Abstract 4340112: ECMO: Beating the Block on a Failing Heart

Case Report: A 26-year-old man with HTN and MDD presented via EMS with 1 day of myalgias, abdominal pain, and hypotension requiring fluid and epinephrine infusion en route after ingesting ~350 mg of amlodipine 2 days prior. Upon arrival he was alert and conversant. Vital signs notable for BP 80/50, HR 120s, EKG: sinus tach. Initial labs: K 3.3, HCO3 13, AG 20, lactate 9.5, Cr 3.6, WBC 11.93, BNP 245, HS-trop 29. TTE showed enlarged RV and RA, LVEF <20%, global hypokinesis. Patient had a PEA arrest with emergent CPR (LUCAS machine used) and early activation of ECMO team for peripheral VA-ECMO cannulation. Glucagon, intralipid, activated charcoal, hydroxocobalamin, and calcium gluconate were given under guidance of toxicology. Right heart catheterization results were HR 89, BP 116/72, RA pressure 26, RV pressure 50/18, PA pressure 46/31 (mean 38), PCWP 35, CO/CI by Fick 12.75/5.72 and CO/CI by thermodilution 11.87/5.33. SVR was 316 dynes. At maximum support he required addition of vasopressin, Angiotensin II, and stress dose steroids to maintain blood pressure while on ECMO support. On Hospital Day 2 (HD2) HS-trop peaked and pressor support was quickly weaned. High-dose insulin euglycemic therapy (HIET) was deferred given persistent vasoplegia and improvement in cardiogenic shock. Repeat TTE showed an improved LVEF of 55%. Patient was decannulated on HD3, after which he required inotropic support for several days. On HD6 he was extubated and neurologically intact. He was discharged on HD14 to a psychiatric rehab facility. Discussion: Dihydropyridine calcium channel blocker (d-CCB) preferentially inhibits L-type calcium channels of vascular smooth muscle. At high doses they lose specificity, acting on calcium channels of cardiac myocytes reducing contractility and chronotropy. Amlodipine is the most common d-CCB involved in poisoning and associated with a high mortality due to prolonged vasoplegia resistant to fluid resuscitation and vasopressors. We present a unique case of a young male with d-CCB toxicity, resulting in hemodynamic circulatory collapse with cardiac arrest successfully supported with early peripheral VA-ECMO. This case report highlights the utility of peripheral VA-ECMO in mixed distributive/cardiogenic shock from d-CCB intoxication resistant to medical therapy, suggesting that d-CCB intoxication can be managed with early initiation of peripheral VA-ECMO as opposed to other reports of high flow central ECMO.