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Fluids, Electrolytes, and Acid - Base Balance

Fluids, Electrolytes, and Acid - Base Balance. Chapter 26. Body Fluids. Body Water Content. Largest component in body Fxn of age, mass, sex, and body fat Adipose tissue ~ 20% Skeletal muscle ~ 75% Infants ~ 73% Low fat and mass Young men and women ~ 60% and 50%

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Fluids, Electrolytes, and Acid - Base Balance

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  1. Fluids, Electrolytes, and Acid - Base Balance Chapter 26

  2. Body Fluids

  3. Body Water Content • Largest component in body • Fxn of age, mass, sex, and body fat • Adipose tissue ~ 20% • Skeletal muscle ~ 75% • Infants ~ 73% • Low fat and mass • Young men and women ~ 60% and 50% • Relationship of adipose to muscle

  4. Fluid Compartments • Intracellular fluid (ICF) ~ 2/3 H20 volume • Extracellular fluid compartment (ECF) ~ 1/3 H2O volume • Plasma • Interstitial fluid (IF) • Other ECF • Lymph • CSF • GI secretions • Synovial fluids

  5. Composition of Body Fluids • Nonelectrolytes • Bonds prevent dissociation in H2O = no charge • Glucose, lipids, and urea • Electrolytes • Dissociate in H2O = charge = conduct electricity • Inorganic salts, acids and bases, and some proteins • Cations w/ (+) charge, anions w/ (-) charge • Greater contribution to fluid shifting (osmolality)

  6. Comparing Compartments (ECF vs ICF) • All ECF similar • Exception proteins b/c to big to diffuse • [Na+] and [Cl- ] predominate • Non-electrolytes ~ 90% & 60% in plasma & IF • ICF • [K +] and [phosphate] (HPO42-) predominate • [Na+] and [Cl- ] lowest • Na +/K + pumps • Renal reabsorption enhances • Non-electrolytes ~ 97% • Fig 26.2

  7. Fluid Movement • Blood and IF exchange at capillaries* • HPb forces protein-free plasma out into IF • OPb sucks H2O out of IF (nondiffusible proteins) • Lymph removes minimal excess • IF and ICF more complex b/c of PM • H20 responds bidirectionally to [gradients] • Ions by active or facilitated transport • Nutrients, gases, and wastes move unidirectionally

  8. Water Balance

  9. Hydration • Intake must equal output ~2500 ml • Increased plasma osmolality (high solutes) = thirst and ADH release  dark urine • Decreased plasma osmolality = inhibits above  light/clear urine

  10. Regulating Intake • Thirst mechanism stimulates drinking • Regulated by hypothalamic osmoreceptors • Increased plasma osmolality causes H2O loss to ECF • Dry mouth from decreased saliva production • Decreased plasma volume • Angiotensin II (Na+ reabsorption) • Moistening of GI mucosaand distension GI tract inhibit • Prevents overconsumption or overdilution • Not fail proof (exercise, heat, athletic events)

  11. Regulating Output • Obligatory H2O losses are unavoidable, but necessary • Insensible from lungs and skin • Sensible w/ sweat, urine, and feces • Kidneys must excrete ingested solutes w/ H2O = urine • Fluid intake, diet, and sweating regulate too • Increased sweating decreases urine output • Relationship of Na+ and H2O

  12. Regulating ADH’s Role • Hypothalamic osmoreceptors • Decreased ECF osmolality inhibits ADH release • Increased ECF osmolality enhances ADH release • Collecting duct reabsorption reflects ADH release • High ADH = little concentrated urine  why? • Low ADH = dilute urine & reduced body fluid volume • Large blood volume and pressure changes also influence • Prolonged fever, vomiting, sweating, diarrhea, burns • Signals arteriole constriction = increasing BP

  13. Dehydration • Output > intake • H2O loss from ECF  H2O from ICF to ECF to equalize • Electrolytes move out too • Causes: hemorrhage, severe burns, vomiting and diarrhea, profuse sweating, H2O deprivation, diuretic abuse • Signs/symptoms • Early: ‘cottonmouth’, thirst, decreased micturition • Prolonged: weight loss, fever, confusion, hypovolemic shock

  14. Hypotonic Hydration • Intake > output • Increases fluid in ALL compartments • Diluted ECF w/normal Na+ H2O from ECF to ICF • Excessive intake of H2O • Reduced renal filtration (renal failure) • Excessive H2O in ICF swells cells • Signs/symptoms • Early: nausea, vomiting, muscular cramping, cerebral edema • Prolonged: disorientation, convulsions, coma, death • IV’s of hypertonic saline to reverse

  15. Edema • Fluid accumulation in IF (only) swells tissues • Increased fluid flow out of blood into IF • Increased BP and permeability • Increases filtration rate • Hindrance of fluid flow from IF into blood • Blocked/removed lymphatic vessels • Low plasma [proteins] • Disruptions • Increased distance for O2 and nutrient diffusion • Blood volume and BP drop = circulation impairment

  16. Electrolyte Balance

  17. Sodium (Na+) Balance • Primary renal function • No known transport maximum • ~ 65% in PCT and ~ 25% in loop of Henle • Controls ECF volume and H2O distribution • Only cation creating OP • Na+ leaks into cells, but pumped out against electrochemical gradient • Water follows salt • [Na+] relatively stable in ECF • Changes effect plasma volume, BP, ICF and IF volumes • Transport coupled to renal acid-base control

  18. Regulating Na+ Balance: Aldosterone • Effects • High  all Na+ reabsorbed • Decrease urinary output and increase blood volume • Inhibited  no Na+ so excreted w/dilute urine • Renin-angiotensin mechanism primary trigger • JG apparatus releases renin  aldosterone release • Decreased BP, [NaCl], or stretch, or SNS stimulation stimulates

  19. Regulating Na+ Balance: ANP • Reduces BP and blood volume • Inhibits vasoconstriction • Inhibits Na+ and H2O retention • Inhibit collecting duct Na+ reabsorption • Suppresses ADH, renin, and aldosterone release • Atrial stretch releases

  20. Regulating Na+ Balance: Other Hormones • Estrogens • Enhance NaCl reabsorption by renal tubules • Enhance H2O retention during menstrual cycles • Cause edema w/ pregnancy • Progesterone • Promotes Na+ and H2O loss • Blocks aldosterone effects at renal tubules  diuretic • Glucocorticoids • Enhance Na + reabsorption • Increase GFR • Promote edema

  21. Regulating K+Balance • Cortical collecting ducts change K+ secretion • [K+] in plasma primarily influences • High K+ in ECF increases secretion for excretion • Stimulates adrenal cortical release of aldosterone • Aldosterone enhances K+ secretion • High ECF K+ stimulates adrenal cortex for release • Renin-angiotensin mechanism

  22. Regulating Ca2+ and PO42- • PTH from parathyroid gland • Activates osteoclast activity in bones • Enhances intestinal absorption of Ca2+ • Kidneys to transform vitamin D to active state • Increases Ca2+and decreases PO42- reabsorption • Calcitonin from thyroid gland • Released w/ increased Ca2+ levels to encourage deposit • Inhibits bone reabsorption

  23. Acid-Base Balance

  24. Acid – Base Review • Acids • Electrolytes that release H+ in solution • Low pH (1 – 6.9) • Proton donors • Acidosis: pH decrease below homeostatic range • Bases • Electrolytes that release OH- in solution • High pH (7.1 – 14) • Proton acceptors • Alkalosis: pH increase above homeostatic range • Homeostatic ranges • Arterial blood 7.4 • Venous blood and IF 7.35 • ICF 7.0

  25. Acid-Base Abnormality • Respiratory imbalances • Respiratory acidosis • Increase in CO2 = increased H+ = decreased pH • From shallow breathing or inhibition of gas exchange • Respiratory alkalosis • Decrease in CO2 PCO2 = decreased H+ = increased pH • From hyperventilation • Metabolic imbalances • Metabolic acidosis • Decrease in HCO3 = lowered pH • From excessive alcohol, diarrhea, starvation • Metabolic alkalosis • Decrease in HCO3 = lowered pH • Excessive vomiting or intake of bases (antacids)

  26. Chemical Buffering Systems • Resist shifts in pH from strong acids and bases • Bicarbonate • Only ECF buffer, but supports ICF • Mixture of H2CO3, NaCl, and NaHCO3 • HCl + NaHCO3 = NaCl + H2CO3 • NaOH + H2CO3 = NaHCO3 + H2O • Phosphate • Mimics bicarbonate • Mixture of dihydrogen (H2PO4-) and monohydrogen phosphate (PO3-) • Effective in urine and ICF • Protein • Plasma and ICF w/highest concentrations • Mixture of carboxyl (COOH) and amine (NH3) groups • Amphoteric molecules can fxn as weak acids or bases

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