Chapter 27 – Water, Electrolytes & Acid-Base (Fluids) 01

Overview

• Focus: Maintenance of body-fluid homeostasis (water, electrolytes, acid–base) – BIOL 2314 • Chapter 27 • Module 1 (Fluids)
• Key variables continually regulated
  • Total body-water (TBW)
  • Distribution between intracellular fluid (ICF) & extracellular fluid (ECF)
  • ECF subdivisions: plasma, interstitial fluid, plus minor components (lymph, cerebro-spinal fluid, synovial fluid, etc.)
  • Osmolality (≈ solute concentration, expressed in $\text{mOsm}\,\text{kg}^{-1}$)
  • Blood pressure/volume
  • Electrolyte composition (especially $\text{Na}^+$, $\text{Cl}^-$, $\text{K}^+$)
  • Acid–base balance (covered in later modules)

Body-Fluid Compartments

• Percent of body mass occupied by water varies with age, sex & adiposity (adipose tissue contains comparatively little water).
• Table 27.1 – Typical percentage distribution
  • Infants
  • TBW ≈ $75\%$
  • ICF ≈ $45\%$
  • ECF ≈ $30\%$
    • Plasma ≈ $4\%$
    • Interstitial fluid ≈ $26\%$
  • Adult males
  • TBW ≈ $60\%$
  • ICF ≈ $40\%$
  • ECF ≈ $20\%$
    • Plasma ≈ $5\%$
    • Interstitial fluid ≈ $15\%$
  • Adult females
  • TBW ≈ $50\%$ (greater adipose proportion)
  • ICF ≈ $35\%$
  • ECF ≈ $15\%$
    • Plasma ≈ $5\%$
    • Interstitial fluid ≈ $10\%$
  • Minor ECF components (<<1 % each): lymph, cerebrospinal fluid (CSF), aqueous/vitreous humors, synovial fluid, serous fluids, etc.

Water Balance – Intake vs. Loss

• Normal daily turnover: $1500{-}3000\,\text{mL day}^{-1}$ (≈ $\pm$ a full kidney/plasma volume every 24 h!)
• Intake sources
  • Ingested liquids & foods ≈ $90\%$ (driven largely by thirst)
  • Metabolic water ≈ $10\%$ (product of aerobic catabolism; major during starvation/desert adaptation)
• Loss routes
  • Sensible (measurable)
  • Urine ≈ $61\%$ of total, primary route for volume & solute regulation
  • Feces ≈ $4\%$ (variable with diet/diarrhea)
  • Insensible (non-perceptible evaporation)
  • Evaporation ≈ $35\%$
    • Diffusion/evaporation across skin (no sweat glands involved)
    • Respiratory water loss (humidification of inspired air)
  • Perspiration (active sweat)
    • Electrolyte content: $\text{Na}^+$, $\text{Cl}^-$, $\text{K}^+$, urea, ammonia
    • In hot environments: additional $100{-}150\,\text{mL}$ for every $1^{\circ}\text{C}$ rise in core/ambient temperature

Fluid Movement – Hydrostatic vs. Osmotic Forces (Fig. 27.3)

• Starling forces govern exchange between plasma & interstitial compartments
  • Hydrostatic pressure (filtration) – pushes water out of blood at arterial end
  • Colloid osmotic pressure (re-absorption) – pulls water into blood at venous end (primarily due to plasma proteins)
• Scenarios
  • (b) Equal osmotic pressure → no net fluid shift; cells unchanged
  • (c) High interstitial osmolality → water exits capillary; cells may shrink (dehydration)
  • (d) High plasma osmolality → water enters capillary; cells may swell (over-hydration)

Variations in Body-Fluid Volume

• Dehydration (negative water balance)
  • Causes: prolonged diarrhea, excessive sweating, vomiting, inadequate intake
  • Early S/Sx: dizziness, dry mouth, headache, lethargy, muscle weakness
  • Severe S/Sx: delirium, dry skin, fever, sunken eyes, ↓ tissue turgor, ↑ blood viscosity
  • ↑ viscosity → ↓ BP, compensatory ↑ HR; can progress to circulatory collapse/heart failure
• Edema (positive interstitial balance)
  • Definition: Interstitial fluid volume exceeds plasma volume
  • Mechanisms
  1. Inflammation → ↑ capillary permeability to proteins → proteins leak into interstitium → local osmotic gradient pulls water out (exudate)
  2. Venous obstruction / heart failure → ↑ venous hydrostatic pressure → filtration > re-absorption; lymphatic return overwhelmed, fluid accumulates

Regulation Mechanisms

• The body uses overlapping negative-feedback loops to keep
  1. ECF osmolality constant (primarily via water handling)
  2. ECF volume/BP constant (primarily via $\text{Na}^+$ handling)

1. Antidiuretic Hormone (ADH / Vasopressin)

• Sensors
  • Hypothalamic osmoreceptors (sense ↑ plasma osmolality ≥ ≈ $1\%$)
  • Arterial & atrial baroreceptors (sense ↓ BP/BV)
• Integration: Hypothalamus → posterior pituitary releases ADH
• Effectors
  • Kidneys: ↑ water reabsorption by making distal convoluted tubule (DCT) & collecting ducts water-permeable (insertion of aquaporin-2)
  • Arterioles: mild vasoconstriction (↑ total peripheral resistance)
• Outcomes (Fig. 27.9/27.10)
  • ↑ BV, ↑ BP; ↓ plasma osmolality + quenched thirst → HOMEOSTASIS RESTORED
• Decreased osmolality produces reverse sequence → ↓ ADH → diuresis

2. Atrial Natriuretic Hormone (ANH / ANP)

• Trigger: Stretch of right atrial wall (↑ venous return/↑ BP)
• Endocrine source: Atrial myocytes release ANH into bloodstream (Fig. 27.8)
• Renal actions
  • ↑ GFR (dilates afferent, constricts efferent arteriole)
  • Inhibits $\text{Na}^+$ & water reabsorption in collecting duct
  • Inhibits renin, aldosterone, and ADH secretion
• Net effect: ↑ urine volume (natriuresis + diuresis) → ↓ BV & BP

3. Renin–Angiotensin–Aldosterone System (RAAS)

• Trigger: ↓ renal perfusion pressure or sympathetic stimulation → juxtaglomerular apparatus releases renin (Fig. 27.7)
• Sequence
  $\text{Renin} + \text{Angiotensinogen} \rightarrow \text{Angiotensin I}$
  $\text{ACE (lungs)}: \text{Ang I} \rightarrow \text{Angiotensin II}$
• Angiotensin II actions
  • Potent vasoconstrictor → rapid ↑ BP
  • Stimulates adrenal cortex (zona glomerulosa) → ↑ aldosterone
• Aldosterone actions
  • ↑ $\text{Na}^+$ reabsorption (and thus water) & $\text{K}^+$ secretion in distal nephron
  • Net: ↓ urine volume, ↑ BV & BP

Hierarchy / Interactions

• ADH primarily corrects osmolality; RAAS & ANH primarily correct volume/pressure, but all interrelate (e.g., Aldosterone indirectly affects osmolality long-term by changing $\text{Na}^+$ content; ADH affects volume acutely).

Thirst Mechanism (Fig. 27.5)

• Stimuli for thirst perception (hypothalamic thirst center)
  1. ↑ ECF osmolality (hypertonicity) sensed by osmoreceptors
  2. ↓ BP/BV sensed by baroreceptors (and by RAAS via Ang II acting centrally)
• Behavioral effector: Water ingestion (slow; ~30 min to absorb)
• Negative feedback: Ingested water ↓ osmolality & ↑ BV → stretch & sensory feedback to hypothalamus → thirst subsides

Clinical & Practical Notes

• Elderly & infants are at higher risk for dehydration/over-hydration → immature or blunted thirst & hormonal responses.
• Certain pathologies
  • Diabetes insipidus: ADH deficiency or renal insensitivity → massive dilute diuresis, hypernatremia
  • SIADH (syndrome of inappropriate ADH): excessive ADH → water retention, hyponatremia, cerebral edema
  • Congestive heart failure: ↓ effective circulatory volume → chronic RAAS activation → edema (despite total BV excess) – rationale for ACE inhibitors & diuretics.
• Environmental/occupational medicine: Heat stroke risk ↑ with high insensible losses; need electrolyte-containing fluids to replace sweat solutes.

Key Numbers & Relationships (quick-reference)

• Normal plasma osmolality: $\approx 275{-}295\,\text{mOsm}\,\text{kg}^{-1}$
• Daily water turnover: $1.5{-}3.0\,\text{L}$
• Starling equilibrium (simplified):
  $\text{Net filtration} = (P<em>c - P</em>i) - (\pi<em>c - \pi</em>i)$
  where $P$ = hydrostatic pressures, $\pi$ = oncotic pressures, subscripts c = capillary, i = interstitium.
• Sweat electrolyte composition (≈ mmol L$^{-1}$)
  • $\text{Na}^+$ ≈ 40-60, $\text{Cl}^-$ ≈ 40-60, $\text{K}^+$ ≈ 4-8, urea ≈ 5-10, ammonia ≈ 1-2.

Concept Integration / Real-World Relevance

• Homeostatic loops are classic negative feedback systems – foundational concept linking physiology & control theory.
• Pharmacology tie-ins
  • ACE inhibitors, ARBs blunt RAAS → treat hypertension & heart failure
  • V2 receptor antagonists (vaptans) counteract SIADH
  • Diuretics exploit nephron segment physiology to manipulate water & Na$^+$ handling.
• Ethical/practical: Safe fluid therapy requires understanding these mechanisms (e.g., avoiding rapid correction of chronic hyponatremia to prevent osmotic demyelination).