Biomedical subjects
Publications and source records attributed to P O Wester.
In congestive heart failure several compensatory mechanisms are operating, and may cause severe disturbances of both the internal and external electrolyte balance. The medical treatment prescribed in congestive heart failure also leads to changes in the handling of electrolytes. These combined effects may prove critical to the patient, especially with regard to the emergence of cardiac arrhythmias.
Diuretic agents influence the renal handling of magnesium, causing increased losses of the ion. Continuing magnesium losses may, in the long term, result in a magnesium deficiency. 296 patients with congestive heart failure or arterial hypertension receiving long term diuretic therapy were studied by skeletal muscle biopsies to assess their magnesium status. 65% of the congestive heart failure patients and 42% of the patients with arterial hypertension were found to have subnormal values for skeletal muscle magnesium. Studies with the potassium-sparing diuretics amiloride, spironolactone and triamterene demonstrate that these drugs significantly increase the muscle magnesium content in patients on long term diuretic treatment for congestive heart failure and/or arterial hypertension--in addition to their well known positive effect on potassium balance.
A series of 676 patients with acute myocardial infarction were evaluated with regard to initial serum potassium level, prior diuretic therapy and occurrence of cardiac dysrhythmias during their first 24 hours in a coronary care unit. Serious dysrhythmias (ventricular tachycardia, ventricular fibrillation, and asystole) were significantly more frequent in hypokalemic patients. In this regard no differences were observed between patients on or off prior diuretic therapy.
Body potassium status is often dosed on serum potassium determinations. However, this parameter is not an adequate guide to the body potassium status, unless several factors are taken into consideration, e.g. acid-base balance and serum creatinine level. Muscle magnesium content is another factor, probably operative through its activation of Na-K-ATPase, which produces the energy necessary for the active transport of potassium into the cell. Magnesium has a membrane-stabilizing effect as well, diminishing the outward movement of potassium from the cell. In case of magnesium deficiency, potassium cannot be transported into the cell in sufficient amounts and the result is an imbalance between the intra- and the extracellular potassium concentration, which in turn may lead to cardiac dysrhythmias.
Twenty patients receiving long term diuretic treatment for arterial hypertension (18 patients) or congestive heart failure (two patients) received magnesium supplementation as aspartate hydrochloride 15 mmol/day for six months. Both systolic and diastolic pressures decreased significantly, by a mean of 12/8 mm Hg. No significant changes were recorded in plasma or urinary electrolytes except for magnesium, 24 hour urinary volumes, or body weight after treatment. The effect of magnesium on blood pressure may be direct or through influences on the internal balance of potassium, sodium, and calcium.
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Long-term diuretic treatment of patients with congestive heart failure is often complicated by hyponatremia and resistance to diuretic treatment, as well as by hypokalemia. Less widely recognized is the increase in intracellular sodium in the presence of hyponatremia, and loss of magnesium, caused by sustained diuretic therapy. Because the sodium pump, which maintains intracellular sodium and potassium against a concentration gradient, is dependent on optimal magnesium levels, we have investigated the influence of magnesium infusions on serum and skeletal muscle levels of sodium and potassium in congestive heart failure patients with electrolyte disturbances. Because aldosteronism, such as accompanies the disease and diuretic treatment, increases intracellular sodium, we have measured intracellular sodium and potassium in six patients given a new aldosterone antagonist (canrenone). It lowered the muscle sodium and raised the muscle potassium and magnesium, and slightly raised the serum sodium. The magnesium infusions, given to eight patients, significantly increased the serum sodium and lowered the muscle sodium levels, and normalized both serum and subnormal muscle potassium levels.
Skeletal muscle biopsies, blood samples, and 24-hour urines, before and after magnesium infusions, were obtained from 12 patients who had undergone jejuno-ileal bypass surgery several years earlier, selected for probable magnesium deficiency on the basis of repeated hypomagnesemia. The patients retained significant amounts of the infused magnesium, and exhibited elevation of low skeletal muscle magnesium and potassium, with concomitant decreases of muscle sodium and chloride. These changes were accompanied by increased urinary calcium and sodium and decreased urinary phosphorus excretion.
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Two cases of ventricular tachycardia (VT), possibly caused by magnesium deficiency, are presented. Skeletal muscle biopsies and blood samples were taken before and after magnesium infusions. These infusions resulted in a significant retention of magnesium, and the VT attacks vanished permanently in one case and temporarily in the other.
Hyperosmolar non-ketotic coma in diabetes is a life-threatening condition. We describe three patients, aged 59-67 years, who developed hyperosmolar coma during the first ten days after admission for stroke. Common to all three were normal plasma osmolality and slightly elevated plasma creatinine levels on admission, treatment with diuretics, parenteral dextrose administration before and low urinary glucose output during the coma. In the five days preceding the coma, total fluid deficits were 3.8, 6.5 and 9.4 1, respectively. In one patient the rate of glucose delivery had clearly exceeded utilization during adequate insulinization, in another a marked reduction in urinary glucose output preceded extreme hyperglycaemia and coma. Two of the three patients died, both from extensive thrombus formation in cerebral arteries and multiple emboli to the lungs. We conclude that enhanced endogenous glucose production and reduced renal clearance of glucose may contribute to precipitate hyperosmolar non-ketotic coma. A close monitoring of fluid and dextrose administration seems mandatory in diabetic stroke patients, in particular if renal function is impaired or if diuretics are given. Insulin treatment should be considered in all diabetic patients during the first days after a stroke.
Tissue concentrations of antimony in lung, liver, and kidney tissue from a group of deceased smelter workers from northern Sweden have been compared with those of a group of persons without occupational exposure from a nearby area. Neutron activation analysis was used to determine the antimony concentration of lung tissue from exposed workers; these concentrations were 12-fold higher than those of referents (p less than 0.001). For lung tissue there was no tendency towards decreased antimony concentrations with time (up to 20 a) after the cessation of exposure, and this result indicates a long biological half-time. The highest values were found for workers who had worked for many years at the roasters and in the arsenic and selenium departments. There was no significant difference between the antimony concentration of the lung tissue from workers who had died of lung cancer and those of persons who died of other malignancies, cardiovascular disease, or other causes. This finding does not however rule out the possibility of a role for antimony in the etiology of lung cancer among smelter workers since multiple factors may have been operating. The antimony concentration of the liver tissue and the kidney cortex did not differ from the corresponding values of the reference group; this finding indicates either a short biological half-time or insignificance for the systemic distribution of antimony.
Eight hyponatraemic patients with severe congestive heart failure, long-term diuretic treatment, oedema, and increasing resistance to diuretic treatment, were studied with skeletal muscle biopsies and serum electrolytes before and after magnesium infusions. The infusions resulted in an increasing serum sodium level, a decrease in muscle sodium and chloride, and an increase in muscle potassium. The effect was probably mediated through the magnesium effect on membrane ATPase.