C h a p t e r 8
Disorders of Fluid, Electrolyte, and Acid–Base Balance
177
Potassium Balance
Potassium (K
+
) is the second most abundant cation in
the body, with 98% located in the intracellular compart-
ment, primarily in skeletal muscle.
30–32
Of the remaining
2% that is in the extracellular compartment, only about
0.4% is measurable in the plasma. This tiny amount is
maintained at a fairly narrow serum concentration of
3.5 to 5.0 mEq/L (3.5 to 5.0 mmol/L).
Regulation of Potassium Balance
Potassium balance is normally regulated by dietary
intake, urine output, and transcompartmental shifts
between the ICF and ECF compartments. The kidneys
are the main source of potassium loss. Approximately
80% to 90% of potassium loss occurs in the urine, with
the remainder being lost in the stools from the gastroin-
testinal tract and in sweat from the skin.
30–34
Potassium is filtered in the glomerulus, reabsorbed
along with sodium and water in the proximal tubule
and with sodium and chloride in the thick ascending
loop of Henle, and then secreted into the late distal and
collecting tubules for elimination in the urine. In con-
trast to other electrolytes, the regulation of potassium
elimination by the kidney is mainly controlled by its
secretion from the blood into the tubular filtrate rather
than through its reabsorption from the tubular filtrate
into the blood (see Chapter 24).
Aldosterone plays an essential role in regulating
potassium elimination in the distal tubule of the kidney.
In the presence of aldosterone, Na
+
is transported back
into the blood and K
+
is secreted in the tubular filtrate
for elimination in the urine. There is also a potassium/
hydrogen exchange mechanism in the collecting tubules
of the kidney. When serum potassium levels increase, K
+
is secreted into the urine and H
+
is reabsorbed, leading
to a decrease in pH and metabolic acidosis; when potas-
sium levels are low, K
+
is reabsorbed and H
+
is secreted
in the urine, leading to an increase in pH and metabolic
alkalosis.
Among the factors that influence the ECF/ICF shift
in potassium are serum osmolality, acid–base bal-
ance, insulin, and increased sympathetic nervous sys-
tem activity (Fig. 8-10). An acute increase in
serum
osmolality
causes water to move out of the cell; this
in turn prompts an increase in K
+
concentration that
causes it to move out into the ECF.
Acid–base disor-
ders
rely on an ECF to ICF cation shift for buffering
of the H
+
ion. In metabolic acidosis, for example, H
+
moves into body cells for buffering, causing K
+
to leave
and move into the ECF. Both insulin and epinephrine
(a
β
-adrenergic sympathetic neurontransmitter) increase
cellular uptake of K
+
by increasing the activity of the
Na
+
/K
+
-adenosine triphosphatase (ATPase) membrane
pump.
4,30–33
Normally, it takes 6 to 8 hours for the
kidneys to eliminate half of potassium that has been
ingested in the diet.
4
After a meal, insulin release not
only serves to regulate blood glucose levels, but also
serves to control serum potassium levels by temporarily
shifting the excess into cells until it can be eliminated
by the kidneys.
Exercise can also produce compartmental shifts in
potassium. Repeated muscle contraction causes potas-
sium to be released into the ECF. Although the increase
usually is small with modest exercise, it can be consid-
erable during exhaustive exercise. Even the repeated
clenching and unclenching of the fist during a blood
draw can cause potassium to move out of cells causing
an artificial elevation in serum potassium levels.
proportionate changes in sodium and water.
Isotonic fluid volume deficit (hypovolemia), which is
characterized by a decrease in ECF volume, causes
thirst, signs of decreased vascular volume, and a
decrease in urine output along with an increase
in urine specific gravity. Isotonic fluid volume
excess (hypervolemia), which is characterized by an
increase in ECF volume, is manifested by signs of
increased vascular volume and edema.
■■
Hyponatremia (sodium deficit) and hypernatremia
(sodium excess) are brought about by
disproportionate losses or gains in ECF sodium
concentration, which cause water to move in or
out of body cells. Because of water movement,
hyponatremia produces an increase in ICF water
causing cells to swell;, whereas hypernatremia
produces an ICF water deficit and cellular
dehydration.
K
Na /K -
ATPase
pump
Na
Epinephrine
Insulin
Intracellular
Extracellular
H
+
K +
+
+
++
+ +
FIGURE 8-10.
Mechanisms regulating transcellular shifts
in potassium.
