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.