Lesson 4: Electrolyte Imbalances

Wendyl A. Recaña, RN, MAN

Electrolyte Imbalances
� Disturbances in electrolyte balances occur in clinical
practice and must be corrected for the patient’s health and
safety.
 TEST   DISORDER
SERUM SODIUM ↑ 145 mEq/L Hypernatremia
135 – 145 mEq/L ↓ 135 mEq/L Hyponatremia
SERUM POTASSIUM ↑ 5.0 mEq/L Hyperkalemia
3.5 – 5.3 mEq/L ↓ 3.5 mEq/L Hypokalemia
SERUM MAGNESIUM ↑ 2.7 mg/dL Hypermagnesemia
1.8 – 2.7 mg/dL ↓ 1.8 mg/dL Hypomagnesemia
SERUM CALCIUM ↑ 10.5 mg/dL Hypercalcemia
8.5 – 10.5 mg/dL ↓ 8.5 mg/dL Hypocalcemia
SERUM PHOSPHORUS ↑ 4.5 mg/dL Hyperphosphatemia
2.5 – 4.5 mg/dL ↓ 2.5 mg/dL Hypophosphatemia

SERUM CHLORIDE ↑ 108 mEq/L Hyperchloremia

96 - 106 mEq/L ↓ 96 mEq/L Hypochloremia
 SIGNIFICANCE OF SODIUM

Normal Sodium Level:135-145 mEqs/L or mmol/L

SIGNIFICANCE OF SODIUM
�Sodium is the most abundant electrolyte in the ECF; its
concentration ranges from 135 to 145 mEq/L (135-145
mmol/L).
�Consequently, sodium is the primary determinant of ECF
osmolality. Decreased sodium is associated with parallel
changes in osmolality.
�Due to its abundance and high concentration, sodium’s
primary role is controlling water distribution throughout
the body.
SIGNIFICANCE OF SODIUM
�In addition, sodium is the primary regulator of ECF
volume.

�Controlling water distribution throughout the body.

�A loss or gain of sodium is usually accompanied by a loss

or gain of water.
 SODIUM DEFICIT
(HYPONATREMIA)
Normal Sodium Level:135-145 mEqs/L or mmol/L
SODIUM DEFICIT (HYPONATREMIA)
�Hyponatremia refers to a serum sodium level that is below
normal (less than 135 mEq/L or 135 mmol/L]).
�Plasma sodium concentration represents the ratio of total
body sodium to total body water.

�A decrease in this ratio can occur:

� Low quantity of total body sodium with a lesser reduction in
total body water (Fluid Volume Deficit)
� Normal total body sodium content with excess total body water
(Fluid Volume Excess)
� Excess of total body sodium with an even greater excess of
total body water (Fluid Volume Excess)
SODIUM DEFICIT (HYPONATREMIA)
�Sodium may be lost by way of:
� Vomiting
� Diarrhea
� Fistulas
� Sweating
� associated with the use of diuretics particularly in combination
with a low-salt diet.
� A deficiency of aldosterone, as occurs in adrenal insufficiency,
also predisposes the patient to sodium deficiency.
�Fistulas
Dilutional Hyponatremia
�Predisposing conditions for this type of hyponatremia
include:
� Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
� Hyperglycemia
� Increased water intake through the administration of
electrolyte-poor parenteral fluids (D5W)
� The use of tap-water enemas
� Irrigation of nasogastric tubes with water instead of normal
saline solution
� It may also be gained by compulsive water drinking
(psychogenic polydipsia)
Syndrome of Inappropriate Antidiuretic
Hormone (SIADH)
�The basic physiologic disturbances in SIADH are
excessive ADH activity.
�With water retention and dilutional hyponatremia, and
inappropriate urinary excretion of sodium in the presence
of hyponatremia.
�Causes:
� Sustained secretion of ADH by the hypothalamus
� Production of an ADH-like substance from a tumor (aberrant
ADH production).
Clinical Manifestations
�Clinical manifestations of hyponatremia depend on the
cause, magnitude, and speed with which the deficit
occurs.
� Poor skin turgor
� Dry mucosa
� Decreased saliva production
� Orthostatic fall in blood pressure
� Nausea
� Abdominal cramping occur
Clinical Manifestations
�Neurologic changes:
� Altered mental status, are probably related to the cellular
swelling and cerebral edema associated with hyponatremia.
� As the extracellular sodium level decreases, the intracellular
fluid becomes relatively more concentrated and pulls water into
the cells
Clinical Manifestations
�In general, patients with an acute decrease in serum
sodium levels have more severe symptoms and higher
mortality rates than do those with more slowly developing
hyponatremia.

�Features of hyponatremia associated with sodium loss and

water gain include:
� Anorexia
� Muscle cramps
� Feeling of exhaustion
Dilutional Hyponatremia
�Due to water intoxication, the patient’s serum sodium
level is diluted by an increase in the ratio of water to
sodium.
�This causes water to move into the cell, so that the patient
develops an ECF volume excess.
�When the serum sodium level drops below 115 mEq/L
(115 mmol/L) signs of increasing intracranial pressure
such as:
� Lethargy
� Confusion
� Muscle twitching
� Focal weakness
� Hemiparesis
� Papilledema
� and seizures, may occur.
Medical Management
�SODIUM REPLACEMENT
� The obvious treatment for hyponatremia is careful
administration of sodium by mouth, nasogastric tube, or the
parenteral route.
� For patients who can eat and drink, sodium is easily replaced,
be-cause sodium is consumed abundantly in a normal diet.
� For those who cannot consume sodium, lactated Ringer’s
solution or iso-tonic saline (0.9% sodium chloride) solution
may be prescribed.
Medical Management
�SODIUM REPLACEMENT
� Sodium must not be increased by greater than 12 mEq/L in 24
hours, to avoid neurologic damage due to osmotic
demyelination and may lead to coma.
Medical Management
�WATER RESTRICTION
� Normal or excess fluid volume, hyponatremia is treated by
restricting fluid to a total of 800 mL in 24 hours.
� It may be necessary to administer small volumes of a
hypertonic sodium solution, such as:
� 3% sodium chloride - contains 513 mEq of sodium
� 5% sodium chloride - contains 855 mEq of sodium.
*Incorrect use of these fluids is extremely dangerous.

� Furosemide to remove excess fluid

� Monitor client in ICU
Medical Management
�If edema exists alone, sodium is restricted
�If edema and hyponatremia occur together, both sodium
and water are restricted.
Nursing Management
�The nurse needs to identify patients at risk for
hyponatremia so that they can be monitored. Early
detection and treatment of this disorder are necessary to
prevent serious consequences.
�For patients at risk, the nurse monitors:
� Fluid intake and output
� Daily body weights
� Abnormal losses of sodium or gains of water are noted.
Nursing Management
�GI manifestations, such as:
� Anorexia
� Nausea
� Vomiting and abdominal cramping, are also noted.
�Central nervous system changes, such as:
� Lethargy
� Confusion
� Muscle twitching
� Seizures.
 SODIUM EXCESS
(HYPERNATREMIA)
Normal Sodium Level:135-145 mEqs/L or mmol/L
SODIUM EXCESS (HYPERNATREMIA)
�Hypernatremia is a higher than normal serum sodium
level (exceeding 145 mEq/L [145 mmol/L]).
�Caused by:
� a gain of sodium in excess of water (FVE), or
� by a loss of water in excess of sodium (FVD).

�As a result, the serum sodium concentration increases and

the increased concentration pulls fluid out of the cell.
Pathophysiology
�A common cause of hypernatremia is fluid deprivation in
unconscious patients who cannot perceive, respond to, or
communicate their thirst (Adrogue & Madias, 2000a).

�Most often affected in this regard are very old, very

young, and cognitively impaired patients.

�Administration of hypertonic enteral feedings without

adequate water supplements leads to hypernatremia.
Pathophysiology
�Watery diarrhea and greatly increased insensible water
loss. (eg, hyperventilation, denuding effects of burns).

�Diabetes insipidus, a deficiency of ADH from the

posterior pituitary gland, leads to hypernatremia if the
patient does not experience, or cannot respond to, thirst or
if fluids are excessively restricted.
Pathophysiology
�Less common causes are:
� Heat stroke
� Near drowning in sea water (which contains a sodium
concentration of approximately 500 mEq/L)
� Malfunction of either hemodialysis or peritoneal dialysis
proportioning systems.
� IV administration of hypertonic saline or excessive use of
sodium bicarbonate also causes hypernatremia.
Clinical Manifestations
�The clinical manifestations of hypernatremia are primarily
neurologic and are presumably the consequence of
cellular dehydration (Adrogue & Madias, 2000a).
Clinical Manifestations
�Moderate Hypernatremia:
� Restlessness and weakness

�Severe Hypernatremia:
� Disorientation,
� Delusions
� Hallucinations
Clinical Manifestations
�Dehydration (resulting in hypernatremia) is often
overlooked as the primary reason for behavioral changes
in the elderly patient.
�If hypernatremia is severe, permanent brain damage can
occur (especially in children).
�Brain damage is apparently due to sub-arachnoid
hemorrhages that result from brain contraction.
Clinical Manifestations
�A primary characteristic of hypernatremia is thirst.
�Thirst is so strong a defender of serum sodium levels in
healthy people that hypernatremia never occurs unless the
person is unconscious or is denied access to water.
Clinical Manifestations
�Rapid Onset
� Severe Vomiting
� Excessive Sweating (diaphoresis)
� Poorly tolerated

�Slow Onset
� CHF, Renal failure
� Cushing’s syndrome
� Excessive salt intake
� Poor water intake
� Fluids shifts massive
What Do You See? FRIED SALT
�Fever (low grade)
�Restless (irritable)
�Increased fluid retention and increased blood pressure
�Edema (peripheral and pitting)
�Decreased Urinary output, dry mouth
�Skin flushed
�Agitation
�Low grade fever
�Thirst
Medical Management
�Hypernatremia treatment consists of a gradual lowering of
the serum sodium level by the infusion of a hypotonic
electrolyte solution (eg, 0.3% sodium chloride) or an
isotonic nonsaline solution(eg, D5W).
�Correct underlying disorder
�Gradual fluid replacement
�Monitor for cerebral edema
�Monitor serum Na+ level
�Seizure precautions
Nursing Management
�Monitor patient’s neurological status
�Monitor vital signs
�Monitor I&O
�Daily weights
�IV replacement
�Administration of ordered medications
�Assess oral membranes and skin integrity
SIGNIFICANCE OF POTASSIUM

Normal Value: 3.5 – 5.3 mEq/L

SIGNIFICANCE OF POTASSIUM
�Potassium is the major intracellular electrolyte;
� 98% of the body’s potassium is inside the cells
� 2% is in the ECF, and it is this 2% that is important in
neuromuscular function

�Potassium influences both skeletal and cardiac muscle

activity.
� Alterations in its concentration change myocardial irritability
and rhythm.
SIGNIFICANCE OF POTASSIUM
�To maintain potassium balance, the renal system must
function because:
� 80% of the potassium is excreted daily from the body by way
of the kidneys
� 20% is lost through the bowel and in sweat.
POTASSIUM DEFICIT
(HYPOKALEMIA)
Normal Value: 3.5 – 5.3 mEq/L
POTASSIUM DEFICIT (HYPOKALEMIA)
�Hypokalemia (below normal serum potassium
concentration)
�Hypokalemia may occur in patients with normal
potassium stores; however:
� when alkalosis is present, a temporary shift of serum potassium
into the cells occurs.

�Can be caused by GI losses, diarrhea, insufficient intake,

non-K+ sparing diuretics (thiazide, furosemide)
POTASSIUM DEFICIT (HYPOKALEMIA)
�Hyperaldosteronism increases renal potassium wasting.
Primary hyperaldosteronism is seen in patients with
adrenal adenomas.

�Hyperinsulinemia - insulin promotes the entry of

potassium into skeletal muscle and hepatic cells.
What Do You See?
�Think S-U-C-T-I-O-N
�Skeletal muscle weakness
�U wave (EKG changes)
� Constipation, ileus
� Toxicity of digitalis glycosides
� Irregular, weak pulse
� Orthostatic hypotension
� Numbness (paresthesia)
Assessment and Diagnostic Findings
�In hypokalemia, the serum potassium concentration is less
than the lower limit of normal.

�Electrocardiographic (ECG) changes can include flat T

waves and/or inverted T waves, suggesting ischemia, and
depressed ST segments.

�An elevated U wave is specific to hypokalemia.

Assessment and Diagnostic Findings
�An elevated U wave is specific to hypokalemia.
Medical Management
�Potassium loss must be corrected daily; administration of
40 to 80 mEq/day of potassium is adequate in the adult if
there are no abnormal losses of potassium.

�For patients at risk for hypokalemia, a diet containing

sufficient potassium should be provided. Dietary intake of
potassium in the average adult is 50 to 100 mEq/day.
Medical Management
�Thorough history taking.
�If the etiology of the loss is unclear, a 24-hour urinary
potassium excretion test can be performed to distinguish
between renal and extrarenal loss.

�Urinary potassium excretion exceeding 20 mEq/24 h with

hypokalemia suggests that renal potassium loss is the
cause.
Medical Management
�What Do We Do?
� Increase dietary K+
� Oral KCl supplements – mild loss of potassium
� IV K+ replacement – severe loss of potassium
� Change to K+-sparing diuretic
� Monitor EKG changes

�REMINDER IV K+ Replacement ()
� Mix well when adding to an IV solution bag
� Concentrations should not exceed 40-60 mEq/L
� Rates usually 10-20 mEq/hr
Nursing Management
�Assess signs of irritability and paresthesia
�Assess cardiac status
� Monitor heart rate and rhythm for irregularities
�Monitor I&O
�Monitor electrolyte status closely
�Follow strict guidelines for replacing potassium via
IV
POTASSIUM EXCESS
(HYPERKALEMIA)
Normal Value: 3.5 – 5.3 mEq/L
POTASSIUM EXCESS (HYPERKALEMIA)
�Hyperkalemia (greater than normal serum potassium
concentration) seldom occurs in patients with normal
renal function.
�It is often due to iatrogenic (treatment-induced) causes.

�More dangerous because cardiac arrest is more frequently

associated with high serum potassium levels.
POTASSIUM EXCESS (HYPERKALEMIA)
�The major cause of hyperkalemia is decreased renal
excretion of potassium.

�Caused by altered kidney function, excessive potassium

supplements, blood transfusions, meds (K+-sparing
diuretics), cell death (injury/trauma)
Clinical Manifestations
�Irritability
�Paresthesia
�Muscle weakness (especially legs)
�EKG changes (tall T wave)
�Nausea, abdominal cramps, diarrhea
Clinical Manifestations
SIGNIFICANCE OF MAGNESIUM

Normal Value: 1.8 – 2.7 mg/dL

SIGNIFICANCE OF MAGNESIUM
�Next to potassium, magnesium is the most abundant
intracellular cation.
�It acts as an activator for many intracellular enzyme
systems and plays a role in both carbohydrate and protein
metabolism.
�Magnesium exerts effects on the cardiovascular system,
acting peripherally to produce vasodilation.
�Regulates muscle contractions
 MAGNESIUM
DEFICIT(HYPOMAGNESEMIA)
Normal Value: 1.8 – 2.7 mg/dL
MAGNESIUM
DEFICIT(HYPOMAGNESEMIA)
�Hypomagnesemia refers to a below normal serum
magnesium concentration.
�Causes:
� Loss of magnesium from the GI tract may occur with
nasogastric suction, diarrhea, or fistulas.
� Lower GI tract has a higher concentration of magnesium than
fluid from the upper tract, diarrhea and intestinal fistulas are
more likely to induce magnesium deficit than nasogastric
suctioning.
MAGNESIUM
DEFICIT(HYPOMAGNESEMIA)
�Causes:
Decreased Intake Decreased Absorption Excessive Loss

Alcoholism Bulimia/purging Diuresis

Anorexia Laxatives Diabetic Ketoacidosis

Hyperalimentaion Chronic Diarrhea Hyperparathyroidism

  Nasogastric drainage Burns/wounds

Clinical Manifestations
� Hypomagnesemia may be accompanied by marked
alterations in mood, such as:
� Apathy
� Depression
� Apprehension
� Extreme agitation
� Ataxia
� Dizziness
� Insomnia
� Confusion
� Delirium
� Auditory or visual hallucinations and frank psychoses may occur
� Altered LOC
Clinical Manifestations
�Neuromuscular:
� Muscle weakness
� Leg/foot cramps
� Hyper deep tendons reflexes
� Chvostek’s & Trousseau’s signs
Clinical Manifestations
Clinical Manifestations
�Cardiovascular
� Tachycardia
� Hypertension
� EKG changes
�Gastrointestinal
� Dysphagia
� Anorexia
� Nausea/vomiting
Medical Management
�Mild
� Dietary replacement
�Severe
� IV or IM magnesium sulfate
�Monitor
� Neuro status
� Cardiac status
� Safety
Medical Management
�Mag Sulfate Infusion
� Use infusion pump - no faster than 150 mg/min
� Monitor vital signs for hypotension and respiratory distress
� Monitor serum Mg++ level q6h
� Cardiac monitoring
� Calcium gluconate as an antidote for over dosage
Nursing Management
�Difficulty in swallowing (dysphagia) may occur in
magnesium-depleted patients, the ability to swallow
should be tested with water before oral medications or
foods are offered.
�Assess level of consciousness
�Evaluate for muscle weakness
�Evaluate for hyperirritable nerves and deep tendon
reflexes
�Assess for potential seizures
�Respiratory Airway
�Monitor cardiac status
 MAGNESIUM
EXCESS(HYPERMAGNESEMIA)
Normal Value: 1.8 – 2.7 mg/dL
MAGNESIUM
EXCESS(HYPERMAGNESEMIA)
�Hypermagnesemia is a greater-than-normal serum
concentration of magnesium.
�The most common cause of hypermagnesemia is renal
failure.
�Hypermagnesemia can occur in a patient with untreated
diabetic ketoacidosis when catabolism causes the release
of cellular magnesium that cannot be excreted because of
profound fluid volume depletion and resulting oliguria.
MAGNESIUM
EXCESS(HYPERMAGNESEMIA)
�Increased serum magnesium levels can also occur in:
� Adrenocortical insufficiency
� Addison’s disease, or hypothermia.
� Excessive use of antacids (eg, Maalox, Riopan, Mylanta) and
laxatives (Milk of Magnesia) also increases serum magnesium
levels.
Clinical Manifestations
�Mildly elevated levels:
� lowered blood pressure due to peripheral vasodilation.
� Nausea, vomiting, soft tissue calcifications, facial flushing, and
sensations of warmth may also occur.

�Higher magnesium concentrations:

� Lethargy
� Difficulty speaking (dysarthria)
� Drowsiness
� Deep tendon reflexes (DTR) are lost, and muscle weakness and
paralysis may develop.
Clinical Manifestations
�Greatly elevated and not treated:
� Coma
� Atrioventricular heart block
� Cardiac arrest
Medical Management
�Avoiding the administration of magnesium to patients
with renal failure.
�Increased fluids if renal function normal
�Loop diuretic if no response to fluids
�Calcium gluconate for toxicity
�Mechanical ventilation for respiratory depression
�Hemodialysis (Mg++-free dialysate)
Nursing Management
� Monitor cognitive status
� Assess vital signs and cardiac status
� Check for muscle weakness and deep tendon reflexes
� Observe flushed skin and diaphoretic appearance
� Monitor serum electrolyte and fluid balance closely as
ordered