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

Exam Tips

• NLE questions often ask about the PRIMARY regulator of fluid balance — always answer KIDNEYS.
• When a question describes a patient with dengue and dropping hematocrit followed by sudden rise, think third-spacing then plasma leakage recovery.
• Memorize: ADH = save water; Aldosterone = save sodium (and water); ANP = lose sodium (and water).
• A 1 kg change in body weight = approximately 1 liter of fluid gained or lost — key for monitoring fluid balance.

Key Points

• Total body water (TBW) = approximately 60% of adult body weight.
• Intracellular fluid (ICF) = about 2/3 of TBW; located inside cells.
• Extracellular fluid (ECF) = about 1/3 of TBW; includes intravascular (plasma) and interstitial fluid.
• Water moves between compartments by OSMOSIS, following osmotic gradients created mainly by sodium (in ECF) and albumin (in plasma).
• Primary regulators of fluid balance: Thirst, ADH (antidiuretic hormone), RAAS (renin-angiotensin-aldosterone system), and ANP (atrial natriuretic peptide).
• The KIDNEYS are the principal organ for fluid and electrolyte homeostasis.
• ADH promotes water reabsorption in the renal collecting ducts (conserves water).
• Aldosterone promotes sodium and water retention in the renal tubules.
• ANP is released by the heart when atrial pressure is high; it promotes sodium and water excretion (opposes aldosterone).
• In the Philippine setting, acute gastroenteritis and dengue-related plasma leakage are major triggers of fluid imbalance.

Definitions

Section Title

Body Fluid Compartments and Fluid Regulation

Common Mistakes

• Confusing ICF and ECF proportions — remember ICF is the LARGER compartment (2/3), ECF is the smaller one (1/3).
• Forgetting that sodium controls ECF osmolality while albumin holds fluid in the intravascular space — these are different mechanisms.
• Thinking the liver regulates fluid balance — the KIDNEYS are the primary organ; the liver produces albumin which affects oncotic pressure.
• Overlooking ANP as a fluid regulator — it is the body's natural 'brake' on fluid retention.

Exam Tips

• Prioritization tip using Maslow: Airway and breathing ALWAYS come before circulation — if FVE causes pulmonary edema and dyspnea, FOWLER'S POSITION comes before diuretics.
• NLE common stem: 'Which finding would the nurse expect in a patient with fluid volume deficit?' — expect rapid weak pulse, flat neck veins, oliguria, increased urine specific gravity.
• Strict I&O and daily weight are the TWO most important nursing monitoring parameters for BOTH FVD and FVE.
• For FVD: give isotonic fluids to EXPAND ECF; for FVE: restrict fluids and sodium, give diuretics.
• In the Philippine community nursing context (PhilHealth, RHU, barangay health center): oral rehydration salts (ORS) are first-line for mild-moderate FVD from gastroenteritis — advocate for this per DOH protocols.

Key Points

• FLUID VOLUME DEFICIT (FVD / Hypovolemia): Loss of ECF — usually isotonic loss of both water AND electrolytes.
• FVD causes in Philippine context: Acute gastroenteritis (vomiting, diarrhea), dengue plasma leakage, hemorrhage, excessive diuresis, third-spacing, and inadequate intake.
• FVD signs: Rapid weak pulse, orthostatic hypotension, flat neck veins, poor skin turgor, dry mucous membranes, oliguria (less than 30 mL/hr), increased thirst, weight loss.
• FVD labs: Rising hematocrit and BUN (hemoconcentration), urine specific gravity above 1.030.
• NURSING PRIORITY in FVD: Restore circulating volume to prevent hypovolemic shock; administer isotonic IV fluids (0.9% NaCl or Lactated Ringer's) as ordered.
• FLUID VOLUME EXCESS (FVE / Hypervolemia): Isotonic expansion of ECF, usually from sodium and water retention.
• FVE causes: Heart failure, renal failure, cirrhosis, over-infusion of IV fluids, excessive sodium intake.
• FVE signs: Bounding pulse, distended neck veins, elevated BP, crackles on auscultation, dyspnea, peripheral/dependent edema, weight gain.
• FVE labs: Decreased hematocrit (hemodilution).
• Most dangerous FVE complication: PULMONARY EDEMA.
• NURSING PRIORITY in FVE with respiratory distress: Position in SEMI- TO HIGH-FOWLER'S to ease breathing — this is the FIRST action.
• For FVD: Institute fall precautions due to orthostatic hypotension.
• Daily weight at the same time with same clothing is the most accurate method to monitor fluid balance.

Definitions

Section Title

Fluid Volume Deficit (Hypovolemia) and Fluid Volume Excess (Hypervolemia)

Common Mistakes

• Confusing FVD with dehydration — FVD is an ISOTONIC loss of ECF (water AND electrolytes); dehydration strictly means water loss alone (hypertonic).
• Failing to check urine output BEFORE administering potassium in a hypovolemic patient — always ensure at least 30 mL/hr urine output.
• Not recognizing that flat neck veins indicate FVD while distended neck veins indicate FVE — opposite findings.
• In FVE with respiratory distress, selecting 'administer diuretics' as the FIRST action instead of positioning — positioning is the immediate priority while waiting for the diuretic to work.
• Forgetting that D5W is isotonic in the bag but becomes HYPOTONIC once dextrose is metabolized in the body.

Exam Tips

• High-yield NLE fact: 'NEVER give potassium by IV push' — if a question presents a nurse pushing undiluted KCl, that is the WRONG action.
• ECG memory aid: 'HIGH K+ = HIGH tent-shaped T (like a PEAK); LOW K+ = LOW flat T with U wave' — think of the K level mirroring the T wave shape.
• For prioritization questions about hyperkalemia: Order of actions is — (1) Calcium gluconate (protect heart), (2) Insulin + dextrose (shift K+), (3) Kayexalate or dialysis (remove K+).
• SIADH pattern in NLE: Low serum sodium + Low serum osmolality + HIGH urine osmolality + NO edema = SIADH (management = fluid restriction).
• Diuretic teaching in Philippine barangay outreach: Remind patients on furosemide to eat potassium-rich foods (bananas, kamote, orange, tomato) and report muscle weakness or cramps.

Key Points

• NORMAL VALUES: Sodium (Na+) = 135–145 mEq/L; Potassium (K+) = 3.5–5.0 mEq/L.
• Sodium is the MAJOR ECF cation and chief determinant of serum osmolality.
• HYPONATREMIA (Na+ below 135 mEq/L): Caused by SIADH, excessive water intake, diuretics, vomiting, diarrhea, adrenal insufficiency.
• Hyponatremia manifestations: NEUROLOGIC from cellular swelling — headache, confusion, muscle cramps, nausea, seizures, coma (severe).
• Hyponatremia management: Fluid restriction if water excess; isotonic 0.9% NaCl if hypovolemic; 3% hypertonic saline ONLY for severe symptomatic cases (given SLOWLY).
• CRITICAL: Correct hyponatremia SLOWLY — rapid correction risks OSMOTIC DEMYELINATION (central pontine myelinolysis).
• HYPERNATREMIA (Na+ above 145 mEq/L): Caused by water deprivation, diabetes insipidus, excess sodium intake, hypertonic tube feedings without adequate water.
• Hypernatremia manifestations: Thirst, dry mucous membranes, restlessness, agitation, neurologic changes from cellular DEHYDRATION.
• Hypernatremia management: Give water orally or HYPOTONIC fluids (0.45% NaCl); correct SLOWLY to avoid cerebral edema.
• Potassium is the MAJOR ICF cation; critical for cardiac and neuromuscular function.
• HYPOKALEMIA (K+ below 3.5 mEq/L): Caused by loop/thiazide diuretics, vomiting, diarrhea, NG suction, alkalosis.
• Hypokalemia manifestations: Muscle weakness, leg cramps, fatigue, decreased bowel sounds, paralytic ileus, cardiac dysrhythmias.
• Hypokalemia ECG: FLATTENED T waves, ST depression, prominent U WAVES.
• HYPERKALEMIA (K+ above 5.0 mEq/L): Caused by renal failure, potassium-sparing diuretics, tissue trauma, acidosis, Addison's disease.
• Hyperkalemia manifestations: Muscle weakness, paresthesias, cardiac dysrhythmias progressing to VF and asystole.
• Hyperkalemia ECG: TALL PEAKED T WAVES, widened QRS — most dangerous cardiac finding.
• NEVER administer potassium by IV PUSH — fatal cardiac arrest risk.
• Safe IV KCl rate: No faster than 10 mEq/hr on a general unit; up to 20 mEq/hr only with continuous cardiac monitoring in ICU setting.
• Always ensure urine output of AT LEAST 30 mL/hr before administering potassium.
• Hyperkalemia priority: IV CALCIUM GLUCONATE stabilizes the cardiac membrane (does NOT lower potassium level).
• To SHIFT K+ into cells (temporarily lower serum K+): Regular insulin + dextrose; sodium bicarbonate (if acidotic); beta-agonists.
• To REMOVE K+ from body: Sodium polystyrene sulfonate (Kayexalate) or dialysis.

Definitions

Section Title

Electrolyte Imbalances: Sodium and Potassium

Common Mistakes

• Saying calcium gluconate 'treats' hyperkalemia by lowering potassium — it only STABILIZES the myocardium; it does not change serum K+ levels.
• Administering IV potassium too fast — the rate of 10 mEq/hr maximum on a general unit is a LEGAL and safety standard under RA 9173 standards of practice.
• Forgetting to check urine output before giving potassium — if the patient is not urinating, potassium will accumulate and worsen hyperkalemia.
• Confusing the ECG findings: PEAKED T waves = Hyperkalemia; FLATTENED T waves with U waves = Hypokalemia.
• Treating hyponatremia too aggressively — rapid correction is MORE DANGEROUS than slow correction; always correct slowly.
• Using hypotonic fluids for hypovolemia — hypotonic fluids shift water into cells and worsen hypotension; use isotonic fluids for hypovolemia.

Exam Tips

• NLE memory aid for calcium signs: 'CATS' — Convulsions, Arrhythmias (hypocalcemia-related), Tetany, Stridor (laryngospasm) = signs of HYPOcalcemia.
• Hypercalcemia mnemonic: 'Stones, Bones, Groans, Moans, Psychic Overtones' — kidney stones, bone pain, abdominal groans (constipation, nausea), muscle moans (weakness), mental status changes.
• Obstetric context (NLE NCM 103): A preeclamptic patient on MgSO4 with absent patellar reflex — STOP the infusion and prepare calcium gluconate (antidote).
• Priority for hypocalcemia: AIRWAY first (laryngospasm risk) before other interventions.
• Calcium gluconate is the antidote for BOTH hypermagnesemia AND hyperkalemia — it is the 'cardiac membrane stabilizer' in both situations.

Key Points

• NORMAL VALUES: Calcium (Ca2+) total = 8.5–10.5 mg/dL; Magnesium (Mg2+) = 1.5–2.5 mEq/L.
• HYPOCALCEMIA (Ca2+ below 8.5 mg/dL): Caused by hypoparathyroidism, thyroidectomy/parathyroidectomy, vitamin D deficiency, pancreatitis, renal failure.
• Hypocalcemia manifestations: NEUROMUSCULAR IRRITABILITY — tetany, paresthesias (numbness/tingling around mouth and fingertips), laryngospasm, seizures.
• TROUSSEAU'S SIGN: Carpal spasm (hand cramping into flexion) when BP cuff inflated above systolic pressure for 3 minutes — positive = hypocalcemia.
• CHVOSTEK'S SIGN: Facial twitching when the facial nerve is tapped just anterior to the ear — positive = hypocalcemia.
• Hypocalcemia PRIORITY: Monitor airway for LARYNGOSPASM (can be fatal); keep IV CALCIUM GLUCONATE at bedside; institute seizure precautions.
• HYPERCALCEMIA (Ca2+ above 10.5 mg/dL): Caused by hyperparathyroidism, malignancy (bone metastasis), prolonged immobilization, thiazide diuretics.
• Hypercalcemia manifestations: Muscle WEAKNESS, decreased deep tendon reflexes, constipation, kidney stones, altered mental status ('moans, groans, bones, stones').
• Hypercalcemia management: Isotonic IV fluids + LOOP diuretics (furosemide) to promote renal excretion; calcitonin; bisphosphonates; encourage mobilization.
• HYPOMAGNESEMIA (Mg2+ below 1.5 mEq/L): Caused by alcoholism, malnutrition, GI losses, prolonged use of loop diuretics.
• Hypomagnesemia manifestations: MIRROR hypocalcemia — tremors, tetany, positive Chvostek's and Trousseau's signs, dysrhythmias including TORSADES DE POINTES.
• Hypomagnesemia often ACCOMPANIES hypokalemia and hypocalcemia — always check all three together.
• Hypomagnesemia management: IV MAGNESIUM SULFATE (MgSO4); monitor deep tendon reflexes during infusion.
• HYPERMAGNESEMIA (Mg2+ above 2.5 mEq/L): Usually from renal failure or excessive Mg intake (antacids, laxatives, obstetric MgSO4 therapy for eclampsia).
• Hypermagnesemia manifestations: Hypotension, LOSS OF DEEP TENDON REFLEXES (DTR) — first sign of toxicity, respiratory DEPRESSION, bradycardia.
• Hypermagnesemia management: STOP magnesium sources; ANTIDOTE = IV CALCIUM GLUCONATE; dialysis if severe.
• Memory aid: Loss of DTR in hypermagnesemia is the EARLIEST sign before respiratory depression — check patellar reflex regularly during MgSO4 therapy.

Definitions

Section Title

Electrolyte Imbalances: Calcium and Magnesium

Common Mistakes

• Confusing which sign is which: TROUSSEAU = blood pressure cuff on the ARM (think 'T' for Tourniquet/Arm); CHVOSTEK = tapping the CHEEK (think 'C' for Cheek).
• Treating hypercalcemia with thiazide diuretics — thiazides CAUSE hypercalcemia by increasing renal calcium reabsorption; use LOOP diuretics (furosemide) instead.
• Forgetting that hypomagnesemia, hypokalemia, and hypocalcemia often occur TOGETHER — if a patient is hypokalemic and not responding to potassium replacement, check MAGNESIUM.
• Not checking deep tendon reflexes during MgSO4 infusion — absent patellar reflex is the signal to STOP the infusion; respiratory depression follows if infusion continues.
• Giving more magnesium for hypermagnesemia — the action is to STOP magnesium and give CALCIUM GLUCONATE as antidote.

Formulas

Exam Tips

• NLE ABG 4-step approach: (1) pH — acidosis or alkalosis? (2) PaCO2 — high or low? Apply ROME-Respiratory Opposite. (3) HCO3- — high or low? Apply ROME-Metabolic Equal. (4) Does the 'other' value support compensation?
• Practice ABG: pH 7.50, PaCO2 30, HCO3- 24 → pH HIGH = alkalosis; PaCO2 LOW and pH HIGH = OPPOSITE → Respiratory Alkalosis; HCO3- normal = no metabolic compensation. Answer: Uncompensated Respiratory Alkalosis.
• DKA pattern: pH 7.20, PaCO2 28, HCO3- 12 → pH LOW = acidosis; HCO3- LOW and pH LOW = EQUAL → Metabolic Acidosis; PaCO2 also LOW = lungs compensating. Answer: Partially Compensated Metabolic Acidosis (Kussmaul respirations explain low PaCO2).
• Common NLE COPD ABG: pH 7.32, PaCO2 60, HCO3- 30 → Respiratory Acidosis with renal compensation (high HCO3- shows kidneys retaining bicarb). Answer: Partially Compensated Respiratory Acidosis.
• Priority nursing action for respiratory acidosis: IMPROVE VENTILATION — reposition to open airway, encourage deep breathing, reduce sedation, prepare for mechanical ventilation if needed.

Key Points

• NORMAL ABG VALUES: pH 7.35–7.45; PaCO2 35–45 mmHg; HCO3- 22–26 mEq/L; PaO2 80–100 mmHg; SaO2 95–100%.
• pH below 7.35 = ACIDOSIS; pH above 7.45 = ALKALOSIS.
• PaCO2 is the RESPIRATORY component — CO2 is an acid; CO2 accumulates (hypoventilation) = acidosis; CO2 is blown off (hyperventilation) = alkalosis.
• HCO3- is the METABOLIC component — HCO3- is a base; loss of HCO3- = acidosis; gain of HCO3- = alkalosis.
• ROME memory aid: Respiratory Opposite — pH and PaCO2 move in OPPOSITE directions in respiratory disorders; Metabolic Equal — pH and HCO3- move in the SAME direction in metabolic disorders.
• 4-STEP ABG INTERPRETATION: (1) Assess pH — acidosis or alkalosis? (2) Assess PaCO2 — respiratory contribution? (3) Assess HCO3- — metabolic contribution? (4) Determine compensation — is the other system compensating?
• RESPIRATORY ACIDOSIS: pH LOW, PaCO2 HIGH — caused by hypoventilation (COPD, respiratory depression, oversedation, neuromuscular disease). Priority = IMPROVE VENTILATION.
• RESPIRATORY ALKALOSIS: pH HIGH, PaCO2 LOW — caused by hyperventilation (anxiety, pain, fever, early salicylate toxicity, mechanical over-ventilation). Manage the underlying cause.
• METABOLIC ACIDOSIS: pH LOW, HCO3- LOW — caused by DKA (diabetic ketoacidosis), renal failure, severe diarrhea, lactic acidosis (shock). KUSSMAUL respirations are a compensatory sign (deep, rapid breathing to blow off CO2).
• METABOLIC ALKALOSIS: pH HIGH, HCO3- HIGH — caused by vomiting, prolonged NG suction, excessive antacids, diuretic overuse.
• COMPENSATION: The system NOT responsible for the primary imbalance tries to return pH toward normal. Partial compensation = pH still abnormal; Full compensation = pH returns to normal range.
• In respiratory problems: KIDNEYS compensate (slow — takes days).
• In metabolic problems: LUNGS compensate (fast — within minutes to hours).

Definitions

Section Title

Acid-Base Balance and ABG Interpretation

Common Mistakes

• Forgetting to assess pH FIRST in ABG interpretation — students often start with PaCO2, which leads to errors.
• Confusing respiratory and metabolic components: PaCO2 is ALWAYS respiratory; HCO3- is ALWAYS metabolic.
• Misapplying ROME: Students write 'Opposite for Metabolic' — OPPOSITE is for RESPIRATORY only. Metabolic = EQUAL direction as pH.
• Not recognizing Kussmaul respirations as COMPENSATION (not the primary problem) — the primary problem is metabolic acidosis, not a respiratory disorder.
• Confusing early vs. late salicylate toxicity: EARLY aspirin toxicity causes RESPIRATORY ALKALOSIS (hyperventilation); LATE toxicity causes METABOLIC ACIDOSIS.
• Thinking compensation means the patient is 'fine' — compensated ABG still indicates an underlying problem that needs treatment.

Exam Tips

• NLE tonicity mnemonic: 'ISO stays, HYPO goes IN, HYPER pulls OUT' — isotonic stays in the vascular space; hypotonic goes into cells; hypertonic pulls fluid out of cells.
• For a patient in hypovolemic shock: ISOTONIC fluid (0.9% NaCl or LR) — never hypotonic (worsens shock) and never hypertonic (risk of fluid overload).
• For a patient with cerebral edema after traumatic brain injury: HYPERTONIC saline or mannitol — pulls water out of brain cells. Avoid hypotonic fluids.
• For a patient with severe symptomatic hyponatremia (seizures, coma): Cautious use of 3% NaCl (hypertonic) — must correct SLOWLY to avoid osmotic demyelination.
• Philippine clinical context: In barangay and RHU settings, nurses often manage oral rehydration therapy (ORS) — ORS is considered isotonic and is appropriate for mild-moderate gastroenteritis-related FVD per DOH-IMCI protocol.

Key Points

• IV fluid TONICITY refers to the osmolality of the solution relative to normal plasma osmolality (275–295 mOsm/kg).
• ISOTONIC solutions (~275–295 mOsm/L): Expand INTRAVASCULAR volume without shifting fluid into or out of cells. Examples: 0.9% NaCl (Normal Saline), Lactated Ringer's (LR), D5W (in the bag — becomes hypotonic in the body once dextrose is metabolized).
• Use isotonic fluids for: Hypovolemia, hemorrhage, shock, pre- and post-operative fluid replacement, hypovolemic FVD.
• HYPOTONIC solutions (below 275 mOsm/L): Have lower osmolality than plasma; water moves INTO the cells (from ECF into ICF). Examples: 0.45% NaCl (Half Normal Saline), 0.33% NaCl.
• Use hypotonic fluids for: Cellular dehydration, hypernatremia (to rehydrate cells).
• AVOID hypotonic fluids in: Increased intracranial pressure (ICP) — water shifts into brain cells, worsening cerebral edema; also avoid in hypovolemia (worsens hypotension by further reducing intravascular volume).
• HYPERTONIC solutions (above 295 mOsm/L): Have higher osmolality than plasma; water moves OUT of cells into the ECF. Examples: 3% NaCl, 5% NaCl, D10W, D5 in 0.9% NaCl, D5 in Lactated Ringer's.
• Use hypertonic fluids for: Severe symptomatic hyponatremia (to correct dangerously low sodium), cerebral edema (to pull water out of brain cells), and hypertonic tube feeding supplementation.
• CAUTION with hypertonic fluids: Monitor CLOSELY for fluid overload and pulmonary edema; 3% NaCl must be given SLOWLY with frequent serum sodium monitoring; administer only in ICU/closely monitored settings.
• KEY TEACHING: D5W is isotonic in the bag, but once metabolized, it provides FREE WATER — effectively hypotonic. Do NOT use as a volume expander for patients with hypovolemia.
• Lactated Ringer's (LR) is the preferred isotonic fluid for burns and trauma — it most closely resembles plasma electrolyte composition.

Definitions

Section Title

IV Fluid Tonicity and Clinical Application

Common Mistakes

• Thinking D5W is always hypotonic — it is isotonic IN THE BAG (before administration) but becomes hypotonic IN THE BODY once dextrose is metabolized. It should not be used as a primary volume expander.
• Using hypotonic fluids (0.45% NaCl) for a patient with increased ICP — this is CONTRAINDICATED because it worsens cerebral edema.
• Using Lactated Ringer's for a hyperkalemic patient — LR contains potassium (4 mEq/L) and can worsen hyperkalemia; use 0.9% NaCl instead.
• Confusing the direction of fluid movement: Hypotonic = water goes INTO cells (cells SWELL); Hypertonic = water comes OUT of cells (cells SHRINK).
• Giving hypertonic saline (3% NaCl) too rapidly — must be given SLOWLY to prevent abrupt fluid shifts, osmotic demyelination risk.