C h a p t e r 8
Disorders of Fluid, Electrolyte, and Acid–Base Balance
181
ICF compartment can be accomplished by the admin-
istration of sodium bicarbonate,
β
-agonists (e.g., nebu-
lized albuterol), or insulin to rapidly decrease the ECF
concentration.
30
Less-emergent measures focus on decreasing or cur-
tailing potassium intake or absorption, increasing renal
excretion, and increasing cellular uptake. Decreased
intake can be achieved by restricting dietary sources of
potassium. The major ingredient in most salt substitutes
is potassium chloride, and such substitutes should not
be given to persons with kidney problems. Increasing
potassium output often is more difficult. Persons with
kidney failure may require hemodialysis or peritoneal
dialysis to reduce serum potassium levels.
Calcium, Phosphorus, and
Magnesium Balance
Calcium, phosphorus, and magnesium are the major
divalent cations in the body. Most of these cations are
deposited in bone, with only a small amount in the ECF.
Homeostatic mechanisms that regulate serum calcium
and phosphorus levels involve three organs—the intes-
tine, kidney, and bone, principally through the complex
interaction of parathyroid hormone and vitamin D
35–37
(Fig. 8-13).
The main function of
parathyroid hormone
(PTH) is
to maintain ECF calcium concentrations.
35,37
It does this
by stimulating the release of calcium and phosphorus
from bone into the ECF; increasing renal reabsorption
of calcium and excretion of phosphorus; and enhancing
the gastrointestinal absorption of calcium and phospho-
rus through its effects on vitamin D synthesis.
Vitamin
D
, which functions as a hormone, is synthesized by the
skin and converted to its active form,
calcitriol
, in the
kidney. The active form of vitamin D has several effects
on the intestines, kidneys, and bone that increase serum
levels of calcium and phosphorus and contribute to their
B
Hypokalemia
C
Hyperkalemia
A
Normal
Depressed
ST segment
Low T
Prominent
U wave
Low P wave
PR
prolongation
PR
prolongation
Widening of QRS
Peaked
T
U
T
R
Q
S
P
Delay in
AV node
FIGURE 8-12.
Comparison of the
(A)
normal
electrocardiogram with electrocardiographic changes that
occur with
(B)
hypokalemia and
(C)
hyperkalemia.
SUMMARY CONCEPTS
■■
Potassium is the second most abundant cation
in the body, with 98% being located in the
intracellular fluid (ICF) compartment.The high ICF
concentration is required for many cell functions,
including maintenance of the osmotic integrity
of cells and acid–base balance, intricate chemical
reactions that transform carbohydrates into
energy, changing glucose into glycogen, and
converting amino acids to proteins. Potassium
also plays a critical role in conducting nerve
impulses and controlling the excitability of
skeletal, cardiac, and smooth muscles.
■■
Potassium is ingested in the diet and eliminated in
the urine, with ICF and extracellular (ECF) levels
being regulated by compartmental shifts between
the ICF and ECF, and mechanisms that adjust renal
excretion with dietary ingestion of potassium.
■■
Hypokalemia, or potassium deficit, can result
from inadequate intake, excessive losses,
or redistribution from the ECF to the ICF
compartments. It is manifested by alterations
in kidney, skeletal muscle, gastrointestinal, and
cardiac function, reflecting the crucial role of
potassium in cell metabolism and neuromuscular
function.
■■
Hyperkalemia, or potassium excess, can result
from decreased elimination of potassium by the
kidney, a transcellular shift in potassium from
the ICF into the ECF compartment, or excessively
rapid intravenous administration of potassium.
It is manifested by alterations in neuromuscular
and cardiac function, the most serious being the
development of serious and even fatal cardiac
arrhythmias.
