Week 2 rsc 325 summer

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Week 2 rsc 325 summer

  1. 1. Fluid, Electrolyte, and Acid-Base Imbalances Gould Chapter 6 Presented by:Mahmoud Kaddoura, PhD, CAGS, MSN, RN 1
  2. 2. Fluid Compartments• Continuous exchange of fluids across membranes separating intracellular and extracellular fluid compartments• Large molecules and those that are ionized less able to cross membranes• About 60% of adults’ body weight is water• About 70% of infants’ body is water• Females – higher percentage of fatty tissue, lower water content than males• Older adults and obese – lower proportion of water 2
  3. 3. Fluid Compartments (Cont’d)• Intracellular compartment (ICF)• Extracellular compartment (ECF) – Intravascular fluid (IVF) or blood – Interstitial fluid (ISF) or intercellular fluid – Cerebrospinal fluid (CSF) – Transcellular fluids • Present in various secretions • Pericardial cavity • Synovial cavities 3
  4. 4. Major Body Fluid Compartments 4
  5. 5. Fluid Compartments in the Body 5
  6. 6. Intake and Output of Water• Amount of water entering the body should equal the amount of water leaving the body.• Control of Water Balance:• Essential for homeostasis• Frequent indications for IV therapy include imbalances of – Body fluids – Electrolytes – Acid-base 6
  7. 7. Sources and Losses of Water 7
  8. 8. Movement of Water• Fluid circulates throughout body via filtration and osmosis.• Water moves between compartments via – Hydrostatic pressure – Osmotic pressure 8
  9. 9. Movements of Water between Compartments 9
  10. 10. Control of Fluid Balance• Achieved through complex mechanisms• Most important regulator of fluid intake is thirst• Primary regulators of fluid output : kidneys – Renin-angiotensin mechanism – Aldosterone – Antidiuretic hormone (ADH)• Thirst mechanism – Osmoreceptors in the hypothalamus• Antidiuretic hormone – Promotes reabsorption of water into blood from kidney tubules• Aldosterone – Determines reabsorption of sodium ions and water• Atrial natiuretic peptide – Regulates fluid, sodium and potassium levels 10
  11. 11. Osmolality• Concentration of osmotic solution• Dependent on number of dissolved solutes in a body fluid – Usually sodium, glucose, or urea• Normal osmolality is 275- 295 mOsm/kg• Changes in osmolality can cause water to move to different compartments – Greatest contributor is sodium – Sodium controlled by hormone aldosterone• Tonicity is relative concentration of intravenous fluid – General term, not precise measurement 11
  12. 12. Osmosis• Water moves from area of low osmolality to areas of high osmolality• Hypertonic intravenous fluid – Water moves from interstitial space to plasma• Hypotonic intravenous fluid – Water moves from plasma to interstitial space• Isotonic intravenous fluid – No fluid shift 12
  13. 13. Movement of fluids and solution tonicity 13
  14. 14. Fluid Balance Disorders• Deficit-fluid-balance disorders – Can cause dehydration or shock – Treated with oral or intravenous fluids• Excess -fluid- balance disorders – Treated with diuretics 14
  15. 15. Fluid Excess – Edema• Edema – excessive amount of fluid in the interstitial compartment – Causes swelling or enlargement of tissue – May be localized or throughout the body – May impair tissue perfusion – May trap drugs in ISF
  16. 16. Capillary Exchange
  17. 17. Causes of Edema• Increased capillary hydrostatic pressure – Due to higher blood pressure or increased blood volume – Forces increased fluid out of capillaries into tissue – Cause of pulmonary edema• Loss of plasma proteins – Particularly albumin – Results in decreased plasma osmotic pressure 17
  18. 18. Causes of Edema (Cont’d)
  19. 19. Causes of Edema (Cont’d)• Obstruction of lymphatic circulation – Causes localized edema • Excessive fluid and protein not returned to general circulation• Increased capillary permeability – Usually causes localized edema • May result from an inflammatory response or infection • Histamines and other chemical mediators increase capillary permeablility – Can also result from some bacterial toxins or large burn wounds and result in widespread edema 19
  20. 20. Causes of Edema (Cont’d)
  21. 21. Effects of Edema• Swelling – Pale or red in color• Pitting edema – Presence of excess interstitial fluid – Moves aside when pressure is applied by finger – Depression – “pit” remains when finger is removed• Increase in body weight – With generalized edema
  22. 22. Effects of Edema (Cont’d)• Functional impairment – Restricts range of joint movement – Reduced vital capacity – Impaired diastole• Pain – Edema exerts pressure on nerves locally – Headache with cerebral edema – Stretching of capsule in organs (kidney, liver)• Impaired arterial circulation – Ischemia leading to tissue breakdown 22
  23. 23. Effects of Edema (Cont’d)• Dental practice – Difficult to take accurate impressions – Dentures do not fit well• Edema in skin – Susceptible to tissue breakdown from pressure
  24. 24. Fluid Deficit – Dehydration• Insufficient body fluid – Inadequate intake – Excessive loss – Both• Fluid loss often measured by change in body weight• Dehydration more serious in infants and older adults• Water loss may be accompanied by loss of electrolytes and proteins, e.g., diarrhea.
  25. 25. Causes of Dehydration• Vomiting and diarrhea• Excessive sweating with loss of sodium and water• Diabetic ketoacidosis – Loss of fluid, electrolytes, and glucose in the urine• Insufficient water intake in older adults or unconscious persons• Use of concentrated formula in infants 25
  26. 26. Manifestations of Dehydration• Decreased skin turgor and dry mucous membranes• Sunken eyes• Sunken fontanelles in infant• Lower blood pressure, rapid weak pulse• Increased hematocrit• Increased temperature• Decreasing level of consciousness• Urine: low volume and high specific gravity
  27. 27. Attempts to Compensate for Fluid Loss• Increasing thirst• Increasing heart rate• Constriction of cutaneous blood vessels• Producing less urine• Concentrating urine 27
  28. 28. Third-Spacing of Fluid• Fluid shifts out of the blood into a body cavity or tissue and can no longer reenter vascular compartment – High osmotic pressure of ISF as in burns – Increased capillary permeability as in some gram- negative infections 28
  29. 29. Intravenous Fluid Therapy• Replaces fluids and electrolytes – Uses crystalloids and colloids• Causes of water and electrolyte loss – Gastrointestinal fluid loss, vomiting, diarrhea, laxatives, suctioning – Perspiration, burns, hemorrhage, excessive diuresis, ketoacidosis
  30. 30. Crystalloids• Contain electrolytes• Used to replace fluids and promote urine output• Capable of leaving plasma and moving to interstitial spaces and intracellular fluid• Compartment entered depends on tonicity of intravenous fluid
  31. 31. Colloids• Molecules too large to easily cross capillary membrane – Stay in intravascular space – Rapidly expand plasma volume• Draw water from intracellular fluid and interstitial spaces into plasma – Increases osmotic pressure
  32. 32. Electrolytes• Positively or negatively charged inorganic molecules• Essential to – Nerve conduction, membrane permeability – Water balance, other critical body functions
  33. 33. Distribution of Major Electrolytes 42
  34. 34. Movements of Electrolytes between Compartments 43
  35. 35. Sodium• Essential for maintaining osmolality, water balance, acid-base balance
  36. 36. Sodium and Water Regulation• Water travels with or toward sodium• Sodium movement is link between water retention, blood volume, and blood pressure• Regulated by kidneys and aldosterone• Sodium major electrolyte in extracellular fluid
  37. 37. Figure 31.3 Renal regulation of sodium and potassium balance
  38. 38. Sodium Imbalance• Review of sodium – Primary cation in ECF – Sodium diffuses between vascular and interstitial fluids – Transport into and out of cells by sodium- potassium pump – Actively secreted into mucus and other secretions – Exists in form of sodium chloride and sodium bicarbonate – Ingested in food and beverages 47
  39. 39. Hyponatremia• Sodium level below 135 mEq/L• Caused by excessive dilution of plasma – Excess antidiuretic hormone (ADH) secretion – Excessive administration of hypotonic intravenous solution• Vomiting, diarrhea, gastrointestinal suctioning, diuretic use• Causes – Losses from excessive sweating, vomiting, diarrhea – Use of certain diuretic drugs combined with low-salt diets – Hormonal imbalances • Insufficient aldosterone • Adrenal insufficiency • Excess ADH secretion – Diuresis – Excessive water intake 48
  40. 40. Hyponatremia and Fluid Shift into Cells
  41. 41. Symptoms of Hyponatremia• Early symptoms – Nausea, vomiting, anorexia, abdominal cramping• Later signs – Altered neurologic function such as confusion, lethargy, convulsions, coma, muscle twitching, tremors
  42. 42. Effects of Hyponatremia• Low sodium levels – Cause fluid imbalance in compartments • Fatigue, muscle cramps, abdominal discomfort or cramps, nausea, vomiting• Decreased osmotic pressure in ECF compartment – Fluid shift into cells • Hypovolemia and decreased blood pressure – Cerebral edema • Confusion, headache, weakness, seizures 51
  43. 43. Treatment of Hyponatremia• Hyponatremia caused by excessive dilution – Treat with loop diuretics to cause an isotonic diuresis• Hyponatremia caused by sodium loss – Treat with oral sodium chloride or intravenous fluids containing salt • Normal saline • Lactated Ringers
  44. 44. Hypernatremia• Sodium level above 145 mEq/L• Most commonly caused by kidney disease• Sodium accumulates – Decreased excretion – High, net water loss (watery diarrhea, fever, burns) – High doses of glucocorticoids or estrogens• Cause is imbalance in sodium and water – Insufficient ADH (diabetes insipidus) • Results in large volume of dilute urine – Loss of the thirst mechanism – Watery diarrhea – Prolonged periods of rapid respiration – Ingestion of large amounts of sodium without enough water 53
  45. 45. Physiology of Hypernatremia• Elevated sodium increases osmolality of plasma – Draws fluid from interstitial space and cells – Causes cellular dehydration• Signs and symptoms – Thirst, fatigue, weakness, muscle twitching – Convulsions, altered mental status, decreased level of consciousness
  46. 46. Effects of Hypernatremia• Weakness, agitation• Dry, rough mucous membranes• edema• Increased thirst (if thirst mechanism is functional)• Increased blood pressure 55
  47. 47. Treatment of Hypernatremia• Can be treated with low-salt diet• Acute hypernatremia treated with hypotonic intravenous fluids or diuretics
  48. 48. Potassium Balance• Essential for – Proper nerve and muscle function• Maintaining acid-base balance• Influenced by aldosterone – For each sodium ion reabsorbed, one potassium ion secreted into renal tubules• Imbalances can be serious , even fatal
  49. 49. Potassium Imbalance• Review of potassium – Major intracellular cation – Serum levels are low with a narrow range – Ingested in foods – Excreted primarily in urine – Insulin promotes movement of potassium into cells – Levels influenced by the acid-base balance – Abnormal potassium levels cause changes in cardiac conduction and are LIFE-THREATENING! 58
  50. 50. Sodium and Potassium Affect Nerve Conduction 59
  51. 51. Causes of Hypokalemia (serum K+ <3.5 mEq/L)• Potassium level below 3.5 mEq/L• Caused by – High doses of loop diuretics – Strenuous muscle activity – Severe vomiting• Excessive losses due to diarrhea• Diuresis associated with some diuretic drugs• Excessive aldosterone or glucocorticoids – i.e., Cushing syndrome• Decreased dietary intake – May occur with alcoholism, eating disorders, starvation• Treatment of diabetic ketoacidosis with insulin
  52. 52. Symptoms of Hypokalemia• Neurons and muscle fibers most sensitive to potassium loss• Muscle weakness, lethargy, anorexia, dysrhythmias, cardiac arrest
  53. 53. Effects of Hypokalemia• Cardiac dysrhythmias – Due to impaired repolarization > cardiac arrest• Interference with neuromuscular function – Muscles less responsive to stimuli• Paresthesias – “pins and needles”• Decreased digestive tract motility• Severe hypokalemia: – Shallow respirations – Failure to concentrate urine – polyuria 62
  54. 54. Treatment of Hypokalemia• Mild- increase dietary intake• Severe – give oral or parenteral potassium supplements
  55. 55. Causes of Hyperkalemia (serum K + >5 mEq/L)• Potassium level above 5 mEq/L• Caused by high consumption of potassium-rich food, dietary supplements• Risk with client taking potassium-sparing diuretics• Accumulates when renal disease causes decreased excretion• Renal failure• Deficit of aldosterone• “Potassium-sparing” diuretics• Leakage of intracellular potassium into the extracellular fluids – In patients with extensive tissue damage• Displacement of potassium from cells by prolonged or severe acidosis
  56. 56. Relationship of Hydrogen and Potassium Ions 65
  57. 57. Symptoms of Hyperkalemia• Most serious are dysrhythmias, and heart block• Other symptoms are muscle twitching, fatigue, parasthesias, dyspnea, cramping, and diarrhea
  58. 58. Effects of Hyperkalemia• Cardiac dysrhythmias – May progress to cardiac arrest• Muscle weakness common – Progresses to paralysis – May cause respiratory arrest – Impairs neuromuscular activity• Fatigue, nausea, paresthesias
  59. 59. Treatment of Hyperkalemia• Restrict dietary sources• Decrease dose of potassium-sparing diuretics• Administer glucose and insulin• Administer calcium to counteract potassium toxicity on heart• Administer polystyrene sulfonate (Kayexalate) and sorbitol to decrease potassium levels
  60. 60. Signs of Potassium Imbalance
  61. 61. Calcium Imbalance• Review of calcium – Important extracellular cation – Ingested in food – Stored in bone – Excreted in urine and feces – Balance controlled by parathyroid hormone (PTH) and calcitonin – Vitamin D promotes calcium absorption from intestine • Ingested or synthesized in skin in the presence of ultraviolet rays • Activated in kidneys
  62. 62. Functions of Calcium• Provides structural strength for bones and teeth• Maintenance of the stability of nerve membranes• Required for muscle contractions• Necessary for many metabolic processes and enzyme reactions• Essential for blood clotting
  63. 63. Causes of Hypocalcemia• Hypoparathyroidism• Malabsorption syndrome• Deficient serum albumin• Increased serum pH• Renal failure
  64. 64. Effects of Hypocalcemia• Increase in the permeability and excitability of nerve membranes – Spontaneous stimulation of skeletal muscle • Muscle twitching • Carpopedal spasm – Tetany• Weak heart contractions – Delayed conduction – Leads to dysrhythmias and decreased blood pressure
  65. 65. Causes of Hypercalcemia• Uncontrolled release of calcium ions from bones – Neoplasms; malignant bone tumors• Hyperparathyroidism• Demineralization due to immobility – Decrease stress on bone• Increased calcium intake – Excessive vitamin D – Excess dietary calcium• Milk-alkali syndrome 74
  66. 66. Effects of Hypercalcemia• Depressed neuromuscular activity – Muscle weakness, loss of muscle tone – Lethargy, stupor, personality changes – Anorexia, nausea• Interference with ADH function – Less absorption of water – Decrease in renal function• Increased strength in cardiac contractions – Dysrhythmias may occur 75
  67. 67. Magnesium Imbalances• Magnesium – Intracellular ion – Hypomagnesemia • Results from malabsorption or malnutrition often associated with alcoholism • Use of diuretics, diabetic ketoacidosis, hyperthyroidism, hyperaldosteronism – Hypermagnesemia • Occurs with renal failure • Depresses neuromuscular function • Decreased reflexes 76
  68. 68. Phosphate Imbalances• Phosphate – Bone and tooth mineralization – Important in metabolism – ATP – Phosphate buffer system – acid-base balance – Integral part of the cell membrane – Reciprocal relationship with serum calcium – Hypophosphatemia • Malabsorption syndromes, diarrhea, excessive antacids – Hyperphosphatemia • From renal failure
  69. 69. Chloride Imbalance• Chloride – Major extracellular anion – Chloride levels related to sodium levels – Chloride and bicarbonate ions can shift in response to acid-base imbalances – Hypochloremia • Usually associated with alkalosis – Early stages of vomiting – loss of hydrochloric acid – Hyperchloremia • Excessive sodium chloride intake
  70. 70. Chloride Shift 79
  71. 71. The Hydrogen Ion and pH Scale 80
  72. 72. Control of Serum pH• Buffer pairs in the blood respond to pH changes immediately.• Respiratory system can alter carbonic acid levels to change pH.• Kidneys can modify the excretion rate of acids and absorption of bicarbonate ions to regulate pH. – Most significant control mechanism – Slowest mechanism
  73. 73. Changes in Acids, Bicarbonate Ion, and Serum pH in Circulating Blood 82
  74. 74. Buffer Systems• Sodium bicarbonate–carbonic acid system – Major ECFbuffer – Controlled by the respiratory system and the kidneys• Other buffering systems: – Phosphate – Hemoglobin – Protein 83
  75. 75. Compensation Mechanisms for pH Imbalance• Compensation is limited and usually short term.• Does not remove the cause of imbalance• Compensation occurs to balance the relative proportion of hydrogen ions and bicarbonate ions in circulation: – Buffers – Change in respiration – Change in renal function 84
  76. 76. Decompensation• Occurs when: – Causative problem becomes more severe – Additional problems occur – Compensation mechanisms are exceeded or fail• Requires intervention to maintain homeostasis• LIFE-THREATENING! 85
  77. 77. Acid-Base Imbalance• Acidosis is excess acid (pH below 7.35)• Alkalosis is excess base (pH above 7.35)• Both symptoms of underlying disorder• Acidosis – Excess hydrogen ions – Decrease in serum pH• Alkalosis – Deficit of hydrogen ions – Increase in serum pH• Both may be fatal if not treated rapidly• Body uses buffers to maintain overall pH within normal limits• Kidneys and lungs collaborate to remove excess metabolic acid 86
  78. 78. Figure 31.4 Acid–base imbalances
  79. 79. Acidosis• May be respiratory , caused by hypoventilation• May be metabolic – Causes: diarrhea, kidney failure, diabetes, excess alcohol, starvation
  80. 80. Respiratory Acidosis• Acute problems – Pneumonia, airway obstruction, chest injuries – Drugs that depress the respiratory control center• Chronic respiratory acidosis – Common with chronic obstructive pulmonary disease• Decompensated respiratory acidosis – May develop if impairment becomes severe or if compensation mechanisms fail
  81. 81. Metabolic Acidosis• Excessive loss of bicarbonate ions to buffer hydrogen – Diarrhea – loss of bicarbonate from intestines• Increased use of serum bicarbonate• Renal disease or failure – Decreased excretion of acids – Decreased production of bicarbonate ions• Decompensated metabolic acidosis – Additional factor interferes with compensation 91
  82. 82. Effects of Acidosis• Impaired nervous system function – Headache – Lethargy – Weakness – Confusion – Coma and death• Compensation – Deep rapid breathing – Secretion of urine with a low pH 92
  83. 83. Changes in Blood Gases with Acidosis 93
  84. 84. Pharmacotherapy of Acidosis• Symptoms affect central nervous system – Lethargy, confusion, coma – Deep, rapid respirations in attempt to blow off excess acid• Goal is to quickly reverse effects of excess acid in blood• Administration of bicarbonate is appropriate pharmacotherapy
  85. 85. Alkalosis• May be respiratory – Cause: hyperventilation due to asthma, anxiety, high altitude• May be metabolic – Prolonged constipation, excess sodium bicarbonate, diuretics that cause potassium depletion, severe vomiting• Respiratory alkalosis – Hyperventilation • Caused by anxiety, high fever, overdose of aspirin • Head injuries • Brainstem tumors• Metabolic alkalosis – Increase in serum bicarbonate ion • Loss of hydrochloric acid from stomach • Hypokalemia • Excessive ingestion of antacids
  86. 86. Effects of Alkalosis• Increased irritability of the nervous system – Causing restlessness – Muscle twitching – Tingling and numbness of the fingers – Tetany – Seizures – Coma 96
  87. 87. Pharmacotherapy of Alkalosis• Symptoms are due to central- nervous- system stimulation – Nervousness, hyperactive reflexes, convulsions – Slow, shallow respirations in attempt to retain acid
  88. 88. Pharmacotherapy of Alkalosis (continued)• Treatment – Administration of ammonium chloride (severe cases) – Administration of sodium chloride with potassium chloride (mild cases)
  89. 89. Role of The Healthcare Provider• Monitor client’s condition• Provide client education• Obtain medical, surgical and drug history• Assess lifestyle and dietary habits• Obtain baseline weight and vital signs, level of consciousness, breath sounds, and urinary output
  90. 90. Role of The Healthcare Provider (continued)• Evaluate electrolytes, CBC, urine specific gravity and urinalysis, BUN and creatinine, total protein and albumin levels, aPTT, aPT or INR, renal and liver function studies)
  91. 91. Colloid Solutions• Monitor fluid-volume status (both deficits and excess)• Assess neurologic status and urinary output• Report hematocrit below 30% to physician immediately• Teach client to report bleeding, hypersensitivity, or fluid-volume overload
  92. 92. Sodium Replacement Therapy• Assess sodium and electrolyte balance• Be alert for signs of hyponatremia or hypernatremia• Monitor serum sodium levels, urine specific gravity, serum and urine osmolarity
  93. 93. Sodium Replacement Therapy (continued)• Client should report symptoms that may relate to fluid overload• Client should drink water or balanced sports drinks to replenish lost fluids and electrolytes
  94. 94. Potassium Replacement Therapy• Monitor for cardiac abnormalities• Contraindicated in cases of severe renal impairment• Do not use with potassium-sparing diuretics• Contraindicated in acute dehydration, heat cramps, clients with digoxin intoxication with AV node disturbance• Take with meals to avoid irritating GI tract
  95. 95. Sodium Bicarbonate Therapy• Monitor arterial blood gas reports• Use cautiously in clients with cardiac disease or renal impairment• Clients should use alternative OTC antacids to prevent excess sodium or bicarbonate from being absorbed into systemic circulation
  96. 96. Ammonium Chloride Therapy• Assess pH in arterial blood-gas levels prior to administration• Contraindicated in presence of liver disease• Infuse slowly to avoid ammonium toxicity, and decrease irritation to veins
  97. 97. Fluid Replacement Agents - Colloids• Prototype drug: dextran 40 (Gentran 40, Hyskon, 10% LMD, Rheomacrodex)• Mechanism of action: to raise oncotic pressure of blood; expands plasma volume within minutes of administration
  98. 98. Dextran
  99. 99. Fluid Replacement Agents – Colloids (continued)• Primary use: as fluid replacement with hypovolemic shock from hemorrhage, surgery, severe burns• Adverse effects: hypersensitivity reactions, fluid overload, hypertension
  100. 100. Electrolytes• Prototype drug: sodium chloride• Mechanism of action: as electrolyte/sodium supplement• Primary use: to treat hyponatremia when serum levels fall below 130mEq/L• Adverse effects: hypernatremia and pulmonary edema
  101. 101. Electrolytes (continued)• Prototype drug: potassium chloride• Mechanism of action: as electrolyte/potassium supplement• Primary use: to treat hypokalemia• Adverse effects: GI irritation, hyperkalemia; contraindicated in clients with chronic renal failure or those taking potassium-sparing diuretic
  102. 102. Potassium chloride
  103. 103. Acid-Base Agents• Prototype: sodium bicarbonate• Mechanism of action: to decrease pH of body fluids• Primary use: metabolic alkalosis caused by receiving too much bicarbonate ion and hypokalemia
  104. 104. Sodium Chloride
  105. 105. Patients receiving drug therapy for fluid-balance, electrolyte, and acid-base disorders• Assessment – Obtain a complete health history – Obtain drug history, including allergies and possible drug interactions – Assess for presence of fluid-volume deficit – Assess for the presence of fluid-volume deficit – Obtain CBC, serum electrolytes, renal function (BUN and serum creatinine), total protein and albumin levels, aPTT, aPT or INR, and liver function studies
  106. 106. Patients receiving drug therapy for fluid-balance,electrolyte, and acid-base disorders (continued) • Diagnoses – Deficient fluid volume – Decreased cardiac output – Fatigue – Activity Intolerance – Deficient Knowledge (drug therapy)
  107. 107. Patients receiving drug therapy for fluid-balance,electrolyte, and acid-base disorders (continued)• Diagnoses – Risk for Falls – Risk for Injury (related to hypotension, dizziness associated with adverse effects) – Risk for Excessive Fluid Volume (related to drug therapy); – Risk for Ineffective Health Maintenance (regarding drug effects and dietary needs)
  108. 108. Drug Therapy for Fluid-Balance,electrolyte, and Acid-Base Disorders• Planning – patient will – Report effects: itching, shortness of breath, flushing, cough, heart palpitations – Exhibit signs of normal fluid volume – Demonstrate an understanding of drug’s action
  109. 109. Patients receiving drug therapy for fluid-balance,electrolyte, and acid-base disorders (continued) • Implementation – Monitor hemodynamic status every 15 to 60 minutes – Monitor for • Hypersensitivity reactions • Circulatory overload • Changes in CBC results • IV sites ( potassium)
  110. 110. Patients receiving drug therapy for fluid-balance,electrolyte, and acid-base disorders (continued) • Implementation – Teach client to • Eat foods rich in potassium (hypokalemia) • Avoid foods rich in potassium and salt substitutes (hyperkalemia)
  111. 111. Patients receiving drug therapy for fluid-balance,electrolyte, and acid-base disorders (continued) • Evaluation –client – Experiences increased urinary output and relief of dehydration, electrolyte values within normal limits). – Is free from, or experiences minimal adverse effects
  112. 112. Patients receiving drug therapy for fluid-balance,electrolyte, and acid-base disorders (continued)• Evaluation –client – Verbalizes an understanding of the drug’s use, adverse effects and required precautions – Demonstrates proper self-administration of the medication (e.g., dose, timing, when to notify provider).
  113. 113. Drugs for Nutritional Disorders 123
  114. 114. Vitamins• Organic substances are needed in small amounts – Promote growth – Maintain health
  115. 115. Vitamins (continued)• Human cells cannot produce vitamins – Exception: vitamin D – Vitamins or provitamins must be supplied in diet – Deficiency will result in disease
  116. 116. Vitamins Serve Important Roles in Function of Body• Vitamin B complex: coenzymes essential to metabolic processes• Vitamin A: precursor of retinol needed for normal vision• Vitamin D: regulates calcium metabolism• Vitamin K: needed to produce prothrombin
  117. 117. Lipid-Soluble Vitamins (A, D, E, K)• Must be ingested with lipids to be absorbed in small intestine• Excess stored in liver and adipose tissue – Can be removed from storage areas and used as needed• Excessive intake can lead to dangerously high levels
  118. 118. Vitamin A
  119. 119. Water-Soluble Vitamins (C, B Complex)• Absorbed with water in digestive tract• Easily dissolved in blood and body fluids
  120. 120. Water-Soluble Vitamins (C, B Complex) (continued)• Excess cannot be stored – Excreted in urine – Must be ingested daily
  121. 121. Folic Acid
  122. 122. Recommended Dietary Allowances (RDAs)• Minimum amount of a vitamin needed to prevent symptoms of deficiency• Need for vitamins and minerals varies among individuals• Supplements should never substitute for healthy diet
  123. 123. Vitamin Pharmacotherapy• Indicated for certain conditions – Poor nutritional intake – Pregnancy – Chronic-disease states
  124. 124. Symptoms of Deficiency• Usually nonspecific; occur over prolonged period• Often result of certain factors – Poverty, fad diets – Chronic alcohol or drug abuse – Prolonged parenteral feeding• Clients often present with multiple deficiencies
  125. 125. Deficiencies in Lipid-Soluble Vitamins• Vitamin A (retinol) – Obtained from foods containing carotenes• Vitamin D – D2 (ergocalciferol)—from dairy products – D3—from ultraviolet light
  126. 126. Deficiencies in Lipid-Soluble Vitamins (continued)• Vitamin E (tocopherols) – Found in plant-seed oils, whole-grain cereals, eggs, certain organ meats – Primary antioxidant
  127. 127. Deficiencies in Lipid-Soluble Vitamins (continued)• Vitamin K—mixture of several chemicals – K1 obtained from plant sources – K2 obtained from microbial flora in colon – Needed for clotting
  128. 128. Deficiencies in Water-Soluble Vitamins• Vitamin C deficiency can cause scurvy• Thiamine (B1) deficiency can cause beriberi• Niacin (B3) deficiency can cause pellagra
  129. 129. Deficiencies in Water-Soluble Vitamins (continued)• Cyanocobalamin (B12) deficiency can cause pernicious or megaloblastic anemia• Deficiencies of riboflavin (B2), folic acid (B9), pyridoxine (B6) – Indicate need for pharmacotherapy with water- soluble vitamins
  130. 130. Minerals• Inorganic substances• Very small amounts needed to maintain normal metabolism• Constitute 4% of body weight• Can be obtained from normal diet• Excess minerals can be toxic
  131. 131. Magnesium
  132. 132. Role of the Nurse• Monitor client’s condition• Provide client education• Obtain medical, surgical, drug history• Assess lifestyle and dietary habits• Obtain description of symptomology and current therapies
  133. 133. Drug Therapy with Fat-Soluble Vitamins• Teach client that excessive vitamin intake can be harmful• Assess for deficiency• Assess for impaired liver function
  134. 134. Drug Therapy with Fat-Soluble Vitamins (continued)• Assess for chronic overdose of vitamins• Consider socioeconomic status and culture of client – Recommend foods that treat deficiency • Recommend foods that are affordable for and liked by client
  135. 135. Water-Soluble Vitamin Therapy• Thiamine administered for hospitalized clients with severe liver disease• Niacin and pyridoxine may cause severe flushing – Expected reaction for client; no permanent harm – Assess women of childbearing age for folic acid deficiency – Prior to attempting or during pregnancy
  136. 136. Water-Soluble Vitamin Therapy (continued)• Recommend multivitamin to avoid overdose• Caution clients with history of kidney stones against using vitamin C• Advise clients taking vitamin C to increase fluid intake• Water-soluble vitamins are not stored in the body – Must be replenished daily
  137. 137. Macromineral Therapy• For mineral deficiencies or eclampsia• Large doses can cause life-threatening adverse effects• Encourage well-balanced diet – Eliminates or reduces need for supplements
  138. 138. Macromineral Therapy (continued) • If calcium prescribed – Inform health-care provider of use of glucocorticoids, thiazide diuretics, tetracyclines – Avoid zinc-rich foods, which impair calcium absorption
  139. 139. Macromineral Therapy (continued) • If phosphorus prescribed – Inform health-care provider if on sodium- or potassium-restricted diet – Immediately report seizure activity; stop drug – Avoid antacids
  140. 140. Macromineral Therapy (continued)• If client is taking magnesium sulfate, immediately report – Changes in consciousness, deep tendon reflexes – Thirst, confusion
  141. 141. Macrominerals• Seven major (macro) minerals – Calcium, chlorine, magnesium, phosphorous – Potassium, sodium, sulfur• Must be obtained daily from dietary sources in amounts of 100 mg or greater
  142. 142. Microminerals (continued)• Nine trace (micro) minerals – Include iron, iodine, fluorine, and zinc• Required daily amount is 20 mg or less
  143. 143. Undernutrition• Many causes – Low dietary intake – Malabsorption disorders – Fad diets – Wasting disorders such as cancer or AIDS
  144. 144. Undernutrition (continued)• Reasons for low dietary intake vary – Poverty, depression, difficulty eating• Nutritional consultation is appropriate
  145. 145. Enteral Nutrition• Provided orally or through feeding tube• Means of meeting client’s nutritional needs
  146. 146. Classification of Enteral Products• Oligomeric (Vivonex, T.E.N., Peptamen)• Polymeric—most common type (Compeat, Sustacal, Ensure)• Modular—given to supplement single nutrient (Casec, Polycose, Microlipid, MCT Oil)• Specialized—given for special disease states (Amin-Aid, Hepatic-Aid II, Pulmocare)
  147. 147. Total Parenteral Nutrition (TPN) • Also known as hyperalimentation • Means of supplying nutrition to clients – Peripheral vein (short term) – Central vein (long term) • Administered through infusion pump for precise monitoring
  148. 148. Vitamin Pharmacotherapy — Lipid –Soluble Vitamins• Prototype drug: Vitamin A• Mechanism of action: – Essential for general growth and development – Necessary for proper wound healing – Essential for the biosynthesis of steroids, – One of the pigments required for night vision
  149. 149. Vitamin Pharmacotherapy — Lipid – Soluble Vitamins (continued)• Primary use: pregnancy, lactation, or undernutrition, night blindness and slow wound healing• Topical forms are available for acne, psoriasis
  150. 150. Vitamin Pharmacotherapy — Lipid – Soluble Vitamins (continued)• Adverse effects: – Acute ingestion, produces serious CNS toxicity- headache, irritability, drowsiness, delirium, and possible coma. – Long-term ingestion of high amounts - drying and scaling of the skin, alopecia, fatigue, anorexia, vomiting, and leukopenia
  151. 151. Vitamin Pharmacotherapy - Water –Soluble Vitamin• Prototype drug: Folic Acid ( Folacin).• Mechanism of action: administered to reverse symptoms of folate deficiency – 1 mg/day of oral folic acid often reverses the deficiency symptoms within 5 to 7 days
  152. 152. Vitamin Pharmacotherapy - Water – Soluble Vitamin (continued)• Primary use: during pregnancy to promote normal fetal growth – Patients with inadequate intake, such as with chronic alcohol abuse.• Adverse effects: uncommon but – Patients may feel flushed following IV injections. – Allergic hypersensitivity to folic acid by the IV route is possible
  153. 153. Mineral Pharmacotherapy - Mineral Supplement• Prototype drug: Magnesium Sulfate• Mechanism of action: – Essential for proper neuromuscular function. – Also serves a metabolic role – in activating certain enzymes in the breakdown of carbohydrates and proteins
  154. 154. Mineral Pharmacotherapy -Mineral Supplement (continued)• Primary use: – Severe hypomagnesemia – To prevent or terminate seizures associated with eclampsia – Oral forms used as cathartics for complete evacuation of the colon – Use of magnesium sulfate is restricted to severe magnesium deficiency
  155. 155. Mineral Pharmacotherapy -Mineral Supplement (continued)• Adverse effects: – Early signs of overdose include • Flushing of the skin, sedation, confusion, intense thirst, and muscle weakness – Extreme levels cause neuromuscular blockade leading to • respiratory paralysis, heart block, and circulatory collapse.
  156. 156. Patients Receiving Vitamin and Mineral Pharmacotherapy• Assessment – Obtain complete health history and complete physical examination – Obtain a history of vitamin deficiencies or hypervitaminosis – Obtain a dietary history noting adequacy of essential vitamins, minerals and nutrients
  157. 157. Patients Receiving Vitamin and Mineral Pharmacotherapy (continued)• Assessment – Note sunscreen use and amount of sun exposure – Obtain weight and vital signs – Evaluate., CBC, electrolytes, hepatic and renal function studies, ferritin and iron levels – Assess for and promptly report adverse effects
  158. 158. Patients Receiving Vitamin and Mineral Pharmacotherapy (continued)• diagnoses – Imbalanced nutrition: less than body requirements – Impaired Health Maintenance, (related to dietary habits, deficient knowledge); – Deficient knowledge, related to drug therapy – Readiness for Enhanced Therapeutic Regimen Management – Risk for Injury (related to adverse drug effects, hypervitaminosis).
  159. 159. Patients Receiving Vitamin and Mineral Pharmacotherapy (continued)• Planning—patient will – Experience maintenance of overall health, symptoms of previous deficiency are absent. – Be free from, or experience minimal adverse effects – Verbalize an understanding of the drug’s use, adverse effects and required precautions – Demonstrate proper self-administration of the medication (e.g., dose, timing, when to notify provider)
  160. 160. Patients Receiving Vitamin and Mineral Pharmacotherapy (continued)• Implementation – Treat the cause: correct the deficiency – Review dietary and supplement history for hypervitaminosis and adverse drug effects. – Monitor the use of fat-soluble vitamins [A, D, E, and K] for possible toxic effects – Monitor liver function
  161. 161. Patients Receiving Vitamin and Mineral Pharmacotherapy (continued)• Implementation – Encourage adequate intake of vitamin and folic- acid rich foods prior to conception – Instruct patient to keep pre-natal vitamins out of reach of children – Ensure adequate hydration if large doses of water- soluble vitamins are taken. – Encourage client to take medication appropriately
  162. 162. Patients Receiving Vitamin and Mineral Pharmacotherapy (continued)• Evaluation – Experiences maintenance of overall health, symptoms of previous deficiency are absent – Is free from, or experiences minimal adverse effects – Verbalizes an understanding of the drug’s use, adverse effects and required precautions – Demonstrates proper self-administration of the medication (e.g., dose, timing, when to notify provider)
  163. 163. Patients Receiving Parenteral Nutrition• Assessment – Obtain complete health history and complete physical examination – Obtain a drug history including allergies, and possible drug interactions – Obtain baseline height, weight and vital signs – Assess for the presence or history of nutritional deficits
  164. 164. Patients Receiving Parenteral Nutrition (continued)• Assessment – Evaluate appropriate laboratory findings (e.g., • CBC, electrolytes, glucose, BUN • hepatic and renal function studies • total protein, serum albumin, lipid profile, serum iron levels – Assess for and promptly report adverse effects
  165. 165. Patients Receiving Parenteral Nutrition (continued)• diagnoses – Risk for infection – Imbalanced nutrition: less than body requirements – Risk for imbalanced fluid volume – Deficient knowledge, related to drug therapy
  166. 166. Patients Receiving Parenteral Nutrition (continued)• Planning—patient will – Experience maintenance or improvement of overall health and nutritional status – Be free from, or experience minimal adverse effects – Verbalize an understanding of the drug’s use, adverse effects and required precautions – Demonstrate proper self-administration of the medication (e.g., dose, timing, when to notify provider)
  167. 167. Patients Receiving Parenteral Nutrition (continued)• Implementation – Monitor vital signs • Observe for signs of infection, such as elevated temperature – Assess patient’s ability to take oral nutrition and encourage small oral feedings if allowed – Assess all access sites (e.g., gastric tube site, I.V. or port sites) frequently for • redness, streaking, swelling, or drainage
  168. 168. Patients Receiving Parenteral Nutrition (continued)• Implementation – Monitor for signs of fluid overload – Observe for signs of hyperglycemia or hypoglycemia • Monitor blood-glucose levels – Monitor renal status – intake and output, daily weight, serum creatinine and BUN
  169. 169. Patients Receiving Parenteral Nutrition (continued)• Implementation – Maintain accurate infusion rate with infusion pump • make rate changes gradually • avoid abruptly discontinuing TPN feeding – Refrigerate TPN solution until 30 minutes before using – Assess for appropriate enteral tube placement before administering any feeding.
  170. 170. Patients Receiving Parenteral Nutrition (continued)• Implementation – Report any fever, chills, malaise, or changes in mental status immediately – Use strict aseptic technique with all I.V. tubing or bag changes, site dressing changes – Instruct patient and/or family in proper self- administration of drug
  171. 171. Patients Receiving Parenteral Nutrition (continued)• Evaluation- patient – Experiences maintenance or improvement of overall health and nutritional status – Is free from, or experiences minimal adverse effects – Verbalizes an understanding of the drug’s use, adverse effects and required precautions – Demonstrates proper self-administration of the medication (e.g., dose, timing, when to notify provider)
  172. 172. Critical Thinking Review Question 1Which of the following mechanisms is the most important regulator of fluid intake?
  173. 173. Critical Thinking Review Question 1 – Choices1. Thirst2. Electrolytes3. Renin–angiotensin4. Kidneys
  174. 174. Critical Thinking Review Question 1 – Answer1. Thirst2. Electrolytes3. Renin–angiotensin4. Kidneys
  175. 175. Critical Thinking Review Question 1 – RationaleRationale: Thirst is the most important regulatorof fluid intake.Cognitive Level: AnalysisNursing Process: AssessmentPatient Need: Physiological Integrity
  176. 176. Critical Thinking Review Question 2Which of the following nursing interventions is most important when caring for a patient receiving a plasma volume expander?
  177. 177. Critical Thinking Review Question 2 – Choices1. Assess the patient for deep vein thrombosis2. Observe for signs of fluid overload3. Encourage fluid intake4. Monitor arterial blood gases
  178. 178. Critical Thinking Review Question 2 – Answer1. Assess the patient for deep vein thrombosis2. Observe for signs of fluid overload3. Encourage fluid intake4. Monitor arterial blood gases
  179. 179. Critical Thinking Review Question 2 – RationaleRationale: Dextran 40, a plasma volumeexpander, causes fluid to move rapidly from thetissues to vascular spaces, which places thepatient at risk for fluid overload.Cognitive Level: AnalysisNursing Process: ImplementationPatient Need: Physiological Integrity
  180. 180. Critical Thinking Review Question 4The patient complains of muscle cramping in the calves, paresthesia of the toes, and the sensation of the heart skipping a beat. These symptoms may indicate which one of the following imbalances?
  181. 181. Critical Thinking Review Question 4 – Choices1. Hypernatremia2. Hypercalcemia3. Hypoglycemia4. Hyperkalemia
  182. 182. Critical Thinking Review Question 4 – Answer1. Hypernatremia2. Hypercalcemia3. Hypoglycemia4. Hyperkalemia
  183. 183. Critical Thinking Review Question 4 – RationaleRationale: Hyperkalemia, a serum potassiumlevel greater than 5 mEq/L, predisposes thepatient to cardiac and muscle irregularities suchas cramping in the calves, paresthesia of thetoes, and palpitations.Cognitive Level: AnalysisNursing Process: DiagnosisPatient Need: Physiological Integrity
  184. 184. Critical Thinking Review Question 5A patient will be sent home on diuretic therapy and will need to increase the amount ofpotassium in the diet. What food choices would the nurse suggest be added?
  185. 185. Critical Thinking Review Question 5 – Choices1. Liver, red meats, lettuce2. Apples, pears, celery, onions3. Bananas, tomatoes, beans, fresh meats4. Potato chips, licorice, rice, corn
  186. 186. Critical Thinking Review Question 5 – Answer1. Liver, red meats, lettuce2. Apples, pears, celery, onions3. Bananas, tomatoes, beans, fresh meats4. Potato chips, licorice, rice, corn
  187. 187. Critical Thinking Review Question 5 – RationaleRationale: Bananas, strawberries, tomatoes,dried beans, and fresh meats are natural sourcesof potassium. The other food items have lowlevels of potassium but may be part of a healthydiet.Cognitive Level: ApplicationNursing Process: ImplementationPatient Need: Physiological Integrity
  188. 188. NCLEX-RN Review Question 6 The nurse weighs the patient and finds thatthere has been a weight gain of 1.5 kg since the previous day. What would be the nurse’s next highest priority?
  189. 189. NCLEX-RN Review Question 6 – Choices1. Check with the patient to see if there have been any dietary changes in the last few days.2. Assess the patient for signs of edema and BP for possible hypertension.3. Contact dietary to change the patient’s diet to reduced sodium.4. Request a diuretic from the patient’s provider.
  190. 190. Critical Thinking Review Question 6 – Answer1. Check with the patient to see if there have been any dietary changes in the last few days.2. Assess the patient for signs of edema and BP for possible hypertension.3. Contact dietary to change the patient’s diet to reduced sodium.4. Request a diuretic from the patient’s provider.
  191. 191. Critical Thinking Review Question 6 – RationaleRationale: A weight gain of 1 kg (approximately2 lb) or more may indicate fluid retention. Signsof fluid retention include hypertension andedema. A complete nursing assessment isneeded to determine other signs or symptomsthat may be present. Checking dietary historymay be considered after the nursing assessmentis completed.
  192. 192. Critical Thinking Review Question 6 – Rationale (cont)Changing diet or medications is part of thecollaborative treatment plan with the healthcare provider.Cognitive Level: AnalysisNursing Process: AssessmentPatient Need: Physiological Integrity
  193. 193. Nutrition Questions 207
  194. 194. Critical Thinking Review Question 1 An older adult has been diagnosed with pernicious anemia and replacement therapy isordered. The nurse will anticipate administering which vitamin, and by what technique?
  195. 195. Critical Thinking Review Question 1 – Choices1. B6, orally in liquid form2. K, via intramuscular injection3. D, by light-box therapy or increased sun exposure4. B12, by intramuscular injection
  196. 196. Critical Thinking Review Question 1 – Answer1. B6, orally in liquid form2. K, via intramuscular injection3. D, by light-box therapy or increased sun exposure4. B12, by intramuscular injection
  197. 197. Critical Thinking Review Question 1 – RationaleRationale: Pernicious anemia results in theinability to absorb vitamin B12 due to the lack ofintrinsic factor in the gut. Replacement therapymust be administered via intramuscularinjection because oral supplementation will notbe absorbed. Pernicious anemia affects vitaminB12 absorption.
  198. 198. Critical Thinking Review Question 1 – Rationale (cont)Cognitive Level: ApplicationNursing Process: ImplementationPatient Need: Physiological Integrity
  199. 199. Critical Thinking Review Question 3The nurse is assessing a patient who is exhibiting generalized weakness, cardiac dysrhythmias, hypertension, loss of deep tendon reflexes, andrespiratory distress. What could be the possible cause of these symptoms?
  200. 200. Critical Thinking Review Question 3 – Choices1. Hypocalcemia2. Hypercalcemia3. Hypomagnesemia4. Hypermagnesemia
  201. 201. Critical Thinking Review Question 3 – Answer1. Hypocalcemia2. Hypercalcemia3. Hypomagnesemia4. Hypermagnesemia
  202. 202. Critical Thinking Review Question 3 – RationaleRationale: Hypomagnesemia should beassessed. Patients experiencinghypomagnesemia may experience generalweakness, dysrhythmias, hypertension, loss ofdeep tendon reflexes, and respiratorydepression.Cognitive Level: AnalysisNursing Process: AssessmentPatient Need: Physiological Integrity
  203. 203. Critical Thinking Review Question 4The patient is a long-time alcoholic. The nurse understands that alcoholism is the most common cause of which vitamin deficiency?
  204. 204. Critical Thinking Review Question 4 – Choices1. Vitamin E2. Vitamin A3. Vitamin D4. Thiamine
  205. 205. Critical Thinking Review Question 4 – Answer1. Vitamin E2. Vitamin A3. Vitamin D4. Thiamine
  206. 206. Critical Thinking Review Question 4 – RationaleRationale: Alcohol is known for its ability toinhibit the absorption of thiamine and folic acid.Alcohol abuse is the most common cause ofthiamine deficiency.Cognitive Level: AnalysisNursing Process: ImplementationPatient Need: Physiological Integrity
  207. 207. Critical Thinking Review Question 5 The patient is a 12-year-old child withhemophilia. The nurse is aware that this patient will require administration of which vitamin to improve the function of clotting factors?
  208. 208. Critical Thinking Review Question 5 – Choices1. Folic acid2. Riboflavin3. Vitamin K4. Vitamin A
  209. 209. Critical Thinking Review Question 5 – Answer1. Folic acid2. Riboflavin3. Vitamin K4. Vitamin A
  210. 210. Critical Thinking Review Question 5 – RationaleRationale: Vitamin K should be given to thepatient to improve clotting. Without vitamin K,abnormal prothrombin is produced and bloodclotting is affected.Cognitive Level: AnalysisNursing Process: ImplementationPatient Need: Physiological Integrity
  211. 211. Critical Thinking Review Question 6 Total parenteral nutrition (TPN) has been ordered for a patient with gastric cancer who isno longer able to maintain oral intake. The nurse notes that the patient has a temperature of 100.4º F. What should the nurse assess first?
  212. 212. Critical Thinking Review Question 6 – Choices1. The date the TPN was ordered2. The patient’s last electrolyte levels, particularly glucose3. The intravenous access site and all IV equipment and TPN bag4. The patient’s last chest x-ray report
  213. 213. Critical Thinking Review Question 6 – Answer1. The date the TPN was ordered2. The patient’s last electrolyte levels, particularly glucose3. The intravenous access site and all IV equipment and TPN bag4. The patient’s last chest x-ray report
  214. 214. Critical Thinking Review Question 6 – RationaleRationale: TPN access sites, tubing, and parenteralnutrition bag are all areas at risk for contamination andfor bacteria to enter the patient. The nurse shouldassess the IV access site for redness, streaking,swelling, or drainage and all tubing and bag for signs ofcracks, cloudiness, or precipitate. Glucose levels andTPN orders will be assessed periodically but do notdirectly contribute to the development of infection.
  215. 215. Critical Thinking Review Question 6 – Rationale (cont)Periodic chest x-ray monitoring may be orderedand should be obtained if adventitious breathsounds are noted.Cognitive Level: ApplicationNursing Process: ImplementationPatient Need: Physiological Integrity

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