Boldios, Psyche Valerie B.

BSN-3A NCM 112 LEC 11/27/21

Electrolytes: Balance and Imbalance

Sodium (Na+)
Normal value: 135 to 145 mEq/L (135 to 145 mmol/L)
Functions:

 Sodium functions in establishing the electrochemical state necessary for muscle contraction and
the transmission of nerve impulses.
 It is the primary determinant of ECF volume and osmolality.
 Sodium has a major role in controlling water distribution throughout the body.

Hyponatremia Hypernatremia
Description: Description:

Hyponatremia refers to a serum sodium level Hypernatremia is a serum sodium level higher than
that is less than 135 mEq/L (135 mmol/L). 145 mEq/L (145 mmol/L).

Causes: Causes:

 Deficiency of aldosterone It can be caused by a gain of sodium in excess of

 High urine sodium concentration
 Anticonvulsants (ie, carbamazepine
[Tegretol], Levetiracetam [Keppra]) and
SSRIs (fluoxetine [Sarafem], sertraline
[Zoloft], paroxetine [Paxil])
 SIADH
water or by a loss of water in excess of sodium:
 Fluid deprivation
 Administration of hypertonic enteral feedings
without adequate water supplements
 Watery diarrhea
 Increased insensible water loss
 diabetes insipidus (central and nephrogenic)
 Heat stroke
 Near drowning in sea water
 Malfunction of hemodialysis or peritoneal
dialysis systems
 IV administration of hypertonic saline or
excessive use of sodium bicarbonate

Clinical Manifestations: Clinical Manifestations:

 Poor skin turgor  Thirst due to dehydration

 Dry mucosa  Dry, swollen tongue and sticky mucous
 Headache membranes
 Decreased saliva production  Flushed skin
 Orthostatic fall in blood pressure  Peripheral and pulmonary edema
 Nausea  Postural hypotension
 Vomiting  Oliguria
 Abdominal cramping occur  Increased muscle tone and deep tendon reflexes
 Altered mental status (DTRs)
 Status epilepticus  Increased body temperature
 Coma In moderate hypernatremia:
 Cerebral edema  Restlessness and weakness
 Anorexia In severe hypernatremia:
 Muscle cramps  Disorientation
 Exhaustion  Delusions
 Brain herniation and compression (de-  Hallucinations
veloped in less than 48 hours)  permanent brain damage can occur (especially in
 Status epilepticus and cerebral pontin children)
 Myelinolysis (developed over 48 hours or
more)
 Pitting edema in patients with SIADH

When the serum sodium level decreases to

less than 115 mEq/L (115 mmol/L):
 Lethargy
 Confusion
 Muscle twitching
 focal weakness
 Hemiparesis
 Papilledema
 Seizures
 Death

Laboratory Findings: Laboratory Findings:

 Serum sodium level is less than 135 mEq/L
 Lower than 100 mEq/L (100 mmol/L) in
SIADH
 Decreased serum osmolality
 Less than 20 mEq/L (20 mmol/L) urinary
sodium content
 Urine specific gravity is low (1.002 to
1.004)
 Serum sodium level exceeds 145 mEq/L (145
mmol/L)
 Serum osmolality exceeds 300 mOsm/kg (300
mmol/L)
 Increased urine specific gravity and urine
osmolality

When hyponatremia is due to SIADH:

 the urinary sodium content is greater than
20 mEq/L urine specific gravity is greater
than 1.012
Management: Management:

Medical Management Medical Management

Sodium Replacement  Infusion of a hypotonic electrolyte solution (eg,

 Lactated Ringer’s solution or isotonic
saline (0.9% sodium chloride) solution as
prescribed
 In patients with SIADH, lithium (Eskalith) or
demeclocycline (Declomycin)
Water Restriction
 Restricting fluid to a total of 800 mL in 24
hours
Pharmacologic Therapy
 AVP receptor antagonists
 IV conivaptan hydrochloride (Vaprisol) for
hospitalized patients
Nursing Management
0.3% sodium chloride) or an isotonic non saline
solution (eg, dextrose 5% in water [D5W])
 Diuretics
 Desmopressin acetate (DDAVP) to treat diabetes
insipidus if it is the cause of hypernatremia
Nursing Management
 Provide fluids at regular intervals
 Enteral feedings or by parenteral route as
prescribed by the doctor
 Monitoring serial serum sodium levels and
observing for changes in neurologic signs

 Detecting and Controlling Hyponatremia

 Encourages foods and fluids with high
sodium content
 Fluid needs are determined by evaluating
fluid I&O, urine specific gravity, and serum
sodium levels.
 Electrolytes: Balance and Imbalance
Potassium (K+)
Normal value: 3.5 to 5.0 mEq/L (3.5 to 5 mmol/L)
Functions:

 Potassium influences both skeletal and cardiac muscle activity.

 Potassium is also important in how nerves and muscles work.
 Potassium levels often change with sodium levels.

Hypokalemia Hyperkalemia
Description: Description:

Hypokalemia (below 3.5 mEq/L [3.5 mmol/L]) Hyperkalemia (greater than 5.0 mEq/L [5 mmol/L])
usually indicates a deficit in total potassium seldom occurs in patients with normal renal function.
stores.
Causes: Causes:

 History  Decreased renal excretion of potassium

 Potassium-losing diuretics, such as the  Rapid administration of potassium
thiazides and loop diuretics  Movement of potassium from the ICF
 Other medications such as corticosteroids, compartment to the ECF compartment
sodium penicillin, carbenicillin, and  Medications such as potassium chloride, heparin,
amphotericin B. ACE inhibitors, NSAIDs, beta-blockers, and
 Vomiting and gastric suction potassium- sparing diuretics
 Diarrhea
 Prolonged intestinal suctioning
 Recent ileostomy
 Villous adenoma
 Hyperaldosteronism
 Patients receiving high-carbohydrate
parenteral nutrition
 Patients who do not eat a normal diet for a
prolonged period
-Elderly people, patients with alcoholism, and
patients with anorexia nervosa
 People with bulimia

Clinical Manifestations: Clinical Manifestations:

 Fatigue  Peaked, narrow T waves

 Anorexia  ST-segment depression
 Nausea  Shortened QT interval
 Vomiting  Prolonged PR interval
 Muscle weakness  Decomposition and widening of the QRS complex
 Leg cramps  Ventricular dysrhythmias and cardiac arrest if
 Decreased bowel motility progresses
 Paresthesias (numbness and tingling)  Paralysis of respiratory and speech muscles
 Dysrhythmias  GI manifestations such as nausea, intermit- tent
 Decreased muscle strength and DTRs intestinal colic, and diarrhea

If prolonged:
polyuria, nocturia and excessive thirst

Laboratory Findings: Laboratory Findings:

 Flat T waves or inverted T waves or both  Metabolic and respiratory acidosis

 Depressed ST segments
 Elevated U wave
 Digitalis toxicity at lower digi- talis levels
 Metabolic alkalosis
 Urinary potassium excretion exceeding 20
mEq/day

Management: Management:

Medical Management Medical Management

 Increased intake in the daily diet
 Oral potassium
 IV replacement therapy (if hypokalemia
cannot be prevented by conventional
measures)
 Administration of 40 to 80 mEq/day of
potassium in the adult if there are no
abnormal losses of potassium
 diet containing sufficient potassium (50 to
100 mEq/day)
 Oral or IV potassium supplements as
prescribed
 Salt substitutes containing 50 to 60 mEq of
potassium per teaspoon
 Potassium chloride
 Potassium acetate or potassium Phosphate
 Restriction of dietary potassium and potassium-
containing medications
 Oral or by retention enema administration of
cation exchange resins (eg, sodium polystyrene
sulfonate [Kayex- alate])
 Emergency Pharmacologic Therapy
 IV calcium gluconate
 IV administration of sodium bicarbonate
 IV administration of regular insulin and a
hypertonic dextrose solution
 Loop diuretics, such as furosemide (Lasix)
 Beta-2 agonists, such as albuterol (Proventil,
Ventolin)
 If the hyperkalemic condition is not transient,
cation exchange resins, peritoneal dialysis,
 as prescribed
Nursing Management
 Preventing Hypokalemia
 Encouraging the patient at risk to eat foods
rich in potassium (when the diet allows)
 Patient education
 Careful monitoring of fluid I&O
 Monitor ECG for changes
 Arterial blood gas values are checked for
elevated bicarbonate and pH levels
 Correcting Hypokalemia oral route is ideal
to treat a mild to moderate hypokalemia
 Administering Intravenous Potassium
stop the potassium infusion if urine volume is
less than 20 mL/h for 2 consecutive hours
hemodialysis, or other forms of renal
replacement therapy
Nursing Management
 Preventing Hyperkalemia
 Encourage the patient to adhere to the
prescribed potassium restriction
 Correcting Hyperkalemia
 Caution patients to use salt substitutes sparingly
if they are taking other supplementary forms of
potassium or potassium-conserving diuretics
potassium-conserving diuretics, such as
spironolactone (Aldactone), triamterene
(Dyrenium), and amiloride (Midamor); potassium
supplements; and salt substitutes should not be
administered to patients with renal dysfunction
 Electrolytes: Balance and Imbalance
Calcium (Ca)
Normal value: 8.6 to 10.2 mg/dL (2.2 to 2.6 mmol/L)
Functions:

 A major component of bones and teeths

 It also transmits nerve impulses and helps regulate muscle contraction and relaxation, including
cardiac muscle
 Calcium is instrumental in activating enzymes that stimulate many essential chemical reactions in
body
 It plays a role in blood coagulation
 Important in neuromuscular activity

Hypocalcemia Hypercalcemia
Description: Description:

Serum calcium value lower than 8.6 mg/dL Serum calcium value greater than 10.2 mg/dL [2.6
[2.15 mmol/L]) occurs in a variety of clinical mmol/L]) is a dangerous imbalance when severe.
situations.

Causes: Causes:

 Primary hypoparathyroidism  Malignancies

 Surgical hypoparathyroidism  Hyperparathyroidism
 Radial neck dissection and is most likely in  Can occur after severe or multiple fractures or
the first 24 to 48 hours after surgery spinal cord injury
 Transient hypocalcemia with massive  Vitamin A and D intoxication
administration of citrated blood  Chronic lithium use
 inflammation of the pancreas  Theophylline toxicity
( pancreatitis)  Cardiac standstill
 Inadequate vitamin D consumption
 Magnesium deficiency
 Medullary thyroid carcinoma
 Low serum albumin level
 Alkalosis
 Alcohol abuse

Medications predisposing to hypocalcemia:

 Aluminum-containing antacids
 Aminoglycosides
 Caffeine
 Cisplatin
 Corticosteroids
 Mithramycin
 Phosphates
 Isoniazid
 Loop diuretics
 Proton pump inhibitors

Clinical Manifestations: Clinical Manifestations:

 Muscular weakness
 Tetany  Constipation
 Numbness  Anorexia
 Tingling of fingers, toes, and circumoral  Nausea and vomiting
region  Polyuria
 Positive Trousseau sign and Chvostek sign  Polydipsia
 Seizures  dehydration
 Carpopedal spasm  Hypoactive deep tendon reflexes
 Hyperactive deep tendon reflexes  Lethargy
 Irritability  Deep bone pain
 Bronchospasm  abdominal cramps
 Anxiety  peptic ulcer symptoms
 Impaired clotting time  Confusion
 Decrease prothrombin  Coma
 Diarrhea  Pathologic fractures
 Decrease BP  Flank pain
 ECG: prolonged QT interval and  Calcium stones
lengthened ST segment  Hypertension
 ECG: shortened ST segment and QT interval,
bradycardia, heart blocks
Other changes associated with hypocalcemia:

 Mental changes such as depression,

impaired memory, confusion, delirium,
and hallucinations

Respiratory effects with decreasing calcium:

 Dyspnea
 Laryngospasm
 Signs and symptoms of chronic
hypocalcemia:
 Hyperactivebowel sounds
 Dry and brittle hair and nails
 Abnormal clotting
Laboratory Findings:
 Evaluate serum albumin levels and arterial
pH.
 Clinicians often discount a low serum
calcium level in the presence of a similarly
low serum albùmin level.
 The ionized calcium level is usually normal
in patients with reduced total serum
calcium levels and concomitant
hypoalbuminemia.
 When the arterial pH increases (alkalosis),
more calcium becomes bound to protein.
 PTH levels are decreased in
hypoparathyroidism
 Magnesium and phosphorus level needs to
be assessed to identify possible causes of
decreased calcium.
Management:
Medical Management
 For acute symptomatic hypocalcemia
 Prompt treatment with IV administration
of a calcium salt.
 Parenteral calcium salts ( includes calcium
gluconate and calcium chloride)
 A 0.9% sodium chloride solution should
not be used with calcium because it
increases renal calcium loss.
 Solutions containing phosphates or
bicarbonates should also not be used with
calcium because they can cause
precipitation when calcium is added.
 The nurse must clarify with the primary
provider and pharmacist which calcium
salt to administer.
- Calcium gluconate yields 4.5
mEq of calcium
- Calcium chloride provides 13.6
mEq of calcium.
 Calcium replacement can cause:
- postural hypotension;
therefore, the patient is kept in
bed during IV infusion, and
Laboratory Findings:
 Cardiovascular changes may include a variety of
dysrhythmias and shortening of QT interval and
ST segment
 Double-antibody PTH test- may be used to
differentiate between primary
hyperparathyroidism and malignancy.
 PTH levels are increased in primary or secondary
hyperparathyroidism and suppressed in
malignancy.
 X-ray may reveal bone changes if the patient
have hypercalcemia secondary to malignancy,
bone cavitations, or urinary calculi.
 Urine calcium can be normal or elevated in
hyperparathyroidism and hypercalcemia caused
by malignancy.
Management:
Medical Management
 Therapeutic aims include:
- decreasing calcium levels
- reversing the process causing the
hypercalcemia.
 Treating the underlying cause:
- chemotherapy for a malignancy
- partial parathyroidectomy for
hyperparathyroidism is essential
 Pharmacologic Therapy
● Administering fluids to dilute serum
calcium and promote its excretion by
the kidneys, mobilizing the
patient,and restricting dietary calcium
intake.
● Administration of 0.9 % sodium
chloride solution temporarily dilutes
the serum calcium level
● Administering IV phosphate can cause
a reciprocal drop in serum calcium.
● Furosemide is often used in
conjunction with the administration
of saline solution and it increases
 blood pressure is monitored. calcium excretion.
● Calcitonin can be used to lower the
Nutritional Therapy serum calcium level - particularly
 Vitamin D therapy ( to increase calcium useful for patients with heart disease
absorption from the GI tract. or kidney injury who cannot tolerate
 Increasing the dietary intake of calcium to large sodium loads.
at least 1000 to 1500 mg/day . ● Skin testing for allergy to salmon
 Calcium supplements must be given in calcitonin is necessary before the
divided doses of mo higher than 500 mg to hormone is given.
promote calcium absorption. ● Calcitonin is given by intramuscular
injection rather than subcutaneously
Calcium containing foods: because patients with hypercalcemia
 Milk products have poor perfusion of subcutaneous
 Green, and leafy vegetables tissue.
 Canned salmon
 Canned sardines For patient with cancer:
 Fresh oysters  Surgery
 Chemotherapy
Nursing Management  Radiation therapy
 Assess for hypocalcemia in at risk patients.
 Seizure precautions are initiated if  Corticosteroids may be used to decrease bone
hypocalcemia is severe. turnover and tubular reabsorption for patients
 Monitor the status of the airway because with:
laryngeal stridor can occur. - sarcoidosis
 The nurse must educate the patient with - myelomas
hypocalcemia about foods that are rich in - lymphomas
calcium. - leukemia
 Advise the patient to consider calcium  IV forms can cause
supplements. - fever
 Emphasize to the patient that alcohol and - transient leukopenia
caffeine in high doses inhibit calcium - eye inflammation
absorption and moderate smoking - nephrotic syndrome
increases urinary calcium excretion. - jaw osteonecrosis
 Cautioned them to avoid the overuse of  Mithramycin- a cytotoxic antibiotic ; inhibits
laxatives and antacids that contain bone resorption, thus lowers the serum calcium
phosphorus because their use decreases levels
calcium absorption.  Inorganic phosphate salts can be given orally or
by nasogastric tube, rectally, or IV.
 IV phosphate therapy is used with extreme
caution in the treatment of hypercalcemia
- it can cause severe calcification in
various tissues
- hypotension
- tetany
- acute kidney injury
Nursing Management
 Monitor for hypercalcemia in at risk patients.
 Interventions such as:
- increasing patient mobility
- encouraging fluids can help prevent
hypercalcemia or at least minimize its
severity.
 Hospitalized patients at risk should be
encouraged to ambulate as soon as possible.
 Educate the importance of frequent ambulation.
 When encouraging oral fluids, the nurse
considers the patient’s likes and dislikes.
 Fluids containing sodium should be given unless
contraindicated because sodium assists with
calcium excretion.
 Patients are encouraged to drink 2.8 to 3.8 L (3-4
quarts) of fluid daily.
 Adequate fiber in the diet is encouraged to offset
the tendency for constipation.
 Safety precautions are implemented, as
necessary, when altered mental status is present.
 The patient and the family should be informed
that these mental changes are reversible with
treatment.
 Increased calcium increases the effects of
digitalis; therefore the patient is assessed for
signs and symptoms of digitalis toxicity .
 Cardiac rate and rhythm are monitored for any
abnormalities.
 Electrolytes: Balance and Imbalance
Magnesium (Mg)
Normal value: 1.3 to 2.3 mg/dL (0.62 to 0.95 mmol/L)

Function:

 Most abundant intracellular cation after potassium

 Acts as an activator for many intracellular enzyme systems
 Plays a role in both carbohydrate and protein metabolism.
 Important in neuromuscular function that acts directly on the myoneural junction
 Produces its sedative effect at the neuromuscular junction
 Inhibits the release of the neurotransmitter acetylcholine
 Increases the stimulus threshold in nerve fibers.
 Affects the cardiovascular system, acting peripherally to produce vasodilation and decreased
peripheral resistance.

Hypomagnesemia Hypermagnesemia
Description: Description:

Hypomagnesemia refers to a below-normal Hypermagnesemia (serum levels over 2.3 mg/dL

serum magnesium concentration (1.3 mg/dL
[0.62 mmol/L]) and is frequently associated
with hypokalemia and hypocalcemia.
[0.95mmol/L]) is a rare electrolyte abnormality,
because the kidneys efficiently excrete magnesium.
A serum magnesium level can appear falsely
elevated if blood specimens are allowed to
hemolyze or are drawn from an extremity with a
tourniquet that was applied too tightly.

Causes: Causes:

 Loss of magnesium from the GI tract may
occur with nasogastric suction, diarrhea,
or fistulas.
 Hypomagnesemia is a common yet often
overlooked imbalance and may occur
with withdrawal from alcohol and
administration of parenteral nutrition.
 The most common causes of significant
hypomagnesemia are said to be diabetes,
alcoholism, and the use of diuretics.
 The most common cause of hypermagnesemia
is renal failure, hence unable to get rid of excess
magnesium and is more susceptible to a build-
up of the mineral in the blood.
 This condition is aggravated when such patients
receive magnesium to control seizures.
 Other causes are:
● adrenal insufficiency
● excessive IV magnesium
administration
● diabetic ketoacidosis
● lithium therapy
● hypothyroidism.
Clinical Manifestations: Clinical Manifestations:

Neuromuscular changes:  Lowered blood pressure because of peripheral

vasodilation
 Hyperexcitability  Nausea
 Muscle weakness  Vomiting
 Tremors  Weakness
 Athetoid movements  Soft-tissue calcifications
 Facial flushing
Others:  Sensations of warmth

 Tetany At higher magnesium concentrations:

 Nystagmus
 Vertigo  Lethargy
 Generalized tonic–clonic or focal seizures  Difficulty speaking (dysarthria)
 Laryngeal stridor  Drowsiness
 Positive Chvostek’s and Trousseau’s sign  DTRs are lost, and muscle weakness and
paralysis may develop.
Hypomagnesemia may be accompanied by  Coma, atrioventricular heart block, and cardiac
marked alterations in mood: arrest can occur when the serum magnesium
level is greatly elevated and not treated.
● Apathy  Platelet clumping
● Depression  Delayed thrombin formation
● Apprehension
● Extreme agitation
● Ataxia
● Dizziness, insomnia, and confusion
● Delirium, auditory or visual
hallucinations, and frank psychosis
may occur

Laboratory Findings: Laboratory Findings:

 On laboratory analysis, the serum  On laboratory analysis

magnesium level is less than 1.3 mg/dL
(0.62 mmol/L).
 Urine magnesium may help identify the
cause of magnesium depletion, and levels
are measured after a loading dose of
magnesium sulfate is administered.
2 Newer Techniques
 Nuclear magnetic resonance
spectroscopy
 Ion-selective electrode
 Both are sensitive and direct means of
measuring ionized serum magnesium
● Serum magnesium level is greater
than 2.3 mg/dL (0.95 mmol/L).
 Increased potassium and calcium are present
concurrently. As creatinine clearance decreases
to less than 3.0 mL/min, the serum magnesium
levels increase.
 ECG findings:
● Prolonged PR interval
● Tall T waves
● Widened QRS
● Prolonged QT interval
● Atrioventricular block.
 levels.
Management:
MEDICAL MANAGEMENT
 Diet modification
● Principal dietary sources of
magnesium include: Green
leafy vegetables, nuts, seeds,
legumes, whole grains,
seafood, peanut butter, and
cocoa.
 Magnesium salts can be administered
orally in an oxide or gluconate form to
replace continuous losses but can
produce diarrhea.
 Patients receiving parenteral nutrition
require magnesium in the IV solution to
prevent hypomagnesemia.
 IV magnesium sulfate must be
administered by an infusion pump and at
a rate not to exceed 150
 mg/min, or 67 mEq over 8 hours.
 Do not administer a bolus dose of
magnesium sulfate too rapidly to avoid
heart block or asystole.
 Vital signs must be assessed frequently
during magnesium administration to
detect changes in cardiac rate or rhythm,
hypotension, and respiratory distress.
 Monitoring urine output is essential
before, during, and after magnesium
administration
 Calcium gluconate must be readily
available to treat hypocalcemic tetany or
hypermagnesemia.
NURSING MANAGEMENT
 Patients receiving digitalis are monitored
closely to avoid digitalis toxicity.
 Implement seizure precautions
 Patients should be screened for
dysphagia
 Teaching plays a major role in treating
magnesium deficit, particularly a deficit
resulting from abuse of diuretic or
Management:
MEDICAL MANAGEMENT
 Avoiding the administration of magnesium to
patients with renal failure
 Carefully monitoring seriously ill patients who
are receiving magnesium salts.
In patients with severe hypermagnesemia:
 All parenteral and oral magnesium salts are
discontinued.
In emergencies, such as respiratory depression or
defective cardiac conduction:
 Ventilatory support
 IV calcium gluconate
In addition:
 Hemodialysis with a magnesium-free dialysate
can reduce the serum magnesium to a safe level
within hours.
 Administration:
● loop diuretics (Lasix)
● Sodium chloride or lactated Ringer’s
IV solution
NURSING MANAGEMENT
If hypermagnesemia is suspected:
 The nurse monitors the vital signs, noting
hypotension and shallow respirations.
 The nurse also observes decreased DTRs and
changes in the level of consciousness.
 Medications that contain magnesium are not
administered to patients with renal failure or
compromised renal function, and patients with
renal failure are cautioned to check with their
health care providers before taking OTC
medications.
 Caution is essential when preparing and
administering magnesium-containing fluids
 laxative medications. parenterally
 Nurse instructs the patient about the
need to consume magnesium-rich foods.
 The nurse provides teaching, counseling,
support, and possible referral to alcohol
abstinence programs or other
professional help.
 Electrolytes: Balance and Imbalance
Phosphorus (P)
Normal value: 2.5 to 4.5 mg/dL (0.8 to 1.45 mmol/L)
Functions:
 Essential to the function of muscle and RBC;
 Formation of ATP and of 2,3-diphosphoglycerate – facilitates the release of oxygen from
hemoglobin;
 Maintenance of acid-base balance, as well as nervous system and the intermediary metabolism
of carbohydrate, protein, and fat;
 Provides structural support to bones and teeth.
Hypophosphatemia Hyperphosphatemia
Description: Serum phosphate level of less Description: Serum phosphorus level that exceeds
than 2.5 mg/dL. 4.5 mg/dL.
Causes: Causes:
 Refeeding after starvation  Acute kidney injury and chronic kidney disease
 Alcohol withdrawal  Excessive intake of phosphorus
 Diabetic ketoacidosis  Vitamin D excess
 Respiratory and metabolic alkalosis  Respiratory and metabolic acidosis
 Low magnesium level  Hypoparathyroidism
 Low potassium level  Volume depletion
 Hyperthyroidism  Leukemia/lymphoma treated with cytotoxic
 Vomiting agents
 Diarrhea  Increased tissue breakdown
 Hyperventilation  Rhabdomyolysis
 Vitamin D deficiency associated with
malabsorptive disorders
 Burns
 Acid-base disorders
 Parenteral malnutrition
 Diuretic and antacid use
Clinical Manifestations: Clinical Manifestations:
 Paresthesia  Tetany
 Muscle weakness  Tachycardia
 Bone pain and tenderness  Anorexia
 Chest pain  Nausea and vomiting
 Confusion  Muscle weakness
 Cardiomyopathy  Signs and symptoms of hypocalcemia
 Respiratory failure  Hyperactive reflexes
 Seizures  Soft tissue calcifications in lungs, heart, kidneys,
 Tissue hypoxia and cornea
 Increased susceptibility to infection
 Nystagmus
Laboratory Findings: Laboratory Findings:
 Serum phosphorus level is less than 2.5  Serum phosphorus level that exceeds 4.5 mg/dL
mg/dL (0.80 mmol/L). (1.5 mmol/L).
 Increased PTH level d/t hyperthyroidism
 Decreased serum magnesium d/t
increased urinary excretion of magnesium
 Increased alkaline phosphatase with
osteoblastic activity
 X-ray may show skeletal changes of
osteomalacia or rickets.
Management:
Medical Management
 Prevention is the goal.
 For prevention: closely monitor serum
phosphate levels and adequate amounts
of phosphorus should be added to
parenteral solutions.
 Severe hypophosphatemia requires
prompt attention:
○ IV phosphorus as sodium or
potassium phosphate with a
rate of 10 mEq/L (monitor for
risk of tissue sloughing and
necrosis).
 Less acute situations: oral phosphorus
replacement.
Nursing Management
 Preventive measures: gradually increasing
solution in parenteral nutrition to avoid
rapid shifts of phosphorus in the cells.
 Careful attention to infection prevention.
 Frequent monitoring of serum
phosphorus levels and reports early signs
of hypophosphatemia (apprehension,
confusion, change in level of
consciousness).
 For mild hypophosphatemia: milk and
milk products, organ meats, nuts, fish,
poultry, and whole grains are
encouraged.
 For moderate hypophosphatemia:
supplements such as Neutra-Phos
capsules, K-Phos, and Fleet Phospho-Soda
as prescribed.
 Serum calcium level is useful for diagnosing the
primary disorder and assessing the effects of
treatments.
 X-ray may show skeletal changes with abnormal
bone development.
 Decreased PTH levels d/t hypoparathyroidism.
 BUN and creatinine levels are used to assess
renal function.
Management:
Medical Management
 Treatment is directed to underlying disorders.
 Vitamin D preparations – to decrease serum
bind phosphorus in the GI tract such as calcitriol
[oral (Rocaltrol); and parenteral (Calcijex,
paricalcitol [Zemplar]].
 Excessive IV administration of calcitriol.
 Administration of Amphojel with meals (long-
term use may cause bone and central nervous
system toxicity).
 Restriction of dietary phosphate, forced diuresis
with a loop diuretic, volume replacement with
saline, and dialysis may lower phosphorus.
 Surgery to remove large calcium and
phosphorus deposits.
Nursing Management
 The nurse monitors patients at risk for
hyperphosphatemia.
 Patients with a prescribed low phosphorus diet
are instructed to avoid phosphorus-rich foods
(hard cheese, cream, nuts, whole-grain cereals,
etc.).
 The nurse instructs to avoid phosphate-
containing laxatives and enemas.
 Patient education regarding recognizing the
signs of impending hypocalcemia.
 Changes in urine output monitoring.
 Electrolytes: Balance and Imbalance
Chloride (Cl)
Normal value: 97 to 107 mEq/L (97 to 107 mmol/L).

Functions:
 Assist in determining osmotic pressure
 Combines with hydrogen to form hydrochloric acid
 Chloride assists in maintaining acid–base balance and works as a buffer in the exchange of
oxygen and carbon dioxide in red blood cells.

Hypochloremia Hyperchloremia
Description: Hypochloremia is a serum Description: Hyperchloremia exists when the serum
chloride level below 97 mEq/L level of chloride exceeds 107 mEq/L (107 mmol/L).
(97 mmol/L). Hypernatremia, bicarbonate loss, and metabolic
acidosis can occur with high chloride levels.

Causes: Causes:
 Administration of chloride-deficient IV  Result of iatrogenically induced hyperchloremic
solutions metabolic acidosis
 Low sodium intake  Stemming from excessive administration of
 Decreased Serum Sodium Levels chloride relative to sodium, most commonly as
 Metabolic Alkalosis 0.9% normal saline solution, 0.45% normal
 Massive Blood Transfusions saline solution, or lactated Ringer’s solution
 Diuretic Therapy  Loss of bicarbonate ions via the kidney or the GI
 Burns tract
 Fever  Acidosis occurs with a decrease in bicarbonate
 Administration of aldosterone, ACTH, ions
corticosteroids, bicarbonate, laxatives  Head trauma,
which decreases serum chloride levels  Increased perspiration,
 Excess adrenocortical hormone production,
 Decreased glomerular filtration

Clinical Manifestations: Clinical Manifestations:

 (PaCO2) increases to 50 mmHg.  Hypervolemia

 Hyperexcitability of muscles  Hypernatremia
 Tetany  Tachypnea
 Hyperactive DTRs  Weakness
 Weakness,  Lethargy
 Twitching  Deep respirations
 Muscle cramps  Rapid respirations
 Cardiac dysrhythmias  Diminished cognitive ability
 Water excess  Hypertension
> If untreated, hyperchloremia can lead to a

Laboratory Findings:
 Chloride level, sodium and potassium
levels are evaluated, because these
electrolytes are lost along with chloride.
 Arterial blood gas analysis identifies the
acid–base imbalance, which is usually
metabolic alkalosis.
 Urine chloride level, which is also
measured, decreases in hypochloremia.
Management:
Medical Management
 Correcting the cause of hypochloremia
and the contributing electrolyte and acid–
base imbalances.
 Normal saline (0.9% sodium chloride) or
half-strength saline (0.45% sodium
chloride) solution is administered by IV to
replace the chloride
 Discontinue If the patient is receiving a
diuretic (loop, osmotic, or thiazide).
 Ammonium chloride to treat metabolic
alkalosis
Nursing Management:
 Nurse monitors the patient’s I&O, arterial
blood gas values, and serum electrolyte
levels.
 Changes in the patient’s level of
consciousness and muscle strength and
movement are reported to the physician
promptly.
 Vital signs are monitored, and respiratory
assessment is carried out frequently.
 The nurse provides and teaches the
patient about foods with high chloride
content.
 Foods high in chloride include tomato
juice, bananas, dates, eggs, cheese, milk,
salty broth, canned vegetables, and
processed meats.
decrease in cardiac output, dysrhythmias, and coma.
Laboratory Findings:
 Serum chloride level is 108 mEq/L (108 mmol/L)
or greater, the serum sodium level is greater
than 145 mEq/L (145 mmol/L),
 Serum pH is less than 7.35,
 Serum bicarbonate level is less than 22 mEq/L
(22 mmol/L).
 Urine chloride excretion increases.
Management:
Medical Management
 Hypotonic IV solutions may be administered to
restore balance.
 Lactated Ringer’s solution may be prescribed to
convert lactate to bicarbonate in the liver,
which increases the bicarbonate level and
corrects the acidosis.
 IV sodium bicarbonate may be administered to
increase bicarbonate levels
 Diuretics may be administered to eliminate
chloride as well.
 Sodium, chloride, and fluids are restricted.
Nursing Management:
 Monitor vital signs, arterial blood gas values,
and I&O to assess the patient’s status and the
effectiveness of treatment.
 Assessment findings related to respiratory,
neurologic, and cardiac systems are
documented, and changes are discussed with
the physician.
 Nurse must teach the patient about the diet
that should be followed to manage
hyperchloremia and maintain adequate
hydration.
 Instruct the patient to refrain from
drinking free water (water without
electrolytes) or bottled water as it
excretes large amounts of chloride.