Page 134 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Abnormalities of Potassium Balance
An abnormal potassium level is the result of a acidosis leads to hyperkalemia. Glucose stimu-
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disorder of K balance or of its distribution be- lates the release of insulin that, by activating
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tween the intracellular and extracellular space. Na /H exchangers, Na -K -2 Cl cotransport-
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An abnormal potassium balance occurs, for ers and Na /K -ATPase, stimulates the uptake
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example, if potassium supply is inadequate of K by the cells. In insulin deficiency or hypo-
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(→ A1). As intravenous infusion of K initially glycemia (when fasting), the cells lose K . The
passes into a compartment, namely plasma, administration of insulin in diabetic hypergly-
that has a relatively low potassium content; cemia (→ p. 286ff.) or food intake by a starving +
Kidney, Salt and Water Balance for Na in the distal tubules and collecting by the cells via ß-receptors and the cellular re- +
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person may lead to dangerous hypokalemia
too rapid K administration can lead to a dan-
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gerous level of hyperkalemia even if there is a
because the cells will be taking up K .
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K deficiency. The secretion of K in exchange
Catecholamines promote the uptake of K
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lease of K from the cells via α-receptors.
duct is the decisive step in the renal elimina-
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The effects of changed plasma K concen-
tion of K (→ A2; see also p. 96ff.). Renal loss
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tration are in part mediated by changes in the
of K occurs, for example, in hyperaldosteron-
membrane potential. Hypokalemia hyperpo-
ism (→ p. 266) or if there is an increased avail-
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larizes, while hyperkalemia depolarizes the K
ability of Na in the distal tubules (→ p. 98 D).
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if: 1) Na reabsorption is impaired in the distal
potential of selective cells. In this way hypo-
tubules, as in hypoaldosteronism; 2) diuretics
kalemia reduces the excitability of nerve cells
acting on the connecting tubule and collecting
(hyporeflexia), skeletal muscles (adynamia),
5 Conversely, renal K elimination is decreased equilibrium potential, and thus the membrane
duct have been administered; or 3) there is a and smooth muscles (gut, bladder, etc.)
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decreased supply of Na (e.g., in renal failure). (→ A6). Conversely, hyperkalemia can increase
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In alkalosis fewer H ions are secreted in the the excitability of the nervous system (hyper-
connecting tubule and collecting duct and reflexia), smooth muscles (→ A7), and skeletal
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more K is lost, while conversely acidosis de- muscles (→ p. 306).
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creases K secretion in the distal nephron. K + In contrast, a decrease in K concentration
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may also be lost via the gut (→ A3). If there is reduces the conductance of the K channels,
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an increased supply of Na or in hyperaldoste- thus decreasing the hyperpolarizing effect of
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ronism, an increased amount of Na is similar- K on the membrane potential. This promotes
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ly absorbed in the colon in exchange for K . the heterotopic automaticity of the heart that
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Even minor shifts of K between intracellu- may even trigger ventricular fibrillation
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lar and extracellular fluid lead to massive chan- (→ p.188ff.). The reduction of K conductance
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ges in plasma K concentration, because the K + is also responsible for delayed repolarization
contentincells is morethan 30 times thatin the of the Purkinje fibers. Hypokalemia often pro-
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extracellular space. Cellular loss of K and hy- duces a prominent U wave in the electrocar-
perkalemia occur, for example, in case of cellu- diogram (ECG) (→ A6). Conversely, hyperkale-
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lar energy deficiency (→ A4), during severe mia increases the K conductance, the action
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physical work (K loss via the muscles), cell potential is shortened, and correspondingly
death (e.g., in hemolysis, myolysis), and in also the ST segment in the ECG (→ A7).
transfusion of blood which has been stored for Lack of potassium promotes the cellular re-
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some time (loss of K from erythrocytes). Fur- tention of H and its secretion in the distal tu-
thermore, hemolysis at the time of blood-tak- bules. This results in an alkalosis (→ p. 86).
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ing can increase the K concentration in the Conversely, K + excess leads to acidosis
plasma and be mistaken for hyperkalemia. (→ p. 88). Hypokalemia also causes polyuria
In (extracellular) alkalosis the cells release (→ p.100) and can ultimately lead to irrevers-
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H in exchange for Na (Na /H exchangers) ible tubular cell damage. Lastly, the release of
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and pump the Na out again in exchange for a number of hormones is abnormal in K defi-
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124 K (Na /K -ATPase) (→ A5). This K uptake by ciency (especially insulin [→ p. 286] and aldo-
the cells causes hypokalemia. Conversely, sterone [→ p. 266]).
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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