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Cheat SheetNLE · Foundations of Medical-Surgical Nursing

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

Everything worth memorising from Fluid, Electrolyte and Acid-Base Imbalances, condensed for NLE reviewers.

Fluid, Electrolyte and Acid-Base Imbalances - Cheat Sheet

Your last-minute revision companion for the most heavily tested chapter in Nursing Practice III. Master body fluid compartments, electrolyte values, ABG interpretation, and priority nursing actions—all in one rapid-fire reference.

Body Fluid Compartments & Water Distribution

Formulas

Total Body Water = 60% of adult body weight

Meaning

TBW—absolute prerequisite; intracellular fluid (ICF) = 2/3 of TBW (~40% body weight); extracellular fluid (ECF) = 1/3 of TBW (~20% body weight)

Watch out

Do NOT confuse ICF and ECF proportions—ICF is always the LARGER compartment (2/3); ECF includes both intravascular (plasma) and interstitial fluid

When to use

Calculating expected fluid shifts and understanding compartment osmolality

1 kg weight change ≈ 1 L fluid change

Meaning

Daily weight gain/loss correlates directly to fluid retention/loss (most reliable bedside assessment)

Watch out

Weight changes >1–2 kg/day are FLUID related, NOT fat; be suspicious of acute weight changes in critically ill patients

When to use

Monitoring fluid status in FVD and FVE patients; weigh daily at same time, same scale, same clothing

Common values

Value

60% of body weight

Symbol

TBW

Quantity

Total body water (adult)

Value

40% body weight (2/3 of TBW)

Symbol

ICF

Quantity

Intracellular fluid

Value

20% body weight (1/3 of TBW)

Symbol

ECF

Quantity

Extracellular fluid

Value

280–300 mOsm/kg

Symbol

Osm

Quantity

Serum osmolality

Important facts

  • Kidneys are the PRIMARY regulator of both fluid AND electrolyte homeostasis
  • Thirst is the FINAL defense mechanism for hypernatremia (affected by age, medications, neurologic injury)
  • ADH (antidiuretic hormone) increases water reabsorption in collecting ducts; SIADH causes inappropriate ADH release → hyponatremia
  • RAAS (renin-angiotensin-aldosterone system) increases sodium reabsorption and vasoconstriction in response to low blood pressure
  • ANP (atrial natriuretic peptide) causes sodium and water LOSS in response to volume overload
  • Osmolality: normal serum osmolality 280–300 mOsm/kg; determines water distribution between ICF and ECF

Key definitions

Osmosis

Example

In hypernatremia, water shifts OUT of cells into ECF, causing cellular dehydration and thirst

Water movement across semipermeable membranes following osmotic gradient (follows solutes, primarily sodium and albumin)

Tonicity

Example

Isotonic 0.9% NaCl stays in ECF; hypotonic 0.45% NaCl moves into cells; hypertonic 3% NaCl pulls water out of cells

Effective osmolality of a solution relative to plasma (determines water movement into or out of cells)

Intracellular Fluid (ICF)

Example

Accounts for 2/3 of total body water; potassium concentration ~140 mEq/L inside cells

Fluid INSIDE cells; comprises ~40% body weight; major cation is K⁺; regulated by Na-K-ATPase pump

Extracellular Fluid (ECF)

Example

Sodium concentration ~140 mEq/L; controls osmolality and blood pressure

Fluid OUTSIDE cells; comprises ~20% body weight; major cation is Na⁺; split into intravascular (plasma) and interstitial

Diagrams to know

  • Body fluid compartments (ICF vs ECF split; ECF subcompartments)
  • Mechanisms of fluid regulation: ADH, RAAS, ANP (cause-effect chain)

Fluid Volume Deficit (FVD/Hypovolemia)

Common values

Value

≥30 mL/hr (or 800–2000 mL/day)

Symbol

UOP

Quantity

Normal urine output

Value

<30 mL/hr or <400–500 mL/day

Symbol

—

Quantity

Oliguria threshold

Value

1.010–1.030

Symbol

USG

Quantity

Urine specific gravity (normal)

Important facts

  • CARDINAL SIGN: Orthostatic hypotension (BP drop >20 mmHg systolic when standing)
  • Weak, rapid (thready) pulse; flat neck veins; poor skin turgor; dry mucous membranes
  • Decreased urine output (oliguria <30 mL/hr); increased urine specific gravity >1.030 (concentration)
  • Hemoconcentration: rising hematocrit, rising BUN (both indicate fluid loss >electrolyte loss)
  • Patient complains of THIRST and WEAKNESS
  • Weight loss is the most RELIABLE indicator (1 kg = ~1 L fluid loss)
  • Priority nursing action: RESTORE CIRCULATING VOLUME and PREVENT HYPOVOLEMIC SHOCK

Key definitions

Fluid Volume Deficit (FVD)

Example

Vomiting, diarrhea, hemorrhage, excessive diuresis, third-spacing (burns, peritonitis), inadequate intake; acute gastroenteritis and dengue plasma leakage are common in Philippine context

Loss of ECF volume; usually ISOTONIC loss (proportional loss of water and electrolytes); hypovolemic shock is the feared complication

Diagrams to know

  • Cascade of FVD → compensatory tachycardia → orthostatic hypotension → shock
  • Signs/symptoms organized by severity (mild to severe)

Fluid Volume Excess (FVE/Hypervolemia)

Common values

Value

1+ = barely visible indent; 2+ = indent <2 sec; 3+ = indent 2–5 sec; 4+ = indent >5 sec, severe

Symbol

—

Quantity

Pitting edema scale

Important facts

  • CARDINAL SIGNS: Bounding pulse, distended neck veins (JVD), elevated blood pressure
  • Pulmonary crackles, dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND)
  • Peripheral and dependent edema (pitting, 1+ to 4+); weight GAIN (most reliable sign)
  • Hemodilution: DECREASED hematocrit, decreased BUN
  • PRIORITY: Semi- to high-Fowler's position if respiratory distress present; restrict sodium and fluids
  • Diuretics given (furosemide)—BUT watch for HYPOKALEMIA as side effect (leading to fatal dysrhythmias)
  • Monitor for worsening pulmonary edema; auscultate breath sounds frequently

Key definitions

Fluid Volume Excess (FVE)

Example

Heart failure, renal failure, cirrhosis, excessive sodium intake, over-infusion of IV fluids (including excessive hypotonic fluids)

Isotonic expansion of ECF from sodium and water RETENTION; pulmonary edema is the life-threatening complication

Diagrams to know

  • FVE progression: sodium/water retention → ECF expansion → edema and pulmonary congestion
  • Signs/symptoms organized by system (cardiac, respiratory, renal, skin)

Sodium Imbalances (Na⁺ = 135–145 mEq/L)

Common values

Value

135–145 mEq/L

Symbol

Na⁺

Quantity

Normal serum sodium

Value

<135 mEq/L (mild <130, moderate 120–130, severe <120)

Symbol

Na⁺

Quantity

Hyponatremia

Value

>145 mEq/L (mild >145, moderate >155, severe >175)

Symbol

Na⁺

Quantity

Hypernatremia

Important facts

  • Hyponatremia: Headache, confusion, muscle cramps, nausea, restlessness → seizures, coma in severe cases
  • Hypernatremia: Thirst (if thirst mechanism intact), dry mucous membranes, restlessness, agitation, confusion → altered mental status
  • CRITICAL: Correct sodium disorders SLOWLY to avoid osmotic demyelination (central pontine myelinolysis) in hyponatremia or cerebral edema in hypernatremia
  • Hyponatremia management: If hypovolemic → 0.9% NaCl (isotonic); if from water excess → FLUID RESTRICTION
  • Hypernatremia management: Provide WATER orally or 0.45% NaCl (hypotonic) IV to correct slowly
  • 3% saline reserved ONLY for severe SYMPTOMATIC hyponatremia (seizures, altered LOC); given with extreme caution and frequent Na⁺ checks
  • Sodium determines serum osmolality; hyponatremia = hypo-osmolar (water moves into cells); hypernatremia = hyperosmolar (water leaves cells)

Key definitions

Hyponatremia (Na⁺ <135 mEq/L)

Example

SIADH, excessive water intake, diuretics, vomiting, diarrhea, adrenal insufficiency; symptoms from brain cell swelling

LOW serum sodium; fundamentally a WATER problem (excess water relative to sodium), NOT a sodium loss problem; causes cellular SWELLING (cerebral edema)

Hypernatremia (Na⁺ >145 mEq/L)

Example

Water deprivation, diabetes insipidus, excess sodium intake, hypertonic feedings without water; symptoms from brain cell dehydration

HIGH serum sodium; fundamentally a WATER DEFICIT problem; causes cellular SHRINKAGE (cellular dehydration)

Diagrams to know

  • Hyponatremia vs hypernatremia: causes, pathophysiology, and management algorithms

Potassium Imbalances (K⁺ = 3.5–5.0 mEq/L) — LIFE-THREATENING

Common values

Value

3.5–5.0 mEq/L (some sources 3.5–5.5)

Symbol

K⁺

Quantity

Normal serum potassium

Value

<3.5 mEq/L

Symbol

K⁺

Quantity

Hypokalemia

Value

>5.0 mEq/L (>6.5 is severe/symptomatic)

Symbol

K⁺

Quantity

Hyperkalemia

Value

10 mEq/hr

Symbol

—

Quantity

Max IV KCl infusion rate (general unit)

Important facts

  • Hypokalemia signs: Muscle weakness, leg cramps, fatigue, decreased bowel sounds/paralytic ileus, CARDIAC DYSRHYTHMIAS (flattened T waves, ST depression, PROMINENT U WAVES)
  • Hyperkalemia signs: Muscle weakness, paresthesias, palpitations, CARDIAC DYSRHYTHMIAS (TALL PEAKED T WAVES, widened QRS, progressing to VF/asystole)
  • PRIORITY NURSING ACTION: CARDIAC MONITORING for BOTH (dysrhythmias are the life threat)
  • NEVER give potassium by IV PUSH—FATAL CARDIAC ARREST
  • Dilute IV KCl and infuse at MAX 10 mEq/hr on general unit (20 mEq/hr only with continuous cardiac monitoring in ICU)
  • MUST confirm urine output ≥30 mL/hr BEFORE giving potassium (ensure renal function)
  • Hypokalemia management: IV KCl (diluted, slow infusion) + encourage K-rich foods (bananas, oranges, potatoes, tomatoes)
  • Hyperkalemia management: (1) PROTECT MYOCARDIUM with IV calcium gluconate (does NOT lower K⁺, just stabilizes membrane); (2) SHIFT K⁺ INTO CELLS with insulin+glucose, beta-agonists, or sodium bicarbonate (if acidotic); (3) REMOVE K⁺ from body with sodium polystyrene sulfonate (Kayexalate) or dialysis

Key definitions

Hypokalemia (K⁺ <3.5 mEq/L)

Example

Furosemide overuse, vomiting from gastroenteritis, or diabetic patient on insulin without adequate potassium intake

LOW serum potassium; caused by GI losses (vomiting, diarrhea, NG suction), diuretics (loop, thiazide), alkalosis, insulinemia; DANGEROUS because of cardiac effects

Hyperkalemia (K⁺ >5.0 mEq/L)

Example

Patient with AKI, ACE inhibitor + spironolactone combination, or crush injury releasing intracellular K⁺

HIGH serum potassium; caused by renal failure, K-sparing diuretics, tissue trauma, acidosis, Addison's disease; FATAL DYSRHYTHMIAS can occur

Diagrams to know

  • Hypokalemia ECG changes vs hyperkalemia ECG changes
  • Hyperkalemia management algorithm: stabilize → shift → remove

Calcium Imbalances (Total Ca²⁺ = 8.5–10.5 mg/dL)

Common values

Value

8.5–10.5 mg/dL (ionized Ca²⁺ 4.5–5.3 mg/dL)

Symbol

Ca²⁺

Quantity

Normal total serum calcium

Value

<8.5 mg/dL

Symbol

Ca²⁺

Quantity

Hypocalcemia

Value

>10.5 mg/dL

Symbol

Ca²⁺

Quantity

Hypercalcemia

Important facts

  • Hypocalcemia: POSITIVE CHVOSTEK'S SIGN (tap facial nerve → facial twitch); POSITIVE TROUSSEAU'S SIGN (inflate BP cuff on arm → carpal spasm)
  • Hypocalcemia: Risk of LARYNGOSPASM (airway emergency); SEIZURES possible
  • PRIORITY for hypocalcemia: Monitor AIRWAY; institute SEIZURE PRECAUTIONS; keep IV calcium gluconate readily available
  • Hypercalcemia: Muscle weakness, DECREASED deep tendon reflexes (opposite of hypocalcemia), constipation (dehydration), kidney stones, confusion/lethargy
  • Hypercalcemia management: IV isotonic fluids + loop diuretics (promote excretion), calcitonin, bisphosphonates; encourage mobilization
  • Parathyroid hormone (PTH) increases serum calcium; vitamin D increases calcium absorption
  • Phosphate inversely related to calcium (high phosphate pulls down calcium)

Key definitions

Hypocalcemia (Ca²⁺ <8.5 mg/dL)

Example

Thyroid surgery complication (parathyroid gland damage) presenting with positive Chvostek's sign and seizure risk

LOW serum calcium; causes neuromuscular irritability (tetany, paresthesias, laryngospasm); caused by hypoparathyroidism, thyroidectomy, vitamin D deficiency, pancreatitis, renal failure

Hypercalcemia (Ca²⁺ >10.5 mg/dL)

Example

Metastatic cancer with bone involvement or hyperparathyroidism causing fatigue and constipation

HIGH serum calcium; causes muscle weakness, kidney stones, altered mental status; caused by hyperparathyroidism, malignancy, prolonged immobilization, thiazides

Diagrams to know

  • Regulation of serum calcium: PTH and vitamin D mechanisms
  • Hypocalcemia vs hypercalcemia: clinical signs organized by system (neuro, GI, cardiac, musculoskeletal)

Magnesium Imbalances (Mg²⁺ = 1.5–2.5 mEq/L)

Common values

Value

1.5–2.5 mEq/L

Symbol

Mg²⁺

Quantity

Normal serum magnesium

Value

<1.5 mEq/L

Symbol

Mg²⁺

Quantity

Hypomagnesemia

Value

>2.5 mEq/L

Symbol

Mg²⁺

Quantity

Hypermagnesemia

Important facts

  • Hypomagnesemia: Tremor, tetany, POSITIVE CHVOSTEK'S and TROUSSEAU'S signs (same as hypocalcemia), dysrhythmias (torsades de pointes), muscle weakness
  • Hypomagnesemia: Often part of TRIAD with hypocalcemia and hypokalemia; MUST correct magnesium to fix calcium and potassium
  • Hypomagnesemia management: IV magnesium sulfate; monitor deep tendon reflexes (become hyperactive)
  • Hypermagnesemia: LOSS OF DEEP TENDON REFLEXES (KEY SIGN), hypotension, respiratory depression, bradycardia, flushing, confusion
  • Hypermagnesemia: IV calcium gluconate is the ANTIDOTE (counteracts Mg effects on neuromuscular junction); dialysis if severe/renal failure
  • Magnesium is cofactor for Na-K-ATPase pump; essential for muscle contraction and nerve transmission

Key definitions

Hypomagnesemia (Mg²⁺ <1.5 mEq/L)

Example

Chronic alcoholic with tremor and tetany, or post-NG suction patient

LOW serum magnesium; causes neuromuscular irritability SIMILAR to hypocalcemia; caused by alcoholism, malnutrition, GI losses; often ACCOMPANIES hypokalemia and hypocalcemia

Hypermagnesemia (Mg²⁺ >2.5 mEq/L)

Example

Pregnant patient on MgSO₄ for preeclampsia developing hypotension and loss of reflexes

HIGH serum magnesium; causes CNS and neuromuscular DEPRESSION (flaccidity); caused by renal failure, excessive Mg intake (antacids, laxatives, obstetric MgSO₄)

Diagrams to know

  • Hypomagnesemia vs hypermagnesemia: clinical effects on neuromuscular system

Acid-Base Balance & ABG Interpretation (pH 7.35–7.45, PaCO₂ 35–45, HCO₃⁻ 22–26)

Formulas

ROME: Respiratory Opposite, Metabolic Equal

Meaning

In respiratory disorders, pH and PaCO₂ move in OPPOSITE directions; in metabolic disorders, pH and HCO₃⁻ move in the SAME direction

Watch out

Do NOT confuse direction of change—use ROME every time to avoid errors; pH is the starting point

When to use

Quick ABG interpretation—determine whether the acid-base disorder is respiratory or metabolic

5-Step ABG Method: (1) Look at pH; (2) Look at PaCO₂; (3) Look at HCO₃⁻; (4) Determine primary disorder; (5) Assess compensation

Meaning

Systematic approach prevents missed diagnoses; compensation is the OPPOSITE system trying to normalize pH

Watch out

Do NOT skip steps; do NOT assume compensation without checking if it's adequate for the primary disorder

When to use

Interpreting every ABG—become automatic with this sequence

Common values

Value

7.35–7.45 (acidemia <7.35, alkalemia >7.45)

Symbol

—

Quantity

pH

Value

35–45 mmHg (respiratory component)

Symbol

—

Quantity

PaCO₂ (partial pressure CO₂)

Value

22–26 mEq/L (metabolic component)

Symbol

—

Quantity

HCO₃⁻ (serum bicarbonate)

Value

80–100 mmHg (oxygenation; <60 is hypoxemia)

Symbol

—

Quantity

PaO₂ (partial pressure O₂)

Value

95–100% (on room air)

Symbol

—

Quantity

SaO₂ (oxygen saturation)

Important facts

  • Normal ABG: pH 7.35–7.45, PaCO₂ 35–45 mmHg, HCO₃⁻ 22–26 mEq/L, PaO₂ 80–100 mmHg, SaO₂ 95–100%
  • Acidosis: pH <7.35; alkalosis: pH >7.45
  • Respiratory component: controlled by LUNGS (hyperventilation ↓ CO₂, hypoventilation ↑ CO₂)
  • Metabolic component: controlled by KIDNEYS (reabsorb HCO₃⁻, excrete H⁺)
  • Compensation is PARTIAL—pH rarely normalizes completely with compensation alone
  • Two PRIMARY disorders can coexist (e.g., respiratory acidosis + metabolic acidosis in a septic patient)
  • Oxygenation (PaO₂, SaO₂) is SEPARATE from acid-base status; check both independently
  • Kussmaul respirations (deep, rapid, fruity-breath) = metabolic acidosis compensation
  • Cheyne-Stokes or slow, shallow breathing = respiratory alkalosis (hypoventilation) compensation

Key definitions

Respiratory Acidosis (pH ↓, PaCO₂ ↑)

Example

COPD exacerbation, sedative overdose, respiratory depression, chest wall paralysis; priority is IMPROVE VENTILATION

Hypoventilation causing CO₂ retention; carbonic acid accumulates; PaCO₂ >45 mmHg

Respiratory Alkalosis (pH ↑, PaCO₂ ↓)

Example

Anxiety, pain, fever, early salicylate toxicity, hypoxemia; priority is address underlying cause and SLOW BREATHING

Hyperventilation blowing off CO₂; PaCO₂ <35 mmHg

Metabolic Acidosis (pH ↓, HCO₃⁻ ↓)

Example

Diabetic ketoacidosis, lactic acidosis (shock), renal failure, diarrhea (loss of HCO₃⁻); KUSSMAUL RESPIRATIONS (deep, rapid) are compensatory

Loss of bicarbonate or accumulation of acid; HCO₃⁻ <22 mEq/L

Metabolic Alkalosis (pH ↑, HCO₃⁻ ↑)

Example

Vomiting (H⁺ loss), prolonged NG suction, excessive antacid/diuretic use; compensatory hypoventilation (slow, shallow breathing)

Gain of bicarbonate or loss of acid; HCO₃⁻ >26 mEq/L

Diagrams to know

  • Acid-base nomogram or 4-quadrant ABG interpretation map
  • Kussmaul vs Cheyne-Stokes respiratory patterns
  • Respiratory vs metabolic disorders: causes, ABG patterns, compensation

Reactions or equations

Respiratory acidosis: ↓pH, ↑PaCO₂ (abnormal >45); compensation: ↑HCO₃⁻

Note

Priority: improve ventilation (oxygen, intubation); kidneys compensate by retaining HCO₃⁻

Conditions

Hypoventilation (COPD, sedation, paralysis, respiratory muscle weakness)

Respiratory alkalosis: ↑pH, ↓PaCO₂ (abnormal <35); compensation: ↓HCO₃⁻

Note

Priority: identify and treat underlying cause; slow breathing rate; rebreather bag may help if anxiety

Conditions

Hyperventilation (anxiety, pain, fever, hypoxemia, early sepsis, salicylate toxicity)

Metabolic acidosis: ↓pH, ↓HCO₃⁻ (abnormal <22); compensation: ↓PaCO₂ (Kussmaul)

Note

Priority: treat underlying cause (insulin for DKA, fluid/perfusion for lactic acidosis); may need IV sodium bicarbonate

Conditions

DKA, lactic acidosis, renal failure, diarrhea (HCO₃⁻ loss), toxic ingestion (aspirin)

Metabolic alkalosis: ↑pH, ↑HCO₃⁻ (abnormal >26); compensation: ↑PaCO₂ (hypoventilation)

Note

Priority: stop GI losses, restore K⁺ (hypokalemia perpetuates alkalosis), IV normal saline; hypoventilation compensation can worsen oxygenation

Conditions

Vomiting (H⁺ loss), NG suction, loop diuretics (K⁺ loss drives alkalosis), excessive antacids

IV Fluid Tonicity & Fluid Replacement

Common values

Value

280–300 mOsm/kg

Symbol

—

Quantity

Normal plasma osmolality

Value

~300 mOsm/kg (isotonic)

Symbol

NS

Quantity

0.9% NaCl (normal saline) osmolality

Value

~150 mOsm/kg (hypotonic)

Symbol

—

Quantity

0.45% NaCl osmolality

Value

~900 mOsm/kg (hypertonic)

Symbol

—

Quantity

3% NaCl osmolality

Important facts

  • Isotonic fluids are FIRST-LINE for most IV replacement because safe and predictable
  • D5W in the BAG is isotonic (because glucose is metabolized), but becomes HYPOTONIC in the body—often called 'free water'
  • Hypotonic fluids move water INTO cells—useful for hypernatremia (high sodium dilutes) but DANGEROUS if brain swelling (increases cerebral edema)
  • Hypertonic fluids pull water OUT of cells—use cautiously; can cause vein irritation, fluid overload, pulmonary edema
  • 3% saline is RESERVED for symptomatic hyponatremia (seizures, altered consciousness) and given SLOWLY with frequent Na⁺ checks
  • Lactated Ringer's is preferred over 0.9% NaCl in trauma/burns because composition closer to ECF (contains K⁺, Ca²⁺, HCO₃⁻)
  • Normal saline (0.9% NaCl) is isotonic but contains NO potassium—prolonged infusion can cause hyperchloremic acidosis
  • Choose fluid tonicity based on patient's sodium level, osmolality, and clinical condition (FVD, FVE, hypernatremia, hyponatremia)

Key definitions

Isotonic Solutions (Osmolality ~300 mOsm/kg, same as plasma)

Example

0.9% NaCl (normal saline), lactated Ringer's, D5W in bag (becomes hypotonic after dextrose metabolized); use in FVD, hemorrhage, shock

Do NOT cause water shift between compartments; expand intravascular volume (ECF) without changing ICF; safe for most situations

Hypotonic Solutions (Osmolality <300 mOsm/kg, lower than plasma)

Example

0.45% NaCl, 0.33% NaCl, D5W after dextrose metabolized; use in hypernatremia, cellular dehydration; AVOID in increased ICP (cerebral edema risk), hypovolemia (worsens shock)

Water moves INTO cells (ICF swelling); dilute ECF; useful for cellular dehydration BUT DANGEROUS in certain conditions

Hypertonic Solutions (Osmolality >300 mOsm/kg, higher than plasma)

Example

3% NaCl, 5% NaCl, D10W, D5 in 0.9% NaCl; use in severe symptomatic hyponatremia, cerebral edema; MONITOR for fluid overload, phlebitis

Water moves OUT of cells (cell shrinkage); pulls fluid from ICF into ECF; used sparingly for severe conditions

Diagrams to know

  • IV fluid tonicity decision tree: patient assessment → choose isotonic vs hypotonic vs hypertonic
  • Water movement in hypotonic vs isotonic vs hypertonic solutions (cell diagram showing ICF/ECF changes)

Chloride, Phosphate, and Other Electrolytes (Brief Reference)

Common values

Value

96–106 mEq/L

Symbol

Cl⁻

Quantity

Normal serum chloride

Value

2.5–4.5 mg/dL

Symbol

PO₄³⁻

Quantity

Normal serum phosphate

Important facts

  • Chloride abnormalities usually SECONDARY to sodium/water problems
  • Phosphate inversely related to calcium—high phosphate pulls serum calcium DOWN
  • Hyperphosphatemia restricts dietary phosphate (dairy, nuts, processed foods) in renal failure
  • Most NLE questions focus on Na⁺, K⁺, Ca²⁺, Mg²⁺; Cl⁻ and PO₄³⁻ less commonly tested

Key definitions

Chloride (Cl⁻)

Example

Prolonged 0.9% saline infusion → high chloride → metabolic acidosis

Normal 96–106 mEq/L; major ECF anion; mirrors sodium; causes hyperchloremic acidosis if excessive

Phosphate (PO₄³⁻)

Example

Hypophosphatemia in hyperparathyroidism; hyperphosphatemia in AKI

Normal 2.5–4.5 mg/dL; inversely related to calcium; essential for energy (ATP); hyperphosphatemia in renal failure

Nursing Process Application & RA 9173 Practice Standards

Important facts

  • PRIORITY INTERVENTIONS for imbalances: Airway/Breathing (if acid-base/pulmonary involvement), Cardiac monitoring (K⁺, Ca²⁺, Mg²⁺ disorders), Prevent complications (seizures, dysrhythmias, shock)
  • ASSESSMENT: Vital signs (orthostatic BP in FVD), skin turgor, mucous membranes, weight, I&O, laboratory values, ABG, ECG changes
  • IMPLEMENTATION: IV access, fluid administration per protocol, electrolyte replacement (diluted, slow), positioning (semi-Fowler's for FVE/respiratory distress)
  • MONITORING: Intake and output (hourly in acute settings), daily weights, vital signs, mental status, cardiac rhythm, urine specific gravity, serum values (K⁺, Na⁺, Ca²⁺, Mg²⁺, pH, HCO₃⁻)
  • PATIENT EDUCATION: Dietary sodium/potassium, medication adherence (diuretics, ACE inhibitors), signs of dehydration/overload, daily weight monitoring (report 1–2 kg/day gain), when to seek help

Key definitions

Nursing Diagnosis (NANDA) Priority in Fluid/Electrolyte/Acid-Base Imbalances

Example

Hypokalemic patient → Priority diagnosis: Risk for decreased cardiac output (dysrhythmia) → Immediate action: Cardiac monitoring and IV KCl replacement

Based on Maslow hierarchy: (1) Ineffective breathing pattern / Impaired gas exchange (if acid-base disorder affects oxygenation); (2) Risk for decreased cardiac output / Dysrhythmia (K⁺, Ca²⁺, Mg²⁺); (3) Risk for injury / Seizures (electrolyte imbalance, altered mental status); (4) Fluid volume deficit / excess; (5) Imbalanced nutrition

RA 9173 Standards & Accountability

Example

Nurse administers IV KCl only after confirming urine output and physician order; documents baseline ECG and subsequent vital signs; reports dysrhythmias to physician immediately

Philippine Nursing Law requires nurses to recognize and report imbalances, monitor therapeutic response, ensure safe IV administration (especially potassium), and document accurately; direct supervision required for complex interventions

Diagrams to know

  • Nursing process for fluid/electrolyte/acid-base imbalance: Assessment → Diagnosis → Planning → Implementation → Evaluation

Must remember

  • 1. POTASSIUM IS LIFE-THREATENING: Hypokalemia → cardiac dysrhythmias (flattened T waves, U waves); hyperkalemia → peaked T waves, widened QRS, VF/asystole. NEVER give potassium by IV push. Dilute and infuse ≤10 mEq/hr on general unit. Check urine output ≥30 mL/hr BEFORE administering.
  • 2. SODIUM DISORDERS ARE WATER PROBLEMS: Hyponatremia = EXCESS WATER (cerebral edema risk); hypernatremia = WATER DEFICIT (cellular dehydration). Correct SLOWLY (8–10 mEq/L per 24 hr) to avoid osmotic demyelination or cerebral edema.
  • 3. NORMAL ELECTROLYTE RANGES (MEMORIZE FOR NLE): Na⁺ 135–145 | K⁺ 3.5–5.0 | Ca²⁺ 8.5–10.5 mg/dL | Mg²⁺ 1.5–2.5 | Cl⁻ 96–106 | Phosphate 2.5–4.5. Most exam questions hinge on recognizing abnormal values.
  • 4. ABG ROME RULE: Respiratory Opposite (pH and CO₂ move opposite), Metabolic Equal (pH and HCO₃⁻ move same direction). Use this every time for interpretation. Normal: pH 7.35–7.45, PaCO₂ 35–45, HCO₃⁻ 22–26, PaO₂ 80–100.
  • 5. CHVOSTEK'S & TROUSSEAU'S SIGNS = HYPOCALCEMIA (AND HYPOMAGNESEMIA): Positive Chvostek's (tap facial nerve → facial twitch); positive Trousseau's (inflate BP cuff → carpal spasm). Institute airway precautions; laryngospasm is a complication.
  • 6. HYPERMAGNESEMIA CAUSES LOSS OF DEEP TENDON REFLEXES: Unlike hypocalcemia (hyperreflexia), hypermagnesemia is characterized by hyporeflexia, hypotension, respiratory depression. IV calcium gluconate is the antidote (counteracts neuromuscular effects).
  • 7. IV FLUID TONICITY & COMPARTMENT SHIFTS: Isotonic (0.9% NaCl, LR) stays in ECF—use for shock/hemorrhage. Hypotonic (0.45% NaCl) moves INTO cells—use for hypernatremia, AVOID in increased ICP. Hypertonic (3% NaCl) pulls water OUT of cells—use for symptomatic hyponatremia/cerebral edema only.
  • 8. HYPERKALEMIA MANAGEMENT: (1) Protect myocardium with IV calcium gluconate (does NOT lower K⁺); (2) Shift K⁺ INTO cells with insulin+glucose, beta-agonist, or sodium bicarbonate; (3) Remove K⁺ from body with Kayexalate or dialysis.
  • 9. DAILY WEIGHT IS MOST RELIABLE FLUID ASSESSMENT: 1 kg weight change ≈ 1 L fluid change. Weigh daily at same time/scale/clothing. Acute weight gain >1–2 kg/day = fluid retention (FVE). Acute weight loss = FVD.
  • 10. PRIORITY NURSING ACTION IN ANY K⁺, Ca²⁺, Mg²⁺ DISORDER = CARDIAC MONITORING: Dysrhythmias are the life threat. Also airway precautions for hypocalcemia (laryngospasm risk) and seizure precautions. Monitor I&O, vital signs, ECG, and laboratory results closely.

Last minute tips

  • TIP #1 — EXAM PATTERN ALERT: NLE heavily tests potassium and sodium imbalances because they are common and life-threatening. If an exam question shows abnormal K⁺ or Na⁺, expect follow-up questions about ECG changes, management, and complications. Read the clinical scenario TWICE before answering.
  • TIP #2 — ABG TRICK: Always START with pH to determine if it's acidosis or alkalosis, THEN look at the responsible system (respiratory or metabolic). Use ROME every time. If pH and PaCO₂ move opposite → respiratory. If pH and HCO₃⁻ move same direction → metabolic. Do not skip the compensation step.
  • TIP #3 — POTASSIUM SAFETY: Any exam question about IV potassium administration must include: (1) dilution confirmation, (2) infusion rate ≤10 mEq/hr, (3) urine output ≥30 mL/hr checked first, (4) cardiac monitoring. If the question does NOT mention these, select the answer that includes them.
  • TIP #4 — FLUID TONICITY QUICK SELECT: FVD/shock = isotonic (0.9% NaCl or LR). Hypernatremia = hypotonic (0.45% NaCl). Symptomatic hyponatremia/cerebral edema = hypertonic (3% saline, slow, central line). If question mentions 'increased ICP,' ELIMINATE hypotonic options immediately.
  • TIP #5 — SIGNS & SYMPTOMS SHORTCUT: Hypocalcemia and hypomagnesemia BOTH present with Chvostek's/Trousseau's signs and muscle irritability. Hypermagnesemia has OPPOSITE (loss of reflexes, flaccidity). Learn these as oppositional pairs—saves mental energy and prevents errors under exam stress.

Comparison tables

Hypokalemia vs Hyperkalemia — ECG and Clinical Presentation

FeatureHypokalemia (K⁺ <3.5)Hyperkalemia (K⁺ >5.0)
ECG ChangesFlattened T waves, ST depression, prominent U waves, prolonged PRTall peaked T waves, widened QRS, prolonged PR, disappearing P wave (severe)
Clinical ManifestationsMuscle weakness, leg cramps, fatigue, decreased bowel sounds, paralytic ileusMuscle weakness, paresthesias, palpitations, cardiac dysrhythmias, cardiac arrest if severe
Common CausesDiuretics (loop, thiazide), vomiting, diarrhea, NG suction, alkalosisRenal failure, K-sparing diuretics, tissue trauma, acidosis, Addison's disease
Priority InterventionIV KCl (diluted, ≤10 mEq/hr on general unit); check urine output ≥30 mL/hr FIRSTIV calcium gluconate (stabilize myocardium); shift K⁺ into cells (insulin+glucose, beta-agonist, bicarb); remove K⁺ (Kayexalate, dialysis)
MonitoringCardiac monitoring, check bowel function, encourage K-rich foodsCardiac monitoring, monitor for dysrhythmias, check urine output, monitor Na⁺ (calcium gluconate contains sodium)

Four Primary Acid-Base Disorders — ABG Patterns and Compensation

DisorderpHPaCO₂HCO₃⁻Primary CauseCompensation
Respiratory Acidosis↓ (<7.35)↑ (>45)Normal or ↑ (kidneys retain HCO₃⁻)Hypoventilation (COPD, sedation, paralysis)Kidneys ↑ HCO₃⁻ reabsorption (slow, takes hours–days)
Respiratory Alkalosis↑ (>7.45)↓ (<35)Normal or ↓ (kidneys lose HCO₃⁻)Hyperventilation (anxiety, pain, fever, hypoxemia)Kidneys ↓ HCO₃⁻ reabsorption (within hours)
Metabolic Acidosis↓ (<7.35)↓ (<35) Kussmaul breathing↓ (<22)DKA, lactic acidosis, renal failure, diarrheaLungs ↓ CO₂ (hyperventilation; occurs within minutes)
Metabolic Alkalosis↑ (>7.45)↑ (>45) shallow breathing↑ (>26)Vomiting, NG suction, diuretics, antacid abuseLungs ↑ CO₂ (hypoventilation; slower, may not be adequate)

Hypocalcemia vs Hypercalcemia — Clinical Presentation and Management

FeatureHypocalcemia (Ca²⁺ <8.5 mg/dL)Hypercalcemia (Ca²⁺ >10.5 mg/dL)
Neuromuscular ManifestationsTetany, paresthesias (tingling), muscle cramps, hyperreflexia, Chvostek's sign +, Trousseau's sign +Muscle weakness, DECREASED reflexes (hyporeflexia), decreased tone, constipation, lethargy
Cardiac ManifestationsProlonged QT interval, dysrhythmias (rare but possible)Shortened QT interval, dysrhythmias
Neurologic ManifestationsSeizures, laryngospasm (airway emergency), altered LOCConfusion, lethargy, polyuria, polydipsia, altered LOC
Common CausesHypoparathyroidism, thyroidectomy, vitamin D deficiency, pancreatitis, renal failure, massive transfusionHyperparathyroidism, malignancy (bone metastases), prolonged immobilization, thiazide diuretics
Management PriorityAirway monitoring (laryngospasm risk); IV calcium gluconate; seizure precautions; treat underlying causeHydration with IV isotonic saline + loop diuretics; mobilization; calcitonin; bisphosphonates; treat underlying cause

Hyponatremia vs Hypernatremia — Pathophysiology and Fluid Management

FeatureHyponatremia (Na⁺ <135 mEq/L)Hypernatremia (Na⁺ >145 mEq/L)
Fundamental ProblemEXCESS WATER (relative to sodium); hypoosmolar; water enters cells → cerebral edemaWATER DEFICIT (relative to sodium); hyperosmolar; water leaves cells → cellular dehydration
Clinical PresentationHeadache, confusion, muscle cramps, nausea, restlessness → seizures, coma (severe)Thirst (if intact), dry mucous membranes, restlessness, agitation → altered LOC, seizures (severe)
Common CausesSIADH, excessive water intake, diuretics (esp. thiazide), vomiting, diarrhea, adrenal insufficiencyWater deprivation, diabetes insipidus, excess sodium intake (hypertonic feedings, excess IV saline), insensible loss (burns, fever)
ManagementIf hypovolemic: 0.9% NaCl; if euvolemic/hypervolemic: FLUID RESTRICTION (most common); 3% saline only for symptomatic (seizures); correct SLOWLY to avoid osmotic demyelinationProvide WATER (oral if can drink) or 0.45% NaCl IV; correct SLOWLY to avoid cerebral edema
Correction RateNo more than 8–10 mEq/L per 24 hr (too fast risks osmotic demyelination/central pontine myelinolysis)No more than 10 mEq/L per 24 hr (too fast risks cerebral edema, seizures)

IV Fluid Tonicity — Selection Based on Clinical Scenario

Fluid TypeOsmolalityWhere Does Water Move?Best Used ForAVOID In
Isotonic (0.9% NaCl, LR, D5W bag)~300 mOsm/kg (same as plasma)Stays in ECF; no shift between ICF/ECFFVD, hemorrhage, shock, most general IV needs—(generally safe)
Hypotonic (0.45% NaCl, 0.33% NaCl, D5W metabolized)<300 mOsm/kg (lower than plasma)INTO cells (ICF swells); ECF dilutesHypernatremia, cellular dehydration, chronic hyperglycemiaIncreased ICP (cerebral edema), hypovolemia (worsens shock), trauma, post-op (swelling risk)
Hypertonic (3% NaCl, 5% NaCl, D10W)>300 mOsm/kg (higher than plasma)OUT OF cells (cells shrink); into ECFSymptomatic hyponatremia (seizures), cerebral edema (osmotic pull of fluid from brain), severe burnsPeripheral veins (risk of phlebitis/thrombosis); use central line preferred; monitor for fluid overload, pulmonary edema

Diagrams

Fluid & Electrolyte Imbalances — Comprehensive Overview

Comprehensive mind map showing all fluid and electrolyte imbalances, their causes, clinical signs, and priority nursing interventions. Organized by disorder type (fluid, sodium, potassium, calcium, magnesium, acid-base, and IV fluids) for quick reference.

ABG Interpretation Step-by-Step Flowchart (ROME Method)

Step-by-step ABG interpretation flowchart using the ROME method. Guides students through pH assessment → identifying primary disorder (respiratory or metabolic) → evaluating compensation. Color-coded for acidosis (red) and alkalosis (teal). Critical for exam success.

Hyperkalemia Management Protocol — Priority Order

Sequence diagram showing the precise 3-step protocol for managing hyperkalemia: (1) Stabilize myocardium with calcium gluconate, (2) Shift K+ into cells with insulin, beta-agonist, or bicarb, (3) Remove K+ with Kayexalate or dialysis. Emphasizes that calcium gluconate does NOT lower K+ but prevents cardiac complications.

Sodium Disorder Decision Tree — Hyponatremia vs Hypernatremia

State diagram showing the decision logic for managing sodium imbalances. Differentiates hyponatremia (excess water, hypoosmolar) from hypernatremia (water deficit, hyperosmolar), includes assessment criteria, treatment decisions, and critical monitoring points. Emphasizes slow correction to prevent complications.

Electrolyte Quick Identification — Sign/Symptom to Diagnosis

Comprehensive diagnostic flowchart based on clinical presentation. Guides students from patient symptoms through systematic questioning to identify the specific electrolyte imbalance. Includes priority treatment for each disorder. Color-coded by disorder type for rapid recognition.

Most Commonly Tested NLE Topics in This Chapter

Pie chart showing the relative emphasis of topics in the NLE. Potassium and sodium imbalances together account for 45% of questions—study these intensively. ABG interpretation is 18% and IV fluid tonicity is 15%. Calcium, magnesium, and volume disorders round out the remaining questions.

Fluid, Electrolyte and Acid-Base Imbalances is chapter 1 of 2 in the Foundations of Medical-Surgical Nursing part of Super Tutor's NLE review. The Philippine Nurse Licensure Examination (PNLE) is given by Professional Regulation Commission (PRC) — Board of Nursing; its dates, format and passing rules are on the NLE page. See the NLE guide.

Study Fluid, Electrolyte and Acid-Base Imbalances in the Super Tutor app

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