Intracellular electrolytes in cardiac failure

Acta Med Scand Suppl. 1986;707:33-6. doi: 10.1111/j.0954-6820.1986.tb18112.x.

Abstract

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.

MeSH terms

  • Aged
  • Aldosterone / blood
  • Body Fluids / metabolism*
  • Catecholamines / metabolism
  • Diuretics / therapeutic use
  • Female
  • Heart Failure / drug therapy
  • Heart Failure / metabolism*
  • Humans
  • Intracellular Fluid / metabolism*
  • Magnesium / metabolism
  • Male
  • Middle Aged
  • Potassium / metabolism
  • Renin-Angiotensin System
  • Sodium / metabolism
  • Sodium-Potassium-Exchanging ATPase / metabolism
  • Water-Electrolyte Balance*

Substances

  • Catecholamines
  • Diuretics
  • Aldosterone
  • Sodium
  • Sodium-Potassium-Exchanging ATPase
  • Magnesium
  • Potassium