Treatment, interventions, and priorities:
Treatments to anticipate include administration
of loop diuretics such as Lasix and
administration of isotonic saline. Priority
intervention is to get patient to excrete excess
calcium through urine. Nurse should encourage
PO fluid intake of at least 3000 mL per day. A
low calcium diet may be prescribed. Pt should be
encouraged to increase weight bearing activity in
order to encourage deposition of calcium in bone
tissue. Drugs which inhibit bone resorption may
also be administered and in the case of
hypercalcemia caused by malignancy drugs
which inhibit osteoclast activity and thus
decrease bone breakdown may be administered.
Priority intervention is to monitor patient for
cardiac changes and CNS depression.
Role in Body: Calcium serves an important
role in bone formation and density. It also has
inhibitory effect on nerve impulses and effects
muscle contraction including cardiac
contraction. Calcium also plays a role in blood
clotting.
Treatment and anticipated interventions:
Primary nursing intervention is on monitoring
any cardiac changes associated with
hypocalcemia. There can be pain associated
with hypocalcemia and this should also be
controlled. Treatment included IV calcium
administration, PO calcium supplements,
increased dietary calcium intake, and possible
increased dietary vitamin D intake or
supplements. Vitamin D is fat soluble and
patients taking vitamin D supplements should
be taught to monitor themselves for symptoms
of toxic vitamin D levels such as N/V/D and
irregular heartbeat.
Signs and Symptoms: Calcium regulates CNS
function and symptoms of hypercalcemia then
include lethargy, weakness, and decreased
reflexes. Other symptoms include decreased
memory, confusion and psychoses, bone pain,
polyuria, anorexia, and even coma. EKG
changes will be present and include shortened
ST segments, shortened QT interval and
ventricular dysrhythmias.
Elevated Values> 10.2
mg/dL(serum)
>2.55 mmol/L (ionized)
Calcium (Ca2+)
Decreased Values<8.6 mg/dL (serum)
<2.15 mmol/L (ionized)
Symptoms and assessment: Fatigue,
depression, anxiety, neuropathies
(especially of mouth), hyperreflexia, and
tetany. Other symptoms include
Trousseau’s sign (contraction of hand upon
blood pressure cuff inflation) and
Chvostek’s sign which is a
hyperexcitability of facial muscles when
tapped on face in front of the tragus of the
ear. EKG changes may be present and
include a prolonged QT interval and
possibly ventricular tachycardia.
Causes: Most often caused by
hyperparathyroidism and then malignancies.
Tumors lead to bone destruction which lead to
increased calcium levels. Vitamin D overdose
can also lead to hypercalcemia. Increased
ionized calcium levels alone indicate some sort
of acidosis. Inactivity and decreased weight
bearing activity can lead to bone destruction and
increased serum calcium levels. Sometimes
hypercalcemia can be caused by excessive
dietary intake, especially in the form of calcium
supplements as antacids.
Labs to consider include: Serum calcium, ionized
calcium, serum albumin (as calcium is largely bound to
albumin), phosphate levels, vitamin D levels(as vitamin D
effects absorption), parathyroid hormone levels, and changes in
pH which will effect calcium binding to albumin.
Geriatric Concerns: Geriatric patients often do not get
exposure to the sun which is the only way to activate vitamin D
which is needed for calcium deposition. The geriatric patient
also commonly does not participate in weight bearing activity
which is necessary to prevent bone breakdown.
Causes: Hypocalcemia can be caused by anything which
decreased parathyroid hormone production. Other
causes include pancreatitis, multiple blood transfusions
as an additive in transfused blood binds with serum
calcium, laxative use, and systematic alkalosis which
increases calcium protein binding, and inadequate
dietary calcium intake.
Treatment, interventions, and priorities:
Treatments for hypernatremia include increased PO
water intake, administration of hypotonic IV fluids,
and control of body temperature if patient presents
with diaphoresis due to overheating. Patients should
also reduce dietary sodium intake. Patients who are
being treated for hypernatremia should have blood
pressure closely monitored closely to avoid a
hypertensive crisis due to excess fluid volume.
Fluids, especially hypotonic fluids, should be
administered in a controlled manner. Fluids
administered too quickly may cause cerebral swelling
and increased intracranial pressure. Priority is to
prevent increased intracranial pressure and
hypertensive crisis.
Role in Body: Main ECF cation. Maintains
ECF osmolality and pressure. Aids in
generation and transmission of nerve impulses
Treatment and anticipated interventions: Fluid
restriction is often adequate treatment for
hyponatremia. If patient is experiencing seizures
IV hypertonic saline may be administered.
Vasopressin may also be administered to combat
effects of ADH in the body. If PT blood pressure is
low this may indicate hypovolemic hyponatremia
and vasopressin should not be administered as it
will cause further fluid loss.
Signs and Symptoms: Thirst, restlessness,
agitation, dry sticky mucosal membranes,
orthostatic hypotension, weakness, lethargy,
decreased skin turgor and increased skin tenting.
Serious late symptoms include seizures and coma.
Elevated value>145 mEq/L
Sodium (Na+)
Decreased value<135 mEq/L
Symptoms and assessment: Symptoms of
hyponatremia are associated with cellular
swelling. These include confusion,
irritability, seizures, dizziness, cold
clammy skin, orthostatic hypotension,
headache, apathy, N/V/D, peripheral
edema, and seizures and coma. Primary
concerns are to provide for patient safety if
actively seizing and to provide for safety if
patient is confused or restless.
Causes: Causes of elevated sodium include excess
administration of hypertonic IV fluids, inadequate
PO water intake, water loss induced by exercise,
cushing’s syndrome, uncontrolled diabetes Mellitus,
hypertonic tube feedings, or excessive isotonic IV
fluid administration.
Labs to consider include: Blood pressure, serum
sodium levels, serum potassium levels, and
creatinine levels to establish kidney functionality.
Geriatric Concerns: The geriatric patient often has
decreased fluid intake which may lead to hypernatremia.
They also commonly eat many sodium rich foods such as
microwave meals which may contribute to hypernatremia
Causes: Often caused by excessive administration of
hypotonic fluids. Also caused by renal failiure and
SIADH which leads to inappropriate fluid retention. Can
also be caused by excessive PO water intake which is
sometimes referred to as “water intoxication.” This is
something which should be considered in populations
with dementia or Alzheimer’s Syndrome as they can be
susceptible to consuming too many liquids. Other causes
include burns, fasting, diuretics, and heart failure.
Treatment, interventions, and priorities: Priority
in the event of hyperkalemia is monitoring of
cardiac function. If hyperkalemia is suspected an
EKG should be done immediately. Common
treatments include elimination of K+ intake,
administration of diuretics or Kayexelate,
increased fluid intake, and administration of
insulin with glucose. Insulin will shift potassium
back into the ICF and glucose will prevent a
sharp drop in blood sugar. Calcium may also be
administered to reduce membrane excitability.
Calcium will be administered to patients
experiencing cardiac changes as it regulates cell
excitability.
Role in Body: Potassium is the main cation in the
ICF. It plays an enormous role in establishing cell
membrane potentials and is thus responsible for muscle
contraction including cardiac function. When new
tissues are forming potassium will move into the cells
and when tissues are breaking down potassium will
leave the tissue cells. Potassium balance is maintained
by the sodium potassium pump.
Treatment and anticipated interventions: The
nurse can anticipate administration of
potassium supplements both oral and IV. IV
potassium is NEVER given as a bolus, and is
NEVER added to a hanging bag. IV bags
should be inverted to evenly distribute
potassium. Rates of infusion are not to exceed
20 mEq/hr. Pt must be excreting 0.5 mL/Kg of
body weight per hour to be eligible for IV
potassium. EKG changes should be closely
monitored when administering potassium.
Signs and Symptoms: Irritability, anxiety,
cramping, diarrhea, weakness (especially of
legs), irregular pulse, twitching, and cardiac
arrest. EKG changes will likely be noted and
include characteristically elevated T waves, ST
depression, and ventricular fibrillation.
Elevated Values> 5.0
mEq/L
Potassium (K+)
Decreased Values<3.5 mEq/L
Symptoms and assessment: Fatigue,
malaise, muscle weakness and cramping,
nausea and vomiting, weak irregular pulse,
polyuria, hyperglycemia and tell tale EKG
changes. EKG changes characteristic of
hypokalemia are ST depression, flat T
waves, bradycardia, and an exaggerated U
wave. Patients may also present with
respiratory depression and GI stasis.
Priority assessment is absolutely the
cardiac assessment and treatment of
cardiac symptoms.
Causes: Extreme potassium intake,
administration of IV potassium, metabolic
acidosis which will move K+ from ICF to ECF,
administration of potassium sparing diuretics,
adrenal insufficiency which decreases
aldosterone which will cause K+ retention, and
administration of ACE inhibitors. The most
common cause of hyperkalemia is renal failure
which leads to aldosterone deficiency which
leads to K+ retention.
Labs to consider include: When assessing potassium
levels one should consider serum potassium levels, Na
levels due to the inverse relationship, and Mg levels as
Mg is crucial to correct sodium potassium pump
function. EKG changes are a very useful and telling
tool when assessing potassium levels and are a
priority as altered potassium levels can have
profound and devastating cardiac effects.
Geriatric Concerns: K+ levels are influenced by many
drugs including insulin, beta blockers and agonists, and ACE
inhibitors. The geriatric patient is often prescribed many drugs
and should be monitored for interaction of the interaction of
prescriptions and potassium levels
Causes: The most common cause of hypokalemia is
excessive fluid loss including diarrhea. The patient on Lasix
or other diuretics should be monitored for hypokalemia.
Increased aldosterone levels will trigger increased urinary
potassium loss. Aldosterone levels will increase when blood
volume is low. If a PT is already experiencing low potassium
levels due to increased water low this mechanism will cause
further potassium loss. Low magnesium levels will also
trigger aldosterone excretion and can lead to hypokalemia.
Metabolic acidosis will cause a shift of K+ from the ECF to
ICF and patients who are in DKA should be monitored for
hypokalemia. Erythropoietin therapy or B12 administration
may also cause hypokalemia.
Treatment, interventions, and priorities:
Elimination of dietary magnesium is often the
first step in treating hypermagnesemia. People
with renal failure should avoid magnesium
supplements. IV calcium may be prescribed to
counteract the effects of increased magnesium
on cardiac tissue and respiratory function. The
nurse can also anticipate the encouragement of
PO fluids to aid the body in excreting excess
serum magnesium. Priority is management of
any cardiac dysrhythmias. The nurse can
anticipate administration of an EKG.
Role in Body: Helps metabolize carbs and protein.
Mostly contained in bones. Helps to regulate cardiac
function and directly acts on neuromuscular junction as
an inhibitory cation.
Treatment and anticipated interventions:
Priority is given to controlling and monitoring
potential cardiac complications related to
hypomagnesemia. An EKG should be
performed and monitored. In extreme cases IV
magnesium may be ordered. This should be
given with great care and the patient should be
closely monitored as rapid administration may
cause cardiac or respiratory arrest. Oral
supplementation and integration of magnesium
rich foods into the diet is often enough to treat
hypomagnesemia.
Signs and symptoms of hypermagnesemia
include: Early hypermagnesemia is
characterized by lethargy, drowsiness, nausea
and vomiting. Deep tendon reflexes are
eventually lost and cardiac and respiratory
function may be profoundly depressed or
cease.
Elevated Values >2.2 mg/dL
Magnesium (Mg)
Decreased Values<1.7 mg/dL
Symptoms and assessment: Symptoms
include those associated with
hypocalcemia such as restlessness,
irritability, muscle twitching, and
hyperreflexia. The patient should be
monitored for potentially life threatening
dysrhythmias such as ventricular
fibrillation or premature ventricular
contractions (PVC’s).
Causes: May be caused by excessive intake of
magnesium. Often this is related to the use of
magnesium containing antacids such as milk of
magnesia. Patients in renal failure may also
experience hypermagnesemia as magnesium is
largely excreted by the kidneys.
Labs to consider include: Magnesium should be assessed
with potassium and calcium as they all play an integral role in
cardiac function.
Geriatric Concerns: Many geriatric patients have a
habitual use of laxatives and antacids containing
magnesium such as Maalox and milk of magnesia.
Causes: Hypomagnesemia is often caused by diarrhea,
vomiting, chronic alcoholism, malnutrition, nasogastric
suctioning, poorly controlled diabetes mellitus, or
poorly controlled hypokalemia. Anything which causes
excessive diuresis should be suspect of causing
hypomagnesemia.
Treatment, interventions, and priorities: Priority
is to treat the underlying cause of the
hyperphosphatemia. If pain is present the patient
should have their pain controlled. Cardiac issues
may be present with this condition and the
treatment of any dysrhythmias should be the
absolute priority. Expected treatments include
eliminating dietary phosphorus (dairy, laxatives),
hydration, and the administration of calcium
supplements as calcium and phosphate have an
inverse relationship. Phosphate binding
medications may also be prescribed in the event
that a patient is renally compromised and is
unable to excrete phosphate adequately.
Role in Body: Phosphate is the primary ICF anion. It
is deposited with calcium in bones and is necessary for
RBC production and is an acid/base buffer. The renal
system is the major route for phosphate excretion.
Treatment and anticipated interventions: We
would expect to treat hypophosphatemia with
PO supplements and a high phosphate diet.
Occasionally IV phosphate administration will
be ordered. If this is the case the patient should
be monitored for signs of acute and serious
hypocalcemia. It may be advisable to monitor
the pateint’s EKG changes.
Signs and Symptoms: Muscle problems such
as tetany can be an indicator of increased
phosphate. Muscle and/or joint pain may also
be an indication of hyperphosphatemia as
when phosphate is present in excess it can bind
with calcium and deposit a precipitate in body
tissue including muscle and joint tissue. Other
signs and symptoms to look for are similar to
those associated with hypocalcemia such as
muscle excitability, muscle weakness, cardiac
issues, confusion, and restlessness.
Elevated Values>4.4 mg/dL
Phosphate (PO43-)
Decreased Values<2.4 mg/dL
Symptoms and assessment: Symptoms of
hypophosphatemia include dysrhythmias,
rhabdomylosis (pain EVERHYWHERE),
muscle and respiratory weakness,
confusion, coma, wasting of magnesium,
calcium, and carbonate. Phosphate is
necessary for RBC production and we may
then expect to see malaise and muscle
weakness.
Causes: Most often caused by renal failure, as
phosphate is largely excreted by the kidneys.
Also may be caused by excessive use of
phosphate containing laxatives or milk. Vitamin
D aids in phosphate absorption and excess
vitamin D may contribute to hyperphosphatemia.
Malignancies may also cause increased
phosphate levels.
Labs to consider include: Calcium should be examined
with phosphate as they have a reciprocal relationship. Vitamin
D should be examined as excess vitamin D can enhance
phosphate absorption.
Geriatric Concerns: The geriatric population often uses
laxatives excessively. Many laxatives contain phosphate and
this may be a cause of hyperphosphatemia. Phosphate also
increases with malignancy, something more common among
the geriatric population
Causes: May be caused by glucose administration,
alcohol withdrawl, respiratory alkalosis, DKA, TPN, or
recovery from starvation. Most commonly
hypophosphatemia is seen in patients who are
malnourished or are recovering from malnourishment.
The next most common cause is TPN which does not
adequately address phosphate needs.
 References

Lewis, S.L., Dirksen, S.R. (2011). Medical Surgical Nursing: Assessment and Management of Clinical Problems (8th edition) . St. Louis, MO: Elsevier

Potter, P.A., Perry, A.G., Stockert, P.A., Hall, A.M. (2013). Fundamentals of Nursing (8th edition). St. Louis, MO: Elsevier