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Fluid, electrolyte and acid base
This document provides an overview of fluid, electrolyte and acid-base balance. It discusses fluid compartments and transport mechanisms including diffusion, filtration, osmosis and active transport. It describes fluid imbalances such as dehydration, hypovolemia, hypervolemia and water intoxication. The document also covers electrolytes including sodium, potassium, regulatory mechanisms and electrolyte imbalances such as hyponatremia, hypernatremia, hypokalemia and hyperkalemia. Clinical presentations and treatment approaches for various fluid and electrolyte disorders are also summarized.
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Fluid, electrolyte and acid base
- 1. Fluid, Electrolyte and Acid-BaseBalance By Nathan Kikku Mubiru Medical Laboratory Scientist (MLSO)
- 3.
- 4. General Concepts • Intake= Output = Fluid Balance • Sensible losses – Urination – Defecation – Wound drainage • Insensible losses – Evaporation from skin – Respiratory loss from lungs
- 5. Fluid Compartments • Intracellular –40%of body weight • Extracellular –20% of body weight –Two types • INTERSTITIAL (between) • INTRAVASCULAR (inside)
- 6. Age-Related Fluid Changes •Full-term baby - 80% • Lean Adult Male - 60% • Aged client - 40%
- 7. Fluid and ElectrolyteTransport • PASSIVE TRANSPORT SYSTEMS – Diffusion – Filtration – Osmosis • ACTIVE TRANSPORT SYSTEM – Pumping – Requires energy expenditure
- 8. Diffusion • Molecules moveacross a biological membrane from an area of higher to an area of lower concentration • Membrane types – Permeable – Semi-permeable – Impermeable
- 9. Filtration • Movement ofsolute and solvent across a membrane caused by hydrostatic (water pushing) pressure • Occurs at the capillary level • If normal pressure gradient changes (as occurs with right-sided heart failure) edema results from “third spacing”
- 10. Osmosis • Movement ofsolvent from an area of lower solute concentration to one of higher concentration • Occurs through a semipermeable membrane using osmotic (water pulling) pressure
- 11. Active Transport System •Solutes can be moved against a concentration gradient • Also called “pumping” • Dependent on the presence of ATP
- 12. Fluid Types • Isotonic •Hypotonic • Hypertonic
- 13. Isotonic Solution • Nofluid shift because solutions are equally concentrated • Normal saline solution (0.9% NaCl)
- 14. Hypotonic Solution • Lowersolute concentration • Fluid shifts from hypotonic solution into the more concentrated solution to create a balance (cells swell) • Half-normal saline solution (0.45% NaCl)
- 15. Hypertonic Solution • Highersolute concentration • Fluid is drawn into the hypertonic solution to create a balance (cells shrink) • 5% dextrose in normal saline (D5/0.9% NaCl)
- 16. Regulatory Mechanisms • Baroreceptorreflex • Volume receptors • Renin-angiotensin-aldosterone mechanism • Antidiuretic hormone
- 17. Baroreceptor Reflex • Respondto a fall in arterial blood pressure • Located in the atrial walls, vena cava, aortic arch and carotid sinus • Constricts afferent arterioles of the kidney resulting in retention of fluid
- 18. Volume Receptors • Respondto fluid excess in the atria and great vessels • Stimulation of these receptors creates a strong renal response that increases urine output
- 19. Renin-Angiotensin-Aldosterone • Renin –Enzyme secretedby kidneys when arterial pressure or volume drops –Interacts with angiotensinogen to form angiotensin I (vasoconstrictor)
- 20. Renin-Angiotensin-Aldosterone • Angiotensin –Angiotensin Iis converted in lungs to angiotensin II using ACE (angiotensin converting enzyme) –Produces vasoconstriction to elevate blood pressure –Stimulates adrenal cortex to secrete aldosterone
- 21. Renin-Angiotensin-Aldosterone • Aldosterone –Mineralocorticoid thatcontrols Na+ and K+ blood levels –Increases Cl- and HCO3- concentrations and fluid volume
- 22. Aldosterone Negative FeedbackMechanism • ECF & Na+ levels drop secretion of ACTH by the anterior pituitary release of aldosterone by the adrenal cortex fluid and Na+ retention
- 23. Antidiuretic Hormone • Alsocalled vasopressin • Released by posterior pituitary when there is a need to restore intravascular fluid volume • Release is triggered by osmoreceptors in the thirst center of the hypothalamus • Fluid volume excess decreased ADH • Fluid volume deficit increased ADH
- 24. Fluid Imbalances • Dehydration •Hypovolemia • Hypervolemia • Water intoxication
- 25. Dehydration • Loss ofbody fluids increased concentration of solutes in the blood and a rise in serum Na+ levels • Fluid shifts out of cells into the blood to restore balance • Cells shrink from fluid loss and can no longer function properly
- 26. Clients at Risk •Confused • Comatose • Bedridden • Infants • Elderly • Enterally fed
- 27. What Do YouSee? • Irritability • Confusion • Dizziness • Weakness • Extreme thirst • urine output • Fever • Dry skin/mucous membranes • Sunken eyes • Poor skin turgor • Tachycardia
- 28. What Do WeDo? • Fluid Replacement - oral or IV over 48 hrs. • Monitor symptoms and vital signs • Maintain I&O • Maintain IV access • Daily weights • Skin and mouth care
- 29. Hypovolemia • Isotonic fluidloss from the extracellular space • Can progress to hypovolemic shock • Caused by: –Excessive fluid loss (hemorrhage) –Decreased fluid intake –Third space fluid shifting
- 30. What Do YouSee? • Mental status deterioration • Thirst • Tachycardia • Delayed capillary refill • Orthostatic hypotension • Urine output < 30 ml/hr • Cool, pale extremities • Weight loss
- 31. What Do WeDo? • Fluid replacement • Albumin replacement • Blood transfusions for hemorrhage • Dopamine to maintain BP • MAST trousers for severe shock • Assess for fluid overload with treatment
- 32. Hypervolemia • Excess fluidin the extracellular compartment as a result of fluid or sodium retention, excessive intake, or renal failure • Occurs when compensatory mechanisms fail to restore fluid balance • Leads to CHF and pulmonary edema
- 33. What Do YouSee? • Tachypnea • Dyspnea • Crackles • Rapid, bounding pulse • Hypertension • S3 gallop • Increased CVP, pulmonary artery pressure and pulmonary artery wedge pressure (Swan- Ganz) • JVD • Acute weight gain • Edema
- 34. Edema • Fluid isforced into tissues by the hydrostatic pressure • First seen in dependent areas • Anasarca - severe generalized edema • Pitting edema • Pulmonary edema
- 35. What Do WeDo? • Fluid and Na+ restriction • Diuretics • Monitor vital signs • Hourly I&O • Breath sounds • Monitor ABGs and labs • Elevate HOB and give O2 as ordered • Maintain IV access • Skin & mouth care • Daily weights
- 36. Water Intoxication • Hypotonic extracellularfluid shifts into cells to attempt to restore balance • Cells swell • Causes: – SIADH – Rapid infusion of hypotonic solution – Excessive tap water NG irrigation or enemas – Psychogenic polydipsia
- 37. What Do YouSee? • Signs and symptoms of increased intracranial pressure – Early: change in LOC, N/V, muscle weakness, twitching, cramping – Late: bradycardia, widened pulse pressure, seizures, coma
- 38. What Do WeDo? • Prevention is the best treatment • Assess neuro status • Monitor I&O and vital signs • Fluid restrictions • IV access • Daily weights • Monitor serum Na+ • Seizure precautions
- 39.
- 40. Electrolytes • Charged particlesin solution • Cations (+) • Anions (-) • Integral part of metabolic and cellular processes
- 41. Positive or Negative? •Cations (+) –Sodium –Potassium –Calcium –Magnesium • Anions (-) –Chloride –Bicarbonate –Phosphate –Sulfate
- 42. Major Cations • EXTRACELLULAR –SODIUM (Na+) • INTRACELLULAR – POTASSIUM (K+)
- 43. Electrolyte Imbalances • Hyponatremia/ hypernatremia •Hypokalemia/ Hyperkalemia • Hypomagnesemia/ Hypermagnesemia • Hypocalcemia/ Hypercalcemia • Hypophosphatemia/ Hyperphosphatemia • Hypochloremia/ Hyperchloremia
- 44. Sodium • Major extracellularcation • Attracts fluid and helps preserve fluid volume • Combines with chloride and bicarbonate to help regulate acid-base balance • Normal range of serum sodium 135 - 145 mEq/L
- 45. Sodium and Water •If sodium intake suddenly increases, extracellular fluid concentration also rises • Increased serum Na+ increases thirst and the release of ADH, which triggers kidneys to retain water • Aldosterone also has a function in water and sodium conservation when serum Na+ levels are low
- 46. Sodium-Potassium Pump • Sodium(abundant outside cells) tries to get into cells • Potassium (abundant inside cells) tries to get out of cells • Sodium-potassium pump maintains normal concentrations • Pump uses ATP, magnesium and an enzyme to maintain sodium-potassium concentrations • Pump prevents cell swelling and creates an electrical charge allowing neuromuscular impulse transmission
- 47. Hyponatremia • Serum Na+level < 135 mEq/L • Deficiency in Na+ related to amount of body fluid • Several types – Dilutional – Depletional – Hypovolemic – Hypervolemic – Isovolemic
- 48. Types of Hyponatremia •Dilutional - results from Na+ loss, water gain • Depletional - insufficient Na+ intake • Hypovolemic - Na+ loss is greater than water loss; can be renal (diuretic use) or non-renal (vomiting) • Hypervolemic - water gain is greater than Na+ gain; edema occurs • Isovolumic - normal Na+ level, too much fluid
- 49. What Do YouSee? • Primarily neurologic symptoms –Headache, N/V, muscle twitching, altered mental status, stupor, seizures, coma • Hypovolemia - poor skin turgor, tachycardia, decreased BP, orthostatic hypotension • Hypervolemia - edema, hypertension, weight gain, bounding tachycardia
- 50. What Do WeDo? • MILD CASE – Restrict fluid intake for hyper/isovolemic hyponatremia – IV fluids and/or increased po Na+ intake for hypovolemic hyponatremia • SEVERE CASE – Infuse hypertonic NaCl solution (3% or 5% NaCl) – Furosemide to remove excess fluid – Monitor client in ICU
- 51. Hypernatremia • Excess Na+relative to body water • Occurs less often than hyponatremia • Thirst is the body’s main defense • When hypernatremia occurs, fluid shifts outside the cells • May be caused by water deficit or over- ingestion of Na+ • Also may result from diabetes insipidus
- 52. What Do YouSee? • Think S-A-L-T – Skin flushed – Agitation – Low grade fever – Thirst • Neurological symptoms • Signs of hypovolemia
- 53. What Do WeDo? • Correct underlying disorder • Gradual fluid replacement • Monitor for s/s of cerebral edema • Monitor serum Na+ level • Seizure precautions
- 54. Potassium • Major intracellularcation • Untreated changes in K+ levels can lead to serious neuromuscular and cardiac problems • Normal K+ levels = 3.5 - 5 mEq/L
- 55. Balancing Potassium • MostK+ ingested is excreted by the kidneys • Three other influential factors in K+ balance : – Na+/K+ pump – Renal regulation – pH level
- 56. Sodium/Potassium Pump • UsesATP to pump potassium into cells • Pumps sodium out of cells • Creates a balance
- 57. Renal Regulation • IncreasedK+ levels increased K+ loss in urine • Aldosterone secretion causes Na+ reabsorption and K+ excretion
- 58. pH • Potassium ionsand hydrogen ions exchange freely across cell membranes • Acidosis hyperkalemia (K+ moves out of cells) • Alkalosis hypokalemia (K+ moves into cells)
- 59. Hypokalemia • Serum K+< 3.5 mEq/L • Can be caused by GI losses, diarrhea, insufficient intake, non-K+ sparing diuretics (thiazide, furosemide)
- 60. What Do YouSee? • Think S-U-C-T-I-O-N – Skeletal muscle weakness – U wave (EKG changes) – Constipation, ileus – Toxicity of digitalis glycosides – Irregular, weak pulse – Orthostatic hypotension – Numbness (paresthesias)
- 61. What Do WeDo? • Increase dietary K+ • Oral KCl supplements • IV K+ replacement • Change to K+-sparing diuretic • Monitor EKG changes
- 62. IV K+ Replacement •Mix well when adding to an IV solution bag • Concentrations should not exceed 40-60 mEq/L • Rates usually 10-20 mEq/hr NEVER GIVE IV PUSH POTASSIUM
- 63. Hyperkalemia • Serum K+> 5 mEq/L • Less common than hypokalemia • Caused by altered kidney function, increased intake (salt substitutes), blood transfusions, meds (K+- sparing diuretics), cell death (trauma)
- 64. What Do YouSee? • Irritability • Paresthesia • Muscle weakness (especially legs) • EKG changes (tented T wave) • Irregular pulse • Hypotension • Nausea, abdominal cramps, diarrhea
- 65. What Do WeDo? • Mild – Loop diuretics (Lasix) – Dietary restriction • Moderate – Kayexalate • Emergency – 10% calcium gluconate for cardiac effects – Sodium bicarbonate for acidosis
- 66. Magnesium • Helps produceATP • Role in protein synthesis & carbohydrate metabolism • Helps cardiovascular system function (vasodilation) • Regulates muscle contractions
- 67. Hypomagnesemia • Serum Mg++level < 1.5 mEq/L • Caused by poor dietary intake, poor GI absorption, excessive GI/urinary losses • High risk clients – Chronic alcoholism – Malabsorption – GI/urinary system disorders – Sepsis – Burns – Wounds needing debridement
- 68. What Do YouSee? • CNS –Altered LOC –Confusion –Hallucinations
- 69. What Do YouSee? • Neuromuscular –Muscle weakness –Leg/foot cramps –Hyper DTRs –Tetany –Chvostek’s & Trousseau’s signs
- 70. What Do YouSee? • Cardiovascular –Tachycardia –Hypertension –EKG changes
- 71. What Do YouSee? • Gastrointestinal –Dysphagia –Anorexia –Nausea/vomiting
- 72. What Do WeDo? • Mild – Dietary replacement • Severe – IV or IM magnesium sulfate • Monitor – Neuro status – Cardiac status – Safety
- 73. Mag Sulfate Infusion •Use infusion pump - no faster than 150 mg/min • Monitor vital signs for hypotension and respiratory distress • Monitor serum Mg++ level q6h • Cardiac monitoring • Calcium gluconate as an antidote for overdosage
- 74. Hypermagnesemia • Serum Mg++level > 2.5 mEq/L • Not common • Renal dysfunction is most common cause – Renal failure – Addison’s disease – Adrenocortical insufficiency – Untreated DKA
- 75. What Do YouSee? • Decreased neuromuscular activity • Hypoactive DTRs • Generalized weakness • Occasionally nausea/vomiting
- 76. What Do WeDo? • Increased fluids if renal function normal • Loop diuretic if no response to fluids • Calcium gluconate for toxicity • Mechanical ventilation for respiratory depression • Hemodialysis (Mg++-free dialysate)
- 77. Calcium • 99% inbones, 1% in serum and soft tissue (measured by serum Ca++) • Works with phosphorus to form bones and teeth • Role in cell membrane permeability • Affects cardiac muscle contraction • Participates in blood clotting
- 78. Calcium Regulation • Affectedby body stores of Ca++ and by dietary intake & Vitamin D intake • Parathyroid hormone draws Ca++ from bones increasing low serum levels (Parathyroid pulls) • With high Ca++ levels, calcitonin is released by the thyroid to inhibit calcium loss from bone (Calcitonin keeps)
- 79. Hypocalcemia • Serum calcium< 8.9 mg/dl • Ionized calcium level < 4.5 mg/Dl • Caused by inadequate intake, malabsorption, pancreatitis, thyroid or parathyroid surgery, loop diuretics, low magnesium levels
- 80. What Do YouSee? • Neuromuscular – Anxiety, confusion, irritability, muscle twitching, paresthesias (mouth, fingers, toes), tetany • Fractures • Diarrhea • Diminished response to digoxin • EKG changes
- 81. What Do WeDo? • Calcium gluconate for postop thyroid or parathyroid client • Cardiac monitoring • Oral or IV calcium replacement
- 82. Hypercalcemia • Serum calcium> 10.1 mg/dl • Ionized calcium > 5.1 mg/dl • Two major causes – Cancer – Hyperparathyroidism
- 83. What Do YouSee? • Fatigue, confusion, lethargy, coma • Muscle weakness, hyporeflexia • Bradycardia cardiac arrest • Anorexia, nausea/vomiting, decreased bowel sounds, constipation • Polyuria, renal calculi, renal failure
- 84. What Do WeDo? • If asymptomatic, treat underlying cause • Hydrate the patient to encourage diuresis • Loop diuretics • Corticosteroids
- 85. Phosphorus • The primaryanion in the intracellular fluid • Crucial to cell membrane integrity, muscle function, neurologic function and metabolism of carbs, fats and protein • Functions in ATP formation, phagocytosis, platelet function and formation of bones and teeth
- 86. Hypophosphatemia • Serum phosphorus< 2.5 mg/dl • Can lead to organ system failure • Caused by respiratory alkalosis (hyperventilation), insulin release, malabsorption, diuretics, DKA, elevated parathyroid hormone levels, extensive burns
- 87. What Do YouSee? • Musculoskeletal – muscle weakness – respiratory muscle failure – osteomalacia – pathological fractures • CNS – confusion, anxiety, seizures, coma • Cardiac – hypotension – decreased cardiac output • Hematologic – hemolytic anemia – easy bruising – infection risk
- 88. What Do WeDo? • MILD/MODERATE – Dietary interventions – Oral supplements • SEVERE – IV replacement using potassium phosphate or sodium phosphate
- 89. Hyperphosphatemia • Serum phosphorus> 4.5 mg/dl • Caused by impaired kidney function, cell damage, hypoparathyroidism, respiratory acidosis, DKA, increased dietary intake
- 90. What Do YouSee? • Think C-H-E-M-O – Cardiac irregularities – Hyperreflexia – Eating poorly – Muscle weakness – Oliguria
- 91. What Do WeDo? • Low-phosphorus diet • Decrease absorption with antacids that bind phosphorus • Treat underlying cause of respiratory acidosis or DKA • IV saline for severe hyperphosphatemia in patients with good kidney function
- 92. Chloride • Major extracellularanion • Sodium and chloride maintain water balance • Secreted in the stomach as hydrochloric acid • Aids carbon dioxide transport in blood
- 93. Hypochloremia • Serum chloride< 96 mEq/L • Caused by decreased intake or decreased absorption, metabolic alkalosis, and loop, osmotic or thiazide diuretics
- 94. What Do YouSee? • Agitation, irritability • Hyperactive DTRs, tetany • Muscle cramps, hypertonicity • Shallow, slow respirations • Seizures, coma • Arrhythmias
- 95. What Do WeDo? • Treat underlying cause • Oral or IV replacement in a sodium chloride or potassium chloride solution
- 96. Hyperchloremia • Serum chloride> 106 mEq/L • Rarely occurs alone • Caused by dehydration, renal failure, respiratory alkalosis, salicylate toxicity, hyperpara-thyroidism, hyperaldosteronism, hypernatremia
- 97. What Do YouSee? • Metabolic Acidosis – Decreased LOC – Kussmaul’s respirations – Weakness • Hypernatremia – Agitation – Tachycardia, dyspnea, tachypnea, HTN – Edema
- 98. What Do WeDo? • Correct underlying cause • Restore fluid, electrolyte and acid-base balance • IV Lactated Ringer’s solution to correct acidosis
- 99.
- 100. Acid-Base Basics • Balancedepends on regulation of free hydrogen ions • Concentration of hydrogen ions is measured in pH • Arterial blood gases are the major diagnostic tool for evaluating acid-base balance
- 101. Arterial Blood Gases •pH 7.35 - 7.45 • PaCO2 35 - 45 mmHg • HCO3 22-26 mEq/L
- 102. Acidosis • pH <7.35 • Caused by accumulation of acids or by a loss of bases
- 103. Alkalosis • pH >7.45 • Occurs when bases accumulate or acids are lost
- 104. Regulatory Systems • Threesystems come into play when pH rises or falls – Chemical buffers – Respiratory system – Kidneys
- 105. Chemical Buffers • Immediateacting • Combine with offending acid or base to neutralize harmful effects until another system takes over • Bicarb buffer - mainly responsible for buffering blood and interstitial fluid • Phosphate buffer - effective in renal tubules • Protein buffers - most plentiful - hemoglobin
- 106. Respiratory System • Lungsregulate blood levels of CO2 • CO2 + H2O = Carbonic acid • High CO2 = slower breathing (hold on to carbonic acid and lower pH) • Low CO2 = faster breathing (blow off carbonic acid and raise pH) • Twice as effective as chemical buffers, but effects are temporary
- 107. Kidneys • Reabsorb orexcrete excess acids or bases into urine • Produce bicarbonate • Adjustments by the kidneys take hours to days to accomplish • Bicarbonate levels and pH levels increase or decrease together
- 108. Arterial Blood Gases(ABG) • Uses blood from an arterial puncture • Three test results relate to acid-base balance – pH – PaCO2 – HCO3
- 109. Interpreting ABGs • Step1 - check the pH • Step 2 - What is the CO2? • Step 3 - Watch the bicarb • Step 4 - Look for compensation • Step 5 - What is the PaO2 and SaO2?
- 110. Step 1 -Check the pH • pH < 7.35 = acidosis • pH > 7.45 = alkalosis • Move on to Step 2
- 111. Step 2 -What is the CO2? • PaCO2 gives info about the respiratory component of acid-base balance • If abnormal, does the change correspond with change in pH? – High pH expects low PaCO2 (hypocapnia) – Low pH expects high PaCO2 (hypercapnia)
- 112. Step 3 –Watch the Bicarb • Provides info regarding metabolic aspect of acid-base balance • If pH is high, bicarb expected to be high (metabolic alkalosis) • If pH is low, bicarb expected to be low (metabolic acidosis)
- 113. Step 4 –Look for Compensation • If a change is seen in BOTH PaCO2 and bicarbonate, the body is trying to compensate • Compensation occurs as opposites, (Example: for metabolic acidosis, compensation shows respiratory alkalosis)
- 114. Step 5 –What is the PaO2 and SaO2 • PaO2 reflects ability to pickup O2 from lungs • SaO2 less than 95% is inadequate oxygenation • Low PaO2 indicates hypoxemia
- 115. Acid-Base Imbalances • RespiratoryAcidosis • Respiratory Alkalosis • Metabolic Acidosis • Metabolic Alkalosis
- 116. Respiratory Acidosis • Anycompromise in breathing can result in respiratory acidosis • Hypoventilation carbon dioxide buildup and drop in pH • Can result from neuromuscular trouble, depression of the brain’s respiratory center, lung disease or airway obstruction
- 117. Clients At Risk •Post op abdominal surgery • Mechanical ventilation • Analgesics or sedation
- 118. What Do YouSee? • Apprehension, restlessness • Confusion, tremors • Decreased DTRs • Diaphoresis • Dyspnea, tachycardia • N/V, warm flushed skin
- 119. ABG Results • Uncompensated –pH < 7.35 – PaCO2 >45 – HCO3 Normal • Compensated – pH Normal – PaCO2 >45 – HCO3 > 26
- 120. What Do WeDo? • Correct underlying cause • Bronchodilators • Supplemental oxygen • Treat hyperkalemia • Antibiotics for infection • Chest PT to remove secretions • Remove foreign body obstruction
- 121. Respiratory Alkalosis • Mostcommonly results from hyperventilation caused by pain, salicylate poisoning, use of nicotine or aminophylline, hypermetabolic states or acute hypoxia (overstimulates the respiratory center)
- 122. What Do YouSee? • Anxiety, restlessness • Diaphoresis • Dyspnea ( rate and depth) • EKG changes • Hyperreflexia, paresthesias • Tachycardia • Tetany
- 123. ABG Results • Uncompensated –pH > 7.45 – PaCO2 < 35 – HCO3 Normal • Compensated – pH Normal – PaCO2 < 35 – HCO3 < 22
- 124. What Do WeDo? • Correct underlying disorder • Oxygen therapy for hypoxemia • Sedatives or antianxiety agents • Paper bag breathing for hyperventilation
- 125. Metabolic Acidosis • Characterizedby gain of acid or loss of bicarb • Associated with ketone bodies – Diabetes mellitus, alcoholism, starvation, hyperthyroidism • Other causes – Lactic acidosis secondary to shock, heart failure, pulmonary disease, hepatic disease, seizures, strenuous exercise
- 126. What Do YouSee? • Confusion, dull headache • Decreased DTRs • S/S hyperkalemia (abdominal cramps, diarrhea, muscle weakness, EKG changes) • Hypotension, Kussmaul’s respirations • Lethargy, warm & dry skin
- 127. ABG Results • Uncompensated –pH < 7.35 – PaCO2 Normal – HCO3 < 22 • Compensated – pH Normal – PaCO2 < 35 – HCO3 < 22
- 128. What Do WeDo? • Regular insulin to reverse DKA • IV bicarb to correct acidosis • Fluid replacement • Dialysis for drug toxicity • Antidiarrheals
- 129. Metabolic Alkalosis • Commonlyassociated with hypokalemia from diuretic use, hypochloremia and hypocalcemia • Also caused by excessive vomiting, NG suction, Cushing’s disease, kidney disease or drugs containing baking soda
- 130. What Do YouSee? • Anorexia • Apathy • Confusion • Cyanosis • Hypotension • Loss of reflexes • Muscle twitching • Nausea • Paresthesia • Polyuria • Vomiting • Weakness
- 131. ABG Results • Uncompensated –pH > 7.45 – PaCO2 Normal – HCO3 >26 • Compensated – pH Normal – PaCO2 > 45 – HCO3 > 26
- 132. What Do WeDo? • IV ammonium chloride • D/C thiazide diuretics and NG suctioning • Antiemetics
- 133. IV Therapy • Crystalloids– volume expander – Isotonic (D5W, 0.9% NaCl or Lactated Ringers) – Hypotonic (0.45% NaCl) – Hypertonic (D5/0.9% NaCl, D5/0.45% NaCl) • Colloids – plasma expander (draw fluid into the bloodstream) – Albumin – Plasma protein – Dextran
- 134. Total Parenteral Nutrition •Highly concentrated • Hypertonic solution • Used for clients with high caloric and nutritional needs • Solution contains electrolytes, vitamins, acetate, micronutrients and amino acids • Lipid emulsions given in addition
- 135.