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Ann Thorac Surg 1995;59:921-927
© 1995 The Society of Thoracic Surgeons

Magnesium Flux During and After Open Heart Operations in Children

Department of Cardiothoracic Surgery, Killingbeck Hospital, and Departments of Clinical Biochemistry, Seacroft Hospital and Leeds General Infirmary, Leeds, United Kingdom

Accepted for publication December 22, 1994.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Hypomagnesemia and depletion of the body's magnesium stores is known to be associated with an increased incidence of both cardiac arrhythmias and neurological irritability. In a two-part prospective study we have evaluated whether magnesium deficiency is a significant occurrence in children treated in the intensive care unit after open heart operations, and subsequently have sought to identify how intraoperative metabolic changes were related to the resultant findings. In 41 children studied after operation the plasma magnesium concentration showed a significant decrease from 0.92 mmol/L (10th to 90th centile, 0.71 to 1.15 mmol/L) immediately after operation to 0.77 mmol/L (0.65 to 0.91 mmol/L) on the following morning. The subsequent change in grouped values was not significant but 14 (34.2%) and 7 (17.1%) possessed values of less than 0.7 mmol/L and 0.6 mmol/L, respectively. The occurrence of cardiac arrhythmias was not statistically related to the occurrence of hypomagnesemia. In 21 children perioperative changes in extracellular and tissue magnesium, potassium, and calcium content were measured. It was found that hemodilution with a prime low in magnesium caused a reduction from a median of 0.81 mmol/L to 0.61 mmol/L (p < 0.01). Plasma potassium level, however, was elevated from 3.7 mmol/L to 4.15 mmol/L (p < 0.05) and the ionized calcium content from 1.17 mmol/L (1.07 to 1.25 mmol/L) to 1.49 mmol/L (1.25 to 2.56 mmol/L) (p = 0.0009). The myocardial content of magnesium did not change significantly but skeletal muscle content was depleted from 6.75 µmol/g (2.85 to 8.35 µmol/g) to 5.65 µmol/g (2.45 to 7.2 µmol/g) (p < 0.01). Urinary excretion ratios of Mg²⁺/creatinine increased by a median 106% from the preoperative value of 0.62 (0.15 to 1.16) to 1.31 (0.59 to 1.43) postoperatively (p < 0.05). We conclude that depletion of total body magnesium occurs during and after open heart operation in children, but cardiac arrhythmias may occur in the absence of low serum concentrations. We suggest that a study evaluating the role of routine magnesium replacement in the prevention of postoperative depletion and its influence on symptomatology would be beneficial.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Magnesium is principally an intracellular electrolyte, 60% of the pool occurring in bone, 35% in muscle, and only 1% of the body pool being in the extracellular compartment [1, 2]. Within the cellular compartment it is bound to numerous enzymes including membrane Na/K adenosine triphosphatase and myosin adenosine triphosphatase playing a role as a coenzyme, and also is bound to adenosine triphosphate. Of the cellular pool 30% is localized to mitochondria, 5% to myofibrils, and almost 60% to the cytosol, but only 1% is free [1].

Magnesium significantly influences the function of excitable tissues [2, 3]. It is essential to the contractility of the heart and maintenance of the resting membrane potential, and acts as a natural calcium antagonist [4, 5]. Deficiency may cause disturbances of myocardial conduction, which are exhibited in the electrocardiogram as a shortened PR interval and ST depression, or arrhythmias such as supraventricular and ventricular tachycardias [6]. Deficiency also may cause neurologic irritability and epileptic seizures [7]. Depletion of extracellular and intracellular magnesium may occur after the use of loop diuretics and intravenous infusion of catecholamines [8, 9]. Cardiopulmonary bypass and open heart operation also have been shown to induce fluctuation in the plasma concentration of magnesium [10].

Hypokalemia is a recognized cause of cardiac arrhythmias after cardiac operations, and hypocalcemia or hypoglycemia of fits. Routine monitoring and replacement therapy for these abnormalities therefore is practiced commonly. It was our experience, however, that the symptoms may occur in the absence of these electrolyte abnormalities but occur secondary to hypomagnesemia. As a result of these observations we undertook first to identify the incidence of hypomagnesemia after open heart operations in children. The results obtained demonstrated a significant incidence; we thus sought to investigate the pattern of change in magnesium metabolism intraoperatively.

In this article we report the results obtained from this two-part study. In addition we report the changes in associated cation concentrations and the change in their tissue content. We discuss pathophysiologic processes that may be responsible for changes and the relevance of changes to clinical practice.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Part One
Forty-one children who required open heart operations to correct major congenital cardiac defects and treatment during recovery in the intensive care unit (ICU) had changes in plasma cation concentration evaluated. Children who had received correction of a secundum atrial septal defect or who required deep hypothermic circulatory arrest were excluded. Their median age was 4.9 years (10th to 90th centiles, 1.5 to 11.8 years), and weight was 15.5 kg (10th to 90th centiles, 9.75 to 25 kg). An attempt was made to collect a sufficient volume of blood on the admission to the preoperative ward in all patients; however, if this required repeated attempts at venipuncture, sampling was abandoned. Blood samples were obtained immediately after operation when patients were admitted to the ICU and on each subsequent morning when children remained in the ICU. The samples were collected in lithium heparin, and concentrations of Mg²⁺, K⁺, total Ca²⁺, albumin, urea, and creatinine were measured. The Ca²⁺ concentration was measured by the cresolphthalein complexone technique (Randox Laboratories Ltd, Crumlin, UK). Magnesium concentrations measured were values of the total plasma content. We elected to evaluate these results uncorrected for albumin concentration as methods of correction have not received extensive evaluation. Measured total calcium concentrations were adjusted for albumin with the following formula: Adjusted total Ca²⁺ concentration (mmol/L) = measured Ca²⁺ (mmol/L) + 0.025 [38 - albumin concentration (g/L)]. The normal values for electrolyte values derived from pooled data in the Yorkshire region were as follows: potassium = 3.5 to 5.0 mmol/L, magnesium = 0.7 to 1.2 mmol/L, and adjusted calcium = 2.1 to 2.7 mmol/L.

Cardiac function was monitored by recording the electrocardiogram and intravascular pressures continuously on standard intensive care monitoring equipment. The occurrence of atrial or ventricular ectopic beats more frequently than five beats a minute was considered abnormal and recorded. Tachycardias caused by abnormal conduction and that caused a reduction in blood pressure also were recorded.

The incidence of magnesium concentrations less than 0.7 mmol/L and 0.6 mmol/L was recorded and the statistical relationship to diuretic administration, the dose of inotropic support, and the incidence of cardiac and neurologic symptoms was documented. The level of significant hypomagnesemia was chosen as 0.6 mmol/L as we have observed previously that pediatric patients with lower plasma concentrations exhibit most symptoms. The results of the first 6 postoperative days only have been analyzed, as after this time the number of patients in the ICU was too low for valid statistical analysis.

Part Two
A group of 21 children had changes in plasma and tissue cation content evaluated during cardiopulmonary bypass (CPB). They had a median age of 3 years (10th to 90th centile, 1.9 to 12 years) and weight of 14.5 kg (10th to 90th centile, 8.5 to 27 Kg). Cardiopulmonary bypass was provided by a nonpulsatile roller pump and a membrane oxygenator, and the patient was cooled to 28°C. The prime volume of 800 mL was constituted of Hartmann's solution and synthetic colloid solution, and in 13 cases blood was added to the solution. The arterial oxygen tension was maintained greater than 20 kPa, and the perfusion pressure was maintained at approximately 50 mm Hg. Diastolic cardiac arrest was induced by the antegrade infusion of 30 mL/kg of St. Thomas's cardioplegia containing 16 mmol/L magnesium and 16 mmol/L potassium. The CPB time was a median of 78 minutes (10th to 90th centile, 50 to 97 minutes) and the ischemic time 48 minutes (10th to 90th centile, 32 to 58 minutes).

Blood specimens were obtained from the patient on induction of anesthesia, from the CPB volume before initiation of bypass, 3 and 30 minutes after the initiation of bypass, and at the end of the procedure. Further samples were collected from the patient on arrival in the ICU. A random urine collection was made preoperatively and immediately after bypass. Electrolyte concentrations measured in the samples of urine were related to creatinine concentration as a ratio. Packed cell volume was measured intraoperatively at the above time points.

Biopsy specimens of cardiac muscle were obtained from the right atrium of patients immediately before the commencement and immediately after completion of support by CPB. Biopsy specimens of skeletal muscle were obtained from rectus muscle visible in the base of the sternotomy wound at the same time points. These samples were collected from areas that had not been subjected to trauma or ischemia. Extraneous fat was removed, after which the samples were weighed and stored at -20°C until the time of analysis.

Blood specimens were collected into lithium heparin anticoagulant, and the concentrations of magnesium, potassium, ionized calcium, albumin, urea, and creatinine were measured. The sample obtained for the measurement of ionized calcium was collected anaerobically. Magnesium concentrations in the blood and urine were measured by atomic absorption spectrophotometry, and the concentration of potassium was measured by flame emission photometry. Plasma albumin concentration was measured with Bromocresol green on a Greiner G450 analyzer (Greiner Instruments, Langenthal, Switzerland). The concentration of ionized calcium was measured with a calcium-selective electrode on an ICAI analyzer (Radiometer, Copenhagen, Denmark). Muscle samples were dissolved with nitric acid, and the contents of magnesium, potassium, and calcium again were measured by atomic absorption spectrophotometry and flame photometry, respectively.

Statistics
Nonparametric statistical tests were used to compare the results of groups. Values have been presented as median values with 10th to 90th centile ranges. The Mann-Whitney U test was used to test the differences between unpaired data groups and the Wilcoxon test for paired data groups. Fisher's exact test was used to test the relation of frequencies of cation abnormalities, and between them and symptoms and treatments. A probability value of p less than 0.05 was accepted as significant.

The two stages of this protocol were evaluated and approved individually by the local hospital ethical committee, and informed consent was obtained from parents of children requiring tissue or blood sampling other than that performed in the course of treatment.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Part One
Forty-one children were treated in the ICU on the first and second postoperative days; on the third and fourth days the number was 28 and 12. The number subsequently remaining in the ICU reduced until on the fifth and sixth days only 9 and 4, respectively, remained.

Preoperative plasma [Mg²⁺] was 0.75 mmol/L (10th to 90th centile, 0.65 to 1.02 mmol/L; n = 12) and did not differ significantly from that obtained on admission to ICU, 0.92 mmol/L (0.72 to 1.15 mmol/L) (Wilcoxon test) (Fig 1). On day 2 the plasma [Mg²⁺] was 0.77 mmol/L (0.65 to 0.91 mmol/L) and was significantly less than that on day 1 (Wilcoxon p < 0.0001), but similar to that on day 3 and subsequent days. Hypomagnesemia at levels less than 0.7 mmol/L and 0.6 mmol/L occurred in 14 (34.2%) and 7 (17.1%) children, respectively. Furosemide was administered to 37 patients in the first day (median dose, 0.65 mg/kg [10th to 90th centile, 0 to 2.35 mg/kg]) and on day 2 (median, 1 mg/kg [0 to 2.8 mg/kg]), and spironolactone was administered to 2 and 10 patients on days 1 and 2 respectively, the dose ranging from 1.6 to 2.5 mg • kg^-1 • day^-1. Administration of these were not related to the occurrence of hypomagnesemia. Twelve patients received intravenous magnesium supplementation to correct hypomagnesemia.

View larger version (19K): [in this window] [in a new window]   Fig 1. . Measured daily plasma [Mg2+] preoperatively and after admission to the intensive care unit. The median and 10th to 90th centiles are presented. (Wilcoxon paired test comparing values with values with the previous day: *p < 0.05, **p < 0.01, ***p < 0.001.)

View larger version (18K): [in this window] [in a new window]   Fig 2. . Measured daily plasma [K+] preoperatively and after admission to the intensive care unit. (See key for Figure 1.)

View larger version (18K): [in this window] [in a new window]   Fig 3. . Measured daily plasma total [Ca+] preoperatively and after admission to the intensive care unit. (See key for Figure 1.)

Part Two
Concentrations of magnesium, potassium, and ionized calcium in the prime were 0.14 mmol/L (10th to 90th centiles, 0.07 to 0.34 mmol/L), 5.75 mmol/L (5.2 to 6.9 mmol/L) and 2.38 mmol/L (1.27 to 6.21 mmol/L), respectively. Hemodilution during initiation of CPB reduced the packed cell volume from 39% (32% to 50%) to 26% (23% to 33%) (p < 0.005). The [Mg²⁺] on induction of anesthesia was 0.81 mmol/L and decreased by 21% (12% to 43%) to 0.63 mmol/L (p < 0.01) (Fig 4). After the administration of cardioplegia the level rose to 1.53 mmol/L (p < 0.01). There was little change in values during the subsequent period of CPB, but the values decreased significantly by the time of admission to the ICU (p < 0.001) and was comparable with preoperative values.

View larger version (21K): [in this window] [in a new window]   Fig 4. . Measured plasma [Mg2+] during cardiopulmonary bypass. The median and 10th to 90th centiles are presented. (See key for Figure 1.)

View larger version (20K): [in this window] [in a new window]   Fig 5. . Measured plasma [K+] during cardiopulmonary bypass. The median and 10th to 90th centiles are presented. (See key for Figure 1.)

View larger version (18K): [in this window] [in a new window]   Fig 6. . Measured plasma ionized [Ca+] during cardiopulmonary bypass. (The result on admission to the intensive care unit was not available in any children.) The median and 10th to 90th centiles are presented. (See key for Figure 1.)

Myocardial Mg²⁺ content did not change significantly from the prebypass value of 4.25 µmol/g of wet tissue (3.35 to 4.85 µmol/g). Skeletal muscle Mg²⁺ content decreased by 17.3% from 6.75 µmol/g (2.85 to 8.35 µmol/g) to 5.65 µmol/g (2.45 to 7.2 µmol/g) (p < 0.01). This change did not correlate with changes in plasma [Mg²⁺]. Myocardial K⁺ content increased by 37% from 58 µmol/g (31.5 to 81.5 µmol/g) to 79 µmol/g (45 to 100.5 µmol/g) (p < 0.005), but the skeletal content did not change significantly from 75.5 µmol/g (26 to 111.5 µmol/g). Myocardial Ca²⁺ content increased significantly by 37.5% from 2.15 µmol/g (1.6 to 4.15 µmol/g) to 3.6 µmol/g (1.3 to 11.25 µmol/g) (p = 0.006), but the 5% increase in skeletal muscle content from 1.15 µmol/L (0.3 to 12.25 µmol/L) to 2.24 µmol/L (4.35 to 0.75 µmol/L) was not significant.

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Occurrence of cardiac arrhythmias or neurologic irritability after correction of congenital intracardiac defects commonly is attributed to deficiencies in plasma potassium, calcium, and glucose, but on many occasions no abnormalities may be demonstrated. The important role of magnesium deficiency in the etiology of these symptoms has been realized increasingly in recent years [5, 7, 9]. Patterns of magnesium deficiency after open heart operations in a pediatric population, however, have not been well defined, and thus the need for magnesium replacement in this population remains largely unaddressed. This study was undertaken first to identify the incidence of hypomagnesemia in children being treated in the intensive care unit after open heart operations and second to identify whether these changes were related directly to intraoperative procedures.

The first part of the study had the primary aim of evaluating the incidence of hypomagnesemia in the ICU. As a significant incidence of hypomagnesemia had not been reported previously in children after open heart operations, the ethical committee granted permission only to measure the plasma [Mg²⁺] in samples being obtained for other routine tests. Subsequent to positive results being obtained the second study was undertaken and ethical approval gained to perform the more detailed and comprehensive evaluation. The presence of ``incomplete'' results in part one of the study therefore must be attributed to difficulties of obtaining sufficiently large blood samples from children.

The results demonstrated a complex pattern of changes in magnesium metabolism occurring during and after open heart operations. An early period of hypomagnesemia occurred after the initiation of CPB and was followed by hypermagnesemia. The plasma level of magnesium returned to normal soon after weaning from CPB and continued to decrease in the subsequent hours. It also was noted that depletion of skeletal muscle magnesium content occurred during CPB but the myocardial content was unaltered. In the ICU a marked reduction in plasma magnesium concentration occurred during the first 24 hours after operation and on the subsequent days. Thus hypomagnesemia less than 0.6 mmol/L was found in 17.1% of patients.

The pattern of change in plasma potassium concentration differed from that of magnesium. It rose significantly throughout the period of CPB. Cardiac muscle content of potassium also rose markedly, but the content in skeletal muscle content did not change significantly. Postoperative hypokalemia was identified in 29.3% of children. Changes in plasma calcium concentration were similar to those of potassium in that a prime with elevated calcium concentration caused hypercalcemia during CPB, which persisted on the first day. Myocardial calcium content was increased and the skeletal muscle content remained relatively unchanged. Postoperative hypocalcemia was identified in only 7.3% of patients. These changes were not statistically related to the occurrence of hypomagnesemia.

In studies comparable with our own the content of magnesium and potassium were measured in samples of atrium and skeletal muscle obtained before open heart operations [11, 12]. Results from these studies concur with our own, demonstrating a higher content of magnesium in skeletal than in cardiac muscle. Tovey and associates [13] demonstrated that the content of magnesium in dehydrated samples of atrium muscle showed a moderate correlation with that of skeletal muscle, and suggested that in some situations changes of the latter may be used as an indirect measure of the former. The results of our own study, however, indicate that the same pattern of change does not occur in the two tissues during and after open heart operations. Therefore in this situation the changes in skeletal muscle magnesium cannot be used as a surrogate measurement of changes in cardiac magnesium.

A dilemma exists in providing an interpretation for the cause and clinical relevance of the patterns of flux identified. The changes in serum and cardiac muscle magnesium content during CPB suggest that magnesium metabolism has not been deranged. This interpretation, however, does not account for the changes in the magnesium metabolism recorded at other times and in other physiologic compartments. Depletion of skeletal muscle content, the marked incidence of postoperative hypomagnesemia, and the increased excretion of magnesium indicate that depletion of a number of physiologic compartments has occurred. A unifying explanation therefore cannot be provided.

The interrelationship of mechanisms causing change in magnesium metabolism are also complex. The first mechanism was the effect of circulating solutions; a prime low in magnesium concentration and cardioplegia high in magnesium concentration caused reciprocal swings in the plasma concentration [10]. The resultant effect of hypermagnesemia was the maintenance of the cardiac content. The finding of a normal cellular content as opposed to one that was high after administration of a hypermagnesemic solution concurs with Quamme and Rabkin's report [1] in which changes in the magnesium content of isolated myocytes were related to the content on magnesium in solutions bathing them. Myocyte content, however, was reported to increase to a maximum beyond which increases of the concentration of magnesium in the bathing solution caused no further rise. Quamme and Rabkin [1] suggested the presence of a controlling mechanism that determined intracellular magnesium content.

A number of pathophysiologic responses to the institution of the procedures of open heart operations also may contribute to the disturbances of magnesium metabolism. Raised levels of circulating catecholamines occurring both intraoperatively and postoperatively cause increased stimulation of myocyte adrenoreceptors and thus an efflux of magnesium [8]. Intraoperative ischemia and the associated depletion of adenosine triphosphate, together with reperfusion injury to the cellular membrane, also may result in a release of the cation into extracellular fluid [14–16]. Finally, administration of loop diuretics such as furosemide induces an increased renal excretion of magnesium together with potassium [9].

The subject of magnesium deficiency and magnesium replacement is more complex than that of potassium deficiency, as the potassium ion has the relatively simple function of influencing the potential difference across cell membranes. The magnesium ion, however, influences a number of membrane transport systems and enzyme systems involved in cellular metabolism and myofibrillar contraction. Administration of magnesium may prevent the toxic effect of catecholamine stimulation of myocytes and thus maintain intracellular adenosine triphosphate content [17, 18].

The presence of overt magnesium depletion exhibited as hypomagnesemia or covert deficiency affecting intracellular content is associated with cardiac arrhythmias. Magnesium in cardioplegia is essential as a protective agent, and administration after myocardial infarction reduced the incidence of ventricular arrhythmias by 77% in the experimental situation and by 50% clinically [6, 16]. Replacement therapy for acute deficiency and ``prophylactic'' replacement in adults after coronary bypass operations have been shown to reduce the incidence of postoperative cardiac arrhythmias [19, 20]. This replacement also has been shown to have the secondary result of rectifying abnormalities of serum concentrations of potassium and calcium. Although the exact mechanism of the antiarrhythmic action of magnesium is not entirely apparent, it is known that increasing extracellular magnesium concentration hyperpolarizes the cell membrane, causing reduced myocardial excitability and attenuating voltage-dependent calcium influx [5, 21].

In our own clinical practice we have addressed the situation of overt deficiencies occurring after pediatric cardiac operations. A number of children within or extraneous to this study have experienced hypomagnesemia postoperatively and have exhibited supraventricular or ventricular arrhythmias and fits in the absence of deranged plasma potassium, calcium, and glucose content. Many of them have been treated successfully by intravenous administration of magnesium sulfate. Subsequent to this study it has been our practice to correct hypomagnesemia revealed by daily evaluation.

The findings of the study have demonstrated that total body magnesium content has been depleted during and after open heart operations in children. Furthermore, there has been an occurrence of cardiac arrhythmias in some of these patients although serum levels of magnesium did not differ between those patients in whom arrhythmias did and did not develop. On the basis of these results we hypothesize that a protocol of routine magnesium replacement after operation may prevent depletion of total body magnesium, reduce the incidence of postoperative arrhythmias, and improve myocardial function after open heart operations. Schuette and associates [22] have suggested that the quantity of magnesium required is best administered intravenously as a slow intravenous infusion rather than as a bolus administration, thus providing the most effective form of replacement. A study that examined the validity of the hypothesis would be required to consider prevention of CPB-induced hypomagnesemia and replacement of losses that follow operation.

In conclusion, in this study we have observed changes in tissue and plasma magnesium content occurring during and after open heart operations in children. We have found that although marked and varying fluxes in plasma magnesium concentration may occur during CPB, intraoperative skeletal muscle depletion of magnesium and postoperative hypomagnesemia were significant findings indicating that depletion of total body magnesium occurred. Cardiac arrhythmias occur in these patients and may be identified in the absence of low serum magnesium concentrations. We suggest that a study is required that investigates the role of routine magnesium replacement after open heart operations in children and its influence on symptomatology.

	Acknowledgments

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
We are grateful to the Killingbeck Children's Heart Surgery Fund, which has provided generous support to this project.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Address reprint requests to Dr Satur, Department of Cardiothoracic Surgery, Killingbeck Hospital, York Rd, Leeds, West Yorkshire, LS14 6UQ, United Kingdom.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Christopher M. R. Satur Cengiz Gebitekin Duncan R. Walker Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Satur, C. M. R. Articles by Walker, D. R. Search for Related Content PubMed PubMed Citation Articles by Satur, C. M. R. Articles by Walker, D. R.