ML

CH 8 - Fluid and Electrolyte Balance

Fluid Compartments

  • Total body water ≈ 60\% of body weight.
    • Intracellular fluid (ICF) – 40\%
    • Fluid located inside all body cells.
    • Extracellular fluid (ECF) – 20\%
    • Interstitial fluid → fluid between cells.
    • Intravascular fluid → plasma / fluid within blood vessels.
    • Transcellular fluid (historically called a “third space”) → fluid in specialized cavities (e.g., pleural, peritoneal, synovial) that can accumulate abnormally.

Forces & Physics of Fluid Balance

  • Osmosis
    • Passive movement of water through a semipermeable membrane.
    • Direction: from an area of higher water (lower solute) concentration → lower water (higher solute) concentration.
  • Osmotic pressure
    • Pressure created by osmosis; drives water across the membrane.
  • Hydrostatic force
    • Physical pressure exerted by fluid in the ECF that pushes water toward its destination (e.g., capillary → interstitium).

Tonicity & Cellular Effects

  • Tonicity = comparative osmotic pressure of 2 solutions separated by a membrane.
    • Isotonic
    • Equal solute concentrations inside & outside the cell.
    • No net water movement → cell volume unchanged.
    • Hypotonic
    • Lower solute concentration outside the cell.
    • Water moves into cell → swelling, potential lysis.
    • Hypertonic
    • Higher solute concentration outside the cell.
    • Water moves out of cell → shrinkage (crenation).
  • Cartoon summary (page image):
    • Hypotonic → “Higher water OUTSIDE” → water IN → cell swells.
    • Isotonic → “Equal solute” → no net movement → normal cell.
    • Hypertonic → “Higher solute OUTSIDE” → water OUT → cell shrinks.

Routes of Fluid Loss

  • Renal: urine.
  • Gastrointestinal: feces / diarrhea, NG suction.
  • Skin: sweat.
  • Emesis.
  • Wound drainage – large draining wounds.

Kidney-Mediated Hormonal Regulation

  • Antidiuretic Hormone (ADH)
    • Trigger: hypovolemia ↑ plasma osmolality.
    • Site: posterior pituitary → kidneys.
    • Action: reabsorb free water in distal nephron → ↑ circulating volume, ↑ BP.
  • Aldosterone
    • Trigger: hypovolemia, hyperkalemia, activation of RAAS.
    • Site: adrenal cortex → kidneys.
    • Action: reabsorb Na^+ (and therefore H_2O); excrete K^+ → ↑ volume & BP.
  • RAAS (Renin-Angiotensin-Aldosterone System)
    1. Kidneys sense ↓ BP → juxtaglomerular apparatus releases renin.
    2. Renin converts angiotensinogen (liver) → angiotensin I.
    3. ACE (lung endothelium) converts angiotensin I → angiotensin II.
    4. Angiotensin II effects:
    • Potent vasoconstriction → ↑ systemic vascular resistance → ↑ BP.
    • Stimulates adrenal cortex → aldosterone release → renal Na^+/H_2O reabsorption.
    • Overall ↑ circulating volume & BP.

Fluid Excess (Hypervolemia / Edema)

  • Definitions
    • Edema → excess fluid in interstitial space.
    • Localized vs. generalized (anasarca).
    • Hypervolemia → excess fluid in intravascular space.
    • Water intoxication → excess intracellular water → cellular rupture.
  • Etiologies
    • Inadequate elimination
    • Hyperaldosteronism, Cushing’s, SIADH, renal failure, liver failure, heart failure.
    • Excessive intake
    • High-sodium diet, psychogenic polydipsia, hypertonic IV fluids, excessive water flushes with enteral feeds.
  • Clinical Manifestations
    • Peripheral & periorbital edema, anasarca, cerebral edema.
    • Respiratory: dyspnea, crackles.
    • Cardiovascular: bounding pulse, tachycardia, JVD, hypertension.
    • Renal: polyuria.
    • Neuro: bulging fontanelles (infants).
    • Rapid weight gain.
  • Diagnostics
    • Physical exam, daily weights, strict I&O, serum chemistry, UA, CBC.
  • Management
    • Compression stockings, elevate limbs, fluid & sodium restriction.
    • Diuretics.
    • In severe cases: cautious hypertonic saline to draw fluid into vasculature.

Fluid Deficit (Dehydration / Hypovolemia)

  • Pathophysiology
    • Total body water below physiologic need.
    • Consequences: ↑ serum osmolality / solute concentration, cellular shrinkage, hypotension.
  • Causes
    • Inadequate intake: poor oral intake, inadequate IV replacement.
    • Excess losses: GI (vomit, diarrhea), diaphoresis, prolonged hyperventilation, hemorrhage, nephrosis.
  • Clinical Manifestations
    • Thirst, altered LOC.
    • ↓ BP, tachycardia, weak/thready pulse, flat jugular veins.
    • Dry mucosa, ↓ skin turgor.
    • Oliguria, weight loss, sunken fontanelles (infants).
  • Diagnostics
    • Hx, exam, daily weight, I&O, labs (chemistry, UA, CBC).
  • Management
    • Treat underlying cause.
    • Volume replacement: oral or IV (often isotonic saline initially).

Electrolyte Overview

  • Electrolytes = charged ions in body fluids.
    • Cations: positive (e.g., Na^+, K^+, Ca^{2+}, Mg^{2+}).
    • Anions: negative (e.g., Cl^-, PO4^{3-}, HCO3^-).
  • Electroneutrality: total cations = total anions within each compartment; critical for physiologic stability.

Normal Laboratory Ranges

  • Sodium: 135!–!145 \text{ mEq/L}
  • Chloride: 98!–!108 \text{ mEq/L}
  • Magnesium: 1.8!–!2.4 \text{ mEq/L}
  • Calcium: 8.6!–!10.2 \text{ mg/dL}
  • Potassium: 3.5!–!5 \text{ mEq/L}
  • Phosphorous: 2.5!–!4.5 \text{ mg/dL}

Detailed Electrolyte Functions & Key Associations

  • Sodium (Na^+)
    • Chief ECF cation; drives serum osmolality & water movement.
    • Couples with Cl^- → acid-base influence.
    • Regulation: kidneys & aldosterone.
    • Clinical correlation: neuro status (confusion, seizures).
  • Chloride (Cl^-)
    • Major ECF anion; partners with Na^+ and water to maintain osmotic balance.
    • Participates in acid-base as part of HCl in stomach, chloride shift in RBCs.
    • Excretion: kidneys, sweat.
  • Magnesium (Mg^{2+})
    • Mostly intracellular; stored in bone & muscle.
    • Supports ATP production, neuromuscular transmission, cardiac rhythm stabilization, BP & glucose regulation.
    • Relationships: direct with calcium, inverse with phosphorus.
  • Potassium (K^+)
    • Dominant ICF cation; critical for resting membrane potential.
    • Extra reservoir in cells for rapid shifts.
    • Regulation: kidneys (aldosterone promotes loss), GI losses possible.
    • Clinical: dysrhythmias (both hyper & hypokalemia).
  • Calcium (Ca^{2+})
    • 99\% in bones/teeth; 1\% for neuromuscular transmission & clotting.
    • Controlled by parathyroid hormone & vitamin D.
    • Excretion: urine, feces.
    • Clinical: muscle cramps, tetany, abnormal reflexes with imbalance.
  • Phosphorous (PO_4^{3-})
    • Largely in bone; essential for ATP, RBC function.
    • Inverse relationship with calcium (↑ P → ↓ Ca^{2+}).
    • Manifestations mirror calcium disorders.

Multimedia / Reinforcement Resources

  • Regulation of Fluids (RAAS, ADH, & BNP) – Simple Nursing video (16 min): https://www.youtube.com/watch?v=xOa0n4nTLT8
  • Electrolyte Memorization Tricks – Simple Nursing video (10 min): https://www.youtube.com/watch?v=N1Db7re91GM

Clinical / Ethical / Practical Connections

  • Proper fluid therapy requires vigilance:
    • Over-resuscitation risks pulmonary edema & organ congestion.
    • Under-resuscitation risks hypoperfusion & acute kidney injury.
  • Understanding RAAS is pivotal for pharmacology (ACE inhibitors, ARBs, aldosterone antagonists) and disease management (heart failure, hypertension).
  • Recognize vulnerable populations (infants, elderly, renal/hepatic failure) for tailored fluid & electrolyte management.
  • Ethical implication: balancing life-saving fluid therapy vs. fluid restriction in palliative contexts—patient comfort and goals of care guide choices.