A.

SODIUM
NORMAL VALUE
135 – 145 135 – 145
mEq/L mmol/L
1. Sodium Deficit (Hyponatremia)
● refers to a serum sodium level below 135 mEq/L or 135 mmol/L
● forms:
1. Acute Hyponatremia
− characterized by onset of symptoms of less than 48 hours
− results from fluid overload
2. Chronic Hyponatremia
− characterized by onset of symptoms of more than 48 hours
− has less serious neurological sequelae
− longer in duration and seen frequently in outpatient settings
3. Exercise-associated Hyponatremia
− occurs during extreme temperature, excessive fluid intake before exercise, or
prolonged exercise
− frequently found in women and in smaller stature

● classifications according to ECF volume:

1. Hypovolemic hyponatremia
− extracellular fluid volume is abnormally decreased
− both water and sodium levels ae decreased in the ECF but sodium loss is greater
than water loss
NONRENAL CAUSES RENAL CAUSES:
vomiting osmotic diuresis
diarrhea salt-losing nephritis,
fistulas adrenal insufficiency
gastric suctioning diuretic use
excessive sweating
cystic fibrosis
burns
wound drainage

2. Isovolemic hyponatremia (euvolemic or dilutional hyponatremia)

− extracellular fluid volume is equal to intracellular volume
− sodium levels may appear low because there is too much fluid in the body
− patient have no signs of fluid volume excess and total body sodium remains
stable
CAUSES
Glucocorticoid deficiency (inadequate fluid filtration by the kidney)
Hypothyroidism (limited water excretion)
Renal failure
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

3. Hypervolemic Hyponatremia
− extracellular fluid volume is abnormally increased
− both waster and sodium levels increase in the extracellular area, but water gain
is greater than sodium gain
− diluted serum sodium and edema occurs
CAUSES
Heart failure
Liver failure
Nephrotic syndrome,
 Excessive administration of hypotonic I.V. fluids
Hyperaldosteronism

● classifications according to actual or relative loss of sodium:

1. Actual hyponatremia
− associated with reduction in serum osmolality
− an actual loss or unavailability of sodium occurs
CAUSES
Excessive diaphoresis
Diuretics (high-ceiling diuretics)
Wound drainage (especially gastrointestinal)
Decreased secretion of aldosterone
Hyperlipidemia
Kidney disease (scarred distal convoluted tubule)
Nothing by mouth
Low-salt diet
Cerebral salt-wasting syndrome
Hyperglycemia

2. Relative hyponatremia
− there is no actual loss of sodium but rather due to hemodilution
CAUSES
Excessive ingestion of hypotonic fluids
Psychogenic polydipsia
Freshwater submersion accident
Kidney failure (nephrotic syndrome)
Irrigation with hypotonic fluids
Syndrome of inappropriate antidiuretic hormone
Heart failure

Clinical manifestations of hyponatremia depends on the cause, magnitude, and speed

with which the deficit occurs.
CLINICAL MANIFESTATION

Headaches Nausea
Mental status changes Vomiting
Seizure Diarrhea
Muscular weakness Abdominal cramps
Dry skin Tachycardia
Pale, dry mucous Hypotension
membrane
CLINICAL DIAGNOSTIC
● Regardless of hyponatremia, the serum sodium level is less than 135 mEq/L.
● Serum osmolality is decreased except in azotemia – accumulation of nitrogenous
wastes.
● Urine sodium is less than 10 mEq/L and low urine specific gravity (1.002 – 1.004) - if
hyponatremia is due to sodium loss in case of increased proximal reabsorption of
sodium secondary to ECF volume depletion.
● Urine sodium is greater than 20 mEq/L and higher urine specific gravity greater than
1.012 - if hyponatremia is due to SIADH which causes pitting edema secondary to
cellular fluid accumulation.

MEDICAL MANAGEMENT
A. Sodium Replacement
● most common treatment:
 − administration of sodium by mouth
− diet modification
− nasogastric tube
− diet modification
− parenteral tube
− Lactated Ringer’s Solution
− 0.9% Sodium Chloride (Isotonic Saline)
− increase of serum sodium must not be 12 mEq/L in 24 hours
to avoid neurologic damage due to demyelination as caused by
rapid infusion of sodium
B. Water Restriction
● for patients with normal or excess fluid volume except in patients with severe
neurologic symptoms (e.g. seizure,or coma) or in traumatic brain injury
C. Pharmacologic Therapy
● AVP receptor antagonists
− pharmacologic agents that treat hyponatremia by stimulating free water
excretion
● IV conivaptan hydrochloride (Vaprisol)
− for patients with moderate to severe symptomatic hyponatremia
− contraindicated to patients with seizures, delirium, or coma
● Tolvaptan (Samsca)
− oral medication indicated for clinically significant hypervolemic and
euvolemic hyponatremia

NURSING MANAGEMENT
A. Monitor patients at risk for hyponatremia.
B. Monitors intake and output and daily body weight.
C. Obtain a thorough history to identify performance athletes which may use salt tablets
to decrease sweating and the prescribed and OTC medications that causes sodium
loss and water retention.
D. Detect and control hyponatremia.
− Monitors I & O and body weight.
− Monitor laboratory values – serum and urine sodium and urine specific
gravity
− Be alert for gastrointestinal manifestations and nervous system changes
that is associated with low sodium levels.
− Encourage patient to eat high-sodium foods and fluids.
− Familiarize the sodium content of parenteral fluids.
− In case of water retention, fluid restriction is highly advised.
− In patients taking lithium, observe for lithium toxicity.

2. Sodium Excess (Hypernatremia)

● refers to a serum sodium level higher than 145 mEq/L or 145 mmol/L
● it can be caused by a gain of sodium in excess of water or by a loss of water in excess of
sodium.
● It can occur in patient with normal fluid volume or in those with FVD or FVE.
● With a water loss 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. This is
both an extracellular and an intracellular FVD
● In sodium excess, the patient ingests or retains more sodium than water.
● classifications according to actual or relative excess of sodium:
1. Actual Hypernatremia
- actual excess of sodium in the extracellular fluid compartment
CAUSES
Hyperaldosteronism
Kidney failure
Corticosteroids
 Cushing’s syndrome or disease
Excessive oral sodium ingestion
Excessive administration of sodium-containing IV fluids

2. Relative Hypernatremia
- no actual excess of sodium in the extracellular fluid compartment or by
increase in serum osmolality
CAUSES
Nothing by mouth
Increased rate of metabolism
Fever
Hyperventilation
Infection
Excessive diaphoresis
Watery diarrhea
Dehydration
DIAGNOSTIC FINDINGS
● Serum sodium level greater than 145 mEq/L.
● Urine specific gravity greater than 1.03 (except in diabetes insipidus, where urine
specific gravity is decreased)
● Serum osmolality greater than 300 mOsm/kg

MEDICAL MANAGEMENT
A. Pharmacologic Therapy
● Restoration of fluid balance when cause is due to fluid loss.
− Administration of hypotonic solutions as prescribed.
● If cause is due to fluid loss and lesser sodium losses
− Administration of hypotonic solutions but slightly higher sodium
concentrations.
● If cause is due to poor renal function
− Administration of diuretics that promote sodium loss – loop diuretics
B. Nutrition Therapy
● Ensuring adequate fluid intake except in patients with kidney problems.
● Dietary sodium restriction

NURSING MANAGEMENT
A. Monitor and record vital signs, especially blood pressure and pulse.
B. Monitor fluid response to IV therapy if patient is under IV fluid replacement.
− Watch for signs of cerebral edema.
− Check for neurological status and report deterioration.
C. Monitor intake ad output of the patient and daily body weight.
D. Assess skin and mucous membrane for signs of breakdown and infection.
E. Monitor patient’s laboratory result - serum sodium level and urine specific gravity.
F. Insert and maintain a patent intravenous line as ordered.
G. Assist patient with oral hygiene.
H. Provide a safe environment for confused or lethargic patients.

B. POTASSIUM (K+)
NORMAL VALUE
3.5 - 5 mEq/L
1. Potassium Deficit (Hypokalemia)
● a serum potassium level below 3.5 mEq/L
● a life threatening condition for it involves all body systems
● symptoms may only after extreme loss of potassium, whereas the rapid reduction of
potassium causes drastic function changes
a. Mild Hypokalemia
− a serum potassium level of less than 3.5 to 3.1 mEq/L
 b. Moderate Hypokalemia
− a serum potassium level of 2.5 to 3 mEq/L
c. Severe Hypokalemia
− a serum potassium level of less than 2.5 mEq/L

WARNING SIGNS

Muscle Paralysis
Paralytic Ileus
Respiratory Arrest
Arrythmias
Cardiac Arrest
Digoxin Toxicity

PATHOPHYSIOLOGY

Low Serum
Potassium

Potassium
shifts from
ECF to ICF

Response to Muscular, GI, and

Increased
Normal Cell Cardiac
Intracellular K+
Stimulus Dysfunction Dysfunction

Actual loss of potassium:

– excessive potassium loss or lesser potassium intake than body requirement
CAUSES
Inappropriate or excessive use of drugs:
Diuretics
Digitalis
Corticosteroids
Increased secretion of aldosterone
Cushing’s syndrome
Diarrhea
Vomiting
Wound drainage (especially gastrointestinal)
Prolonged nasogastric suction
Heat-induced excessive diaphoresis
Kidney disease impairing reabsorption of potassium
Nothing by mouth

Relative decrease of potassium

– total body potassium levels are normal but the potassium distribution between fluid
spaces is abnormal, diluted by excess water, or movement of K+ from ECF to ICF
 CAUSES
Alkalosis
Hyperinsulinism
Hyperalimentation
Total parenteral nutrition
Water intoxication
IV therapy with potassium-poor solutions

CLINICAL MANIFESTATION:

Anorexia Malaise
Nausea Drowsiness
Vomiting Muscular weakness
Diarrhea Confusion
Abdominal distention Mental depression
Dysrhythmias Diminished deep tendon reflexes
Vertigo Respiratory paralysis
Polyuria

DIAGNOSTIC FINDINGS
● Serum potassium level less than 3.5 mEq/L
● Increased 24-hour urine level
● Elevated pH and bicarbonate levels
● Slightly elevated serum glucose level
● Characteristic ECG changes
– ST segment depression, flat or inverted t waves, increased u waves
● Decreased serum magnesium level
● Increased digoxin level (if patient is taking the drug)

MEDICAL MANAGEMENT
A. Pharmacologic Therapy
PRIORITIES:
− prevent potassium loss
− increase serum potassium levels
− ensure patient safety
● The amount and route of potassium replacement depends on the degree of loss
● agents:
− Potassium chloride, Potassium gluconate, Potassium citrate
▪ not to be given through IM or SQ for it is an irritant
▪ oral preparations to be given during or after meals but never to take
on empty stomach
▪ given intravenously for severe hypokalemia
✔ NEVER GIVE POTASSIUM BY INTRAVENOUS PUSH OR BOLUS
- DILUTE IN A SOLUTION.
✔ DO NOT GIVE WITH INSULIN.
● Avoid use of diuretics that increases excretion of potassium through kidneys:
loop and thiazide diuretics
B. Nutrition Therapy
● Ensuring adequate food intake of foods rich in potassium.
● Only prevents further loss of potassium.

NURSING MANAGEMENT
PRIORITIES:
− ensuring adequate oxygenation
− patient safety for falls prevention
− prevention of injury from potassium administration
 − monitoring the patient’s response to therapy

A. Assess the patient’s respiratory rate, depth, and pattern. Notify physician
immediately if respirations become shallow and rapid. Keep a handheld
resuscitation bag at the bedside of a patient with severe hypokalemia.
− Hypokalemia may weaken or paralyze respiratory muscles.
B. Monitor vital signs, especially pulse and blood pressure.
− Hypokalemia is commonly associated with hypovolemia, which can cause
orthostatic hypotension.
C. Check heart rate and rhythm and ECG tracings in a patient with a serum potassium
level with severe hypokalemia.
− Hypokalemia is commonly associated with hypovolemia, which may create
tachyarrhythmias.
D. Monitor heart rate and rhythm and ECG tracings of a patient receiving a potassium
infusion of more than 5 mEq/hour or a concentration of more than 40 mEq/L of fluid.
E. Monitor serum potassium levels.
− Changes in serum potassium levels can lead to serious cardiac
complications.
F. Check the prescription carefully to ensure that the patient receives the correct
amount of potassium.
G. Check IV site for phlebitis or infiltration. Assess the IV site hourly, and ask the patient
whether he or she feels burning or pain at the site.
H. Encourage patient to eat food and drink fluids rich in potassium but low in sodium
content.
I. Implement safety measures by eliminating hazards and assisting in ambulation.

2. Potassium Excess (Hyperkalemia)

● a serum potassium level above 5 mEq/L
● less common than hypokalemia and commonly occurs in patients undergoing medical
conditions
● a life threatening condition for it involves all body systems
a. Mild Hyperkalemia
− a serum potassium level of greater than 5 to 6 mEq/L
b. Moderate Hyperkalemia
− a serum potassium level of 6.1 to 7 mEq/L
c. Severe Hyperkalemia
− a serum potassium level of greater than 7 mEq/L

PATHOPHYSIOLOGY

K+ Intake

K+

Neuromuscular
Potassium shifts Increased Response to
and
from ICF to Extracellular K+ Less Stimulus
Cardiac Sx

Actual increase of potassium:

– excessive potassium reabsorption or intake than body requirement
CAUSES
Overingestion of potassium-containing foods or medications:
Salt substitutes
Potassium chloride
Rapid infusion of potassium-containing IV solution
 Bolus IV potassium injections
Transfusions of whole blood or packed cells
Adrenal insufficiency (Addison’s disease, adrenalectomy)
Kidney failure
Potassium-sparing diuretics
Angiotensin-converting enzyme inhibitors (ACEIs)

Relative increase of potassium

– movement of potassium from the cells into the blood
CAUSES
Tissue damage
release, or spilling, of potassium into the serum
Hyperuricemia
Acidosis
moves potassium outside the cells
Uncontrolled diabetes mellitus

CLINICAL MANIFESTATIONS

Nausea Muscle weakness

Diarrhea Flaccid paralysis
Intestinal colic Paresthesia
Abdominal distention Cramps
Oliguria or anuria Irritability
Tachycardia Bradycardia Anxiety
Dysrhythmias

DIAGNOSTIC FINDINGS
● Serum potassium level more than 5 mEq/L
● Arterial blood gas may reveal both a metabolic and respiratory acidosis.
● Electrocardiograph tracing shows peaked T waves initially.

MEDICAL MANAGEMENT
PRIORITIES:
− rapidly reducing the serum potassium level
− preventing recurrences
− ensuring patient safety during the electrolyte imbalance

EMERGENCY MANAGEMENT
Administer IV Calcium Gluconate through slow IV push.
contains 4.5 mEq of calcium
calcium antagonizes the action of hyperkalemia on the heart but does not reduce
the serum potassium concentration
monitor blood pressure for possible hypotension
stop infusion if bradycardia occurs
effect lasts for 30 minutes

Administer sodium bicarbonate

indicated for patients in severe metabolic acidosis
alkalinize the plasma, shift potassium into the cells, and furnish sodium to
antagonize the cardiac effects of potassium
effect starts within 30 – 60 minutes and lasts for hours

Administer regular insulin and hypertonic dextrose solution

provides a temporary shift of potassium into the cell
onset of action within 30 minutes and lasts for hours
 A. Pharmacologic Therapy
● the main medical intervention for hyperkalemia
● restores normal potassium balance by enhancing potassium excretion and
promoting the movement of potassium from the extracellular fluid (ECF) into the
cells
− Potassium-excreting diuretics
▪ for patients with normal kidney function
▪ increases potassium excretion through urine
▪ e.g. loop diuretics (Furosemide)
− Cation exchange resins
▪ indicated for patients with kidney problems
▪ contraindicated for patients with paralytic ileus
– at risk for intestinal perforation
▪ given orally or through retention enema which promotes intestinal
sodium absorption and potassium excretion
▪ look out for signs of hypomagnesemia and hypocalcemia
▪ e.g. sodium polystyrene sulfonate (Kayexelate)
− Insulin
▪ increases activity of the sodium-potassium pumps
▪ enhances potassium movement back into the cells from the
extracellular space to temporarily reduce serum potassium levels
− Intravenous fluids containing glucose and insulin
▪ decreases serum potassium levels
▪ hypertonic solutions infused through a central line or a vein with
high blood flow to avoid inflammation
B. Cardiac Monitoring
● obtained immediately to detect changes
● for early recognition of dysrhythmias and other manifestations of hyperkalemia
on cardiac muscles
C. Dialysis
● indicated for patients with dangerously high potassium levels
● also indicated for patients not responding to other treatments

NURSING MANAGEMENT
PRIORITIES:
− monitoring to prevent cardiac complications
− patient safety for falls prevention
− monitoring the patient’s response to therapy
− health teaching

A. Monitor vital signs. Anticipate cardiac monitoring if the patient’s serum potassium
level exceeds 6 mEq/L.
− A patient with ECG changes may need aggressive treatment to prevent
cardiac arrest.
B. Monitor for signs of hyperkalemia especially patient at risk of it.
C. Monitor intake and output. Report an output of less than 30 ml/hour.
− An inability to excrete potassium adequately may lead to dangerously high
potassium levels.
D. Monitor the serum potassium level and related laboratory test results.
− A patient with a serum potassium level greater than 6 mEq/L requires
cardiac monitoring because asystole may occur as hyperkalemia makes
depolarization of cardiac muscle easier and shortens repolarization times.
E. Administer prescribed medications, and monitor the patient for their effectiveness
and for adverse effects.
● Regulate IV flow rate with solution containing potassium so that no more than
10 mEq of KCl is administered per hour.
 ● For a patient receiving repeated insulin and glucose treatment, check for clinical
signs and symptoms of hypoglycemia, including muscle weakness, syncope,
hunger, and diaphoresis.
● Observe patient for manifestations of hypokalemia and hypoglycemia.
● Encourage the patient to retain Kayexalate enemas for 30 to 60 minutes. Monitor
the patient for hypokalemia when administering this drug on 2 or more
consecutive days.
● Administer prescribed antidiarrheals, and monitor the patient’s response.
● Monitor the patient’s digoxin level if he’s taking this medication.
− The patient may be at risk for digoxin toxicity.
F. Eliminate sources of extra potassium.
● Stop potassium-containing infusions.
● Keep IV access open.
● Withhold oral potassium supplements.
● Provide a potassium-restricted diet.
G. Implement safety measures if the patient has muscle weakness. Advise patient to ask
for help before attempting to get out of bed and walk. Continue to evaluate muscle
strength.
H. Compare recent ECG tracings with the baseline tracings or with the tracings obtained
when the patient’s serum potassium level was close to normal.
I. Conduct health teaching on diet, drugs and recognition of the manifestations of
hyperkalemia – focus on the prevention and early detection of hyperkalemia.

C. CALCIUM (CA++)
Total Calcium
Ionized Calcium NORMAL VALUE
NORMAL VALUE 4.5 – 5.1 mg/dL
8.5 – 10.5 mg/dL

1. Calcium Deficit (Hypocalcemia)

● a serum calcium level below 8.5 mg/dL (total calcium) or 4.5 mg/dL (ionized calcium)
Actual loss of calcium:
– a reduction of total body calcium that occurs when the absorption of calcium from
the gastrointestinal tract slows or when calcium is lost from the body
CAUSES

Inadequate oral intake of calcium End-stage kidney disease

Lactose intolerance Kidney failure—polyuric phase
Malabsorption syndromes: Diarrhea
Celiac sprue Steatorrhea
Crohn’s disease Wound drainage (especially gastrointestinal)
Inadequate intake of vitamin D
Relative decrease of calcium:
– total body calcium amount remains to be normal, but serum calcium levels are low
which occurs when unbound calcium levels are reduced or decreased parathyroid gland
function
CAUSES

Hyperproteinemia Immobility
Hyperphosphatemia Removal or destruction of
Alkalosis parathyroid glands
Medications: Calcium chelators or
binders, Citrate, Mithramycin,
Penicillamine, Sodium cellulose
phosphate (Calcibind), Aredia
Acute pancreatitis
OTHER CAUSES
 Impaired calcium absorption calcitonin – decreases
laxative abuse calcium resorption
anticonvulsants interfering diuretics: loop diuretic
vitamin D metabolism
high intestinal phosphorous Hypomagnesemia
levels Hypoalbuminemia
Severe burns and infections
Excessive calcium loss

CLINICAL MANIFESTATIONS
Numbness
Tingling of fingers, toes, and circumoral region
Positive Trousseau and Chvostek sign
Seizures
Carpopedal spasm
‘ Hyperactive deep tendon reflexes
Irritability
Bronchospasm
Anxiety
Diarrhea
Hypotension

PATHOPHYSIOLOGY

Ca++ excretion

Ca++ or Vit. D
Intake or
Absorption

Release of PTH

PTH draws Ca
from Bone

Renal and Intracellular

Hypocalcemia Neuromuscular and
Intestinal Hypocalcemia
Overwhelms Cardiac Sx
Calcium causes Cell
PTH
Absorption Dysfunction

DIAGNOSTIC FINDINGS
● Serum calcium below normal levels.
− Total serum calcium level less than 8.5 mg/dl.
− Ionized calcium level below 4.5 mg/dl
(the definitive method to diagnose hypocalcemia)
● Low albumin levels.
● Impaired clotting time.
● Decreased prothrombin levels.
● Electrocardiograph tracing show prolonged QT interval and lengthened ST segments.
Differentiating Chvostek and Trousseau Signs

Chvostek Sign Trousseau Sign

- a contraction of the facial muscles - a carpopedal spasm induced by

elicited in response to light tap over inflating a blood pressure cuff for 1 –
the facial nerve in front of the ear 4 minutes above systolic blood
pressure

MEDICAL MANAGEMENT
PRIORITIES:
− restore normal calcium levels
− preventing complications
EMERGENCY MANAGEMENT
Administer IV Calcium Gluconate or Calcium Chloride
contains 4.5 mEq of calcium
contraindicated for patients with digitalis medications
effect lasts for 30 minutes
stop infusion if bradycardia occurs
observe IV site for infiltration

DO NOT USE 0.9% NaCl solution.

increases renal calcium loss

A. Pharmacologic Therapy
● direct calcium replacement either through oral or intravenously that will
enhance absorption of calcium
− Aluminum hydroxide
− Vitamin D
● decrease nerve and muscle response
− Magnesium Sulfate
− Muscle relaxants
B. Nutrition Therapy
● increase dietary intake of calcium through a high-calcium diet
− milk products
− green, leafy vegetables
− canned salmon
− canned sardines
− fresh oysters
● vitamin D therapy

NURSING MANAGEMENT
PRIORITIES:
− monitoring to prevent complications
− patient safety
− monitoring the patient’s response to therapy
− health teaching
Patients at risk of hypocalcemia
A. Obtain a complete medical history. Note whether the patient has ever had neck
surgery.
 − Hypoparathyroidism may develop either immediately or several years after
neck surgery
B. Obtain a list of medications the patient is taking; the list may help determine the
underlying cause of hypocalcemia.
C. Assess the patient carefully, especially if he has had parathyroid or thyroid surgery
or has received massive blood transfusions.
D. If the patient is breast-feeding, assess for adequate vitamin D intake and exposure to
sunlight.
E. Assess the effects of symptoms on the patient’s ability to perform activities of daily
living.
F. If your patient is recovering from parathyroid or thyroid surgery, keep calcium
gluconate, which ensures a quick response to signs of a sudden drop in calcium
levels, at the bedside.

Patients with hypocalcemia

A. Ask a patient who has chronic hypocalcemia if he has a history of fractures.
B. If the patient is recovering from parathyroid or thyroid surgery.
● Monitor vital signs, and assess the patient frequently.
● Monitor respiratory status, including rate, depth, and rhythm.
● Watch for stridor, dyspnea, and crowing.
C. If the patient shows overt signs of hypocalcemia, keep a tracheotomy tray and a
handheld resuscitation bag at the bedside in case laryngospasm occurs.
D. Place the patient on a cardiac monitor, and evaluate for heart rate and rhythm
changes. Notify the practitioner if the patient develops arrhythmias, such as
ventricular tachycardia or heart block.
E. Check the patient for Chvostek’s sign or Trousseau’s sign.
F. Monitor a patient receiving I.V. calcium for arrhythmias, especially if also taking
digoxin.
− Calcium and digoxin have similar effects on the heart.
G. Administer medications as prescribed.
● Administer I.V. calcium replacement therapy carefully.
− Ensure the patency of the intravenous. line because infiltration can cause
tissue necrosis and sloughing.
● Give oral calcium supplements 1 to 1 1⁄2 hours after meals. If GI upset occurs,
give the supplement with milk.
H. Monitor pertinent laboratory test results, including calcium levels, albumin levels,
and those of other electrolytes such as magnesium. Remember to check the ionized
calcium level after every 4 units of blood transfused.
I. Implement safety precautions.
● Take precautions for seizures such as padding bed side rails.
● Reorient a confused patient.
● Provide a calm, quiet environment.
● Adjust the lighting of the environment
● Provide health teaching on description, causes, and treatment for hypocalcemia,
dietary sources of calcium, prescribed medications, importance of exercise, the
need to report pain during IV calcium infusion, and the warning signs to look for
and when to report them.

2. Calcium Excess (Hypercalcemia)

● a serum calcium level above 10.5 mg/dL (total calcium) or 5.1 mg/dL (ionized calcium)
● suggests either that the amount of serum calcium is so great that the normal calcium-
controlling mechanisms cannot keep pace or that at least one control mechanism is not
functioning properly
Actual excess of calcium:
CAUSES
Excessive oral intake of calcium
 Excessive oral intake of vitamin D
Kidney failure
Use of thiazide diuretics

Relative excess of calcium

CAUSES
Hyperparathyroidism
Malignancy:
Direct invasion (cancers of breast, lung, prostate, and osteoclastic bone and multiple myeloma)
Indirect resorption (liver cancer, small cell lung cancer, and cancer of the adrenal gland)
Hyperthyroidism
Immobility
Use of glucocorticoids
Dehydration

PATHOPHYSIOLOGY

Ca++ Resorption

Calcium shifts to ECF

Overwhelms Kidney
Excretion of Calcium

Excess Calcium shifts

to ICF

Affects skeletal and cardiac

Membrane excitability muscles and nervous Signs and Symptoms
system

CLINICAL MANIFESTATIONS
Altered level of consciousness
Flabby muscles
Pathologic fractures
Deep pain over bony areas
Decreased deep tendon reflexes
Constipation
Anorexia
Abdominal pain
Apparent bone thinning
Flank pain
Renal calculi
Tachycardia Bradycardia
Hypertension Hypotension
Hypoactive or absent bowel sounds
Abdominal distention

WARNING SIGNS
Paralytic Ileus
Stupor
Arrythmias: Bradycardia
Coma
DIAGNOSTIC FINDINGS
● Serum magnesium above normal levels.
− Total serum calcium level more than 10.5 mg/dl.
− Ionized calcium level above 5.1 mg/dl
(the definitive method to diagnose hypercalcemia)
● Radiologic examination reveals pathologic fractures.
● Electrocardiograph tracing show shortened QT interval, prolonged PT interval,
flattened T waves, and heart block.

MEDICAL MANAGEMENT
PRIORITIES:
− restore normal calcium levels
− preventing complications

A. Pharmacologic Therapy
● involves preventing increases in calcium, as well as drugs to lower calcium levels
− Loop Diuretics
▪ enhances excretion of calcium
▪ e.g. furosemide
− Calcium Chelators
▪ helps lower calcium levels by binding excess calcium
▪ e.g. plicamycin (Mithracin) and penicillamine
− Intravenous 0.9% NaCl
▪ temporarily dilutes the serum calcium level and increases urinary
calcium excretion by inhibiting tubular reabsorption of calcium
− Intravenous Phosphate
▪ causes a reciprocal drop in serum calcium
− Calcitonin (Calcimar) – given IM
▪ reduces bone resorption, increases the deposition of calcium and
phosphorus in the bones, and increases urinary excretion of
calcium and phosphorus
▪ useful for patients with heart disease or kidney injury who cannot
tolerate large sodium loads
− Bisphosphonates (etidronate), and Prostaglandin synthesis inhibitors
(aspirin, NSAIDs)
▪ prevents hypercalcemia by inhibiting calcium resorption from bone
B. Dialysis
● used when severe hypercalcemia causes life-threatening cardiac problems and
drug therapy may not reduce serum calcium levels fast enough to prevent death
● can either be hemodialysis or peritoneal dialysis
C. Cardiac Monitoring
● to identify dysrhythmias and decreased cardiac output

NURSING MANAGEMENT
PRIORITIES:
− monitoring to prevent complications
− patient safety
− monitoring the patient’s response to therapy
− health teaching
A. Monitor vital signs and assess the patient frequently.
B. Watch the patient for arrhythmias. Assess neurologic and neuromuscular function,
and report changes.
C. Monitor the patient’s fluid intake and output.
D. Monitor serum electrolyte levels, especially calcium.
− To determine the effectiveness of treatment and to detect new imbalances
that might result from therapy.
 E. Insert and maintain I.V. access. Normal saline solution is usually administered at a
rate of 200 to 500 ml/hour. Monitor the patient for signs of pulmonary edema, such
as crackles and dyspnea.
F. Ensure patient is properly hydrated before administering diuretics to avoid volume
depletion.
G. Encourage the patient to drink 3 to 4 L of fluid daily unless contraindicated
− To stimulate calcium excretion from the kidneys and to decrease the risk of
calculi formation
H. Assess for renal calculi.
● Strain the urine for calculi.
● Assess for flank pain which indicates presence for renal calculi.
I. Watch for signs and symptoms of digitalis toxicity - anorexia, nausea, vomiting, or an
irregular heart rate.
J. Ambulate the patient as soon as possible.
− To prevent bones from releasing calcium.
K. Handle a patient who has chronic hypercalcemia gently to prevent pathologic
fractures.
● Reposition bedridden patients frequently.
● Perform active or passive range-of-motion exercises to prevent complications
from immobility.
L. Provide a safe environment.
● Keep side rails raised as needed, the bed in its lowest position, and the wheels
locked.
● Make sure the patient’s belongings and call button are within reach.
M. Provide health teaching on description, causes, and treatment for hypercalcemia,
importance of increased fluid intake, dietary guidelines, prescribed medications,
warning signs to look for and when to report them, and avoidance of supplements
that contains calcium.

D. Magnesium (Mg++)

NORMAL VALUE
1.5 – 2.5 mEq/L

1. Magnesium Deficit (Hypomagnesemia)

● a serum magnesium level below 1.5 mEq/L.

CAUSES
Malnutrition
Starvation
Diarrhea
Steatorrhea
Celiac disease
Crohn’s disease
Ethanol ingestion
Medications
diuretics
aminoglycoside antibiotics
cisplatin,
amphotericin B
cyclosporine
Citrate (blood products)

CLINICAL MANIFESTATION

Neuromuscular irritability signs

Positive Chvostek and Trousseau Insomnia
 Mood changes Vomiting
Arrythmias Increased tendon reflexes
Anorexia Elevated blood pressure

PATHOPHYSIOLOGY

Mg++ excretion

Mg++ Intake or Absorption

Intracellular Mg
Cell starves for Skeletal Muscle Weakness
moves out of the
Magnesium Hyperirritable muscles
cell

DIAGNOSTIC FINDING
● Serum magnesium below 1.5 mEq/L.
● May have low albumin, potassium, and calcium levels.
● Elevated serum digoxin (for patients taking digoxin).
● Electrocardiograph tracing shows prolonged PR interval, widened QRS complex,
prolonged QT interval, depressed ST segment, broad, flattened T wave, prominent U
wave.
● Nuclear magnetic resonance spectroscopy and the ion selective electrode
- sensitive and direct means of measuring ionized serum magnesium levels

MEDICAL MANAGEMENT
PRIORITIES:
− restore normal magnesium levels
− preventing complications
A. Pharmacologic Therapy
● for severe hypomagnesemia
− Intravenous or Intramuscular Magnesium Sulfate
● for mild hypomagnesemia
− Oral magnesium chloride
− Oral magnesium oxide
B. Nutrition Therapy
● indicated for mild hypomagnesemia
● increase dietary intake of magnesium through a high-magnesium diet
 − green, leafy − whole grains
vegetables − seafoods
− nuts − peanut butter
− seeds − cocoa
− legumes

NURSING MANAGEMENT
PRIORITIES:
− monitoring to prevent complications
− patient safety
− monitoring the patient’s response to therapy
− health teaching
A. Assess the patient’s mental status and report changes. Reorient him as needed.
B. Monitor and record the patient’s vital signs. Report findings that indicate hemodynamic
instability
● Assess the patient’s vital signs every 15 minutes.
● If in respiratory distress, assess for a sharp decrease in blood pressure.
● Monitor the patient’s respiratory status.
− A magnesium deficiency can cause laryngeal stridor and compromise the
airway.
C. Evaluate the patient’s neuromuscular status regularly.
● Check for hyperactive DTRs, tremors, and tetany.
● Check for Chvostek’s and Trousseau’s signs if hypocalcemia is also suspected.
D. Check the patient for dysphagia before giving food, oral fluids, or oral medications.
− Hypomagnesemia may impair his ability to swallow.
E. Connect the patient to a cardiac monitor if his magnesium level is below 1 mEq/L. Watch
the rhythm strip closely for arrhythmias .
F. Monitor the patient if he has lost an excessive amount of fluid, which may occur as a
result of fistula drainage or prolonged diarrhea.
− A patient who has experienced excessive fluid loss is at risk for magnesium
deficiency.
G. Monitor the patient’s urine output at least every 4 hours.
− Magnesium generally isn’t administered if urine output is less than 10 ml in 4
hours.
J. Monitor closely for signs and symptoms of digoxin toxicity in patients taking digoxin -
nausea, vomiting, and bradycardia.
− Magnesium deficiency enhances the pharmacologic action of digoxin.
K. Monitor serum magnesium levels for patients taking certain medication such as insulin,
loop or thiazide diuretics, torsemide, aminoglycosides, amphotericin, cisplatin,
cyclosporin, gentamicin.
− These medications can contribute to low magnesium levels.
L. Monitor the patient’s serum electrolyte levels, and notify the practitioner if the serum
potassium level or calcium level is low.
− Both hypocalcemia and hypokalemia can cause hypomagnesemia.
M. Monitor the patient if nothing given per orem or I.V. fluids without magnesium salts.
− Prolonged administration of magnesium-free fluids can result in low serum
magnesium levels.
N. Establish and maintain a patent I.V. line in case your patient needs intravenous
magnesium replacement or I.V. fluids.
O. Administer medication supplements as prescribed.
 ● When administering a magnesium sulfate infusion, be aware that I.V. magnesium
sulfate comes in various concentrations.
● Ensure a proper order stating how many grams or milliliters of a particular
concentration to administer, the volume of desired solution for dilution, and the
length of time for infusion.
● Intramuscular magnesium are is to be given through the deep gluteal muscle.
Alternate sites for multiple injections.
− I.M. injections of magnesium are painful.
● Check the cardiac monitor frequently and assess the patient closely for signs of
magnesium excess - hypotension and respiratory distress. Keep calcium gluconate
at the bedside in case such signs occur.
P. Implement safety precautions.
● Institute seizure precautions. If a seizure occurs, report the type of seizure, its length,
and the patient’s behavior during the seizure. After the seizure, reorient the patient
as needed.
● Ensure the patient’s safety at all times.
Q. Provide health teaching on hypomagnesemia, its risk factors, treatment, prescribed
medications, avoidance of drugs that decreases serum magnesium, consumption of a
high magnesium diet, and the warning signs to look for and when to report them.

2. Magnesium Excess (Hypermagnesemia)

● a serum magnesium level above 2.5 mEq/L
● a rare electrolyte abnormality for the kidneys efficiently excrete magnesium
● can sometimes be false elevated if blood specimens are allowed to hemolyze or extracted from
an extremity with tourniquet applied too tightly
CAUSES
Increased magnesium intake:
Magnesium-containing antacids and laxatives
IV magnesium replacement
Decreased kidney excretion of magnesium resulting from kidney disease

CLINICAL MANIFESTATIONS
Flushing
Hypotension
Muscle weakness
Drowsiness
Hypoactive reflexes
Depressed respirations
Cardiac arrest
Coma
Diaphoresis
Tachycardia Bradycardia

DIAGNOSTIC FINDINGS
● Serum magnesium above 2.5 mEq/L.
● Increased potassium and calcium levels.
● Decreasing creatinine clearance to less than 3.0 mL/min.
● Electrocardiograph tracing shows prolonged PR interval, widened QRS complex,
prolonged QT interval, depressed ST segment, broad, flattened T wave, prominent U
wave.

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PATHOPHYSIOLOGY

Mg++ Intake

Mg++ Excretion

Elevated Serum
Mg++

Suppression of
Acetylcholine

Acetylcholine
Level

Neuromuscula
Cell
r Transmission
Excitability
Level of Consciousness

Respiratory Distress
Neuromuscular
and CNS
Depression
Arrythmia
Cardiac Complications

MEDICAL MANAGEMENT
PRIORITIES:
− restore normal magnesium levels
− preventing complications

A. Pharmacologic Therapy
● for patients with normal renal function in order to facilitate increased excretion of
magnesium to the urine and increase urine output for patients with
− Intravenous fluid of 0.9% NacL or Lactated Ringer’s solution
● for patients not responding to increasing urine output
− Loop diuretics
● in case of hypermagnesemia emergency
− 10% Calcium gluconate
▪ antagonizes the cardiovascular and neuromuscular effects of
magnesium
B. Hemodialysis
● indicated for patients with severe renal dysfunction
● utilizes magnesium-free dialysate

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NURSING MANAGEMENT
PRIORITIES:
− monitoring to prevent complications
− patient safety
− monitoring the patient’s response to therapy
− health teaching
A. Monitor vital signs frequently.
● Stay especially alert for hypotension and respiratory depression, which are
indicators of hypermagnesemia.
● Notify the practitioner immediately if the patient’s respiratory status deteriorates.
B. Check for flushed skin and diaphoresis.
C. Assess the patient’s neuromuscular system, including DTRs and muscle strength.
D. Monitor laboratory tests and report abnormal results.
● Monitor serum electrolyte levels and other laboratory test results that reflect renal
function, such as blood urea nitrogen and creatinine levels.
● Monitor the patient for hypocalcemia, which may accompany hypermagnesemia.
− A low serum calcium level suppresses parathyroid hormone secretion.
E. Monitor urine output.
− The kidneys excrete most of the body’s magnesium.
F. Evaluate the patient for changes in mental status.
● If his LOC decreases, institute safety measures.
● Reorient patient if confused.
G. Prepare the patient for continuous cardiac monitoring. Assess ECG tracings for pertinent
changes.
H. Always be prepared for occurrence of hypermagnesemia emergency.
● Administer resuscitation drugs, maintain a patent airway, and provide calcium
gluconate, as ordered.
● Prepare the patient for dialysis, as ordered, if the patient’s magnesium level
becomes dangerously high.
● Provide mechanical ventilation which may be needed if the patient has
compromised respiratory function.
● Provide a temporary pacemaker, which may be inserted for the patient with
bradyarrhythmias.
I. Establish I.V. access and maintain a patent I.V. line.
● Provide adequate fluids, both I.V. and oral, if prescribed, to help your patient’s
kidneys excrete excess magnesium.
● When giving large volumes of fluids, remember to keep accurate intake and output
records and to watch closely for signs of fluid overload and kidney failure.
● Avoid giving your patient medications that contain magnesium.
J. Provide health teaching on hypermagnesemia and its risk factors, hydration
requirements, dietary modifications, prescribed and needed to avoid medications,
warning signs and symptoms and when to report them, and dialysis if indicated.

E. Phosphorous (HPO4)

NORMAL VALUE
1.8 – 2.6 2.5 – 4.5
mEq/L mg/dL
1. Phosphorous Deficit (Hypophosphatemia)
● a serum phosphorous level below 1.8 mEq/L or 2.5 mg/dL
● an abnormally low content of phosphorous in lean tissues

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 ● three main processes:
(1) decreased absorption of phosphorus
(2) increased excretion of phosphorus
(3) intracellular phosphorus shift

a. Severe Hypophosphatemia
− a serum phosphorous level less than 1 mg/dL
CAUSES

Malnutrition Kidney failure

Starvation Malignancy
Use of aluminum hydroxide Hyperglycemia
–based antacids Hyperalimentation
Use of magnesium-based Respiratory alkalosis
antacids Uncontrolled diabetes mellitus
Hyperparathyroidism Alcohol abuse
Hypercalcemia

CLINICAL MANIFESTATIONS
Paresthesia
Muscle weakness
Bone pain and tenderness
Chest pain
Confusion
Nystagmus
Cardiomyopathy
Respiratory failure
Seizures
Tissue hypoxia
Increased susceptibility to infection

DIAGNOSTIC FINDINGS
● Serum phosphorous below 2.5 mg/dL; ; severe hypophosphatemia is less than 1 mg/dL.
● Elevated serum creatine due to rhabdomyolysis.
● Accompanying electrolyte imbalance: decreased serum magnesium may be decreased to
increased urinary excretion and increased serum calcium levels.
● Increase level of alkaline phosphatase.
● Radiologic examination shows skeletal changes of osteomalacia or rickets.

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PATHOPHYSIOLOGY
Intestinal Absorption Renal Elimination Shift of Phosphorous to ICF

Phosphorou
s Level

Cellular
Energy Stores

Musculoskeletal Cardiac Hematologic

Neurologic Effects
Effects Effects Effects

MEDICAL MANAGEMENT
PRIORITIES:
− prevention of hypophosphatemia
− restore normal phosphorous levels
− preventing complications
A. Pharmacologic Therapy
● for moderate hypophosphatemia
− oral replacement of phosphorous with vitamin D supplementation
● for serum phosphorous levels below 1 mg/dL with serious manifestations
− intravenous phosphorous
B. Nutrition Therapy
● increase dietary intake of phosphorous through a phosphorous-rich diet
− fish
− beef − organ meats
− chicken − nuts
− pork − whole-grain breads and cereal

NURSING MANAGEMENT
PRIORITIES:
− monitoring to prevent complications
− patient safety
− monitoring the patient’s response to therapy
− health teaching
A. Monitor vital signs, level of consciousness, and neurologic status.
− Hypophosphatemia can lead to respiratory failure, low cardiac output,
confusion, seizures, or coma.
● Monitor the patient’s temperature at least every 4 hours. Check WBC counts. Follow
strict sterile technique in changing dressings, and report signs of infection.
B. In patients with severe hypophosphatemia, monitor the rate and depth of respirations.

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 ● Report signs and symptoms of hypoxia, such as confusion, restlessness, increased
respiratory rate and, in later stages, cyanosis.
● If possible, take steps to prevent hyperventilation.
− Hyperventilation worsens respiratory alkalosis and can lower phosphorus
levels.
● Check arterial blood gas results and pulse oximetry levels to monitor the
effectiveness of ventilation.
C. Monitor the patient for evidence of heart failure related to reduced myocardial
functioning - crackles, shortness of breath, decreased blood pressure, and tachycardia.
D. Assess the patient frequently for evidence of decreasing muscle strength - weak hand
grasps or slurred speech.
E. Administer prescribed phosphorus supplements.
− Oral supplements may cause diarrhea.
● Vitamin D may also be ordered with the oral phosphate supplements to increase
absorption.
● Mix oral supplements with juice to improve taste.
F. Establish and maintain a patent intravenous line.
G. Record the patient’s fluid intake and output.
H. Administer medication supplements as prescribed.
● Administer an analgesic, if ordered.
● Infuse phosphorus solutions slowly, using an infusion device to control the rate.
● Watch for signs of hypocalcemia, hyperphosphatemia, and I.V. infiltration during
infusion.
− Potassium phosphate can cause tissue sloughing and necrosis.
● Monitor serum phosphate levels every 4 hours.
I. Carefully monitor serum electrolyte levels, especially calcium and phosphorus levels, as
well as other pertinent laboratory test results. reort any abnormalities.

J. Implement safety precautions.

● Make sure the patient maintains bed rest, if ordered.
● Keep the bed in its lowest position, with wheels locked and side rails raised.
● If the patient is at risk for seizures, pad the side rails and keep an artificial airway at
the patient’s bedside.
● Orient the patient as needed. Keep clocks, calendars, and familiar personal objects
within his sight.
● Assist the patient with ambulation and activities of daily living, if needed, and keep
essential objects near him.
K. Provide health teaching on hypophosphatemia, its risk factors, treatment, prescribed
medications, consumption of a high-phosphorous diet, and the warning signs to look for
and when to report them.

2. Phosphorous Excess (Hyperphosphatemia)

● a serum phosphorous level above 2.6 mEq/L or 4.5 mg/dL
● reflects the kidney’s inability to excrete excess phosphorous
● commonly occurs with increase release of phosphorous from damaged cell

a. Severe Hyperphosphatemia
− a serum phosphorous level at 6 mg/dL or higher
CAUSES
Decreased kidney excretion resulting from kidney disease
Tumor lysis syndrome
Increased intake of phosphorus

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 Hypoparathyroidism
Destruction of cells

CLINICAL MANIFESTATIONS
Tetany
Tachycardia
Anorexia
Nausea
Vomiting
Muscle weakness
Flaccid paralysis
Signs and symptoms of hypocalcemia
Hyperactive reflexes
Soft tissue calcifications in lungs, heart, kidneys, and cornea

PATHOPHYSIOLOGY

Phosphorous Intake
Vitamin D

Renal Insult or
Failure

Glomerular
Filtration Rate

Ineffective Renal
Filtration of
Phosphorous

Phosphorous shifts Phosphorou

to ECF from ICF s Level

Compound
Phosphorous binds Formation of Insoluble
Deposits on Soft
with calcium Compounds
Tissues
DIAGNOSTIC FINDINGS
● Serum phosphorous level above 2.6 mEq/L or 4.5 mg/dL.
● Serum calcium level below 8.5 mg/dL.
● Radiologic examination may reveal skeletal changes resulting from osteodystrophy
(defective bone development) in chronic hyperphosphatemia.
● Increased blood urea nitrogen and creatine levels – worsening renal function.
● Electrocardiograph tracing shows characteristics of hypocalcemia – prolonged QT
interval.

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MEDICAL MANAGEMENT
PRIORITIES:
− prevention of hyperphosphatemia
− restore normal phosphorous levels
− preventing complications
− treatment of underlying causes
A. Pharmacologic Therapy
● to decrease absorption of phosphorous at gastrointestinal tract
− Aluminum
− Magnesium
− Calcium gel
− Phosphate-binding antacids
● for phosphorous levels at 6 mg/dL with normal renal functioning
− intravenous 0.9% NaCl
● to increase renal excretion of phosphorous
− acetazolamide (Diamox)
B. Nutrition Therapy
● decrease dietary intake of phosphorous through a low-phosphorous diet by
avoiding:
− fish
− beef − organ meats
− chicken − nuts
− pork − whole-grain breads and cereal

C. Dialysis
● can either be hemodialysis of peritoneal dialysis
● indicated for patients with chronic renal failure or extreme case of
hyperphosphatemia with symptomatic hypocalcemia

NURSING MANAGEMENT
PRIORITIES:
− monitoring to prevent complications
− monitoring the patient’s response to therapy
− health teaching

Patients at risk for hyperphosphatemia.

A. Monitor the patient carefully.
B. Use caution when administering phosphorus in intravenous infusions, enemas, and
laxatives.
− Extra phosphorus may cause hyperphosphatemia.

Patients with hyperphosphatemia.

A. Focus on careful monitoring, safety measures, and interventions to restore normal serum
phosphorus levels.
B. Monitor vital signs.
● Keep in mind the symptoms of hypocalcemia.
● If symptoms of hypocalcemia worsens, notify physician immediately.
● Notify also the physician for signs and symptoms of calcification – oliguria, visual
impairment, irregular heart rate or palpitations, and popular eruptions.
C. Monitor fluid intake and output.
● If urine output falls below 30 ml/hour, immediately notify the physician immediately.

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 − Decreased urine output can seriously affect renal clearance of excess serum
phosphorus.

D. Carefully monitor serum electrolyte levels, especially calcium and phosphorus. Report
changes immediately.
● Monitor BUN and serum creatinine levels.
− Hyperphosphatemia can impair renal tubules when calcification occurs.
E. Administer prescribed medications, monitor their effectiveness, and assess the patient
for possible adverse reactions.
● Give antacids with meals to increase their effectiveness in binding phosphorus.
F. Prepare the patient for possible dialysis if hyperphosphatemia is severe
G. Provide health teaching on hyperphosphatemia, its risk factors, treatment, prescribed
medications, avoidance of medications that contain phosphorous, consumption of a
low-phosphorous diet, and the warning signs to look for and when to report them.

F. Chloride (Cl-)

NORMAL VALUE
96 - 106 mEq/L

1. Chloride Deficit (Hypochloremia)

● a deficiency of chloride in the extracellular fluid
● a serum chloride level below 96 mEq/L

CAUSES
Decreased chloride intake
Excessive chloride losses
Vomiting
Diarrhea
Severe diaphoresis
Gastric surgery
Nasogastric suction
Gastrointestinal tube drainage
Metabolic alkalosis
Untreated diabetic ketoacidosis
Addison’s disease
Rapid removal of ascitic fluid during paracentesis
Heart failure – caused by hemodilution
Medications:
Bicarbonate
Corticosteroids
Laxatives
Theophylline
Diuretics – loop, osmotic, and thiazide

CLINICAL MANIFESTATIONS
Hyperexcitability of the nerves and muscles – tremors, twitching
Tetany
Hyperactive deep tendon reflexes
Muscle hypertonicity
Slow and shallow breathing
Hypotension – with severe chloride and ECF losses
Agitated or irritable

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 WARNING SIGNS
Arrythmias
Coma
Respiratory arrest
Seizure

PATHOPHYSIOLOGY

Chloride Intake or
Absorption

Chloride Loss

Sodium and
Bicarbonate Retention
by Kidneys

Bicarbonate
Ions in ECF Arrythmia

Seizure
pH Elevation Hypochloric
Metabolic Alkalosis
Coma

Respiratory Arrest

DIAGNOSTIC FINDINGS
● Serum chloride below 98 mEq/L.
● Serum sodium below 135 mEq/L � hyponatremia.
● Serum pH greater than 7.45 and bicarbonate level greater than 26 mEq/L � metabolic
alkalosis.

MEDICAL MANAGEMENT
PRIORITIES:
− treatment of underlying cause of hypochloremia
− restore normal chloride levels
− preventing complications
A. Pharmacologic Therapy
● for chloride replacement given intravenously
− 0.9% Sodium Chloride
− 0.45% Sodium Chloride
● discontinuation of diuretics: loop, osmotic, or thiazide
● treatment of metabolic alkalosis
− Ammonium chloride
▪ an acidifying intravenous agent

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 ▪ dosage depends on the patient’s weight and serum chloride levels
▪ metabolized by the liver and effect lasts for 3 days
▪ contraindicated for patients with hepatic or renal impairment
B. Nutrition Therapy
● increase dietary intake of chloride through a chloride-rich diet

NURSING MANAGEMENT
PRIORITIES:
− monitoring to prevent complications
− patient safety
− monitoring the patient’s response to therapy
− health teaching

A. Monitor LOC, muscle strength, and movement.

B. Notify the physician if the patient’s condition worsens.
C. Monitor vital signs, especially respiratory rate and pattern, and observe for worsening
respiratory function.
D. Monitor cardiac rhythm.
− Hypokalemia may be present with hypochloremia.
E. Monitor and record serum electrolyte levels, especially chloride, sodium, potassium, and
bicarbonate. Also assess arterial blood gas results for acid-base imbalance.
F. Offer foods high in chloride (tomato juice or salty broth) if patient is alert and can
swallow without difficulty.
G. Administer medication supplements as prescribed.
● Insert an I.V. line as ordered, and keep it patent.
● Administer chloride and potassium replacements as ordered.
● If administering ammonium chloride, assess the patient for pain at the infusion site
and adjust the rate, if needed.
− Do not give in patients with severe hepatic impairment for ammonium chloride
is metabolized in the liver.
● Use normal saline solution to flush the patient’s nasogastric tube.

H. Accurately measure and record intake and output, including the volume of vomitus and
gastric contents from suction and other gastrointestinal drainage tubes.
I. Implement safety precautions.
● Make sure the patient maintains bed rest, if ordered.
● Keep the bed in its lowest position, with wheels locked and side rails raised.
● If the patient is at risk for seizures, pad the side rails and keep an artificial airway at
the patient’s bedside.
● Orient the patient as needed. Keep clocks, calendars, and familiar personal objects
within his sight.
● Assist the patient with ambulation and activities of daily living, if needed, and keep
essential objects near him.
J. Provide health teaching on hypochloremia, its risk factors, treatment, prescribed
medications, and the warning signs to look for and when to report them.

2. Chloride Excess (Hyperchloremia)

● an excess of chloride in the extracellular fluid exceeding 108 mEq/L
● associated with other acid-base imbalance such as metabolic acidosis, and rarely occurs alone
● has an inverse relationship with bicarbonate

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 CAUSES

Increase intake and absorption Hyperaldosteronism

Increased intake of sodium Hypernatremia
Water loss Drug-related retention
Anastomoses of the ureter Ammonium chloride
and intestines Ion exchange resin
Dehydration (Kayexelate)
Renal failure Carbonic anhydrase
Respiratory alkalosis inhibitors - acetazolamide
Hyperparathyroidism

CLINICAL MANIFESTATIONS
Metabolic acidosis s/sx
Tachypnea
Lethargy
Weakness
Diminished cognitive ability
Deep, rapid respirations
(Kussmaul’s respirations)
Unconsciousness (late)
Agitated
Dyspnea
Tachycardia
Pitting edema

PATHOPHYSIOLOGY

Chloride Intake
Absorption
Retention

Sodium Level

Water loss worsen S/Sx of Metabolic

Cl- accumulation Acidosis

Bicarbonate
Level
DIAGNOSTIC FINDINGS
● Serum chloride level greater than 106 mEq/L.
● Serum sodium level greater than 145 mEq/L.
● Serum pH less than 7.35.
● Serum bicarbonate less than 22 mEq/L.

MEDICAL MANAGEMENT
PRIORITIES:
− treatment of underlying cause
− restore fluid, electrolyte, and acid-base balance
− preventing complications
− treatment of underlying causes
D. Pharmacologic Therapy
● Intravenous fluid therapy
− Lactated Ringer’s Solution

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 ▪ converts lactate to bicarbonate in the liver which increase serum
bicarbonate and correct acidosis
● for severe hyperchloremia
− Sodium bicarbonate
▪ administered intravenously to raise serum bicarbonate levels
▪ leads to renal excretion of chloride ions and correction of acidosis

NURSING MANAGEMENT
PRIORITIES:
− monitoring to prevent complications
− monitoring the patient’s response to therapy
− health teaching
A. Monitor vital signs, including cardiac rhythm.
B. Continually assess the patient, paying particular attention to the neurologic, cardiac, and
respiratory examinations. Immediately report changes to the physician.

C. Look for changes in the respiratory pattern that may indicate a worsening of the acid-
base imbalance.
D. Insert an I.V. line and maintain its patency.
● Administer I.V. fluids and medications as ordered.
● Watch for signs of fluid overload.
● Watch out for overcompensation when administering sodium bicarbonate such as
metabolic alkalosis.
● Watch for signs of hypokalemia as potassium is forced into the cells.
E. Evaluate muscle strength, and adjust activity level accordingly.
F. Restrict fluids, sodium, and chloride, if ordered.
G. Monitor and record serum electrolyte levels and arterial blood gas results.
H. Monitor and record fluid intake and output.
I. Focus on careful monitoring, safety measures, and interventions to restore normal
chloride levels.
J. Provide health teaching on hyperchloremia, its risk factors, treatment, prescribed
medications, dietary restrictions, importance of fluid replenishment, and the warning
signs to look for and when to report them.

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