Anesth Analg 2003;96:1617-1620
© 2003 International Anesthesia Research Society
PEDIATRIC ANESTHESIA
The Effects of Magnesium Prime Solution on Magnesium Levels and Potassium Loss in Open Heart Surgery
Wang Jian, MSc,
Liu Su, MD, and
Liang Yiwu, MD
Department of Cardiac Surgery, Second Hospital of Hebei Medical University, Shijiazhuang, People’s Republic of China
Address correspondence and reprint requests to Wang Jian, MSc, Department of Cardiac Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, P. R. China. Address e-mail to wangjian91{at}hotmail.com
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Abstract
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In this study, we examined the effects of magnesium supplementation in the cardiopulmonary bypass (CPB) prime solution on pediatric patients’ magnesium levels and potassium loss with open heart surgery. Forty pediatric patients undergoing heart surgery were randomly assigned either magnesium sulfate (magnesium group, n = 20; 0.25 mmol/kg) or saline (placebo group; n = 20) supplementation to the prime solution. Ionized magnesium (IMg) and urinary magnesium and potassium were mea- sured at defined time points during and after CPB. In the magnesium group, IMg concentration was larger during CPB but not after CPB. IMg decreased in the early stages of CPB in the placebo group and decreased to an even smaller level 24 h after CPB. Urinary magnesium levels in the magnesium group were larger than those in the placebo group during and after CPB, and urinary potassium concentrations reached significantly smaller levels 24 h after CPB (44.2 ± 2.9 versus 60.9 ± 2.6 mmol/L; P < 0.01). We conclude that the addition of magnesium into prime solution maintains normal IMg levels and prevents potassium flux during the perioperative period.
IMPLICATIONS: In our study, we demonstrate that a magnesium prime solution can prevent hypomagnesemia during and after cardiopulmonary bypass (CPB) and decrease the urinary potassium loss after CPB in pediatric patients undergoing open heart surgery.
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Introduction
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Magnesium plays an important role in human physiology and affects the function of cardiovascular processes, such as vascular smooth muscle tone, myocardial conduction, and cardiac excitability and contractility. Magnesium deficiency can impair cardiac conduction, increase the risk for arrhythmias, predispose to coronary artery spasm, and contribute to neurological irritability (1,2). Hypomagnesemia and its effects during the perioperative period have been documented in pediatric patients undergoing cardiopulmonary bypass (CPB), but few measures have been taken to prevent it. The purpose of this study was to examine the effects of magnesium supplementation in the prime solution on the pediatric patient’s magnesium levels and potassium loss during the perioperative period.
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Methods
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After IRB approval and written, informed consent, 40 pediatric patients with normal heart, liver, and kidney function undergoing open heart surgery with CPB for repair of ventricular septal defect were enrolled in the study between October 2001 and April 2002. Patients with pulmonary hypertension or chronic arrhythmia and those receiving medication prescribed for the control of these conditions were excluded from the study. All operations were conducted at our center, and the anesthetic management and surgical techniques were standardized. The induction of anesthesia was accomplished with halothane, fentanyl, and midazolam. Heparinization was achieved with a heparin dose of 3 mg/kg, and the activated clotting time was controlled at >450 s. Red blood cells were added to the prime solution to maintain the patient’s hematocrit level >20% as necessary. CPB was maintained with a Stocket SIII roller pump with a membrane oxygenator. The cardioplegic solution consisted of a cold hyperkalemic crystalloid cardioplegia containing 1.2 mmol/L of MgSO4.
Forty patients were prospectively and randomly assigned to add magnesium sulfate (magnesium group, n = 20; 0.25 mmol/kg) or saline (placebo group; n = 20) to the prime solution. Samples of arterial blood were collected at defined time points: t1, 24 h before surgery; t2, before CPB; t3, at onset of CPB; t4, at rewarming; t5, at the termination of CPB; and t6, t7, t8, and t9—1, 2, 6, and 24 h, respectively, after CPB. Samples were measured immediately on a Stat Profile M analyzer (Nova Biomedical, Waltham, MA) for ionized magnesium (IMg), blood gases, hematocrit level, electrolytes, ionized calcium (Ca2+), lactate, and glucose. Urine samples were also collected at the same time points as blood sampling, and urinary magnesium concentration was measured. Urinary potassium concentration was analyzed for the entire 24 h after CPB. Calcium and potassium were supplemented to normal levels after CPB. No patient received magnesium after CPB. Continuous electrocardiographic documentation of arrhythmias was performed for 24 h after CPB. The occurrence of atrial or ventricular ectopic beats and tachycardias was recorded.
Demographic and clinical variables were analyzed by using Fisher’s exact test for categorical variables and Student’s t-test for continuous variables. Chi-square tests were performed to assess the probability of dysrhythmias between the two treatment groups. The data were presented as mean ± SD. All statistical procedures were performed with SPSS statistical software (SPSS Inc., Chicago, IL). Statistical significance was considered as P < 0.05.
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Results
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There were no demographic differences between patients in the placebo group and magnesium group (Table 1). The levels of IMg before surgery were similar between the two groups. The patients in the magnesium group had a large IMg blood concentration during CPB and had normal levels during the postoperative period. IMg levels were significantly less for patients in the placebo group (Fig. 1). Creatinine, potassium, and Ca2+ levels were within the reference range for patients in both groups throughout the entire study. There was no difference in the amount of calcium, potassium, and furosemide supplementation required for each study group. There was no difference in urinary magnesium between the two treatment groups before CPB. However, urinary magnesium was significantly less for patients in the placebo group during and after CPB than for those in the magnesium group (Fig. 2). Urine samples 24 h after CPB were collected together and showed that urinary potassium concentration in the magnesium group (44.2 ± 2.9 mmol/L) was less than that (60.9 ± 2.6 mmol/L; P < 0.01) in the placebo group. After aortic cross-clamp removal, five patients (25%) in the placebo group experienced ventricular fibrillation (VF), whereas two patients (10%) with VF were observed in the magnesium group. The probability of VF occurring in the placebo group was estimated to be twice as much as in the magnesium group. However, the difference did not reach statistical significance. Dysrhythmias were noted by continuous electrocardiography monitoring. No ventricular dysrhythmia occurred, and all dysrhythmias were either atrial or junctional in nature.
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Figure 1. Mean ionized magnesium concentration in the magnesium group (top line) and placebo group (bottom line) at each blood-sampling time point: t1, 1 day before surgery; t2, before CPB; t3, at the onset of CPB; t4, at rewarming; t5, at the termination of CPB; and t6, t7, t8, and t9—1, 2, 6, and 24 h, respectively, after CPB. P < 0.01, t3–t9. CPB = cardiopulmonary bypass.
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Figure 2. Mean urinary magnesium concentration in the magnesium group (top line) and the placebo group (bottom line) at the same time points as blood sampling. P < 0.01, t3–t9.
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Discussion
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Our investigation demonstrates that the prime solution with magnesium supplementation prevents hypomagnesemia during and after CPB. The mechanism for hypomagnesemia in pediatric patients undergoing heart surgery is multifactorial. One factor is that the volume of the prime solution in children is large compared with the patient’s circulating blood volume. The role of hemodilution as a causative factor in hypomagnesemia may be significant with the magnesium-free prime solution. Perioperative renal magnesium losses can occur after the administration of loop or thiazide diuretics. Munoz et al. (3) have demonstrated that neonates have the most frequency of ionized hypomagnesemia during cooling on CPB. Preoperative ionized hypomagnesemia was also a common finding in patients with congenital heart defects who were older than one month.
Fox et al. (4) have demonstrated that IMg decreased with the onset of CPB, and a statistically significant decrease was seen in children. Depletion of total body magnesium also occurs during and after open heart operations in children (5). In our study, we prevented hypomagnesemia during and after CPB in the magnesium group. During CPB, there were large levels of IMg in the magnesium group, but they were transient. One hour after CPB, IMg returned to normal ranges. Whether large levels of magnesium are beneficial during hypothermic CPB is unknown. This concentration of magnesium sulfate (0.25 mmol/L) administered to the prime solution did not appear to result in toxic sequelae, such as heart block, bradycardia, or ascension of the arteriotony.
Patients with ionized hypomagnesemia have been shown to have normal levels of total magnesium (6). Because significant changes to the IMg can take place independently of total magnesium 24 hours after CPB (7), we used the measurement of IMg to analyze the magnesium levels.
Magnesium has a major influence on myocardial tissues, has an essential role in the maintenance of resting membrane potential, and attenuates the electrophysiologic effects of hyperkalemia (8). Magnesium also has been shown to reduce platelet aggregation (9), to inhibit the catecholamine release associated with stressful events, such as tracheal intubation, and to reduce systemic and coronary vascular resistance (10). Therefore, adequate levels of magnesium during and after CPB should be maintained. With normal kidney function, the surplus magnesium can flux with urine. In our study, urinary magnesium in the magnesium group was larger than in the placebo group. This can reflect the magnesium saturation in the body’s fluid.
Potassium flux is also a problem after CPB. Under the condition of hypomagnesemia, cells cannot fully absorb potassium and increase potassium flux across cell membranes. In our study, urinary potassium concentrations of the placebo group were larger than those of the magnesium group. We demonstrated that adding magnesium to the prime solution can decrease the incidence of urinary potassium flux after CPB and maintain a potassium balance.
In our patients, the probability of VF in the placebo group was almost twice that of the magnesium group; however, this did not reach statistical significance. Ventricular recovery after hypothermic cardioplegic arrest may be related to the calcium antagonist properties of magnesium, including the inhibition of voltage-dependent calcium channels and increased mitochondrial and sarcoplasmic reticulum calcium uptake that attenuates calcium overload after reperfusion (11). Magnesium supplementation in pediatric patients undergoing surgery for congenital heart defects during the perioperative period has been shown to enhance myocardial recovery (12). After CPB, normalization of myocardial cell function is dependent on the restoration of oxidative metabolism (repletion of cellular oxidative adenosine triphosphate stores), and magnesium deficiency may contribute to the depletion of adenosine triphosphate and subsequent poor myocardial performance (13). The addition of extracellular magnesium to the prime solution may serve to reduce ischemia-associated cellular magnesium losses and accelerate the resumption of normal metabolism and contractile function of the heart.
The results of our study demonstrate that adding magnesium to the prime solution can prevent hypomagnesemia during and after CPB and can decrease the urinary potassium loss after CPB. Therefore, routine supplementation of magnesium sulfate may be helpful for pediatric patients undergoing cardiac surgery with CPB.
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References
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Accepted for publication February 10, 2003.
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Abstract
Introduction
