A 46-year-old man was brought to our emergency department with general malaise 14 h after ingesting 1210 mg amlodipine besylate (amlodipine) and 936 mg candesartan cilexetil (candesartan) in a suicide attempt. He had a history of hypertension, but no known history of mental illness. Upon arrival at the emergency department, his vital signs were as follows: Glasgow Coma Scale score, 13 (E3V4M6); blood pressure, 60/39 mmHg; heart rate, 95 b.p.m. (sinus rhythm); respiratory rate, 30 breaths/min; and blood oxygen saturation, 93% on a reservoir oxygen mask at 10 L/min. Blood tests revealed elevated lactate concentration and metabolic acidosis. The 12-lead electrocardiogram findings were as follows: heart rate, 91 b.p.m.; normal sinus rhythm; right bundle branch block; and no QTc prolongation. The transthoracic echocardiogram findings were as follows: visually estimated ejection fraction, 20%; no asynergy; and no valvular disease. Based on the patient's medical history, we suspected acute amlodipine and candesartan intoxication that led to shock. However, despite our attempts to improve his condition with fluid resuscitation and the administration of high-dose noradrenaline and vasopressin, there was no improvement in the patient's blood pressure or lactic acidosis. To maintain the patient's blood calcium levels, we administered calcium gluconate and regularly monitored the levels using arterial blood gas tests. Hyperinsulinemia-euglycemia therapy was initiated at a rate of 0.5 U/kg/h, without a bolus to avoid hypoglycemia and hypokalemia. Additionally, we administered lipid emulsion and glucagon. Unfortunately, the patient's vital signs, ejection fraction, and left ventricular outflow tract velocity time integral showed no improvement. We considered using methylene blue, but it was unavailable at our hospital. In addition to distributive shock, we suspected impaired cardiac function contributing to the catecholamine-refractory hypotension, suggesting cardiogenic shock. Consequently, we decided to intubate the patient and initiate VA-ECMO approximately 4 h after arrival. Following the initiation of VA-ECMO, we observed a gradual improvement in blood lactate concentration and metabolic acidosis, and we simplified our management approach by discontinuing hyperinsulinemia-euglycemia therapy, lipid emulsion, and glucagon. Despite the improvement observed with VA-ECMO, the patient still required catecholamines for several days to maintain mean arterial pressure, indicating persisting refractory distributive shock. Over time, the patient's requirement for catecholamines decreased, and cardiac function gradually improved, ultimately leading to successful weaning from VA-ECMO on day 5 of hospitalization. Although the patient experienced renal failure due to the intoxication, renal replacement therapy was not deemed necessary. Finally, the patient was extubated on day 9 and discharged on day 18 without experiencing any complications related to VA-ECMO. Blood levels of amlodipine and candesartan were determined. The maximum blood concentrations of amlodipine and candesartan were 536.9 and 8.1 mg/mL, respectively, on day 1.