BackFluid, Electrolyte, and Acid-Base Balance: Study Notes
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Fluid, Electrolyte, and Acid-Base Balance
Body Fluids and Fluid Compartments
The human body is composed of a significant proportion of water, which varies with age, sex, and tissue type. Understanding the distribution and regulation of body fluids is essential for maintaining homeostasis.
Water Content by Age and Tissue:
Infants: ~73% water (due to low bone mass and fat)
Adults: Water content declines with age; elderly may have as low as 45% water
Sex differences: Males generally have more water (more muscle, less fat) than females
Fluid Compartments:
Intracellular Fluid (ICF): Fluid within cells; ~2/3 of total body water
Extracellular Fluid (ECF): Fluid outside cells; subdivided into:
Plasma: Fluid portion of blood; ~1/3 of ECF
Interstitial Fluid (IF): Fluid between cells in tissues; ~2/3 of ECF
Transcellular Fluid: Specialized ECF compartments (lymph, cerebrospinal fluid, synovial fluid, etc.); grouped with IF for composition
Composition of Body Fluids
Body fluids consist of water and solutes, which are classified as electrolytes or nonelectrolytes.
Electrolytes: Compounds that dissociate into ions in water (e.g., inorganic salts, acids, bases, some proteins)
Nonelectrolytes: Do not dissociate in water; mostly organic (e.g., glucose, creatinine, urea, proteins)
Major Ion Composition
ECF: High in Na+, Cl-, HCO3-; low in K+
ICF: High in K+, Mg2+, HPO42-, proteins; low in Na+
Fluid Movement Between Compartments
Water moves freely between compartments, driven by changes in solute concentration (osmosis). Solutes are not equally distributed, and any change in solute concentration can cause water to shift between compartments.
Regulation of Water Intake and Output
Homeostasis requires a balance between water intake and output.
Intake: Ingested food and water (major source), metabolic water
Output: Insensible loss (exhaled air, skin), sensible loss (urine, sweat, feces)
Regulation of Water Intake
Thirst Mechanism: Controlled by the hypothalamus, triggered by:
Osmoreceptors (detect changes in osmolality)
Dry mouth (decreased saliva)
Decreased blood volume/pressure (baroreceptors, angiotensin II)
Thirst can be quenched quickly, but is not always an accurate indicator of hydration.
Regulation of Water Output
Obligatory Water Loss: Unavoidable loss via kidneys, respiration, feces
Antidiuretic Hormone (ADH):
Released in response to increased ECF osmolality or decreased blood volume
Promotes insertion of aquaporins in distal collecting duct, increasing water reabsorption
Absence of ADH results in dilute urine
Disorders of Water Balance
Imbalances can result from mismatched intake and output or improper distribution between compartments.
Dehydration: Loss of water and/or solutes; causes include hemorrhage, burns, vomiting, diarrhea, sweating, deprivation, diuretics. Symptoms: thirst, dry skin, concentrated urine, confusion, fever, hypovolemic shock.
Hypotonic Hydration (Overhydration): Excess water, insufficient electrolytes; can cause edema, cramps, neuronal damage, death. Often due to excessive water intake during prolonged activity without electrolyte replacement.
Edema: Accumulation of fluid in interstitial space; impairs gas exchange, increases diffusion distance. Results from imbalance in water movement out of and into blood.
Regulation of Electrolytes (Na+, K+, Ca2+, HPO42-)
Electrolyte balance is crucial for nerve, muscle, and cellular function.
Intake: Food and fluids (unprocessed foods preferred; processed foods high in Na+)
Losses: Sweat, feces, urine, vomit
Role of Sodium (Na+)
Most abundant ECF ion; regulates osmotic pressure and fluid balance
Water follows sodium
Concentration: Maintained short-term by water movement; long-term by ADH and thirst
Total Content: Affects ECF volume and blood pressure; regulated by baroreceptors, osmoreceptors, hormones (RAA, ANP)
Hormonal Regulation:
Aldosterone: Increases Na+ reabsorption in DCT and collecting ducts; also increases water reabsorption if ADH is present
Atrial Natriuretic Peptide (ANP): Inhibits Na+ reabsorption, ADH, renin, and aldosterone release
Estrogens: Similar to aldosterone at high levels (can cause bloating)
Neural Control: Baroreceptor reflex adjusts sympathetic output to kidneys based on blood pressure
Potassium (K+) Balance
Regulated by secretion in collecting ducts; controlled by ECF K+ concentration
Aldosterone enhances K+ secretion
Calcium (Ca2+) and Phosphate (HPO42-)
Bone is a reservoir for both ions
Regulated primarily by parathyroid hormone (PTH):
Stimulates osteoclasts (releasing Ca2+ and HPO42- from bone)
Increases Ca2+ reabsorption, decreases HPO42- reabsorption in kidneys
Stimulates calcitriol formation (increases Ca2+ absorption in intestine)
When Ca2+ is high, PTH is inhibited, and calcitonin promotes bone formation
Anions
Cl- generally follows Na+ in excretion/retention
Other anions are excreted if their concentration exceeds renal transport maximum
pH Regulation
Maintaining blood pH (7.35–7.45) is vital for enzyme function and metabolic processes.
Sources of H+
Metabolic processes: protein breakdown, glucose and fatty acid metabolism, CO2 transport
Chemical Buffer Systems
Bicarbonate Buffer System:
Equation:
Buffers strong acids/bases; abundant due to CO2 solubility
Phosphate Buffer System:
Important in ICF and urine; works similarly to bicarbonate system
Protein Buffer System:
Amino acid side groups (NH2, COOH) act as weak acids/bases
Hemoglobin and plasma proteins buffer blood and ICF
Respiratory Regulation of pH
External respiration adjusts blood pH via CO2/H2CO3 equilibrium
Equation:
Increased ventilation raises pH (removes CO2); decreased ventilation lowers pH
Renal Regulation of pH
The kidneys provide long-term pH regulation by excreting or reabsorbing H+ and HCO3-.
Regulate nonvolatile acids (phosphoric, lactic, ketone bodies)
Normally secrete H+ and reabsorb HCO3-
H+ can be secreted or reabsorbed in the proximal convoluted tubule (PCT)
HCO3- can be reabsorbed or produced in PCT and collecting duct
pH Imbalance (Pathology/Abnormalities)
Abnormal pH can be classified as respiratory or metabolic in origin.
Type | Cause | pH Change | Key Features |
|---|---|---|---|
Respiratory Acidosis | CO2 retention (e.g., shallow breathing, pneumonia, emphysema) | pH falls | Impaired gas exchange |
Respiratory Alkalosis | Hyperventilation (stress, pain) | pH rises | CO2 flushed from blood |
Metabolic Acidosis | Low HCO3- (alcohol, diarrhea, lactic acid, ketoacidosis, starvation, kidney failure) | pH falls | Excess acid or loss of base |
Metabolic Alkalosis | Vomiting, diuretics, antacid overuse | pH rises | Loss of acid or excess base |
Compensation for Abnormalities
Respiratory Compensation:
For metabolic acidosis: Increased breathing rate/depth lowers CO2
For metabolic alkalosis: Slow, shallow breathing retains CO2
Renal Compensation:
For acidosis: Retain HCO3-, secrete H+
For alkalosis: Reabsorb H+, secrete HCO3-
Key Equations
Bicarbonate buffer:
Example
Example of Compensation: In diabetic ketoacidosis (a metabolic acidosis), the body compensates by increasing respiratory rate (Kussmaul breathing) to lower CO2 and raise pH.
Additional info: The above notes expand on the original lecture outline by providing definitions, context, and examples for each major concept, as well as a summary table for acid-base imbalances and their compensations.