NCM 112: Fluids and Electrolytes

1st Semester A/Y 2020-2021

Activity No. 1

Fluid Volume Disturbances:

FVD results from loss of body fluids and occurs more Deficient fluid volume r/t inadequate
Hypovolemia or Fluid volume deficit (FVD)
rapidly when coupled with decreased fluid intake fluid intake as evidenced by acute weight
occurs when loss of ECF volume exceeds the
alone if the decreased intake is prolonged. loss and oliguria.
intake of fluid.
Hypervolemia or Fluid volume excess (FVE) Fluid volume overload r/t excessive
refers to an isotonic expansion of the ECF FVE may be related to simple fluid overload or sodium-containing fluid intake as
caused by the abnormal retention of water and diminished function of the homeostatic mechanisms evidenced by edema in lower
sodium in approximately the same proportions responsible for regulating fluid balance. extremities.
in which they normally exist in the ECF.
Hyponatremia primarily occurs due to an imbalance
Electrolyte Imbalances: of water rather than sodium. The urine sodium value
Deficient serum sodium level secondary
Hyponatremia or Sodium deficit refers to a assists in differentiating renal from nonrenal causes
to use of diuretics as evidenced by
serum sodium level that is less than 135 of hyponatremia. Low urine sodium occurs as the
anorexia, nausea, and vomiting.
mEq/L (135 mmol/L). kidney retains sodium to compensate for nonrenal
fluid loss.
Hypernatremia can be caused by a gain of sodium in
excess of water or by a loss of water in excess of Serum sodium level excess secondary to
Hypernatremia or Sodium excess a
sodium. With a water loss, the patient loses more water deprivation as evidenced by thirst,
serum sodium level higher than 145 mEq/L
water than sodium; as a result, the serum sodium elevated body temperature, and
(145 mmol/L).
concentration increases and the increased lethargy.
concentration pulls fluid out of the cell.
 Hypokalemia it may occur in patients with normal
potassium stores: When alkalosis (high blood pH) is
present, a temporary shift of serum potassium into
the cells occurs.

Hypokalemia or Potassium deficit serum Vomiting and gastric suction frequently lead to Deficient serum potassium deficit
potassium level below 3.5 mEq/L (3.5 hypokalemia, because potassium is lost when gastric secondary to vomiting and gastric
mmol/L); usually indicates a deficit in total fluid is lost and because potassium is lost through the suction as evidenced by fatigue and
potassium stores kidneys in response to metabolic alkalosis. muscle weakness.

Because relatively large amounts of potassium are

contained in intestinal fluids, potassium deficit occurs
frequently with diarrhea, which may contain as much
potassium as 30 mEq/L.
In older adults, there is an increased risk of
hyperkalemia due to decreases in renin and
aldosterone as well as an increased number of
comorbid cardiac conditions.

Hyperkalemia or Potassium excess Major causes of hyperkalemia are decreased renal

(serum potassium level greater than 5 mEq/L [5 excretion of potassium, rapid administration of Risk for electrolyte imbalance r/t
mmol/L]) seldom occurs in patients with potassium, and movement of potassium from the ICF metabolic acidosis
normal renal function compartment to the ECF compartment.

Hyperkalemia is commonly seen in patients with

untreated kidney injury, particularly those in whom
potassium levels increase as a result of infection or
excessive intake of potassium in food or medications

Hypocalcemia or Calcium deficit serum
calcium value lower than 8.6 mg/dL
(2.15 mmol/L)
Older adults and those with disabilities, who spend an
increased amount of time in bed, have an increased Risk for electrolyte imbalance r/t
risk of hypocalcemia, because bed rest increases hypoparathyroidism
bone resorption.
Not only is hypocalcemia associated with thyroid and
parathyroid surgery, but it can also occur after radical
neck dissection and is most likely in the first 24 to 48
hours after surgery.
Transient hypocalcemia can occur with massive
administration of citrated blood (i.e., massive
hemorrhage and shock), because citrate can combine
with ionized calcium and temporarily remove it from
the circulation.
Inflammation of the pancreas causes the breakdown
of proteins and lipids. It is thought that calcium ions
combine with the fatty acids released by lipolysis,
forming soaps. As a result of this process,
hypocalcemia occurs and is common in pancreatitis.
Hypocalcemia may be related to excessive secretion
of glucagon from the inflamed pancreas, which
results in increased secretion of calcitonin.

Hypercalcemia or Calcium excess
(serum calcium value greater than 10.2 mg/dL
[2.6 mmol/L]) is a dangerous imbalance when
severe
Hypomagnesemia or Magnesium deficit
a below-normal serum magnesium
concentration (1.3 mg/dL [0.62 mmol/L])
Malignant tumors can produce hypercalcemia by
various mechanisms. The excessive PTH secretion
associated with hyperparathyroidism causes
increased release of calcium from the bones and Serum calcium level excess secondary to
increased intestinal and renal absorption of calcium. prolonged immobilization as evidenced
by muscular weakness and constipation
Bone mineral is lost during immobilization, and
sometimes this causes elevation of total (and
especially ionized) calcium in the bloodstream.
An important route of magnesium loss is the GI tract; Serum magnesium level deficiency
such loss can occur with nasogastric suction, diarrhea, secondary to diabetic ketoacidosis as
or fistulas. Because fluid from the lower GI tract has a evidenced by (+) Troussea’s and
higher concentration of magnesium (10 to 14 mEq/L) Chvostek’s signs
than fluid from the upper tract (1 to 2 mEq/L), losses
from diarrhea and intestinal fistulas are more likely to
induce magnesium deficit than are those from gastric
suction.
Hypomagnesemia occurs if losses are prolonged and
magnesium is not replaced through IV infusion.
Because the distal small bowel is the major site of
magnesium absorption, any disruption in small bowel
function can lead to it.
During nutritional replacement, the major cellular
electrolytes move from the serum to newly
synthesized cells. Therefore, if the enteral or
parenteral feeding formula is deficient in magnesium
content, serious hypomagnesemia will occur.

Hypermagnesemia or Magnesium excess
serum magnesium level higher than 3.0 mg/dL
(1.25 mmol/L)
Hypermagnesemia can occur in patients 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.
Risk for electrolyte imbalance r/t
Decreased elimination of magnesium or its increased
excessive IV magnesium administration
absorption due to intestinal hypomotility from any
cause can contribute to hypermagnesemia.
Lithium intoxication can also cause an increase in
serum magnesium levels.
Extensive soft tissue injury or necrosis as with trauma,
shock, sepsis, cardiac arrest, or severe burns can also
result in hypermagnesemia.

Hypophosphatemia or Phosphorus deficit A administration of calories to patients with severe
below-normal serum concentration of
inorganic phosphorus; below 2.5 mg/dL (0.8 from overzealous intake or administration of simple
mmol/L)
Hyperphosphatemia or Phosphorus excess
a serum phosphorus level that exceeds 4.5
mg/dL (1.45 mmol/L)
Phosphorus deficiency is an abnormally low content
of phosphorus in lean tissues that may exist in the
absence of hypophosphatemia. It can be caused by an
intracellular shift of potassium from serum into cells,
by increased urinary excretion of potassium, or by
decreased intestinal absorption of potassium.
Hypophosphatemia may occur during the
Low serum phosphorus level r/t
protein–calorie malnutrition. It is most likely to result refeeding after starvation as evidenced
by bone pain and tenderness.
carbohydrates.
Excess phosphorus binding by antacids may decrease
the phosphorus available from the diet to an amount
lower than required to maintain serum phosphorus
balance. The degree of hypophosphatemia depends
on the amount of phosphorus in the diet compared to
the dose of antacid.
Kidney injury can lead to hyperphosphatemia. Other
causes include increased intake, decreased output, or
a shift from the intracellular to extracellular space.
Symptoms that do occur usually result from Deficient serum phosphorus level r/t
decreased calcium levels and soft issue calcifications. acute renal failure as evidenced by
tetany and tachycardia.
Because of the reciprocal relationship between
phosphorus and calcium, a high serum phosphorus
level tends to cause a low serum calcium
concentration.

Hypochloremia or Chloride deficit a
serum chloride level below 97 mEq/L (97
mmol/L)
Hyperchloremia or Chloride excess exists
when the serum level of chloride exceeds
107 mEq/L (107 mmol/L)
Hypochloremia can occur with GI tube drainage,
gastric suctioning, gastric surgery, and severe
vomiting and diarrhea. Administration of chloride
deficient IV solutions, low sodium intake, decreased
serum sodium levels, metabolic alkalosis, massive
blood transfusions, diuretic therapy, burns, and fever
may cause hypochloremia.
Risk for electrolyte imbalance secondary
Administration of aldosterone, ACTH, corticosteroids, to untreated diabetic ketoacidosis
bicarbonate, or laxatives decreases serum chloride
levels as well. As chloride decreases (usually because
of volume depletion), sodium and bicarbonate ions
are retained by the kidney to balance the loss.
Bicarbonate accumulates in the ECF, which raises the
pH and leads to hypochloremic metabolic alkalosis.
High serum chloride levels are almost exclusively a
result of iatrogenically induced hyperchloremic
metabolic acidosis, stemming from excessive
administration of chloride relative to sodium
This condition can also be caused by the loss of
bicarbonate ions via the kidney or the GI tract with a Serum chloride level excess r/t head
corresponding increase in chloride ions. Chloride ions injury (sodium retention) as evidenced by
in the form of acidifying salts accumulate, and tachypnea, lethargy, and deep rapid
acidosis occurs with a decrease in bicarbonate ions. respirations
Head trauma, increased perspiration, excess
adrenocortical hormone production, and decreased
glomerular filtration can lead to a high serum chloride
level.
Reference:

Cheever, K. H., Hinkle, J. L., Smeltzer, S. C., & Cheever, B. L. (2008). Brunner & Suddarth's Textbook of Medical-Surgical Nursing (11th ed.).
Philadelphia: Wolters Kluwer.