. Nursing care: treat underlying cause (insulin for DKA, dialysis for renal failure), monitor respiratory status, give sodium bicarbonate if ordered for severe cases.
Explanation
Loss of bicarbonate or accumulation of acids lowers pH; Kussmaul breathing is the hallmark compensatory sign.
Metabolic alkalosis: causes, compensation, and nursing care
Answer: Causes: prolonged vomiting or NG suction, excessive antacid use, loop/thiazide diuretics, excessive bicarbonate intake (pH >7.45, HCO3 >26). Compensation: lungs hypoventilate (slow, shallow respirations) to retain CO2. Nursing care: treat underlying cause, replace fluids and electrolytes (K+, Cl-), monitor respiratory status, give antiemetics if vomiting.
Explanation
Loss of gastric acid (HCl) or excess bicarbonate raises pH; respiratory compensation is often limited because hypoventilation also causes hypoxia.
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