Congestive heart failure (CHF) represents a pathophysiologic state in which cardiac output is inadequate to meet the metabolic needs of multiple organ systems. The primary pathologic event in CHF is a marked, sustained reduction in the intrinsic contractility of the heart. A review of the current knowledge regarding the etiology and progression of CHF reveals that it is associated with profound biochemical, peripheral hemodynamic (increased peripheral vascular resistance), and electrolyte disturbances. In addition to sodium and water retention, CHF is often associated with hypokalemia and hypomagnesemia as well as tissue deficits in K and Mg. Cardiac glycosides and diuretics (loop and distal types) often exacerbate, or result in, hypokalemia and hypomagnesemia, which may lead to cardiac arrhythmias and sudden cardiac death. Deficits in extracellular and vascular tissue Mg lead to peripheral vasoconstriction; this together with K deficits and the release of neurohumoral substances may be responsible in large measure for the increase in peripheral vascular resistance commonly noted in CHF. More attention must be paid to the careful monitoring of electrolyte levels (Na, K, Mg) in tissues (possibly lymphocytes) and plasma of CHF patients. Deficits in either K or Mg must be corrected in CHF. The nonspecific vasodilator properties of Mg2+ together with its ability to unload the heart should be considered as an important adjunct tool in the management of CHF.