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
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
8. Movement of Water
• Fluid circulates throughout body via filtration
and osmosis.
• Water moves between compartments via
– Hydrostatic pressure
– Osmotic pressure
8
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. 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. 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
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. 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
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
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
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. 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. 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. 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. 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. 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. Attempts to Compensate
for Fluid Loss
• Increasing thirst
• Increasing heart rate
• Constriction of cutaneous blood vessels
• Producing less urine
• Concentrating urine
27
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. 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. 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.
32. 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
33.
34.
35.
36.
37.
38.
39. Electrolytes
• Positively or negatively charged inorganic
molecules
• Essential to
– Nerve conduction, membrane permeability
– Water balance, other critical body functions
45. 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
46. Figure 31.3 Renal regulation of sodium and potassium balance
47. 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
48. 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
50. Symptoms of Hyponatremia
• Early symptoms
– Nausea, vomiting, anorexia, abdominal cramping
• Later signs
– Altered neurologic function such as confusion,
lethargy, convulsions, coma, muscle twitching,
tremors
51. 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
52. 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
53. 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
54. 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
56. Treatment of Hypernatremia
• Can be treated with low-salt diet
• Acute hypernatremia treated with hypotonic
intravenous fluids or diuretics
57. 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
58. 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
60. 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
61. Symptoms of Hypokalemia
• Neurons and muscle fibers most sensitive to
potassium loss
• Muscle weakness, lethargy, anorexia,
dysrhythmias, cardiac arrest
62. 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
63. Treatment of Hypokalemia
• Mild- increase dietary intake
• Severe – give oral or parenteral potassium
supplements
64. 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
66. Symptoms of Hyperkalemia
• Most serious are dysrhythmias, and heart
block
• Other symptoms are muscle twitching,
fatigue, parasthesias, dyspnea, cramping, and
diarrhea
67. 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
68. 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
70. 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
71. 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
72. Causes of Hypocalcemia
• Hypoparathyroidism
• Malabsorption syndrome
• Deficient serum albumin
• Increased serum pH
• Renal failure
73. 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
74. 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
75. 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
76. 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
77. 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
78. 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
81. 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
82. Changes in Acids, Bicarbonate Ion, and Serum
pH in Circulating Blood
82
83. Buffer Systems
• Sodium bicarbonate–carbonic acid system
– Major ECFbuffer
– Controlled by the respiratory system and the
kidneys
• Other buffering systems:
– Phosphate
– Hemoglobin
– Protein
83
84. 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
85. 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
86. 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
89. Acidosis
• May be respiratory , caused by
hypoventilation
• May be metabolic
– Causes: diarrhea, kidney failure, diabetes, excess
alcohol, starvation
90. 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
91. 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
92. 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
94. 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
95. 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
96. Effects of Alkalosis
• Increased irritability of the nervous system
– Causing restlessness
– Muscle twitching
– Tingling and numbness of the fingers
– Tetany
– Seizures
– Coma
96
97. Pharmacotherapy of Alkalosis
• Symptoms are due to central- nervous- system
stimulation
– Nervousness, hyperactive reflexes, convulsions
– Slow, shallow respirations in attempt to retain acid
98. Pharmacotherapy of Alkalosis
(continued)
• Treatment
– Administration of ammonium chloride (severe
cases)
– Administration of sodium chloride with potassium
chloride (mild cases)
99. 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
100. 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)
101. 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
102. 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
103. 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
104. 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
105. 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
106. 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
107. 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
109. 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
110. 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
111. 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
113. 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
115. 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
117. 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)
118. 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
119. 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)
120. 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)
121. 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
122. 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).
125. Vitamins (continued)
• Human cells cannot produce vitamins
– Exception: vitamin D
– Vitamins or provitamins must be supplied in diet
– Deficiency will result in disease
126. 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
127.
128. 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
135. 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
137. 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
138. Deficiencies in Lipid-Soluble
Vitamins
• Vitamin A (retinol)
– Obtained from foods containing carotenes
• Vitamin D
– D2 (ergocalciferol)—from dairy products
– D3—from ultraviolet light
139. Deficiencies in Lipid-Soluble
Vitamins (continued)
• Vitamin E (tocopherols)
– Found in plant-seed oils, whole-grain cereals,
eggs, certain organ meats
– Primary antioxidant
140. 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
141. Deficiencies in Water-Soluble
Vitamins
• Vitamin C deficiency can cause scurvy
• Thiamine (B1) deficiency can cause beriberi
• Niacin (B3) deficiency can cause pellagra
142. 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
143. 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
145. 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
146. Drug Therapy with Fat-Soluble
Vitamins
• Teach client that excessive vitamin intake can
be harmful
• Assess for deficiency
• Assess for impaired liver function
147. 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
148. 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
149. 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
150. 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
151. 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
152. 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
153. Macromineral Therapy (continued)
• If client is taking magnesium sulfate,
immediately report
– Changes in consciousness, deep tendon reflexes
– Thirst, confusion
154. 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
155.
156. Microminerals (continued)
• Nine trace (micro) minerals
– Include iron, iodine, fluorine, and zinc
• Required daily amount is 20 mg or less
157. Undernutrition
• Many causes
– Low dietary intake
– Malabsorption disorders
– Fad diets
– Wasting disorders such as cancer or AIDS
158. Undernutrition (continued)
• Reasons for low dietary intake vary
– Poverty, depression, difficulty eating
• Nutritional consultation is appropriate
160. 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)
161. 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
162. 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
163. 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
164. 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
165. 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
166. 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
167. 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
168. 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
169. 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.
170. 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
171. 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
172. 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).
173. 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)
174. 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
175. 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
176. 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)
177. 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
178. 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
179. 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
180. 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)
181. 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
182. 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
183. 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.
184. 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
185. 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)
186. Critical Thinking Review
Question 1
Which of the following mechanisms is the most
important regulator of fluid intake?
189. Critical Thinking Review
Question 1 – Rationale
Rationale: Thirst is the most important regulator
of fluid intake.
Cognitive Level: Analysis
Nursing Process: Assessment
Patient Need: Physiological Integrity
190. Critical Thinking Review
Question 2
Which of the following nursing interventions is
most important when caring for a patient
receiving a plasma volume expander?
191. Critical Thinking Review
Question 2 – Choices
1. Assess the patient for deep vein thrombosis
2. Observe for signs of fluid overload
3. Encourage fluid intake
4. Monitor arterial blood gases
192. Critical Thinking Review
Question 2 – Answer
1. Assess the patient for deep vein thrombosis
2. Observe for signs of fluid overload
3. Encourage fluid intake
4. Monitor arterial blood gases
193. Critical Thinking Review
Question 2 – Rationale
Rationale: Dextran 40, a plasma volume
expander, causes fluid to move rapidly from the
tissues to vascular spaces, which places the
patient at risk for fluid overload.
Cognitive Level: Analysis
Nursing Process: Implementation
Patient Need: Physiological Integrity
194. Critical Thinking Review
Question 4
The 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?
197. Critical Thinking Review
Question 4 – Rationale
Rationale: Hyperkalemia, a serum potassium
level greater than 5 mEq/L, predisposes the
patient to cardiac and muscle irregularities such
as cramping in the calves, paresthesia of the
toes, and palpitations.
Cognitive Level: Analysis
Nursing Process: Diagnosis
Patient Need: Physiological Integrity
198. Critical Thinking Review
Question 5
A patient will be sent home on diuretic therapy
and will need to increase the amount of
potassium in the diet. What food choices would
the nurse suggest be added?
201. Critical Thinking Review
Question 5 – Rationale
Rationale: Bananas, strawberries, tomatoes,
dried beans, and fresh meats are natural sources
of potassium. The other food items have low
levels of potassium but may be part of a healthy
diet.
Cognitive Level: Application
Nursing Process: Implementation
Patient Need: Physiological Integrity
202. NCLEX-RN Review
Question 6
The nurse weighs the patient and finds that
there has been a weight gain of 1.5 kg since the
previous day. What would be the nurse’s next
highest priority?
203. NCLEX-RN Review
Question 6 – Choices
1. 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.
204. Critical Thinking Review
Question 6 – Answer
1. 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.
205. Critical Thinking Review
Question 6 – Rationale
Rationale: A weight gain of 1 kg (approximately
2 lb) or more may indicate fluid retention. Signs
of fluid retention include hypertension and
edema. A complete nursing assessment is
needed to determine other signs or symptoms
that may be present. Checking dietary history
may be considered after the nursing assessment
is completed.
206. Critical Thinking Review
Question 6 – Rationale (cont)
Changing diet or medications is part of the
collaborative treatment plan with the health
care provider.
Cognitive Level: Analysis
Nursing Process: Assessment
Patient Need: Physiological Integrity
208. Critical Thinking Review
Question 1
An older adult has been diagnosed with
pernicious anemia and replacement therapy is
ordered. The nurse will anticipate administering
which vitamin, and by what technique?
209. Critical Thinking Review
Question 1 – Choices
1. B6, orally in liquid form
2. K, via intramuscular injection
3. D, by light-box therapy or increased sun
exposure
4. B12, by intramuscular injection
210. Critical Thinking Review
Question 1 – Answer
1. B6, orally in liquid form
2. K, via intramuscular injection
3. D, by light-box therapy or increased sun
exposure
4. B12, by intramuscular injection
211. Critical Thinking Review
Question 1 – Rationale
Rationale: Pernicious anemia results in the
inability to absorb vitamin B12 due to the lack of
intrinsic factor in the gut. Replacement therapy
must be administered via intramuscular
injection because oral supplementation will not
be absorbed. Pernicious anemia affects vitamin
B12 absorption.
213. Critical Thinking Review
Question 3
The nurse is assessing a patient who is exhibiting
generalized weakness, cardiac dysrhythmias,
hypertension, loss of deep tendon reflexes, and
respiratory distress. What could be the possible
cause of these symptoms?
216. Critical Thinking Review
Question 3 – Rationale
Rationale: Hypomagnesemia should be
assessed. Patients experiencing
hypomagnesemia may experience general
weakness, dysrhythmias, hypertension, loss of
deep tendon reflexes, and respiratory
depression.
Cognitive Level: Analysis
Nursing Process: Assessment
Patient Need: Physiological Integrity
217. Critical Thinking Review
Question 4
The patient is a long-time alcoholic. The nurse
understands that alcoholism is the most
common cause of which vitamin deficiency?
218. Critical Thinking Review
Question 4 – Choices
1. Vitamin E
2. Vitamin A
3. Vitamin D
4. Thiamine
219. Critical Thinking Review
Question 4 – Answer
1. Vitamin E
2. Vitamin A
3. Vitamin D
4. Thiamine
220. Critical Thinking Review
Question 4 – Rationale
Rationale: Alcohol is known for its ability to
inhibit the absorption of thiamine and folic acid.
Alcohol abuse is the most common cause of
thiamine deficiency.
Cognitive Level: Analysis
Nursing Process: Implementation
Patient Need: Physiological Integrity
221. Critical Thinking Review
Question 5
The patient is a 12-year-old child with
hemophilia. The nurse is aware that this patient
will require administration of which vitamin to
improve the function of clotting factors?
222. Critical Thinking Review
Question 5 – Choices
1. Folic acid
2. Riboflavin
3. Vitamin K
4. Vitamin A
223. Critical Thinking Review
Question 5 – Answer
1. Folic acid
2. Riboflavin
3. Vitamin K
4. Vitamin A
224. Critical Thinking Review
Question 5 – Rationale
Rationale: Vitamin K should be given to the
patient to improve clotting. Without vitamin K,
abnormal prothrombin is produced and blood
clotting is affected.
Cognitive Level: Analysis
Nursing Process: Implementation
Patient Need: Physiological Integrity
225. Critical Thinking Review
Question 6
Total parenteral nutrition (TPN) has been
ordered for a patient with gastric cancer who is
no 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?
226. Critical Thinking Review
Question 6 – Choices
1. The date the TPN was ordered
2. The patient’s last electrolyte levels,
particularly glucose
3. The intravenous access site and all IV
equipment and TPN bag
4. The patient’s last chest x-ray report
227. Critical Thinking Review
Question 6 – Answer
1. The date the TPN was ordered
2. The patient’s last electrolyte levels,
particularly glucose
3. The intravenous access site and all IV
equipment and TPN bag
4. The patient’s last chest x-ray report
228. Critical Thinking Review
Question 6 – Rationale
Rationale: TPN access sites, tubing, and parenteral
nutrition bag are all areas at risk for contamination and
for bacteria to enter the patient. The nurse should
assess the IV access site for redness, streaking,
swelling, or drainage and all tubing and bag for signs of
cracks, cloudiness, or precipitate. Glucose levels and
TPN orders will be assessed periodically but do not
directly contribute to the development of infection.
229. Critical Thinking Review
Question 6 – Rationale (cont)
Periodic chest x-ray monitoring may be ordered
and should be obtained if adventitious breath
sounds are noted.
Cognitive Level: Application
Nursing Process: Implementation
Patient Need: Physiological Integrity
