Motivation: The standard ACLS catechism is that: "If you see torsades de pointes, give magnesium." During the ACLS protocol, torsades is, I think, the only point where magnesium enters into the algorithm. While supplementing someone with mag the other day, I wondered what the evidence was for use of magnesium in torsades and other rhythms. I was a bit surprised to learn that the ACLS guideline for torsades is based mostly on two (quoted from the official ACLS publication) observational studies. The major study in Circulation appeared in 1988 and is reviewed here:
Paper: "Treatment of torsade de pointes with magnesium sulfate" Tzivoni, D. et. al. Circulation (1988), 77: 392-397.
Methods: An unblinded, uncontrolled study in which 12 consecutive patients who developed torsades de pointes (TdP) with QT prolongation were treated with magnesium (2g IV bolus over 1 to 2 minutes followed in most patients with a continuous infusion). Five additional patients with polymorphic ventricular tachycardia with normal QT interval were also treated with magnesium.
Results:
Patients: Of 12 patients with TdP (10 men and 2 women) and prolonged QT, six had ischemic heart disease, two had valvular rheumatic heart disease, two had atrial arrhythmia, and two did not have known heart disease. Nine of the twelve patients were also on antiarrhythmic therapy. The mean corrected QTc was 640 msec. The five patients with polymorphic VT with normal QT interval who received magnesium all had chronic ischemic heart disease.
Patients with prolonged QTc: In nine of the twelve patients, a single bolus of magnesium stopped TdP. In the other three patients, TdP was stopped after second Mag bolus. In eight of 12 patients, potassium levels were below 3.5, which was repleted with oral and intravenous potassium. The mean QTc did not change after magnesium bolus. Magnesium levels were available in eight patients, and all were normal.
Patients without prolonged QTc: In the five patients with polymorphic ventricular tachycardia, none responded to multiple boluses of magnesium.
Discussion: One of the major points of the paper for me is that sometimes amazing results trump poorly designed studies. Most of the patients had multiple confounders, including hypokalemia and concurrent anti-arrhythmic administration, but achieving a 100% response rate really makes this paper landmark. And, really since the publication of the paper, magnesium has become the standard therapy of choice for TdP. There were a couple of other interesting points in the paper as well. The first is that not every polymorphic ventricular tachycardia responds to magnesium - only polymorphic v-tach in patient with prolonged QTc can be properly called TdP. Also, while magnesium bolus is key, the precipitating factor for TdP is not hypomagnesemia since magnesium levels were normal. Finally, repleting potassium and other electrolytes are pretty important too!
Paper: "Treatment of torsade de pointes with magnesium sulfate" Tzivoni, D. et. al. Circulation (1988), 77: 392-397.
Methods: An unblinded, uncontrolled study in which 12 consecutive patients who developed torsades de pointes (TdP) with QT prolongation were treated with magnesium (2g IV bolus over 1 to 2 minutes followed in most patients with a continuous infusion). Five additional patients with polymorphic ventricular tachycardia with normal QT interval were also treated with magnesium.
Results:
Patients: Of 12 patients with TdP (10 men and 2 women) and prolonged QT, six had ischemic heart disease, two had valvular rheumatic heart disease, two had atrial arrhythmia, and two did not have known heart disease. Nine of the twelve patients were also on antiarrhythmic therapy. The mean corrected QTc was 640 msec. The five patients with polymorphic VT with normal QT interval who received magnesium all had chronic ischemic heart disease.
Patients with prolonged QTc: In nine of the twelve patients, a single bolus of magnesium stopped TdP. In the other three patients, TdP was stopped after second Mag bolus. In eight of 12 patients, potassium levels were below 3.5, which was repleted with oral and intravenous potassium. The mean QTc did not change after magnesium bolus. Magnesium levels were available in eight patients, and all were normal.
Patients without prolonged QTc: In the five patients with polymorphic ventricular tachycardia, none responded to multiple boluses of magnesium.
Discussion: One of the major points of the paper for me is that sometimes amazing results trump poorly designed studies. Most of the patients had multiple confounders, including hypokalemia and concurrent anti-arrhythmic administration, but achieving a 100% response rate really makes this paper landmark. And, really since the publication of the paper, magnesium has become the standard therapy of choice for TdP. There were a couple of other interesting points in the paper as well. The first is that not every polymorphic ventricular tachycardia responds to magnesium - only polymorphic v-tach in patient with prolonged QTc can be properly called TdP. Also, while magnesium bolus is key, the precipitating factor for TdP is not hypomagnesemia since magnesium levels were normal. Finally, repleting potassium and other electrolytes are pretty important too!
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