Venoarterial Extracorporeal Membrane Oxygenation for Calcium Channel Blocker Toxicity: Does the Left Ventricle Matter?

To the Editor: We were very interested in two articles recently published in the ASAIO Journal regarding the use of extracorporeal membrane oxygenation (ECMO) for calcium channel blocker (CCB) overdose. The first, a meta-analysis of published cases (n = 26), found a survival of 84.6% in patients who required extracorporeal support in the setting of CCB toxicity.1 This study was followed by an analysis of the Extracorporeal Life Support Organization (ELSO) registry, reporting a much lower survival of 40.6% (n = 98).2 The significant difference in survival may be due to a small sample size or publication bias. However, it could also be due to a confounder and critical missing element: the degree of cardiac dysfunction. One might assume that the decision to pursue venoarterial ECMO in patients with acute CCB overdose who exhibit end-organ malperfusion despite optimal medical therapy depends mainly on the underlying cause of shock, whether it is due to low systemic vascular resistance or low cardiac output. Both pathways are plausible because CCB overdose can result in refractory vasodilation and cardiotoxicity. In cases of cardiogenic shock, VA-ECMO is warranted while awaiting the resolution of CCB toxicity. However, the literature has not yet addressed an important question: What if cardiac function is preserved? Traditional teaching suggests that using VA-ECMO to bypass a functioning cardiopulmonary system would not provide any physiological benefit. Accordingly, the inappropriate (by this logic) use of VA-ECMO in patients with preserved cardiac function in the registry analysis could account for the mortality difference. Despite this, our center has encountered several cases that indicate a benefit of VA-ECMO in acute CCB overdose with preserved cardiac function. Both patients presented from an outside center after massive amlodipine ingestion. Despite high-dose insulin, methylene blue, and maximal vasopressor support, they could not sustain an appropriate mean arterial pressure (MAP). They exhibited signs of end-organ malperfusion, including worsening lactic acidosis and anuria. Both patients underwent bedside percutaneous VA-ECMO cannulation. Following cannulation, their hemodynamics improved dramatically, and they were decannulated after several days. Ultimately, they were liberated from mechanical ventilation, achieved full renal recovery, and were safely discharged. We propose that VA-ECMO altered the trajectory of these patients’ course despite a primary physiological insult of vasoplegia. There are possible physiological explanations for this observation. In cases of refractory vasoplegia, adding ECMO flow can lead to a net increase in cumulative output (ECMO plus native cardiac output), MAP, and oxygen delivery. This may reverse the cycle of anaerobic metabolism and multi-organ failure. Furthermore, VA-ECMO can serve as a safety net when cardiac dysfunction is delayed or obscured by inotropes and low afterload. While these explanations are speculative, they certainly merit further investigation. We applaud the authors of both studies for drawing attention to a specific group of patients who may benefit from extracorporeal support. It is crucial to explore the significance of cardiac dysfunction in this group of patients. Until then, we propose the following: In settings of acute CCB toxicity with worsening end-organ perfusion despite optimal medical management, VA-ECMO should be offered, regardless of ventricular function, provided there are no significant contraindications.