Authors: Ahmed Sarsar , Fathima Murthaza , Mohamed Abdou

Abstract

Introduction
Calcium channel blocker (CCB) overdose is a leading cause of cardiovascular drug-related mortality, typically presenting with refractory hypotension, bradycardia, and metabolic acidosis . While initial therapy—including calcium, high-dose insulin euglycemia therapy (HIET), and vasopressors—remains the mainstay of management, extracorporeal membrane oxygenation (ECMO) serves as a salvage intervention in cases of refractory cardiogenic shock. A systematic review reported an 84.6% survival rate with ECMO in CCB overdose, reinforcing AHA recommendations to VA-ECMO in refractory shock unresponsive to maximal medical therapy . We report a case of amlodipine-induced vasoplegic shock successfully managed with VA-ECMO.

Case Presentation:
A 37-year-old woman with hypertension and hypothyroidism presented 15 hours after ingesting 220 mg of amlodipine and 6 g of paracetamol in a suicide attempt. She was hypotensive and acidotic despite early fluid resuscitation, High-dose insulin euglycemic therapy, vasopressors, glucagon, and intralipid. She then deteriorated to refractory vasoplegic shock with pulmonary edema requiring mechanical ventilation. A worsening acidosis with elevating lactate were in her serial blood gas . Persistent hemodynamic instability despite maximal medical therapy prompted bedside initiation of femoral-femoral VA-ECMO, with successful decannulation after three days and uncomplicated discharge.

Discussion
This case illustrates the challenges faced in CCB overdose, where a combination of vasoplegia and cardiogenic shock happen. Peripheral vasodilation is a primary effect of dihydropyridines such as amlodipine when used therapeutic doses; however, loss of pharmacologic selectivity  is seen in cases of massive overdose leading to impairment of the cardiac contractility and causing a mixed cardiogenic-distributive shock phenotype. The process of starting  ECMO usually takes a place after failure of the conventional treatments and due to the patient’s refractory shock despite maximal medical therapy ECMO was initiated which is consistent with systematic reviews reporting an 84.6% survival rate in CCB overdose patients managed with ECMO. ECMO’s efficacy in CCB overdose derives from its ability to bypass cardiopulmonary dysfunction, thereby maintaining organ perfusion while endogenous drug clearance occurs . 

The rapid improvement of the patient’s hemodynamic post-cannulation in this case is consistent with prior reports of ECMO reversing vasoplegia within 48–72 hours. The patient’s persistent tachycardia reflects the predominant vasodilation typical of dihydropyridine toxicity. Although HIET remains first-line therapy, its vasodilatory effects limit efficacy in severe vasoplegic shock, highlighting the importance of early ECMO to prevent irreversible organ damage. The minimal effect here of intralipid emulsion supports ECMO as the preferred intervention in refractory cases despite the fact that it has theoretical benefits for lipophilic CCBs.

Conclusion
This case reflects the importance of early recongition of shock and initation of VA-ECMO in case of severe amlodipine overdose before an irrerversible shock develops. Prompt multidisciplinary coordination and early involvement of the ECMO team are vital to improving outcomes in these complex toxicologic emergencies

Keywords: "CCB overdose" "ECMO" "Amlodipine" "dihydropyridine"