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Utility of magnesium sulfate in the treatment of rapid atrial fibrillation in the emergency department: a systematic review and meta-analysis

Hoffer, Megana; Tran, Quincy K.b,c; Hodgson, Ryana; Atwater, Matthewa; Pourmand, Alia

Author Information
European Journal of Emergency Medicine: August 2022 - Volume 29 - Issue 4 - p 253-261
doi: 10.1097/MEJ.0000000000000941



In the emergency department (ED), magnesium sulfate is used to treat multiple emergent medical conditions including preeclampsia/eclampsia, acute asthma attacks, migraines, and cardiac dysrhythmias. Among those conditions, magnesium sulfate is the first-line agent for treatment of eclampsia and torsades des pointes (TdP), and is a secondary agent in asthma exacerbations and migraine therapy [1,2].

Cardiac dysrhythmias are a common and potentially life-threatening presenting symptom in the ED setting, however, magnesium is not currently used routinely for treatment or prevention of cardiac dysrhythmias except in the case of TdP. Nonetheless, magnesium sulfate has been studied extensively in the cardiology literature for use in the treatment and prevention of cardiac dysrhythmias and, in particular, for the treatment of supraventricular tachycardias including atrial fibrillation.

In the cardiology literature, magnesium sulfate has been shown to provide antidysrhythmic benefit when given prophylactically following cardiac surgery. A Cochrane Review in 2013 concluded that magnesium sulfate was effective in the prevention of postoperative atrial fibrillation [3]. Prophylactic magnesium sulfate has been demonstrated in several randomized controlled trials (RCTs) to reduce the risk of supraventricular tachycardias, including atrial fibrillation, atrial tachycardia, and supraventricular tachycardia postoperatively [4–11]. Similarly, there is evidence that coadministration of magnesium sulfate with other antidysrhythmic medications reduces the rate of arrhythmias [12,13]. Low serum magnesium has also been associated with a greater risk for development of cardiac dysrythmias [14]. There is also evidence that magnesium may decrease early-after-depolarizations (EADs) and suppress induced dysrhythmias [15–23].

In a cross-sectional analysis of US ED data, there were 3.9 million ED visits from 2007 to 2014 with atrial fibrillation as a primary diagnosis, resulting in an average 67% admission rate. The same data indicate an upward trend in ED visits for atrial fibrillation during that same time period. In a cost analysis during this time period, there was a 37% increase in annual adjusted cost of admitted patients with atrial fibrillation to a total of 10.1 billion annually in 2014 [24].

Taking into consideration the apparent benefits of magnesium supplementation in similar inpatient settings and the high rate that rapid atrial fibrillation is observed in the ED, it is a question of interest whether the addition of magnesium may improve our ability to safely and effectively treat this cardiac dysrhythmia in the ED. This systemic review and meta-analysis aim to examine the existing evidence for use of magnesium in the treatment of rapid atrial fibrillation in the ED.


Study selection criteria

Prior to the beginning our study, we created a protocol according to the Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) protocols statement, and we conducted our study according to PRISMA guidelines [25].

We used the Patient, Intervention, Comparison, Outcome framework to guide our inclusion criteria


We included randomized control trials, all observational studies (prospective and retrospective studies) of adult patients (age > 18 years) who presented to EDs with atrial fibrillation and rapid ventricular responses


Patients with atrial fibrillation and rapid ventricular responses were treated with intravenous magnesium alone or along with other pharmacological agents.


The control group included patients with atrial fibrillation and rapid ventricular responses but were treated with other pharmacological agents, without intravenous magnesium.


Our primary outcome was the difference in ventricular heart rate (HR) before and after treatment at the earliest assessment by the authors. Our secondary outcomes of interest included the percentage of patients who converted from atrial fibrillation to sinus rhythm. We also investigated the rate of any complications or any major complications, as defined by the authors.

Search criteria

We searched PubMed and SCOPUS databases from their conception up to 30 June 2021.

We excluded studies that did not have full text, and we also excluded conference abstracts, any reviews, or case reports. We further excluded studies that did not specify whether the clinical setting was in the ED. We screened the bibliographies of included full-text studies for additional eligible studies but did not find any. We also contacted the corresponding author of an included study to request further data but did not receive any responses. This study was registered with PROSPERO, an international database of prospectively registered systematic reviews (CRD42021260097).

Search strategy

We used the search (“emergency service, hospital”[MeSH Terms] OR (“emergency”[All Fields] AND “service”[All Fields] AND “hospital”[All Fields]) OR “hospital emergency service”[All Fields]) AND (“magnesium”[MeSH Terms] OR “magnesium”[All Fields] OR “magnesium’s”[All Fields] OR “magnesiums”[All Fields]) AND (Atrial fibrilation).

We included further detail search terms in Appendix 1, Supplemental digital content 1,

Selection process

After the search, we imported our search results to the website Covidence (, Melbourne, Australia), which helps to manage the screening of our titles, abstracts, full-text articles, and duplicates. Multiple reviewers (M.P., C.P., A.P., and Q.K.T.) worked independently to screen each title and abstract for eligible studies. A third investigator adjudicated any differences. Any title and abstract would need at least two agreements to proceed to the full-text review stage. The same process again is repeated for the full-text stage. Only full-text articles receiving agreements from at least two investigators were included in the final analyses.

Risk of bias assessment

We used the Cochrane’s Risk-of-Bias tool to assess the quality of the included studies [26]. The Cochrane’s Risk-of-Bias tool assesses risk of bias in five domains: randomization, deviations from the study protocol, outcome measurement, selection of the reported result, and bias due to missing outcomes data. The overall risk of bias of the entire study is based on the worst score of any single domain, which is ranked as low, high, or some concerns. For quality assessment, two investigators graded the included studies independently. Any discrepancy was adjudicated by consensus between the two investigators and a third investigator as an arbiter, if necessary.

Statistical analysis

We presented the information from each study as percentage or mean (±SD) as appropriate. When the authors expressed continuous variables as median (±interquartile range), we converted median into mean as previously described, for ease of reporting [27].

Random-effects meta-analysis was performed when any two studies reported the same outcome. We expressed the outcome of continuous variables, such as HR before and after treatment, as standardized difference of means (SDM), because some studies reported HR as mean, whereas few others reported them as median. We defined the magnitude of effect between interventions and control as small if the SDM value was 0.2 or less; an SDM value of approximately 0.5 was considered a moderate magnitude of effect, and an SDM value of at least 0.8 was considered a large magnitude of effect size for the interventions [28]. We reported the results from random-effect meta-analysis of categorical outcome (percentages of patients whose cardiac rhythm converted to sinus rhythm) as odd ratio (OR) and 95% confidence interval (CI).

For heterogeneity, we used both the Cochrane’s Q-statistic and the I2 value. The Q-statistic tests against the null hypothesis that all studies within our meta-analysis would share similar effect size. The I2 value shows whether the variance between studies’ effect size is due to true difference and not by chance.

We also performed a sensitivity analysis of our primary outcome by using one-study-removed random-effect meta-analysis. The one-study-removed sensitivity analysis systemically removed each individual study, whereas meta-analysis was performed with the rest of the study. The sensitivity analysis aimed to identify any single study that significantly influenced the effect size of the study. Furthermore, to assess the dose-effect of magnesium, we performed exploratory meta-regressions with continuous independent variables. Our meta-regression involved baseline serum magnesium at ED presentation, initial dose of magnesium, and total dosage of magnesium as independent variables. For studies that used a single dose of magnesium, we treated the single dose as both a loading dose and a maintenance dose.

For publication bias, we used both Egger test and Begg test. An Egger test’s or Begg test’s P-value > 0.05 would indicate low risk for publication bias. We did not use the funnel plot because of the small number of studies included in our meta-analysis. For another publication bias assessment, we used the Orwin’s fail-safe N test. This Orwin’s fail-safe N test would predict the number of missing or number of future studies that could have changed the effect size of our primary outcome.

All meta-analysis, sensitivity analysis, meta-regressions, and publication bias assessment were performed with the Comprehensive Meta-Analysis software (, Englewood, New Jersey, USA). Any variable with two-tailed P-value < 0.05 was considered statistically significant.


Study selection

The initial literature search identified 395 studies. We reviewed 11 full-text articles and included five studies in the final analysis (Fig. 1). All five studies [29–33] were RCTs. All five studies reported the change of HR before and after treatment, when compared with control treatment, although they did not report the proportions of patients who achieved rate control. Four studies [29–32] reported the percentages of patients whose rhythms were converted to sinus rhythm. One study [34] investigated the effect of magnesium but did not include a control group, so it was not included in our final analysis.

Fig. 1.:
PRISMA flow diagram for study selection. PRISMA, Preferred Reporting Items for Systematic reviews and Meta-Analyses.

We identified two additional systematic reviews comparing magnesium treatments with other antiarrhythmic medication [35,36]. However, these studies were not involving ED settings, so they were excluded.

Risk of bias assessment

All studies included in our meta-analysis were randomized trials. The risk of bias from five included studies were assessed by the using five qualities of the Cochrane’s Risk-of-Bias tool (Appendix 2, Supplemental digital content 1, Only one study from Hays et al. [29] demonstrated some concerns for risk of bias. The rest of the studies were graded as low risk for bias.

Summary of studies

Our meta-analysis included 815 patients who presented to the ED with atrial fibrillation and rapid ventricular rate, 328 (40%) patients were part of the control group, whereas 487 patients (60%) received magnesium. One study [32] contained one control group and two treatment arms: one treatment group was treated with ‘low dose’ of magnesium, whereas the second treatment group received ‘high dose’ of magnesium. Since this study reported separate outcomes for control, ‘low dose’, and ‘high dose’ groups, respectively, we analyzed the effect of ‘low dose’ and ‘high dose’ magnesium compared with the control group separately [35].

All studies reported treatment of control groups with placebo up to their first assessments of treatment efficacy. After the first assessments, any additional antiarrhythmic medication for both the control groups and the magnesium group was left at the discretion of the treating physicians. Four studies [34–37] used other antidysrhythmic agents besides magnesium. Digoxin was the most common antidysrhythmic agent in three studies [29,30,33]. On the other hand, Chu et al. [31] reported that only a small number of patients in their study received amiodarone, while Zouche et al. [33] did not use any additional antidysrhythmic agents.

Only four studies reported the systolic blood pressure before treatment [29,31–33], and only two studies reported systolic blood pressure after treatment for placebo group [29,31]. Therefore, we did not perform assessment of blood pressure between control and magnesium groups.

Four studies [29,30,32,33] reported the prevalence of any complications from the treatment.

Primary outcome

Five of the RCTs reported the change in HR after treatment with magnesium and control [29–33]. Bouida et al.[32] reported two separate groups of patients who were given ‘low dose’ and ‘high dose’ of magnesium, compared with a control group. As a result, we performed meta-analysis from these two separate groups [32].

Most studies reported the time intervals for HR reduction within 4–6 h of magnesium administration [29–33]. However, two studies reported patients’ HRs at 12 h [33] and 24 h [32] after first administration of magnesium.

The baseline HR for placebo group before treatment was 136 beats per minute, and the group’s HR after treatment was 119 bpm. On the other hand, baseline HR for magnesium group was 137 bpm. At the first assessment, the average HR for the magnesium group after treatment was 108 bpm.

Our random-effects meta-analysis showed a standardized mean difference (SMD) of HR reduction of 0.34 between magnesium versus control groups, which was statistically significant (SMD, 0.34; 95% CI, 0.21–0.47; P < 0.001) (Fig. 2a). Our prediction interval also suggested that, for future studies similar to those included in our analysis, magnesium infusion would be associated with a small magnitude of reduction of HR (SMD, 0.2) to a moderate magnitude of reduction (SMD, 0.5) (Fig. 2a). The P-value for the Q-statistic was 0.39, which suggested that the effect size from our study would be similar to the true effect size. The I2 value was 4%, which demonstrated that only 4% of variance between our studies’ effect sizes and the true effect size was due to true difference. In other words, there was low likelihood that our study’s findings would be different from the true effect size.

Fig. 2.:
(a) Forest plot of random-effects meta-analysis comparing heart rate difference before and after treatment with magnesium or control. The difference was expressed as standardized mean difference (SMD). (b) Forest plot of random-effects meta-analysis comparing rates of sinus conversion between treatment with magnesium or control. (c) Sensitivity analysis of meta-analysis comparing heart rate difference before and after treatment.

Sensitivity analysis using one-study-removed random-effects meta-analysis (Fig. 2c) demonstrated that the overall SMD of HR reduction between magnesium treatment and control was consistently between 0.33 and 0.36 and was well within the 95% CI of the pooled studies. The analysis showed that no individual studies overly affected the effect size of our study.

For our publication bias assessment, the P-values for both Egger’s test and Begg’s test were 0.38 and 0.45, respectively. This suggested that our meta-analysis was associated with low likelihood of having publication bias. Furthermore, the Orwin’s fail-safe N test demonstrated that it would take nine missing or future studies with very small SMD to reduce the effect of magnesium on HR reduction. In other words, nine missing or future studies need to have a SMD between magnesium treatment and control groups of 0.1 (very small effect in HR reduction) to reduce the effect of magnesium to SMD from 0.34 to 0.2 (small effect in HR reduction).

Secondary outcome: rates of sinus conversion

Only three RCTs reported the rate of conversion to sinus rhythm [30–32]. Treating patients with magnesium infusion was not statistically associated with higher likelihood of achieving sinus conversion (OR, 1.46; 95% CI, 0.726–2.94; P = 0.29) (Fig. 2b). The P-value for the Q-statistic test was 0.09, which suggested that our study’s effect size would be similar to the true effect size. Furthermore, the I2 value was 53%, which demonstrated that up to 53% of difference between our studies’ effect size and the true effect size was true difference and not by chance.

Other outcomes: any complications and major complications

Four studies reported rates of complications [29,30,32,33], whereas three studies reported the prevalence of major complications [30,32,33]. Most authors defined major complications as hypotension or bradycardia. Minor complications included flushing, headache, nausea, etc. Patients receiving magnesium infusion were associated with a five-time higher likelihood of having ANY complications (OR, 5.33; 95% CI, 2.3–12.3; P < 0.001) (Fig. 3a). On the other hand, patients receiving magnesium infusion had a similar prevalence of major complications, when compared with patients receiving control treatment (OR, 2.2; 95% CI, 0.62–8.09; P = 0.22).

Fig. 3.:
(a) Forest plot of random-effects meta-analysis comparing the prevalence of any complications as reported by the authors. (b) Forest plot of random-effects meta-analysis comparing the prevalence of major complications as reported by the authors such as hypotension and bradycardia. (c) Results from multivariable meta-regressions measuring association of serum magnesium concentrations and the magnitude of heart rate reductions before and after treatments.

Effect of serum magnesium level and magnesium dose

Our exploratory meta-regressions demonstrated that the baseline (pretreatment) serum magnesium levels were not related to the SMD of HR reduction after receiving magnesium treatment (Fig. 3c). In contrast, the initial loading dose of magnesium [correlation coefficient (corr. coeff), −0.13; 95% CI, 0.25–0.20; P = 0.02] was negatively correlated with the magnitude of the SMD of HR reduction, whereas the maintenance dose of magnesium up to 6 hours (corr. coeff, 0.17; 95% CI, 0.06–0.28; P = 0.01) was positively correlated with the magnitude of SMD of HR reduction. In other words, higher maintenance magnesium dose for up to 6 h was associated with larger HR reductions.


Our random-effect meta-analysis demonstrated that magnesium infusion was associated with significant reduction in HR among patients who presented to ED with atrial fibrillation and rapid ventricular rates. However, treatment with magnesium was associated with neither higher rates of sinus conversion nor higher rates of major complications. Furthermore, our primary finding was associated with very low heterogeneity, which suggested that our result might not be much different from the true effect size.

To our knowledge, this is the first meta-analysis evaluating the use of magnesium to treat atrial fibrillation in the EDs. A previous meta-analysis by Onalan et al. [35] involved studies that used magnesium for treatment of atrial fibrillation; however, it also included other arrhythmias such as supraventricular tachycardia and was not limited to ED setting. As a result, our study provides further evidence for the use of magnesium in the treatment of patients with atrial fibrillation with rapid ventricular rates in the ED setting.

The role of magnesium in treating cardiac arrhythmias is not fully understood but may be attributable to prevention of EADs [37]. Magnesium may abolish or diminish the amplitude of EAD, by blocking calcium influx via L-type calcium channels. Thus, EADs are unable to reach threshold potential, thus preventing the triggering of dysrhythmias [37,38]. Magnesium also may reduce dysrhythmias by reducing the inward potassium current, resulting in fewer EAD [39]. Although more studies are necessary to confirm our observations, our findings suggested that magnesium is a good candidate to treat patients with atrial fibrillation and rapid ventricular rates, and further, magnesium has a good safety profile when compared with other frequently used agents such as metoprolol or diltiazem. Our study demonstrated that the unadjusted rate of major complications (hypotension and bradycardia) from magnesium infusion was 11/456 (2.4%) (Fig. 3b). In contrast, a recent study reported that the rate of hypotension among ED patients treated with metoprolol or diltiazem was 23 or 39%, respectively [40].

Due to the variabilities in magnesium dosages, further studies about the dose-effect are necessary to provide more evidence about the benefit–risk ratios of magnesium treatments. Our exploratory multivariable meta-regressions demonstrated that higher initial loading dose of magnesium was not correlated with larger reduction of HRs among patients who received magnesium. This effect was likely derived from the result of the 2019 Bouida study’s group of patients who were given the ‘large dose’ of magnesium. Patients in this group were given up to 9 g of loading dose of intravenous magnesium, but these patients did not achieve higher HR reductions at 4 h when compared with those who received the ‘low-dose’ (4.5 g) magnesium infusion. In contrast, a higher maintenance dose was correlated with an increased HR reduction. Therefore, we recommended that starting with a small loading dose of magnesium then eventually reaching 3–4 g over a period of 4–6 h would be associated with larger HR reductions while avoiding high rates of major complications.

Further studies are also necessary to investigate whether magnesium can either be used as a single therapy for patients with rapid atrial fibrillation and rapid ventricular rates, or as an adjunct therapy in addition to other rate-controlled agents in the ED. Additionally, further studies are necessary to investigate the benefit/risk ratio of using magnesium infusion in addition to other agents such as metoprolol or diltiazem, given that use of either metoprolol or diltiazem is associated with increased risk of hypotension [40].


Our meta-analysis has several limitations. A limited number of studies were available since we were interested exclusively in the ED setting in an effort to provide a more homogenous setting, acuity level, and relevance to the specialty of Emergency Medicine. Some of these studies involved smaller patient populations, which would be at risk of ‘small study effects’, when the effect sizes are artificially larger than the true effect size. Furthermore, there was a lack of standardized placebo/control treatment across all studies. Additionally, variability in the dosage of magnesium prevented us from drawing conclusions on the best practice of using magnesium infusion for patients who presented to ED with atrial fibrillation and rapid ventricular rates. The studies’ authors only reported the ventricular HRs before and after treatment and not reported the proportion of rate control. Therefore, although magnesium was associated with rate reductions, compared with the control group, some patients still had atrial fibrillation with rapid ventricular rate.


Magnesium sulfate has been used successfully in the treatment of rapid atrial fibrillation in the ED setting, both as an independent agent and as an adjunct to other medication for rate control. Further randomized control studies in the ED setting using magnesium as a single agent comparing to other medications are necessary to confirm our observations.


Conflicts of interest

There are no conflicts of interest.


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atrial fibrillation; emergency department, magnesium

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