Intracellular electrolytes in cardiac failure.
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.
D000368:Aged; D000450:Aldosterone / Q000097:blood; D001826:Body Fluids / Q000378:metabolism*; D002395:Catecholamines / Q000378:metabolism; D004232:Diuretics / Q000627:therapeutic use; D005260:Female; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism*; D006801:Humans; D007424:Intracellular Fluid / Q000378:metabolism*; D008274:Magnesium / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011188:Potassium / Q000378:metabolism; D012084:Renin-Angiotensin System; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014882:Water-Electrolyte Balance
D002395:Catecholamines; D004232:Diuretics; D000450:Aldosterone; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D008274:Magnesium; D011188:Potassium