40: Out of the Frying Pan and into the Fire - Amlodipine Toxicity - Cardiogenic Shock and ARDS

Introduction: Amlodipine, a calcium channel blocker, acts on L-type calcium channels with high affinity for smooth muscle, causing peripheral vasodilation and myocardial depression. Although cardiovascular collapse is the hallmark of amlodipine overdose, acute respiratory distress syndrome (ARDS) is rare. Two mechanisms have been proposed: inhibition of endothelin-1 stimulated surfactant secretion by type II alveolar epithelial cells leading to alveolar collapse, and selective precapillary vasodilation causing excessive fluid leakage from capillaries into the alveoli. Case Presentation: A 25-year-old female presented after ingesting 60 tablets each of alprazolam (0.5 mg) and nebivolol (5 mg), and 105 tablets of amlodipine (5 mg) over three days. She arrived in cardiogenic shock with high anion gap metabolic acidosis and complete heart block. The patient was mechanically ventilated and managed with temporary transvenous pacing and vasopressors. Intravenous glucagon and intralipid therapy were administered. Due to refractory shock, Retrieval VA-ECMO was initiated, and she was transferred to our center Charcoal Hemadsorption was performed for 12-hour sessions at 24-hour intervals. Extracorporeal support was weaned and removed after 72 hours as cardiac function improved without vasopressors. Four hours post-decannulation, the patient’s hemodynamics deteriorated, with a decreased P/F ratio and reduced urine output. Empirical antibiotics were started after cultures, and sustained low-efficiency dialysis (SLED) was initiated. Chest X-ray showed bilateral basal consolidation consistent with ARDS. The patient underwent two cycles of prone ventilation. Bronchoalveolar lavage cultures were negative, allowing antibiotic de-escalation. She was successfully extubated on day 8. Conclusion: While cardiovascular collapse dominates amlodipine overdose, ARDS, though uncommon, can mislead diagnosis toward infection or fluid overload. Prompt identification and lung-protective ventilation are vital. Careful monitoring and recognizing the hidden complications is essential for timely Initiation, maintenance and weaning of extracorporeal support. Limitations: Management challenges include the requirement of specialized ECMO centers, high costs, and limited large-scale studies.

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ASAIO Journal
Published
2026-02-01
DOI
https://doi.org/10.1097/01.mat.0001180848.60863.39
Primary Topic
Poisoning and overdose treatments
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article

40: Out of the Frying Pan and into the Fire - Amlodipine Toxicity - Cardiogenic Shock and ARDS

Varun Kumar
ASAIO Journal
Poisoning and overdose treatments
article

40: Out of the Frying Pan and into the Fire - Amlodipine Toxicity - Cardiogenic Shock and ARDS

Varun Kumar
article en

Abstract

Introduction: Amlodipine, a calcium channel blocker, acts on L-type calcium channels with high affinity for smooth muscle, causing peripheral vasodilation and myocardial depression. Although cardiovascular collapse is the hallmark of amlodipine overdose, acute respiratory distress syndrome (ARDS) is rare. Two mechanisms have been proposed: inhibition of endothelin-1 stimulated surfactant secretion by type II alveolar epithelial cells leading to alveolar collapse, and selective precapillary vasodilation causing excessive fluid leakage from capillaries into the alveoli. Case Presentation: A 25-year-old female presented after ingesting 60 tablets each of alprazolam (0.5 mg) and nebivolol (5 mg), and 105 tablets of amlodipine (5 mg) over three days. She arrived in cardiogenic shock with high anion gap metabolic acidosis and complete heart block. The patient was mechanically ventilated and managed with temporary transvenous pacing and vasopressors. Intravenous glucagon and intralipid therapy were administered. Due to refractory shock, Retrieval VA-ECMO was initiated, and she was transferred to our center Charcoal Hemadsorption was performed for 12-hour sessions at 24-hour intervals. Extracorporeal support was weaned and removed after 72 hours as cardiac function improved without vasopressors. Four hours post-decannulation, the patient’s hemodynamics deteriorated, with a decreased P/F ratio and reduced urine output. Empirical antibiotics were started after cultures, and sustained low-efficiency dialysis (SLED) was initiated. Chest X-ray showed bilateral basal consolidation consistent with ARDS. The patient underwent two cycles of prone ventilation. Bronchoalveolar lavage cultures were negative, allowing antibiotic de-escalation. She was successfully extubated on day 8. Conclusion: While cardiovascular collapse dominates amlodipine overdose, ARDS, though uncommon, can mislead diagnosis toward infection or fluid overload. Prompt identification and lung-protective ventilation are vital. Careful monitoring and recognizing the hidden complications is essential for timely Initiation, maintenance and weaning of extracorporeal support. Limitations: Management challenges include the requirement of specialized ECMO centers, high costs, and limited large-scale studies.

ASAIO JournalVol. 72(Supplement 1)
Kovai Medical Center and Hospital (IN)
Good health and well-being
Openalex Percentile: Top 67%
Poisoning and overdose treatments
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