NLE Foundations of Medical-Surgical Nursing — Fluid, Electrolyte and Acid-Base ImbalancesSummary

Total body water represents approximately 60% of adult body weight and is divided into two main compartments: the intracellular fluid (ICF) compartment, which comprises about two-thirds (40% of body weight), and the extracellular fluid (ECF) compartment, which comprises about one-third (20% of body weight). The ECF is further subdivided into intravascular fluid (plasma, 5% of body weight) and interstitial fluid (15% of body weight). Water moves between compartments by osmosis, following osmotic gradients created primarily by sodium in the ECF and potassium in the ICF. In a 70-kg adult, approximately 42 kg is water (60%), 28 kg is ICF (40%), and 14 kg is ECF (20%). This distribution is critical because electrolyte and water imbalances shift this ratio and cause clinical manifestations.

Fluid balance is maintained by four primary regulatory mechanisms: (1) Thirst—triggered by osmoreceptors when serum osmolality exceeds 295 mOsm/kg or when blood volume drops 10–15%; (2) Antidiuretic Hormone (ADH)—released from the posterior pituitary in response to increased osmolality or decreased blood volume, promoting water reabsorption in the kidney's collecting duct; (3) Renin-Angiotensin-Aldosterone System (RAAS)—activated by decreased renal perfusion or sodium depletion, leading to aldosterone release, which promotes sodium and water retention in the distal tubule; (4) Atrial Natriuretic Peptide (ANP)—released from atrial myocytes when volume expands, promoting sodium and water excretion. The kidneys are the primary regulators of both fluid and electrolyte homeostasis, filtering approximately 180 L of plasma daily and reabsorbing 99% of filtered water and electrolytes while excreting 1–2 L of urine. Dysfunction in any regulatory mechanism leads to imbalance.

FVD is the loss of extracellular fluid volume, usually reflecting isotonic loss of both water and electrolytes in similar proportions (e.g., losses of sodium and chloride). Common causes include vomiting, diarrhea, hemorrhage, excessive diuresis, third-spacing (fluid shifting to non-functional spaces like peritoneal cavity in peritonitis), and inadequate intake. In the Philippine context, acute gastroenteritis and dengue-related plasma leakage into tissue spaces are frequent triggers. Manifestations result from decreased circulating volume and compensatory mechanisms: rapid, weak, thready pulse; orthostatic hypotension (SBP drop >20 mmHg or DBP drop >10 mmHg on standing); flat neck veins; poor skin turgor; dry mucous membranes; decreased urine output (oliguria, <30 mL/hr); intense thirst; weight loss (0.5–1 kg daily); elevated hematocrit and blood urea nitrogen (hemoconcentration); and urine specific gravity >1.030. Mental status may range from alert to anxious to confused (if severe). The nursing diagnosis is Deficient Fluid Volume related to [cause] as evidenced by [manifestations].

FVE is the isotonic expansion of the extracellular fluid compartment, usually resulting from sodium and water retention together (excess occurs in both plasma and interstitial fluid). Causes include heart failure (decreased cardiac output triggers RAAS), renal failure (inability to excrete sodium and water), cirrhosis (decreased plasma osmotic pressure and RAAS activation), excessive sodium intake, and over-infusion of IV fluids (especially normal saline). Manifestations result from expanded circulating and interstitial volume: bounding, full pulse; distended (engorged) neck veins (>2 cm above sternal angle when supine); elevated blood pressure; presence of crackles or wheezes on lung auscultation; dyspnea (especially orthopnea); peripheral edema (pitting) and dependent edema (sacral edema if bedbound); weight gain (0.5–1 kg daily); and decreased hematocrit (hemodilution). Pulmonary edema is the most feared complication, presenting with pink frothy sputum, severe dyspnea, and altered mental status. The nursing diagnosis is Excess Fluid Volume related to [cause] as evidenced by [manifestations], often with additional diagnoses such as Activity Intolerance or Risk for Pulmonary Edema.

Sodium (normal 135–145 mEq/L) is the major extracellular cation and the chief determinant of serum osmolality and water distribution between compartments. Sodium disorders are fundamentally water problems, not sodium problems. **Hyponatremia (Na⁺ <135 mEq/L)** is caused by excessive water intake, SIADH (syndrome of inappropriate antidiuretic hormone), diuretics, vomiting, diarrhea, adrenal insufficiency, or chronic renal disease. Manifestations are largely neurologic from acute cellular swelling: headache, confusion, muscle cramps, nausea, lethargy, seizures (if severe and acute), and coma. Severity depends on rate of onset—acute hyponatremia (<48 hours) is more symptomatic than chronic. Management depends on volume status: in hypovolemic hyponatremia, give 0.9% NaCl to restore volume; in hypervolemic hyponatremia (e.g., heart failure), restrict fluids; in euvolemic hyponatremia (e.g., SIADH), restrict fluids. **Critical point: Correct hyponatremia slowly**—a rise of no more than 8–10 mEq/L in 24 hours is recommended. Rapid correction risks osmotic demyelination (central pontine myelinolysis), a devastating complication causing permanent neurologic damage. Hypertonic 3% saline is reserved for severe symptomatic hyponatremia (seizures, altered mental status) and must be given cautiously with frequent serum sodium checks. **Hypernatremia (Na⁺ >145 mEq/L)** is caused by water deprivation (elderly, unconscious patients), diabetes insipidus (central or nephrogenic), excess sodium intake (hypertonic feedings, saline infusions), or excessive water losses (diarrhea, fever). Manifestations reflect cellular dehydration: intense thirst, dry mucous membranes, restlessness, agitation, lethargy, and seizures in severe cases. Management involves providing water orally or via hypotonic IV fluids (0.45% NaCl or 0.33% NaCl) to correct slowly, avoiding rapid correction which risks cerebral edema (water rushes into cells). Both hypo- and hypernatremia require frequent serum sodium monitoring and patient education.

Potassium (normal 3.5–5.0 mEq/L) is the major intracellular cation and is critical to cardiac excitability and neuromuscular function. Both extremes are potentially fatal because of dysrhythmias. **Hypokalemia (K⁺ <3.5 mEq/L)** is caused by loop or thiazide diuretics (most common), vomiting, diarrhea, nasogastric suction, insulin administration, and alkalosis (hydrogen ions shift out of cells in exchange for potassium). Manifestations include muscle weakness (especially legs), leg cramps, fatigue, decreased bowel sounds or paralytic ileus, and cardiac dysrhythmias. ECG changes are characteristic: **flattened or inverted T waves, ST depression, and prominent U waves**—a U wave is a distinctive finding in hypokalemia. Severe hypokalemia can cause life-threatening dysrhythmias like atrial fibrillation. Management includes IV potassium replacement, but **CRITICAL safety point: Never administer potassium by IV push**—this can cause sudden hyperkalemia and fatal cardiac arrest. Potassium must be diluted in IV fluid and infused no faster than **10 mEq/hr** on a general unit (up to 20 mEq/hr only with continuous cardiac monitoring in an intensive care setting). Before administering any IV potassium, ensure adequate urine output (at least 30 mL/hr) to prevent potassium accumulation in renal failure. Oral potassium supplements (KCl liquid) are an alternative if GI function is intact. Encourage potassium-rich foods (bananas, oranges, potatoes, tomatoes, leafy greens). **Hyperkalemia (K⁺ >5.0 mEq/L)** is caused by renal failure (inability to excrete), potassium-sparing diuretics (spironolactone, amiloride), ACE inhibitors, tissue trauma (burns, crush injuries release intracellular K⁺), acidosis (hydrogen ions shift into cells; potassium shifts out), and Addison's disease (adrenal insufficiency leads to sodium loss and potassium retention). Manifestations include muscle weakness, paresthesias (tingling in fingers, toes, tongue), and cardiac dysrhythmias. ECG changes are ominous: **tall, peaked (tented) T waves**, widened QRS complex, and prolonged PR interval—these indicate serious myocardial irritability and risk of ventricular fibrillation and asystole. Management prioritizes **protecting the myocardium first** (not lowering potassium level, which takes longer). **IV calcium gluconate** (or calcium chloride) stabilizes the cardiac membrane by decreasing myocardial excitability—it acts within 1–3 minutes but does NOT lower the serum potassium level (this is a common NLE trap). To actually shift potassium into cells (temporary measure): give **regular insulin plus dextrose** (insulin drives glucose and potassium into cells), beta-2 agonists like albuterol (nebulized or IV), or **sodium bicarbonate** if the patient is acidotic (alkalosis shifts potassium into cells). To remove potassium from the body (permanent): administer sodium polystyrene sulfonate (Kayexalate/Sorbitex, an ion-exchange resin) orally or rectally, or arrange dialysis in renal failure. Monitor cardiac rhythm continuously and obtain serial potassium levels.

Calcium (normal total 8.5–10.5 mg/dL; ionized Ca⁺² 4.5–5.3 mg/dL) is critical for neuromuscular transmission, cardiac contractility, and bone metabolism. Note that serum calcium is affected by serum albumin—a low albumin falsely lowers total calcium (use the correction formula: add 0.8 mg/dL for every 1 g/dL drop in albumin below 4 g/dL). **Hypocalcemia (total Ca²⁺ <8.5 mg/dL)** is caused by hypoparathyroidism, thyroidectomy or parathyroidectomy (parathyroid gland removal), vitamin D deficiency (dietary, malabsorption, or renal disease causing impaired conversion to active form), acute pancreatitis (calcium is sequestered in fatty tissue), chronic renal failure (inability to activate vitamin D), and hyperphosphatemia (elevated phosphate binds calcium). Manifestations reflect neuromuscular hyperexcitability from decreased threshold for nerve firing: paresthesias (tingling around lips, fingers, toes), muscle cramps, tetany (involuntary muscle contractions), **positive Trousseau's sign** (carpal spasm when blood pressure cuff is inflated for 3 minutes—indicates latent tetany), **positive Chvostek's sign** (facial twitch when the facial nerve is tapped anterior to the ear), and laryngospasm (life-threatening airway closure). Seizures and cardiac dysrhythmias can occur. Priority nursing interventions include **monitoring airway for laryngospasm** (keep suction and intubation equipment available), instituting seizure precautions, keeping IV calcium gluconate at bedside for rapid administration, and monitoring cardiac rhythm. **Hypercalcemia (total Ca²⁺ >10.5 mg/dL)** is caused by hyperparathyroidism (most common in outpatient settings), malignancy (bone metastases release calcium; PTHrP hormone stimulates calcium release), prolonged immobilization (especially in young, healthy people—bed rest triggers bone resorption), thiazide diuretics (increase renal reabsorption of calcium), and thyrotoxicosis. Manifestations reflect decreased neuromuscular excitability (opposite of hypocalcemia): muscle weakness, **decreased or absent deep tendon reflexes**, constipation (decreased GI motility), polydipsia and polyuria (calcium causes nephrogenic diabetes insipidus), kidney stones (hypercalciuria), and altered mental status (lethargy, confusion, coma—'stones, bones, groans, and psychiatric overtones' is a teaching mnemonic). Management includes **IV isotonic fluids** (0.9% NaCl) and **loop diuretics** (furosemide) to promote urinary calcium excretion, calcitonin (rapid onset, brief duration) to inhibit bone resorption, bisphosphonates (slower onset, longer duration) to inhibit bone resorption, and mobilization (to promote calcium resorption and reduce bone resorption). Avoid thiazides and thiazide-like diuretics.

Magnesium (normal 1.5–2.5 mEq/L) is critical for neuromuscular function, cardiac excitability, enzyme function, and protein synthesis. Approximately 50–60% of magnesium is intracellular; 20–30% is protein-bound; only 10–15% is ionized (physiologically active). Serum magnesium levels may not reflect total body stores, making hypomagnesemia easy to miss. **Hypomagnesemia (Mg²⁺ <1.5 mEq/L)** is caused by alcoholism (poor nutritional intake and increased urinary losses), malnutrition, chronic diarrhea, diuretics, proton pump inhibitors (reduce absorption), and nasogastric suction. Manifestations are similar to hypocalcemia (neuromuscular hyperexcitability): tremor, tetany, weakness, positive Chvostek's and Trousseau's signs, and cardiac dysrhythmias (including torsades de pointes, a polymorphic ventricular dysrhythmia). **Important: Hypomagnesemia frequently accompanies and contributes to hypokalemia and hypocalcemia**—if a patient with hypokalemia does not respond to potassium replacement, check magnesium and calcium levels and correct hypomagnesemia first. Management includes IV magnesium sulfate (MgSO₄)—typical dose is 1–2 g IV over 5–60 minutes depending on acuity. Monitor deep tendon reflexes frequently; hyperreflexia indicates adequate magnesium; loss of reflexes indicates magnesium excess (toxicity) and dose should be reduced. Ensure adequate urine output before giving magnesium. Oral magnesium supplements are an alternative if GI function is intact. **Hypermagnesemia (Mg²⁺ >2.5 mEq/L)** usually occurs only in renal failure or from excessive exogenous magnesium intake (antacids containing magnesium hydroxide, mineral oil laxatives, magnesium-containing cathartics, or obstetric therapy with magnesium sulfate for preeclampsia). Manifestations reflect depressed neuromuscular transmission: hypotension, flaccid muscle weakness, **loss of deep tendon reflexes** (absent reflexes are a cardinal sign), respiratory depression (can progress to respiratory failure if severe), bradycardia, and altered mental status. This constellation—loss of reflexes, weakness, hypotension—is distinctive and easily recognized on the NLE. Management includes stopping all magnesium sources, giving IV **calcium gluconate** (the antidote for magnesium excess, similar to its role in hyperkalemia—it antagonizes magnesium effects on the myocardium), and dialysis in severe hypermagnesemia or renal failure.

Arterial blood gas analysis measures pH, PaCO₂ (partial pressure of carbon dioxide), HCO₃⁻ (bicarbonate), PaO₂ (partial pressure of oxygen), and SaO₂ (oxygen saturation). Normal ranges are: pH 7.35–7.45, PaCO₂ 35–45 mmHg, HCO₃⁻ 22–26 mEq/L, PaO₂ 80–100 mmHg (at sea level, decreases with altitude), SaO₂ 95–100%. The body maintains pH through the bicarbonate buffer system: H⁺ + HCO₃⁻ ⇌ H₂CO₃ ⇌ CO₂ + H₂O. The lungs control CO₂ elimination (respiratory component); the kidneys control HCO₃⁻ reabsorption and H⁺ excretion (metabolic component). **Stepwise ABG Interpretation Method:** (1) **Look at pH**—below 7.35 indicates acidosis, above 7.45 indicates alkalosis. (2) **Look at PaCO₂ (respiratory component)**—in respiratory disorders, CO₂ and pH move in opposite directions (remember **ROME**: Respiratory Opposite). A high CO₂ with low pH = respiratory acidosis (hypoventilation). A low CO₂ with high pH = respiratory alkalosis (hyperventilation). (3) **Look at HCO₃⁻ (metabolic component)**—in metabolic disorders, HCO₃⁻ and pH move in the same direction (Metabolic Equal). A low HCO₃⁻ with low pH = metabolic acidosis. A high HCO₃⁻ with high pH = metabolic alkalosis. (4) **Determine primary disorder and compensation**—the system that initiated the pH change is the primary problem; the opposite system responds to restore pH (compensation). Compensation never fully corrects pH (pH remains abnormal). **Four Primary Acid-Base Disorders:** **Respiratory Acidosis** (pH <7.35, PaCO₂ >45): hypoventilation from COPD (chronic obstructive pulmonary disease—most common cause), respiratory depression (drugs, anesthesia), oversedation, neuromuscular weakness, chest wall restriction, or pneumonia. Acute respiratory acidosis is life-threatening. Manifestations include headache, confusion, drowsiness, restlessness, and dysrhythmias. Priority nursing intervention: improve ventilation (oxygen, assist with breathing, treat underlying cause). **Respiratory Alkalosis** (pH >7.45, PaCO₂ <35): hyperventilation from anxiety, pain, fever, sepsis, pulmonary embolism, or early salicylate toxicity. Manifestations include lightheadedness, dizziness, paresthesias, tetany, and syncope (from cerebral vasoconstriction). Priority intervention: manage underlying cause, slow breathing (reassurance, rebreathing into paper bag only if anxiety). **Metabolic Acidosis** (pH <7.35, HCO₃⁻ <22): caused by increased acid production (diabetic ketoacidosis, lactic acidosis from shock, alcoholic ketoacidosis), loss of bicarbonate (diarrhea), or renal inability to excrete acid (chronic kidney disease). Manifestations include Kussmaul respirations (deep, rapid breathing—compensatory hyperventilation to blow off CO₂), headache, lethargy, and dysrhythmias. Priority intervention: treat underlying cause (insulin for DKA, fluids for shock, dialysis for renal failure). The anion gap (AG = Na⁺ − (Cl⁻ + HCO₃⁻); normal 8–16) helps classify metabolic acidosis: high AG (>16) = excess acids (DKA, lactic acidosis); normal AG (<16) = bicarbonate loss or renal acidosis. **Metabolic Alkalosis** (pH >7.45, HCO₃⁻ >26): caused by loss of acid (vomiting, nasogastric suction), gain of bicarbonate (excessive antacids), or hyperaldosteronism (sodium and water retention, potassium loss). Manifestations include hyperventilation (compensatory), weakness, and altered mental status. The key to management is identifying the volume status: **volume-responsive alkalosis** (from vomiting or NG suction—patient is typically hypovolemic) responds to **normal saline and potassium chloride replacement**; **volume-resistant alkalosis** (from hyperaldosteronism or diuretic abuse—patient is euvolemic or hypervolemic) requires spironolactone or other treatment of underlying cause. Hypokalemia worsens metabolic alkalosis and prevents correction until potassium is repleted. **Mixed Disorders:** Complex patients may have two or three simultaneous acid-base disorders. For example, a patient with COPD (chronic respiratory acidosis) who has an acute exacerbation with vomiting (adding metabolic alkalosis) requires careful interpretation.

IV fluids are classified by osmolality relative to plasma (normal serum osmolality ~295 mOsm/kg). Matching fluid tonicity to the clinical need prevents complications. **Isotonic solutions** (osmolality ~250–310 mOsm/kg) have osmolality similar to plasma and do not cause net water movement across cell membranes. Examples: **0.9% NaCl (normal saline)** — 154 mEq/L Na⁺, 154 mEq/L Cl⁻, commonly used for maintenance and restoration of intravascular volume; **Lactated Ringer's (LR)** — contains sodium, potassium, calcium, chloride, and lactate (which is metabolized to bicarbonate), more physiologic than saline because lactate buffers acidosis and it contains potassium; **5% dextrose in water (D5W)** — isotonic in the bag (25 g dextrose in 500 mL = 5% dextrose + water) but becomes hypotonic once the dextrose is metabolized (cells consume dextrose, leaving free water). Isotonic fluids expand the intravascular volume (and interstitial fluid to a lesser extent) without shifting fluid across cell membranes, making them ideal for **hypovolemia, hemorrhage, and shock**. Use isotonic fluids for acute fluid losses and to maintain circulating volume. Caution: 0.9% NaCl contains higher chloride (154 mEq/L) than plasma (96–106 mEq/L), potentially causing hyperchloremic acidosis with large volumes; LR is preferred in many settings. **Hypotonic solutions** (osmolality <250 mOsm/kg) have lower osmolality than plasma and cause **water to move into cells** (hypotonic relative to ECF, so water leaves ECF and enters ICF). Examples: **0.45% NaCl (half-normal saline)** — 77 mEq/L Na⁺, 77 mEq/L Cl⁻; **0.33% NaCl (one-third normal saline)**; **5% dextrose in 0.45% NaCl (D5W in 0.45%)** or **5% dextrose in 0.9% saline (D5W in 0.9%)** — when the dextrose is metabolized, these become hypotonic. Hypotonic fluids are used for **cellular dehydration (when cells are shrunken from hypernatremia or hyperglycemia) and to provide free water without excessive sodium**. They are ideal for **hypernatremia correction** (water enters cells to rehydrate them). **Caution—major contraindications**: (1) Do NOT use hypotonic fluids in **increased intracranial pressure (ICP)**—if cells in the brain swell from hypotonic fluid, cerebral edema worsens and ICP rises, potentially causing herniation; (2) Do NOT use in **hypovolemic shock**—hypotonic fluids worsen hypotension because water leaves the vasculature, decreasing circulating volume. **Hypertonic solutions** (osmolality >310 mOsm/kg) have higher osmolality than plasma and cause **water to move out of cells** (cells shrink). Examples: **3% NaCl (hypertonic saline)** — 513 mEq/L Na⁺, used only for **severe symptomatic hyponatremia** (seizures, altered mental status) or **cerebral edema**; **10% dextrose (D10W)** — high dextrose concentration; **5% dextrose in 0.9% NaCl (D5 in 0.9% NaCl)** or **5% dextrose in lactated Ringer's (D5LR)**. Hypertonic fluids pull water out of cells and into the ECF, expanding the intravascular volume and reducing intracellular fluid volume. They are used for **severe symptomatic hyponatremia** (to raise sodium and shrink swollen brain cells) and **cerebral edema** (to reduce intracranial pressure). **Caution**: (1) Hypertonic fluids can cause **fluid overload and pulmonary edema**—give slowly and monitor closely; (2) **3% NaCl must be given through a central line** (peripheral line can cause phlebitis); (3) Monitor serum sodium closely (goal is to raise no more than 8–10 mEq/L in 24 hours to avoid osmotic demyelination); (4) Extravasation of hypertonic fluid into tissue causes necrosis. **Clinical Selection Summary:** (1) **Hypovolemia, hemorrhage, shock** → Isotonic (0.9% NaCl, LR, D5W once dextrose metabolized); (2) **Hypernatremia, cellular dehydration** → Hypotonic (0.45% NaCl, 0.33% NaCl); (3) **Severe hyponatremia with symptoms, cerebral edema, increased ICP** → Hypertonic (3% saline); (4) **Maintenance fluids** (no active losses) → Hypotonic + dextrose (e.g., D5W with 0.45% NaCl).

The nursing process provides a systematic framework for managing complex fluid, electrolyte, and acid-base disorders in accordance with RA 9173 (Philippine Nursing Act of 2002) standards of practice. **Assessment (Data Collection):** Gather subjective data (patient history of vomiting, diarrhea, thirst, weakness, dyspnea) and objective data (vital signs, physical examination for edema/dehydration signs, weight changes, intake and output, laboratory values—electrolytes, ABG, osmolality, BUN, creatinine, hematocrit). Assess level of consciousness, neuromuscular status (reflexes, Chvostek's, Trousseau's), breath sounds (crackles = pulmonary edema), neck vein distention, skin turgor and mucous membranes, and urine color/characteristics. Calculate estimated deficit or excess based on weight changes and clinical presentation. **Nursing Diagnoses (per NANDA):** Common diagnoses include: Deficient Fluid Volume related to [cause] as evidenced by [manifestations]; Excess Fluid Volume related to [cause] as evidenced by [manifestations]; Imbalanced Nutrition: Less Than Body Requirements (if severe deficits); Decreased Cardiac Output (if dysrhythmias); Risk for Electrolyte Imbalance; Acute Confusion (if altered mental status); Risk for Falls (if orthostatic hypotension); Risk for Seizures (if hypocalcemia, hyponatremia). **Planning (Goals and Outcomes):** Establish SMART goals: maintain vital signs within normal range, restore serum electrolytes to normal, achieve I&O balance, patient will verbalize understanding of fluid/sodium restrictions, prevent complications (shock, dysrhythmias, seizures, pulmonary edema). **Interventions (Implementation):** (1) **Restore or Maintain Circulation** (priority per Maslow)—establish IV access, administer fluids at prescribed rate, monitor vital signs q15min initially then q4h as stable, assess for signs of shock or fluid overload. (2) **Monitor I&O Meticulously**—record all intake (oral, IV, medications, tube feeding) and output (urine, emesis, diarrhea, drainage, insensible losses via respiration/perspiration; estimate insensible at 30–50 mL/kg/day depending on fever, humidity). Weigh daily at the same time (before breakfast, after voiding), noting that 1 kg gain/loss ≈ 1 L fluid. (3) **Administer Medications as Ordered**—IV fluids (isotonic, hypotonic, or hypertonic per diagnosis), diuretics (monitor electrolytes, especially potassium), potassium supplements (never IV push; dilute and give over 10+ minutes), calcium, magnesium, bicarbonate, or insulin per ABG/electrolyte results. (4) **Position and Breathing Support**—high-Fowler's for dyspnea/pulmonary edema; assist with coughing, deep breathing, or oxygen to prevent respiratory complications. (5) **Restrict or Encourage Fluids/Sodium**—per physician order; educate patient on restrictions. (6) **Monitor Cardiac Status**—continuous cardiac monitor if potassium or calcium disorder; listen for dysrhythmias; obtain ECGs as ordered. (7) **Institute Safety Precautions**—fall precautions (orthostatic hypotension, weakness), seizure precautions (hypocalcemia, severe hyponatremia, high fevers). (8) **Frequent Reassessment**—repeat vital signs, physical examination, I&O, weight; obtain lab values (electrolytes, ABG, osmolality) per protocol; assess for improvement or worsening. **Evaluation (Outcomes):** Did fluid volume status improve (vitals stable, I&O balanced, weight stable, no edema or dehydration signs)? Are electrolytes normalized? Is ABG normalized? Are complications prevented? Does patient understand discharge teaching (fluid/sodium restrictions, medications, signs to report)? Document response to interventions and adjust plan as needed. **Documentation:** Follow Philippine medical record standards; document all I&O, weights, vital signs, assessment findings, electrolyte/ABG values, medications given, patient response, and teaching provided.

Sodium is the major ECF cation and chief determinant of serum osmolality. Water follows osmotic gradients created by sodium (and albumin), moving from areas of low sodium concentration to areas of high sodium concentration. Hyponatremia (low Na⁺) draws water INTO cells (cells swell, neurologic symptoms); hypernatremia (high Na⁺) pulls water OUT of cells (cells shrink, thirst, altered mental status). This relationship is fundamental—'hyponatremia is a water problem' because low sodium creates an osmotic gradient that traps water intracellularly.

Potassium and hydrogen ions shift between intracellular and extracellular compartments based on pH. Acidosis (low pH, excess H⁺) causes H⁺ to shift into cells; K⁺ shifts out in exchange (secondary hyperkalemia). Alkalosis (high pH, deficit H⁺) causes H⁺ to shift out of cells; K⁺ shifts in (secondary hypokalemia). This relationship means acid-base disorders predictably cause secondary electrolyte shifts—e.g., DKA (metabolic acidosis) causes hyperkalemia; nasogastric suction (metabolic alkalosis) causes hypokalemia.

Both calcium and magnesium regulate neuromuscular transmission. Hypocalcemia and hypomagnesemia both increase neuromuscular excitability (tetany, Chvostek's, Trousseau's, seizures). Hypercalcemia and hypermagnesemia both decrease neuromuscular excitability (weakness, hyporeflexia). Hypokalemia also causes muscle weakness but through a different mechanism (decreased resting membrane potential). Additionally, hypomagnesemia prevents correction of hypokalemia and hypocalcemia—all three deficiencies often coexist in chronic diuretic use.

The heart's electrical conduction system is exquisitely sensitive to electrolyte imbalances. ECG changes reflect these disturbances: Hypokalemia → flattened T waves, prominent U waves, ST depression. Hyperkalemia → tall peaked T waves, widened QRS, prolonged PR (progressive toxicity). Hypocalcemia → prolonged QT interval. Hypermagnesemia → prolonged PR and QT intervals (similar to hypocalcemia). Hypomagnesemia → shortened QT interval. These ECG findings are not random; they reflect the electrolyte's effect on myocardial repolarization and conduction velocity.

The respiratory system rapidly controls CO₂ (and thus pH) through changes in minute ventilation. Hypoventilation (decreased respiratory rate or depth) retains CO₂, causing respiratory acidosis. Hyperventilation (increased respiratory rate or depth) blows off CO₂, causing respiratory alkalosis. The kidneys slowly control HCO₃⁻ (metabolic pH) over hours to days through reabsorption and excretion. In primary respiratory disorders, the kidneys compensate by adjusting HCO₃⁻. In primary metabolic disorders, the lungs compensate by adjusting ventilation (manifest as Kussmaul respirations in metabolic acidosis or slow shallow breathing in metabolic alkalosis).

Osmolality determines the direction of water movement between compartments. Isotonic fluids (osmolality ~295 mOsm/kg) do not cause net water shifts; they expand the ECF proportionally (plasma and interstitial). Hypotonic fluids (osmolality <250 mOsm/kg) are hypotonic to plasma; water moves INTO cells (ICF expands, cells swell). Hypertonic fluids (osmolality >310 mOsm/kg) are hypertonic to plasma; water moves OUT of cells (ICF shrinks, ECF expands). This osmotic principle determines the clinical effects and appropriate uses of each fluid type.

Aldosterone, released by the adrenal cortex in response to RAAS activation or elevated K⁺, acts on the distal tubule to increase sodium reabsorption and potassium excretion (in exchange for sodium). This creates an inverse relationship: when sodium is retained, potassium is excreted (and vice versa). Conditions causing aldosterone excess (primary hyperaldosteronism, secondary to volume depletion or renal disease) result in hypernatremia, hypokalemia, and metabolic alkalosis (from potassium loss and H⁺ excretion). Conditions causing aldosterone deficiency (Addison's disease) result in hyponatremia, hyperkalemia, and metabolic acidosis.

These three factors maintain water balance in an integrated feedback system. Rising osmolality (>295 mOsm/kg) triggers thirst (prompting water intake) and ADH release (promoting water reabsorption in kidneys). Both actions lower osmolality back toward normal. Falling osmolality (<280 mOsm/kg) suppresses thirst and ADH release, allowing urinary water loss (dilute urine) that raises osmolality back to normal. Disruption of any component causes imbalance—e.g., SIADH overrides the normal feedback and causes excessive ADH release despite low osmolality, resulting in hyponatremia and water retention.