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

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Presentation on theme: "Fluids, Electrolytes, and Acid - Base Balance Chapter 26."— Presentation transcript:

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 H 2 0 volume Extracellular fluid compartment (ECF) ~ 1/3 H 2 O volume – Plasma – Interstitial fluid (IF) Other ECF – Lymph – CSF – GI secretions – Synovial fluids

5 Composition of Body Fluids Nonelectrolytes – Bonds prevent dissociation in H 2 O = no charge – Glucose, lipids, and urea Electrolytes – Dissociate in H 2 O = 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] (HPO 4 2- ) 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* – HP b forces protein-free plasma out into IF – OP b sucks H 2 O out of IF (nondiffusible proteins) – Lymph removes minimal excess IF and ICF more complex b/c of PM – H 2 0 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 H 2 O loss to ECF – Dry mouth from decreased saliva production – Decreased plasma volume – Angiotensin II (Na + reabsorption) Moistening of GI mucosa and distension GI tract inhibit – Prevents overconsumption or overdilution – Not fail proof (exercise, heat, athletic events)

11 Regulating Output Obligatory H 2 O losses are unavoidable, but necessary – Insensible from lungs and skin – Sensible w/ sweat, urine, and feces Kidneys must excrete ingested solutes w/ H 2 O = urine Fluid intake, diet, and sweating regulate too – Increased sweating decreases urine output – Relationship of Na + and H 2 O

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 H 2 O loss from ECF  H 2 O from ICF to ECF to equalize – Electrolytes move out too – Causes: hemorrhage, severe burns, vomiting and diarrhea, profuse sweating, H 2 O 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 +  H 2 O from ECF to ICF Excessive intake of H 2 O Reduced renal filtration (renal failure) Excessive H 2 O 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 O 2 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 H 2 O 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 H 2 O 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 H 2 O retention during menstrual cycles – Cause edema w/ pregnancy Progesterone – Promotes Na + and H 2 O 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 Ca 2+ and PO 4 2- PTH from parathyroid gland – Activates osteoclast activity in bones – Enhances intestinal absorption of Ca 2+ Kidneys to transform vitamin D to active state – Increases Ca 2+ and decreases PO 4 2- reabsorption Calcitonin from thyroid gland – Released w/ increased Ca 2+ 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 CO 2 = increased H + = decreased pH From shallow breathing or inhibition of gas exchange – Respiratory alkalosis Decrease in CO 2 P CO 2 = decreased H + = increased pH From hyperventilation Metabolic imbalances – Metabolic acidosis Decrease in HCO 3 = lowered pH From excessive alcohol, diarrhea, starvation – Metabolic alkalosis Decrease in HCO 3 = 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 H 2 CO 3, NaCl, and NaHCO 3 HCl + NaHCO 3 = NaCl + H 2 CO 3 NaOH + H 2 CO 3 = NaHCO 3 + H 2 O Phosphate – Mimics bicarbonate – Mixture of dihydrogen (H 2 PO 4 - ) and monohydrogen phosphate (PO 3 - ) – Effective in urine and ICF Protein – Plasma and ICF w/highest concentrations – Mixture of carboxyl (COOH) and amine (NH 3 ) groups – Amphoteric molecules can fxn as weak acids or bases


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