Body fluid: all the water and dissolved solutes in fluid compartments.
Mechanisms regulate: total volume, distribution, concentration of solutes, and pH.
Exchange between compartments occurs only at two sites:
Cell membranes separate intracellular fluid from interstitial fluid.
Capillary walls are thin enough for exchange between plasma and interstitial fluids.
Fluid volumes in each compartment are kept constant. Water follows electrolytes, requiring their balance.
Total body water for a 150 lb male: 40L.
Fluid compartment distribution:
65% Intracellular Fluid (ICF) - 26L
35% Extracellular Fluid (ECF) - 14L
25% Interstitial Fluid - 10L
8% Blood Plasma & Lymph - 3.2L
2% Transcellular Fluid (CSF, synovial fluid, etc.) - 0.8L
Body water comprises 45-75% of body weight, which declines with age.
Gain from ingestion and metabolic processes (2500 mL/day).
Loss normally equals gain through urine, feces, sweat, and breathing.
Routes of loss include urine, feces, expired breath, sweat, and cutaneous transpiration.
Loss varies with environmental conditions and physical activity.
Respiratory loss increases in cold/dry air or heavy exertion.
Perspiratory loss rises with hot/humid conditions or intense physical work.
Types of water loss:
Insensible water loss: breathing and skin evaporation.
Obligatory water loss: minimum urine output (400 mL/day) required for excretion.
Metabolic water formation is unregulated and based on ATP needs.
Main regulator: intake regulation affecting thirst.
Stimulators for thirst include dry mouth, osmoreceptors in hypothalamus, decreased blood volume causing drop in BP and angiotensin II release.
Drinking restores body water levels back to normal.
Causes:
Increased blood osmolarity, stimulated by antidiuretic hormone (ADH).
Thirst center activation and dry mouth sensation lead to water ingestion, resulting in blood rehydration.
Short-term effects: inhibition of thirst upon rehydration.
Long-term effects: sustained impact on fluid homeostasis.
Short-term inhibition: cooling and moistening of the mouth and gastrointestinal tract.
Long-term inhibition: rehydration of blood reduces blood osmolarity, ceasing osmoreceptor response and reducing salivation.
Excess water or solute elimination primarily through urination.
Salty meal consumption demonstrates interaction of three hormones, affecting Na+ and water balance.
Water follows salt; excreting Na+ leads to concurrent water excretion, decreasing blood volume.
Hormonal regulation includes:
Angiotensin II and aldosterone facilitating Na+ and Cl- reabsorption, increasing fluid volume.
Atrial natriuretic peptide (ANP) promotes natriuresis (Na+ excretion), decreasing blood volume.
Increased filtration rates reduce water and Na+ reabsorption.
ADH influences thirst and assists in water reabsorption by enhancing permeability of collecting duct cells.
ADH secretion increases with significant blood volume decreases, severe dehydration, vomiting, diarrhea, sweating, or burns.
Normally, intracellular and interstitial fluids have the same osmolarity, preventing cell swelling or shrinking.
Water intoxication can cause swollen cells if plasma Na+ concentration falls too low due to rapid plain water consumption or improper rehydration post-diarrhea/vomiting.
Fluid Deficiency:
Volume depletion (hypovolemia) with normal osmolarity.
Common causes: hemorrhage, severe burns, chronic vomiting, and diarrhea.
Dehydration:
Total body water decreases, osmolarity increases.
Causes include lack of water intake, diabetes, profuse sweating, and diuretics.
Infants are particularly vulnerable due to higher metabolic rates and surface area-to-volume ratios.
Profuse sweating- causes fluid loss.
Blood volume and pressure drop while osmolarity rises.
Blood absorbs tissue fluid to replace loss.
Fluid is drawn from intracellular fluid (ICF).
Volume excess (hypervolemia): Na+ and water retention leads to isotonic ECF.
Possible causes: aldosterone hypersecretion, congestive heart failure.
Hypotonic hydration: more water retained than Na+, leading to hypotonic ECF and cellular swelling.
Highest concern: pulmonary and cerebral edema.
Relationship between fluid intake and kidney compensation capabilities.
Kidneys manage excess fluid intake well, but struggle with inadequate intake.
Fluid Deficiency: Volume depletion, decreased total body water, isotonic & hypertonic conditions.
Fluid Excess: Volume excess, high total body water, isotonic & hypotonic states.
Functions:
Control osmosis between compartments.
Maintain acid-base balance and carry electrical current.
Cofactors for enzymatic activity.
Concentrations expressed in mEq/liter for plasma, interstitial, and intracellular fluids.
Plasma contains proteins; interstitial fluid does not, affecting blood colloid osmotic pressure.
Na+ and Cl- are predominant in ECF.
K+ and phosphates are prominent in ICF, alongside protein anions.
Membrane potentials are largely sodium-driven.
Na+ accounts for 90-95% of ECF osmolarity.
Na+-K+ pump creates gradients for solute cotransport, generating heat.
Sodium bicarbonate (NaHCO3) plays a significant role in pH buffering.
Primary concern: dietary excess excretion (0.5 g/day necessary; diets often contain 3-7 g/day).
Hormones involved:
Aldosterone: increases renal Na+/K+ pumps, reabsorbing more Na+ and reducing K+.
ADH: increases water reabsorption without Na+ retention.
ANP promotes Na+ and water excretion, lowering BP/volume.
Hypernatremia: Plasma sodium > 145 mEq/L, causing water retention, hypertension, edema.
Hyponatremia: Plasma sodium < 130 mEq/L, resulting from excess body water, quickly corrected by excretion.
Most abundant cation in ICF; crucial for osmolarity, membrane potential, and Na+-K+ pump function.
90% K+ in glomerular filtrate reabsorbed by PCT; DCT and cortical collecting ducts secrete K+ based on blood levels.
Stimulated by hypotension, hyponatremia, and hyperkalemia, leading to increased Na+ reabsorption and K+ secretion.
Supports fluid balance and Na+ concentration for urine output.
Most dangerous electrolyte imbalances.
Hyperkalemia: Acute increases in ECF K+ make muscle cells excitable, while chronic increases result in decreased excitability.
Hypokalemia: Results from sweating, chronic vomiting, laxatives, leading to muscle weakness, reduced reflexes, and arrhythmias.
Hyperkalemia: Increases extracellular K+, causing membrane depolarization and heightened excitability.
Hypokalemia: Lowers extracellular K+, resulting in hyperpolarization and reduced excitability, risking muscle function.
Key for ECF osmolarity, stomach acidity, and pH regulation.
Follows Na+, K+, and Ca2+ passively to maintain balance.
Hyperchloremia: Result of dietary excess IV saline.
Hypochloremia: Typically linked to hyponatremia affecting pH balance.
Essential for skeletal mineralization, muscle contraction, second messenger signaling, exocytosis, and blood clotting.
Regulated by PTH, calcitriol (vitamin D), and calcitonin, affecting bone metabolism and urinary excretion.
Hypercalcemia: Caused by acidosis, hyperparathyroidism, inhibiting depolarization and causing weakness/arrhythmias.
Hypocalcemia: Increased Na+ permeability leads to excitation, with severe cases resulting in tetanus and potential death.
Important in nucleic acids, phospholipids, ATP production, and buffering pH, primarily concentrated in ICF.
Renal control with reabsorption influenced by parathyroid hormone; body tolerates wide variability in phosphate levels.
Major extracellular anion acting as a primary pH buffer, regulated mainly by kidneys that synthesize and excrete bicarbonate as needed.
Acts as a cofactor for metabolic processes, contributing to nerve and muscle function; urinary excretion varies based on calcium status and other factors.
Critical in maintaining H+ concentration within 7.35 - 7.45 pH range.
Regulation mechanisms include buffer systems, respiratory CO2 exhalation, and kidney H+ excretion.
Act to prevent rapid pH changes, some transforming strong acids/bases into weaker forms; key systems include protein, carbonic acid-bicarbonate, and phosphate buffers.
Effective in plasma and intracellular fluids, using hemoglobin in RBCs and albumin in plasma for H+ buffering.
Functions in both ECF and ICF; bicarbonate can act as a weak base, with critical roles in metabolism and respiration.
Buffers strong acids in intracellular environments and urine, maintaining optimal pH balance in accordance with metabolic needs.
Changes in breathing rate adjust blood pH; faster respiration decreases pCO2, raising pH, while slower respiration can lower it.
Excrete H+ from metabolic processes and synthesize bicarbonate, crucial for managing blood pH and addressing acidosis or alkalosis.
Acidosis: Blood pH < 7.35; causes depression of CNS.
Alkalosis: Blood pH > 7.45; causes nervous system excitability leading to spasms and convulsions.
Respiratory system adjusts ventilation for rapid compensation, while renal compensation is slower but more effective for prolonged imbalances.
Evaluated by systemic arterial blood pH, bicarbonate concentration, and PCO2; identify respiratory vs metabolic causes based on these markers.
Infants have higher body water content prone to disturbances, high fluid turnover, immature kidney function, and higher metabolic demands.
Age-related decline in intracellular fluid volume, muscle mass, and renal function complicates fluid and electrolyte balance.