Fluid & Electrolyte Balance – Comprehensive CAT Review Notes

Homeostasis & Fluid Balance

• Homeostasis = the body’s ability to maintain internal stability despite external changes.

  • Central to this is fluid balance (water + electrolytes).

  • Key electrolytes repeatedly referenced: Na⁺, K⁺, Cl⁻, Mg²⁺, Ca²⁺, HCO₃⁻.

Osmolality

• Definition: Concentration of solutes per kilogram of solvent.

• Serum (plasma) osmolality

  • Normal: 285\text{–}295\,\text{mOsm/kg}.

  • >295 ➔ blood too concentrated (dehydration).

  • <285 ➔ blood too diluted (over-hydration).

  • Major solutes that drive the value: sodium, glucose, urea.

• Urine osmolality

  • Normal: 50\text{–}1200\,\text{mOsm/kg}.

  • High value ⇒ kidneys holding water (concentrated urine).

  • Low value ⇒ kidneys releasing water (dilute urine).

• Clinical links

  • Dehydration: high serum osmolality + concentrated urine.

  • Over-hydration: low serum osmolality + dilute urine (but urine may be concentrated if kidneys are compensating).

• Ongoing nursing assessments

  • Strict I&O, daily weights.

  • Lab review (Na⁺, BUN, creatinine, glucose, osmolality).

  • Physical: edema, skin turgor, mucous membranes, neuro status, BP.

Major Fluid Compartments

• Intracellular (ICF)

  • Inside cells; ≈67 % of body water.

  • Functions: metabolism, energy production, cellular repair.

• Interstitial (part of ECF)

  • Between cells; ≈25 % of body water.

  • Cushions, “padding” for tissues; site of edema accumulation.

• Intravascular (plasma)

  • In blood vessels; ≈8 % of body water.

  • Transports nutrients, hormones, wastes.

• IV fluids first enter intravascular space, then shift based on tonicity & body need.

Transport Mechanisms

• Osmosis: Water moves across a semipermeable membrane from low-solute to high-solute area to equalize concentration.

  • Example: 0.45 % NaCl (hypotonic) pulls water into dehydrated cells; monitor for edema & cerebral swelling (confusion, headache, seizures).

• Diffusion: Passive spread of particles (electrolytes, gases) from high to low concentration.

  • O₂ diffuses from alveoli (high) to blood (low).

  • K⁺ & Na⁺ shift until electrochemical equilibrium.

• Active transport (Na⁺/K⁺ pump)

  • Pumps 3\,\text{Na}^+ out & 2\,\text{K}^+ in per 1\,\text{ATP}.

  • Maintains nerve impulses, muscle contraction, cardiac rhythm.

  • Med example: digoxin inhibits pump—therapeutic window, risk of toxicity.

Thirst Mechanism

• Lamina terminalis (near hypothalamus) senses serum osmolality.

  • ↑ osmolality (dehydration) ➔ triggers thirst.

  • ↓ osmolality (over-hydration) ➔ turns thirst off.

• Populations at risk for "blunted" thirst: elderly, dementia patients, infants.

  • Nursing: offer fluids, monitor I&O, assess dehydration signs.

Antidiuretic Hormone (ADH / Vasopressin)

• Released from posterior pituitary when osmolality ↑, BP ↓, or volume ↓.

• Acts on nephron to reabsorb water ➔ ↑ plasma volume, ↓ urine output.

• Excess or deficiency will appear in fluid status & serum Na⁺ trends.

Kidney Function Essentials

• Filters ≈50 gal (180 L) blood/day.

• Removes wastes (urea, creatinine) & extra water; selectively reabsorbs needed solutes.

• Key labs: BUN, creatinine, \text{GFR}, electrolytes, osmolality.

• Output goal: ≥0.5 mL/kg/hr (≈30 mL/hr adult).

• Fluid-balance manifestations: edema, BP changes, weight gain/loss.

Fluid Loss Pathways

• Sensible (measurable): urine, liquid stool, emesis, wound/NG drainage, measurable sweat, blood loss.

• Insensible (unmeasurable): respiration, evaporation from skin, water in formed stool.

  • Dehydrated patient signs: poor skin turgor, sunken eyes, dry mucosa, chapped lips, dark concentrated urine, low BP.

Core Electrolyte Principles

• Electrolytes = charged minerals regulating heart rhythm, muscle/nerve function, fluid distribution, acid–base balance.

• Small deviations can be life-threatening.

• Causes of imbalance: vomiting, diarrhea, diuretics, IV fluids, kidney disease, burns, endocrine disorders.

Potassium (K⁺)

• Normal: 3.5\text{–}5.0\,\text{mEq/L}.

• Major intracellular cation; vital for neuromuscular & cardiac conduction.

• Dietary sources: bananas, oranges/juice, cantaloupe, apricots, avocados, white beans, lentils, coconut water, tomato juice.

Hypokalemia (<3.5; critical <3.0 adult, <2.5 infant)

• Causes

  • Meds: loop/thiazide diuretics (non-K⁺-sparing), amphotericin-B, laxative abuse.

  • GI loss: vomiting, diarrhea.

  • ↓ intake, alcoholism.

• Manifestations

  • Mild (3.0–3.5): often asymptomatic; may see fatigue, muscle weakness, constipation.

  • Severe (<3): arrhythmias, hypotension, respiratory paralysis.

• Diagnostics: serum BMP/CMP, continuous ECG.

• Treatment

  • Oral or IV K⁺ (central line for >10 mEq/hr), high-K⁺ foods.

  • Address cause; review meds.

Hyperkalemia (>5.0; critical >6.1 adult, >8.0 newborn)

• Causes: renal failure (#1), K⁺-sparing diuretics, dehydration, diabetes, burns/trauma, transfusions, excessive intake.

• Manifestations: early asymptomatic; later muscle weakness, flaccid paralysis, fatal arrhythmias, heart failure.

• Diagnostics: BMP/CMP, ECG (peaked T-waves, wide QRS, sine wave).

• Treatment

  • Calcium gluconate (cardiac membrane stabilization).

  • Loop diuretics, insulin + D50, sodium bicarb, albuterol, kayexalate, dialysis in extreme cases.

  • Dietary K⁺ restriction; avoid K⁺ salt substitutes.

Sodium (Na⁺)

• Normal: 135\text{–}145\,\text{mEq/L}.

• Main extracellular cation; governs neuro & neuromuscular function, fluid distribution, BP.

• High-Na⁺ foods: processed meats (deli, bacon, ham, hot dogs), canned soups/veg, bread/rolls, cheese, condiments (ketchup, BBQ, soy), fast food (Big Mac + fries ≈1500 mg), sports drinks (Gatorade).

Hyponatremia (<135; critical <120)

• Commonest cause: excess water intake (dilutional).

• Other causes: thiazide diuretics, GI loss, alcohol, severe burns, heart/liver/renal failure.

• Manifestations

  • Mild: general malaise, nausea.

  • Moderate: lethargy, confusion, headache, restlessness, irritability.

  • Severe/critical: muscle twitching, seizures, death.

• Diagnostics: BMP/CMP, urine Na⁺, osmolality.

• Treatment

  • Fluid restriction, hypertonic saline (3 %) if severe & neuro sx (slow correction!), discontinue causative meds.

  • Teach: urine color chart (pale yellow ideal), plan electrolyte drinks during intense activity.

Hypernatremia (>145; critical >160)

• Causes: water loss (dehydration, sweating, burns), impaired thirst (elderly, infants), CKD, diabetes.

• Manifestations

  • Mild: confusion, lethargy, irritability.

  • Severe: muscle twitching, seizures, death.

• Diagnostics: BMP/CMP, plasma osmolality test.

• Treatment

  • IV free water replacement (D5W) or hypotonic saline – slowly to prevent cerebral edema.

  • Identify/correct underlying cause; oral free water if able.

Calcium (Ca²⁺)

• Normal total Ca²⁺: 8.5\text{–}10.5\,\text{mg/dL} (ionized 4.4–5.4 mg/dL).

• 99 % in bones/teeth.

• Functions: bone structure, muscle contraction, nerve impulse, coagulation, hormone secretion, cardiac rhythm.

• Absorption requires Vitamin D (raises Ca²⁺ absorption from 10-15 % to 30-45 %).

• Dietary sources: milk, yogurt, cheese, leafy greens (spinach, kale, bok choy), canned salmon/sardines.

Hypocalcemia (<8.5)

• Causes: laxatives, long-term glucocorticoids, loop diuretics, PPIs, Vit D deficiency, menopause, multiple transfusions, low Mg²⁺ or high phosphate.

• Manifestations

  • Numbness/tingling (fingers, toes, perioral).

  • Muscle cramps/spasms.

  • Positive Chvostek sign (facial twitch when tapping cheek).

  • Positive Trousseau sign (carpal spasm with BP cuff inflation).

  • May progress to seizures, laryngospasm.

• Diagnostics: BMP/CMP, ionized Ca²⁺.

• Treatment

  • Mild: dietary Ca²⁺ + Vit D.

  • Severe/symptomatic: IV calcium gluconate or chloride.

Hypercalcemia (>10.5)

• Causes: malignancy (bone metastasis, PTH-secreting tumors), Vit D toxicity, thiazide diuretics, lithium, prolonged immobility, CKD.

• Manifestations

  • GI: constipation, abdominal pain, nausea, vomiting, anorexia (loss of appetite).

  • Skeletal: bone pain, muscle weakness.

  • Neuro: lethargy, confusion, coma.

  • Renal: polyuria, kidney stones.

• Diagnostics: BMP/CMP, PTH level, CT/X-ray for underlying etiology.

• Treatment

  • Mild/no sx: ↑ oral hydration, limit Ca²⁺/Vit D.

  • Symptomatic: oral phosphate (binds Ca²⁺), IV isotonic saline + loop diuretics, bisphosphonates, calcitonin.

  • Severe: hemodialysis.

Magnesium (Preview – details not covered in lecture)

• Mentioned as 1 of 4 electrolytes to focus on; lecture ran out of time. Review normal 1.5\text{–}2.5\,\text{mEq/L} independently.

Integrated Clinical Connections

• Electrolyte shifts frequently present first as neurologic or cardiac changes—continuous assessment and ECG monitoring critical.

• Always relate:

  • Lab value ↔ physical assessment ↔ underlying cause ↔ treatment/intervention.

• Quality documentation of I&O, daily weights, edema grading, mental status, and vitals reinforces safe care and prepares you for Med-Surg I, Pharmacology, and CAT exam.

Ethical/Practical Implications

• IV fluid administration is NOT benign; nurses must reassess for cerebral edema, pulmonary edema, electrolyte shifts.

• Elderly & cognitively impaired patients rely on nurses to detect subtle signs (thirst blunting, early confusion).

• Patient education: diet options (allergies, preferences, chewing ability), medication side-effects, and when to seek help (muscle cramps, palpitations, seizures).

High-Yield Numbers & Quick Reference

• Serum osmolality: 285\text{–}295\,\text{mOsm/kg}

• Urine osmolality: 50\text{–}1200\,\text{mOsm/kg}

• Na⁺: 135\text{–}145\,\text{mEq/L} (critical <120, >160)

• K⁺: 3.5\text{–}5.0\,\text{mEq/L} (critical <3.0, >6.1)

• Ca²⁺ (total): 8.5\text{–}10.5\,\text{mg/dL}

• Key fluid loss: ≥0.5 mL/kg/hr urine output target

  Magnesium: Physiology & Sources

  • Second-most abundant intracellular cation after potassium.

  • 50\text{–}60\% of total body Mg is stored in bone; remainder in muscle & soft tissue.

  • Core functions

    • Regulates nerve impulse transmission & skeletal/ smooth/ cardiac muscle contraction.

    • Stabilises blood pressure & modulates vascular tone.

    • Participates in carbohydrate metabolism → maintains serum glucose.

    • Structural support for bone & teeth (with Ca & P).

    • Essential co-factor in >300 enzymatic reactions: protein, DNA & RNA synthesis.

  • Dietary acquisition

    • Whole foods: leafy greens (spinach, kale), nuts/seeds (almonds, cashews, pumpkin seeds), legumes (black beans, chick-peas, lentils), whole grains (quinoa, brown rice, oats, whole-wheat bread), fatty fish (salmon, mackerel), avocado, banana, dark chocolate \ge 70\% cocoa.

    • Fortified products: breakfast cereals, plant milks (almond, soy), selected breads & snack bars.

    • Supplements (Mg oxide, citrate, glycinate, etc.) if ordered.

  Normal & Critical Serum Mg Values

  • Reference laboratory range (adult): 1.6\text{–}2.6\,\text{mg·dL}^{-1} (facility specific).

  • Critical

    • Severe hypomagnesaemia < 0.5\,\text{mg·dL}^{-1}.

    • Severe hypermagnesaemia > 3.0\,\text{mg·dL}^{-1} (life-threatening threshold rises to >12\,\text{mg·dL}^{-1}).

  Hypomagnesaemia

  • Aetiology

    • Medication losses: loop & thiazide diuretics, certain aminoglycosides, proton-pump inhibitors.

    • ↓ Intake: poor diet, general under-nutrition.

    • ↓ GI absorption: Crohn’s, coeliac disease.

    • ↑ GI losses: severe diarrhoea, pancreatitis.

    • ↑ Renal excretion: uncontrolled T2DM (osmotic diuresis), alcohol use disorder, post-burn diuresis.

    • Associated electrolyte shifts: hypokalaemia, hypocalcaemia.

  • Clinical presentation (usually at <1.2\,\text{mg·dL}^{-1})

    • Mild–moderate: nausea, vomiting, anorexia, fatigue, generalised weakness.

    • Severe: neuromuscular irritability (tetany, cramps, spasticity), paraesthesias, seizures, personality/ mood change, arrhythmias & coronary/ peripheral vasospasm— potentiated when combined with other dyselectrolytaemias.

  • Diagnostics

    • Serum Mg on BMP/CMP; always assess concurrent K^+ & Ca^{2+}.

    • 12-lead ECG for dysrhythmia.

  • Management

    • Oral Mg salts for mild–moderate deficit (observe for diarrhoea).

    • IV Mg sulfate for severe or symptomatic cases (telemetry required).

    • Correct underlying cause; reinforce Mg-rich diet.

  Hypermagnesaemia

  • Criticality scale

    • Moderate symptoms above 7\,\text{mg·dL}^{-1}.

    • Severe/ life-threatening at >12\,\text{mg·dL}^{-1}.

  • Causes

    • Renal insufficiency/ failure (most common: impaired excretion).

    • Excess intake: Mg-containing laxatives, antacids, over-supplementation.

    • Drug-induced: lithium, chronic opioids.

    • Massive tissue injury/ trauma (cellular release).

  • Symptom progression

    1. Mild – nausea, dizziness, lethargy, confusion.

    2. Moderate – worsening confusion, somnolence, blurred vision, headache, flushing, constipation.

    3. Severe – flaccid paralysis, respiratory depression, profound hypotension, bradycardia → AV block, seizure, coma, cardiac arrest.

  • Work-up mirrors hypomagnesaemia (BMP/CMP ± ECG).

  • Treatment

    • Mild: discontinue Mg sources (OTC antacids/ laxatives/supplements).

    • Moderate: IV Ca^{2+} (gluconate or chloride) as physiological antagonist; IV loop diuretics + isotonic saline to enhance renal excretion.

    • Severe/ anuric renal failure: emergent haemodialysis.

    • Continuous monitoring of cardiac rhythm, BP, neuromuscular status; serial Mg labs.

  Dehydration (Water Loss > Sodium Loss)

  • Definition: Pure H₂O deficit → hypernatraemia & ↑ plasma osmolality.

  • Contributing factors

    • GI fluid loss (vomiting, diarrhoea).

    • Excessive perspiration (fever, heat exposure).

    • Polyuria (e.g., uncontrolled DM, diuretics).

    • Fever, ↓ fluid intake, impaired thirst (elderly, infants, benzodiazepines, SSRIs).

  • Manifestations

    • Mild–moderate: thirst, dry mucosa, lethargy, cognitive slowing, ↓ skin turgor, oliguria (concentrated urine).

    • Severe: tachycardia, hypotension (↓ preload), shock, coma → multi-organ failure if uncorrected.

  • Diagnostics: BMP/CMP (hypernatraemia), ↑ serum osmolality, urine specific gravity >1.030.

  • Therapy

    • Oral rehydration solutions if alert.

    • IV hypotonic: D5W or 0.45\% NS, infused slowly to prevent cerebral oedema.

  Fluid Volume Deficit: Hypovolaemia

  • Loss of both water & electrolytes → ↓ circulating volume.

  • Aetiology: haemorrhage, diarrhoea/ vomiting, severe burns (capillary leak), third-spacing (ascites, pancreatitis), excessive sweating, over-diuresis, major trauma.

  • S/S (progressive)

    • Early: thirst, dry mucous membranes, tenting skin (unreliable in elderly), ↓ urine output.

    • Progression: lethargy, muscle weakness, orthostatic hypotension, tachycardia (compensatory).

    • Severe: confusion, tachypnoea, chest pain, palpitations, oliguria, hypovolaemic shock (>20\% blood volume loss) → MODS.

  • Diagnostics

    • BMP/CMP: dyselectrolytaemias.

    • ↑ BUN/Cr (prerenal); CBC may show ↑ haemato­crit (hemoconcentration) or ↓ if haemorrhage.

    • Urine specific gravity high.

  • Treatment

    • Mild: oral fluids/electrolytes.

    • Moderate–severe: isotonic IV 0.9\% NS or Lactated Ringer’s; PRBC transfusion if haemorrhagic.

  Fluid Volume Excess: Hypervolaemia

  • Excess Na^+ & H₂O in ECF.

  • Common causes: CHF (↓ cardiac output → RAAS activation), CKD (↓ urine output), cirrhosis/ ESLD (portal HTN, ↓ albumin → ascites), drugs (vasodilators, CCBs).

  • Hallmark findings

    • Rapid weight gain, peripheral/ sacral oedema.

    • Cardiopulmonary: JVD, bounding pulse, hypertension, crackles/ rales, dyspnoea; severe → pulmonary oedema & respiratory distress.

  • Work-up: Daily weights, oedema grading, BMP/CMP (variable Na^+), urine Na^+ to assess renal handling.

  • Management

    • Loop diuretics (furosemide); thiazides if mild.

    • Fluid & sodium restriction.

    • Daily weights, I&O charting.

    • Haemodialysis in refractory CKD; paracentesis for tense ascites.

  Blood Components & Their Uses

  • Whole blood seldom transfused—components are targeted via centrifugation (≈60\% plasma / 40\% cells).

  • Red Blood Cells (PRBC)

    • Carry O2 & remove CO2; lifespan 120 days; production \approx2\times10^6 cells·s^{-1}.

    • 1 unit PRBC raises Hb by \approx1\,\text{g·dL}^{-1} & Hct by 3\%.

    • Typical trigger: Hb < 7\text{–}8\,\text{g·dL}^{-1} (patient/context dependent).

    • Rough rule: Hct \approx Hb \times 3 (e.g., Hb 10\Rightarrow Hct\sim30\%).

  • Platelets

    • Indicated when count < 20{,}000\,\text{µL}^{-1} or active bleeding.

    • Single transfusion may pool platelets from up to 10 donors.

  • Plasma (FFP)

    • Contains clotting factors, proteins, electrolytes; stored frozen & thawed → Fresh Frozen Plasma.

    • Utilised for coagulopathy, massive transfusion, liver failure, burns.

    • Fractionation yields derivatives (albumin, factor VIII, immunoglobulin, etc.).

  • Cryoprecipitate: rich in fibrinogen, factor VIII, XIII & vWF.

  • Granulocytes (WBC) rarely transfused—reserved for severe neutropenia unresponsive to G-CSF.

  • Autologous donation: patient pre-donates own blood for elective surgery; NOT acceptable to most Jehovah’s Witnesses.

  ABO & Rh Blood Grouping

  • Four ABO phenotypes: A, B, AB, O — determined by surface antigens.

  • Rh factor: D antigen present (Rh+) or absent (Rh-).

  • Incompatible transfusion → immune-mediated haemolysis (life-threatening).

  • Compatibility ensured by:

    • Type & screen (ABO/Rh).

    • Cross-match: recipient plasma + donor RBC; agglutination = incompatible.

    • Plasma & platelets require ABO/Rh typing but not formal cross-match.

  Transfusion Procedure & Safety Checklist

  1. Obtain informed consent & baseline vitals.

  2. Large-bore IV (18\text{–}20 G) patent; gather Y-tubing, 0.9\% NS only.

  3. Retrieve blood—must begin within 30 min & complete within \le4 h.

  4. Two RNs verify at bedside: patient ID, unit number, ABO/Rh, expiration.

  5. Remain with patient first 15 min; repeat vitals at 15 min, facility protocol, end of transfusion & +1 h.

  Acute Transfusion Reactions (within 24 h)

  • Acute haemolytic (ABO incompatible): fever, chills, flank pain, haemoglobinuria → DIC, renal failure.

  • Febrile non-haemolytic: temp rise >1\,^{\circ}\text{C} from donor WBC cytokines.

  • Allergic: urticaria → anaphylaxis.

  • TRALI: non-cardiogenic pulmonary oedema.

  • TACO: circulatory overload from rapid infusion.

  Immediate Nursing Actions

  • STOP transfusion, keep IV line with 0.9\% NS.

  • Re-check identifiers, notify provider & blood bank.

  • Send blood bag, tubing, patient blood & urine to lab.

  • Supportive care: O₂, fluids, meds as ordered.

  Delayed Transfusion Reactions ( >24 h – weeks)

  • Delayed haemolytic TR: mild, often unnoticed.

  • TA-GVHD: donor T-cells attack host; usually fatal.

  Acid–Base Balance Essentials

  • pH = “power of H^+”.

    • Normal arterial range 7.35\text{–}7.45.

    • <6.9 or >7.8 incompatible with life.

  • Homeostatic controls

    1. Chemical buffers (instant): bicarbonate, phosphate, proteins.

    2. Respiratory (minutes, transient): adjust CO_2 via rate/depth.

    • ↑ RR → ↓ CO_2 → ↓ H^+ (alkalinises).

    • ↓ RR → ↑ CO_2 → ↑ H^+ (acidifies).

    1. Renal (hours–days, powerful): reabsorb/ excrete HCO_3^- & H^+.

  • Renal impairment => high risk of uncorrected acidosis/ alkalosis.

  Arterial Blood Gas (ABG) Parameters

  • pH : acid–base status.

  • PaCO_2 (35–45 mmHg): respiratory component.

  • HCO_3^- (22–26 mEq·L^{-1}): metabolic component.

  • PaO2 (80–100 mmHg) & SaO2 (95–100 %) assess oxygenation.

  • Disorders named by primary cause

    • Respiratory acidosis/ alkalosis \Rightarrow driven by PaCO_2.

    • Metabolic acidosis/ alkalosis \Rightarrow driven by HCO_3^-.

  (NB: Full ABG interpretation is mastered in Med-Surg.)

  Self-Study — Intravenous Therapy (Required Reading)

  • Calculate IV flow rates & titration.

  • Principles of rehydration therapy.

  • Selecting, initiating & maintaining IV tubing/ infusion pumps.

  • Peripheral vs central venous access devices.

  • Recognition & management of IV-related complications (infiltration, phlebitis, CLABSI, air embolus, catheter occlusion).

Study & Exam Tips

• Memorize normal ranges & critical alarms; practice converting mg/dL ↔ mEq/L if needed.

• Sketch fluid compartments & Na⁺/K⁺ pump for quick recall.

• Pair electrolyte with primary body systems affected (Na⁺ ⇄ neuro, K⁺ ⇄ cardiac, Ca²⁺ ⇄ muscles/bone, Mg²⁺ ⇄ cardiac/neuromuscular).

• Use case scenarios (vomiting child, kidney-failure adult, marathon runner) to rehearse cause–effect–treatment chains.

• Expect fill-in-the-blank items straight from these lecture slides—review every bolded value, sign, and nursing action.