Key points are not available for this paper at this time.
BACKGROUND: Patients with severe decompensated congestive heart failure (CHF) commonly exhibit acid-base and electrolyte disturbances mainly due to the activation of several neurohumoral mechanisms as well as to drugs regularly used in this population. Magnesium deficit is not infrequently observed in CHF patients but its pathophysiology remains less well-studied as compared with other electrolyte alterations, such as hypokalemia. However, there is evidence that early detection and correction of magnesium abnormalities could obviate potentially deleterious arrhythmogenic effects. AIM: To assess the incidence of magnesium level disorders and analyze the underlying pathophysiological mechanisms in patients with CHF. METHODS: Eighty-six consecutive CHF patients (NYHA class III or IV) admitted to our hospital over a period of 5 years were studied. Patients with diabetes mellitus, liver or renal failure, and chronic obstructive lung disease were excluded. All patients received conventional treatment with digoxin, diuretic agents and an angiotensin converting enzyme inhibitor. On admission, blood and urine electrolytes and renal function parameters were determined. Arterial blood gases and serum anion gap determinations were also performed. RESULTS: Hypomagnesemia was found in 15 n=15 (17.4%) CHF patients. The majority of these patients also exhibited other electrolyte abnormalities, such as hypokalemia, hypocalcemia and hypophosphatemia. Inappropriate magnesiuria (fractional excretion of magnesium >4%) was evident in eight hypomagnesemic patients. A variety of associated conditions, including poor dietary intake, also favored magnesium depletion. CONCLUSION: Magnesium deficit is a common electrolyte disorder in CHF (NYHA class III/IV) patients and several interrelated mechanisms are implicated in its pathogenesis. Clinicians' awareness of the incidence of hypomagnesemia in this population as well as its related pathophysiology could be useful for the early detection and appropriate treatment to inhibit its arrhythmogenic potential.
Milionis et al. (Fri,) studied this question.