306 Fluids and Electrolytes

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KristaDavis
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306 Fluids and Electrolytes
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2012-09-10 23:32:46
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306 Fluids Lytes
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Exam 1
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  1. Sites of fluids and electrolytes:
    • Intracellular: body cells
    • Extracellular: 
    • -tissue space between cells
    • -blood that fills the vascular compartment
    • -transcellular (3rd space-- CSF, peritoneal, joints)
  2. What spaces make up the "3rd Space" (Transcellular)
    • Cerebral Spinal Fluid
    • Pepritoneal Cavity
    • Joints
  3. Functions of Body Fluids:
    • Transports gases, nutrients and wastes
    • Generates electrical activity
    • Transforms food into energy
    • Maintains overall function
  4. Factors Affecting Fluid Volume and Composition:
    • **Environmental Stress and Disease
    • –Increase fluid loss

    –Impair fluid intake

    • –Interfere with mechanisms that regulate fluid volume,
    • composition, and distribution
  5. What 2 parts work together to distribute fluids properly?
    ICF & ECF
  6. –Larger of the two compartments, makes up approximately two thirds of the body water in healthy adults
    –Consists of fluid contained within all cells in the body
    Intracellular Compartment (ICF)
  7. –Smaller, contains the remaining one third of body water
    –Contains the fluids outside cells: interstitial or tissue
    spaces, blood plasma, transcellular spaces
    Extracellular Compartment (ECF)
  8. Total Water percentage in body:
    60%
  9. Intracellular Water %
    40% body weight
  10. Extracellular Water %
    20% body weight
  11. Composition of the ECF, Plasma, and Interstitial Fluids:
    • *Large amounts of sodium (Na+) and chloride (Cl-)
    • *Moderate amounts of bicarbonate (HC03-)
    • *Small quantities of potassium (K+), calcium (Ca+2), magnesium (Mg+2), and Phosphate (P+)
  12. Composition of the ICF:
    •Large amounts of potassium (K+)

    • •Small amounts of sodium,
    • chloride, bicarbonate, and phosphate

    •Moderate amounts of magnesium

    •Almost no calcium
  13. Molecules that dissociate in solution to form ions:
    ex: NaCl --> Na+  + Cl-
    Electrolytes
  14. Non-electrolytes ______ dissociate in solution:
    • DO NOT
    • (ex: Glucose does NOT dissociate)
  15. The movement of molecules along a concentration gradient
    from an area of higher concentration to one of lower concentration
    Diffusion
  16. The movement of water across a semipermeable membrane from the side of the membrane with the lesser number of particles and greater concentration of water to the side with the greater number of particles and lesser concentration of water
    Osmosis
  17. Water follows ____
    Solutes

    • ex: 
    • Blood= +water, -solute
    • Cell= -water, +solute
    • (water rushes in cell toward the solute)
  18. Concentration of particles in 1 kg (1 L) of water
    Osmolarity
  19. Normal serum osmolality 
    280 - 295 mOsm/L
  20. •The ability of a solution to change the internal water volume of cells
    Tonicity
  21. What are solutions classified according to?
    How much they cause a cell to shrink or swell
  22. Isotonic
    neither shrink nor swell (equal)
  23. Hypotonic
    Cell swells
  24. Hypertonic
    Cell shrinks
  25. Solutes
    Particles
  26. Solution
    Fluid
  27. Capillary - Interstitial Fluid Exchange
    • •Factors favoring movement out of capillary
    • –Capillary filtration pressure
    • (hydrostatic pressure)
    • –Interstitial colloid pressure
    • (tissue oncotic pressure)

    • Factors favoring the movement of fluid back into the capillary
    • –Capillary colloid osmotic pressure (plasma proteins)
    • –Tissue Hydrostatic pressure
  28. Lymph drainage 
  29. Contributions to Edema (swelling)
    –Increase in the capillary filtration pressure (Ex: dependent edema)

    • –Decrease in the capillary colloidal osmotic pressure (loss of
    • serum proteins); burns, kidney and liver disease

    –Increased capillary permeability

    –Obstruction to lymph flow - lymphedema
  30. Methods for Assessing Edema:
    •Daily weight

    •Visual assessment

    •Measurement of the affected part

    •Application of finger pressure to assess for pitting edema
  31. 3rd Space Accumulation
    •Accumulation in transcellular spaces (Ex: CSF, peritoneal, joints)

    •Contributes to body weight but not to fluid reserve or function

    •Peritoneal cavity - acites

    •Pleural cavity - hydrothorax
  32. Water intake through :
    • Liquids/Foods
    • Metabolic reactions
  33. Water loss through:
    –Respiratory tract (expiration)

    –GI tract

    –Skin (perspiration)

    –Kidneys (urine our put)
  34. Normal sodium Levels:
    135-147 mEq/L
  35. Functions of Sodium
    • –Controls ECF osmolality
    • –Participates in active transport (Na+/K+ pump)
    • –Action potentials of muscle, neuron
  36. Where does Sodium enter?
    GI, Meds, IV solutions
  37. Where/How is Sodium lost?
    •kidney, GI, skin

    –Vomiting, diarrhea, enemas, sweat, burns can increase sodium losses
  38. What is they main regulator of sodium?
    Kidney
  39. How does the kidney monitor arterial pressure?
    • It retains sodium when arterial pressure is low.
    • It eliminates sodium when arterial pressure is high.
  40. What is the rate of arterial pressure coordinated by? And what increases reabsorbtion of Na? What decreases the reabsorbtion? 
    • Sympathetic Nervous System and the renin-angiotensin-aldosterone system (RAAS).
    • Aldosterone increases reabsorption of Na
    • Atrial Natriuretic Peptide (ANP) decreases reabsorbtion.
  41. *Primary Regulator of water intake:
    Thirst
  42. Absence of Thirst
    Adipsia
  43. Decreased sensation of thirst:
    Hypodypsia
  44. Excessive Thirst:
    Polydipsia
  45. Regulator of water reabsorbtion that acts on the kidneys...
    Antidiuretic Hormone (ADH)
  46. High Osmolarity causes:
    –Thirst --->  increased water intake

    –ADH release ---> water reabsorbed from urine
  47. Low osmolarity causes:
    –Lack of thirst ---> decreased water intake

    –Decreased ADH release ---> water lost in urine
  48. Factors that affect the release of ADH
    • •Severe pain
    • •Nausea
    • •Trauma
    • •Surgery
    • •Certain anesthetic
    • •Some analgesic drugs 
  49. Abnormality of ADH in Diabetes insipidus
    Deficiency or decreased response to blood volume
  50. –Occurs because of a defect in the synthesis or release of ADH
    •Central or neurogenic diabetes insipidus 
  51. Occurs because the kidneys do not respond to ADH
    Nephrogenic diabetes insipidus 
  52. Fluid Results of Diabetes
    Excessive urination, excessive thirst (if not able to communicate thirst – dehydration)
  53. Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
    •Failure of normal negative feedback system to inhibit ADH – most often from neoplasias, lung and neurologic diseases

    Retention of H2O even when serum sodium levels are too low (dilutional hyponatremia).

    Increase GFR suppresses RAA system

    Suppression of aldosterone → low sodium reabsorption. Serum Na osmolality low; Urine osmolality high
  54. Features of SIADH (Syndrome of Inappropriate Antidiuretic Hormone)
    • Hypotonic hyponatremia
    • Natriuresis
    • Urine osmolality exceeds plasma osmolality
    • Other blood values may also be low
  55. Causes of Fluid Deficit
    •Inadequate fluid intake

    •Excessive gastrointestinal fluid losses

    •Excessive renal losses

    •Excessive skin losses

    •Third-space losses
  56. Causes of Fluid Excess:
    •Inadequate sodium and water elimination

    •Excessive sodium intake in relation to output

    •Excessive fluid intake in relation to output, water intoxication
  57. Water and Electrolytes lost in isotonic proportions:
    Isotonic Fluid Volume Deficit 
  58. Causes of Isotonic Fluid Volume Deficit:
    • –Inadequate fluid intake, excessive GI, renal, or skin losses
    • –Third space losses
  59. Manifestations of Isotonic Fluid Volume Deficit–
    –Weight loss;

    –Increased: ADH, thirst, urine osmolality and SG;

    –Decreased: urine output, loss of skin or tissue turgor, BV and BP
  60. Treatment of Isotonic Fluid Volume Deficit:
    Isotonic Fluid Replacement
  61. •Gain of sodium and water in isotonic proportion
    Isotonic Fluid Volume Excess
  62. Cause of Isotonic Fluid Volume Excess
    • –Decrease in Na and H2O elimination by kidney
    • (CHF, RF)
    • –Excessive Na intake, meds, IV fluids
    • Cushing’s syndrome – corticoid increases Na retention
  63. Manifestation of Isotonic Fluid Volume Excess:
    –Wt gain, edema, increased blood volume and pressure, pulmonary edema
  64. Treatment for Isotonic Fluid Volume Excess:
    diuretics, restricted Na diet
  65. Low serum Na levels ( < 135 mEq/L) 
    Hyponatremia
  66. Causes of Hyponatremia
    Excessive sodium losses, inadequate sodium intake, replacement with Na free fluids; excessive water intake, SIADH
  67. water retained, diluting Na
    Hypotonic (dilutional) hyponatremia
  68. elevated total fluid volume in hyponatremia:
    hypervolemic
  69. Decreased total fluid volume in hyponatremia:
    Hypovolemic
  70. Normal total fluid volume in hyponatremia:
    Isovolemic
  71. Water moves into ECF due to an increase in other molecules:
    Hypertonic hyponatremia
  72. Manifestations of Hyponatremia
    GI (abdominal cramps, N/V/), headache, changes in LOC, seizures, (coma -cerebral edema), edema, muscle cramps, weakness, fatigue, 
  73. Treatment of Hyponatremia:
    •–Lab values, signs & symptoms; loop diuretics, saline solutions
  74. Serum sodium  > 147 mEq/L
    Hypernatremia
  75. Who is at the greatest risk for hypernatrimia?
    Infants and Children
  76. What casues Hypernatremia
    –Excessive intake of Na (salt water drowning, IV )

    –Loss of water (diarrhea, excessive sweating, hypertonic tube feedings, diabetes insipidus)

    –Inability to respond to thirst
  77. Manifestations of Hypernatremia:
    Dehydration: Wt loss, thirst, dry mucous membranes, decreased urine output and BV (tachycardia, weak thready pulse), loss of tissue turgor, agitation, coma
  78. Treatment for Hypernatremia:
    Lab values; Replacement of fluids (ORT)
  79. POTASSIUM (K)
    •Normal level is 3.5-5.5 mEq/L

    •Maintains intracellular osmolarity

    •Controls cell resting potential

    •Needed for Na+/K+ pump

    •Exchanged for H+ to buffer changes in blood pH
  80. Hypokalemia _______ muscle
    contraction; hyperkalemia _____ muscle contraction.
    Decreases; Increases
  81. Potassium Balance
    • Gains – dietary
    • Losses – mainly by kidney

    • Regulations
    • –Kidney – Regulates retention and elimination of K+.

    •Aldosterone causes K+ to be

    •K+-H+ shift: When K+ is increased in serum: K+ secreted into tubule, H+ reabsorbed into blood → drop pH, metabolic acidosis. If serum K+ ↓: K+ reabsorbed, H+ secreted → rise in pH, metabolic alkalosis

    –Transcellular shifts between intracellular and extracellular as needed to regulate K levels

     
  82. Transcellular Shift to regulate K
  83. Serum potassium < 3.5 mEq/L
    Hypokalemia
  84. What causes Hypokalemia
    Poor nutrition, excessive losses (GI, renal, skin), diuretics
  85. What are the manifestations of Hypokalemia
    CV- EKG changes, dysrhythmias

    Postural hypotension

    GI- anorexia, N/V, constipation, paralytic ileus

    Neuromuscular- weakness, fatigue

    Muscle cramps

    Paresthesia

    CNS- irritability, confusion

    Acid-base disorders
  86. Treatment of Hypokalemia
    Lab values; Dietary, oral supplements, IV
  87. Hypokalemia _______ resting potential away from threshold
    (low blood potassium)
    • Lowers
    • (cells fire less easily)
  88. Serum potassium > 5.5 mEq/L
    Hyperkalemia
  89. Causes of Hyperkalemia
    –Excessive intake of potassium (oral potassium supplements, infusion of potassium containing parenteral fluids

    –Release from intracellular compartment (Burns, tissue trauma, crushing injury, extreme exercise)

    • Inadequate elimination by kidneys
    • -Renal failure, adrenal insufficiency, (Addison’s decr aldosterone)
  90. Manifestations of Hyperkalemia
    Neuromuscular- initially- muscle cramps

    Then, inactivation of sodium channels- decrease excitability and Paresthesia Cardiovascular- Serious- EKG changes
  91. Treatment of Hyperkalemia
    Lab values, symptoms, ECG; Calcium can reverse membrane excitability, IV glucose & insulin cause K+ to → cells. Dietary restrictions
  92. Hyperkalemia ________ resting potential toward threshold
    • RAISES
    • –Cells fire more easily
    • –When resting potential reaches threshold, Na+ gates open and won’t close
  93. What are the major divalent cations in the body?
    • Calcium
    • Phosphate
    • Magnesium
  94. How are the major divalent cations of the body (calcium, phosphate, and magnesium) regulated?
    –Ingested in the diet

    –Absorbed from the intestine

    –Filtered in the glomerulus of the kidney

    –Reabsorbed in the renal tubules

    –Eliminated in the urine
  95. Normal Level of Calcium
    Normal serum level 8.5 – 11.0 mg/dL
  96. Function of Calcium:
    • *Most is stored in bone
    • *Blocks sodium gates
    • *Clotting
    • *Intracellularly needed for muscle contraction
    • *Acts as a messenger in hormone and neurotransmitter pathways
  97. Regulation of Calcium
    • *Vitamin D- Maintains plasma levels of calcium and phosphate by increasing
    • *Intestinal absorption

    PTH- low calcium levels cause a release of PTH, removing calcium from bone, decreasing calcium elimination from kidney,  increasing phosphate elimination

    • *Hypoparathyroidism (low PTH)- yields hypocalcemia
    • *Hyperparathyroidism (high PTH)- yields hypercalcemia
    •  
    • *Calcitonin- decreases  serum calcium levels, stores excess in bone

    *Calcium balance inverse to phosphate- If calcium decreases, phosphate increases

     
  98. Hypocalcemia Levels
    Serum calcium < 8.5 mg/dL
  99. What causes Hypocalcemia?
    –Impaired ability to move Ca from bone: Decreased PTH (hypoparathyroidism, Mg deficiency, Vit D deficiency)

    –Abnormal losses (from kidney, pancreatitis)

    Protein binding– alkalosis causes Ca to bind to protein, lowering free levels
  100. Manifestations of Hypocalcemia:
    –Blocks Na channels, so nerves fire more easily: Paresthesia, tetany, muscle cramps, convulsions

    –Chvostek’s and Trousseau’s sign

    –CV – hypotension, cardiac arrhythmias (heart block, V fib), failure to respond to calcium mediated drugs (digitalis, NE, dopamine)
  101. Treatment for Hypocalcemia:
    Lab values: ↓Ca, ↓PTH, ↑Phosphate; Acute: IV calcium solutions; Chronic: oral and dairy supplements
  102. Trousseau's Sign -- ischema-induced carpal spasm that can occur with hyopcalcemia or hypomagnesia
  103. Hypercalcemia levels
    Serum calcium > 11.0 mg/dL
  104. What causes hypercalcemia
    –Increased intestinal absorption (Excessive Vitamin D and calcium, milk-alkali syndrome – calcium + antacids)

    • –Increased bone resorption - Increased levels of parathyroid
    • hormone, malignant neoplasms, prolonged immobilization

    –Decreased elimination - Thiazide diuretic, lithium therapy
  105. Manifestations of Hyprecalcemia:
    –Blocks more Na channels, decreased neural excitability, muscle weakness, lethargy, stupor, coma

    –CV – increased contractility, hypertension, AV block

    –GI – anorexia, N/V, constipation, pancreatitis

    –Renal – kidney stones, impair concentration of urine, thirst, polyuria
  106. Treatment for Hypercalcemia:
    •Lab values, symptoms; Rehydration, diuretics to eliminate Na and Ca in urine
  107. Roles of Phosphate in the body:
    •Plays a major role in bone formation

    •Essential to certain metabolic processes:

    –The formation of ATP and the enzymes needed for metabolism of glucose, fat, and protein

    •Incorporated into the nucleic acids of DNA and RNA and the phospholipids of the cell membrane

    •Serves as an acid-base buffer in the extracellular fluid and in the renal excretion of hydrogen ions

    •Needed for normal function of red blood cells, white blood cells and platelets

    •PTH promotes bone loss of P into serum
  108. Normal levels of Phosphate in the body:
    2.0-6.0 mg/dL
  109. Hypophosphatemia levels:
    Serum phosphate < 2.0 mg/dL

     
  110. Causes of Hypophosphatemia:
    –Malnutrition, insufficient intestinal absorption - high Mg, Ca, Al inhibit absorption of P (antacids), glucocorticoids, alcoholism

    –Transcompartmental shifts - insulin moves glucose and P into cells.

    –Increased renal losses –DKA, drugs
  111. Manifestations of Hypophosphatemia:
    • **Same as increase in calcium
    • Blood- platelet and WBC impairment, hemolytic anemia
    • Neuro- tremors, confusion, coma
    • Musculoskeletal- bone pain, osteomalacia, Rickets
  112. Treatment of Hypophosphatemia:
    Dietary, oral, or IV replacement therapy
  113. Hyperphosphatemia levels:
    Serum phosphate > 6.0 mg/dL
  114. What causes Hyperphosphatemia?
    –Failure of kidneys to excrete P (RF)

    –Shift of P from ICF to ECF (burns, tissue injury)

    –Ingestion of phosphates (laxatives, antacids, enemas)
  115. Manifestations of Hyperphosphatemia:
    **Same as decrease in calcium (see hypocalcemia)
  116. Treatment of Hyperphosphatemia:
    •Lab values; Dietary restriction, phosphate binders, hemodialysis ESRD
  117. ROLES of Magnesium:
    •Cofactor in rx (essential for ATP)

    •Involved in DNA replication, transcription

    •Assists Na/K pump

    •Heart contraction

    •Necessary for PTH function

    •Nerve conduction, ion transport, binds to Ca receptors

    •Regulation: Ingested in diet, excreted by kidneys. Reabsorption stimulated by PTH, inhibited by ↑Ca levels

    •Mg and K levels change together: ↓Mg = ↓K
  118. Normal level of Magnesium:
    1.8-2.4 mg/dL
  119. Levels for Hypomagnesemia:
    Serum magnesium < 1.8 mg/dL
  120. What causes Hypomagnesemia?
    –Malnutrition, excessive Ca intake, alcoholism, diuretics, DKA
  121. Manifestations of Hypomagnesemia:
    –Neuromuscular – ↑ in excitability, muscle weakness, tetany, + Babinski’s, Chvostek’s, Trousseau’s signs, disorientation, psychotic symptoms

    –Cardiovascular - Tachycardia, hypertension, cardiac dysrhythmias

    –Often occurs in combination with hypocalcemia and hypokalemia
  122. Hypermagnesemia Levels:
    Serum magnesium > 2.4 mg/dL
  123. What causes Hypermagnesemia:
    –Excessive intake: laxatives, Mg antacids, IV administration of magnesium for treatment of preeclampsia, excessive use of oral magnesium-containing medications

    Decreased Excretion: Kidney disease, Acute renal failure
  124. Manifestations of Hypermagnesemia:
    –↑Mg suppresses PTH → hypocalcemia, blocks ACh release → muscle weakness, blockade, or respiratory paralysis

    –CV – Hypotension, ↓ BP, arrhythmias

    Neuro – Confusion, coma, hyporeflexive
  125. Treatment for Hypermagnesemia:
    Lab values; IV calcium

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