Search PubMed⌕ Search

Biomedical subjects

T Dyckner

Publications and source records attributed to T Dyckner.

At least 37 records · Page 2Linked to original sources
PubMed1984

Problems with potassium and magnesium in diuretic-treated patients.

Treatment with thiazides and loop diuretics increase the urinary excretion of potassium and magnesium and the body content of these ions are reduced after long-term treatment. The diuretic-induced magnesium deficiency influences the potassium metabolism. Magnesium is a necessary activator of Na-K-ATPase, which supplies the Na-K pump with energy. Lack of magnesium will therefore impair the pumping of sodium out of the cell and of potassium into the cell. The change of the relationship between extra and intracellular potassium may induce cardiac arrhythmias. Certain groups of patients, such as patients on digitalis therapy, patients with secondary hyperaldosteronism, elderly patients with insufficient dietary habits, and heavy drinkers, run an additional risk of developing potassium/magnesium disturbances. In young patients with uncomplicated essential hypertension, the risk is probably very small.

Diuretics↗
PubMed1984

Magnesium deficiency in congestive heart failure.

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.

Cardiac Output↗
PubMed1984

Intracellular magnesium loss after diuretic administration.

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.

Diuretics↗
PubMed1984

Cardiac dysrhythmias in patients with acute myocardial infarction. Relation to serum potassium level and prior diuretic therapy.

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.

Aged↗
PubMed1984

Intra-/extracellular shifts of potassium after the administration of Mg in patients with cardiovascular diseases.

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.

Cardiovascular Diseases↗
PubMed1983

Effect of magnesium on blood pressure.

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.

Aged↗
PubMed1982

Magnesium treatment of diuretic-induced hyponatremia with a preliminary report of a new aldosterone-antagonist.

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.

Aged↗
PubMed1982

Magnesium deficiency following jejunoileal bypass operations for obesity.

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.

Adult↗
PubMed1982

Magnesium deficiency contributing to ventricular tachycardia. Two case reports.

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.

Aged↗
PubMed1981

Effects of magnesium infusions in diuretic induced hyponatraemia.

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.

Aged↗
PubMed1981

Diuretic treatment and magnesium losses.

Therapy with most kinds of diuretics causes increased urinary excretion of both potassium and magnesium and after long term treatment the skeletal muscle content of these ions is reduced. Magnesium is known activator of Na-K-ATP:ase, which provides the energy for the sodium-potassium pump. Thus, lack of magnesium may impair the pumping of sodium out from the cell and potassium into the cell. Three studies are presented which agree with this theory. In one study the correlation between potassium in serum and potassium in muscle was, among other factors, found to be dependent on the content of muscle magnesium. In another study it was found in hypokalemic patients that muscle potassium could not be corrected by potassium supplementation if there was a concomitant magnesium deficiency. In the third study it was found that muscle potassium increased after magnesium infusion but not after potassium infusion.

Creatinine↗