Prof. Jose M Antigua
Electrolytes
 A substance that is dissolved in solution and
some of its molecules split or dissociate into
electrically charged atoms or ions.
Slide 2
Body Fluid Compartments
 Fluid in each of the body compartments
contains electrolytes.
 Each compartment has a particular
composition of electrolytes, which differs
from that of other compartments.
 To function normally, body cells must have
fluids and electrolytes in the right
compartments and in the right amounts.
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 Whenever an electrolyte moves out of a
cell, another electrolyte moves in to take
its place.
 The numbers of cations and anions must
be the same for homeostasis to exist.
 Compartments are separated by semi
permeable membranes.
Slide 5
Electrolyte Movement
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Intravascular Compartment
 Refers to fluid inside a blood vessel
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Intracellular Compartment
 Refers to all fluid inside the cell.
 Most bodily fluids are inside the cell
Slide 12
Intracellular fluid
Provides the cell with internal fluid
necessary for cellular function.
Approximately 40% to 50% of body
weight (two thirds of total body
water).
Electrolytes: potassium (primary),
magnesium, phosphate.
Slide 13
The Extracellular Compartment
 Refers to fluid outside the cell.
 The extracellular compartment includes the interstitial
fluid, (intravascular and interstitial) which is fluid
between cells (sometimes called the third space), blood,
lymph, bone, connective tissue, water, and trans cellular
fluid.
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 Transport system for cellular waste, oxygen,
electrolytes, and nutrients; help regulate
body temperature; lubricate and cushion
joints.
 Approximately 20% to 30% of body weight
(one third of total body water).
 Vascular: circulating plasma volume.
 Interstitial: fluid surrounding tissue cells.
 Electrolytes: sodium (primary), chloride,
bicarbonate.
Slide 16
Third-Spacing
 Is the accumulation and sequestration of
trapped extracellular fluid in an actual or
potential body space as a result of disease or
injury.
 The trapped fluid represents a volume loss and is
unavailable for normal physiological processes.
 Fluid may be trapped in body spaces such as the
pericardial, pleural, peritoneal, or joint
cavities; the bowel; or the abdomen, or
within soft tissues after trauma or burns.
 Assessing the intravascular fluid loss caused by third-
spacing is difficult.
The loss may not be reflected in weight changes or intake and
output records and may not become apparent until after
organ malfunction occurs.
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Edema
 Is an excess accumulation of fluid in the
interstitial space.
 Localized edema occurs as a result of
traumatic injury from accidents or surgery,
local inflammatory processes, or burns.
 Generalized edema, also called anasarca, is
an excessive accumulation of fluid in the
interstitial space throughout the body and
occurs as a result of conditions such as
cardiac, renal, or liver failure.
Slide 20
The Inflammatory
Response
Slide 21
Elsevier items and derived items © 2011, 2008, 2005,
2002 by Saunders, an imprint of Elsevier Inc.
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Body Fluid
 Body fluids transport nutrients to the cells and
carry waste products from the cells.
 Total body fluid (intracellular and extracellular)
amounts to about 60% of body weight in the
adult, 55% in the older adult, and 80% in the
infant.
 Thus, infants and older adults are at a higher risk
for fluid-related problems than younger adults;
children have a greater proportion of body water
than adults, and the older adult has the least
proportion of body water.
Slide 24
Constituents of Body Fluids
 Body fluids consist of water and dissolved
substances.
 The largest single fluid constituent of the body is
water.
 Some substances, such as glucose, urea, and
creatinine, do not dissociate in solution; that is,
they do not separate from their complex forms into
simpler substances when they are in solution.
 Other substances do dissociate; for example, when
sodium chloride is in a solution, it dissociates, or
separates, into two parts or elements.
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Urea
Slide 28
Osmosis
 Osmotic pressure is the force that draws
the solvent from a less concentrated
solute through a selectively permeable
membrane into a more concentrated
solute, thus tending to equalize the
concentration of the solvent.
 If a membrane is permeable to water but
not to all the solutes present, the
membrane is a selective or
semipermeable membrane.
Slide 29
Osmosis
 Osmosis is the movement of solvent molecules
across a membrane in response to a
concentration gradient, usually from a solution
of lower to one of higher solute concentration.
 When a more concentrated solution is on one
side of a selectively permeable membrane and a
less concentrated solution is on the other side, a
pull called osmotic pressure draws the water
through the membrane to the more
concentrated side, or the side with more
solute.
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Filtration
Is the movement of solutes and
solvents by hydrostatic pressure.
The movement is from an area of
higher pressure to an area of lower
pressure.
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Hydrostatic Pressure
 Hydrostatic pressure is the force exerted by the
weight of a solution.
 When a difference exists in the hydrostatic
pressure on two sides of a membrane, water and
diffusible solutes move out of the solution that
has the higher hydrostatic pressure by the
process of filtration.
 At the arterial end of the capillary, the
hydrostatic pressure is higher than the osmotic
pressure; therefore, fluids and diffusible solutes
move out of the capillary.
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Lymph channels
At the venous end, the osmotic
pressure, or pull, is higher than the
hydrostatic pressure, and fluids and
some solutes move into the capillary.
The excess fluid and solutes
remaining in the interstitial spaces
are returned to the intravascular
compartment by the lymph channels.
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Lymph Channels of the Body
Slide 46
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Osmolality
 Osmolality refers to the number of
osmotically active particles per kilogram
of water; it is the concentration of a
solution.
 In the body, osmotic pressure is
measured in milliosmoles (mOsm).
 The normal osmolality of plasma is
270 to 300 milliosmoles/kilogram
(mOsm/kg) water.
Slide 48
Slide 49
Concepts of Fluid and Electrolyte
Balance (continued)
 Body fluid replacement
Orally ingested liquids
 Water in foods
 Water formed by oxidation of foods
 Maintaining fluid and electrolyte balance
 Kidneys, adrenal glands play major role
 Antidiuretic hormone from pituitary gland
regulates osmotic pressure of extracellular fluid
by regulating amount of water reabsorbed by
kidneys.

Slide 50
 Description
Fluid Volume Deficit
 Dehydration occurs when fluid intake of the body is
insufficient to meet fluid needs of body
 Types of fluid volume deficits
 Isotonic dehydration: Water and electrolytes lost in equal
proportions.
 Hypotonic dehydration: Electrolyte loss exceeds water
loss.
 Hypertonic dehydration: Water loss exceeds electrolyte
loss.
 Causes of fluid volume deficits
 Hemorrhage
 Excessive perspiration
 Hyperventilation
 Prolonged fever, vomiting, and diarrhea
 End-stage renal failure
 Diabetes insipidus
Slide 51
Elsevier items and derived items © 2011, 2008, 2005,
2002 by Saunders, an imprint of Elsevier Inc.
Slide 52
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FLUID VOLUME DEFICIT
 Dehydration occurs when the fluid intake
of the body is not sufficient to meet the
fluid needs of the body.
 The goal of treatment is to:
a) Restore fluid volume,
b) Replace electrolytes as needed, and
c) Eliminate the cause of the fluid volume
deficit.
Slide 54
Fluid imbalances
Sensible fluid loss: fluid loss of
which an individual is aware, as in
urine.
Insensible fluid loss: fluid loss of
which an individual is not aware
(approximately 600 to 900 mL of fluid
is lost every 24 hours through the skin
and lungs in a healthy adult).
Slide 55
Causes of fluid deficit
 Decreased fluid intake.
 Loss of fluid through the gastrointestinal tract, as in
vomiting, nasogastric suctioning, diarrhea.
 Excessive excretion due to renal disease;
inappropriate antidiuretic hormone secretion (DI).
 Iatrogenic loss due to overuse of diuretics or
inadequate replacement of fluid loss.
 Increased insensible fluid loss through skin and
lungs due to febrile state, increased respiratory rates.
 Loss of fluid through impaired integrity of the skin as
in burns, wounds, and hemorrhages.
Slide 56
Types of Fluid Volume Deficits
Isotonic Dehydration
 Water and dissolved electrolytes are lost in
equal proportions.
 Known as hypovolemia; isotonic
dehydration is the most common type of
dehydration.
 Isotonic dehydration results in decreased
circulating blood volume and inadequate
tissue perfusion.
Slide 57
Causes of Fluid Volume Deficits
Isotonic Dehydration
a. Inadequate intake of fluids and solutes
b. Fluid shifts between compartments
c. Excessive losses of isotonic body fluids
Slide 58
Intravenous fluid replacement
therapy
Isotonic solutions
 Used to expand ECF volume and for intravascular
dehydration.
Solutions.
 D5W: 5% dextrose in water (physiologically hypotonic).
 0.9% NaCl (normal saline solution).
 Lactated Ringer’s solution.
May be used to dilute medications or to keep the vein
open.
Slide 59
NURSING PRIORITY
 In D5W the dextrose is metabolized
rapidly, leaving free water to be
absorbed.
 It does not replenish electrolytes.
 Contraindicated for clients with head
injuries.
 Used with caution in children, potential
for increase in intracranial pressure.
Slide 60
Hypertonic Dehydration
 Water loss exceeds electrolyte loss.
 The clinical problems that occur result
from alterations in the concentrations
of specific plasma electrolytes.
 Fluid moves from the intracellular
compartment into the plasma and
interstitial fluid spaces, causing cellular
dehydration and shrinkage.
Slide 61
Elsevier items and derived items © 2011, 2008, 2005,
2002 by Saunders, an imprint of Elsevier Inc.
Slide 62
Hypertonic Dehydration
Conditions that increase fluid loss, such as:
excessive perspiration, hyperventilation,
ketoacidosis, prolonged fevers, diarrhea,
early-stage renal failure, and diabetes
insipidus.
Slide 63
Hypotonic solutions
 Solutions containing more water and
less basic electrolytes.
 0.45% or half-strength NaCl (normal
saline solution).
 May be used to replenish cellular fluid.
 Monitor closely for intravascular fluid loss,
hypotension, changes in level of
consciousness, and edema.
Slide 64
Hypotonic Dehydration
Electrolyte loss exceeds water loss.
The clinical problems that occur result
from fluid shifts between
compartments, causing a decrease in
plasma volume.
Fluid moves from the plasma and
interstitial fluid spaces into the cells,
causing a plasma volume deficit and
causing the cells to swell.
Slide 65
Hypotonic Dehydration
Causes
a. Chronic illness
b. Excessive fluid replacement (hypotonic)
c. Renal failure
d. Chronic malnutrition
Slide 66
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Hypertonic solutions
 Administered slowly; can cause intravascular
volume overload; carefully monitor serum
sodium, lung sounds, and blood pressure.
 Solutions.
 Dextrose 5% in 0.45% or half-strength NaCl
(normal saline).
 Dextrose 5% in 0.9% NaCl (normal saline).
 Dextrose 5% in Lactated Ringer’s.
 Used to treat situations of hyponatremia and
hypovolemia.
Slide 68
Assessment
 In children Assess skin turgor on the
abdomen or the inner thigh (unless
abdominal distention is present).
 In older adult Assess skin turgor on the
sternum or below the clavicle.
 In adults Assess skin turgor on the back of
hand and anterior forearm.
 Infants and children: poor perfusion, poor
capillary refill resulting in mottled skin** color
changes.
Slide 69
Mottled skin
Slide 70
Fluid Volume Deficit
 Assessment
Tachycardia
 Hypotension
 Tachypnea
 Lethargy to coma state
 Oliguria
 Nonelastic skin turgor
 Dry skin
 Mucous membranes
 Decreased bowel sounds
 Constipation
 Thirst
 Interventions
 Rehydrate client as prescribed
 Administer medications to correct cause(s) as prescribed
Slide 71

Nursing intervention
 Maintain accurate intake and output records.
 Obtain accurate daily weight.
 Daily weight is the most reliable indicator of
fluid loss or gain in all clients, regardless of age.
 Accurate daily weight: same time each day
(preferably before breakfast), same scales, same
clothing. NOTE: 1 L of fluid equals 2.2 lb or 1 kg.
 Evaluate for presence of edema.
 Maintain intravenous (IV) replacement fluids at
prescribed flow rate.
Slide 72
Fluid Volume Excess
Causes
 Inadequately controlled intravenous (IV)
therapy
 Renal failure
 Long-term corticosteroid therapy
 Excessive sodium ingestion
 Rapid infusion hypertonic-hypotonic solutions
 Excessive sodium bicarbonate therapy
 Syndrome of inappropriate secretion of
antidiuretic hormone (SIADH)
Slide 73
Fluid Volume Excess
 Assessment
Bradycardia
 Hypertension
 Distended neck veins
 Tachypnea
 Moist crackles
 Altered level of consciousness
 Pitting, dependent edema
 Diarrhea
 Ascites
 Polyuria
 Interventions
 Administer diuretics as prescribed
 Restrict sodium and fluid intake as prescribed

Slide 74
Fluid Volume Excess
 Description
 Fluid intake or fluid retention exceeds fluid
needs of the body
 Types
 Isotonic overhydration

Excessive fluid in extracellular fluid compartment
 Hypertonic overhydration

Rare, but may be caused by excessive sodium intake
 Hypotonic overhydration


Known as water intoxication
Excessive fluid moves into intracellular space and
all body fluid compartments expand
Slide 75
Overhydration
Slide 76
Volume Expanders: 2 Types.
 Crystalloids and Colloids.
 Crystalloids are aqueous solutions of
mineral salts or other water-soluble
molecules.
 Colloids contain larger insoluble
molecules, such as gelatin; blood itself is a
colloid.
Slide 77
 Crystalloids are those substances which
are easily crystallized from their aqueous
solution.
 Colloids contain much larger particles
than crystalloids (1 – 200 nm).
 Crystalloids contain much smaller
particles than colloids (<1 nm).
 Colloids do not pass through the plasma
membrane of the cell.
Slide 78
 Colloids are better than crystalloids at
expanding the circulatory volume, because
their larger molecules are retained more
easily in the intravascular space and increase
osmotic pressure.
 Colloids are gelatinous solutions that
maintain a high osmotic pressure in the
blood.
 Examples: albumin, dextran, hydroxyethyl
starch (or hetastarch), Haemaccel and
Gelofusine.
Slide 79
Hyponatremia
Serum sodium level less than 135 mEq/L
Causes:
1. Increases in excretion
 Excessive diaphoresis
 Diuretics
 Vomiting
 Diarrhea
 Wound drainage, especially gastrointestinal
 Renal disease
 Decreased secretion of aldosterone
2. Inadequate intake
 Nothing by mouth
 Low-salt diet
Slide 80
3. Diluted serum sodium
 Excessive ingestion of hypotonic fluids or
irrigation with hypotonic fluids.
 Renal failure
 Freshwater drowning
 Syndrome of inappropriate antidiuretic
hormone secretion
 Hyperglycemia (act as an osmotic active
substance diluting sodium in plasma).
 Congestive heart failure
Slide 81
Assessment
 Changes in pulse and blood pressure,
depending on vascular volume
 Shallow respirations
 Skeletal muscle weakness
 Diminished deep tendon reflexes
 Increased gastrointestinal motility,
(hyperactive bowel sounds)
 Polyuria
 Decreased specific gravity
Slide 82
Slide 83
Hyponatremia
 Interventions
 Accurate monitoring of body systems related
to impact of changes in serum sodium status
 Monitor cardiovascular, respiratory,
neuromuscular, cerebral, renal, and
gastrointestinal status.
 Increase daily dietary sodium intake as
prescribed
 Bacon, butter, canned foods, luncheon
meats, table salt.
Slide 84
Elsevier items and derived items © 2011, 2008, 2005,
2002 by Saunders, an imprint of Elsevier Inc.
Slide 85
 If hyponatremia is accompanied by a fluid
volume deficit (hypovolemia), IV sodium
chloride infusions are administered to restore
sodium content and fluid volume.
 If hyponatremia is accompanied by fluid volume
excess (hypervolemia), osmotic diuretics
(Manitol) are administered to promote the
excretion of water rather than sodium.
 If caused by inappropriate or excessive secretion
of antidiuretic hormone, medications that
antagonize antidiuretic hormone may be
administered. See the list….
Slide 86
Vasopressin Receptor Antagonist
Unselective (mixed V1A/V2)
 Conivaptan
V1A selective (V1RA)
 Relcovaptan
V1B selective (V3RA)
 Nelivaptan
V2 selective (V2RA)
 Lixivaptan
 Mozavaptan
 Satavaptan
 Tolvaptan
Slide 87
 Instruct the client to increase oral sodium
intake and inform the client about the
foods to include in the diet.
 If the client is taking lithium (Lithobid),
monitor the lithium level, because
hyponatremia can cause diminished
lithium excretion, resulting in toxicity.
Hyponatremia precipitates lithium toxicity in
a client taking lithium (Lithobid).
Slide 88
Hypernatremia
Serum sodium level exceeds 145 mEq/L
Causes:
1. Decreased sodium excretion
 Corticosteroids
 Cushing’s syndrome
 Renal failure
 Hyperaldosteronism
 Increased sodium intake: excessive oral sodium
ingestion or excessive administration of sodium containing IV fluids.
Slide 89
Decreased water intake: nothing by
mouth.
Increased water loss: increased rate of
metabolism, fever, hyperventilation,
infection, excessive diaphoresis,
watery diarrhea, diabetes insipidus
Slide 90
Hypernatremia
 Assessment
 Changes in pulse and blood pressure in
response to vascular volume
 Irregular muscle contractions
 Diminished to absent deep tendon reflexes
 Altered cerebral function
 Increased specific gravity
 Oliguria
 Dry skin
Slide 91
Interventions
 Monitor cardiovascular, respiratory, neuromuscular,
cerebral, renal, and integumentary status.
 If the cause is fluid loss, prepare to administer IV
infusions.
 If the cause is inadequate renal excretion of sodium,
prepare to administer diuretics that promote sodium
loss.
 Restrict sodium and fluid intake as prescribed
Monitor the client closely for signs of a potassium
imbalance.
A potassium imbalance can cause cardiac
dysrhythmias that can be life-threatening.
Slide 92
Hypokalemia
 Serum
potassium level less than 3.5 mEq/L
 Potassium deficit is potentially life-threatening
because everybody system is affected.
 Causes
 Total body potassium loss
 Inadequate intake
 Movement of potassium from extracellular
to intracellular fluid
 Dilution of serum potassium
Slide 93
Causes
1. Actual total body potassium loss
 Excessive use of medications such as diuretics or
corticosteroids
 Increased secretion of aldosterone, such as in
Cushing’s syndrome
 Vomiting, diarrhea
 Wound drainage, particularly gastrointestinal
 Prolonged nasogastric suction
 Excessive diaphoresis
 Renal disease impairing reabsorption of
potassium.
Slide 94
2. Inadequate potassium intake: nothing by
mouth
3. Movement of potassium from the extracellular
fluid to the intracellular fluid
• Alkalosis
• Hyperinsulinism
4. Dilution of serum potassium
• Water intoxication
• IV therapy with potassium-poor solutions
Slide 95
Hypokalemia (continued)
 Assessment
 Thready, weak pulses
 Orthostatic hypotension
 Changes in electrocardiogram (ECG), such as ST depression
and flat or inverted T wave
 Shallow respirations
 Lethargy to coma state
 Skeletal muscle weakness
 Deep tendon hyporeflexia
 Decreased GI motility
 Polyuria
 Decreased specific gravity
Slide 96
Slide 97
Hypokalemia (continued)
 Interventions
 Accurate monitoring of body systems related to impact of
changes in serum potassium status.
 Take precautions when administering.
potassium IV.
 Maximum infusion rate should be 5 to 10 mEq/hr as
prescribed.
 If client receiving more than 10 mEq/hr, place on
cardiac monitor, infuse using IV controller.
 Instruct client not to take oral potassium
supplements, if prescribed, on empty stomach.
 Instruct client about increasing dietary potassium with
foods, such as bananas, fish, oranges, potatoes, meat,
raisins, spinach, tomatoes.
Slide 98
Interventions
Monitor cardiovascular, respiratory,
neuromuscular, gastrointestinal, and
renal status, and place the client on a
cardiac monitor.
Monitor electrolyte values.
Administer potassium supplements
orally or intravenously, as prescribed.
Slide 99
Oral Potassium Supplements
 Oral potassium supplements may cause nausea
and vomiting, and they should not be taken on
an empty stomach; if the client complains of
abdominal pain, distention, nausea, vomiting,
diarrhea, or gastrointestinal bleeding, the
supplement may need to be discontinued.
 Liquid potassium chloride has an unpleasant
taste and should be taken with juice or another
liquid.
Slide 100
 IV administered potassium
 Institute safety measures for the client experiencing
muscle weakness.
 If the client is taking a potassium-losing diuretic, it
may be discontinued; a potassium sparing diuretic may
be prescribed.
 Instruct the client about foods that are high in
potassium content.
Potassium is never administered by IV push,
intramuscular, or subcutaneous routes.
IV potassium is always diluted and
administered using an infusion device.
Slide 101
Precautions Intravenously
Administering Potassium
The maximum recommended infusion rate is 5 to 10
mEq/hr, never to exceed 20 mEq/hr under any
circumstances.
Potassium is never given by intravenous (IV) push or by the
intramuscular or subcutaneous route.
A dilution of no more than 1 mEq/10 mL of solution is
recommended.
After adding potassium to an IV solution, rotate and invert
the bag to ensure that the potassium is distributed evenly
throughout the IV solution.
Ensure that the IV bag containing potassium is properly
labeled.
Slide 102
A client receiving more than 10 mEq/hr should be
placed on a cardiac monitor and monitored for
cardiac changes, and the infusion should be
controlled by an infusion device.
Potassium infusion can cause phlebitis; therefore the
nurse should assess the IV site frequently for signs of
phlebitis or infiltration.
If either occurs, the infusion should be stopped
immediately.
Assess renal function before administering
potassium, and monitor intake and output during
administration.
Slide 103
Slide 104
Hyperkalemia
Serum potassium level exceeds 5.1 mEq/L
Causes
1. Excessive potassium intake
 Over ingestion of potassium-containing foods or
medications, such as potassium chloride or salt
substitutes
 Rapid infusion of potassium-containing IV solutions
2. Decreased potassium excretion
 Potassium-sparing diuretics
 Renal failure
 Adrenal insufficiency, such as in Addison’s disease
.
Slide 105
Potassium-sparing diuretics
Amiloride
Eplerenone (Inspra)
Spironolactone (Aldactone)
Triamterene (Dyrenium)
Slide 106
3. Movement of potassium from the
intracellular fluid to the extracellular
fluid.
Tissue damage
Acidosis
Hyperuricemia
Hyper catabolism
Slide 107
Slide 108
Interventions
1. Monitor cardiovascular, respiratory, neuromuscular, renal,
and gastrointestinal status; place the client on a cardiac
monitor.
2. Discontinue IV potassium (keep the IV catheter patent)
and hold oral potassium supplements.
3. Initiate a potassium-restricted diet.
4. Prepare to administer potassium-excreting diuretics if
renal function is not impaired.
5. If renal function is impaired, prepare to administer sodium
polystyrene sulfonate (Kayexalate), a cation exchange resin
that promotes gastrointestinal sodium absorption and
potassium excretion.
Slide 109
6. Prepare the client for dialysis if potassium levels
are critically high.
7. Prepare for the IV administration of hypertonic
glucose with regular insulin to move excess
potassium into the cells.
8. Monitor renal function.
9. When blood transfusions are prescribed for a
client with a potassium imbalance, the client
should receive fresh blood, if possible;
transfusions of stored blood may elevate the
potassium level because the breakdown of older
blood cells releases potassium.
Slide 110
10. Teach the client to avoid foods high
in potassium
11. Instruct the client to avoid the use of
salt substitutes or other potassiumcontaining substances.
Monitor the serum potassium level
closely when a client is receiving a
potassium-sparing diuretic.
Slide 111
Kayexalate Administration
Oral
 Give as a suspension in a small quantity of water or in syrup.
Usual amount of fluid ranges from 20–100 mL or approximately
3–4 mL/g of drug.
Rectal
 Use warm fluid (as prescribed) to prepare the emulsion for
enema.
 Administer at body temperature and introduce by gravity,
keeping suspension particles in solution by stirring.
 Flush suspension with 50–100 mL of fluid; then clamp tube and
leave it in place.
 Urge patient to retain enema at least 30–60 min but as long as
several hours if possible.
 Irrigate colon (after enema solution has been expelled) with 1 or
2 quarts flushing solution (non-sodium containing).
 Drain returns constantly through a Y-tube connection.
 Store remainder of prepared solution for 24 h; then discard.
Common Food Sources
 Avocado
 Oranges
 Bananas
 Potatoes
 Cantaloupe
 Pork, beef, veal
 Carrots
 Raisins
 Fish
 Spinach
 Mushrooms
 Strawberries
 Tomatoes
Slide 113
Hypocalcemia
Serum calcium level lower than 8.6 mg/dL
Causes
1. Inhibition of calcium absorption from the
gastrointestinal tract
 Inadequate oral intake of calcium
 Lactose intolerance
 Malabsorption syndromes such as celiac sprue
or Crohn’s disease
 Inadequate intake of vitamin D
 End-stage renal disease
Slide 114
2. Increased calcium excretion
 Renal failure, polyuric phase
 Diarrhea
 Steatorrhea
 Wound drainage, especially gastrointestinal
3. Conditions that decrease the ionized fraction of calcium
 Hyperproteinemia
 Alkalosis
 Medications such as calcium chelators or binders
 Acute pancreatitis
 Hyperphosphatemia
 Immobility
 Removal or destruction of the parathyroid glands
Slide 115
Slide 116
(A) Chvostek’s sign. (B,C) Trousseau’s sign
Slide 117
Interventions
1. Monitor cardiovascular, respiratory,
neuromuscular, and gastrointestinal status; place
the client on a cardiac monitor.
2. Administer calcium supplements orally or calcium
intravenously.
3. When administering calcium intravenously,
warm the injection solution to body
temperature before administration and
administer slowly; monitor for
electrocardiographic changes, observe for
infiltration, and monitor for hypercalcemia.
Slide 118
4. Administer medications that increase calcium absorption.
a. Aluminum hydroxide reduces serum phosphorus levels,
causing the counter effect of increasing calcium levels.
b. Vitamin D aids in the absorption of calcium from the
intestinal tract.
5. Provide a quiet environment to reduce environmental
stimuli.
6. Initiate seizure precautions.
7. Move the client carefully and monitor for signs of a
pathological fracture.
8. Keep 10% calcium gluconate available for treatment of
acute calcium deficit.
9. Instruct the client to consume foods high in calcium
Slide 119
Normal Value
Ca+ 8.6 to 10 mg/dL
 Cheese
 Collard greens
 Milk and Soy milk
 Rhubarb
 Sardines
 Spinach
 Tofu
 Yogurt
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Hypercalcemia
 Serum calcium level that exceeds 10 mg/dL.
Causes
1. Increased calcium absorption
 a. Excessive oral intake of calcium
 b. Excessive oral intake of vitamin D
2. Decreased calcium excretion
 a. Renal failure
 b. Use of Thiazide diuretics
Slide 121
3. Increased bone resorption of calcium
 a. Hyperparathyroidism
 b. Hyperthyroidism.
 c. Malignancy (bone destruction from metastatic
tumors)
 d. Immobility
 e. Use of glucocorticoids
4. Hemoconcentration
 a. Dehydration
 b. Use of lithium
 c. Adrenal insufficiency
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Slide 123
Interventions
1. Monitor cardiovascular, respiratory, neuromuscular,
renal, and gastrointestinal status; place the client on a
cardiac monitor.
2. Discontinue IV infusions of solutions containing calcium
and oral medications containing calcium or vitamin D.
3. Discontinue Thiazide diuretics and replace with diuretics
that enhance the excretion of calcium.
4. Administer medications as prescribed that inhibit
calcium resorption from the bone, such as phosphorus,
calcitonin (Calcimar), bisphosphonates, and
prostaglandin synthesis inhibitors (aspirin, nonsteroidal
anti-inflammatory drugs).
Slide 124
5. Prepare the client with severe hypercalcemia for
dialysis if medications fail to reduce the serum
calcium level.
6. Move the client carefully and monitor for signs of a
pathological fracture.
7. Monitor for flank or abdominal pain, and strain the
urine to check for the presence of urinary stones.
8. Instruct the client to avoid foods high in calcium
A client with a calcium imbalance is at risk for a
pathological fracture.
Move the client carefully and slowly; assist the client
with ambulation.
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HYPOMAGNESEMIA
Serum magnesium level lower than 1.6 mg/dL
Normal Value 1.6 to 2.6 mg/dL
Causes
1. Insufficient magnesium intake
 a. Malnutrition and starvation
 b. Vomiting or diarrhea
 c. Malabsorption syndrome
 d. Celiac disease
 e. Crohn’s disease
2. Increased magnesium secretion
 a. Medications such as diuretics
 b. Chronic alcoholism
3. Intracellular movement of magnesium
 a. Hyperglycemia
 b. Insulin administration
 c. Sepsis
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Slide 127
Interventions
1. Monitor cardiovascular, respiratory,
gastrointestinal, neuromuscular, and central
nervous system status; place the client on a
cardiac monitor.
2. Because hypocalcemia frequently accompanies
hypomagnesemia, interventions also aim to
restore normal serum calcium levels.
3. Administer magnesium sulfate by the IV
route in severe cases (intramuscular
injections cause pain and tissue damage);
monitor serum magnesium levels frequently.
Slide 128
4. Initiate seizure precautions.
5. Monitor for diminished deep tendon
reflexes, suggesting Hypermagnesemia,
during the administration of magnesium
6. Oral preparations of magnesium may cause
diarrhea and increase magnesium loss.
7. Instruct the client to increase the intake of
foods that contain magnesium
Slide 129
Common Food Sources
 Avocado
 Peanut butter
 Canned white tuna
 Peas
 Cauliflower
 Pork, beef, chicken
 Green leafy
vegetables, such as
spinach and broccoli
 Potatoes
 Milk
 Raisins
 Yogurt
 Oatmeal
Slide 130
HYPERMAGNESEMIA
Is a serum magnesium level that exceeds 2.6
mg/dL
Causes
1. Increased magnesium intake
 a. Magnesium-containing antacids and
laxatives
 b. Excessive administration of magnesium
intravenously
2. Decreased renal excretion of magnesium as a
result of renal insufficiency
Slide 131
Slide 132
Interventions
1. Monitor cardiovascular, respiratory, neuromuscular, and
central nervous system status; place the client on a cardiac
monitor.
2. Diuretics are prescribed to increase renal excretion of
magnesium.
3. Intravenously administered calcium chloride or calcium
gluconate may be prescribed to reverse the effects of
magnesium on cardiac muscle.
4. Instruct the client to restrict dietary intake of magnesiumcontaining foods.
5. Instruct the client to avoid the use of laxatives and antacids
containing magnesium.
Calcium gluconate is the antidote for magnesium overdose
Slide 133
HYPOPHOSPHATEMIA
Serum phosphorus level lower than 2.7 mg/dL
Normal Value 2.7 to 4.5 mg/dL
2. A decrease in the serum phosphorus level is accompanied
by an increase in the serum calcium level.
Causes
1. Insufficient phosphorus intake:
• a. malnutrition and starvation
2. Increased phosphorus excretion
 a. Hyperparathyroidism
 b. Malignancy
 c. Use of magnesium-based or aluminum hydroxide–based
antacids
3. Intracellular shift
 a. Hyperglycemia
 b. Respiratory alkalosis
Slide 134
Assessment
1. Cardiovascular
 a. Decreased contractility and cardiac output
 b. Slowed peripheral pulses
2. Respiratory:
• a. shallow respirations
3. Neuromuscular
 a. Weakness
 b. Decreased deep tendon reflexes
 c. Decreased bone density that can cause fractures
and alterations in bone shape
 d. Rhabdomyolysis
Slide 135
4. Central nervous system
 a. Irritability
 b. Confusion
 c. Seizures
5. Hematological
 a. Decreased platelet aggregation and
increased bleeding
 b. Immunosuppression
Slide 136
Interventions
1. Monitor cardiovascular, respiratory, neuromuscular,
central nervous system, and hematological status.
2. Discontinue medications that contribute to
hypophosphatemia.
3. Administer phosphorus orally along with a vitamin D
supplement.
4. Prepare to administer phosphorus intravenously
when serum phosphorus levels fall below 1 mg/dL
and when the client experiences critical clinical
manifestations.
5. Administer IV phosphorus slowly because of the
risks associated with Hyperphosphatemia.
Slide 137
6. Assess the renal system before administering
phosphorus.
7. Move the client carefully, and monitor for signs of a
pathological fracture.
8. Instruct the client to increase the intake of the
phosphorus-containing foods while decreasing the
intake of any calcium-containing foods
A decrease in the serum phosphorus level is
accompanied by an increase in the serum calcium
level.
An increase in the serum phosphorus level is
accompanied by a decrease in the serum calcium level.
Slide 138
Common Food Sources
Fish
Organ meats
Nuts
Pork, beef, chicken
Whole-grain breads and cereals
Slide 139
HYPERPHOSPHATEMIA
Is a serum phosphorus level that exceeds 4.5
mg/dL
2. Most body systems tolerate elevated serum
phosphorus levels well.
3. An increase in the serum phosphorus level is
accompanied by a decrease in the serum calcium
level.
4. The problems that occur in hyperphosphatemia
center on the hypocalcemia that results when
serum phosphorus levels increase.
Slide 140
Causes
1. Decreased renal excretion resulting from renal
insufficiency
2. Tumor lysis syndrome (hematologic ca: nonHodgkin’s lymphoma or acute leukemia)
hyperuricemia, hyperkalemia,
hyperphosphatemia, and hypocalcemia
3. Increased intake of phosphorus, including
dietary intake or overuse of phosphatecontaining laxatives or enemas
4. Hypoparathyroidism
Slide 141
Assessment
Slide 142
Interventions
1. Interventions entail the management of hypocalcemia.
2. Administer phosphate-binding medications that
increase fecal excretion of phosphorus by binding
phosphorus from food in the gastrointestinal tract.
3. Instruct the client to avoid phosphate-containing
medications, including laxatives and enemas.
4. Instruct the client to decrease the intake of food that is
high in phosphorus.
5. Instruct the client in medication administration: take
phosphate-binding medications, emphasizing that they
should be taken with meals or immediately after meals.
Slide 143