Nursing 50 Exam 6

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Nursing 50 Exam 6
2011-05-07 17:28:13
Fluid Electrolytes Acid Base

nursing 50 exam 6
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  1. What % of the Body is H2O?
    What are the main functions of H2O in the body?
    What factors change H20 Composition in the body?
    • 60%
    • Temperature Maintenance, Elimination of Wastes, Transportation
    • Fat- increased fat cells = decreased H20, H2O decreases with age, Premature babies have incresed H20, Females have less H2O than males
  2. What are the different types of solutes found in the body?
    • Electrolytes: Anions and Cations
    • Nonelectrolytes: Glucose, Urea, Creatinine, Bilirubin
  3. What is the most abundant Cation in the ICF and ECF?
    • ICF- Potassium
    • ECF- Sodium
  4. What is the most abundant Anion in the ICF and ECF?
    • ICF-Phosphate
    • ECF- Chloride
  5. Intracellular fluids
    • Fluids contained in cells
    • 2/3 of body h20. ~27L
    • ~42% of body weight
  6. Extracellular fluids
    • Fluid spaces between cells (interstitial and lymph)
    • 1/3 of body h20
    • ~20% of body wt
  7. Interstitial fluid and lymph
    • Fluid surrounding cells
    • Reserve fluids to replace plasma
  8. Intravascular fluid/plasma
    • Liquid portion of the blood
    • Least stable to fluid changes
  9. Transcellular Space
    • Fluid secreted and absorbed by epithelial cells
    • CSF, GI tract, Pleural, Synovial, and Peritoneal fluid spaces
    • Doesn't change very much
  10. First Spacing
    Normal distribution of fluid
  11. Second Spacing
    Abnormal accumulation of Interstitial fluid (peripheral edema)
  12. Third Spacing
    Accumulation of fluid in areas that usually have no/limited fluids. (ascites)
  13. Hypotonic Solution
    • Solution that has lower osmolality (less solutes) than cells
    • Leads to water moving into cells and possible lysis (especially neurons)
  14. Isotonic Solution
    Solution that has the same osmolality of the cells
  15. Hypertonic Solution
    • Solution that has more solutes than the cells
    • Leads to water moving out of the cells causing cell shrinkage (especially neurons)
  16. Osmotic Pressure
    • The pulling force (pulls water) of a solution.
    • The higher the osmolality the higher the osmotic pressure
  17. Oncotic Pressure
    The pulling force of colloids (large molecules)
  18. How does Renin-Angiotensin work?
  19. How does Aldosterone work?
  20. How does ADH work?
  21. Factors affecting aldosterone Secretion
  22. Thirst Mechanism
    • Stimulated by thirst receptors in the hypothalmus
    • Primary protection against hyperosmolality
    • Occurs with even small fluid losses
    • Stimulates ADH and Aldosterone secretion
    • Response is diminished in the elderly
  23. Atrial Natriuretic Peptide (ANP)
    • Cardiac hormone found in atria and released when BP/Blood Volume too high in atrium.
    • Decreases aldosterone and ADH, Leads to increased glomerular filtration rate (GFR), Increases h20 secretion which decreases blood volume and BP.
  24. How much does one liter of H2O weigh?
    2.2 lbs or 1 kg
  25. Sources of Fluid Gains
    • Oxidative Metabolism
    • Oral Fluids
    • Solid Foods
    • Fluid Therapy (parenteral, enteral etc)
  26. Sources of Fluid Losses
    • Kidneys
    • Skin
    • Lungs
    • GI tract
    • Abnormal-Diarrhea, vomiting, NG suction
    • Third space losses-clinically depleted but sx of overload too.
  27. Causes of Fluid Volume Excess (5)
    • Renal Disease
    • Too rapid IV infusion
    • Steroid Therapy-causes stress response
    • Production of ADH
    • Cadiac Disease-HF
  28. Assessment findings of Fluid Volume Excess (11)
    • Wt Gain-best measure
    • Distended neck veins
    • Distended peripheral veins
    • Slow emptying of peripheral veins (when are raised)
    • Bounding, full pulse
    • Elevated BP
    • Edema
    • Crackles, SOB, Dyspnea
    • Polyuria-decreased specific gravity (lower osmolality)
    • Decreased Hct
    • Pulmonary edema
  29. Causes of Fluid volume deficit (7)
    • Blood loss
    • Fluid loss from GI (D&V)
    • Profuse sweating
    • Polyuria (hyperglycemia, DM, diuretics, Diabetes insipidous)
    • Fever
    • Third Spacing
    • Decreased intake
  30. Assesment finding for Fluid Volume Defecit (14)
    • Altered mental status
    • Dry Mucous membranes
    • Flushed dry skin
    • decreaseed skin turgor
    • increased pulse
    • slow filling peripheral veins
    • orthostatic changes, decreased BP
    • increased Hct
    • changes in temp
    • thirsty
    • decreased urine output with increased specific gravity
    • wt loss
    • signs of shock
    • Tenting (skin turgor)
  31. Serum Osmolality
    • The number of osmotically active particles in the serum
    • 280-300 Osm/kg
  32. Hematocrit
    • Percentage of whole blood that is made up of RBCs.
    • -Increases with dehydration and decreases with overhydration
    • Males- 42-52%
    • Females- 37-48%
  33. Urea Nitrogen (BUN)
    • A byproduct of hepatic protein metabolism
    • High BUN = decreased renal function
    • Can also be affected by hydration and protein intake
    • BUN 8-25mg/dl
  34. Urine Osmolality Range
    • 24hr urine collection measuring solute concentration
    • Will be increased with FVD/SIADH
    • Will be decreased with FVE/Diabetes Insipidus
    • 50-1400 mOsm/kg (avg 500-800)
  35. Urine Specific Gravity
    • Another measure for the osmolality of urine
    • 1.010-1.020
  36. Sx of Diabetes Mellitus R/T Fluid Volume
    • Sweet Urine
    • Osmotic diuresis
    • Increased SG
    • Three polys
  37. Sx of Diabetes Insipidus R/T Fluid Volume
    • (Damage to hypothalmus/pituitary)
    • Decreased ADH
    • Decreased SG
    • 2 Polys
    • -Will show signs of FVD except there will be increased dilute urine output
  38. SIADH in relation to Fluid Volume
    • syndrome of inappropriate antidiuretic hormone hypersecretion
    • Increased ADH
    • Decreased Serum Na+
    • May have decreased urine output
    • Increased SG
    • -Will have signs of FVE except decreased urine output with a high specific gravity
  39. What is the disease?
    Decreased intake, Increased Output
    K+ WNL
    Glu WNL
    Na+, Cl-, BUN increased
    Sx- restless, disoriented, confused
    Diabetes Insipidus
  40. What is wrong?
    R- 24
    T 101.6
    Mucous normal
    No Edema
    Decreased bowel sounds
    Decreased urine
    Increased SG
    Sx-HA, dizziness, N/V, Confusion
    SIADH (cellular swelling)
  41. What is wrong?
    Increased fluid in vascular space- increased capillary hyrostatic pressure --> Increased fluids in ICF
    Decreased Potassium
    Sx- thirst, Nausea, muscle weakness, malaise, Irregular HR, diminished peripheral pulses, no tenderness in abd, changes in EKG
    Hypokalemia (CHF)
  42. What is wrong?
    Hct, BUN increased
    Cap Refill decreased
    Pulse deficit
    Dark concentrated urine
    Mental confusion and dampening
    Shiny skin
    Soft abd with pain
    Muscle twitches/tremors
    Dry Mucous
  43. Sodium
    -Normal Value
    -Where is it found
    -Where is it absorbed
    -Where is it eliminated
    -What are its major functions
    • -135-145 mEq/L
    • -Most abundant Cation in ECF
    • -GI tract
    • -Urine, Feces, Perspiration
    • -Regulating osmolality-- maintains fluid volume; generation and transmission of impulses in nerves and muscles; helps regulate acid-base
  44. How is sodium regulated
    • -The same mechanisms as H20
    • Thirst
    • ADH
    • Aldosterone
    • ANP
  45. Etiology of Hyponatremia
    • Associated with ECF imbalances
    • -Inadequate sodium intake
    • -Increased excretion or dilution of serum sodium (excess h20)
  46. Risk Factors for Hyponatremia (3)
    • Loss of Sodium-GI, Sweating, Diuretics
    • Gain of H20- Hypotonic tube feedings, increased H20 intake, hypotonic IV solutions, CHF, Liver cirrhosis, D5W because dextrose is metabolized quickly leaving just h20.
    • SIADH- head injury, AIDS, malignant tumors, medications
  47. Clinical Manifestations of Hyponatremia
    • Caused by inracellular shift of H20
    • CNS mostly-lethargy, confusion, aprehension, muscle twitching, HA
    • Coma
    • GI-abd cramps, anorexia, N/V
    • If <118 very high risk of Seizures
  48. Hyponatremia lab Values
    • Na < 135 mEq/L
    • Serum Osmolality < 280 mOsm/kg
    • Specific gravity decreased Except with SIADH
  49. Nursing Interventions for Hyponatremia
    • Fluid Restriction - 1000ml/24hr
    • 3% Saline when dangerously low
  50. Hypernatremia etiology
    • Excess water loss or overall sodium excess
    • Typically occurs with decreased free water intake
  51. Hypernatremia risk factors
    • Loss of fluids - insensible water loss, V/D
    • Water Deprivation - excess salt intake, IV saline solution, hyperosmolar tube feedings
    • Diabetes Insipidus
    • Excess Aldosterone secretion
  52. Hypernatremia Manifestations
    • CNS- fatigue, restlessness, drecreased LOC, disorientation, convulsions
    • CV-signs of FVD
  53. Hypernatremia lab values
    • Sodium > 145
    • Serum osmolality > 297
    • SG increased except with diabetes insipidus
  54. Potassium
    -Where is it located
    -Main functions
    • -3.5 - 5.0 mEq/L
    • Major cation in ICF
    • -Regulates metabolic activities, transmission and conduction of nerve impulses, cardiac conduction, smooth muscle contraction.
  55. Regulation of Potassium (4)
    • Dietary Intake
    • Kidneys- primary regulator of potassium balance
    • Aldosterone
    • Insulin
  56. Hypokalemia etiology
    • Changes of serum potassium reflective of ECF levels not total body levels.
    • Loss of potassium from the body or movement of potassium into the cells.
    • Rarely a result of inadequate intake
  57. Hypokalemia risk factors
    • Reduction in body potassium- increased urinary losses, GI losses, diaphoresis, medications- thiazides and loop diuretics, increased aldosterone secretion
    • Intracellular shifts-alkalosis, increased insulin, tissue repair (trauma, burns)
  58. Hypokalemia Clinical Manifestations
    • Cardiac
    • CV: irregular pulse rate, weak, thready, ECG changes, digitalis toxicity is potentiated,
    • GI-abdominal distention, hyperactive bowel sounds
    • NM- leg cramps, decreased muscle tone, decreased DTRs
  59. Hypokalemia lab values
    • Serum K+ < 3.5
    • ABG- Metabolic alkalosis, or respiratory alkalosis
    • EKG- ST segment depression, flattened T wave, presence of a U wave, wentricular dysrhythmias
    • Maybe decreased Ca and Mg
    • Look at EKG to see digitalis toxicity if plasma levels are normal
  60. Hypokalemia interventions
    • No more than 10-20 mEq K+ IV per hour.
    • Anything greater than 10 mEq must be on heart monitor.
    • NO IV push
  61. Hyperkalemia Etiology
    • Occurs because of an increased intake of Potassium, decreased urinary excretion of K+, or movement of K+ out of cells.
    • -Anything that causes cells to break- even tourniquets
  62. Risk Factors of Hyperkalemia
    • High intake of potassium- IV potassium
    • Decreased excretion- renal failure, medications- K+ sparing diuretics, ACE inhibitors, NSAIDS, Adrenal insufficiency (Addison's disease)
    • Movement of Potassium out of cells- acidososis, insulin deficiency, tissue catabolism, crush injuries
  63. Clinical Manifestations of Hyperkalemia
    • Cardiac
    • CV: Irregular, slow HR, decreased BP, ECK changes
    • NM- Muscle cramps, Early-muscle twitching, Late- ascending muscle paralysis
    • GI- Hyperactive BS, diarrhea
  64. Lab Values for Hyperkalemia
    • Serum K+ > 5mEq/L
    • -Careful not to leave tourniquet on too long because may lyse cells releasing K+ and giving a false reading.
    • ABG- may show metabolic or respiration acidosis
    • ECG- tall thin T waves, prolonged PR interval, ST depression, widened QRS and loss of P wave
  65. Hyperkalemia treatment
    • Administer glucose and insulin as ordered
    • Administer calcium gluconate (careful with digoxin)
    • Administer Kayexalate
    • Dialysis if ordered
  66. Calcium
    -Main function
    • 4.3-5.3 mEq/L (ionized) or 8.5-10.5 mg/dl (total)
    • Primarily combined with phosphorus to form mineral salts of bone and teeth. ,1% located in ECF, 99% in bone.
    • Bone tissue, sedative effect on nerve cells, helps develop cardia action potential and muscle contraction
  67. Regulation of Calcium
    • Parathyroid hormone
    • Matabolites of Vitamin D
    • Calcitonin
  68. Hypocalcemia etiology
    • Total Ca levels may decrease with increased Ca loss, altered intestinal absorption, altered regulation
    • May be caused by elevated phosphorus or decreased magnesium
  69. Risk Factors for Hypocalcemia (9)
    • Hyperphosphatemia
    • Medications-loop diuretics
    • Impaired Vit D metabolism
    • Hypoparathyroidism
    • Hypomagnesemia
    • Acute Pancreatitis
    • Chronic Alcoholism
    • Rapid Blood Transfusion
    • Post partial parathyroidectomy or thyroidectomy
  70. Clinical Manifestations of Hypocalcemia
    • CNS- numbness, tingling, increasd DTRs, positive trousseau's and chvostek's sign, muscle cramps,
    • CV cardiac dysrhythmias
    • Increased bleeding
    • NM Excitability
  71. Hypocalcemia lab values
    • Serum Ca++ < 8.5mg/dL
    • Ionized Ca++ < 4.3 mEq/L
    • Usually increased phosphate
  72. Hypocalcemia treatment
    • Administer IV calcium (caution as ordered)
    • Administer po calcium and Vit D as ordered
    • May need phosphorus binding antacids
    • Seizure precautions
    • Observe for bleeding/bruising
  73. Hypercalcemia Etiology
    Usually when calcium moves from bone to ECF
  74. Risk factors for Hypercalcemia (7)
    • Hyperparathyroidism
    • Malignancies
    • Prolonged Immobilization
    • Pagets disease
    • Renal Failure
    • Medications- thiazide diuretics
    • Increased Ca++ intake
  75. Clinical Manifestations of Hypercalcemia
    • CNS- lethargy, weakness, depressed DTR,
    • CV- dysrhythmias
    • Musculoskeletal- pathologic fx, bone pain
    • GI- anorexia, N/V, Constipation
    • Renal- flank pain, polyuria
    • NM- decreased excitability, responses
  76. Hypercalcemia lab values
    • Total serum Ca++ > 10.5 mg/dL
    • Ionized Ca++ > 5.3 mEq/L
    • Increased parathyroid hormone possibly (hyperparathyroidism)
    • X-Ray may show osteoporosis, bone cavitation, urinary calculi.
    • Decreased phosphorus
  77. Hypercalcemia treatment
    • Mild hypercalcemia requires no treatment
    • Safety
    • Monitor for signs of digoxin toxicity (Ca++ potentiates toxicity)
    • Administer saline and loop diuretics
    • Avoid Vitamin D
    • Encourage acid-ash fluids
    • Increase fluid intake
    • Monitor Renal Fx
    • Assess for kidney stones
  78. Phosphorus
    • 1.8-2.6 mEq/L ir 2.6-4.5 mg/dL
    • Primary anion found in the ICF. Found as phosphate in the body. 85% found in bones and teeth, 14% in soft tissue, <1% in ECF, Combined in a 1;2 ration with calcium
  79. Regulation of Phosphorus (6)
    • Dietary Intake
    • Intestinal Absorption
    • Parathyroid hormone
    • Vitamin D
    • Calcium levels
    • Kidneys
  80. Hypophosphatemia Etiology
    • Can be transient intracellular fluid shift, increased urinary losses, decreased itestinal absorption, or increased cellular use.
    • -It can occur even when total body phosphorus stores are normal
  81. Hypophosphatemia Risk Factors (6)
    • TPN use
    • Hyperparathyroidism
    • Medications- thiazide diuretics
    • Alcoholism
    • DKA
    • Insuilin
  82. Hypophosphatemia Clinical Manifestations
    • Majority of sx due to decreased ATP.
    • CNS- Mental changes, slurred speech, seizures
    • Neuromuscular- muscle weakness, myalgia,
    • Hematologic- anemia, bruising and bleeding
    • CV- dysrhythmias
  83. Hypophosphatemia Lab Values
    • Serum phosphorus < 1.7 mEq/L
    • PTH level will be elevated in hyperparathyroidism
    • May also have increased Ca++
  84. Hypophosphatemia treatment
    • Administer phosphate slowly
    • Asses LOC, orientation, neuro status with each VS check
    • Assess muscle strength
    • Assist with ambulation
    • Encourage intake of foods high in phosphorus
    • Pain management
    • Monitor for cardiac or pulmonary complications
  85. Hyperphosphatemia Etiology
    Excessive intatke, extracellular fluid shifts, cellular destruction w/ movement of phosphorus out of the cell, decreased urinary losses.
  86. Hyperphosphatemia Clinical Manifestations
    • Very few sx, most are as a result of hypocalcemia.
    • Same sx of hypocalcemia
  87. Hyperphosphatemia risk factors (7)
    • Acute and chronic renal failure
    • Hypoparathyroidism
    • Volume depletion
    • Excessive phosphorus supplement
    • Increased Vit D
    • Neoplastic disease
    • Increased tissue breakdown (crush injuries)
  88. Hyperphosphatemia Lab Values
    • Serum phosphate > 2.6 mEq/L (be careful not to lyse cells when handling specimen)
    • Xrays may show skeletal changes
    • PTH level decreased
    • BUN and Creatinine may show signs of renal failure
    • Ca++ may be decreased
  89. Hyperphosphatemia treatment
    • Administer phosphate binders
    • Administer stool softeners
    • Limit food high in phosphorus
    • Avoid Vit D products
    • Monitor for signs of hypocalcemia
    • Monitor renal fx
  90. Magnesium
    -Main function
    • 1.5-2.0 mEq/L
    • Most abundant intracellular cation. 50-60% in Bone, 1% located in ECF, the rest ICF. 1/3-1/4 bound to protein
    • Activates enzymes involved in CHO and Protein metabolism, affects intracellular potassium levels by triggering sodium-potassium pump, neurno transmission in NM and CNS, myocardial fx.
  91. Regulation of Magnesium (3)
    • GI absorption
    • Renal Excretion
    • Parathyroid hormone
  92. Hypomagnesium Etiology
    • Usually a shift into intracellular space.
    • Decreased GI absorption
    • Increased urinary or GI loss
  93. Hypomagnesemia Risk Factors (4)
    • Inadequate intake- chronic alcoholism, administration of Mg free solutions
    • Inadequate absorption- Cancer, Colitis, Pancreatic insufficiency
    • GI/Urinary Losses- prolonged vomiting, NG suctions, Prolonged diarrhea, DKA, Medications- loop diuretics
    • Intracellular shifts- Insulin
  94. Hypomagnesmia Clinical Manifestations
    • CNS- irritability with tremors, disorientation and confusion
    • Increased DTRs and Chvostek's and Trousseaus signs
    • CV- tachycardia, dysrhythmias
    • GI- N/V anorexia
  95. Hypomagnesemia Lab Values
    • Serum magnesium < 1.5 mEq/L
    • Serum ionized magnesium level is a better indicator
    • Urinary magnesium to ID renal cause (also Alb, K+, Ca++)
    • EKG changes
    • Maybe tachycardia/dysrhythmias
    • Afib
  96. Hypomagnesemia Treatment
    • Administer MgSO4
    • Encourage foods high in Magnesium
    • Seixure precautions
    • Asses LOC and Neuro status with each VS check
    • Monitor pts taking digoxin
  97. Hypermagnesemia Etiology
    Almost exclusively in renal disease who have increased magnesium intake (pregnancy too)
  98. Hypermagnesemia Risk Factors (4)
    • Renal failure
    • Addisons Disease
    • Medications- antacids, laxatives
    • Preeeclamptics on MgSO4
  99. Hypermagnesemia Clinical Manifestations
    • CNS- depression, somnolence, lethargy
    • NM- Weakness, decreased DTRs
    • CV- hypotension, bradycardia, flushing sensation, possible cardiac arrest, pulmonary depression
  100. Hypermagnesemia lab values
    • Serum Magnesium > 2.5 mEq/L
    • ECG changes
    • AV block with sever levels
  101. Hypermagnesemia treatment
    • Asses LOC, Neuro, DTR with each VS check
    • Administer .45% NaCl and diuretic to enhance excretion
    • Administer calcium gluconate as ordered
    • Prepare for dialysis if necessary
  102. Chloride
    Lab Value
    Main function
    • 100-108 mEq/L
    • Most abundant extracellular anion, makes up 2/3 plasma anions, 80% found in ECF
    • Assessing the anion gap, metabolic acid-base balance, regulation of osmotic pressure and H20 balance
  103. Chloride Regulation (2)
    • GI
    • Kidneys
  104. Hypochloremia Etiology
    Increased admin of bicarb, renal excretion of acid, decreased sodium intake
  105. Hypochloremia Risk Factors (8)
    • Hyponatremia
    • Excessive admin of Bicarb
    • Excessive GI loss
    • Diaphoresis
    • Emphysema
    • Pneumonia
    • Pulmonary Edema
    • Resp Acidosis
  106. Hypochloremia Clinical Manifestations
    • NM- hyperexcitability, twitching, tremors
    • Resp- slow/shallow breathing
    • CV- hypotension with severe Chloride and ECF losses
  107. Hypochloremia Lab Values
    • Serum Chloride < 100 mEq/L
    • Maybe decreased sodium and increased HCO3
  108. Hypochloremia treatment
    • Encourage foods high in Na and Cl
    • Administer acid inhibitors
    • No Diuretics
    • Assess neuro status and LOC with VS checks
  109. Hyperchloremia Etiology
    Occurs with other fluid and electrolyte imbalances-hypernatremia, hypovolemia, metabolic acidosis
  110. Hyperchloremia risk factors (5)
    • Seme as hypernatremia
    • Decreased Bicarb
    • Metabolic acidosis
    • Ingestion of excessive chloride
    • Kaexalate
  111. Hyperchloremia Clinical Manifestations
    • NM-weakness, lethargy,
    • Resp- deep, rapid
    • CV- risk of dysrhytmia
  112. Hyperchloremia Lab Values
    • Serum chloride > 108 mEq/L
    • Maybe elevated Na
    • Decreased Bicarb
  113. Hyperchloremia treatment
    • Administer IV Hydration
    • Replace bicarb to increase pH
    • Monitor LOC and Resp
    • Monitor Na and Cl
    • Diuretics to excrete chloride
  114. Buffers
    • First line of defense for acid-base imbalances. Act immediately but are only 50% effective.
    • -Include Bicarbonate, phosphate and protein buffer systems.
  115. Respiratory system in relation to acid-base balance
    Hypoventilation effects?
    Hyperventilation effects?
    • Second line of defense against imbalance. Occurs within minutes to hours.
    • Controlled by respiratory center in the medulla
    • Hypo- retains CO2 which leads to acidosis
    • Hyper- blows off CO2 which leads to alkalosis
  116. Kidney in relation to acid-base balance
    • Most effective mechanism for imbalances.
    • Secretes/Reabsorbs H+ and HCO3- and electrolytes (Na, Cl)
  117. pH normal Value
    7.35-7.45 (7.4)
  118. PaCO2
    -Normal Value
    -Hyper/Hypoventilation effects
    • Partial pressure of CO2 in arterial blood
    • 35-45mmHg
    • Hyper--> <35mmHg
    • Hypo---> >45mmHg
  119. PaO2
    -Normal Value
    -What it means
    • Partial pressure of Oxygen in arterial blood. No role in acid-base regulation.
    • 80-100mmHg
    • If <60 -- can lead to anaerobic metabolism and metabolic acidosis. Also will decrease oxygen saturation
    • Hypoxemia can lead to hyperventilation which can cause respiratory alkalosis
  120. Oxygen saturation
    -Normal Value
    • Percentage of hemoglobin saturated by oxygen
    • 95-99%
  121. Base Excess
    -Normal Value
    -What values mean
    • The amount of blood buffer (HCO3) that exists
    • +/- 2
    • > +2 = base excess- alkalosis
    • < -2 = base defecit - acidosis
  122. Bicarbonate Function
    -Normal Value
    • Major renal component of acid-base balance. Excreted and reproduced by the kidneys to maintain normal acid-base. Primary buffer in ECF.
    • 22-30 mmol/L
  123. Anion Gap
    -Normal Value
    -Increase? Normal? Decrease?
    • Reflects anions not routinely measured. To determine cause of metabolic acidosis/alkalosis
    • 12mEq/L +/- 2
    • Increase- lactic acidosis/ketoacidosis
    • Normal- hyperchloremic acidosis or renal insufficiency. (or HCO3 loss)
    • Decrease-loss of colloids
  124. How to obtain ABG sample
    • -Use a peripheral artery
    • -Heparinized syringe
    • -Do not allow air to enter syringe
    • -Place sample in crushed ice and take to lab immediately
    • -Must be 15-20 minutes after a procedure
    • -Apply pressure for >5 minutes
  125. Respiratory Acidosis Etiology
    • Hypoventilation
    • Acute- medications (anesthetics, narcotics), painful breathing, infection, underdeveloped lungs.
    • Chronic- COPD
  126. Respiratory Acidosis Sx
    • Acute
    • CNS- dilated blood vessels in brain- HA, drowsiness, confusion, fullness in head, stupor, unconsciousness
    • GI- nausea
    • NM- lack of response, decreased DTR, lethargy
    • CV- Increased K+ and Ca++ possibly leading to dysrhthmia

    • Chronic COPD
    • dyspnea, activity intolerance, accessory muscle use, barrel chested
  127. Respiratory Acidosis Treatment
    • Acute: TCDB, Try to clear lungs- percussion, suctioning, spirometer, splint for pain, bronchodilators,
    • Chronic: Careful of oxygenation which can lead to further respiratory depression
  128. Respiratory Acidosis
  129. Respiratory Acidosis ABG Values
  130. Respiratory Alkalosis
  131. Respiratory Alkalosis ABG Changes
  132. Metabolic Acidosis
  133. Metabolic Acidosis ABG changes
  134. Metabolic Alkalosis
  135. Metabolic Alkalosis ABG changes
  136. Respiratory Alkalosis Etiology
    • Hyperventilation
    • Pain, Fear/Anxiety, Labor, Fever, Medications, hypoxic stimulation due to lung disease
  137. Respiratory Alkalosis Sx
    • CNS- brain blood vessels constricted- lightheadedness, dizziness, vertigo, blurred vision, faintness
    • Muscle cramps
    • Nausea
  138. Respiratory Alkalosis Treatment
    • Have patient make a conscious effort to slow breathing, breathe into a bag, also treat any fluid deficit due to hyperventilation. Oxygenation treatment for chronic hyperventilation.
    • *Treat respiratory issues before treating cause (pain, fever, etc)
  139. Metabolic Acidosis Etiology
    • Either a gain in acid or a loss of base.
    • Usually lower GI losses.
    • GI loss of HCO3
    • Renal Failure/Dysfunction- H+ retention and HCO3 excretion
    • Cellular Shifts- H+ movement out of cells
    • Overproduction of Acid- DM, decreased insulin, anorexia, malnutrition
    • Increased lactic acid from anaerobic metabolism, hemorrhage, shock
  140. Metabolic Acidosis Sx
    • CNS-depression, HA confusion, drowsiness, stupor, LOC
    • NM- Decreased DTR, lethargy, stupor, decreased sensory
    • Flush warm skin
    • Nausea
    • Increased Respirations- Kussmal respirations
    • Increased Ca++, Cl-, and K+
  141. Metabolic Acidosis Treatment
    • Dietary counseling, DM management.
    • Assess LOC, NM reflexes, Skin
  142. Metabolic Alkalosis Etiology
    • Gain in Base or Loss of Acid
    • Upper GI loss
    • GI loss- vomiting, suctioning (Decreased Cl- & H+ and Increased HCO3-)
    • K+ depleting diuretics (renal loss of H+)
    • Cellular Shifts of Ions (K+/H+)
    • High intake of bases-baking soda and antacids
    • Fluid Volume Defecit---> decreased BP in Kidneys--> ADH---> H+ excretion
  143. Metabolic Alkalosis Sx
    • CNS-brain blood vessel constriction- dizziness, faintness, lightheadedness, blurred vision,
    • NM- more excitability, tingling, spasms, cramping
    • GI- Nausea
    • Respirations decreased- trying to compensate
  144. Metabolic Alkalosis Treatment
    • Increase Potassium intake (Will lead to increased H+ levels)
    • Hydration
    • Ambulation assist due to muscle weakness
    • Monitor heart function
  145. Isotonic IV solutions
    -3 Types
    • Solutions with about the same concentration of osmotically active particles in the ECF so little fluid shifts into and out of cells.
    • -275-295 mOsm/L
    • Dextrose 5% in Water, 0.9% Sodium Chloride (NS), Lactated Ringers
  146. Dextrose 5% in Water
    -Indications for use
    -Precautions for use
    • For simple dehydration, fluid loss, and hypernatremia
    • D5 is broken down quickly just leaving H20 so it becomes a hypotonic solution which can lead to cerebral edema; doesn't provide adequate calories for sustained nutrition and can cause protein breakdown
  147. 0.9% Sodium Chloride (NS)
    -Indications for use
    • Shock, hyponatremia, blood transfusions, resuscitation, metabolic alkalosis, hypercalcemia, fluid replacement in diabetic ketoacidosis
    • Can lead to overload- CHF, edema, hypernatremia
  148. Lactated Ringers
    -Indications for use
    -What electrolyte is missing?
    • Dehydration, burns, lower GI fluid loss, acute blood loss, hypovolemia (caused by 3rd spacing)
    • Magnesium
    • Renal failure-contains K+ (causes hyperkalemia), Liver disease- pt can't metabolize lactate, pH > 7.5 (will increase Bicarb if liver is working)
  149. Hypotonic Solutions
    • Less concentrated than extracellular fluid so fluid shifts into cells causing cell to swell
    • >275 mOsm/L
    • 0.45% Sodium Chloride (1/2 NS)
  150. 0.45% Sodium Chloride (1/2 NS)
    -Indications for use
    • Water replacement, hypertonic dehydration, sodium and chloride depletion, GI fluid loss from suctioning/vomiting, diabetic ketoacidosis (after NS and before D5)
    • May cause CV collapse, increased ICP
    • Liver disease, Trauma (stroke, head trauma), Burns
  151. Hypertonic Solutions
    -3 Types
    • Solutions that draw fluids from intracellular space causing cells to shrink
    • >295mOsm/L
    • Dextrose 5% in Half Normal Saline; Dextrose 5% in Normal Saline; Dextros 10% in Water
  152. Dextrose 5% in Half Normal Saline
    -Indications for use
    • Diabetic ketoacidosis after initial NS and 1/2 NS to prevent hypoglycemia and cerebral edema
    • Use only if glucose <250mg/dL
  153. Dextrose 5% in Normal Saline
    -Indications for Use
    • For hypotonic dehydration, SIADH, Addisonian crisis (adrenal dysfunction)
    • CHF, Pulmonary Edema
  154. Dextrose 10% in Water
    -Indications for use
    Primarily for water replacement, parenteral nutrition when glucose is required.
  155. Colloids
    -What they do
    -When to use
    -2 examples
    • Increases plasma fluid by pulling fluid into bloodstream using oncotic pressure. Prevents edema during surgery
    • When crystalloid therapy doesn't work. Monitor closely
    • Albumin, Dextran
  156. Contraindications for using UE peripheral IV line
    Mastectomy, lymphectomy, AV fistula
  157. Needle gauge vs needle diameter.
    For increased fluids over short amount of time?
    Routine IV fluid admin?
    • Larger gauge # = smaller needle diameter
    • Want a larger gauge (smaller #)
    • Want a smaller gauge (larger #)
  158. Macrodrip IV Tubing
    Must check order to set the drip rate. Will be 10, 15, or 20 drip rate
  159. Microdrip IV Tubing
    Drip rate will always be 60
  160. Volutrol
    • A second container to hold part of the main bag so that the mainline bag cannot be completely infused into a pt.
    • Will always have a microdrip
  161. Blood IV Tubing
    Must always be used for transfusion
  162. Angiocatheter
    -best gauge?
    -Bigger or smaller gauge better?
    • 18
    • Bigger, if it is too small blood cells might break when squeezing through small diameter especially when administering quickly
  163. What must be hung with blood transfusions?
  164. Infiltration v. Phlebitis Sx
    • Both- Pain, edema/swelling, inflammation
    • Infiltration- pallor Cool skin temp
    • Phlebitis- Erythema, Warm Skin Temp
  165. Whole Blood Transfusions
    -Indications for use
    -Special Considerations
    • Massive hemorrhage, exchange transfusions
    • Used rarely
  166. Packed RBC transfusions
    -Indications for use
    -Special Considerations
    • Severe anemia, acute blood loss
    • Less danger of fluid overload, the absence of leukocytes reduces the risk of hemolytic febrile reactions
  167. Fresh frozen plasma transfusions
    -Indications for use
    -Special Considerations
    • Liquid portion of blood seperated from blood, rich in clotting factors but no platelets
    • For bleeding caused by deficiency in clotting factors, sometimes for hypovolemic shock
    • Must be used within 2 hours of thawing, this transfusion is being replaced by others for treating hypovolemic shock such as albumin and plasma expanders
  168. Factor VIII
    -Special Considerations
    • An essential blood clotting factor concentrated from plasma
    • For hemophiliacs
    • Careful of build up of Factor VIII antibodies
  169. Albumin Transfusion
    -Indications for use
    -Special Considerations
    • Hypovolemic shock, hypoalbuminemia
    • Doesn't transmit viruses because it is heat treated, Hyperosmolar so it draws fluid into the intravenous space using oncotic pressure
  170. Platelet Transfusion
    -Indications for Use
    -Special Considerations
    • For thrombocytopenia bleeding
    • Can be kept at room temperature for 1-5 days
  171. Blood transfusion nursing considerations
    • Do not leave patient for first 15 minutes to monitor for any signs of reaction.
    • If there is any reaction stop transfusion and NS since continuing the NS would infuse the rest of the blood in the line. -Start a new IV line with just NS