the acute effects of magnesium in atrial fibrillation and flutter with a rapid ventricular rate

The acute effects of magnesium in atrial fibrillation and flutter with a rapid ventricular rate

Steve Walker, James Taylor, Richard Harrod

Steve Walker MBBS (Formerly) Senior Registrar Emergency IDepartment Royal Melbourne Hospital

James Taylor MBBS DA(UK) FACEM Staff Specialist Emergency Department Dandenong Oistrict Hospital

Richard Harrod MBBS FACEM Staff Specialist Emergency Department Royal Melbourne Hospital

Address for correspondence: Dr Steve Walker C/O CareFlight PO Box 3589 Parramatta NSW 2124

Abstract A prospective, randomised, placebo

controlled, double blinded trial to assess the efficacy of intravenous magnesium sulphate (20mmol over 30 minutes) versus placebo in parients presenting to the emergency department with rapid atrial fibrillation and flutter. The end points were slowing of the ventricular rate and reversion to sinus rhythm. A total of 41 patients were enrolled. The mean decrease in heart rate 30 minutes after commencing the infiision was 24.1 /min for the magnesium group compared to 11.0/min for the placebo group (different at the 95% level of significance). The mean decrease in heart rate and the reversion rate four hours after commencing the infusion were the same at the 95% level of significance for the two groups. We conclude that magnesiimi has a significant effect in the acute slowing of ventricular rate but no effect in achieving reversion to sinus rhythm.

Introduction Atrial fibrillation and atrial flutter with a

rapid ventricular rate are common emergency department presentations. Digoxin, which has traditionally been used to treat these conditions, is not ideal as it has a relatively slow onset of action, a low rate of reversion to sinus rhythm and commencement of therapy is often delayed until the serum potassium is known". Furthermore, class II and IV antiarrhythmic drugs are sometimes required to temporarily slow the ventricular rate until digoxin takes effecf-«.

Emergency Medicine 1996 • Vol 8 207

Stfvc Walker, janifi Taiilor, RicharJ Harwd

While a number of alternative antiarrhythmic agents to digoxin, in particular class Ic and class III drugs have been studied, none of these has proven ideal due to significant side effects and frequent contraindicahons to their use"'".

Recently there have been some favourable case reports and small studies on the use of magnesium in the treatment of supraventricular tachyarrhythmias"".

The aim of our study was to establish the efficacy of a single dose of magnesium in addition to standard management in the acute treatment of rapid atrial fibrillation and flutter. The measured end points were slowing of the ventricular rate and reversion to sinus rhythm.

Method A prospective, randomised, placebo

controlled, double blinded trial was conducted in the emergency departments of Royal Melbourne Hospital and Dandenong Hospital. Approval was obtained from the Ethics Committee at each hospital.

Patients presenting to the emergency department with atrial fibrillation or flutter with a rapid ventricular rate that met the inclusion criteria (Table 1) were entered.

After arrival in the emergency department a preliminary assessment and 12 lead ECG were

performed. If the inclusion criteria were met, the study was explained and informed consent obtained.

The patient was then randomised to receive either an infusion of magnesium sulphate ZOmmol (5g) diluted to 20ml with normal saline, or an infusion of normal saline 20ml, administered over 30 minutes by syringe pump. The study infusion was double blinded and no other antiarrythmic drug was administered during its infusion. After the study infusion was completed the patient could receive digoxin at the discretion of the treating physician, although no antiarrhythmic other than digoxin could be administered for the remainder of the trial. The parient remained monitored in the emergency department for four hours at which point the study was concluded.

The data recorded in the emergency department included the rhythm and the electrical ventricular rate prior to administration of the study Infusion, upon completion of the infusion, and four hours after commencing the infusion. Reversion to sinus rhythm and any adverse effects were noted.

Statistical analysis was performed by the Australian Bureau of Statistics. Values for heart rates were reported as mean standard deviation beats per minute. The mean reduction in heart

Table 1. Criteria for inclusion, exclusion, withdrawal

Inclusion criteria 1. Atrial fibrillation and flutter with a ventricular rate of greater than 100 per minute 2. Duration of arrhythmia less than 48 hours (onset defined as an acute development of palpitations).

Exclusion criteria 1. Lack of informed consent (either refusal of the patient to give consent, or inability to obtain consent due

to the medical condition of the patient). Evidence of haemodynamic instability: a) systolic arterial pressure < 90mmHg, or b) respiratory distress due to left ventricular failure. Widened QRS complex (le >120msec) unless identical in morpfiology to previously recorded ECGs in sinus rhythm and therefore considered likely to be of supraventricular origin. Presence of chest pain or ECG changes consistent with acute myocardial infarction. The acute administration of anti-arrhythmic agents other than digoxin (see withdrawal criteria below). This did not exclude patients who were already taking these drugs as maintenance therapy (eg. patients on verapamil or p-blockers for hypertension). Atrial fibrillation and flutter occurring in the setting of a drug overdose. Patients known to have renal impairment (le serum creatinine > 0.15 mmol/L).

Withdrawal criteria 1. Patient withdraws consent, 2. Deterioration in condition of patient:

a) drop in systolic arterial pressure of greater than 30mmHg b) drop in heart rate to less than 50/min. or c) increasing respiratory distress due to left ventricular failure.

3. Decision to administer anti-arrhythmic agents other than digoxin.

208 Emergency Medicine W46 • Vol H

The acute effects of magnesium in atruil fibriUatuni and flutter with a rapid ventricular rate

rate in the various treatment groups was investigated using the Students t test. The percentage of patients who had a heart rate less than 100/min after 30 minutes and 240 minutes was investigated using Chi Square analysis. A result was deemed to be meaningful if it reached the 95% level of significance.

Results Forty-one patients were enrolled in the study.

Thirty seven had atrial fibrillation and four had atrial flutter. These two groups were considered together for the purposes of analysis. Twenty-one patients received magnesium and 20 received placebo.

The variables analysed were the mean reduction in heart rate between 0,30, and 240 minutes, the percentage of patients with a rate less than 100/min after 30 niinutes and after 240 minutes, the percentage of patients who reverted to sinus rhythm within 240 minutes and the incidence of side effects.

The mean heart rates of the two groups at the time of entry into the study were identical, being 144 ±24.6/min for the magnesium group and 145 ±20.6/min for the placebo group.

There was a significant difference in heart rate between the two groups after 30 nunutes. Those receiving magnesium experienced a mean decrease of 24.1/min with a mean rate of 120 ±20.6/min, while the placebo recipients experienced a mean decrease of 11/min with a mean rate of 134 ±21.0/min. There was also a significant difference in the proportion of patients with a heart rate less than 100/min at 30 minutes, with five of the 21 (24%) patients receiving magnesium having a rate less than 100/min compared to one of the 20 (5%) placebo recipients. Only one patient reverted within 30 minutes (Table 2).

Table 2. Data at 30 minutes (after completion of study infusion)

Magnesium Placebo Number of patients 21 20 Initial heart rate/mm 144 ±24.6 145 ±20.6 Mean decrease 24.1 I T Median decrease 20 10.5* Heart rate/min at

30 minutes 120 ±20.6 134 ±21.0* Number of patients witfi rate < 100 5 (24%) 1 (5%)*

Number of patients who reverted 0 1 (5%)

*= different at the 95% limit of significance.

There were no significant differences between the two groups after 240 minutes. Those receiving magnesium experienced a mean decrease in heart rate of 45.7/min with a mean rate of 98 ±24.4/min, while the placebo recipients experienced a mean decrease of 41.5/ min with a mean rate of 104 ±25.3/min. These differences were not significant. Similarly there was no significant difference in the proportion of patients with a heart rate less than 100/min with 14 of the 21 (67%) magnesium recipients having a rate less than 100/min compared to 11 of the 20 (55%) placebo recipients. The groups were also the same with respect to reversion to sinus rhythm with four of the 21 (19%) magnesium recipients having reverted compared to nine of the 20 (45%) placebo recipients (Table 3).

Table 3. Data at 240 minutes (at completion of study)

Magnesium Placebo Number of patients Initial heart rate/min (viean decrease Median decrease Heart rate/min at

240 minutes Number of patients with rate < 100

Number of patients who reverted

21 144 ±24.6 45.7 40

98 ±24.4

14(67%)

4 (19%)

20 145 ±20.6 41.5 39

104 ±25.3

11 (55%)

9 (45%)

There was a significant difference in side effects reported between the two groups. Nine of the 21 (43%) magnesium recipients reported sweating and flushing during the administration of the study infusion, compared to none of the 20 placebo recipients.

Discussion At a cellular level, magnesium stabilises ceU

membranes by increasing the cellular uptake of potassium. Magnesium acts as a coenzyme for Na/K ATPase and also by modulating potassium channels"*"^"- '̂̂ -" ^l It also facilitates the maintenance of a low intracellular concentration of calcium, high intracellular levels of calcium being associated with the development of after-potentials and triggered arrhythmias"'-''". In vitro, magnesium infusions are known to slow the intrinsic rate of the canine sinus node and have been shown to slow intra-atrial, AV nodal and intraventricular conduction in humans'''^''-". It is thus not surprising that attention has recently focused on the use of magnesium as an antiarrhythmic agent.


Steve Walker, James Taylor, Richard Harrod

Magnesium is now recommended for various arrhythmias including torsades de pointes and resistant ventricular fibrillahon-"''. It has also been used for many years for a variety of non-cardiac conditions, notably pre-eclampsia"-^. It has been administered to thousands of patients with only minor adverse effects such as transient flushing of the skin occurring with rapid bolus doses of 8-lOmmol'*-^'.

Compared to currently used agents, magnesium has a number of potential advantages, including few contraindications to its use, its apparent safety, its low cost, a more rapid onset of action and its immediate use without needing to wait for laboratory test results prior to administration '"^''^i.

Figure. Heart rate versus time for magnesium and placebo

^ Initial heart rate

I I Heart rate at 30 minutes

• Heart rate at 240 minutes

Magnesium Placebo

Our results show that magnesium is effective in slowing the heart rate of patients presenting with rapid atrial fibrillation and flutter While this difference at 30 minutes is modest, it is statistically significant (Figure).

Four hours after administration of the study infusion there was no significant difference in the mean heart rate between the patients who received magnesium and those who received placebo. Only 14 of the 21 (67%) magnesium recipients had received digoxin at the discretion of the treating physician by this time, compared to 19 of the 20 (95%) placebo recipients. It is possible that the differential use of digoxin following the study infusion occurred because magnesium achieved a useful reduction in heart rate altering the perceived need for digoxin. The data for those 33 patients who received digoxin was analysed. The 14 magnesium recipients had an initial heart rate of 150 ±20.1 /min, a mean decrease of 48.4/min, and a rate of 101 ±27.4/ min at 240 min while the 19 placebo recipients had an initial heart rate of 145 ±21.1 /min, a mean decrease of 40.5/min, and a rate of 105 ±25.8/min at 240 minutes. Although the

difference in the mean heart rate decrease between the magnesium and the placebo groups is larger for this sub-group than in the study population as a whole, it still is not statistically significant (Table 4).

Table 4. Data at 240 minutes (at completion of study) for tJiose 33 patients who received digoxin

Number of patients Initial heart rate/min Mean decrease Median decrease Heart rate /min at

240 minutes Number of patients with rate < 100

Number of patients who reverted

Magnesium Placebo 14 19 150±20.1 145+21. 48.4 40.5 45 38

101 ±27,4 105 ±25.i

9(64%) 10(53%)

4 (29%) 8 (42%)

There was also no significant difference in the proportion of patients who reverted to sinus rhythm during the 240 minute study period. Amongst those 33 patients who received digoxin, four out of 14 (29%) magnesium recipients reverted compared to 8 out of 19 (42%) placebo recipients. This difference was not statistically significant and a larger study would be needed to define the effect of magnesium on reversion to sinus rhythm (Table 4).

There was a strong correlation between magnesium administration and the occurrence of symptoms such as sweating and flushing. TTiese are recognised side effects of intravenous magnesium and have been reported in other studies and are cited in the manufacturer's product information'"^'. They are thought to be due to vasodilation secondary to enhanced production of prostacyclin^'-^. These symptoms were all of mild severity, transient and in no case necessitated cessation of the study infusion.

One patient was withdrawn from the study. This was a previously healthy 48 year old man who had presented following an acute episode of dizziness and presyncope. He was found to be in atrial fibrillation at a rate of 160/min and was entered into the trial. He received magnesium as the study infusion. Fifteen minutes after commencing the infusion (after lOmmol magnesium had been administered) the patient felt faint and dizzy and developed profound bradycardia. He then lost consciousness and was noted to be pulseless, with the monitor showing asystole. The infusion was ceased and external cardiac compression was commenced. After 20 seconds the patient

210 Emergency Medicine 1W6 • Vol 8


reverted back to atrial fibrillation at a rate of 110/min and promptly regained consciousness with no neurological deficit. After review by the cardiology team and admission to the coronary care unit, he was successfully reverted to sinus rhythm with flecainide 80mg IV. About 20 minutes after reversion the patient again became dizzy and presyncopal with a sinus bradycardia at 35/min which responded promptly to atropine 0.6 mg IV. The patient had no further adverse events. On more detailed questioning he reported several previous similar episodes. A Holter monitor and echocardiogram were both subsequently normal and he remained symptom free.

A Medline™ search failed to show any similar reports in the literature. It is difficult to make recommendations on the basis of one case, but it would seem prudent not to administer magnesium to patients suspected of having episodes of bradyarrhythmia (eg patients with sick sinus syndrome or patients with a history of presyncope or syncope despite only a moderately rapid tachyarrhythmia). Patients should certainly be monitored and closely observed when parenteral magnesium is given.

Our results need to be interpreted in the light of a small sample size. Despite the study being conducted over a period of 12 months in two hospitals with busy emergency departments, we were only able to enlist a total of 41 patients. The major reason for this was the strict exclusion criteria.

It is accepted practice only to revert atrial fibrillation without prior anticoagulation if it has been present for less than 48 hours, because of the risk of systemic embolism. Consequently, only patients whose arrhythmia had definitely been present for less than this time were eligible. Many patients presented with atrial fibrillation and flutter of uncertain duration and were thus excluded.

Another criterion which limited the number enrolled was a normal QRS complex width, unless an identical widened complex was documented in previous ECGs in sinus rhythm. A significant number of patients with rapid atrial fibrillation and flutter had a wide QRS complex and were thus ineligible.

Finally, many patients with rapid atrial fibrillation and flutter have haemodynamic instability, left ventricular failure or chest pain suggestive of angina, which also were exclusion criteria.

Despite the above limitations and consequent small sample size of our study, it is one of the larger studies published in the literature. A Medline™ search was performed and only two studies have been published on the acute effects of magnesium on atrial fibrillation and flutter.

One single blinded study comprised 57 patients"* and compared magnesium to verapamil for all supraventricular tachyarrhythmias with no placebo group. It included 12 patients with paroxysmal SVT, leaving 45 with atrial fibrillation or flutter of whom 21 received magnesium. The magnesium recipients received an initial dose of lOnmiol over 15 minutes, followed by a infusion of 0.04mmol/min for up to 24 hours. There was a significant reduction in heart rate over 30 minutes of 25/min in the magnesium group and 57% (12 of 21) of these patients reverted within four hours.

The other study was a randomised, double blind trial comparing magnesium to placebo in which all patients subsequently received digoxin^'. It comprised 15 patients with atrial fibrillation, seven of whom received magnesium. The magnesium group received a bolus of Smmol, followed by an infusion of 4 mmol/hour for four hours. There was a significant reduction in heart rate over 30 minutes of 20/mijn, and 14% (1 of 7) of these patients reverted within four hours.

The dose of magnesium, rate of administration, some patient characteristics (e.g. the duration of the arrhythmia prior to entry into the trial) and other medications studied differed between all three studies. This together with the small numbers in each study make it difficult to compare them. However, all studies concluded that magnesium caused a significant reduction in ventricular rate within 30 rriinutes. The effect of magnesium on reversion to sinus rhythm remains unclear (Table 5).

Table 5. Comparison of data between different studies

Number of patients given magnesium Reduction in heart rate over 30 minutes Reduction in heart rate over 4 hours Number of patients reverted within 4 hours

Gullestad'" 21 25 34

12(57%)

Hay^^ 7

20 39

1 (14%)

Walker 21 24.1 45.7

4 (19%)


Steve Walker, James Taylor. Richard Harrod

A limitation of our study is that patients who were haemodynamically compromised were ineligible. It is in these patients that the early onset of action of magnesium might have the most practical benefit by rapidly causing a modest decrease in heart rate while waiting for other agents to take effect. Having demonstrated that magnesium appears safe, consideration should be given to conducting a similar trial including such patients, to establish whether magnesium is indeed beneficial in the compromised patient.

Our study did not aim to determine the overall management of patients presenting to the emergency department with atrial fibrillation and flutter. Issues such as the necessity for admission, anticoagulation, appropriate timing of reversion, chemical versus electrical reversion, the acute use of newer antiarrhythmic agents and the need for maintenance therapy were beyond the scope of the study.

Conclusions We conclude that the use of a single dose of

intravenous magnesium sulphate has a significant effect in the acute slowing of the ventricular rate in rapid atrial fibrillation and flutter. The magnitude of this decrease was comparable to that seen in other similar studies"*'^'. Magnesium sulphate was ineffective in achieving reversion to sinus rhythm, Ln contrast to previous reports'". With the exception of one case of transient asystole, there were no complications associated with the use of magnesium. Sweating and flushing were experienced by 43% of the patients. These symptoms were only mild and in no case required cessation of the infusion.

Acknowledgments We would like to ttiank ttie emergency department staff of ttie Royal tvlelbourne Hospital and the Dandenong Hospital for tlieir help in this trial We also appreciate the support from Dr Leanne Grigg, Director of Cardiology. Royal Ivlelbourne Hospital and Eng Chee and Janine Lloyd from the Australian Bureau of Statistics.

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(Accepted: 26 June 1996)

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the acute effects of magnesium in atrial fibrillation and flutter with a rapid ventricular rate

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