الفهرس 
PHYSIOLOGY AND HOMEOSTASIS OF POTASSIUM
Renal handling of potassiumOnly 14 pages are availabe for public view
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Abstract
Potassium plays a key role in maintaining cell function.
Almost all cells possess an Na+-K+-ATPase, which pumps
Na+ out of the cell and K+ into the cell and leads to a K+
gradient across the cell membrane (K+
in>K+
out) that is partially
responsible for maintaining the potential difference across the
membrane which is critical to the function of cells, particularly
in excitable tissues, such as nerve and muscle. The body has
developed numerous mechanisms for K+ homeostasis.
The kidney is primarily responsible for maintaining total
body K+ content by matching K+ intake with K+ excretion.
Adjustments in renal K+ excretion occur over several hours;
therefore, changes in extracellular K+ concentration are initially
buffered by movement of K+ into or out of skeletal muscle. The
regulation of K+ distribution between the intracellular and
extracellular space is referred to as internal K+ balance. The
most important factors regulating this movement under normal
conditions are insulin and catecholamines.
Despite mechanisms to maintain K+ homeostasis,
hypokalemia is frequently encountered in clinical practice.
Transient causes of hypokalemia are due to cellular shift,
whereas sustained hypokalemia can be manifested by either
inadequate intake or excessive K+ loss. Hypokalemia resulting
from excessive K+ loss can be due to renal or extrarenal losses.
The cause and source of hypokalemia can be assessed by obtaining a clinical history and conducting a physical
examination, with particular attention paid to volume and acid
base status of the patient.
The severity of the manifestations of hypokalemia tends
to be proportionate to the degree and duration of the reduction
in serum potassium. Symptoms generally do not become
manifest until the serum potassium is below 3.0 meq/L, unless
the serum potassium falls rapidly or the patient has a
potentiating factor, such as a predisposition to arrhythmia due
to the use of digitalis. Symptoms usually resolve with
correction of the hypokalemia.
Cellular redistribution is a more important cause of
hyperkalemia than hypokalemia. It is important to note that as
little as a 2% shift of intracellular K+ to the extracellular fluid
will result in a serum K+of 8 mEq/l.Disturbances in serum K+
concentration due to cell shifts are generally transient in
nature, whereas sustained hyperkalemia is due to impaired
renal excretion. Metabolic acidosis promotes K+ exit from
cells dependent upon the type of acid present. Mineral acidosis
(NH4Cl or HCl) causes the greatest efflux of K+ from cells,
whereas organic acidosis (i.e., lactic, β-hydroxybutyric, or
methylmalonic acid) results in no significant efflux of K+.
Hyperkalemia associated with lactic acidosis is the result of
cell ischemia. The most serious manifestations of hyperkalemia are
muscle weakness or paralysis, cardiac conduction
abnormalities, and cardiac arrhythmias. These manifestations
usually occur when the serum potassium concentration is ≥7.0
meq/L with chronic hyperkalemia or possibly at lower levels
with an acute rise in serum potassium.
Pseudohyperkalemia should be excluded before
concluding that hyperkalemia is due to cell shift or abnormal
renal K+ excretion. Pseudohyperkalemia is the result of release
of K+ from cells during the phlebotomy procedure, or specimen
processing, and is defined by a serum K+concentration 0.5
mEq/l greater than the plasma K+ concentration.
The goals of therapy in hypokalemia are to prevent or
treat life threatening complications (arrhythmias, paralysis,
rhabdomyolysis, and diaphragmatic weakness), to replace the
potassium deficit, and to diagnose and correct the underlying
cause. The urgency of therapy depends upon the severity of
hypokalemia, associated and/or comorbid conditions.
The urgency of treatment of hyperkalemia varies with the
presence or absence of the symptoms and signs associated with
hyperkalemia, the severity of the potassium elevation, and the
cause of hyperkalemia.Potassium a major intra cellular cation is intimately
involved in the maintenance of resting membrane potential.
Hypo or hyperkalemia can cause disturbances of muscle,
nerve and cardiac cell excitability. These three excitable cells
are closely associated with anaesthesia. The absolute levels of
potassium, presence of symptoms, acute or chronic
disturbance and associated risk factors should be borne in
mind perioperatively.