1.

ELECTROLYTE IMBALANCES

 Electrolyte imbalances can occur in healthy people as a result of changes in fluid intake
and output.
 These imbalances are usually mild and are easily corrected.
 Severe electrolyte imbalances are life threatening.
 People at greater risk for severe imbalances are older clients, clients with chronic renal or
endocrine disorders, clients who are mentally impaired, and clients who are taking drugs
that alter fluid and electrolyte levels,
 Ill people are at some risk for electrolyte imbalances.

1.1. SODIUM IMBALANCES:

 Sodium is the most abundant electrolyte in the ECF. It ranges from 135 to 145 mEq/L
(135 to 145 mmol/L).
Functions:
 Regulates the fluid volume of ECF.
 Maintain plasma volumes and regulates size of the vascular space.
 Controls body H2O distribution by maintaining the osmotic equilibrium between ICF and
ECF  because it does not easily cross the cell wall membrane and because of its
abundance and high concentration in the body.
 Aid in conduction of nerve impulses
 Control muscle contractility especially cardiac muscle
 Maintenance of neuromuscular irritability and acid-base balance

 Sodium is regulated by ADH, thirst, and the renin-angiotensin-aldosterone system

of the body.
 A loss or gain of sodium is usually accompanied by a loss or gain of
water.

The two most common sodium imbalances are Sodium Deficit and Sodium Excess.

A. SODIUM DEFICIT (HYPONATREMIA)

 Hyponatremia refers to a serum sodium level below 135 mEq/L (135 mmol/L).
Normal values: 135 to 145 mEq/L (mmol/L).

Pathophysiology

 Hyponatremia primarily occurs due to an imbalance of water rather than sodium 

because sodium is the major cation in the blood and interstitial fluid and maintains the
osmolarity of these fluids.

 2 Mechanisms involved that can cause problems of Hyponatremia are:

1. First mechanism is a change in cell excitability  as the sodium level in the blood
and other ECF decreases, the difference in sodium levels between the ECF and the
cellular fluid also decreases.
 Less sodium is present to move across the excitable membrane resulting in
slower membrane depolarization.

2. The second mechanism is the movement of water from the ECF space into the
cells  cells swells and their functions are impaired.
Common Causes of Hyponatremia:

 Actual Sodium Deficit

Increased Sodium Excretion
 Excessive diaphoresis
 Diuretics (high-ceiling diuretics)
 Wound drainage (especially gastrointestinal)
 Decreased secretion of aldosterone
 Hyperlipidemia
 Renal disease ( scarred distal convoluted tubule)

 Inadequate Sodium Intake

 NPO
 Low-salt diet

 Relative Sodium Deficits

Dilution of Serum Sodium
 Excessive ingestion of hypotonic solution
 Psychogenic polydipsia
 Freshwater drowning
 Renal failure (nephrotic syndrome)
 Irrigation with hypotonic fluids
 Syndrome of inappropriate antidiuretic hormone secretion
 Hyperglycemia
 Congestive heart failure

 Hyponatremia can result from the loss of total body sodium, the movement of sodium
from the blood to other fluid spaces, or the dilution of serum from excessive water in
the plasma.

Clinical Manifestations:

 The manifestations of hyponatremia are caused by its effects on excitable cellular

activity. The cells especially affected are those involved in cerebral, neuromuscular, and
gastric smooth muscle functions.

 Cerebral Manifestations:
= Changes in cerebral function are the most obvious problems of hyponatremia  these
changes may be seen as either depressed activity or excessive activity (and sometimes
both).
 Behavioral or personality changes – result from cerebral edema and increased
intracranial pressure such as irritability and agitation.
 Headache  coma  death.
 Closely observe and document client’s behavior and level of
consciousness.

 Neuromuscular Manifestations:
= Assess the client’s neuromuscular status for any changes from baseline.
 Generalized skeletal muscle weakness – occurs bilaterally and is worse in the legs
and arms.
 Diminished muscle tone and deep tendon reflexes.

 Gastrointestinal Manifestations:
= The smooth muscle of the GI system responds to decreased serum sodium levels with
increased motility causing:
 Nausea
 Diarrhea
  Abdominal cramping
 Hyperactive bowel sounds – listen to bowel sounds (with rushes and gurgles over
the splenic flexure and in the lower left quadrant.
 Bowel movements are frequent and watery.
 Peristaltic movements may be palpated and may be visible on the
abdominal surface.

 Cardiovascular Manifestations:
= Hyponatremia has a little effect on cardiac muscle contractility but cardiac output is
changed with hyponatremia.
= When hyponatremia occurs with changes in blood volumes, these fluid changes alter
cardiac function.
 Normovolemic
 Rapid pulse rate
 Normal blood pressure.
 Hypovolemic (decreased plasma volume or fluid deficit)
 Rapid pulse rate
 Pulse quality thready and weak
 Decreased diastolic pressure. Severe hypotension when moving from lying
to sitting position to a standing position.
 Central venous pressure normal or low
 Flat neck veins in supine position
 Hypervolemic (increased plasma volume or fluid excess)
 Cardiac changes include a full-pulse, rapid, bounding pulse with normal or
high blood pressure.
 Central venous pressure is normal or high – depending on how well the
left ventricle handles the extra fluid.

 Respiratory Manifestations:
 Late manifestations related to skeletal muscle weakness:
 Shallow, ineffective respiratory movements
 Hypervolemia
 Pulmonary edema
 Rapid, shallow respiration
 Moist crackles

 Renal Manifestations:
 Increased urine output
 Decreased urine specific gravity

 Integumentary:
 Dry skin
 Pale, dry mucous membrane

 Serum Sodium Level < 115 mEq/L (mmol/L):

 Signs of increasing intracranial pressure such as:
 Lethargy
 Confusion
 Muscle twitching
 Focal weakness
 Hemiparesis
 Papilledema
 Seizure  DEATH may occur.
Assessment and Diagnostic Findings:

 Assessment includes the history and physical examination including a focused neurologic
examination; evaluation of signs and symptoms as well as laboratory results;
identification of IV fluids, and review of all medications the patient is taking.

 Na level less than 135mEq/L – regardless of the cause of hyponatremia.

 In SIADH – may be lower than 100 mEq/L (mmol/L).
 Urine specific gravity is low (1.002 to 1.004).
 Hyponatremia due to SIADH – urine specific gravity is greater than 1.012
 Serum osmolality less than 280mOsm/kg.

Medical Management:

 The key to treating hyponatremia is assessment including identifying patients who are at
risk and recognizing that the rapidity of the onset of hyponatremia is of primary
importance.
 Mild Hyponatremia:
 Restrict fluid intake
 Oral Na supplements
 Hyponatremia related to hypovolemia:
 Isotonic fluid such as NS or LR – to restore both sodium and fluid volume.
 High Na foods
 Severe Hyponatremia:
 Requires treatment to ICU.
 Hypertonic saline solution such as 3% or 5% NaCl infusion causes water to shift
out of cells may lead to intravascular overload and brain damage – must be given
in small-volume. Monitor the infusion rate and client’s response.
 Fluid volume overload prevented with slow infusion of furosemide – usually
administered simultaneously.
 Hyponatremia related to Fluid excess:
 Drug therapy
= Osmotic Diuretics such as mannitol (Osmitrol) – promotes excretion of water
rather than sodium.
 Assess the client hourly for signs of excessive fluid loss and increased sodium
levels.
= Hyponatremia caused by inadequate secretion of ADH includes agents that
antagonize ADH such as lithium and demeclocycline (Declomycin).

Nursing Interventions:

 Electrolyte Management: Hyponatremia

 Identify and monitor patient at risk of hyponatremia – early detection of this disorder are
necessary to prevent serious consequences.
 Monitor for electrolyte imbalances associated with hyponatremia (ex: hypokalemia,
metabolic acidosis, and hypoglycaemia) as appropriate.
 Monitor for renal loss of sodium (oliguria).
 Monitor intake and output.
 Weigh client daily and monitor trends.
 Monitor for indications of fluid overload or retention (ex: crackles, elevated CVP or
PCWP (pulse capillary wedge pressure), edema, neck vein distention and ascitis) as
appropriate.
 Administer hypertonic (3% to 5%) saline at 3 ml/kg/hr or per policy for rapid correction
of hyponatremia, as appropriate.
 Maintain fluid restriction (total of 800 mL in 24 hours), as appropriate.
  Monitor for neurologic and/or neuromuscular manifestations of hyponatremia (ex:
lethargy, increased ICP, confusion, headache, seizures, coma, fatigue, tremors,
apprehension, muscle weakness, and hyperreflexia).
 Monitor for cardiovascular manifestations of hyponatremia (ex: elevated blood pressure,
cold and clammy skin, and hypo or hypovolemia).
 For patient taking lithium – the nurse observes for lithium toxicity, particularly when
sodium is lost by abnormal route.
 Supplemental salt and fluid are administered.
 For all patients on lithium therapy – adequate salt intake should be ensured.

B. SODIUM EXCESS (HYPERNATREMIA)

Hypernatremia is a serum sodium level higher than 145 mEq/L (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.
 In sodium excess, the patient ingests or retains more sodium than water.

Pathophysiology:

 As serum sodium level rises  increases sodium levels between ECF and ICF  causing
an increase in osmolarity levels of the ECF  this problem causes water to move from
the cells into the ECF to dilute the hyperosmolar ECF as hypernatremia persists or
worsens, compensatory actions cause severe cellular dehydration.

Common Causes of Hypernatremia:

 Actual Sodium Excesses

Decreased Sodium Excretion
 Hyperaldosteronism
 Renal failure
 Corticosteroids
 Cushing syndrome or disease

 Increased Sodium Intake

 Excessive oral sodium ingestion
 Excessive administration of sodium-containing IV fluids

 Relative Sodium Excesses

Decreased Water Intake
 Nothing by mouth

 Increased Water Loss

 Increased rate of metabolism
 Fever
 Hyperventilation
 Infection
 Excessive diaphoresis
 Watery diarrhea
 Dehydration

Clinical Manifestations:

 The manifestations of hypernatremia vary with the severity of imbalance and whether a
fluid imbalance is also present. Rapid increase in serum sodium cause more obvious and
severe symptoms.
 The manifestations of hypernatremia involve changes in excitable membrane activity,
especially cerebral, neuromuscular, and cardiac functions.
 Thirst – is the primary characteristic of hypernatremia. It is a strong defender of serum
sodium level.

 Central Nervous System Manifestations:

 Altered cerebral function is the most common problem of hypernatremia.
 Assess the client’s mental status for attention span, recall of recent events,
and cognitive function.
 In hypernatremia with normal or decreased fluid volume  the client may
have a short attention span and may be agitated or confused about recent
events  seizures may occur if serum sodium continues to rise.
 When hypernatremia occurs with blood volume overload  client may be
lethargic, drowsy, stuporous and even comatose.

 Neuromuscular Manifestations:
 Skeletal muscles responses vary with the degree of sodium increases.
 Mild or early hypernatremia
 Spontaneous muscle twitching
 Irregular muscle contraction
 Severe hypernatremia – as it worsens, the muscles and nerves are less able
to respond to a stimulus.
 Skeletal muscle weakness – the muscles become progressively
weaker with rigid paralysis.
 Diminished or absent deep tendon reflexes
= Assess neuromuscular status by observing for twitching in
muscle group.

 Cardiovascular Manifestations:
 Decreased cardiac contractility – Increased serum sodium slows movement of
calcium into the heart cells  which decreases contractility.
 Diminished cardiac output
 Heart rate and blood pressure respond to vascular volume
 Assess cardiac status by measuring blood pressure and the rate and quality
of the apical and peripheral pulses.
 Pulse rate and blood pressure may be normal, above normal or
below normal depending on the fluid volume and how rapidly the
imbalance occurred.
 Hypernatremia with hypovolemia
 Pulse rate is increased and peripheral pulses are difficult to palpate
and are easily blocked.
 Hypotension and severe orthostatic (postural) hypotension are
present and pulse pressure is reduced.
 Hypernatremia with hypervolemia
 Slow to normal bounding pulses
 Peripheral pulses are full and difficult to block.
 Distended neck veins even in upright position.
 Increased diastolic blood pressure

 Respiratory Manifestations:
 Problems associated with pulmonary edema when hypernatremia is accompanied
by hypervolemia.

 Renal Manifestations:
 Decreased urine output
 Increased urine specific gravity

 Integumentary Manifestations:
 Dry, flaky skin
  Presence or absence of edema related to accompanying fluid volume changes

Assessment and Diagnostic Findings:

 Increased serum sodium level exceeds 145 mEq/L (145 mmol/L) and serum osmolality
exceeds 300 mOsm/kg (300 mmol/L)
 Increased urine specific gravity and urine osmolality – the kidneys attempt to conserve
water (provided the water loss is from a route other than the kidneys).
 Patients with nephrogenic or central diabetes insipidus have hypernatremia and produce a
dilute urine with a urine osmolality less than 250 mOsm/kg.

Common Nursing Diagnoses and Collaborative Problems;

 Excess Fluid Volume related to excess sodium intake

 Decreased Cardiac Output related to poor cardiac contractility
 Risk for Falls related to skeletal muscle weakness
 Impaired Memory related to fluid and electrolyte imbalances
 Readiness for Enhanced Nutrition related to the need for dietary sodium restrictions
 Potential for Pulmonary Edema

Medical Management:

 Treatment of hypernatremia consists of gradual lowering of serum sodium level.

 Other interventions used when sodium levels become life-threatening include:
Hemodialysis and blood ultrafiltration.

 Drug Therapy
 Hypotonic IV infusions, usually 0.225% or 0.45% NaCl are prescribed -
when hypernatremia is caused by fluid loss. It is used to restore fluid
balance
 Isotonic NaCl solutions – for hypernatremia caused by fluid and sodium
losses as fluid replacement.
 Diuretics such as furosemide (Lasix, Furoside), bumetanide (Bumex), and
ethacrynic acid (Edecrine) – for hypernatremia caused by poor renal
excretion of sodium to promote sodium loss.
 Desmopressin acetate (DDAVP) – a synthetic antidiuretic hormone, may
be prescribed to treat diabetes insipidus if it is the cause of hypernatremia.
 Assess the client hourly for symptoms of excessive fluid, sodium or
potassium losses.

 Diet Therapy
 Mild hypernatremia can be prevented or corrected by ensuring adequate water
intake.
 Dietary sodium restriction – may be needed to prevent sodium excess when
renal problems are present.
 Collaborate with the dietitian to teach the client how to determine the
sodium content of foods, beverages, and drugs.
 Stress the importance of adhering to the diet.
 Fluid restriction must be followed.

Nursing Management:

Electrolyte Management: Hypernatremia

 Monitor for indications of dehydration (ex: decreased sweating, decreased urine,
decreased skin turgor, and drymucousmembrane).
 Monitor vital signs as appropriate.
 Weigh client daily and monitor trends.
  Promote comfort measures to decrease thirst.
 Maintain patent IV access.
 Monitor intake and output.
 Provide frequate oral hygiene.
 Administer isotonic (0.9%) saline, hypotonic (0.45%) saline, hypotonic (5%)
dextrose, or diuretics, as appropriate, based on fluid status and urine osmolality.
 Maintain sodium restrictions.

2.2 POTASSIUM IMBALANCES

 Potassium is the major intracellular electrolyte; 98% of the body’s potassium is inside
the cells. The remaining 2% is in the ECF and is important in neuromuscular function.
 Potassium influences both skeletal and cardiac muscle activity.
Ex: alterations in its concentration change myocardial irritability and rhythm.
 The normal serum potassium concentration ranges from 3.5 to 5.0 mEq/L (mmol/L).
 The normal ICF potassium level is about 140 mEq/L (mmol/L).
 Potassium control also occurs through the kidney function, because about 80% of
potassium removed from the body occurs via the kidney.
 Aldosterone is the only hormone that enhances kidney excretion of potassium.

A. HYPOKALEMIA

 Is a serum potassium level below 3.5 mEq/L (mmol/L).

 A common electrolyte imbalance which can be life threatening because every
system is affected.
 The severity of problems caused by hypokalemia is related to how rapidly the
serum potassium level drops.

Pathophysiology:

 Low serum potassium levels increases the difference in the amount of potassium between
the fluid inside the cells (ICF) and the fluid outside the cells (ECF)  as a result, the cell
membranes of all excitable tissues such as nerve and muscle are less responsive to normal
stimuli.
 When the loss of ECF potassium is gradual  cells adjust and cellular potassium
decreases in proportion to the ECF potassium level  potassium difference between the
2 fluid spaces remained unchanged  symptoms of hypokalemia may not appear until
the potassium loss is extreme.
 Rapid reduction of serum potassium levels  causes dramatic changes in function.
 Hyperkalemia may result either from an actual total body potassium loss or from
movement of potassium from the ECF to the ICF  causing a relative decrease in ECF
potassium level.

Common Causes of Hypokalemia:

 Actual Potassium Deficits:

 Inappropriate or excessive use of drugs
 Diuretics
 Digitalis
 Corticosteroids
 Increased secretion of aldosterone
 Cushing’s syndrome
 Diarrhea – large amounts of potassium (30 mEq/L) are contained in the intestinal
fluids, potassium deficit may occur.
 Vomiting
  Wound drainage (especially gastrointestinal) (recent ileostomy and villous
adenoma – a tumor of the intestinal tract characterized by excretion of potassium-
rich mucus).
 Prolonged nasogastric suction – potassium is actually lost when gastric fluid is
lost.
 Heat-induced excessive diaphoresis
 Renal disease impairing reabsorption of potassium
 Nothing by mouth

 Relative Potassium Deficits:

 Alkalosis – is caused by the kidneys’ response to an extreme lack or loss of
potassium, which can occur when people take certain diuretic medications.
 Hyperinsulinism – above normal level of insulin in the blood. Insulin promotes
entry of potassium into skeletal muscle and hepatic cells  patients with
persistent insulin hypersecretion may experience hypokalemia  often seen in
patients receiving high-carbohydrate parenteral nutrition.
 Hyperalimentation – administration of nutrients by intravenous feeding especially
to patients who cannot ingest food through the alimentary tract.
 Total parenteral nutrition – is a method of feeding that bypasses the
gastrointestinal tract. Fluids are given into a vein to provide most of the necessary
nutrients the body needs.
 Water intoxication – a potentially life-threatening condition caused by drinking
too much water which leads to hyponatremia and disturbances in mental functions
which may result to seizure, coma and death.
 IV therapy with potassium-poor solutions

Clinical Manifestations:

 Potassium deficiency can result in widespread derangements in physiologic function.

 Severe hypokalemia can cause death through cardiac or respiratory arrest.

 Gastrointestinal: Anorexia, nausea, vomiting, diarrhea, ileus, distention, decrease bowel

motility
 Musculoskeletal: Muscle weakness, paralysis, leg cramps, muscle flabbiness,
paresthesias, decreased muscle strength and tendon reflexes.
 Cardiovascular: Dysrrhythmias, vertigo, postural hypotension, flattened T wave or
inverted T waves, depressed ST segments prominent U wave, slow weak pulse
 Respiratory: Shallow respirations, shortness of breath
 Neurologic: Fatigue, lethargy, confusion, depression
 Renal: Polyuria, nocturia, decreased serum osmolality

Diagnostic Findings:

 ECG changes:
 Depressed ST segment
 Flattened or inverted T wave
 Prominent U wave – extreme hypokalemia
 Decrease K level
 Elevated pH and bicarbonate level
 Decrease serum Mg level
 Increase 24H urine level

Medical Management:

 If hypokalemia cannot be prevented by conventional measures such as increased intake in

the daily diet or by oral potassium supplements for deficiencies, then it is treated
cautiously with IV replacement therapy.
  Oral potassium chloride (available in tablet and liquid form) – used to correct potassium
deficits.
 K+ is extremely irritating to the gastric mucosa, the drug must be taken with
H2O, juice or during meals.

 Potassium chloride, potassium acetate, potassium phosphate  parenteral or IV route.

 KCl should never be given IM or given as a bolus IV push undiluted.
 If given IV, it should be diluted a concentration of less than 80 mEq/L as
recommended.
 10mEq/L diluted in 50-100ml administered within 30 min. to 1 hour.
Maximum concentration of potassium that should be administered thru a
peripheral IV line is 20 mEq/100 ml and the rate no faster than 10 to 20 mEq/L
concentration greater than 20 mEq/100 should be administered thru a central IV
catheter.
 Mix IV solutions when adding KCl as incorporation.
 NPO and post-op clients should be on maintenance dose at 20 to 40 mEq/L in the
IV.
 Renal function should be monitored thru BUN and creatinine levels and urine
output.

Common Nursing Diagnoses and Collaborative Problems:

 Impaired Physical Mobility related to skeletal muscle weakness

 Decreased Cardiac Output related to dysrhythmia
 Risk for Fall related to skeletal muscle weakness
 Constipation related to smooth muscle atony
 Potential for Respiratory Insufficiency

Nursing Intervention:

 Interventions for hypokalemia aim to prevent potassium loss, increase serum potassium
levels and provide a safe environment.
 Drug and nutrition therapies help restore normal serum potassium levels.
 The priorities for nursing care of patient with hypokalemia are: ensuring adequate
oxygenation, patient safety for falls prevention, and prevention of injury from
potassium administration and monitoring the patient’s response to therapy.
 Monitor patients who are at risk – implement safety measures who have muscle weakness
from hypokalemia.
 Eliminating hazards and assisting with ambulation.
 Encouraging the patient at risk to eat foods rich in potassium – helps prevent further loss
but supplementation is needed to restore normal potassium levels.
 Monitor heart rate and rhythm such as hypotension, broad T wave, U wave, tachycardia
and weak pulse.
 Assess respiratory rate, depth and pattern – hourly for severe hypokalemia.
 Check oxygen saturation by pulse oximetry to determine breathing effectiveness.
 Assess respiratory muscle effectiveness by checking patient’s ability to cough.
 Examine face, oral mucosa and nailbeds for pallor or cyanosis.
 Evaluate arterial blood gas values for decreased blood oxygen levels (hypoxemia)
and increased arterial carbon dioxide levels (hypercapnia).
 Administer prescribed supplemental potassium (PO, NG, or IV) as prescribed.
 Prevent/reduce irritation from potassium(is a severe tissue irritant) supplement –
administer PO or NG potassium supplements during or after meals to minimize GI
irritation, dilute IV potassium adequately, administer IV supplement slowly and apply
topical anesthetics to IV sites.
 MIO – because 40mEq of K is lost per 1L of urine output.
 Diuresis put the patients at risk for serious K loss – but for patients with
hypokalemia who needs diuretics, potassium-sparing diuretics such as
 spironolactone (Aldactone), triumterene (Dyrenium) and amiloride (Midamor) –
they increase urine output without increasing potassium loss.
 Monitor serum K level.
 Monitor for signs of hypokalemia-related metabolic alkalosis.
 Provide teaching.
 Stop drugs that cause hypokalemia e.g. diuretics, laxatives.

B. HYPERKALEMIA

Hyperkalemia – is a serum potassium level higher than 5.0 mEq/L (mmol/L).

 The normal range for serum potassium values is narrow but a slight increase above
normal values can affect excitable tissues, especially the heart  cardiac arrest.

Pathophysiology:

 A high serum potassium level decreases the potassium difference between the ICF and
the ECF  this decreased difference increases cell excitability, as a result excitable
tissues respond to less intense stimuli  causing altered cardiac function (the heart is
very sensitive to serum potassium increases).
 Sudden rises in serum potassium levels between 6 and 7 mEq/L  cause severe
problems.
 Hyperkalemia may result from an actual increase in total body potassium or from the
movement of potassium from the cells to the blood.
 Hyperkalemia are rare in people with normal kidney function but most cases occur in
hospitalized patients and those undergoing medical treatment. Those that are at a greater
risk are the chronically ill patients, debilitated patients and the older adults.

3 Major Causes of Hyperkalemia:

1. Decreased renal excretion of potassium – commonly seen in patients with untreated renal
failure or as a result of infection.
2. Rapid administration of potassium – particularly those in whom potassium levels increase
due to excessive intake of potassium in food or medications.
3. Movement of potassium from the ICF compartment to the ECF compartment – patients
with hypoaldosteronism or Addison’s disease are at risk because deficient adrenal
hormones leads to sodium loss and potassium retention.

Common Causes of Hyperkalemia:

 Actual Potassium Excesses:

 Over ingestion of containing K foods or medicines – potassium chloride, heparin,
ACE (angiotensin-converting enzyme) inhibitors, captopril, NSAIDs, potassium
sparing diuretics.
 Salt substitutes
 Rapid infusion of K+ containing IV solutions
 Bolus of IV K+ injections
 Transfusion of whole blood or packed cells
 Adrenal insufficiency (Addison’s disease, adrenalectomy)
 Renal failure

 Relative Potassium Excesses:

 Tissue damage such as in burns, crushing injuries or severe trauma – causes an
elevated ECF potassium level.
 Acidosis – potassium moves out of the cells and into the ECF.
 Hyperuricemia
 Uncontrolled diabetes mellitus
Clinical Manifestations:

 Ask about chronic illnesses particularly renal disease and diabetes mellitus, recent
medical or surgical treatment, and urine output, including frequency and amount of
voiding.
 Ask about drug use, particularly potassium-sparing diuretics and ACE inhibitors.
 Diet history – intake of potassium-rich foods and use of salt substitutes.

 Cardiovascular Changes: the most severe problems from hyperkalemia and are
the most common cause of death.
 Bradycardia, hypotension and ECG changes: Tall, peaked T waves,
prolonged PR intervals, flat or absent P waves and wide QRS complexes.
 As serum potassium rises  heartbeat generated outside the normal
conduction system in the ventricle (ectopic beats) may appear  complete
heart block, asystole and ventricular fibrillation may occur  life-
threatening complication of severe hyperkalemia.

 Neuromuscular Changes:
 Skeletal muscle twitching such as tingling and burning sensations
followed by numbness in the hands and feet and around the mouth
(paresthesia) – early stages of hyperkalemia.
 As hyperkalemia worsens  muscle twitching changes to weakness
followed by flaccid paralysis. The weakness moves up from the hands and
feet and affects the muscles of the arms and legs.

 Intestinal Changes:
 Increased motility – causing diarrhea and spastic colonic activity.
 Bowel sounds are hyperactive, with audible rushes and gurgles.
 Bowel movements are frequent and watery.

Diagnostic Findings:

 Laboratory data confirms hyperkalemia (potassium level over 5.0 mEq/L).

 Levels of other electrolytes, hematocrit and haemoglobin are elevated – caused by
dehydration.
 Elevated serum creatinine, and BUN, decreased blood pH and normal or low
hematocrit and haemoglobin levels – caused by renal failure.

 ECG changes: Tall, peaked T waves, prolonged PR intervals, flat or absent P waves and
wide QRS complexes.
 Arterial blood gas analysis – may reveal both a metabolic and respiratory acidosis.
 Correcting the acidosis helps correct hyperkalemia.

Medical Management:
 Drug Therapy is the main medical intervention.
 Potassium level between 5.0 to 5.5 mEq/L – restriction of dietary K intake.
 If potassium excess is due to metabolic acidosis – correcting the acidosis with
NaHCO3 which promotes K+ uptake into the cells.
 Improving urine output usually decreases the elevated serum K+ level. Potassium-
wasting diuretics (furosemide) can be used.

Severe Hyperkalemia:
 Intravenous Ca gluconate infusion or Ca chloride to decrease the antagonistic effect of
K+ excess in the myocardium – monitor BP for hypotension which may result from the
rapid IV administration of Ca gluconate.
  IV infusion of insulin and glucose or NaHCO3 to promote K+ uptake into the cells – help
decrease serum potassium levels (usually 100 ml of 10% to 20% glucose with 10 to 20
units of regular insulin). This is a hypertonic solution.
 Observe patient manifestations of hypokalemia and hypoglycaemia during this
therapy.
 Loop diuretics – increase excretion of water by inhibiting Na, K, Cl reabsorption in the
ascending loop of henle and distal renal tubule
 Beta – 2 agonist, such as albuterol – is highly effective in decreasing potassium.
 Kayexelate (polysterane sulfonate) may be given orally or rectally – This treatment
stimulates the exchange of a K ion for a Na ion that promotes the intestinal sodium
absorption. The K ion is then excreted in the stool. Sorbitol may be combined with
kayexelate to prevent constipation.
 Peritoneal Dialysis or Hemodialysis – if potassium levels are dangerously high.
Nursing Interventions:
 Interventions for hyperkalemia are aimed at rapidly reducing the serum potassium level,
preventing recurrences and ensuring patient safety during the electrolyte imbalance.
 The priorities for nursing care of patient with hyperkalemia are:
 Close monitoring to prevent cardiac complications – allows for the early
recognition of dysrhythmias and other manifestations of hyperkalemia on cardiac
muscle.
 Assess vital signs, monitor cardiovascular status.
 Anticipate cardiac monitoring and a 12 lead ECG.
 Refer if the patient’s heart rate falls below 60 beats per minute or if
the T waves become spiked.
 Patient safety for falls prevention - Implement safety measures.
 Monitoring the patient’s response to therapy
 Monitor serum potassium levels
 Assess motor and sensory function
 Monitor neurologic status
 Be prepared to give calcium gluconate by slow IV infusion in
acute cases of hyperkalemia – monitor BP for hypotension which
may result from rapid IV administration of Ca gluconate.
 Prepare the patient for the possibility of dialysis – those with
chronic renal failure.
 Great care should be taken to administer and monitor potassium
solutions closely.
 Health teaching – is the key to the prevention of hyperkalemia and early detection
of complication.
 Patient at risk for hyperkalemia includes diet (avoid foods high in
potassium and use of salt substitutes), drugs (Administer insulin
and glucose and sodium bicarbonate as or ordered) and recognition
of the manifestations of hyperkalemia.
 2.3 CALCIUM IMBALANCES

 Calcium (Ca+) is a mineral with functions closely related to those of phosphorous and
magnesium.
 Calcium is an ion having 2 positive charges (divalent cation) that exist in the body in a
bound form and an ionized (unbound or free) form.
 Bound calcium is usually attached to serum proteins, especially albumin.
 Ionized calcium is present in the blood and other ECF as free calcium which is
in active form and must be kept within a narrow range in the ECF.
 More than 99% of the body’s calcium is located in the skeletal system; it is a major
component of bones and teeth.
 About 1% of skeletal calcium is rapidly exchangeable with blood calcium and the rest is
more stable and only slowly exchanged.

Functions:

 Maintaining bone strength and density

 Activating enzymes
 Allowing skeletal and cardiac muscle contraction
 Controlling nerve impulse transmission
 Allowing blood clotting

 Calcium enters the body by dietary intake and absorption through the intestinal tract.
Dairy products are common foods high in calcium and absorption of dietary calcium
requires the active form of vitamin D.
 PTH and Calcitonin – controls the serum calcium level.
 As ionized calcium decreases  the parathyroid glands secrete PTH  increases
calcium absorption from the GI tract, increases calcium reabsorption in the renal
tubule and releases calcium from the bones.
 When calcium increases excessively  the thyroid gland secretes calcitonin 
which inhibits calcium reabsorption from the bone and decreases the serum
calcium concentration and increasing kidney excretion of calcium in the urine.

 The body functions best when calcium levels are maintained between 9.0 and 10.5
mg/dl or between 2.25 and 2.75 mmol/L.

A. CALCIUM DEFICIT (HYPOCALCEMIA)

 Hypocalcemia is a total serum calcium level below 9.0 mg/dl or 2.25 mmol/L.
 A patient may have a total body calcium deficit (as in osteoporosis) but has a normal
serum calcium level. Elderly people and those with disabilities, who spend an amount of
time in bed, have an increased risk of hypocalcemia because bed rest increased bone
resorption.

Pathophysiology:

 Calcium is stored in the bone, with only a small amount of total calcium present in the
ECF  has a major effect on its function.
 Low calcium levels  increases sodium movement across excitable membranes 
allowing depolarization to occur more easily and at inappropriate times.
 Acute hypocalcemia  results in the rapid onset of life-threatening manifestations, even
when the serum calcium level is not very low.
 Chronic hypocalcemia  occurs slowly overtime  excitable membrane manifestations
may not be severe because the body has adjusted to the gradual reduction of serum
calcium levels.
Common Causes of Hypocalcemia:

Actual Calcium Deficit:

 Inadequate oral intake of calcium
 Lactose intolerance
 Malabsorption syndrome
 Celiac sprue – an autoimmune disease that affects the digestive tract that interfers
with the digestion and absorption of food nutrients.
 Crohn’s disease – is an inflammatory bowel disease that may affect any part of
the GI tract.
 Inadequate intake of vitamin D
 End-stage kidney disease
 Renal failure –polyuric phase
 Diarrhea
 Steatorrhea – fatty stools and foul-smelling.
 Wound drainage (especially gastrointestinal)

Relative Calcium Deficit:

 Hyperproteinemia
 Alkalosis
 Calcium chelators or binders
 Citrate – from massive administration of citrated blood (ex: massive hemorrhage and
shock) because citrate can combine with ionized calcium and temporarily remove it from
circulation.
 Mithramycin
 Penicillamine
 Sodium cellulose phosphate (Calcibind)
 Aredia
 Acute pancreatitis – causes breakdown of protein and lipids. Calcium ions combine with
fatty acids released by lipolysis  forming soaps  causing hypocalcemia.
 Hyperphosphatemia – causes reciprocal drop of serum calcium level.
 Immobility
 Removal of obstruction of parathyroid glands – on the first 24 to 48 hours after surgery.

Clinical Manifestations;

 Diet history is important to assess for the risk of hypocalcemia. Ask the patient about his
or her intake of dietary products and whether a calcium supplement is taken regularly.
 Report of frequent painful muscle spasm (“charley horses”) in the calf or foot during rest
or sleep – one indicator of hypocalcemia.
 Other information that may indicates possible hypocalcemia: History of recent
orthopaedic surgery or bone healing; endocrine disturbances and treatment; history of
thyroid surgery, therapeutic irradiation of the upper chest and neck area, or a recent
anterior neck injury.
 Most manifestations of acute hypocalcemia are caused by overstimulation of the nerves
and muscles.

 Neuromuscular Changes:
 Tetany – is the most characteristic manifestations of hypocalcemia and
hypomagnesemia which refers to the entire symptoms complex induced by
increased neural excitability.
 Paresthesia occurs at first with sensations of tingling that affects the lips, nose
and ears and numbness.
 If hypocalcemia continues or worsen  actual muscle twitching or painful
cramps and spasms occur.
 Assess hypocalcemia by testing for Trousseau’s and Chvostek’s sign.
  Cardiovascular Changes:
 Heart rate may be slower or slightly faster than normal with a weak, thready
pulse.
 Severe hypocalcemia  severe hypotension and ECG changes of prolonged ST
interval and a prolonged QT interval.

 Intestinal Changes:
 Increased peristaltic activity  hyperactive bowel sounds.
 Painful abdominal cramping and diarrhea

 Skeletal Changes:
 Most common with chronic hypocalcemia.
 Calcium is moved from the bone storage sites  causing a loss of bone density
(Osteoporosis).
 The bones are thinner, more brittle and fragile  breaks easily with even slight
trauma.
 Vertebrae become more compact and may bend forward  leading to an overall
loss of height.
 Ask about changes in height and any unexplained bone pain.
 Observe for spinal curvatures and any unusual bumps or protrusions in
bone areas that may indicate old fractures.

Common Nursing Diagnoses and Collaborative problems:

 Acute Pain related to hypocalcemia-induced muscle spasms and hyperactive gastric

motility
 Decreased Cardiac Output related to hypocalcemia-induced dysrhythmias or reduced
myocardial contractility
 Deficient knowledge (dietary calcium) related to lack of exposure
 Risk for Injury related to bone density loss

Diagnostic Findings:

 Decreased calcium levels

 ECG changes - prolonged ST interval and a prolonged QT interval.

Medical Management:

 Acute symptomatic hypocalcemia is life-threatening and requires prompt treatment with

IV administration of a calcium salt.
 Parenteral salts include calcium gluconate, calcium chloride and calcium
gluceptate.
 Special precaution: Too-rapid IV administration of calcium can cause
cardiac arrest, preceded by bradycardia. Therefore, calcium should be
diluted in D5W and administered as a slow IV bolus or a slow IV infusion
using volumetric infusion pump.
 For patients receiving digitalis-derived medications – IV
administration of calcium is dangerous because calcium ions exert
an effect similar to that of digitalis and can cause digitalis toxicity
with adverse cardiac effects.
 A 0.9% sodium chloride solution should not be used with calcium because
they cause precipitation when calcium is added.
 Calcium replacement can cause postural hypotension  the patient is kept
in bed during IV infusion and blood pressure is monitored.
 Vitamin D may be instituted to increase calcium absorption from the GI
tract.
  Aluminum hydroxide, calcium acetate or calcium carbonate antacids may
be prescribed – to decrease elevated phosphorous levels before treating
hypocalcemia in patient with chronic renal failure.

 Increasing dietary intake of calcium to at least 1000 to 1500 mg/day in adult.

 Calcium-containing foods include: milk products; green, leafy vegetables;
canned salmon; sardines and fresh oyster.
 Hypomagnesemia can also cause tetany – if the tetany responds to
IV calcium, then a low magnesium level is considered as a possible
cause in chronic renal failure.

Nursing Management:

 Observe for hypocalcemia in at-risk patients.

 Seizure precautions if hypocalcemia is severe.
 The status of airway is closely monitored because laryngeal stridor can occur.
 Keeping emergency equipment (ex: oxygen, suction) at bedside.
 Keep emergency cart equipped with emergency drugs and endotracheal
tray.
 Padding the siderails of the bed.
 Nutrition Therapy
 High-calcium diet – for mild hypocalcemia and those with chronic conditions.
 Calcium supplements – is considered if sufficient calcium is not consumed in the
diet. Must be taken with meals.
 Environmental management is needed – because the excitable membranes of the nervous
system and the skeletal system are overstimulated in hypocalcemia.
 Interventions to reduce stimulation include:
 Keeping the room quiet
 Limiting visitors
 Adjusting the lighting
 Using a soft but reassuring voice
 Injury prevention strategies are needed – because the patient with long-standing calcium
loss may have brittle, fragile bones that fracture easily and cause little pain.
 When lifting or moving a patient with fragile bones – use a lift sheet rather than
pulling the patient.
 Observe for normal range of joint motion and for unusual surface bumps or
depressions over bony areas.
 B. CALCIUM EXCESS (HYPERCALCEMIA)

 Hypercalcemia is a total serum calcium level above 10.5 mg/dl or 2.75 mmol/L. which
is a dangerous imbalance when severe; in fact hypercalcemic crisis has a mortality rate as
high as 50% if not treated promptly.

Pathophysiology:

 Hypercalcemia is either cause by the greater amount of serum calcium that the normal
calcium-controlling mechanism (parathyroid gland) cannot cope or that one control
mechanism is not functioning properly.
 Hypercalcemia causes excitable tissues to be less sensitive to normal stimuli, thus
requiring a stronger stimulus to response.
 The excitable tissues mostly affected by hypercalcemia are: the heart, muscles, nerves,
and intestinal smooth muscles.
 Calcium is needed by many of the enzymes involved in blood clotting.
 Hypercalcemia causes faster clotting times and excessive clotting from
hypercalcemia occurs more easily in vessels with slow blood flow.

Common Causes of Hypercalcemia:

Actual Calcium Excesses

 Excessive oral intake of calcium
 Excessive oral intake of vitamin D
 Renal failure
 Use of thiazide diuretics – can cause slight elevation of calcium levels because they
potentiate the action of PTH on the kidneys  reducing urinary calcium excretion.

Relative Calcium Excesses

 Hyperparathyroidism – causes increased released of calcium from the bones and
increased intestinal and renal absorption of calcium.
 Malignancy – are the most common causes of hypercalcemia.
 Direct invasion (cancer of the breast, lung, prostate and osteoclastic bone and
multiple myeloma)
 Indirect resorption ( liver cancer, small cell lung cancer and cancer of the adrenal
glans)
 Hyperthyroidism
 Immobility – causes elevation of total (especially ionized) calcium in the bloodstream.
 Use of glucocorticoids
 Dehydration

Clinical Manifestations:

 The manifestations of hypercalcemia are related to severity and how quickly the
imbalances occur.
 The patient with mild but rapidly occurring calcium excess usually has more severe
problems than the patient whose imbalance is severe but has developed slowly.

 Cardiovascular Changes – are the most serious and life-threatening problems of

hypercalcemia.
 Mild hypercalcemia – at first causes increased heart rate and blood pressure.
 Severe or prolonged calcium imbalance – Slowed heart rate because it depresses
electrical conduction.
 Measure pulse rate and blood pressure.
 Cyanosis and pallor – it indicates a poor tissue blood flow.
 Examine ECG tracings for dysrhythmias, especially a shortened
QT interval.
  Assess for slowed or impaired blood flow – hypercalcemia allows blood clot to
form more easily whenever blood flow is poor. Blood clotting is more likely in
the lower legs, the pelvic region, areas where blood flow is blocked by internal or
external constrictions, and areas where venous obstruction occurs.
 Measure and record calf circumference.
 Assess for temperature, color and capillary refill to determine the
blood flow to and from the area.

 Neuromuscular Changes:
 Severe muscle weakness and decreased deep tendon reflexes with paresthesia.
 Bone pain may also be present.
 Patient may have an altered level of consciousness that can range from confusion,
impaired memory, slurred speech, and lethargy to coma.
 Mild psychotic behaviour or problems can occur also.

 Intestinal Changes – are first reflected as decreased peristalsis.

 Constipation
 Anorexia, nausea, vomiting and abdominal pain are common  Dehydration.
 Bowel sounds are hypoactive or absent.
 Abdomen increases in size – because the intestinal contents remain in the tract
instead of moving forward.
 Assess abdominal size by measuring abdominal girth.

 Renal Changes:
 Excessive urination – due to disturbed renal tubular function produced by
hypercalcemia.
 Severe thirst may occur with polyuria secondary to high calcium load.

 Chronic hypercalcemia  they may develop symptoms similar to peptic ulcer disease
because hypercalcemia increases the secretion of hydrochloric acid and pepsin in the
stomach.
 The more severe symptoms tend to appear when serum calcium level is approximately
16 mg/dL (4 mmol/L) or higher. However, some patients become profoundly disturbed
with serum calcium levels of only 12 mg/dL (3 mmol/L).
 These symptoms can be resolved once serum calcium levels return to normal
after treatment.
 Hypercalcemic Crisis – refers to an acute rise in the serum calcium levels to 17 mg/dL
(4.3 mmol/L) or higher.
 Severe thirst and polyuria are often present.
 Muscle weakness, intractable nausea, abdominal cramps, constipation, or
diarrhea, peptic ulcer symptoms, bone pain, lethargy, coma, and confusions 
This condition is very dangerous and may result to cardiac arrest.

Assessment and Diagnostic Findings:

 Serum calcium level is greater than 10.2 mg/dL (2.6 mmol/L)

 Cardiovascular changes – include dysrhythmias (ex. Heart block) and shortening of QT
intervals and ST segments. PR interval is sometimes prolonged.
 Double-antibody PTH test may be used to differentiate between primary
hyperparathyroidism and malignancy as a cause of hypercalcemia.
 Increased PTH levels – indicates primary or secondary hyperparathyroidism and
suppressed in malignancy.
 X-rays may reveal bone changes if the patient has hypercalcemia secondary to
malignancy, bone cavitation and renal calculi.
Medical Management:

 Therapeutic management for hypercalcemia include: decreasing the serum calcium

level and reversing the process causing hypercalcemia.
 Treating the underlying cause (ex. Chemotherapy for malignancy, partial
parathyroidectomy for hyperparathyroidism) is essential.

 Pharmacologic Therapy:
 IV administration of 0.9% sodium chloride solution – temporarily dilutes the
serum calcium and increases urinary calcium excretion.
 Administering IV phosphate – can cause a reciprocal drop in serum calcium.
 Furosemide (Lasix) – often used in conjunction with administration of saline
solution by causing diuresis and it increases calcium excretion.
 Often overlooked, fluids and medications that contain calcium and dietary
sources of calcium should be stopped. (D/C IV with calcium ex: PLR).
 Calcitonin – can be used to lower the serum calcium level and is particularly
useful for patients with heart disease or renal failure who cannot tolerate large
sodium loads.
 Although several forms are available, calcitonin derived from salmon is
commonly used. ( Skin testing for allergy to salmon calcitonin is
necessary before the hormone is administered)  systemic allergic
reactions are possible because this hormone is protein; resistance to the
medication may develop later because of antibody formation.
 Calcitonin is administered by intramuscular (IM) injection rather than
subcutaneously – because patients with hypercalcemia have poor
perfusion of subcutaneous tissue.
 For patient with cancer – treatment is directed at controlling the condition by:
 Surgery
 Chemotherapy
 Radiation therapy
 Corticosteroids – may be used to decreased bone turnover and tubular
reabsorption (ex: patients with myelomas, lymphomas and leukemias).
 Mithramycin – a cytotoxic antibiotic inhibits bone resorption thus lowers serum
calcium levels.
 Inorganic phosphate salts (Phospho-Soda, Neutra-Phos) can be administered
orally or by NGT.
 Dialysis – for life-threatening hypercalcemia.

Nursing Management:

 Interventions for hypercalcemia aim to reduce serum calcium levels through drug therapy
and dialysis.
 It is important to monitor hypercalcemia in at-risk patients.
 Rehydration and cardiac monitoring are also important.
 Increasing patient mobility and increasing fluids – can help prevent
hypercalcemia or at least minimize its severity.
 Hospitalized patients at risk for hypercalcemia should be encouraged to ambulate
as soon as possible.
 Outpatients – are instructed about the importance of frequent ambulation.
 Oral fluids
 The nurse should consider the patient’s likes and dislikes.
 Fluids containing sodium should be administered unless contraindicated –
because sodium assists with calcium excretion.
 Encouraged patient to drink at least 3 to 4 quarts of fluid daily.
 Adequate fiber in the diet – to offset the tendency for constipation.
  Safety precautions are implemented as necessary, when mental symptoms are
present.
 The patient and family are informed that these mental changes are
reversible with treatment.

 Drug therapy
 Preventing increases in calcium, as well as drugs to lower calcium levels.
 IV solutions containing calcium (ex: Ringer’s Lactate) are stopped.
 Oral drugs containing calcium or vitamin D (ex: calcium-based antacids)
are discontinued.
 IV normal saline (0.9% sodium chloride) – as fluid volume replacement which
can help restore normal serum calcium levels because sodium increases kidney
excretion of calcium.
 Thiazide diuretics are discontinued and replaced with diuretics that enhance the
excretion of calcium such as furosemide, (Lasix, Furoside).
 Calcium chelators (calcium-binders) such as plicamycin (Mithracin) and
penicillamine (Cuprimine, Pedramine) – helps lower serum calcium levels.
 Drugs to prevent hypercalcemia include agents that inhibit resorption from bones
such as phosphorous, calcitonin (Calcimar), biphosphonates (etidronate) and
prostaglandin synthesis inhibitors (aspirin, NSAIDs).

 Dialysis – is used when severe hyperglycemia causes life-threatening cardiac problems

and drug therapy may not reduce serum calcium levels fast enough to prevent death.
 Prepare patient for a possible hemodialysis or blood ultrafiltration (a procedure
used to treat fluid overload (extra fluid and salts) in the body – used for rapid
calcium reduction.

 Cardiac monitoring – because increased calcium increases the effects of digitalis

(Digoxin).
 Assess for signs and symptoms of digitalis toxicity such as confusion,
irregular pulse, loss of appetite, nausea and vomiting, diarrhea,
palpitations and vision changes (blurred vision, blind spots).
- Other symptoms such as decreased consciousness, decreased urine
output, difficult breathing when lying down, excessive nighttime
urination and overall swelling.
 Identify dysrhythmias and decreased cardiac output.
 Compare recent ECG tracings with the patient’s baseline tracings.
 Look for changes in T waves and the QT interval and changes in rate and
rhythm.