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fluid and electrolyte imbalance

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here's short description on fluid and electrolyte imbalances, hope it helps you out !!

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fluid and electrolyte imbalance

  1. 1. Name: laxmi thapa & ravisha pokhrel B.sc nursing 3rd year College of medical sciences, bharatpur
  2. 2.  Help maintain body temperature and cell shape  Helps transport nutrients gases and wastes
  3. 3.  The desirable amount of fluid intake and loss in adults ranges from 1500 to 3500 mL each 24 hours. Ave= 2500 mL  Normally INTAKE = OUTPUT FLUID IMBALANCEFLUID IMBALANCE • Changes in ECF volume = alterations in sodium balance • Change in sodium/water ratio = either hypoosmolarity or hyperosmolarity • Fluid excess or deficit = loss of fluid balance • As with all clinical problems, the same pathophysiologic change is not of equal significance to all people • For example, consider two persons who have the same viral syndrome with associated nausea and vomiting
  4. 4. It is an abnormally decreased or increased fluid volume or rapid shift from one compartment of body fluid to another Hypovolemia Hypervolemia
  5. 5. • May occur as a result of:May occur as a result of: • Reduced fluid intakeReduced fluid intake • Loss of body fluidsLoss of body fluids • Sequestration (compartmentalizing) of body fluidsSequestration (compartmentalizing) of body fluids PathophysiologyPathophysiology DECREASED FLUID VOLUMEDECREASED FLUID VOLUME Stimulation ofStimulation of thirst center inthirst center in hypothalamushypothalamus Person complains ofPerson complains of thirstthirst ↑↑ ADH SecretionADH Secretion ↑↑ Water resorptionWater resorption ↓↓ Urine OutputUrine Output Renin-Angiotensin-Renin-Angiotensin- Aldosterone SystemAldosterone System ActivationActivation ↑↑ Sodium andSodium and Water ResorptionWater Resorption ↑↑ Urine specific gravity exceptUrine specific gravity except with osmotic diuresiswith osmotic diuresis
  6. 6. acute weight loss Oliguria Low bp Sunken eyes Dizziness Weakness Decreased skin turgor Concentrated urine
  7. 7. • Fluid Management • 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 clients cardiovascular status. • Diet therapy – Mild to moderate dehydration. Correct with oral fluid replacement.
  8. 8. Monitor & measures fluids at least every 8 hours and sometimes hourly Monitor daily body weight Monitor vital signs Observe for weak, rapid pulse and orthostatic hypotension Monitor urine concentration by measuring urine specific gravity Assess degree of oral and mucous membrane moisture
  9. 9.  To prevent hypovolemia, the nurse identifies patient at risk and takes measures to minimize fluid loss. For ex: the patient has diarrhoea, measures should be implemented to control diarrhoea and replacement fluid administered. This includes antidiarrheal medication and small volume of oral fluids at frequent intervals
  10. 10.  It refers to an isotonic expansion of the ECF caused by abnormal retention of water and sodium in approximately the same proportion in which they normally exist in the ECF.  It is most often secondary to an increase in total body water.
  11. 11.  Common Causes: Congestive Heart Failure Early renal failure IV therapy Excessive sodium ingestion SIADH Corticosteroid
  12. 12.  Signs/Symptoms Increased BP Weight gain Bounding pulse Venous distention Pulmonary edema  Dyspnea  Orthopnea (diff. breathing when supine)  crackles
  13. 13.  Pharmacological therapy Diuretics such as thiazide diuretics and loop diuretics Thiazide diuretics: hydrochlorothiazide Loop diuretics: furosemide, torsemide  Potassium supplement
  14. 14. I/O chart at regular intervals to identify excessive fluid retention Breath sound are assessed at regular intervals in at risk patient particularly if parenteral fluid are being administered Monitor the degree of edema in most dependent parts of body such as feet & ankles
  15. 15.  If renal function is so severely impaired that pharmacologic agents cannot act efficiently, other modalities are considered to remove sodium and fluid from the body. Haemodialysis or peritoneal dialysis may be used to remove nitrogenous wastes and control potassium and acid base balance and to remove sodium and fluid. Continuous renal replacement therapy may also be required
  16. 16.  IF it is important to detect FVE before the condition become severe. Intervention include promoting rest, restricting sodium intake , monitoring parenteral fluid therapy and administering appropriate medications  Regular rest periods may be beneficial because bed rest favours diuresis of fluid  Sodium and fluid restriction should be instituted as indicated  Fowlers position should be maintain to promote lung expansion
  17. 17. • Controls and regulates volume of body fluidsControls and regulates volume of body fluids • Its concentration is the major determinant of ECF volumeIts concentration is the major determinant of ECF volume •Participates in the generation and transmission of nerveParticipates in the generation and transmission of nerve impulsesimpulses • Eliminated primarily by the kidneys, smaller in fecesEliminated primarily by the kidneys, smaller in feces • Salt intake affects sodium concentrationsSalt intake affects sodium concentrations • Sodium is conserved through reabsorption in the kidneys, aSodium is conserved through reabsorption in the kidneys, a process stimulated by aldosteroneprocess stimulated by aldosterone • Normal value: 135-145 mEq/LNormal value: 135-145 mEq/L
  18. 18.  Refers to the serum sodium concentration less than 135 mEq/L  Common with thiazide diuretic use, but may also be seen with loop and potassium-sparing diuretics as well  Occurs with marked sodium restriction, vomiting and diarrhea, SIADH, etc. The etiology may be mulfactorial  May also occur postop due to temporary alteration in hypothalamic function, loss of GI fluids by vomiting or suction, or hydration with nonelectrolyte solutions  Postoperative hyponatremia is a more serious complication in premenopausal women. The reasons behind this is unknown  Therefore monitoring serum levels is critical and careful assessment for symptoms of hyponatremia is important for all postoperative patients
  19. 19. Sodium loss from the intravascular compartmentSodium loss from the intravascular compartment Diffusion of water into the interstitial spacesDiffusion of water into the interstitial spaces Sodium in the interstitial space is dilutedSodium in the interstitial space is diluted Decreased osmolarity of ECFDecreased osmolarity of ECF Water moves into the cell as a result of sodium lossWater moves into the cell as a result of sodium loss Water moves into the cell as a result of sodium lossWater moves into the cell as a result of sodium loss Extracellular compartment is depleted of waterExtracellular compartment is depleted of water CLINICAL SYMPTOMSCLINICAL SYMPTOMS
  20. 20. Muscle Weakness APATHY Postural hypotensi on Nausea and Abdominal Cramps Weight Loss In severe hyponatremia: mental confusion, delirium, shock and comaIn severe hyponatremia: mental confusion, delirium, shock and coma
  21. 21.  Contributing Factors  Excessive diaphoresis  Wound Drainage  NPO  CHF  Low salt diet  Renal Disease  Diuretics
  22. 22.  Assessment findings:  Neuro - Generalized skeletal muscle weakness. Headache / personality changes.  Resp.- Shallow respirations  CV - Cardiac changes depend on fluid volume  GI – Increased GI motility, Nausea, Diarrhea (explosive)  GU - Increased urine output Plasma osmolality: 2Na + glucose/18 + BUN/2.8
  23. 23.  Interventions/Treatment Restore Na levels to normal and prevent further decreases in Na. Drug Therapy –  (FVD) - IV therapy to restore both fluid and Na. If severe may see 2-3% saline.  (FVE) – Administer osmotic diuretic (Mannitol) to excrete the water rather than the sodium. Increase oral sodium intake and restrict oral fluid intake.
  24. 24. • A serum sodium level above 145 mEq/L is termedA serum sodium level above 145 mEq/L is termed hypernatremiahypernatremia • May occur as a result of fluid deficit or sodiumMay occur as a result of fluid deficit or sodium excessexcess • Frequently occurs with fluid imbalanceFrequently occurs with fluid imbalance • Develops when an excess of sodium occurs without aDevelops when an excess of sodium occurs without a proportional increase in body fluid or when waterproportional increase in body fluid or when water loss occurs without proportional loss of sodiumloss occurs without proportional loss of sodium • Risk Factors: excess dietary or parenteral sodiumRisk Factors: excess dietary or parenteral sodium intake, watery diarrhea, diabetes insipidus, damageintake, watery diarrhea, diabetes insipidus, damage to thirst center, too young, too old, those withto thirst center, too young, too old, those with physical or mental status compromise, and peoplephysical or mental status compromise, and people with hypothalamic dysfunctionwith hypothalamic dysfunction
  25. 25. Increased Sodium concentration in ECFIncreased Sodium concentration in ECF Osmolarity risesOsmolarity rises Water leaves the cell by osmosis and entersWater leaves the cell by osmosis and enters the the extracellular compartmentsthe the extracellular compartments Dilution of fluids in ECFDilution of fluids in ECF Cells are water depletedCells are water depleted Suppression of aldosteroneSuppression of aldosterone secretionsecretion Sodium is exreted in theSodium is exreted in the urineurine CLINICAL SYMPTOMSCLINICAL SYMPTOMS
  26. 26. Dry, sticky mucousDry, sticky mucous membranesmembranes Firm, rubberyFirm, rubbery tissue turgortissue turgor Manic excitementManic excitement TachycardiaTachycardia DEATHDEATH
  27. 27.  Assessment findings: Neuro - Spontaneous muscle twitches. Irregular contractions. Skeletal muscle wkness. 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 r/t fluid volume changes.
  28. 28.  Interventions/Treatment Drug therapy Lowering of serum sodium level by infusion of hypotonic electrolyte solution Diuretics also may be prescribed to treat sodium gain Desmopressin acetate to treat diabetes insipidus if it is cause of hypernatremia Diet therapy  Mild – Ensure water intake
  29. 29.  The nurse should assess for abnormal looses of water or low water intake and for large gains of sodium as might occur with ingestion of OTC medication that have high sodium content  The nurse should obtain a medication history, because some prescription medications have a high sodium content  The nurse also notes the patients thirst or elevated body temperature and evaluates it in relation to other clinical sign and symptoms
  30. 30. The more K, the less Na. The less K, the more NaThe more K, the less Na. The less K, the more Na • Plays a vital role in such processes such as transmission ofPlays a vital role in such processes such as transmission of electrical impulses, particularly in nerve, heart, skeletal,electrical impulses, particularly in nerve, heart, skeletal, intestinal and lung tissue; CHON and CHO metabolism; andintestinal and lung tissue; CHON and CHO metabolism; and cellular building; and maintenance of cellular metabolism andcellular building; and maintenance of cellular metabolism and excitationexcitation • Assists in regulation of acid-base balance by cellularAssists in regulation of acid-base balance by cellular exchange with Hexchange with H •Sources: bananas, peaches, kiwi, figs, dates, apricots,Sources: bananas, peaches, kiwi, figs, dates, apricots, oranges, prunes, melons, raisins, broccoli, and potatoes, meat,oranges, prunes, melons, raisins, broccoli, and potatoes, meat, dairy productsdairy products •Normal value: 3.5 – 5 mEq/LNormal value: 3.5 – 5 mEq/L
  31. 31.  Serum level is below 3.5 meq/l (3.5 mmol/L) usually indicates a deficit in potassium store
  32. 32. = Action Potential= Action Potential Nerve and Muscle ActivityNerve and Muscle Activity LowLow ExtracellularExtracellular K+K+ Increase inIncrease in restingresting membranemembrane potentialpotential The cellThe cell becomes lessbecomes less excitableexcitable
  33. 33. Sodium is retained in the body through resorption by theSodium is retained in the body through resorption by the kidney tubuleskidney tubules Potassium is excretedPotassium is excreted Aldosterone is secretedAldosterone is secreted Use of certain diuretics such as thiazides and furosemide, and corticosteroidsUse of certain diuretics such as thiazides and furosemide, and corticosteroids Increased urinary outputIncreased urinary output Loss of potassium in urineLoss of potassium in urine
  34. 34.  Administration od 40- 80 meq/day of potassium is adequate in adult if there are no abnormal losses of potassium  Dietary intake of potassium in average adult is 50-100meq/day  When dietary intake is inadequate for any reason, oral or IV potassium supplements may be prescribed
  35. 35.  The nurse needs to monitor for its early presence in patients at risk  Fatigue, anorexia, muscle weakness, decreased bowel motility, paraesthesia and dysrhythmias are signal that warrant assessing the serum potasium concentration
  36. 36.  Interventions  Assess and identify those at risk  Encourage potassium-rich foods  K+ replacement (IV or PO)  Monitor lab values  D/c potassium-wasting diuretics  Treat underlying cause
  37. 37.  Serum potassium level greater than 5meq/L  Less common than hypokalaemia , but it is usually dangerous
  38. 38.  Contributing factors:  Increase in K+ intake  Renal failure  K+ sparing diuretics  Shift of K+ out of the cells
  39. 39.  In non acute situations, restriction of dietary potassium and potassium containing medications may correct the imbalance  Administration either orally or by retention enema of cation exchange resins  EMERGENCY PHARMACOLOGIC THERAPYEMERGENCY PHARMACOLOGIC THERAPY  If serum potassium level are dangerously elevated, it may be necessary to adm. IV calcium gluconate  Monitor blood pressure
  40. 40. Patients at risk for potassium excess need to be identified and closely monitored for signs of hyperkalemia Nurse should monitor I/O and observe for signs of muscle weakness and dysrythmias Serum potassium level as well as BUN , creatinine, glucose & arterial blood gas values are monitored for patient at risk for developing hyperkalemia
  41. 41.  Interventions Need to restore normal K+ balance: Eliminate K+ administration Inc. K+ excretion  Lasix  Kayexalate (Polystyrene sulfonate) Infuse glucose and insulin Cardiac Monitoring
  42. 42.  HYPOCHLOREMIA is a serum chloride level below 97meq/L (97mmol/L)
  43. 43.  Irritability  Tremors  Muscle cramps  Hyperactive deep tendon reflexes  Slow shallow respiration  Coma  seizures
  44. 44. Correcting the cause of hypochloremia and contributing electrolytes and acid- base imbalances Normal saline (0.9% sodium chloride) or half strength saline(0.45% sodium chloride) solution is administered by IV to replace the chloride
  45. 45.  Monitor the patient I/O, arterial blood gas values and serum electrolyte levels  Changes in pts level of consciousness, muscle strength and movement and reported to the physician promptly  Vital signs are monitored and respiratory assessment is carried out frequently  Educate the pt about food with high chloride content which include tomato juice, banana, eggs, cheese etc
  46. 46.  Serum level of chloride exceeds 107 meq/L  Hypernatremia, bicarbonate loss and metabolic acidosis can occur with high chloride levels
  47. 47.  Tachypnea  Weakness  Lethargy  Deep and rapid respiration  Hypertension  Dimnished cognitive ability  If untreated it leads to:If untreated it leads to:  Decrease in cardiac output, dysrhythmiasDecrease in cardiac output, dysrhythmias and comaand coma
  48. 48.  Correcting the cause of underlying cause of hyperchloremia and restoring electrolyte fluid and acid base balance are essential  Hypotonic IV solution may be administered to restore balance  Lactated ringers solution may be prescribed to convert lactate to bicarbonate in liver  Diuretics may be administered to eliminate chloride as well  Sodium chloride and fluid are restricted
  49. 49. Monitoring vital sign , arterial blood gas values and I/O is important to assess the patients status and the effectiveness of treatment Assessment findings related to respiratory, neurologic and cardiac systems are documented and changes are discussed with physician Educate about the diet
  50. 50.  More than 90% of body’s calcium is located in the skeletal system  The normal total serum calcium level is 8.6- 10.2 mg/dl (2.2 to 2.6 mmol/L)
  51. 51.  The serum calcium value lower than 8.6mg/dl  Occurs in variety of clinical situation  Older people and those with disabilities, who spend on increased amount of time in bed have an increased risk of hypocalcaemia because bed rest increases bone resorption
  52. 52.  Contributing factors:  Dec. oral intake  Lactose intolerance  Dec. Vitamin D intake  End stage renal disease  Diarrhea
  53. 53.  Contributing factors (cont’d): Acute pancreatitis Hyperphosphatemia Immobility Removal or destruction of parathyroid gland
  54. 54.  Numbness  Tingling of finger, toes and circumoral region  Anxiety  Hyperactive deep tendon reflex  Bronchospasm  diarrhoea
  55. 55.  Assessment findings:  Neuro –Irritable muscle twitches.  Positive Trousseau’s sign.  Positive Chvostek’s sign.  Resp. – Resp. failure d/t muscle tetany.  CV – Dec. HR., dec. BP, diminished peripheral pulses  GI – Inc. motility. Inc. BS. Diarrhea
  56. 56.  Interventions/Treatment  Drug Therapy  Calcium supplements  Vitamin D  Diet Therapy  High calcium diet  Prevention of Injury  Seizure precautions
  57. 57.  Status of airway is clearly monitored  Safety precaution to be taken if confusion is present  Educate the patient about hypocalcemia, and calcium containing foods like milk, yogurt, cheese, sea fruit, legumes, fruits  Avoid overuse of laxatives and antacids
  58. 58.  serum calcium value greater than 10.2 mg/dl  It is a dangerous imbalance when severe infact, hypercalcemic crisis has a mortality rate as high as 50% if not treated promptly
  59. 59.  Contributing factors:  Excessive calcium intake  Excessive vitamin D intake  Renal failure  Hyperparathyroidism  Malignancy  Hyperthyroidism
  60. 60.  Muscular weakness  Constipation  Anorexia  Nausea & vomiting  Dehydration  Hypoactive deep tendon reflexes  Calcium stones
  61. 61.  Assessment findings:  Neuro – Disorientation, lethargy, coma, profound muscle weakness  Resp. – Ineffective resp. movement  CV - Inc. HR, Inc. BP. , Bounding peripheral pulses, Positive Homan’s sign. Late Phase – Bradycardia, Cardiac arrest  GI – Dec. motility. Dec. BS. Constipation  GU – Inc. urine output. Formation of renal calculi
  62. 62.  Interventions/Treatment  Eliminate calcium administration  Drug Therapy  Isotonic NaCL (Inc. the excretion of Ca)  Diuretics  Calcium reabsorption inhibitors (Phosphorus)  Cardiac Monitoring
  63. 63.  Increasing patient mobility and encouraging fluids  Encourage to drink 2.8 to 3.8L of fluid daily  Adequate fiber in diet is encouraged  Safety precaution are implemented
  64. 64.  It is indicated by value below 2.5 mg/dl
  65. 65.  Contributing Factors:  Malnutrition  Starvation  Hypercalcemia  Renal failure  Uncontrolled DM
  66. 66.  Paresthesia  Muscle weakness  Bone pain & tenderness  Chest pain  Confusion  Cardiomyopathy  Seizures  Tissue hypoxia
  67. 67.  Assessment findings: on lab analysis, serum phosphate level is less than 2.5 mg/L Serum magnesium may be decreased due to increased urinary excretion of magnesium X-ray may show skeletal changes of rickets
  68. 68.  MANAGEMENT  Treat underlying cause  Oral replacement with vit. D  IV phosphorus (Severe)  Serum phosphate level should be closely monitored  Diet therapy  Foods high in oral phosphate
  69. 69.  Identify the patient at risk for hypophosphatemia  Close monitoring of patient  Vital signs and monitor serum phosphorous level  Check the level of consciousness  Health education
  70. 70.  Serum phosphorus level that exceeds 4.5mg/dl (1.45 mmol/L)
  71. 71.  Tetany  Tachycardia  Anorexia  Nausea & vomiting  Muscle weakness  Hyperactive reflexes
  72. 72.  Administration of vit.D such as calcitriol which is available both oral ( Rocaltrol) & parenteral ( Calajex, paricalcitol forms)  Calcium binding antacids  Administration of amphojel with meals  Restriction of dietary phosphate, forced diuresis with loop diuretics volume replacement with saline
  73. 73.  Surgery may be indicated for removal of large calcium and phosphorus deposits  Dialysis may also lower phosphorus
  74. 74.  The nurse monitor patient at risk for hyperphosphatemia  If low phosphorus diet is prescribed, patient is instructed to avoid phosphorus rich food such as hard cheese, cream, nuts, meats etc  Nurse instruct patient to avoid phosphate containing laxatives and enemas  Monitoring for chnages in urine output
  75. 75.  HYPOMAGNESEMIAHYPOMAGNESEMIA  Refers to below normal serum magnesiumRefers to below normal serum magnesium concentration 1.3mg/dl (0.62 mmol/L)concentration 1.3mg/dl (0.62 mmol/L)  It is frequently associated with hypokalemiaIt is frequently associated with hypokalemia
  76. 76.  Contributing factors:  Malnutrition  Starvation  Diuretics  Aminoglcoside antibiotics  Hyperglycemia  Insulin administration
  77. 77.  Neuromuscular irritability  Mood changes  Anorexia  Vomiting  Increased bp  Increased deep tendon reflex  insomnia
  78. 78.  Assessment findings: *Neuro - Positive Trousseau’s sign. Positive Chvostek’s sign. Hyperreflexia. Seizures *CV – ECG changes. Dysrhythmias. HTN *Resp. – Shallow resp. *GI – Dec. motility. Anorexia. Nausea
  79. 79.  Mild magnesium deficiency can be corrected by diet alone  Magnesium salt can be administered orally in an oxide or gluonate form  Vital signs must be assessed frequently  Calcium gluconate must be readily available to treat  IV.mgso4
  80. 80.  Observe for its sign and symptom  Safety precaution are institued  Due to dysphagia, patient should be screened  Health education
  81. 81.  Serum magnesium level higher than 2.3 mg/dl  It is a rare electrolyte abnormality because kidney efficiently excrete magnesium
  82. 82.  Contributing factors:  Increased Mag intake  Decreased renal excretion
  83. 83.  Flushing  Hypotension  Muscle weakness  Drowsiness  Depressed respiration  Cardiac arrest  diaphoresis
  84. 84.  Assessment findings: serum magnesium level is greater than 2.3mg/dl creatinine clearance decreases to less than 3.0ml/min ECG finding: prolonged PR interval : tall T waves : widened QRS
  85. 85.  Administration of magnesium  Ventilatory support  IV calcium gluconate  Administration of loop diuretics and sodium chloride  Administration of lactated ringers IV solution
  86. 86.  Risk for hypermagnesemia are identified and assessed  Monitor vital signs, noting hypotension and shallow respiration  Observe for decreased deep tendon reflex and changes in level of consciousness  Caution is essential when preparing and medicating magnesium containing fluid parenterally

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