Chapter 25: Fluids, Electrolytes & Acid–Base Balance – Exam Review

Body Fluids

  • Total body water (TBW) depends on:
    • Age: neonates \approx 75\% TBW ↓ to \approx 45\% in elderly.
    • Gender / body composition: ♂ > ♀ because muscle (water-rich) > adipose (water-poor).
    • Fat content: ↑ fat ⇒ ↓ water; ↑ lean mass ⇒ ↑ water.
  • Compartments & volumes (average adult):
    • Intracellular fluid (ICF): \approx \tfrac{2}{3} \text{TBW}.
    • Extracellular fluid (ECF): \approx \tfrac{1}{3} \text{TBW} → plasma (20 %) + interstitial (80 %).
  • Solute composition
    • ICF: \text{K^+},\;\text{Mg^{2+}},\;\text{PO_4^{3-}} dominant.
    • ECF: \text{Na^+},\;\text{Cl^-},\;\text{HCO_3^-} dominant.
  • Electrolytes dissociate into ions → multiply particle number → exert high osmotic pressure; nonelectrolytes (glucose, lipids, urea) do not.
  • Fluid shifts driven by opposing hydrostatic vs. osmotic pressures across capillary & cell membranes; water moves toward higher osmolarity.

Fluid Balance

  • Water gain: beverages/food \approx 2500\,\text{mL day}^{-1} + metabolic water.
  • Water loss: urine (largest), insensible (skin/lungs), sweat, feces.
  • Thirst mechanism (hypothalamus): triggered by ↑ ECF osmolarity, ↓ plasma volume/BP via \text{Ang II}, or dry mouth; quenched as soon as GI distends & osmolarity falls.
  • Water output control (kidney):
    • Obligatory loss \approx 500\,\text{mL} to excrete solutes.
    • Facultative loss adjusted by ADH level.
  • Dehydration: water output > intake; ECF osmolarity ↑, cells shrink → hypovolemia, hypotension.
  • Hypotonic hydration (water intoxication): excess water intake or impaired excretion; ECF osmolarity ↓, cells swell → hyponatremia, cerebral edema.

Hormonal Regulation (DCT & CD)

  • Angiotensin II
    • Stimulus: ↓ BP/BV detected by JG cells; renin converts angiotensinogen → \text{Ang I}; ACE converts \text{Ang I} \to \text{Ang II}.
    • Effects: vasoconstriction, ↑ ALDO & ADH, ↑ thirst.
  • Antidiuretic Hormone (ADH)
    • ↑ ADH → very concentrated, low-volume, dark yellow urine.
    • ↓ ADH → dilute, high-volume, pale/clear urine.
  • Aldosterone (ALDO)
    • ↑ ALDO → Na(^+)/water reabsorption ⇒ low-volume, concentrated urine.
    • ↓ ALDO → Na(^+) loss ⇒ high-volume, dilute urine.
  • Atrial Natriuretic Peptide (ANP)
    • ↑ ANP → natriuresis & diuresis ⇒ very dilute, large-volume, clear urine.
    • ↓ ANP → reduced Na(^+) loss ⇒ smaller, more concentrated urine.

Acid–Base Imbalances

  • Acids
    • Fixed (non-volatile): sulfuric, phosphoric, lactic, keto acids; source = metabolism; kidneys excrete \text{H^+} & regenerate \text{HCO_3^-}.
    • Volatile: \text{CO_2} from aerobic metabolism; lungs expel via ventilation.
  • Buffering systems
    • Physiological: respiratory (minutes) & renal (hours–days).
    • Chemical (instant): bicarbonate, phosphate, protein systems.
  • Bicarbonate buffer: \text{H2CO3} \leftrightarrow \text{H^+} + \text{HCO_3^-}; adds base → drive right; adds acid → drive left.
  • Respiratory disturbances
    • Respiratory acidosis: hypoventilation → \uparrow \text{PCO}2, \downarrow pH; renal compensation \uparrow \text{HCO3^-}.
    • Respiratory alkalosis: hyperventilation → \downarrow \text{PCO}2, \uparrow pH; renal compensation \downarrow \text{HCO3^-}.