week 2 rsc 325 summer
TRANSCRIPT
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Fluid, Electrolyte, and Acid-Base ImbalancesGould Chapter 6
Presented by:
Mahmoud Kaddoura, PhD, CAGS, MSN, RN
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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
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Fluid Compartments (Cont’d)
• Intracellular compartment (ICF)• Extracellular compartment (ECF)
– Intravascular fluid (IVF) or blood– Interstitial fluid (ISF) or intercellular fluid– Cerebrospinal fluid (CSF)– Transcellular fluids
• Present in various secretions• Pericardial cavity• Synovial cavities
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Major Body Fluid Compartments
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Fluid Compartments in the Body
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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
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Sources and Losses of Water
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Movement of Water
• Fluid circulates throughout body via filtration and osmosis.
• Water moves between compartments via– Hydrostatic pressure – Osmotic pressure
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Movements of Water between Compartments
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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
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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
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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
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Movement of fluids and solution tonicity
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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
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
Capillary Exchange
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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
Causes of Edema (Cont’d)
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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
Causes of Edema (Cont’d)
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
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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
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
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.
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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
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
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Attempts to Compensate for Fluid Loss
• Increasing thirst• Increasing heart rate• Constriction of cutaneous blood vessels• Producing less urine• Concentrating urine
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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
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
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
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
Electrolytes
• Positively or negatively charged inorganic molecules
• Essential to– Nerve conduction, membrane permeability– Water balance, other critical body functions
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Distribution of Major Electrolytes
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Movements of Electrolytes between Compartments
Sodium
• Essential for maintaining osmolality, water balance, acid-base balance
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
Figure 31.3 Renal regulation of sodium and potassium balance
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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
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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
Hyponatremia and Fluid Shift into Cells
Symptoms of Hyponatremia
• Early symptoms– Nausea, vomiting, anorexia, abdominal cramping
• Later signs– Altered neurologic function such as confusion,
lethargy, convulsions, coma, muscle twitching, tremors
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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
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
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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
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
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Effects of Hypernatremia
• Weakness, agitation• Dry, rough mucous membranes• edema• Increased thirst (if thirst mechanism is
functional)• Increased blood pressure
Treatment of Hypernatremia
• Can be treated with low-salt diet• Acute hypernatremia treated with hypotonic
intravenous fluids or diuretics
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
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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!
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Sodium and Potassium Affect Nerve Conduction
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
Symptoms of Hypokalemia
• Neurons and muscle fibers most sensitive to potassium loss
• Muscle weakness, lethargy, anorexia, dysrhythmias, cardiac arrest
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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
Treatment of Hypokalemia
• Mild- increase dietary intake• Severe – give oral or parenteral potassium
supplements
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
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Relationship of Hydrogen and Potassium Ions
Symptoms of Hyperkalemia
• Most serious are dysrhythmias, and heart block
• Other symptoms are muscle twitching, fatigue, parasthesias, dyspnea, cramping, and diarrhea
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
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
Signs of Potassium Imbalance
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
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
Causes of Hypocalcemia
• Hypoparathyroidism • Malabsorption syndrome• Deficient serum albumin• Increased serum pH• Renal failure
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
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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
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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
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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
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
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
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Chloride Shift
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The Hydrogen Ion and pH Scale
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
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Changes in Acids, Bicarbonate Ion, and Serum pH in Circulating Blood
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Buffer Systems
• Sodium bicarbonate–carbonic acid system– Major ECFbuffer– Controlled by the respiratory system and the
kidneys• Other buffering systems:
– Phosphate– Hemoglobin– Protein
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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
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Decompensation
• Occurs when:– Causative problem becomes more severe– Additional problems occur– Compensation mechanisms are exceeded or fail
• Requires intervention to maintain homeostasis
• LIFE-THREATENING!
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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
Figure 31.4 Acid–base imbalances
Acidosis
• May be respiratory , caused by hypoventilation
• May be metabolic– Causes: diarrhea, kidney failure, diabetes, excess
alcohol, starvation
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
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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
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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
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Changes in Blood Gases with Acidosis
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
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
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Effects of Alkalosis
• Increased irritability of the nervous system– Causing restlessness– Muscle twitching– Tingling and numbness of the fingers– Tetany– Seizures– Coma
Pharmacotherapy of Alkalosis
• Symptoms are due to central- nervous- system stimulation– Nervousness, hyperactive reflexes, convulsions– Slow, shallow respirations in attempt to retain acid
Pharmacotherapy of Alkalosis (continued)
• Treatment– Administration of ammonium chloride (severe
cases)– Administration of sodium chloride with potassium
chloride (mild cases)
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
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)
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
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
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
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
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
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
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
Dextran
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
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
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
Potassium chloride
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
Sodium Chloride
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
Patients receiving drug therapy for fluid-balance, electrolyte, and acid-base disorders (continued)
• Diagnoses– Deficient fluid volume– Decreased cardiac output– Fatigue– Activity Intolerance– Deficient Knowledge (drug therapy)
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)
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
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)
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)
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
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).
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Drugs for Nutritional Disorders
Vitamins
• Organic substances are needed in small amounts– Promote growth– Maintain health
Vitamins (continued)
• Human cells cannot produce vitamins– Exception: vitamin D– Vitamins or provitamins must be supplied in diet– Deficiency will result in disease
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
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
Vitamin A
Water-Soluble Vitamins (C, B Complex)
• Absorbed with water in digestive tract• Easily dissolved in blood and body fluids
Water-Soluble Vitamins (C, B Complex) (continued)
• Excess cannot be stored– Excreted in urine– Must be ingested daily
Folic Acid
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
Vitamin Pharmacotherapy
• Indicated for certain conditions– Poor nutritional intake– Pregnancy– Chronic-disease states
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
Deficiencies in Lipid-Soluble Vitamins
• Vitamin A (retinol)– Obtained from foods containing carotenes
• Vitamin D– D2 (ergocalciferol)—from dairy products– D3—from ultraviolet light
Deficiencies in Lipid-Soluble Vitamins (continued)
• Vitamin E (tocopherols)– Found in plant-seed oils, whole-grain cereals,
eggs, certain organ meats– Primary antioxidant
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
Deficiencies in Water-Soluble Vitamins
• Vitamin C deficiency can cause scurvy• Thiamine (B1) deficiency can cause beriberi
• Niacin (B3) deficiency can cause pellagra
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
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
Magnesium
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
Drug Therapy with Fat-Soluble Vitamins
• Teach client that excessive vitamin intake can be harmful
• Assess for deficiency• Assess for impaired liver function
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
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
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
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
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
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
Macromineral Therapy (continued)
• If client is taking magnesium sulfate, immediately report– Changes in consciousness, deep tendon reflexes– Thirst, confusion
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
Microminerals (continued)
• Nine trace (micro) minerals– Include iron, iodine, fluorine, and zinc
• Required daily amount is 20 mg or less
Undernutrition
• Many causes– Low dietary intake– Malabsorption disorders– Fad diets– Wasting disorders such as cancer or AIDS
Undernutrition (continued)
• Reasons for low dietary intake vary– Poverty, depression, difficulty eating
• Nutritional consultation is appropriate
Enteral Nutrition
• Provided orally or through feeding tube• Means of meeting client’s nutritional needs
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)
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
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
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
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
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
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
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
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
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.
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
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
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).
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)
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
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
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)
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
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
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
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)
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
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
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.
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
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)
Critical Thinking ReviewQuestion 1
Which of the following mechanisms is the most important regulator of fluid intake?
Critical Thinking ReviewQuestion 1 – Choices
1. Thirst 2. Electrolytes 3. Renin–angiotensin 4. Kidneys
Critical Thinking ReviewQuestion 1 – Answer
1. Thirst 2. Electrolytes 3. Renin–angiotensin 4. Kidneys
Critical Thinking ReviewQuestion 1 – Rationale
Rationale: Thirst is the most important regulator of fluid intake.Cognitive Level: AnalysisNursing Process: AssessmentPatient Need: Physiological Integrity
Critical Thinking ReviewQuestion 2
Which of the following nursing interventions is most important when caring for a patient
receiving a plasma volume expander?
Critical Thinking ReviewQuestion 2 – Choices
1. Assess the patient for deep vein thrombosis 2. Observe for signs of fluid overload3. Encourage fluid intake 4. Monitor arterial blood gases
Critical Thinking ReviewQuestion 2 – Answer
1. Assess the patient for deep vein thrombosis 2. Observe for signs of fluid overload3. Encourage fluid intake4. Monitor arterial blood gases
Critical Thinking ReviewQuestion 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: AnalysisNursing Process: ImplementationPatient Need: Physiological Integrity
Critical Thinking ReviewQuestion 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?
Critical Thinking ReviewQuestion 4 – Choices
1. Hypernatremia 2. Hypercalcemia 3. Hypoglycemia 4. Hyperkalemia
Critical Thinking ReviewQuestion 4 – Answer
1. Hypernatremia 2. Hypercalcemia 3. Hypoglycemia 4. Hyperkalemia
Critical Thinking ReviewQuestion 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: AnalysisNursing Process: DiagnosisPatient Need: Physiological Integrity
Critical Thinking ReviewQuestion 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?
Critical Thinking ReviewQuestion 5 – Choices
1. Liver, red meats, lettuce 2. Apples, pears, celery, onions 3. Bananas, tomatoes, beans, fresh meats 4. Potato chips, licorice, rice, corn
Critical Thinking ReviewQuestion 5 – Answer
1. Liver, red meats, lettuce 2. Apples, pears, celery, onions 3. Bananas, tomatoes, beans, fresh meats 4. Potato chips, licorice, rice, corn
Critical Thinking ReviewQuestion 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: ApplicationNursing Process: ImplementationPatient Need: Physiological Integrity
NCLEX-RN ReviewQuestion 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?
NCLEX-RN ReviewQuestion 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.
Critical Thinking ReviewQuestion 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.
Critical Thinking ReviewQuestion 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.
Critical Thinking ReviewQuestion 6 – Rationale (cont)
Changing diet or medications is part of the collaborative treatment plan with the health care provider.Cognitive Level: AnalysisNursing Process: AssessmentPatient Need: Physiological Integrity
207
Nutrition Questions
Critical Thinking ReviewQuestion 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?
Critical Thinking ReviewQuestion 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
Critical Thinking ReviewQuestion 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
Critical Thinking ReviewQuestion 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.
Critical Thinking ReviewQuestion 1 – Rationale (cont)
Cognitive Level: ApplicationNursing Process: ImplementationPatient Need: Physiological Integrity
Critical Thinking ReviewQuestion 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?
Critical Thinking ReviewQuestion 3 – Choices
1. Hypocalcemia 2. Hypercalcemia 3. Hypomagnesemia 4. Hypermagnesemia
Critical Thinking ReviewQuestion 3 – Answer
1. Hypocalcemia 2. Hypercalcemia 3. Hypomagnesemia 4. Hypermagnesemia
Critical Thinking ReviewQuestion 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: AnalysisNursing Process: Assessment Patient Need: Physiological Integrity
Critical Thinking ReviewQuestion 4
The patient is a long-time alcoholic. The nurse understands that alcoholism is the most
common cause of which vitamin deficiency?
Critical Thinking ReviewQuestion 4 – Choices
1. Vitamin E 2. Vitamin A 3. Vitamin D 4. Thiamine
Critical Thinking ReviewQuestion 4 – Answer
1. Vitamin E 2. Vitamin A 3. Vitamin D 4. Thiamine
Critical Thinking ReviewQuestion 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: AnalysisNursing Process: ImplementationPatient Need: Physiological Integrity
Critical Thinking ReviewQuestion 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?
Critical Thinking ReviewQuestion 5 – Choices
1. Folic acid2. Riboflavin 3. Vitamin K 4. Vitamin A
Critical Thinking ReviewQuestion 5 – Answer
1. Folic acid2. Riboflavin 3. Vitamin K 4. Vitamin A
Critical Thinking ReviewQuestion 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: AnalysisNursing Process: ImplementationPatient Need: Physiological Integrity
Critical Thinking ReviewQuestion 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?
Critical Thinking ReviewQuestion 6 – Choices
1. The date the TPN was ordered 2. The patient’s last electrolyte levels,
particularly glucose3. The intravenous access site and all IV
equipment and TPN bag 4. The patient’s last chest x-ray report
Critical Thinking ReviewQuestion 6 – Answer
1. The date the TPN was ordered 2. The patient’s last electrolyte levels,
particularly glucose3. The intravenous access site and all IV
equipment and TPN bag 4. The patient’s last chest x-ray report
Critical Thinking ReviewQuestion 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.
Critical Thinking ReviewQuestion 6 – Rationale (cont)
Periodic chest x-ray monitoring may be ordered and should be obtained if adventitious breath sounds are noted. Cognitive Level: ApplicationNursing Process: ImplementationPatient Need: Physiological Integrity