Download Intravenous magnesium for cardiac arrhythmias: jack of all trades

Magnesium Research 2008; 21 (1): 65-8
RECENT ADVANCES AND OPINIONS IN MAGNESIUM RESEARCH
Intravenous magnesium for cardiac
arrhythmias: jack of all trades
Kwok-Ming Ho
Department of Intensive Care, Royal Perth Hospital, Perth, Australia
Copyright © 2017 John Libbey Eurotext. Téléchargé par un robot venant de 88.99.165.207 le 06/05/2017.
Correspondence: K.-M. Ho, Department of Intensive Care, Royal Perth Hospital, Perth, WA 6000, Australia
<[email protected]>
Abstract. Intravenous magnesium has been used to prevent and treat many different types of cardiac arrhythmia. It has diverse electrophysiological actions on the
conduction system of the heart; including prolonging sinus node recovery time, and
reducing automaticity, atrioventricular nodal conduction, antegrade and retrograde
conduction over an accessory pathway, and His-ventricular conduction. Intravenous magnesium can also homogenise transmural ventricular repolarisation.
Because of its unique and diverse electrophysiological actions, intravenous magnesium has been reported to be useful in preventing atrial fibrillation and ventricular
arrhythmias after cardiac and thoracic surgery; in reducing the ventricular response
in acute onset atrial fibrillation, including for patients with Wolff-Parkinson-White
syndrome; in the treatment of digoxin induced supraventricular and ventricular
arrhythmias, multifocal atrial tachycardia, and polymorphic ventricular tachycardia
or ventricular fibrillation from drug overdoses. Intravenous magnesium is, however,
not useful in monomorphic ventricular tachycardia and shock-resistant ventricular
fibrillation. Large randomised controlled studies are needed to confirm whether
intravenous magnesium can improve patient centre outcomes in different cardiac
arrhythmias.
doi: 10.1684/mrh.2008.0130
Key words: antiarrhythmics, atrial fibrillation, rhythm control
Magnesium has many significant physiological and
pharmacological effects on different organ systems.
Intravenous magnesium has a high therapeutic to
toxic ratio and minimal negative inotropic effect [1],
and as such, it has been used in the prevention and
treatment of many different types of cardiac arrhythmia. Cardiac arrhythmia is, however, a common presentation of a diverse spectrum of diseases. Even
within the same class of arrhythmia, such as atrial
fibrillation or ventricular tachycardia, it can still be
caused by different arrhythmogenic mechanisms
from different underlying diseases. It is, therefore,
unrealistic to expect intravenous magnesium to be
useful in preventing or treating all types of cardiac
arrhythmias. Furthermore, animal studies have
shown that both the pro-arrhythmic effects of hypomagnesaemia and the anti-arrhythmic effects of magnesium depend on the underlying causes of the
arrhythmia and the condition of the heart [2-4]. This
review aims to briefly summarise the electrophysiological effects of intravenous magnesium and its
effects on different types of cardiac arrhythmia.
While intravenous magnesium chloride may have different actions from magnesium sulphate [5], magnesium sulphate is the most widely available intravenous preparation and almost exclusively used in
many of the studies cited in this review.
Electrophysiological effects of intravenous
magnesium
Intravenous magnesium has been shown to have a
number of electrophysiological actions on the conduction system of the heart. The mechanism of
its actions may include calcium antagonism at the
L- and T-type calcium channels [6], regulation of
energy transfer, and in supraphysiological doses,
magnesium decreases the outward potassium current density resulting in membrane stabilisation and
it also acts as an indirect antagonist of digoxin at the
sarcolemma Na(+)-K(+)-ATPase pump [7, 8].
65
K.-M. HO
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In the supraventricular conduction pathway, magnesium can reduce automaticity [9], increase sinus
node recovery time (at high doses) [10], and reduce
atrioventricular nodal conduction without affecting
atrial-atrial conduction [11]. Magnesium can also
block the antegrade and retrograde conduction over
an accessory pathway [12-14], and has a dominant
effect on the slow atrioventricular nodal (AVN) pathway in patients with dual AVN physiology [15].
In the ventricular conduction pathway, magnesium
suppresses prematurely triggered activity, prolongs
the His-ventricular conduction [16], and homoge-
nises transmural ventricular repolarisation [4, 17]
without affecting autonomic nervous activity [18].
Homogenisation of ventricular repolarisation
is believed to explain the anti-arrhythmic effect of
magnesium in prolonged QT syndrome [17]. Magnesium appears to have no effect on excitable gap
arrhythmias associated with a fixed anatomic substrate (e.g. monomorphic ventricular tachycardia)
[4, 19].
Table 1. Possible indications for intravenous magnesium as an anti-arrhythmic agent.
Rhythm and clinical condition
Atrial fibrillation (AF)
- Prevention in cardiac and thoracic surgery
- Treatment of chronic AF
- Digoxin toxicity with Wolff-Parkinson-White
syndrome
- Treatment of acute onsetAF
Benefits
Reference
Reduces the incidence of AF
Reduces rapid ventricular response
Reduces rapid ventricular response
[20, 21]
[8]
[14, 23]
Reduces rapid ventricular response
Improves conversion to sinus rhythm and reduces
the incidence of torsades de points polymorphic
ventricular tachycardia when used with ibutilide
[22, 24, 25]
Multifocal atrial tachycardia
Reduces rapid ventricular response and converts
some patients to sinus rhythm
[26]
Paroxysmal supraventricular tachycardia
Converts to sinus rhythm (less effective than
[12, 27, 28]
adenosine but may help if no response to adenosine)
Ventricular premature complexes
- Prevention in cardiac surgery
- Treatment in heart failure patients with
hypomagnesaemia
Ventricular tachycardia (VT)
- Digoxin toxicity
- Class Ic anti-arrhythmic toxicity (e.g. pilsicainide)
Polymorphic VT (torsades de pointes)
- Prolonged QT
(congenital and acquired)
(e.g. haloperidol, amiodarone)
Ventricular fibrillation (VF)
Amitriptyline poisoning
Intravenous magnesium was reported to be not
useful in the following conditions
Community cardiac arrest with shock-resistant VF
Monomorphic VT
66
Reduces the incidence
Reduces the incidence
[29, 30]
[31]
Converts to stable junctional rhythm
Converts to sinus rhythm
[32]
[33]
Converts to sinus rhythm
[34-36]
Converts to sinus rhythm
[37]
[38, 39]
[4, 19]
INTRAVENOUS MAGNESIUM FOR CARDIAC ARRHYTHMIAS: JACK OF ALL TRADES
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Effects of intravenous magnesium on different
types of cardiac arrhythmia
Due to its unique but diverse electrophysiological
effects, intravenous magnesium has been reported to
be effective in the prevention and treatment of a
variety of cardiac arrhythmias (table 1).
Intravenous magnesium is useful in preventing
atrial fibrillation and ventricular arrhythmias after
cardiac and thoracic surgery [20, 21], reducing the
ventricular response in acute onset atrial fibrillation
[22] (including in patients with Wolff-ParkinsonWhite syndrome [23]), improving rhythm control
with ibutilide [24, 25], treatment of digoxin induced
supraventricular and ventricular arrhythmias, multifocal atrial tachycardia [26], polymorphic ventricular
tachycardia with a prolonged QT interval, and ventricular fibrillation from amitriptyline overdoses.
Intravenous magnesium can also be considered as a
second line drug in the treatment of supraventricular
tachycardia when adenosine is not effective [27].
Intravenous magnesium is, however, not useful in
monomorphic ventricular tachycardia and shockresistant ventricular fibrillation.
Apart from being effective in controlling many cardiac arrhythmias, intravenous magnesium also has
less significant detrimental haemodynamic effects
on the cardiovascular system compared to other
anti-arrhythmic agents, including amiodarone or calcium channel blockers; although minor symptoms of
flushing, tingling, and dizziness are common after
intravenous magnesium [22]. Evidence that supports
the use of intravenous magnesium in many different
types of cardiac arrhythmias is, however, based on
case reports, animal studies, and randomised controlled studies that evaluated physiological endpoints only [20, 22]. None of the published randomised controlled studies on intravenous
magnesium have demonstrated a significant reduction in mortality.
Conclusion
Intravenous magnesium appears to be useful in the
prevention and treatment of a variety of cardiac
arrhythmias. It is, however, not useful in monomorphic ventricular tachycardia and shock-resistant
ventricular fibrillation. We must also be aware that
the successful prevention or treatment of cardiac
arrhythmias is only, at best, a surrogate end-point of
effectiveness. Large randomised controlled studies
are needed to confirm whether intravenous magnesium can improve patient centre outcomes in different cardiac arrhythmias.
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