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FLUIDS AND ELECTOLYTE DISORDERS DR. PADMAJA PALLAVI PANDEY

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  1. 1. DR. PADMAJA PALLAVI PANDEY
  2. 2. INTRODUCTION: FLUIDS & ELECTROLYTE DISORDERS Objectives Fluid Balance Solute Homeostasis Regulation of Body Water Volume Abnormalities Fluid Volume Deficit Fluid Volume Excess
  3. 3. CONT. Basic Metabolic Panel Electrolytes Sodium - Hyponatremia & Hypernatremia Potassium - Hypokalemia & Hyperkalemia Calcium Hypocalcemia & Hypercalcemia Magnesium Hypomagnesemia & Hypermagnesemia
  4. 4. OBJECTIVES Recognize common fluid and electrolyte disorders Clinical presentations Management
  5. 5. 5 Total body water (TBW)
  6. 6. 6 Fluid compartments are separated by membranes that are freely permeable to water but impermeable to solutes. Movement of fluids is due to: hydrostatic pressure differentials osmotic pressure differentials
  7. 7. 7 Fluid Balance
  8. 8. 8 Fluid Balance(Contd) The body tries to maintain homeostasis of fluids and electrolytes by regulating: Volumes Solute charge and osmotic load
  9. 9. 9 Solute Homeostasis Electrolytes charged particles Cations positively charged ions Na+, K+ , Ca++, H+ Anions negatively charged ions Cl-, HCO3 - , PO4 3- Non-electrolytes - Uncharged particles Proteins, urea, glucose, O2, CO2
  10. 10. 10 Maintained by: Ion transport Water movement Kidney function These functions act to keep body fluids: Electrically neutral Osmotically stable (specified number of particles per volume of fluid) Solute Homeostasis
  11. 11. 11 Where sodium goes, water follows. Diffusion movement of particles down a concentration gradient. Osmosis diffusion of water across a selectively permeable membrane Active transport movement of particles up a concentration gradient; requires energy Solute Homeostasis
  12. 12. 12
  13. 13. 13 Regulation of body water The default is get rid of it The control processes include: Release of ADH (antidiuretic hormone) Thirst
  14. 14. Regulation of body water Any of the following: Decreased amount of water in body Increased amount of Na+ in the body Increased blood osmolality Decreased circulating blood volume Results in: Stimulation of osmoreceptors in hypothalamus Release of ADH from the posterior pituitary Increased thirst And thus: water consumption and conservation
  15. 15. 15 Volume Abnormalities Isotonic fluid loss ECF volume, weight loss, dry skin and mucous membranes, urine output: hypovolemic shock
  16. 16. 16 Volume Abnormalities Isotonic fluid gain ECF volume, weight gain, decreased hematocrit, diluted plasma proteins, distended neck veins, B.P: anasarca
  17. 17. 17 Volume Abnormalities Edema the accumulation of fluid within the interstitial space Causes: increased hydrostatic pressure venous obstruction, lymphedema, CHF, renal failure lowered plasma osmotic pressure (protein loss) liver failure, malnutrition, burns increased capillary membrane permeability Inflammation, SIRS, sepsis
  18. 18. 18 Volume Abnormalities Edema the accumulation of fluid within the interstitial space. Results in: increased distance for diffusion impaired blood flow slower healing increased risk of infection pressure sores over bony prominences impaired organ function (brain, liver, gut, kidney)
  19. 19. Fluid Volume Deficit (Hypovolemia, Isotonic Dehydration) Common Causes Hemorrhage Vomiting Diarrhea Burns Diuretic therapy Fever Impaired thirst
  20. 20. Clinical Manifestations Signs/Symptoms Weight loss Thirst Orthostatic changes in pulse rate and BP Weak, rapid pulse Decreased urine output Dry mucous membranes Poor skin turgor
  21. 21. Treatment/Interventions (FVD) Fluid Management Diet therapy Mild to moderate dehydration. Correct with oral fluid replacement. Oral rehydration therapy Solutions containing glucose and electrolytes. E.g., Pedialyte, Rehydralyte. IV therapy Type of fluid , ordered depends on the type of dehydration and the patients cardiovascular status.
  22. 22. Fluid Volume Excess Common Causes: Congestive Heart Failure Early renal failure IV therapy Excessive sodium ingestion SIADH Corticosteroid
  23. 23. Clinical Manifestations Signs/Symptoms Increased BP Bounding pulse Venous distention Pulmonary edema Dyspnea Orthopnea (difficulty in breathing , when supine) Crackles
  24. 24. Treatment/Interventions (FVE) Drug therapy Diuretics may be ordered if renal failure is not the cause. Restriction of sodium and saline intake I/O Weight
  25. 25. Basic Metabolic Panel Na + Cl- BUN Ca++ Glu Mg++ K+ CO3 -- Cr Phos-- 25
  26. 26. 26 Electrolytes
  27. 27. Basic Metabolic Panel Na + Cl- BUN Ca++ Glu Mg++ K+ CO3 -- Cr Phos-- 27
  28. 28. Sodium (Na+) Bulk cation of extracellular fluid change in SNa reflects change in total body Na+ Principle active solute for the maintenance of intravascular & interstitial volume Absorption: throughout the GI system via active Na, K- ATPase system Excretion: urine, sweat & feces
  29. 29. CONT. Kidneys are the principal regulator 2/3 of filtered Na+ is reabsorbed by the proximal convoluted tubule, increase with contraction of extracellular fluid 145 mEq / L Due to Na + or water Water moves from ICF ECF Cells dehydrate
  30. 44. CONT. Due to: Excess Na intake (hypertonic IV solution) Excess Na retention (oversecretion of aldosterone) Loss of pure water Long term sweating with chronic fever Respiratory infection water vapor loss Diabetes (mellitus or insipidus) polyuria Insufficient intake of water (hypodipsia)
  31. 45. CONT. Contributing Factors :- Hyperaldosteronism Renal failure Corticosteroids Increase in oral Na intake Na containing IV fluids Decreased urine output with increased urine concentration.
  32. 46. CONT. Contributing Factors(Contd) :- Diarrhea Dehydration Fever Hyperventilation
  33. 47. CONT. Assessment findings:- Neuro - Spontaneous muscle twitches . Irregular contractions. Skeletal muscle weakness . Diminished deep tendon reflexes Resp. Pulmonary edema CV Diminished CO. HR and BP depend on vascular volume. GU Dec. urine output. Inc. specific gravity. Skin Dry, flaky skin. Edema related to fluid volume changes.
  34. 48. CONT. Evaluation :- Volume Serum sodium, osmolality, BUN/Creatinine Urine sodium, osmolality.
  35. 49. CONT. Interventions/Treatment :- Drug therapy (FVD) .45% NS. If caused by both Na and fluid loss, will administer NaCL . If inadequate , renal excretion of sodium, will administer diuretics. Diet therapy Mild Ensure water intake
  36. 50. CONT. Calculate the free water deficit: 0.6 x wt (kg) x (patients sodium/140 - 1) Correct the free water deficit at a rate of 1mEq/L/hr Check serum Na q4hr Use isotonic salt-free IV fluid
  37. 51. Basic Metabolic Panel Na + Cl- BUN Ca++ Glu Mg++ K+ CO3 -- Cr Phos-- 52
  38. 52. Potassium (K+) Normal range: 3.5-5.0 Largely contained intra-cellular SK does not reflect total body K Important roles: contractility of muscle cells, electrical responsiveness Principal regulator: kidneys
  39. 53. CONT. Daily requirement 1-2 mEq/kg Complete absorption in the upper GI tract Kidneys regulate balance 10-15% filtered is excreted Aldosterone: increase K+ & decrease Na+ excretion Mineralocorticoid & glucocorticoid increase K+ & decrease Na+ excretion in stool
  40. 54. CONT. Solvent drug Increase in Sosmo water moves out of cells K+ follows. Increase 0.6 SK /Increase 10 of Sosmo Evidence of solvent drug in diabetic ketoacidosis Acidosis Low pH shifts K+ out of cells (into serum) High pH shifts K+ into cells 0.3-1.3 mEq/L K+ change / 0.1 unit change in pH in the opposite direction
  41. 55. HYPOKALEMIA (5.0mEq/L) Serum K+ > 5.5 mEq / L Check for renal disease Massive cellular trauma Insulin deficiency Addisons disease Potassium sparing diuretics Decreased blood pH Exercise pushes K+ out of cells Pathophysiology :- An inc. in K+ causes increased excitability of cells.
  42. 60. CONT. Contributing Factors :- Increase in K+ intake Renal failure K+ sparing diuretics Shift of K+ out of the cells
  43. 61. CONT. Interventions/Treatment :- Need to restore normal K+ balance: Eliminate K+ administration Inc. K+ excretion Lasix Kayexalate (Polystyrene sulfonate) Cardiac Monitoring
  44. 62. CONT. 10% Calcium Gluconate or Calcium Chloride Insulin (0.1U/kg/hr) and IV Glucose Metabolic alkalosis (if the patient is acidemic) 1 L H20 with 150meq of NaHCO3 Hemodialysis
  45. 63. Basic Metabolic Panel Na + Cl- BUN Ca++ Glu Mg++ K+ CO3 -- Cr Phos-- 66
  46. 64. Calcium Normal range: 8.8-10.1 with half bound to albumin Ionized (free or active)calcium: 4.4-5.4 relevant for cell function Majority is stored in bone Hypoalbuminemia falsely decreased calcium Cac = Cam + [0.8 x (Albn Alb m)]
  47. 65. CONT. Roles: Coagulation Cellular signals Muscle contraction Neuromuscular transmission Controlled by parathyroid hormone and vitamin D
  48. 66. HYPOCALCEMIA (10.5mg/dl) Contributing Factors :- Excessive calcium intake Excessive vitamin D intake Renal failure Hyperparathyroidism Malignancy Hyperthyroidism
  49. 73. CONT. Assessment findings :- Neuro Disorientation, lethargy, coma, profound muscle weakness Resp. Ineffective resp. movement CV - Inc. HR, Inc. BP. , Bounding peripheral pulses, Positive Homans sign. Late Phase Bradycardia, Cardiac arrest GI Dec. motility. Dec. BS. Constipation GU Inc. urine output. Formation of renal calculi
  50. 74. CONT. Interventions/Treatment :- Eliminate calcium administration Drug Therapy Isotonic NaCL (Inc. the excretion of Ca) Diuretics Calcium reabsorption inhibitors (Phosphorus) Cardiac Monitoring
  51. 75. Basic Metabolic Panel Na + Cl- BUN Ca++ Glu Mg++ K+ CO3 -- Cr Phos-- 78
  52. 76. Magnesium Normal range: 1.5-2.3 60% stored in bone 1% in extracellular space Necessary cofactor for many enzymes Renal excretion is primary regulation
  53. 77. HYPOMAGNESEMIA (2.0mEq/L) Contributing Factors :- Increased Mag intake Decreased renal excretion
  54. 81. CONT. Assessment findings :- Neuro Reduced or weak DTRs. Weak voluntary muscle contractions. Drowsy to the point of lethargy. CV Bradycardia, peripheral vasodilatation, hypotension. ECG changes.
  55. 82. CONT. Interventions/Treatment :- Eliminate contributing drugs Administer diuretic Calcium gluconate reverses cardiac effects Diet restrictions
  56. 83. THANK YOU