FLUIDS AND

ELECTROLYTES
FUNDAMENTAL CONCEPTS intravascular space in which the
kidneys then receive less blood and
attempt to compensate by
AMOUNT AND COMPOSITION OF BODILY decreasing urine output.
FLUIDS  Other s/sx that indicate an intravascular
fluid volume deficit include:
 ~60% of the total weight. o Increased HR
 Influenced by age, gender, and body fat. o Decreased BP
 Percentage of body fluid: o Decreased central venous pressure
o Young > old
(CVP))
o Men > women o Edema
o Obese > thin o Increased body weight
 Fat cells – little water. o Imbalances in fluid I and O.
 Muscle, skin, and blood – highest water.  Occur in patients who have:
 Two fluid compartments: o Hypocalcemia
o Intracellular space (2/3, primarily in o Decreased iron intake
the skeletal muscle mass) o Severe liver diseases
o Extracellular space (1/3)
o Alcoholism
 Extracellular fluid (ECF) compartment –
o Hypothyroidism
o Intravascular fluid space –
o Malabsorption
 Contains plasma.
o Immobility
 ~3L of the average 6L of
o Burns
blood volume is made up of
plasma. o Cancer
 The remaining 3L is made up
of erythrocytes, leukocytes, ELECTROLYTES
and thrombocytes.
o Interstitial fluid space –  Active chemicals classified as –
 Contains the fluid that o Cations – (+) charges.
surrounds the cell and totals  Sodium
about 11-12L in an adult.  Potassium
 Example – lymph.  Calcium
o Transcellular fluid space –  Magnesium
 ~1L.  Hydrogen ions
 Examples – cerebrospinal, o Anions – (-) charges.
pericardial, synovial,  Chloride
intraocular, and pleural fluids;  Bicarbonate
sweat; and digestive  Phosphate
secretions.  Sulfate
 Proteinate ions
Third Fluid Shift Or “Third Spacing” –  Milliequivalents (mEq) – expression of
 Loss of ECF into a space that does not electrolyte concentration.
contribute to equilibrium between the ICF o mEq is defined as being equivalent
and ECF. to the electrochemical activity of 1
 Early evidence: mg of hydrogen.
o A decrease in urine output despite  In a solution, cations and anions are equal
adequate fluid intake which occurs in mEq per liter.
because fluid shifts out of the  Electrolyte concentrations in the ICF differ
from those in the ECF. It is customary to
FLUIDS AND
ELECTROLYTES
measure the electrolytes in the most
accessible portion of the ECF, namely, the
plasma.
 Na+ ions
o Major cations in the ECF.
o Concentration affects the overall
concentration of the ECF, thus
responsible in regulating the volume
of body fluid.
o Na+ retention > fluid retention.
o Na+ loss > fluid loss.
 K+ and PO4-
o Major electrolytes in the ICF.
o K+ is low in ECF and can only
tolerate small changes.
 Cell membrane pumps –
o Exchange sodium and potassium
ions to maintain the high
extracellular concentration of sodium
and high intracellular concentration
of potassium.
 Hydrostatic pressure –
o The pressure exerted by the fluid on
the walls of the blood vessel.
o Normal movement of fluids through
the capillary wall into the tissues
depends on HP at both the arterial
and the venous ends of the vessel
and the osmotic pressure exerted by
the protein of plasma.
o The direction of fluid movement
depends on the differences in these
two opposing forces (hydrostatic vs.
osmotic pressure).
REGULATION OF BODY FLUID
COMPARTMENTS
Osmosis and Osmolality –
FLUIDS AND
ELECTROLYTES
 Osmosis –
o Shifting of fluid through a
 Movement of water and solutes occurs from
an area of high hydrostatic pressure to an
area of low hydrostatic pressure.
semipermeable membrane from the
region of low solute (more water) to  Examples:
the region of high solute (less o The kidneys filter approximately
water) until the solutions are of 180L of plasma per day.
equal concentration. o Passage of water and electrolytes
 Osmolality – from the arterial capillary bed to the
o Refers to the concentration of interstitial fluid; in this instance, the
dissolved particles in a unit of fluid. hydrostatic pressure results from the
o The higher the number of dissolved pumping action of the heart.
particles, the higher the osmolality.
Sodium-Potassium Pump –
o Osmolality influences the movement
of water.  Moves molecules from an area of low
 Tonicity – concentration to that of high concentration.
o The ability of all solutes to cause an  Actively moves sodium from the cell into the
osmotic driving force that promotes ECF, and potassium into the cell.
water movement from one  Requires energy to be spent for the
compartment to another. movement to occur against a concentration
o The control of tonicity determines gradient (active transport).
the normal state of cellular
hydration and cell size.
o Sodium, mannitol, glucose, and SYSTEMIC ROUTES OF GAINS AND LOSSES
sorbitol are effective osmoles
(capable of affecting water
movement).
 Osmotic pressure –
o The amount of hydrostatic pressure
needed to stop the flow of water by
osmosis. It is primarily determined
by the concentration of solutes.
 Oncotic pressure –
o The osmotic pressure exerted by
proteins (e.g., albumin).
 Osmotic diuresis – Kidneys –
o The increase in urine output caused  Daily urine volume: 1-2 L.
by the excretion of substances such  Output: ~1 mL/kg/hour (all age groups).
as glucose, mannitol, or contrast
agents in the urine. Skin –

Diffusion –  Sensible perspiration – the visible water and

electrolyte loss through the skin (sweating).
 Movement of substance from an area of o Solutes in sweat – Na+, K+, Cl-
higher concentration to one of lower
o Actual sweat loss: 0-1000 mL or
concentration.
more every hour (depending on
 It occurs through the random movement of
factors).
ions and molecules.
 Insensible perspiration – a nonvisible form
Filtration – of water loss.
FLUIDS AND
ELECTROLYTES
o

o
Continuous water loss by
evaporation: ~600 mL/day
Fever greatly increases insensible
o Using this formula –

water loss through the lungs and the

skin, as does loss of the natural skin
barrier (through major burns).
Lungs –
 Factors affecting serum and urine
 Insensible loss: ~300 mL/day osmolality:
 Much greater with increased respiratory rate
or depth, or in a dry climate.
Gastrointestinal Tract –

 Usual loss: 100-200 mL/day.

 Fluid that circulates through the GI every
24 hours: ~8 L.
 Bulk of fluid is normally reabsorbed in the
small intestine.
 Diarrhea and fistulas can cause large
losses.

Osmolarity –
LABORATORY TESTS FOR EVALUATING
 Describes the concentration of solutions
FLUID STATUS
and is measured in milliosmoles per liter
Osmolality – (mOsm/L).
 Normal value: within 10 mOsm of the
 Concept: measured osmolality.
o The concentration of fluid that
affects the movement of water Urine specific gravity –
between fluid compartments by
 Concept:
osmosis.
o Measures the kidneys’ ability to
o Measures the solute concentration
excrete or conserve water.
per kilogram in blood and urine.
o Compared to the weight of distilled
o A measure of a solution’s ability to
water, which has a specific gravity of
create osmotic pressure and affect
1.000.
the movement of water.
 Normal value: 1.010 to 1.025.
o Measured as milliosmoles per
 Procedures:
kilogram of water (mOsm/kg).
o Can be measured at bedside by
 Normal levels –
placing a calibrated hydrometer or
o Serum osmolality – reflects the
urinometer in a cylinder of ~20mL of
concentration of sodium (alongside
urine.
BUN and glucose).
o Can also be assessed with a
 200 to 300 mOsm/kg.
refractometer or dipstick with a
o Urine osmolality – determined by
reagent for this purpose.
urea, creatinine, and uric acid.
 Interpretation:
 200 to 800 mOsm/kg.
o Varies inversely with urine volume;
 Estimating serum osmolality at bedside:
normally, the larger the volume of
o Doubling the serum sodium level, or
FLUIDS AND
ELECTROLYTES
o
urine, the lower the specific gravity
is.
Less reliable indicator of
concentration than urine osmolality;
increased glucose or protein in urine
can cause a falsely elevated specific
gravity.
Blood Urea Nitrogen (BUN) –
 Concept:
o Measures urea nitrogen, an end-
product of protein metabolism by the
liver.
o Amino acid breakdown produces
large amounts of ammonia
molecules, which are absorbed into
the bloodstream. Ammonia
molecules are converted into urea
and excreted in the urine.
 Normal value: 10-20 mg/dL (3.6-7.2
mmol/L).
 Factors that increase BUN:
o Decreased renal function.
o GI bleeding.
o Dehydration.
o Increased protein intake.
o Fever.
o Sepsis.
 Factors that decrease BUN:
o End-stage liver disease.
o Low-protein diet.
o Starvation.
o Any condition that results in
expanded fluid volume (e.g.,
pregnancy).
Creatinine –
 Concept:
o Measures creatinine, an end-product
of muscle metabolism.
o Better indicator of renal function than
BUN because it does not vary with
protein intake and metabolic state.
 Normal serum creatinine: ~0.7-1.4 mg/dL
(62-124mmol/L).
 Interpretation:
o
o
Concentrations depends on lean body
mass and varies from person to person.
Serum creatinine levels increase when
renal function decreases.
Hematocrit –
 Concept:
o Measures the volume percentage of
RBC in whole blood.
 Normal range:
o 42%-52% for males
o 35%-47% for females.
 Conditions that increase hematocrit –
o Dehydration
o Polycythemia
 Conditions that decrease hematocrit –
o Overhydration
o Anemia
Urine sodium –
 Concept:
o Used to assess volume status and
are useful in the diagnosis of
hyponatremia and acute renal
failure.
o Values change with sodium intake
and status of fluid volume:
 As sodium intake increases,
excretion increases.
 As the circulating fluid
volume decreases, sodium is
conserved.
 Normal urine sodium levels:
o 75-100 mEq/24 hours (75-
200mmol/24hours).
o A random specimen usually contains
more than 40mEq/L of sodium.
HOMEOSTATIC MECHANISMS
Kidney Functions –
 Filters 180 L of plasma every day in the
adult.
 Excretes 1-2 L of urine.
 Act both autonomously and in response to
bloodborne messengers, such as
FLUIDS AND
ELECTROLYTES

aldosterone and antidiuretic hormone
(ADH).
Major functions of kidneys:
Other Mechanisms –
o Regulation of ECF volume and
osmolality by selective retention and
excretion of body fluids.
o Regulation of normal electrolyte
levels in the ECF by selective
electrolyte retention and excretion.
o Regulation of pH of the ECF by
retention of hydrogen ions.
o Excretion of metabolic wastes and
toxic substances.
Heart and Blood Vessel Functions –
 Pumping action of the heart circulates blood
through the kidneys under sufficient
pressure to allow for urine formation.
 Failure of this pumping action interferes with
renal perfusion and thus with water and
electrolyte regulation.
Lung Functions –
 Lungs remove ~300 mL of water daily in the
normal adult through exhalation.
 Play major role in maintaining acid-base
balance.
Pituitary Functions –
 Antidiuretic Hormone (ADH) from the
pituitary gland controls the retention and
excretion of water by the kidneys and
regulates blood volume to maintain the
osmotic pressure of the cells.
Adrenal Functions –
 Increase in aldosterone secretion from the
adrenal cortices of the adrenal gland causes
increased sodium and fluid retention, as
well as potassium loss. Conversely, a
decreased in aldosterone level also
increases sodium and fluid loss, as well as
potassium retention.
 Large quantities of cortisol can also
produce sodium and fluid retention.
Parathyroid Functions –
 Parathyroid hormones (PTH) promote
bone resorption, calcium absorption from
the intestines, and calcium reabsorption
from the renal tubules.
 Baroreceptors – responds to changes in
the circulating blood volume and regulate
sympathetic and parasympathetic neural
activity as well as endocrine. Usually, when
arterial pressure decreases, baroreceptor
impulses through the vasomotor center also
decreases. This stimulates the sympathetic
nervous system and inhibits the
parasympathetic nervous system that result
in vasoconstriction, activation of RAAS, and
the eventual release of more aldosterone.
The outcome is an increase in cardiac rate,
conduction, contractility, and an increase in
circulating blood volume.
 Renin-Angiotensin-Aldosterone System
(RAAS) – decreased in renal perfusion
activates RAAS which then stimulates the
release of Renin from the kidneys. Renin
acts on angiotensinogen from the liver to
form Angiotensin I. An enzyme called
Angiotensin-converting enzyme (ACE)
also acts on angiotensin I and transform it to
Angiotensin II, a potent vasoconstrictor
which results in increase arterial perfusion
and stimulates thirst. Increased release of
renin results in the release of more
aldosterone.
 Antidiuretic Hormone and Thirst – both
have important roles in maintaining sodium
concentration and oral intake of fluids.
o Oral intake – controlled by the thirst
center located in the hypothalamus.
As serum concentration or
osmolality increases or blood
volume decreases, neurons in the
hypothalamus are stimulated by the
intracellular dehydration; thirst then
occurs.
o Water excretion – controlled by
ADH, aldosterone, and
baroreceptors. ADH determines
whether the urine that is excreted is
concentrated or dilute.
FLUIDS AND
ELECTROLYTES
 Osmoreceptors – located in the surface of
the hypothalamus, they sense changes in
sodium concentration. As osmotic pressure
tachycardia, hyperthyroidism,
subarachnoid hemorrhage, and
small cell lung cancer.
increases, the neurons become dehydrated o Level decreases in chronic heart
and quickly release impulses to the failure and with the use of
posterior pituitary, which increases the medications such as urea and
release of ADH, which then travels in the prazosin.
blood to the kidneys where it alters the
permeability to water, causing increased
reabsorption of water and decreased urine
output.

 Release of Atrial Natriuretic Peptide –

increased release of ANP decreases blood INTRAVENOUS SOLUTIONS
pressure and volume. Normal value of ANP
in plasma is 20-77 pg/mL (20-77 ng/L). Isotonic Solutions -

 IV fluids that have similar concentrations as

o Level increases in acute heart
blood.
failure, paroxysmal supraventricular
FLUIDS AND
ELECTROLYTES
 Because of this, the fluid stays in the
intravascular and osmosis does not cause
fluid movement between compartments.
 Examples of hypotonic solutions:

o 0.45% NaCl (half-strength saline)

 Used for patients with FLUID VOLUME
DEFICIT (FVE) to raise blood pressure.
 Too much isotonic fluid can cause FLUID
VOLUME EXCESS.
 Examples of isotonic solutions:
o 0.9 % NaCl (isotonic, also known as
normal saline [NS])
 Na+ 154 mEq/L
 Cl- 154 mEq/L
 (308 mOsm/L)
 Also available with varying
concentrations of dextrose
(the most frequently used is
a 5% dextrose
concentration).
o Lactated Ringer’s solution
(Hartmann’s solution)
 Na+ 130 mEq/L
 K+ 4 mEq/L
 Ca++ 3 mEq/L
 Cl- 109 mEq/L
 Lactate (metabolized to
bicarbonate)
 Also available with varying
concentrations of dextrose
(the most frequently used is
a 5% dextrose
concentration).
o 5% dextrose in water (D5W)
 No electrolytes
 50g of dextrose
Hypotonic Solutions –
 Na+ 77 mEq/L
 Cl- 77 mEq/L
 (154 mOsm/L)
 Also available with varying
concentrations of dextrose
(most commonly 5%
concentration).
Hypertonic Solutions –
 IV fluids that have higher concentration of
dissolved particles than blood.
 Causes an increased of dissolved solutes in
the intravascular space compared to the
cells which causes osmotic movement of
water out of the cells and into the
intravascular space to dilute the solutes in
the blood.
 Used to draw water away from the bloated
tissues and back into the bloodstream.
 Examples of hypertonic solutions:
o 3% NaCl (hypertonic saline)
 Na+ 513 mEq/L
 Cl- 513 mEq/L
 (1026 mOsm/L)
o 5% NaCl (hypertonic solution)
 Na+ 855 mEq/L
 Cl- 855 mEq/L
 (1710 mOsm/L)

 IV fluids that have a lower concentration of

dissolved solutes than blood.
 It results in decreased concentration of
dissolved solutes in the blood as compared
to the intracellular space which causes an
osmotic movement of water from the
intravascular compartment into the
intracellular space.
 Used to treat cellular dehydration.
 Too much fluid movement out of the
intravascular compartment into cells,
cerebral edema can occur.
FLUIDS AND
ELECTROLYTES
FLUID VOLUME DISTURBANCES 

Thirst
Decreased or delayed capillary refill
 Decreased central venous pressure
HYPOVOLEMIA (FLUID VOLUME DEFICIT)  Cool, clammy, pale skin related to
peripheral vasoconstriction
 A condition that occurs when loss of
extracellular fluid (ECF) exceeds the intake  Anorexia
of fluid.  Nausea
 It occurs when water and electrolytes are  Lassitude
lost in the same proportion as they exist in  Muscle weakness
normal body fluids, so that the ratio of  Cramps
serum electrolytes to water remains the
Assessment and Diagnostic Findings –
same.
 Not the same with dehydration because  Blood urea nitrogen (BUN) and
dehydration refers to loss of water alone Creatinine – a volume-depleted patient has
with increased serum sodium levels. a BUN elevated out of proportion to the
serum creatinine (normal – 10:1 to 20:1).
Pathophysiology –

 Results from loss of body fluids and occurs o Normal BUN: 6 to 24 mg/dL (2.1 to
more rapidly when coupled with decreased 8.5 mmol/L)
fluid intake. o Normal Creatinine:
 May also develop with a prolonged period of  For men – 0.7 to 1.3 mg/dL
inadequate intake. (61.9 to 114.9 µmol/L)
 Causes include:  For women – 0.6 to 1.1
o Abnormal fluid losses, such as from mg/dL (53 to 97.2 µmol/L)
vomiting, diarrhea, GI suctioning,
and sweating.  Hematocrit – the hematocrit level is greater
o Decreased intake, as in nausea or than normal because the plasma volume
lack of access to fluids. does not increase to achieve the
o Third-spacing normovolemic anemic state.
o Diabetes insipidus.
o Normal for male: 41-50%
o Adrenal insufficiency
o Normal for female: 36-48%
o Osmotic diuresis
o Hemorrhage
 Serum electrolytes –
o Coma

Clinical Manifestations – o Potassium is decreased or elevated.

 Hypokalemia occurs with GI
Severity depends on the degree of fluid loss. and renal losses.
 Acute weight loss  Hyperkalemia occurs with
 Decreased skin turgor adrenal insufficiency.
 Oliguria o Sodium is decreased or elevated.
 Concentrated urine  Hyponatremia occurs with
increased thirst and ADH
 Orthostatic hypotension due to volume
release.
depletion
 Hypernatremia results from
 Weak, rapid heart rate
increased insensible losses
 Flattened neck veins
and diabetes insipidus.
 Increased temperature
FLUIDS AND
ELECTROLYTES
 Urine specific gravity – increased in
relation to the kidneys’ attempt to conserve
water and is decreased with diabetes
insipidus.
o Normal: 1.005 to 1.030
 Urine osmolality – can be greater than 450
mOsm/kg, because the kidneys try to
compensate by conserving water.
o Normal: 250-900 mOsm/kg (250-900
mmol/kg)
Gerontologic Considerations –
 Requires careful assessment of:
o Intake and output of fluids from all
sources.
o Daily weight.
o Side effects and interactions of
medications.
o Prompt reporting and management
of disturbances.
o Skin turgor over the forehead or the
sternum.
 Functional assessment of the ability of the
elderly patient to determine fluid and food
needs and to obtain adequate intake.
 Recognize that some elderly patients
deliberately restrict their fluid intake to avoid
embarrassing episodes of incontinence.
 Remind elderly patient without
cardiovascular and renal dysfunction to
drink adequate fluids, particularly in warm or
humid weather.
Medical Management –
 Oral fluid is preferred if deficit is not severe.
 IV route is needed if acute or severe.
o Isotonic electrolyte solutions are
frequently used to treat hypotensive
patients with FVD because they
expand plasma volume –
 Lactated ringer’s solution
 90% sodium chloride
o Hypotonic electrolyte solution is
given if patient becomes
normotensive to provide both
electrolytes and water for renal
excretion of metabolic wastes –
 0.45% sodium chloride
 Accurate assessment of I&O, weight, vital
signs, central venous pressure, level of
consciousness, breath sounds, and skin
color should be performed to determine
when therapy should be slowed to avoid
volume overload.
 Fluid Challenge Test – done if patient is
not excreting enough urine to determine
whether the depressed renal function is
caused by reduced renal blood flow
secondary to FVD or by acute tubular
necrosis.
o Example – administering 100-200
mL of normal saline solution over 15
minutes. The goal is to provide fluids
rapidly enough to attain adequate
tissue perfusion without
compromising the cardiovascular
system. The response for patients
with FVD but normal renal function is
increased in urine output and
increase in BP and central venous
pressure.
Nursing Management –
 Monitor and measure fluid I&O at least
every 8 hours or hourly.
o Normal: 30 mL/hour or more.
 Monitor body weight.
o An acute loss of 0.5 kg (1lb)
represents fluid loss of ~500 mL.
o 1 L of fluid = 1kg or 2.2 lb.
 Monitor vital signs closely.
o Weak, rapid pulse.
o Orthostatic hypotension.
o Decreased in body temperature.
 Monitor skin and tongue turgor regularly.
 Assess the degree of oral mucous
membrane moisture.
o Dry mouth.
 Monitor urine concentration by measuring
urine specific gravity.
o USG is greater than 1.020.
 Assess cerebral and peripheral perfusion.
o Alteration in mental function.
FLUIDS AND
ELECTROLYTES
o
o
Cold extremities.
Low central venous pressure – if
cardiopulmonary function is normal.
Preventing Hypovolemia –
 Identifies patients at risk and takes
measures to minimize fluid losses. For
example:
o Patient w/ diarrhea – control
diarrhea (i.e., antidiarrheal
medications) and administer
replacement fluids (oral fluids).
Correcting Hypovolemia –
 Oral fluids with considerations on like and
dislikes.
 Fluid replacement with consideration on the
type of fluid lost.
 Assist with frequent mouth care and
provides nonirritating fluids if patient has
mouth discomfort.
 Offer small volumes of oral rehydration
solutions (i.e., Rehydrate, Elete, Cytomax).
 Antiemetics may be needed if nausea is
present before oral fluid replacement.
 Therapy may need to be initiated by an
alternative route if deficit cannot be
corrected by oral fluids (enteral or
parenteral).
 Isotonic fluids are prescribed to increase
ECF volume.
HYPERVOLEMIA (FLUID VOLUME EXCESS)
 Refers to an isotonic expansion of the ECF
caused by the abnormal retention of water
and sodium in approximately the same
proportion in which they normally exist in
the ECF.
 Secondary to an increase in the total body
sodium content which leads to an increase
in total body water.
 Serum sodium concentration is essentially
normal.
Pathophysiology –
 May be related to simple fluid overload or
diminished function of the homeostatic

mechanisms responsible for regulating fluid
balance.
Contributing factors:
o Heart failure
o Renal failure
o Cirrhosis of the liver
 Other factors:
o Consumption of excessive amounts
of table or other table salts.
o Excessive administration of sodium-
containing fluids may predispose a
patient with impaired regulatory
mechanism to a serious FVE as
well.
Clinical Manifestations –
 Edema
 Distended neck veins
 Crackles (abnormal lung sounds).
 Tachycardia
 Increased BP
 Increased pulse pressure
 Increased central venous pressure
 Increased weight
 Increased urine output
 Shortness of breath and wheezing
Assessment and Diagnostic Findings –
 BUN – may decreased because of plasma
dilution, low protein intake, and anemia.
 Hematocrit – may also decreased because
of plasma dilution, low protein intake, and
anemia.
 Serum and urine osmolality – both
decreased due to excessive retention of
water.
 Urine sodium level – increased.
 Chest x-ray – pulmonary congestion.
Medical Management –
 Directed at the causes:
o Discontinuing the infusion if related
to excessive administration of
sodium-containing fluids.
 Symptomatic treatment:
o Diuretics
o Restricting fluid and sodium.
FLUIDS AND
ELECTROLYTES
Pharmacologic Management –
 Diuretics – prescribed when dietary
restriction of sodium is insufficient to reduce
edema.
o Thiazide diuretics – block sodium
reabsorption in the distal tubule
where only 5% to 10% of filtered
sodium is reabsorbed.
 For mild to moderate
hypervolemia.
o Loop diuretics – can cause greater
loss of both sodium and water
because they block sodium
reabsorption in the ascending limb of
the loop of Henle where 20% to 30%
of filtered sodium is normally
reabsorb.
 For severe hypervolemia
Side Effects:
o Hypokalemia – with all diuretics
except those that work in the last
distal tubule of the nephrons.
o Hyperkalemia – can occur with
diuretics that work in the last distal
tubule especially in patients with
decreased renal function.
o Hyponatremia – due to increase
release of ADH secondary to
reduction in circulating volume.
o Decreased magnesium – occurs
with loop and thiazide due to
decreased reabsorption and
increase excretion of magnesium.
 Potassium supplements – to prevent
hypokalemia.
Dialysis –
 May be used to remove nitrogenous wastes
and control potassium and acid-base
balance, and to remove sodium and fluid.
 Continuous renal replacement therapy may
also be required.
Nutritional Therapy –
 Dietary restriction of sodium (from a mild
restriction as little as 250 mg/day).
 Use lemon juice, onions, and garlic as
substitute flavorings.
 Be cautious in using salt substitute in
patients taking potassium-sparing diuretics
as they contain potassium.
 Patients may need to use distilled water if
the local water supply is very high in
sodium.
 Avoid water softeners that add sodium to
water in exchange for other ions, such as
calcium.
 Protein intake may be increased in patients
who are malnourished or who have low
serum protein levels to increase oncotic
pressure and pull fluid out of the tissues into
vessels for excretion by the kidneys.
Nursing Management –
 Regularly measure I & O.
 Weigh patient daily and note for rapid
weight gain.
 Assess breath sounds at regular intervals.
 Monitors the degree of edema in the most
dependent parts of the body, such as feet
and ankles in ambulatory patients and the
sacral region in patients confined to bed.
Preventing Hypervolemia –
 Sodium-restricted diet.
 Avoidance of over-the-counter medications
without first checking with a health care
provide because the substance may contain
sodium.
 Consider hidden sources of sodium, such
as water supply or use of water softeners if
fluid retention persists despite adherence to
prescribed diet.
Detecting and Controlling Hypervolemia –
 Promoting rest
o Bed rest favors diuresis of edema
fluid may be due to diminished
venous pooling and the subsequent
increase in effecting circulating
blood volume and renal perfusion.
 Restricting sodium intake.
 Monitoring parenteral fluid therapy.
FLUIDS AND
ELECTROLYTES


Administering appropriate medications.
Place patient in semi-Fowler’s position if
dyspnea or orthopnea is present.
 Turn and reposition patient at regular
intervals because edematous tissue is
prone to skin breakdown.
 Teach patient to monitor response to
therapy by documenting fluid I & O and
body weight changes.
 Emphasize to patient the importance of
adhering to treatment regimen.
Teaching Patients About Edema –

 Edema can occur as a result of increased

capillary fluid pressure, decreased capillary
oncotic pressure, or increased interstitial
oncotic pressure, causing expansion of the
interstitial fluid compartment.
 Edema can be localized or generalized.
Severe generalized edema is called
anasarca.
 Edema can occur when there is a change in
capillary membrane increasing the
formation of interstitial fluid and decreasing
its removal.
 Increased ECF volume is caused by:
o Sodium retention.
o Burns and infections.
o Obstruction to lymphatic outflow.
o A plasma albumin level of less than
1.5 to 2 g/dL.
o Decrease in plasma oncotic
pressure.
 Kidneys retain sodium and water when ECF
is low as a result of decreased cardiac
output form heart failure.
 Ascites is a form of edema causing
shortness of breath and a sense of pressure
because of pressure on the diaphragm.
Other Treatments –

 Diuretic therapy
 Restriction of fluids and sodium.
 Elevation of the extremities.
 Application of anti-embolism stockings.
 Paracentesis
 Dialysis
 Continuous renal replace therapy.
FLUIDS AND
ELECTROLYTES
SODIUM IMBALANCES
Sodium is the most abundant electrolyte in the
ECF:
 Normal concentration: 135-145 mEq/L
(135-145 mmol/L).
 Primary determinant of ECF volume and
osmolality.
 Regulated by ADH, thirst, and the RAAS.
Functions of sodium:
 Controlling water distribution throughout the
body.
 Establish the electrochemical state
necessary for muscle contraction and the
transmission of nerve impulses.
Syndrome of Inappropriate Antidiuretic
Hormone (SIADH):
 A condition in which the body makes too
much ADH.
 SIADH can be the result of:
o Sustained secretion of ADH by the
hypothalamus.
o Production of an ADH-like substance
from a tumor (aberrant ADH
production).
o Conditions affecting the central
nervous system
 Over secretion of arginine vasopressin
(AVP) can cause SIADH.
SODIUM DEFICIT (HYPONATREMIA)
 Serum sodium level: < 135 mEq/L (135
mmol/L).
 Plasma sodium concentration represents
the ratio of total body sodium to total body
water.
 A hyponatremic state can be superimposed
on an existing fluid volume deficit (FVD) or
fluid volume excess (FVE).
Pathophysiology –
 Occurs due to an imbalance of water rather
than sodium.
 Urine sodium assists in differentiating renal
from nonrenal causes of hyponatremia.
o Low urine sodium occurs as the
kidney retains sodium to
compensate for nonrenal fluid loss
(i.e., vomiting, diarrhea, sweating).
o High urine sodium concentration is
associated with renal salt wasting
(i.e., diuretic use).
 Dilutional hyponatremia when a person
consumes too much water without an
adequate intake of electrolytes. The ECF
volume is increased without any edema.
 Deficiency in aldosterone, as occurs in
adrenal insufficiency.
 Use of certain medications, such as
anticonvulsants (i.e., carbamazepine
[Tegretol], levetiracetam [Keppral]) and
SSRIs (fluoxetine [Sarafem], sertraline
[Zoloft], paroxetine [Paxil]).
 SIADH is seen in both hyponatremia and
hypernatremia. It includes excessive ADH
activity with:
o Water retention and dilutional
hyponatremia.
o Inappropriate excretion of sodium in
the presence of hyponatremia
Clinical Manifestations –
 General –
o Poor skin turgor
o Dry mucosa
o Headache
o Decreased saliva production
o Orthostatic fall in blood pressure
o Nausea, vomiting, and abdominal
cramping.
 Neurologic changes probably related to
the cellular swelling and cerebral edema
associated with hyponatremia, including:
o Altered mental status
o Status epilepticus
o Coma
FLUIDS AND
ELECTROLYTES
 Acute decreases in sodium, developing
in less than 48 hours, may be associated
with brain herniation and compression of o


SIADH:
↓ Specific gravity (1.002-
1.004)

midbrain structures.  Urinary sodium content is >

 Chronic decreases in sodium, 20 mEq/L
developing after 48 hours or more, can  Specific gravity is usually >
occur in status epilepticus and cerebral 1.012
pontine myelinolysis.
 Features of hyponatremia associated
Medical Management –
with sodium loss and water gain:
o Anorexia  Sodium Replacement –
o Muscle cramps o Careful administration of sodium by
o Feeling of exhaustion mouth, nasogastric tube, or a
 When serum sodium level is < 115 mEq/L parenteral route.
(115 mmol/L), signs of increasing
intracranial pressure such as:  Example – lactated ringer’s
o Lethargy solution or isotonic saline
o Confusion (0.9% NaCl) for patients who
o Muscle twitching cannot consume sodium.
o Focal weakness
o Hemiparesis o Serum sodium must not be
o Papilledema increased by more than 12 mEq/L in
24 hours to avoid neurologic
o Seizures
damage due to osmotic
o Death
demyelination.

Assessment and Diagnostic Findings –  May occur when serum

sodium exceeds 140 mEq/L
 Focused neurologic examination too rapidly or in the presence
 Evaluation of signs and symptoms of hypoxia or anoxia.
o Weight gain  May produce lesions that
o No peripheral edema, but pitting show symmetric myelin
edema due to fluid accumulation destruction affecting all the
inside the cells. fiber tracts that cause
 Identification of current IV fluids paraparesis, dysarthria,
 Review of all medications the patient is dysphagia, and coma.
taking  Usual serum sodium
 Laboratory results: requirement – approximately
o Serum sodium level: 100 mEq – provided there
 Any cause: < 135 mEq/L are not excessive losses.
 SIADH: < 100 mEq/L
o ↓ Serum osmolality o In SIADH:
o Primary sodium loss:
 Urinary sodium content is <  Hypertonic saline solution
20 mEq/L (20 mmol/L) – alone cannot change the
suggesting ↑ proximal plasma sodium
reabsorption of sodium concentration. Excess
secondary to ECF volume sodium would be excreted
depletion. rapidly in highly concentrated
urine.
FLUIDS AND
ELECTROLYTES  With the addition of diuretic
furosemide (Lasix), urine is
not concentrated, and
isotonic urine is excreted to
effect a change in water
balance.
 Lithium (Eskalith) or
demeclocycline (Declomycin)
can antagonize the osmotic
effect of ADH on the
medullary collecting tubule.
 Water Restriction –
o In patients with normal or excess
fluid volume, hyponatremia is –
 Treated by restricting fluid to
a total of 800 mL in 24 hours.
o If neurologic symptoms are
severe (seizures, delirium, coma),
as well as in traumatic brain injury –
 Administer small volumes of
a hypertonic sodium solution.
 The prescribed volume of
hypertonic saline solution
depends on the patient’s
weight and on current and
desired serum sodium levels.
 Incorrect use is dangerous
because 1 L of 3% NaCl
contains 513 mEq of sodium
and 1 L of 5% NaCl contains
855 mEq of sodium.
o NURSING ALERT: Highly
hypertonic sodium solutions (2% to
23% sodium chloride) should be
administered only in intensive care
settings under close observation,
because only small volumes are
needed to elevate the serum sodium
concentration from a dangerously
low level. These fluids are
administered slowly and in small
volumes, and the patient is
monitored closely.
o If edema and hyponatremia occur
together, both sodium and water are
restricted.
 Pharmacologic Therapy –
o AVP receptor antagonists –
 Treat hyponatremia by
stimulating free water
excretion.
o IV conivaptan hydrochloride
(Vaprisol) –
 Limited to the treatment of
hospitalized patients with
moderate-severe
symptomatic hyponatremia.
 Contraindicated in patients
with seizure, delirium, or
coma, which warrant the use
of hypertonic saline.
Nursing Management –
 Identify and monitor patients at risk of
hyponatremia.
 Monitors fluid I&O as well as body weight.
 Note abnormal losses of sodium or gains of
water, as well as GI manifestations such as:
o Anorexia
o Nausea
o Vomiting
o Abdominal cramping
 As well as CNS changes, such as:
o Lethargy
o Confusion
o Muscle twitching
o Seizures
 Close monitoring of serum sodium, urine
sodium, and specific gravity.
 Elderly considerations –
o Frequent cause of confusion
o Administration of prescribed and
OTC medications that cause sodium
loss or water retention
o Diminished sense of thirst or loss of
access to food or fluids
Detecting and Controlling Hyponatremia –
 With abnormal losses of sodium who
can consume a general diet –
FLUIDS AND
ELECTROLYTES
o Encourages patient to consume
foods and fluid with high sodium
content. For example:
 Broth made with one beef
cube contains approximately
900 mg of sodium.
 8 oz of tomato juice contains
approximately 700 mg of
sodium
o Be familiar with the sodium content
of parenteral fluids.
 If primary problem is water retention –
o Restrict fluid intake to administer
sodium.
 In normovolemia or hypervolemia –
o Administration of sodium
predisposes a patient to fluid volume
overload.
 In severe hyponatremia –
o Therapy is to elevate the serum
sodium level only enough to alleviate
the neurologic signs and symptoms.
 Generally recommended that serum
sodium concentration be increased to not >
125 mEq/L (125 mmol/L) with hypertonic
saline solution.
 For patients taking lithium –
o Observes for lithium toxicity,
particularly when sodium is lost by
an abnormal route. In such
instances, supplemental salt and
fluid are administered.
o Instructed not to use diuretics
without close medical supervision.
o Adequate salt intake should be
ensured.
 Excess water supplements are avoided in
patient receiving isotonic or hypotonic
enteral feedings particularly if normal
sodium loss occurs or water is being
abnormally retained (as in SIADH).
 Evaluate fluid I&O, urine specific gravity,
and serum sodium levels to know actual
fluid needs.
SODIUM EXCESS (HYPERNATREMIA)
 Serum sodium level: > 145 mEq/L (145
mmol/L).
 Can be caused by a gain of sodium more
than water or by a loss of water in excess of
sodium.
 Can occur in patients with normal fluid
volume or in FVD or FVE patients.
 With a water loss:
o The patient loses more water than
sodium, as a result, the serum
sodium concentration increases, and
the increased concentration pulls
fluid out of the cell.
 In sodium excess:
o The patient ingests or retains more
sodium than water.
Pathophysiology –
 Common cause is fluid deprivation in
unconscious patients who cannot perceive,
respond to, or communicate their thirst.
 Administration of hypertonic enteral
feedings without adequate water
supplements.
 Watery diarrhea and greatly increased
insensible water loss (e.g.,
hyperventilation, denuding effects of burns).
 Diabetic insipidus which is a decreased
ability to concentrate urine due to a defect in
the kidney tubules that interferes with water
reabsorption can cause hypernatremia if the
patient does not experience or can respond
to thirst, or if fluids are excessively
restricted.
 Less common causes:
o Heat stroke
o Near drowning in seawater
o Malfunction of hemodialysis or
peritoneal dialysis systems
o IV administration of hypertonic saline
o Excessive use of sodium
bicarbonate.
Clinical Manifestations –
 Primarily neurologic and are due to
increased plasma osmolality caused by an
increase in plasma sodium concentrations.
FLUIDS AND
ELECTROLYTES
 Water moves out of the cell into the ECF,
resulting in cellular dehydration and a more
concentrated ECF.
 Moderate hypernatremia –
o Restlessness
o Weakness
 Severe hypernatremia –
o Disorientation
o Delusions
o Hallucinations
o Permanent brain damage due to
hemorrhages that result from brain
contractions.
 Other signs include:
o Dry, swollen tongue and sticky
mucous membranes
o Flushed skin
o Peripheral and pulmonary edema
o Postural hypotension
o Oliguria
o Increased muscle tone
o Deep tendon reflexes
o Mild ↑ in body temperature
Assessment and Diagnostic Findings –
 Serum sodium level > 145 mEq/L (145
mmol/L)
 Serum osmolality > 300 mOsm/kg (300
mmol/L)
 ↑ urine specific gravity
 ↑ urine osmolality
 Patients with nephrogenic or central
diabetes insipidus have hypernatremia and
produce a dilute urine with a urine
osmolality of < 250 mOsm/kg.
Medical Management –
 Gradual lowering of the serum sodium level
by the infusion of a:
o Hypotonic electrolyte solution
(e.g., 0.3% NaCl) – safer choice
because it allows for gradual
reduction in the serum sodium level,
thereby decreasing the risk of
cerebral edema.
o Isotonic saline solution (e.g.,
dextrose 5% in water [D5W]) –

indicated when water needs to be
replaced without sodium.
Diuretics to treat sodium gain.
 Serum sodium level is reduced at a rate
no faster than 0.5 to 1 mEq/L/hour to allow
sufficient time for readjustment through
diffusion across fluid compartments.
 Desmopressin acetate (DDAVP) – to treat
diabetes insipidus if it is the cause of
hypernatremia.
Nursing Management –
 Monitoring of fluid I&O.
 Assess for abnormal losses of water or low
water intake and for large gains of sodium,
as might occur with ingestion of OTC
medications that have a high sodium
content (e.g., Alka-Seltzer).
 Obtain medication history.
 Notes the patient’s thirst or ↑ body
temperature and evaluates it in relation to
other clinical signs.
 Monitors for changes in behavior, such as
restlessness, disorientation, and lethargy.
Preventing Hypernatremia –
 Provide fluids at regular intervals,
particularly in debilitated or unconscious
patients who are unable to perceive or
respond to thirst.
 If fluid intake remains inadequate, consults
with the physician to plan an alternative
route for intake, either by enteral feedings or
by the parenteral route.
o Enteral feedings – sufficient water
should be administered to keep the
serum sodium and BUN within
normal limits.
 For diabetes insipidus – adequate water
intake must be ensured.
Correcting Hypernatremia –
 If parenteral fluids are necessary, monitor
the patient’s response to the fluids by
FLUIDS AND
ELECTROLYTES
reviewing serial serum sodium levels and by
observing for changes in neurologic signs.
o Gradual decrease in serum sodium
level – neurologic signs should
improve.
o Too rapid reduction – renders the
plasma temporarily hypo-osmotic to
the fluid in the brain tissue, causing
movement of fluid into the brain cells
and causing dangerous cerebral
edema.
FLUIDS AND
ELECTROLYTES
POTASSIUM IMBALANCES
Major intracellular electrolyte (98% of the
body’s potassium is inside the cells, 2% is in
the ECF):
 Normal potassium concentration: 3.5-5.0
mEq/L (3.5-5 mmol/L).
 Excretion: 80% in the kidneys, 20% is lost
through the bowel and in the sweat.
 Regulated by kidneys by adjusting the
amount of potassium that is excreted in the
urine.
o As serum potassium levels ↑, so
does the potassium level in the renal
tubular cell.
o A concentration gradient occurs,
favoring the movement of potassium
into the renal tubule and excretion of
potassium in the urine.
 Aldosterone also increases the excretion of
potassium by the kidneys.
 Kidneys do not conserve potassium as well
as they conserve sodium, thus it may still be
lost in urine in the presence of a potassium
deficit.
 Imbalances are commonly associated with
various disease, injuries, medications (e.g.,
NSAIDS and ACE inhibitors), and acid-base
imbalances.
Functions of potassium:
 Influences both skeletal and cardiac muscle
activities.
POTASSIUM DEFICIT (HYPOKALEMIA)
 Serum potassium concentration: < 3.5
mEq/L (3.5 mmol/L).
 May occur in patients with normal
potassium stores and in patients with
alkalosis as serum potassium temporarily
shifts into the cells.
Pathophysiology –
 Potassium-losing diuretics, such as the
thiazides and loop diuretics.
 Other medications, including
corticosteroids, sodium penicillin,
carbenicillin, and amphotericin B.
 Gastrointestinal loss of potassium:
o Vomiting and gastric suction –
partly because potassium is lost
when gastric fluid is lost and
because potassium is lost through
the kidneys in response to metabolic
alkalosis.
o Diarrhea – because relatively large
amounts of potassium are contained
in intestinal fluids, so potassium
deficit occurs in diarrhea which may
contain as much as 30 mEq/L.
o Prolonged intestinal suctioning,
recent ileostomy, and villous
adenoma (a tumor of the intestinal
tract characterized by excretion of
potassium-rich mucus).
 Alterations in acid-base balance because
hydrogen and potassium ions shift between
the cells and the ECF:
o Respiratory or metabolic alkalosis
– promotes the transcellular shift of
potassium and can have a variable
and unpredictable effect on serum
potassium.
o Example: hydrogen ions move out of
the cells in alkalotic states to help
correct the high pH, and potassium
ions move in to maintain an
electrically neutral state.
 Hyperaldosteronism increases renal
potassium wasting and can lead to severe
potassium depletion.
 Persistent hypersecretion of insulin
because insulin promotes the entry of
potassium into skeletal muscles and hepatic
cells.
 Patients who do not eat normal diet for a
prolonged period are at risk of hypokalemia.
FLUIDS AND
ELECTROLYTES
 Patients with bulimia through self-induced
vomiting, misuse of laxatives, diuretics, and
enemas.
 Magnesium depletion causes renal
potassium loss and must be corrected first;
otherwise, urine loss of potassium will
continue.
Clinical Manifestations –

 Can result in widespread derangements in

physiologic functions.
 Severe hypokalemia can cause death
through cardiac and respiratory arrest.
 Clinical signs rarely develop before the
serum potassium level has decreased to < 3
mEq/L (3 mmol/L) unless the rate of decline
has been rapid.
 Manifestations include:
o Fatigue
o Anorexia
o Nausea and vomiting
o Muscle weakness
o Leg cramps
o Decreased bowel motility
o Paresthesia (numbness and tingling)
o Dysrhythmias
 If prolonged, can lead to an inability of the
kidneys to concentrate urine, causing dilute
urine (resulting in polyuria, nocturia) and
excessive thirst.
 Potassium depletion suppresses the release
of insulin resulting in glucose intolerance.  Increased sensitivity to digitalis,
predisposing the patient to digitalis toxicity
 Decreased muscle strength and deep
at lower digitalis levels.
tendon reflex.
 Metabolic alkalosis.
Assessment and Diagnostic Findings –  24-hour urinary potassium excretion test
can be performed to distinguish between
 Serum potassium concentration < 3.5
renal and extrarenal loss.
mEq/L (3.5 mmol/L).
 ECG changes can include:
o > 20 mEq/day with hypokalemia
o Flat T waves or inverted T waves
suggests that renal potassium loss is
or both, suggesting ischemia, and the cause.
depressed ST segments.
o Elevated U wave is specific to Medical Management –
hypokalemia.
 Increased intake in the daily diet or by oral
potassium supplements.
 If not treated by conventional measures, it is
treated cautiously with IV replacement
therapy:
FLUIDS AND
ELECTROLYTES
o
o
Must be corrected daily.
Administration of 40-80 mEq/day of
potassium is adequate in the adult if
there are no abnormal losses of
potassium.
 Patients at risk for hypokalemia –
o Diet containing sufficient potassium
is provided.
o Dietary intake of potassium in the
average adult is 50-100 mEq/day.
o Example foods: fruits and
vegetables, legumes, whole grains,
milk, and meat.
 If dietary intake is inadequate –
o Oral or IV potassium supplements.
o Many salt substitutes contain 50-60
mEq of potassium per teaspoon and
may be sufficient to prevent
hypokalemia.
 If oral is not feasible, IV route is indicated:
o Indicated with severe hypokalemia.
o Example: KCl, potassium acetate, or
potassium phosphate.
Nursing Management –
 Monitor patients at risk of hypokalemia.
 Look for signs and symptoms of
hypokalemia:
o Fatigue
o Anorexia
o Muscle weakness
o Decreased bowel motility
o Paresthesia
o Dysrhythmias
 Assess serum potassium concentrations if
signs are noted.
 If available, the ECG may provide useful
information.
 For example, patient receiving digitalis who
are at risk for potassium deficiency should
be monitored closely for signs of digitalis
toxicity because hypokalemia potentiates
the action of digitalis.
Preventing Hypokalemia –
 Encourage patients at risk to eat foods rich
in potassium (when diet allows).
 If hypokalemia is caused by the abuse of
laxatives or diuretics, patient education may
help alleviate the problem.
 Part of the health history and assessment
should be directed at identifying problems
that are amenable to prevention through
education.
 Careful monitoring of fluid I&O.
 ECG is monitored for changes.
 ABG values are checked for ↑ bicarbonate
and pH levels.
Correcting Hypokalemia –
 Oral administration of potassium
supplements for mild to moderate
hypokalemia.
 Care should be exercised when
administering potassium, particularly in
older adults who have lower lean body
mass and total body potassium levels and
therefore lower potassium requirements.
 Nursing Alert: Oral potassium supplements
can produce small-bowel lesions; therefore,
the patient must be assessed for and
cautioned about abdominal distention, pain,
or GI bleeding.
Administering IV Potassium –
 Potassium should be administered only
after urine flow has been established.
 A decrease in urine volume to < 20 mL/hour
for 2 consecutive hours is an indication to
stop the potassium infusion until the
situation is evaluated.
 When oliguria occurs, potassium
administration can cause the serum
potassium concentration to rise
dangerously.
 Maximum concentration of potassium in a
medical-surgical unit through a peripheral IV
line is 20 mEq/100 mL and the rate no
faster than 10-20 mEq/hour.
 Concentrations of potassium > 20 mEq/L
should be administered through a central IV
catheter using an infusion pump with the
patient monitored by ECG.
 Caution must be used when selecting the
correct premixed solution of IV fluid
FLUIDS AND
ELECTROLYTES

containing KCl as the concentrations range
from 10-40 mEq/100 mL.
Renal function should be monitored through
BUN and Creatinine levels and urine output
if the patient is receiving potassium
replacement.
 During potassium replacement, smooth
muscle hyperactivity can lead to hyperactive
bowel sounds, a sign of hyperkalemia.
POTASSIUM EXCESS (HYPERKALEMIA)
 Serum potassium concentration: > 5.0
mEq/L (5.0 mmol/L).
 Seldom occurs in patients with normal renal
function.
 Often caused by iatrogenic (treatment-
induced) causes.
 Less common than hypokalemia but more
dangerous because cardiac arrest is more
frequently associated with high serum
potassium levels.
Pathophysiology –
 Major causes:
o Decreased renal excretion of
potassium
o Rapid administration of potassium
o Movement of potassium from the
ICF compartment to the ECF
compartment.
 Commonly seen in patients with untreated
renal failure, particularly those in whom
potassium levels increase because of
infection or excessive intake of potassium in
food or medications.
 Hypoaldosteronism or Addison’s
disease because deficient adrenal
hormones lead to sodium loss and
potassium retention.
 Medications including potassium chloride,
heparin, ACE inhibitors, NSAIDs, beta-
blockers, and potassium-sparing diuretics.
 Acute and chronic renal failure with
glomerular filtration rate of less than 10-20%
of normal.
 Improper use of potassium supplements,
especially if salt substitutes are used.
 In acidosis – potassium ions move out of
the cells and into the ECF.
 Intensive trauma, as in burns, crushing
injuries, or severe infections.
 Lysis of malignant cells after
chemotherapy.
 Pseudo-hyperkalemia may occur because
of:
o Use of a tight tourniquet around an
exercising extremity while drawing
blood sample, producing hemolysis
of the sample before analysis.
o Other causes:
 Marked leukocytosis (WBC >
200,000/mm3)
 Thrombocytosis (platelet
count > 1 million/mm3)
 Drawing blood above the site
where potassium is infusing
 Familial pseudo
hyperkalemia – potassium
leaks out of the RBC while
the blood is awaiting
analysis.
 Nursing Alert: Potassium supplements are
extremely dangerous for patients who have
impaired renal function and thus decreased
ability to excrete potassium. Even more
dangerous is the IV administration of
potassium to such patients, because serum
levels can rise very quickly. Aged (stored)
blood should not be administered to patients
with impaired renal function, because the
serum potassium concentration of stored
blood increases due to red blood cell
deterioration. It is possible to exceed the
renal tolerance of any patient with rapid IV
potassium administration, as well as when
large amounts of oral potassium
supplements are ingested.
Clinical Manifestations –
 Most important consequence is its effect on
the myocardium.
 Cardiac effects of ↑ serum potassium > 7
mEq/L (7 mmol/L) are not usually
significant, but always present when the
level is 8 mEq/L (8 mmol/L) or greater.
 As plasma potassium level rises,
disturbances in cardiac conduction occurs.
FLUIDS AND
ELECTROLYTES
 Earliest changes occurring at a serum
potassium level > 6 mEq/L (6 mmol/L) are:
o Peaked, narrow T waves
o ST-segment depression
o Shortened QT interval
 If serum potassium level continues to
increase:
o The PR interval becomes
prolonged and is followed by the
disappearance of the P waves.
o There is decomposition and
widening of the QRS complex.
o Ventricular dysrhythmias and
cardiac arrest may occur at any
point in this progression.
 Severe hyperkalemia causes skeletal
muscle weakness and even paralysis,
related to a depolarization block in the
muscle.
 Ventricular conduction is slowed.
 Rapidly ascending muscular weakness
leading to flaccid quadriplegia.
 Paralysis of respiratory and speech
muscles can also occur.
 GI manifestations, such as nausea,
intermittent intestinal colic, and diarrhea.
Assessment and Diagnostic Findings –
 Serum potassium level > 5.0 mEq/L (5.0
mmol/L).
 ECG changes.
 ABG analysis may reveal both metabolic
and respiratory acidosis.
Medical Management –
 ECG must be obtained immediately to
detect changes:
o Shortened repolarization and
peaked T waves are seen
essentially.
o To verify results, a repeat serum
potassium level should be obtained
from a vein without an IV infusing a
potassium-containing solution.
 Non-acute situations:
o Restriction of dietary potassium and
potassium-containing medications
may correct the imbalance.
 Administration of cation exchange resins
(e.g., sodium polystyrene sulfonate
[Kayexalate]) either orally or by retention
enema in patients with renal impairment – to
prevent serious hyperkalemia.
o Exchange resins cannot be used if
the patient has a paralytic ileus.
 Emergency Pharmacologic Therapy –
o Serum potassium level
dangerously elevated –
administer calcium gluconate as it
antagonizes the action of
hyperkalemia on the heart.
 Monitor blood pressure to
detect hypotension which
FLUIDS AND
ELECTROLYTES may result from the rapid
administration of calcium
gluconate.
 Identify patients at risk for potassium excess
(e.g., those with renal failure).
 Observe for signs of muscle weakness and
 ECG should be continuously dysrhythmias.
monitored during  Note for presence of paresthesia and GI
administration – the symptoms such as nausea and intestinal
appearance of bradycardia is colic.
in indication to stop infusion.  Monitor serum potassium levels, as well as
 Parenteral administration of BUN, creatinine, glucose, and ABG values.
calcium sensitizes the heart
to digitalis and may Preventing Hyperkalemia –
precipitate digitalis toxicity.
 Encourage patient to adhere to the
prescribed potassium restriction.
o IV administration of sodium
bicarbonate may be necessary to Correcting Hyperkalemia –
alkalinize the plasma, cause a
temporary shift of potassium into the  Care is taken to administer and monitor
cells, and furnish sodium to potassium solutions closely.
antagonize the cardiac effects of  Particular attention is paid to the solution’s
potassium. concentration and rate of administration.
 Potassium is not added to parenteral
 Begin within 30-60 minutes solutions on the nursing units but in the
and may persist for hours. pharmacy.
 IV administration is via volumetric infusion
o IV administration of insulin and pump.
hypertonic dextrose solution  Caution patients to use salts substitute
causes a temporary shift of sparingly if they are taking other
potassium into the cells. supplementary forms of potassium or
o Loop diuretics, such as furosemide potassium-conserving diuretics.
(Lasix), increase excretion of water  Potassium-conserving diuretics, such as
by inhibiting sodium, potassium, and spironolactone (Aldactone), triamterene
chloride reabsorption in the (Dyrenium), and amiloride (Midamor);
ascending loop of Henle and distal potassium supplements; and salt substitutes
renal tubule. should not be administered to patients with
o Beta-2 agonists, such as albuterol renal dysfunction.
(Proventil, Ventolin), are highly
effective in decreasing potassium
but remains controversial because
they can cause tachycardia and
chest discomfort. Only use in the
absence of ischemic heart disease.
o If hyperkalemic condition is not
transient, actual removal of
potassium from the body is
required through cation exchange
resins, peritoneal dialysis,
hemodialysis, or other forms of renal
replacement therapy.
Nursing Management –
FLUIDS AND
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CALCIUM IMBALANCES
More than 99% of the body’s calcium is in the
skeletal system while 1% of skeletal calcium is
rapidly exchangeable with blood calcium and rest is
more stable and only slowly exchanged:
 Calcium outside the bone circulates in the
serum, partly bound to protein, and partly
ionized.
 Normal total serum calcium level: 8.6-
10.2 mg/dL (2.2-2.6 mmol/L.
 Normal ionized serum calcium level: 4.5-
5.1 mg/dL (1.1-1.3 mmol/L)
Calcium Function:
 Transmitting nerve impulses and helps
regulate muscle contraction and relaxation
(e.g., cardiac muscle).
 Instrumental in enzyme activation, and
blood coagulation.
Three forms of calcium in plasma:
 Ionized
 Bound
 Complex
Calcium mechanism:
 Calcium is absorbed from foods in the
presence of normal gastric acidity and
vitamin D.  released by lipolysis, forming soaps.
 Excreted in feces, remainder excreted in
urine.  pancreatitis.
 Serum calcium level is controlled by PTH
and calcitonin.  from the inflamed pancreas,
 As ionized serum calcium decreases, the
parathyroid glands secrete PTH. This, in
turn, increases calcium absorption from the
GI tract, increases calcium reabsorption
from the renal tubule, and releases calcium
from the bone.
 Suppression of PTH secretion is caused by
the increase in calcium ion concentration.
 Excessive increase in calcium results in the
secretion of calcitonin by thyroid gland
(inhibits calcium reabsorption from the bone
and decreases the serum calcium
concentration).
Calcium Deficit (Hypocalcemia):
 Serum calcium value: < 8.6 mg/dL or 2.15
mmol/L. 
 In some cases, a patient may have a total-
body calcium deficit (as in osteoporosis) but
a normal serum calcium level.
 Older adults and those with disabilities, who
spend an increased amount of time in bed,
have an increased risk of hypocalcemia
because bed rest increases bone resorption
Pathophysiology –
 Several factors can cause hypocalcemia,
including primary hypoparathyroidism
and surgical hypoparathyroidism.
o Not only associated with thyroid and
parathyroid surgery but can also
occur after radical neck dissection.
o 28-48 hours after surgery. 
 Transient Hypocalcemia- occurs with
massive administration of citrated blood
(i.e., massive hemorrhage and shock). 
o Since citrate can combine with
ionized calcium, temporarily remove
it from circulation. 
 Inflammation of the pancreas- breakdown
of proteins and lipids.
o It is thought that calcium ions
combine with the fatty acids
o Hypocalcemia = common in
 
o Excessive secretion of glucagon
increasing calcitonin (which
reduces calcium) secretion.
 Kidney Injuries
o Patients frequently have elevated
serum phosphate levels. 
o Note: High phosphate levels or
Hyperphosphatemia cause calcium
levels in the blood to drop.
 Other causes of hypoCa:
o vitamin D consumption
o magnesium deficiency
o medullary thyroid carcinoma
o low serum albumin levels
o alkalosis, and alcohol abuse
 Medications predisposing to hypocalcemia:
o aluminum-containing antacids
FLUIDS AND
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o
o
o
aminoglycosides
caffeine, cisplatin
Corticosteroids
o Mithramycin
o Phosphates
o Isoniazid
o loop diuretics
o and proton pump inhibitors.
Clinical Manifestations –
 Tetany – refers to the entire symptom
complex induced by increased neural
excitability. Caused by spontaneous
discharges of both sensory and motor fibers
in peripheral nerves.
o Sensation of tingling may occur in
the tips of the fingers, around the
mouth, and less commonly, in the
feet.
o Spasms of the muscles of the
extremities.
o Hyperactive DTRs.
 Chvostek sign – Consists of twitching of
muscles enervated by the facial nerve when
the region of about 2 cm anterior to the
earlobe, just below the zygomatic arch, is
tapped.
 Trousseau sign – a carpopedal spasm
induced by inflating a blood pressure cuff on
the upper arm to about 20 mmHg above
systolic pressure.
 Seizures – hypocalcemia increases the
irritability of the CNS and PNS.  precipitation).
 Other changes:
o Mental changes – depression,
impaired memory, confusion,
delirium, and hallucinations.
o Prolonged qt interval (ecg)-
prolongation of the st segment, and
torsades de pointes, a type of
ventricular tachycardia, may occur.  o Aluminum hydroxide, calcium
o Respiratory effects- dyspnea and
laryngospasm.
 Chronic hypocalcemia –
o Hyperactive bowel sounds
o Dry and brittle hair and nails
o And abnormal clotting
 Osteoporosis – associated with prolonged
low intake of calcium and represents a total-
body calcium deficit.
o Characterized by loss of bone mass,
which causes bones to become
porous and brittle and therefore
susceptible to fracture.
Medical Management –
 Acute symptomatic hypocalcemia –
o IV administration of calcium salt.
o Parenteral calcium salt includes:
 Calcium gluconate
 Calcium chloride – not used
as often because it is more
irritating and can cause
sloughing of tissue if it
infiltrates
o IV administration of calcium is
particularly dangerous in patients
receiving digitalis-derived
medications.
 Could cause digitalis toxicity,
w/ adverse cardiac effects.
 IV site must be observed
often for any evidence of
infiltration because of the risk
of extravasation and
resultant cellulitis or necrosis.
 0.9% sodium chloride
solution should not be used
with calcium (increases renal
calcium loss). 
 Solutions containing
phosphates or bicarbonate -
should not be used with
calcium (could cause
o Calcium replacement → causes
postural hypotension; patient is kept
in bed during IV infusion, BP is
monitored.
 Nutritional Therapy –
o Vitamin D therapy – to increase
calcium absorption from the GI tract
acetate, or calcium carbonate
antacids – decrease elevated
phosphorus levels before treating
hypocalcemia in the patient with
CKD.
o Dietary calcium intake increased
(1000-1500 mg/day in adult)
o Calcium supplements – divided
doses of no higher than 500 mg to
promote calcium absorption
o Calcium-containing foods – like milk
products; green, leafy vegetables;
FLUIDS AND
ELECTROLYTES
o
canned salmon; canned sardines;
and fresh oysters.
Hypomagnesemia → tetany; if the
tetany responds to IV calcium, a low
magnesium level is considered as a
possible cause in CKD.

Nursing Management –
 Assess for hypocalcemia in at-risk patients.
 Seizure precautions are initiated if
hypocalcemia is severe.
 Status airway closely monitored –
laryngeal stridor can occur.
 Safety precautions are taken, as indicated,
if confusion is present
 Educate pt about foods that are rich in
calcium. 
 Advice the pt to consider calcium
supplements if sufficient calcium is not
consumed in the diet.
 Alcohol and caffeine in high doses inhibit
calcium absorption.
 Moderate cigarette smoking increases
urinary calcium excretion.
 Cautioned to avoid the overuse of
laxatives and antacids that contain
phosphorus (decreases calcium
absorption).
 
FLUIDS AND
ELECTROLYTES
MAGNESIUM IMBALANCES
Most abundant intracellular cation after potassium:
 Normal range: 1.3 to 2.3 mg/dL (0.62 to
0.95 mmol/L)
 1/3 of serum Mg – bound to protein
 2/3 of serum Mg – exist as free cations
(active component)
Functions of Magnesium
 Acts as an activator for many intracellular
enzyme systems
 Plays a role in both carbohydrate and
protein metabolism.
 Important in neuromuscular function. Acts
directly on the myoneural junction.
Variations in the Mg level affect
neuromuscular irritability and contractility
o Excess Mg: Diminished the
excitability of the muscle cells.
o Deficit Mg: Increases
neuromuscular irritability and
contractility.
 Affects the cardiovascular system, acting
peripherally to produce vasodilation and
decreased peripheral resistance.
 It is predominantly found in bone and soft
tissues and eliminated by the kidneys.
MAGNESIUM DEFICIT (HYPOMAGNESEMIA)
 Less than 1.3 mg/dL [0.62 mmol/L] in
magnesium concentration.
 Frequently associated with hypokalemia
and hypocalcemia.
Magnesium is like calcium in two aspects:
1. It is the ionized fraction of magnesium that
is primarily involved in neuromuscular
activity and other physiologic processes,
and
2. Magnesium levels should be evaluated in
combination with albumin levels.
 About 30% of magnesium is protein
bound, principally to albumin.
 Decreased serum albumin level can
also reduce the measured total
magnesium concentration; however,
it does not reduce the Zionized
plasma magnesium concentration.
Pathophysiology –
 ↓ intake of magnesium.
 Electrolyte imbalances (hypokalemia,
hypocalcemia).
 Wasting of magnesium in kidneys (due to
loop diuretics, thiazide, cyclosporine)
 Malabsorption in the GI tract (r/2 Crohn’s
disease, celiac disease).
 Medications (proton-pump inhibitors).
 Alcohol (due to poor dietary intake).
 Glycemic issues (Diabetic Ketoacidosis,
insulin resistance)
Clinical Manifestations – mostly excitable
 Tetany
 Involuntary movements
 Hyperreflexia
 (+) Chvostek sign
 (+) Trousseau sign – r/2 hypocalcemia.
 ECG changes:
o Prolonged QRS, Depressed ST
segment
 Cardiac dysrhythmias:
o Premature ventricular contractions
o Supraventricular tachycardia
o Torsades de pointes (a form of
ventricular tachycardia)
o Ventricular fibrillation.
 Irritability
 Weak respirations
 Hypertension
 GI issues – nausea, ↓ bowel sounds and
motility.
 Digitalis toxicity from digoxin is associated
with low Mg
 Diuretic therapy is associated to renal loss
of Mg.
Assessment and Diagnostic Findings –
 Less than 1.3 mg/dL (0.62 mmol/L)
FLUIDS AND
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 Levels are measured after a loading dose of
magnesium sulfate is administered
o
o
Peanut butter
Pork
 2 newer diagnostic techniques are sensitive o Oatmeal
and direct of measuring Mg o Fish (canned tuna and mackerel)
o Nuclear magnetic resonance o Cauliflower
spectroscopy o Chocolate
o Ion-selective electrode o Legumes
Medical Management – o Nuts
o Orange
 Diet: If mild Mg deficiency o Milk
o Green leafy vegetables, nuts, seeds,
legumes, whole grains, seafood,
peanut butter, and cocoa. MAGNESIUM EXCESS (HYPERMAGNESEMIA)
 Magnesium salts: Orally, Oxide or
gluconate form to replace continuous losses  > 2.3 mg/dL [0.95 mmol/L
but can produce diarrhea  Rare electrolyte abnormality: Kidneys
 Magnesium IV solution: Infusion pump, @ efficiently excrete magnesium
rate not to exceed 150 mg/min, or 67 mEq  Mg can appear falsely elevated: Blood
over 8 hours specimens are hemolyzed or drawn from an
 Parenteral administration of magnesium extremity with a tight tourniquet
 Bolus dose of magnesium sulfate: Can
Pathophysiology –
produce cardiac conduction alterations (e.g
heart block or asystole)  Renal failure
 Frequent VS assessment: To detect o Most common cause of
changes in cardiac rate or rhythm, hypermagnesemia
hypotension, and respiratory distress. o Patients with advanced renal
 Urine output monitoring: Before, during failure –
and after. Notify physician if <100mL over 4  Have at least a slight
hrs elevation in serum
 Calcium gluconate: Readily available to magnesium levels
treat hypocalcemic tetany or  Aggravated when receiving
hypermagnesemia Mg to control seizures
 Untreated diabetic ketoacidosis
Nursing Management –
o Hypermagnesemia can occur when
 Monitor cardiac, GI, respiratory, catabolism causes the release of
neurological status. cellular magnesium that cannot be
 Administer K+ oral supplements. excreted because of profound fluid
 Oral Ca+ supplements with vitamin D or volume depletion and resulting
10% Ca+ gluconate. oliguria.
 Administer magnesium sulfate IV route –  Patients treated for hypertension of
o Monitor magnesium levels pregnancy or treated for low
o Check DTR hypomagnesemia.
 Place in seizure precautions. o Hypermagnesemia can result from
 Oral magnesium may cause diarrhea that excessive magnesium
can waste magnesium. administration.
 Encourage magnesium-rich foods –  Other conditions cause HyperMg:
o Avocado o Adrenocortical insufficiency
o Green-leafy vegetables o Addison’s disease
o Hypothermia
FLUIDS AND
ELECTROLYTES
o Excessive use of magnesium-based
antacids (eg, Maalox, Riopan,
Mylanta)
QT interval, as well as an
atrioventricular block

o Laxatives (Milk of Magnesia)

o Medications that decrease GI
motility, including opioids and
Medical Management –
anticholinergic
o Decreased elimination of
magnesium or its increased
absorption due to intestinal
hypomotility
o Lithium intoxication
o Extensive soft-tissue injury or
necrosis as with trauma, shock,
sepsis, cardiac arrest, or severe
burns
Clinical Manifestations – very lethargic
 Depressed CNS and peripheral
neuromuscular junction
 Low blood pressure: Because of
peripheral vasodilation
 GI issues: nausea, vomiting
 Weakness
Nursing Management –
 Soft-tissue calcifications
 Facial flushing
 Sensations of warmth
 Lethargy (profound), difficulty speaking
(dysarthria), and drowsiness
 ↓ reflex – DTRs are lost, and muscle
weakness and paralysis
 Depressed respiratory center: Serum
magnesium levels exceed 10 mEq/L (5
mmol/L)
 Coma, atrioventricular heart block, and
cardiac arrest
 Platelet clumping and delayed thrombin
formation
Assessment and Diagnostic Findings –
 Avoid administration of magnesium to
patients with renal failure
 Carefully monitoring seriously ill patients
who are receiving magnesium salts
 All parenteral and oral magnesium salts are
discontinued: Severe case
 Hemodialysis with a magnesium-free
dialysate can reduce the serum magnesium
to a safe level within hours.
 Administration of loop diuretics (Lasix) and
sodium chloride or lactated Ringer’s IV
solution enhances magnesium excretion in
patients with adequate renal function.
 IV calcium gluconate antagonizes the
cardiovascular and neuromuscular effects of
magnesium.
 Monitor cardiac, respiratory, neurological
GI, and renal system status.
 Place on ECG for cardiac monitoring.
 Ensure safety due to lethargy.
 Avoid giving patient in renal failure
magnesium-containing antacids/laxatives.
 Avoid foods high in magnesium.
 Loop diuretics and thiazides (except in renal
failure).
 Dialysis.
 Administration of IV calcium – watch for
infiltration.

 > 2.3 mg/dL (0.95 mmol/L)

 Increased potassium and calcium are
present
 Creatinine clearance decreases to less than
3.0 mL/mins
 ECG:
o Prolonged PR interval, tall T waves,
a widened QRS, and a prolonged
FLUIDS AND
ELECTROLYTES
PHOSPHORUS IMBALANCES  Other conditions that cause
hypophosphatemia:
o Medications:
Critical constituent of all the body’s tissues  Antacids (e.g., aluminum
hydroxide-based +
 Normal serum phosphorus level: 2.5 to magnesium-based) – causes
4.5 mg/dL (0.8 to 1.45 mmol/L) in adults. malabsorption of
 Stored mainly in bones, regulated by phosphates.
kidneys and parathyroid hormone.  Carbonic anhydrase
Functions of Phosphorus: inhibitors (acetazolamide
[Diamox])
 Essential to the function of muscle and red o Lack of vitamin D
blood cells. o Hyperparathyroidism – inhibition of
 Formation of adenosine triphosphate (ATP) phosphate reabsorption by PTH.
and of 2,3- diphosphoglycerate, which o Oncogenic osteomalacia – wasting
facilitates release of oxygen from of phosphates by kidneys causing ↓
hemoglobin. levels and softening of the bones.
 Maintenance of acid–base balance, as well o Pulmonary issues – respiratory
as the nervous system and the intermediary alkalosis, diabetic ketoacidosis.
metabolism of carbohydrate, protein, and fat o Hyperglycemia – excretion of
 Provides structural support to bones and glucose leads to excretion of
teeth. phosphates.
 85% of phosphorus is located in bones and o Alcoholism – affects absorption of
teeth, 14% in soft tissue, and less than 1% phosphates.
in the ECF. o Thermal burns – shifting of
phosphates into cells.
o Electrolyte imbalances:
PHOSPHORUS DEFICIT  Hypercalcemia
(HYPOPHOSPHATEMIA)  Hypomagnesemia
 Hypokalemia
 < 2.5 mg/dL (0.8 mmol/L)
o Heat stroke
 May occur under a variety of circumstances
o Poor dietary intake
in which total body phosphorus stores are
normal o Hepatic encephalopathy
 Caused by an intracellular shift of potassium o Acute volume expansion, osmotic
from serum into cells, by increased urinary diuresis, use of carbonic anhydrase
excretion of potassium, or by decreased inhibitors (acetazolamide [Diamox]),
intestinal absorption of potassium and some malignancies
o Chronic diarrhea or severe
Pathophysiology – potassium restriction
 Occur during the administration of Clinical Manifestations –
calories to patients with severe protein–
calorie malnutrition (anorexia nervosa or  Neurologic manifestations:
alcoholism, elderly debilitated patients who o Irritability
are unable to eat) – sudden ↑ in blood sugar o Fatigue
releases insulin and calcium resulting into o Apprehension
depletion. o Weakness
 Receive parenteral nutrition if the o Numbness
phosphorus loss is not corrected. o Paresthesias
FLUIDS AND
ELECTROLYTES
o Dysarthria
o Dysphagia
o Diplopia
o Confusion, seizures, and coma.
 Breathing problems due to respiratory
muscle weakness – may result to hypoxia.
 Muscle damage
 Rhabdomyolysis – necrosis of muscles
releases myoglobulin into blood which is
toxic to kidneys (s/sx: tea-colored urine &
muscle weakness).
 Decreased reflexes (e.g., ↓ DTR)
 Osteomalacia (bone fractures, deformities)
 Low cardiac output
 Low platelet aggregation resulting bruising
and bleeding
 Muscle weakness/pain
 Infection
 Insulin resistance (Hyperglycemia)
Assessment and Diagnostic Findings –
 Less than 2.5 mg/dL (0.80 mmol/L) in adults
 PTH levels are increased
 Alkaline phosphatase is increased with
osteoblastic activity
 May decrease due to:
o Glucose or insulin administration
o Increased urinary excretion of
Magnesium
 X-rays may show skeletal changes of
osteomalacia or rickets
Medical Management –
 Closely monitored and correction initiated
before deficits become severe
 Adequate amounts of phosphorus should be
added to parenteral solutions, and attention
should be paid to the phosphorus levels in
enteral feeding solutions
 Aggressive IV phosphorus correction is
usually limited to the patient whose serum
phosphorus levels decrease to less than 1
mg/dL (0.3 mmol/L) and whose GI tract is
not functioning.
 IV preparations of phosphorus are available
as sodium or potassium phosphate (10
mEq/h). Site should be carefully monitored
because tissue sloughing, and necrosis can
occur with infiltration
Nursing Management –
o Identifies patients who are at risk for
hypophosphatemia and monitors them
o Preventive measures involve gradually
introducing the solution to avoid rapid
shifts of phosphorus into the cells
o Careful attention should be given to
preventing infection
o Frequently monitors serum phosphorus
levels and documents
o Report early signs of hypophosphatemia
(apprehension, confusion, change in level of
consciousness)
o Mild: Foods such as milk and milk products,
organ meats, nuts, fish, poultry, and whole
grains should be encouraged
o Moderate: Supplements such as
o Neutra-Phos capsules (250 mg
phosphorus/capsule;
o 7 mEq sodium and potassium), K-
Phos (250 mg phosphorus/tablet;
o 14 mEq potassium), and Fleet’s
Phospho-Soda (815 mg
phosphorus/5 mL) may be
prescribed
o Oral phosphorus with vitamin D.
o Watch patient on TPN for muscle pain and
weakness.
o Ensure patient safety (r/2 bone fracture
and confusion).
o Phosphate < 1 mg/dL – administer IV
phosphate when renal status is good, BUN
is normal, Crea is normal:
o Watch Ca+ level
o Monitor phosphate level
o Monitor EKG.
PHOSPHORUS EXCESS
(HYPERPHOSPHATEMIA)
 > 4.5 mg/dL (1.45 mmol/L) in adults
Pathophysiology –
 Renal failure
FLUIDS AND
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o Most common condition that can
lead to hyperphosphatemia.
 Other causes:
o Phospho-soda overuse – e.g.,
phosphate-containing laxatives and
enema.
o Vitamin D overuse.
o Hypoparathyroidism
o Chemotherapy for neoplastic
disease
o Administration of total parenteral
nutrition.
o Metabolic or respiratory acidosis
o Diabetic ketoacidosis
o Acute hemolysis
o High phosphate intake
o Profound muscle necrosis
o Increased phosphorus absorption
o Metastatic calcification: primary
complication of increased
phosphorus.
o Occurs when the calcium–
magnesium product (calcium
magnesium) exceeds 70 mg/dL.
Clinical Manifestations –
 Tetany: Most important short-term
consequence
 Low serum calcium concentration
 Tingling sensations in the fingertips and
around the mouth
 Anorexia, nausea, vomiting, bone and joint
pain, muscle weakness, hyperreflexia, and
tachycardia
 Soft-tissue calcification: Major long-term
consequence
o occurs mainly in patients with a
reduced glomerular filtration rate
 Precipitation of calcium phosphate in non-
osseous sites, decrease urine output,
impaired vision, and palpitations
Assessment and Diagnostic Findings –
 Serum phosphorus level exceeds 4.5 mg/dL
(1.5 mmol/L) in adults
 Serum calcium level is useful also for
diagnosing the primary disorder and
assessing the effects of treatments.
 X-rays may show skeletal changes with
abnormal bone development
 PTH levels are decreased in
hypoparathyroidism
 BUN and creatinine levels are used to
assess renal function
Medical Management –
o Treatment is directed at the underlying
disorder
o Vitamin D preparations, such as calcitriol,
which is available in both oral (Rocaltrol)
and parenteral (Calcijex, paricalcitol
[Zemplar]) forms
o Calcium-binding antacids (calcium
carbonate or calcium citrate)
o Administration of Amphojel
o Restriction of dietary phosphate, forced
diuresis with a loop diuretic, volume
replacement with saline, and dialysis
o Surgery may be indicated for removal of
large calcium and phosphorus deposits.
o Dialysis
Nursing Management –
o Monitors patients at risk for
hyperphosphatemia
o Avoid phosphorus-rich foods such as
hard cheeses, cream, nuts, meats, whole-
grain cereals, dried fruits, dried vegetables,
kidneys, sardines, sweetbreads, and foods
made with milk
o Instructs the patient to avoid phosphate-
containing substances such as laxatives
and enemas
o Teaches the patient to recognize the signs
of impending hypocalcemia and to monitor
for changes in urine output.
FLUIDS AND
ELECTROLYTES
CHLORIDE IMBALANCES o Neuro status – very confused and at
risk for injury.
o Seizure precautions
 Normal serum chloride: 95-105 mEq/L o Respiratory status
 Role: o I and O
o Acid-base balance o Vital signs
o Digestion o Daily weight
 Regulated by kidneys, excreted in kidneys,  Monitor laboratory values – ↑ carbohydrates
sweat, and GI juices. and ↓ potassium.
 ↑ chloride = ↑ sodium and vice versa.  Administration of normal saline (0.9%)
 ↑ chloride = ↓ bicarbonate and vice versa. o Add chloride and sodium.
 Chloride imbalances can lead to K+  Sources of chloride foods –
alterations. o Tomate
o Table salt
o Olives
CHLORIDE DEFICIT (HYPOCHLOREMIA) o Processed meats
 Serum chloride < 95 mEq/L. o Seafoods
o Canned foods
Pathophysiology –

 GI-related (vomiting, gastric juices,

ileostomy). CHLORIDE EXCESS (HYPERCHLOREMIA)
 Use of diuretics (e.g., thiazides).  Serum chloride > 105 mEq/L.
 Burns
 Cystic fibrosis – defective Cystic Fibrosis Pathophysiology –
Transmembrane Conductance Regulator  ↑ sodium intake
(CFTR) protein leading to excessive loss of
 Not drinking enough
sodium and chloride in sweat which results
 ↓ bicarbonate (r/2 to loss of body fluids
in hypochloremia and hyponatremia.
through vomiting, diarrhea, sweating, fever)
 Fluid volume overload (heart failure,
 Conn’s syndrome – adrenal glands make
SIADH)
too much aldosterone which retains sodium
 Metabolic alkalosis – related to increase in
and water.
bicarbonate which decreases chloride.
 Medications (androgens, corticosteroids,
Clinical Manifestation – estrogens, diuretics).
 Metabolic acidosis
 Dehydration –  Diabetic insipidus or diabetic coma.
o ↑ heart rate
 Kidney failure or kidney disorders.
o ↓ blood pressure
o Fever Clinical Manifestations –
o Vomiting
 Fatigue
o Diarrhea
 Restless, really agitated.
o Lethargy
 ↑ reflexes (seizure/coma)
Nursing Management –  Extreme thirst
 ↓ urine output, dry mouth/skin
 Monitor sodium level.
 Assess for signs and symptoms of Nursing Management –
hyponatremia.
FLUIDS AND
ELECTROLYTES
 Hold sodium chloride infusions and sodium
chloride-rich foods.
 Administer lactated ringer’s solution.
 Collect I & O, vital signs.
 Monitor laboratory values on chloride,
sodium, potassium, and bicarbonate.
FLUIDS AND
ELECTROLYTES
ACID-BASE IMBALANCES
Normal ABG values:
 PO2: 80-100 mmHg
 PaCO2: 35-45 mmHg
 pH: 7.35-7.45
 HCO3: 22-26 mEq/L
 O2 Sat: 95-100%
METABOLIC ALKALOSIS
Laboratory values indicating metabolic alkalosis:
 pH: > 7.45 (increased)
 HCO3: > 26 (increased)
 PaCO2: > 45 (increased – partially
compensated) or normal (uncompensated)
Pathophysiology –
 Excessive loss of hydrogen (acidic) ions
which increases bicarbonate (alkalotic).
 Body tries to compensate in respiratory
system by causing hypoventilation to keep
CO2 resulting in bradypnea (RR < 12 bpm).
Etiology –
 Hyperaldosteronism – water and sodium
retention which causes to lose hydrogen
ions and potassium while retaining
bicarbonate.
 Loop diuretics (Lasix) and Thiazides –
cause wasting of hydrogen ions in the
kidneys (e.g., chloride) which increases
bicarbonate.
 Alkali ingestion – foods that contain high
alkali (e.g., baking soda, antacids, milk).
 Anticoagulants – administration of citrated
blood which is metabolized by the body as
bicarbonate.
 Loss of fluids – vomiting and nasogastric
suctioning.
 ↑ sodium bicarbonate administration.
Clinical Manifestation –
 Bradypnea
 Hypokalemia – tetany, tremors, EKG
changes.
Nursing Management –
 For vomiting – administer antiemetics
(Zofran).
 Stop suctioning.
 Stop diuretics.
 Watch ABG values and for respiratory
distress.
 Diamox may be ordered – a diuretic that
reduces reabsorption of bicarbonate.
o Watch for potassium levels, might
cause hypokalemia.
METABOLIC ACIDOSIS
Laboratory values indicating metabolic alkalosis:
 pH: < 7.35 (decreased)
 HCO3: < 22 (decreased)
 PaCO2: < 35 (decreased – partially
compensated) or normal (uncompensated)
Pathophysiology –
 Too much build-up of acid in the body fluids
with ↓ bicarbonate levels.
 Happens in diabetic ketoacidosis which
produces ketones (acids).
 Decreased acid secretion in the kidneys as
in renal failure.
 Loss of bicarbonate (e.g., diarrhea).
 To compensate, hyperventilation occurs to
expel CO2 causing rapid, deep, and shallow
respiration (Kussmaul breathing).
Etiology –
 Caused by high and normal anion gap –
determined by calculating laboratory results
to measure difference between anions and
cations in the body.
o High anion – conditions that cause
the body to produce too much acid
and not enough bicarbonate:
 Aspirin toxicity
 Carbohydrates not
metabolized due to
insufficient O2 to breakdown
FLUIDS AND
ELECTROLYTES pyruvic acid, thus turning it to
lactic acid.
 Kidney insufficiency
 Diarrhea
 DKA
 Intake of high fats
o Normal anion – conditions that
cause the body to lose bicarbonate:
 Ostomy drainage
 Fistula
 Carbonic anhydrase
inhibitors
Clinical Manifestation –

 Kussmaul breathing
 Confusion
 Weakness
 ↓ blood pressure
 Hyperkalemia
 Nausea/vomiting
Nursing Management –

 Watch for respiratory distress.

 Watch for electrolyte – increased in
potassium.
 Monitor neuro status/seizure.
 Renal failure – dialysis, I and O, electrolyte,
BUN, Creatinine monitoring.
 For DKA – give insulin.