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Introduction: High dose insulin (HDI) and intravenous lipid emulsion (ILE) have emerged as treatment options for severe calcium channel blocker (CCB) and beta-blocker (BB) toxicity. Insulin causes increased glucose uptake into cardiac myocytes and affects various intra-cellular pathways resulting in positive inotropic effects. ILE therapy is theorized to work by sequestering highly lipophilic compounds and preventing them from reaching their site of action. It provides a fatty acid substrate to stressed myocardial cells and improves the function of calcium ion membrane channels on myocardial cells therefore increasing inotropy and chronotropy. Case Series Description: The first patient was a 35 year old male who arrived in the emergency department (ED), in bradycardic arrest (20 beats/min) without a measurable blood pressure (BP). He ingested 30-amlodipine 5mg (150mg), 47-metoprolol 25mg (1.2g), and 57-verapamil ER 180mg (10.3g). He was given atropine, glucagon, and calcium along with infusions of dopamine, epinephrine, and glucagon with return of measurable vital signs. After return of a palpable femoral artery pulse and subsequent intubation for mental status the patient was transferred to the medical intensive care unit (MICU). HDI was initiated with a 1unit/kg (83 units) bolus, an insulin infusion 1unit/kg/hr (80 units/hr), and D10% infusion at 100ml/hr approximately five hours after arrival to the ED. The glucagon infusion and dopamine were discontinued within one hour of the HDI bolus. Due to the amount of medication ingested and persistent shock it was decided to start ILE therapy. It was started approximately seven hours after arrival to the ED and included a bolus of ILE 20% 1.5ml/kg (130ml) and an infusion of 0.25ml/kg/min for 60min. The epinephrine was discontinued approximately an hour after initiation of the ILE. On hospital day three the patient started to spontaneously move his extremities and was extubated with a full neurological recovery. The second patient was a 59 year old male who presented after a witnessed suicide attempt where he ingested approximately 60-metformin (30g), 30-amlodipine (3g), 30-lisinopril (3g), and simvastatin of an unknown quantity. He received activated charcoal and calcium prior to arrival. Upon arrival to the ED, he was hypotensive (78/36 mmHg) and bradycardic (54 beats/minute). His initial pH was 7.2 showing a severe lactic acidosis with an anion gap of 17, and a lactate of 6.6mmol/L. He was started on norepinephrine and a sodium bicarbonate infusion for his severe metabolic acidosis. Approximately six hours after arrival, the patient received HDI [bolus-1unit/kg (70units), infusion-1unit/kg/hr (70 units/hr)], ILE [bolus-1.5ml/kg (105ml), infusion (0.25ml/kg/min for 60min)], and D10% at 100ml/hr. Six hours after initiation of HDI the dextrose infusion was converted to D20% due to hypoglycemia. He was initiated on continuous renal replacement therapy in the MICU. While the drip was running, the patient's BGs were checked hourly and 25g of dextrose was administered for any BG <100mg/dL. HDI was continued for 55 hours after initiation with a mean BG of 121 ± 43 (57-223)mg/dL. He experienced one episode of hypoglycemia (BG < 70mg/dL). After discontinuation of the insulin drip, the patient was transferred to the general medicine floor where his renal function improved over the next few days. He was discharged neurologically intact back to his institution.