That Prolonged QT Warning?! Magnesium for Cardiac Arrhythmias

You get a pop-up warning in the electronic medical record about potentially adverse interaction with a prolonged QT interval. What’s the risk, right? Afraid of a little torsades de pointes? Can’t we just give some prophylactic magnesium and call it a day? Let’s see if there’s any literature out there…

First off, let’s review magnesium. A prominent role of magnesium in the body is functioning as a de facto calcium antagonist which will inhibit the torsades de pointes mechanism.1 Furthermore, it’s part of the treatment for digoxin-induced arrhythmias in addition to the antibody fragments. Though not classically an antiarrhythmic, magnesium may convert some arrhythmias and prior work shows low magnesium may be proarrhythmogenic.2

Hypermagnesium is relatively uncommon, especially in the critically ill. However, if it does occur, toxicity manifests as neuromuscular symptoms or EKG changes, starting with widening of the QRS.1 Severe magnesium toxicity may lead to cardiac arrest but can be treated with calcium gluconate or dialysis in addition to standard resuscitative interventions.

Hypomagnesium is more common and is seen in 65% of intensive care patients.3 More pertinent to the undifferentiated ED patient, we consider administering magnesium when attempting to avert ventricular arrhythmias. For torsades de pointes, 2g of magnesium sulfate is the drug of choice. Though solid clinical data is lacking, small studies have demonstrated suppression of monomorphic ventricular tachycardia.4 A meta-analysis by Shiga et al in 2004 showed how it has potential (at least in the cardiac surgery population) to be used prophylactically to avert supraventricular and ventricular arrhythmias.5 So, in short, it’s unclear how low our threshold for giving prophylactic magnesium should be when there’s risk of prolonged QT. Strong evidence is lacking; however, the cardiac surgery population appears to get some benefit.

References
1. Herroeder S, Schönherr ME, De hert SG, Hollmann MW. Magnesium–essentials for anesthesiologists. Anesthesiology. 2011;114(4):971-93.
2. Moran JL, Gallagher J, Peake SL, Cunningham DN, Salagaras M, Leppard P: Parenteral magnesium sulfate versus amiodarone in the therapy of atrial tachyarrhythmias: A prospective, randomized study. Crit Care Med 1995; 23:1816–24
3. Rubeiz GJ, Thill-Baharozian M, Hardie D, Carlson RW: Association of hypomagnesemia and mortality in acutely ill medical patients. Crit Care Med 1993; 21:203–9Rubeiz, GJ Thill-Baharozian, M Hardie, D Carlson, RW
4. Ceremuzynski L, Gebalska J, Wolk R, Makowska E: Hypomagnesemia in heart failure with ventricular arrhythmias. Beneficial effects of magnesium supplementation. J Intern Med 2000; 247:78–86
5. Shiga T, Wajima Z, Inoue T, Ogawa R. Magnesium prophylaxis for arrhythmias after cardiac surgery: a meta-analysis of randomized controlled trials. Am J Med. 2004;117(5):325-33.

Don’t Forget The Right Ventricle

The Right Ventricle

The right ventricle (RV) has been getting more coverage lately from the Wilcox et al review article in Annals to the continued coverage in many critical care circles where anesthesia and emergency medicine overlap.(1)  Furthermore, the increased presence of VADs and physiology-centric thinking in the resuscitation units of the ED require facility with manipulation of the RV.

Danger with Positive Pressure

The RV’s lower pressures, structural design, and interdependence with the left ventricle (LV) create unfavorable hemodynamic interactions for the RV and positive pressure ventilation.(2) Most easily appreciated when separating preload and afterload, the conceptual challenge with positive pressure is seen in the following diagram from derangedphysiology.com. Intrathoracic pressure from either non-invasive or mechanical ventilation decreases RA preload and increases RV afterload. Proceed with caution when intubating pulmonary hypertension or RV failure patients.

Structure

Anatomically, the RV is crescent-shaped in longitudinal cross-section and triangular in axial cross-section. The deep longitudinal fibers of the RV pull it from apex to base of the heart. Additionally, there is small contribution from inward motion of the RV free wall as well as left ventricular traction on the RV.

Ventricular Interdependence

Compared to the LV, the RV’s thin wall and lower resistance circuit means it contracts throughout systole; it has no isovolumic relaxation phase. Any acute rise in right sided pressures (e.g. PE, tamponade, RV infarct) push the septum to the left, impairing LV diastolic filling and contractility.

References

  1. Wilcox SR, Kabrhel C, Channick RN. Pulmonary Hypertension and Right Ventricular Failure in Emergency Medicine. Ann Emerg Med. 2015;66(6):619-28.
  2. Deranged Physiology: Effects of Positive Pressure Ventilation on Cardiovascular Physiology. Deranged Physiology. http://www.derangedphysiology.com/main/core-topics-intensive-care/mechanical-ventilation-0/Chapter%202.1.7/effects-positive-pressure-ventilation-cardiovascular-physiology. Accessed March 14, 2017.
  3. Ibrahim BS. Right Ventricular Failure. European Society of Cardiology. https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-14/Right-ventricular-failure. Published December 12, 2016. Accessed March 14, 2017.