Sodium

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Na

Sodium (Na+) is the dominant electrolyte in the ECF. Sodium is the chief base of the
blood. The normal serum level is 135-145 mEq/L.

Na+ affects the fluid volume of the ECF and is regulated, in part, by:
 aldosterone
 renal blood flow

 renin secretion
 antidiuretic hormone (ADH) due to its effect on water
 estrogens
 carbonic anhydrase enzyme

Sodium (Na+) and potassium (K+) exchange with hydrogen (H+) in the kidney tubule to
maintain electrolyte and acid-base balance.

The regulation of the body’s water and electrolyte status by the kidneys is influenced
by the ECF sodium concentration.

Sodium does not cross the cell membrane easily. The sodium pump is required to
provide the energy to move sodium across the membrane.

Sodium has important physiologic functions including:

 neuromuscular irritability
 conduction of nerve impulses and muscle contraction
 osmotic pressure of the ECF
 acid-base balance
 water balance
 gland secretions
Sodium is the determinant of the osmolality (tonicity) of body fluids since it is the main
cation in the ECF.

Imbalances in which the gain or loss of fluid and sodium occur together in equal
proportions are referred to as isotonic, or isoosmolar, fluid imbalance.

This content is discussed in the section of this program called Fluid Imbalances.

Sodium imbalances are referred to as osmolar imbalances. There is either too much
or too little sodium in relation to the amount of water. The terms are
therefore hyperosmolar or hypoosmolar.

Hypernatremia and hyponatremia are terms which also are used to reflect sodium
levels.

Hyponatremia
It is due to sodium loss (solute deficit) or water gain. This is a hypoosmolar state.

The result of the hypoosmolar imbalance is that water leaves the ECF and moves into
the cell, causing cell swelling.

Hyponatremia with water excess results from:


 excess intake of water/forcing hypotonic fluids
 inability of kidneys to excrete water (renal failure)

 retention of water (as in heart failure or cirrhosis of the liver)


 excess tap water enemas
 excess intravenous fluids of dextrose in water
 SIADH (syndrome of inappropriate antidiuretic hormone secretion)

True hyponatremia is relatively uncommon. The hypoosmolar state where there is


hyponatremia with dehydration (sodium deficit in excess of water) result from:
 poor salt intake

 diuretic drugs which cause Na+ loss


 burn wounds or wound drainage
 cystic fibrosis
 adrenal insufficiency (Na+ lost in urine)
 fluid loss replaced with water only
 salt wasting nephritis
 excessive gastrointestinal loss
o loss of bile
o nasogastric suction along with ice chips or water by mouth
o using water only for NG tube irrigations

Manifestations of hyponatremia (hypoosmolar state) where there is reduced Na+ and


excess water reflect failure of swollen cells to transmit electrical impulses.
Neurological symptoms are due to cerebral edema and altered nerve conduction.
Findings include:
 serum Na+ < 1.35 mEq/L
 mental confusion, headache

 altered levels of consciousness, coma


 hyperirritability, anxiety
 tremors, seizures
 hyperreflexia, muscles weakness, twitching
 nausea, vomiting: abdominal cramps
 edema and weight gain

Clinical findings in hyponatremia with dehydration include those of hypovolemia:


 serum Na+ < 1.35 mEq/L
 hypotension

 tachycardia
 cold, clammy skin
 decreased skin turgor
 dry mucous membranes
 weight loss
 seizures, hyperirritability

The treatment for a hyponatremia (hypoosmolar) state is to:


 treat the cause first

 restrict oral and intravenous water intake


 increase dietary sodium
 change IV fluids to normal saline
In a hyperosmolar state, there is too much sodium in relation to the amount of water.
There will either be a deficit of body fluid with hypernatremia or hypernatremia in
excess of the amount of water.

In either case, the ECF becomes hypertonic, water leaves the cell and the cell
shrinks.

Causes for hyperosmolar imbalance where there is hypernatremia and fluid deficit
include situations when water loss exceeds sodium loss or when there is inadequate
water intake. Such situations could include:
 decreased water intake due to:

o Inability to swallow
o mental confusion, loss of consciousness
o debilitated state
o anorexia, depressed thirst mechanism
o inability to communicate need for water
 excessive water loss, without sodium loss, through burn wounds, sweating,
mechanical ventilation, coughing, polyuria
 failure of kidney to reabsorb water
 diabetes insipidus
 Cushing's syndrome
 renal tubular disease
 excessive use of osmotic diuretics

Another hyperosmolar imbalance is that where there is excess Na+ in relation to the
amount of water. This imbalance represents a gain of sodium without water loss.
Water will pour out of cells into the ECF. Causes of this form of hypernatremia
include:
 excess sodium containing intravenous solutions

 excess salt intake

The indication of a hyperosmolar imbalance include:


 serum sodium level > 145 mEq/L, serum osmolarity > 295 mOsm/kg

 intense thirst
 dry, sticky mucous membranes, dry, rough, red tongue
 flushed, dry skin, poor skin turgor
 oliguria
 low-grade fever
 weakness, lethargy which can progress to coma
 irritability, agitation, convulsions, tremors
 increased deep tendon reflexes, nuchal rigidity
 circulatory overload, shock, respiratory distress and renal failure can occur if the
hyperosmolar state continues

Treatment of hypernatremia, hyperosmolar states, includes:


 gradual reduction of serum sodium to prevent cerebral edema

 us D5 / ¼ % or .45% saline solution (avoids overcorrection causing deficit)


 monitor urine output and serum sodium levels
 administer fluids cautiously
 restrict sodium intake

Prevention of the problem is the best treatment. Remember, if a person is unable to


ask for fluids, or obtain fluids themselves-think of hypernatremia.

The person who experiences extreme thirst, who can obtain fluids will not develop
hypernatremia.

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