Potassium And Magnesium
J Intensive Care Med. 2005 Jan-Feb;20(1):3-17.
Magnesium deficiency in critical illness.
Tong GM, Rude RK.
University of Southern California, School of Medicine, Los Angeles, CA 90089-9317, USA.
Magnesium (Mg) deficiency commonly occurs in critical illness and correlates with a higher mortality and worse clinical outcome in the intensive care unit (ICU). Magnesium has been directly implicated in hypokalemia, hypocalcemia, tetany, and dysrhythmia. Moreover, Mg may play a role in acute coronary syndromes, acute cerebral ischemia, and asthma. Magnesium regulates hundreds of enzyme systems. By regulating enzymes controlling intracellular calcium, Mg affects smooth muscle vasoconstriction, important to the underlying pathophysiology of several critical illnesses. The principle causes of Mg deficiency are gastrointestinal and renal losses; however, the diagnosis is difficult to make because of the limitations of serum Mg levels, the most common assessment of Mg status. Magnesium tolerance testing and ionized Mg2+ are alternative laboratory assessments; however, each has its own difficulties in the ICU setting. The use of Mg therapy is supported by clinical trials in the treatment of symptomatic hypomagnesemia and preeclampsia and is recommended for torsade de pointes. Magnesium therapy is not supported in the treatment of acute myocardial infarction and is presently undergoing evaluation for the treatment of severe asthma exacerbation, for the prevention of post-coronary bypass grafting dysrhythmias, and as a neuroprotective agent in acute cerebral ischemia.
Intern Med. 2004 May;43(5):410-4.
Depressive state and paresthesia dramatically improved by intravenous MgSO4 in Gitelman’s syndrome.
Enya M, Kanoh Y, Mune T, Ishizawa M, Sarui H, Yamamoto M, Takeda N, Yasuda K, Yasujima M, Tsutaya S, Takeda J.
Third Department of Internal Medicine, Gifu University School of Medicine, 40 Tsukasa-machi, Gifu 500-8705.
A 69-year-old woman was referred to our department for evaluation of hypokalemia, which had been treated by oral potassium for more than ten years. She complained of headache, knee joint pain, sleeplessness and paresthesia in extremities and, most prominently, depression. Laboratory data suggested Gitelman’s syndrome, which is caused by mutations in the gene encoding the thiazide-sensitive Na-Cl cotransporter. Direct sequencing of the gene in this patient revealed homozygous mutation R964Q in exon 25.
Intravenous supplement of MgSO4 dramatically improved both the depression and the paresthesia, suggesting that hypomagnesemia played a role in the clinical manifestations.
Am J Ther. 2006 Mar-Apr;13(2):101-8.
Prevention of thiazide-induced hypokalemia without magnesium depletion by potassium-magnesium-citrate.
Odvina CV, Mason RP, Pak CY.
Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX 75390-8885, USA.
Thiazide can cause magnesium depletion, which may exaggerate renal potassium wasting and hypokalemia. The purpose of this double-blind, randomized trial was to compare the metabolic effects of potassium-magnesium-citrate (K-Mg-citrate) and potassium chloride (KCl) during long-term treatment with thiazide. Twenty-two normal volunteers received hydrochlorothiazide 50 mg/d. Ten subjects concurrently took K-Mg-citrate (42 mEq K/d and 21 mEq Mg/d), and 12 subjects were given KCl 42 mEq/d. Serum potassium concentration remained unchanged during K-Mg-citrate supplementation, with a change from baseline of 21.7% over 6 months, compared with 26.4% with KCl supplementation. Serum electrolytes were normal and not significantly different between K-Mg-citrate and KCl. During K-Mg-citrate treatment, serum magnesium increased significantly by about 10%, associated with an adequate increase in urinary magnesium and a nonsignificant increase in monocyte and free muscle magnesium. Serum magnesium was unchanged, and monocyte and free muscle magnesium showed a nonsignificant decline during KCl supplementation. K-Mg-citrate provided an alkali load, increasing urinary pH, and reducing urinary undissociated uric acid. It also increased urinary citrate and tended to lower the saturation of calcium oxalate. KCl supplementation lacked these actions. K-Mg-citrate prevents thiazide-induced hypokalemia without provoking metabolic alkalosis. It seems to prevent magnesium depletion. By providing an alkali load, it retards the propensity for the crystallization of uric acid and probably of calcium oxalate. Though not conclusive, KCl supplementation may be less effective than K-Mg-citrate in maintaining normokalemia because of a subtle magnesium wasting. Moreover, KCl is devoid of protective action toward crystallization of stone-forming salts.
Acta Med Scand Suppl. 1986;707:33-6.
Intracellular electrolytes in cardiac failure.
Wester PO, Dyckner T.
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.
Arch Intern Med. 1988 Aug;148(8):1801-5.
The effect of intravenous magnesium therapy on serum and urine levels of potassium, calcium, and sodium in patients with ischemic heart disease, with and without acute myocardial infarction.
Rasmussen HS, Cintin C, Aurup P, Breum L, McNair P.
Medical Department P/Chest Clinic, Bispebjerg Hospital.
Serum concentrations of magnesium, potassium, calcium, and sodium were determined on admission of 224 patients to the hospital and after 2, 4, and 6 days in hospital; all were admitted to the hospital with suspected acute myocardial infarction (AMI). On admission, the patients were randomly allocated to 48 hours of treatment with magnesium intravenously or placebo. One hundred twenty-three patients had AMI (of whom 53 [43%] were treated with magnesium) and 101 had their suspected AMI disproven (of whom 51 [50%] were treated with magnesium). In a supplementary study, serum and urine levels of magnesium, potassium, calcium, and sodium, together with serum levels of parathyroid hormone, were determined before and after intravenous magnesium treatment in six patients with AMI and six patients with ischemic heart disease but without AMI. In both studies, magnesium therapy was associated with significant alterations in extracellular ion homeostasis. Serum concentrations of potassium decreased during the initial days of hospitalization in the patients treated with placebo, but increased slightly in the patients treated with magnesium infusions. These increments in the serum concentrations of magnesium and potassium correlated significantly. The increase in the serum concentration of potassium after magnesium infusions was due to a reduced renal potassium excretion level (from 71.3 to 49.4 mmol/24 h), indicating the existence of a divalent-monovalent cation exchange mechanism in the nephron. This hypothesis was supported by the observation that renal sodium excretion likewise decreased after magnesium infusions (from 83.2 to 59.2 mmol/24 h). Serum concentration of calcium decreased significantly after magnesium treatment (from 2.35 mmol/L on admission to 2.15 mmol/L after 24 hours in the hospital) in the AMI group, in contrast to the placebo-treated patients, where no significant fluctuations in serum concentration of calcium were detected during the initial six days. This decrease in serum concentration of calcium was due to a marked increase in renal calcium excretion (from 3.43 mmol/24 h before to 6.59 mmol/24 h after magnesium infusion). A correlation between increments in serum magnesium concentration and decrements in serum calcium concentration was detected. No change in serum levels of parathyroid hormone was found before and after magnesium infusions. Both serum and urine levels of magnesium significantly increased after magnesium treatment to levels above the upper normal limits (serum magnesium concentration increased from 0.81 to 1.21 mmol/L, urine magnesium excretion levels from 3.57 to 16.57 mmol/24 h for both serum and urine changes.
Kardiol Pol. 2003 Nov;59(11):402-7.
Acute coronary syndrome: potassium, magnesium and cardiac arrhythmia. [Article in English, Polish] Maciejewski P, Bednarz B, Chamiec T, Gorecki A, Lukaszewicz R, Ceremuzynski L.
Department of Cardiology, Postgraduate Medical School, Grochowski Hospital, Warsaw, Poland.
BACKGROUND: Cardiac arrhythmia is often present in patients with acute coronary syndrome (ACS) and may be due to the electrolyte imbalance. AIM: To assess the prevalence and clinical significance of electrolyte imbalance in ACS. METHODS: Serum potassium and magnesium levels were measured within the first few hours in 204 consecutive patients with ACS admitted to our department over a period of 23 months. Cardiac arrhythmia was documented using continuous ECG monitoring, telemetry or standard ECG. RESULTS: Hypokalemia was observed in 34% of patients, and was significantly associated with the occurrence of life-threatening ventricular arrhythmias (26% of patients with potassium level <4 mmol/l vs 11.9% of patients with normokalemia, p<0.001). No relationship was found between potassium level and supraventricular arrhythmias or in-hospital mortality. Decreased magnesium serum concentration was found in 22% of patients but was not significantly associated with cardiac arrhythmias or mortality. CONCLUSIONS: Hypokalemia and hypomagnesemia are often present in patients with ACS. The former is associated with dangerous ventricular arrhythmias. Early assessment of electrolyte serum concentration is needed in order to implement proper supplementation.
Crit Care Med. 2003 Apr;31(4):1082-7.
Development of ionized hypomagnesemia is associated with higher mortality rates.
Soliman HM, Mercan D, Lobo SS, Melot C, Vincent JL.
Department of Intensive Care, Erasme University Hospital, Free University of Brussels, Belgium.
OBJECTIVE: Previous studies have shown a wide variation in the prevalence of total serum hypomagnesemia in intensive are unit (ICU) patients and in associated mortality rates. As the ionized part of magnesium is the active portion, we sought to define the prevalence of ionized hypomagnesemia in critically ill patients and to evaluate its relationship with organ dysfunction, length of stay, and mortality. DESIGN: Prospective observational study. SETTING: A 31-bed, medical-surgical, university hospital ICU. PATIENTS: A total of 446 consecutive patients admitted to the ICU over a 3-month period. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The ionized magnesium level (normal value, 0.42-0.59 mmol/L) was measured at admission and then every day until discharge from the ICU. At admission, 18% of patients had ionized hypomagnesemia, 68% had normal ionized magnesium levels, and 14% had ionized hypermagnesemia. There was no significant difference in the length of stay or in the mortality rate between these three groups of patients. Hypomagnesemic patients more frequently had total and ionized hypocalcemia, hypokalemia, and hypoproteinemia. A total of 23 patients developed ionized hypomagnesemia during their ICU stay; these patients had higher Acute Physiology And Chronic Health Evaluation II (14.9 +/- 5.4 vs. 11.0 +/- 6.2) and Sequential Organ Failure Assessment (SOFA; 7.1 +/- 5.4 vs. 3.9 +/- 2.8) scores at admission (p <.01 for both), a higher maximum SOFA score during their ICU stay (10.0 +/- 5.6 vs. 4.4 +/- 3.2, p <.01), a higher prevalence of severe sepsis and septic shock (57 vs. 11%, p <.01), a longer ICU stay (15.4 +/- 15.5 vs. 2.8 +/- 4.7 days, p <.01), and a higher mortality rate (35% vs. 12%, p <.01) than the other patients. The major risk factors for developing hypomagnesemia during the ICU stay were a prolonged ICU stay, treatment with diuretics, and sepsis. CONCLUSION: Development of ionized hypomagnesemia during an ICU stay is associated with a worse prognosis. It is often associated with the use of diuretics and the development of sepsis. Monitoring of ionized magnesium levels may have prognostic, and perhaps therapeutic, implications.
J Am Coll Nutr. 1990 Apr;9(2):114-9.
Effect of intravenous epinephrine on serum magnesium and free intracellular red blood cell magnesium concentrations measured by nuclear magnetic resonance.
Ryzen E, Servis KL, Rude RK.
Department of Internal Medicine, University of Southern California, Los Angeles.
Hypomagnesemia is a common clinical finding in hospitalized patients and can cause hypocalcemia, cardiac arrhythmias, muscular weakness, and hypokalemia. Hypomagnesemia usually implies cellular magnesium (Mg) depletion, but stress and some clinical conditions which raise serum catecholamine concentrations may lower serum Mg (sMg) concentrations. To help investigate the mechanism and degree of the effect of catecholamines on sMg concentration, we gave intravenous epinephrine (0.1 microgram/kg/min) to 12 normal volunteers for 2 hours. The sMg concentration fell from 1.86 +/- 0.04 mg/dl to 1.63 +/- 0.05 mg/dl (mean +/- SEM, p less than 0.01). Pre-infusion intracellular free Mg (Mg++) in red blood cells (RBC) as measured by nuclear magnetic resonance spectrophotometry (NMR) was 171 +/- 7.6 microM and did not differ significantly from post-infusion RBC Mg++, 186 +/- 12.6 microM. Total blood mononuclear cell Mg content and urine Mg excretion also did not change. These data suggest that epinephrine has a small but significant effect on the lowering of sMg concentrations. Endogenous catecholamine release during stress or acute illness may therefore contribute to the hypomagnesemia seen in acutely ill patients. Our data also suggest that hypomagnesemia seen under conditions of acute stress may not always imply depleted tissue Mg stores. As no absolute change in cellular Mg or in urinary Mg excretion was demonstrated, acute intracellular shifts of Mg into blood cells and/or urinary Mg losses may not account for the hypomagnesemia. The prevalence and clinical consequences of stress hypomagnesemia require further investigation.
Crit Care Med. 1996 Jan;24(1):38-45.
Magnesium repletion and its effect on potassium homeostasis in critically ill adults: results of a double-blind, randomized, controlled trial.
Hamill-Ruth RJ, McGory R.
Department of Anesthesiology, University of Virginia Health Sciences Center, Charlottesville 22908, USA.
OBJECTIVES: The aims of this study were to evaluate the safety and efficacy of magnesium replacement therapy and to determine its effect on potassium retention in hypokalemic, critically ill patients. DESIGN: A prospective, double-blind, randomized, placebo-controlled trial. SETTING: A surgical intensive care unit (ICU). PATIENTS: A total of 32 adult surgical ICU patients were admitted to the study on the basis of documented hypokalemia (potassium of < 3.5 mmol/L) within the 24-hr period before entering the study. Patients were randomized to receive either placebo (n = 15) or magnesium sulfate (n = 17). One patient from each group was excluded from the study due to failure to complete the full series of doses. INTERVENTIONS: Patients received a “test dose” of either magnesium sulfate (2 g, 8 mmol) or placebo (5% dextrose in water) infused over 30 mins every 6 hrs for eight doses. The next schedule test dose was held if hypermagnesemia (magnesium of > 2.8 mg/dL [> 1.15 mmol/L]) was documented at any time during the study. Routine replacements of potassium and magnesium continued during the duration of the study, when clinically indicated, for serum potassium concentrations of 3.5 mmol/L or serum magnesium concentrations of < 1.8 mg/dL (< 0.74 mmol/L). MEASUREMENTS AND MAIN RESULTS: Age, weight, and Acute Physiology and Chronic Health Evaluation II scores were recorded on entry into the study. Just before administration of each test dose, blood was drawn for magnesium and potassium, bicarbonate, pH, and glucose determinations, and an aliquot of the preceding 6 hrs urine collection was sent for magnesium and potassium determinations. Serum calcium, phosphate, urea nitrogen, and creatinine concentrations were measured daily. The amounts of magnesium and potassium administered via parenteral nutrition, tube feeding, and replacement infusions were calculated for each 6-hr interval. The amounts of magnesium and potassium excreted in the urine were similarly assessed. The groups showed no differences with regard to age, weight, Acute Physiology and Chronic Health Evaluation II scores, or initial serum magnesium concentration. Initial potassium, bicarbonate, pH, calcium, phosphate, glucose, blood urea nitrogen, and creatinine values were not different between groups. Patients receiving magnesium sulfate showed a statistically significant increase in serum magnesium concentration at 6 hrs when compared with placebo, as well as with itself at time 0 (p < .0001), a difference maintained throughout the study. Compared with the placebo group, the total amount of elemental magnesium administered was significantly greater in the treatment group (1603 +/- 124 vs. 752 +/- 215 mg [65.7 +/- 5.8 vs. 30.8 +/- 8.8 mmol], p < .0001), as was urine magnesium excretion (1000 +/- 156 vs. 541 +/- 68 mg [41.0 +/- 6.4 vs. 22.2 +/- 2.8 mmol] p < .0001). However, the net magnesium balance (total magnesium in – total urine magnesium) was significantly more positive in the treatment group (612 +/- 180 vs. 216 +/- 217 mg [25.1 +/- 7.4 vs. 8.9 +/- 8.9 mmol], p < .005). The treatment and control groups had the same serum potassium concentrations and did not receive different amounts of potassium (245 +/- 39 vs. 344 +/- 45 mmol, respectively, p = .06), although the treatment group required less potassium replacement/6 hrs by 30 hrs compared with itself at time 0 (p < .05). Despite the same serum potassium values, the net potassium balance for 48 hrs was positive in the treatment group (+ 72 +/- 32 mmol) and negative in the control group (-74 +/- 95 mmol, p < .05). There were no complications associated with the magnesium sulfate administration. CONCLUSIONS: Magnesium sulfate administered according to the above regimen safety and significantly increases the circulating magnesium concentration. Despite greater urine magnesium losses in the treatment group, this group exhibited significantly better magnesium retention.
Influence of intravenous Mg++ solutions on renal excretion of potassium, sodium, calcium, chloride, intraleukocytic potassium and peripheral vascular resistance: a metabolic and hemodynamic study in normal volunteers.
Glanzer K, Schlebusch H, Sorger M, Pannenbecker D, Kruck F.
In an open randomized crossover trial 8 healthy male volunteers received an intravenous infusion of potassium chloride, potassium/magnesium chloride, potassium-(D,L)-aspartate, and potassium/magnesium-(D,L)-aspartate. Equimolar amounts of potassium (27.75 mmol) and magnesium (13.9 mmol) were given in a 500-ml volume during 24 h. During two 9-day periods subjects were maintained on a constant diet with a daily intake of 80 mmol potassium and 60 mmol magnesium. Infusions were administered on day 5 and 7 of each period. Serum and urine electrolyte concentrations as well as intraleukocyte potassium were measured before, during, and after the tests; cardiac output and systemic vascular resistance were determined by impedance cardiography. Potassium and magnesium containing solutions did not influence renal elimination of potassium, and also the circadian rhythm of potassium excretion did not show any change. The elimination of sodium, calcium, potassium, and chloride rose significantly over the corresponding control values during magnesium infusions, but not when potassium salts were given. The increase of calcium excretion after Mg++ is most probably due to suppression of parathyroid hormone. Intraleukocyte potassium was not affected significantly by the various infusions, indicating that intracellular compartments are completely filled. There was no evidence that the anion (D,L-aspartate or chloride) had a significant effect on all measured variables. Mean arterial blood pressure and peripheral vascular resistance were not altered significantly during the infusions.
Arch Intern Med. 1988 Nov;148(11):2415-20.
Magnesium metabolism. A review with special reference to the relationship between intracellular content and serum levels.
Marshfield Clinic, WI 54449.
Magnesium (Mg++) is a ubiquitous element in nature, playing a role in photosynthesis and many metabolic functions in humans. All enzymatic reactions that involve adenosine triphosphate have an absolute requirement for Mg++. Levels of Mg++ are controlled by the kidneys and gastrointestinal tract and appear closely linked to calcium, potassium, and sodium metabolism. The clinical manifestations and causes of abnormal Mg++ status are protean. Testing for altered Mg++ homeostasis is problematic. Serum levels, which are those generally measured, reflect only a small part of the total body content of Mg++. The intracellular content can be low, despite normal serum levels in a person with clinical Mg++ deficiency. Future directions in research related to intracellular content of Mg++ are discussed. Treatment of altered Mg++ status depends on the clinical setting and may include the addition of a potassium/Mg++-sparing drug to an existing diuretic regimen. Guidelines for therapy are given.
Alcohol Clin Exp Res. 1992 Oct;16(5):986-90.
Oral magnesium supplementation improves metabolic variables and muscle strength in alcoholics.
Gullestad L, Dolva LO, Soyland E, Manger AT, Falch D, Kjekshus J.
Department of Internal Medicine, Baerum Hospital, Sandvika, Norway.
Magnesium deficiency is common among chronic alcoholics, but the knowledge of oral magnesium supplementation to this group is limited. We, therefore, randomized 49 chronic alcoholics, moderate to heavy drinkers for at least 10 years to receive oral magnesium or placebo treatment for 6 weeks according to a double-blind protocol. Effects on metabolic variables and muscle strength were analyzed. Significant reduction of aspartate-aminotransferase (ASAT), alanine-aminotransferase (ALAT) and gamma-glutamyl-transpeptidase (GGT) were seen after magnesium, whereas no change was observed with placebo. Bilirubin decreased in both groups. Serum Na, Ca, and P increased significantly during magnesium therapy compared with no statistically significant change in the placebo group. Serum K and Mg increased slightly after magnesium supplementation and decreased in the placebo group, resulting in a significant difference between the two groups at the end of the study. Muscle strength increased significantly during magnesium treatment, contrasting to no change with placebo. Blood pressure, heart rate, hematological variables, serum lipids (cholesterol, HDL, TG), glucose tolerance, and creatinine were unchanged in the two groups after treatment. Alcohol consumption was similar before and during the trial and does not explain the differences between the two groups The results shows that short-term oral magnesium therapy may improve liver cell function, electrolyte status, and muscle strength in chronic alcoholics.
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