| Pharmacodynamics |
The potassium ion is in the principle intracellular cation of
most body tissues. Potassium ions participate in a number of essential
physiological processes including the maintenance of intracellular
tonicity, the transmission of nerve impulses, the contraction of
cardiac, skeletal and smooth muscle, and the maintenance of normal renal
function. The intracellular concentration of potassium is approximately
150 to 160 mEq per liter. The normal adult plasma concentration is 3.5
to 5 mEq per liter. An active ion transport system maintains this
gradient across the plasma membrane. Potassium is a normal dietary
constituent and under steady-state conditions the amount of potassium
absorbed from the gastrointestinal tract is equal to the amount excreted
in the urine. The usual dietary intake of potassium is 50 to 100 mEq
per day. Potassium depletion will occur whenever the rate of potassium
loss through renal excretion and/or loss from the gastrointestinal tract
exceeds the rate of potassium intake. Such depletion usually develops
as a consequence of therapy with diuretics, primarily or secondary
hyperaldosteronism, diabetic ketoacidosis, or inadequate replacement of
potassium in patients on prolonged parenteral nutrition. Depletion can
develop rapidly with severe diarrhea, especially if associated with
vomiting. Potassium depletion due to these causes is usually accompanied
by concomitant loss of chloride and is manifested by hypokalemia and
metabolic alkalosis. Potassium depletion may produce weakness, fatigue,
disturbances of cardiac rhythm (primarily ectopic beats), prominent
U-waves in the electrocardiogram, and, in advanced cases, flaccid
paralysis and/or impaired ability to concentrate urine. If potassium
depletion associated with metabolic alkalosis cannot be managed by
correcting the fundamental cause of the deficiency, e.g., where the
patient requires long-term diuretic therapy, supplemental potassium in
the form of high potassium food or potassium chloride may be able to
restore normal potassium levels. In rare circumstances (e.g., patients
with renal tubular acidosis) potassium depletion may be associated with
metabolic acidosis and hyperchloremia. In such patients, potassium
replacement should be accomplished with potassium salts other than the
chloride, such as potassium bicarbonate, potassium citrate, potassium
acetate, or potassium gluconate. |
| Toxicity |
The administration of oral potassium salts to persons with normal
excretory mechanisms for potassium rarely causes serious hyperkalemia.
However, if excretory mechanisms are impaired, of if potassium is
administered too rapidly intravenously, potentially fatal hyperkalemia
can result. It is important to recognize that hyperkalemia is usually
asymptomatic and may be manifested only by an increased serum potassium
concentration (6.5-8.0 mEq/L) and characteristic electrocardiographic
changes (peaking of T-waves, loss of P-wave, depression of S-T segment,
and prolongation of the QT interval). Late manifestations include muscle
paralysis and cardiovascular collapse from cardiac arrest (9-12 mEq/L). |
