| In congestive heart failure (CHF) there are several compensatory
mechanisms operating which may influence electrolyte metabolism. The
activation of the renin-angiotensin-aldosterone system causes
retention of sodium (Na) and losses of potassium (K) and magnesium
(Mg). The secondary hyperaldosteronism may give rise to high
intracellular Na and low intracellular K through a direct
permeability effect on the cell membrane. The Mg deficiency may lead
to a further increase of intracellular Na and decrease of
intracellular K since Mg is a necessary ion for the function of the
Na-K pump. In 297 patients with diuretic treated CHF we found that
42% had hypokalemia, 37% hypomagnesemia and 12% hyponatremia. We also
found that 57% had excess muscle Na, 52% had depletion of muscle K
and 43% had low muscle Mg. We have also shown that the low muscle K
cannot be corrected by K supplementation when there is a concomitant
Mg deficiency and that Mg infusions may change the disturbed relation
between extra- and intracellular electrolytes towards normal.
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