Physician Assistant - Cardiothoracic Surgery S Setauket, New York, United States
Disclosure(s):
Amy Butcher, PA-C: No financial relationships to disclose
Background: High dose insulin euglycemic therapy (HIET) can treat beta-blocker toxicity by increasing glucose and pyruvate uptake in myocardial cells with the risk of hypokalemia from altered intracellular buffering. Various HIET protocols allow relative hypokalemia to 2.5 mEq/L with an adequate safety profile.
Methods: A 36-year-old male with a history of cocaine use and non-ischemic cardiomyopathy (LVEF 40%) presented unresponsive after intentional beta-blocker overdose. He remained obtunded and bradycardic (HR 39beat/min) despite naloxone and glucagon and required intubation and epinephrine infusion (0.1 mcg/kg/min). Toxicology recommended high dose insulin euglycemic therapy (HIET), glucagon, and calcium chloride infusions for beta-blocker toxicity. Insulin infusion was initiated at 0.25 units/kg/hr (goal rate of 0.5-1 unit/kg/hr) with an initial serum potassium of 3.2 mEq/L (recommended tolerance to 2.5-2.8 mEq/L). 4 hours after HIET initiation, the patient became profoundly bradycardic (17beats/min) with escalation of pressors. A transvenous pacer was placed and pacing was initiated at 80beat/min with hemodynamic recovery and HIET was uptitrated to 1 unit/kg/hr.
The patient suffered a polymorphic ventricular tachycardia (VT) arrest requiring 19 minutes of CPR, defibrillation at 360Jx3, and double sequential defibrillation at 720Jx2. After return of spontaneous circulation, the ECMO team was initiated for emergent cannulation. The patient had recurrent VT arrest with transvenous pacer repositioned given concern for R-on-T, and lidocaine infusion was initiated at 4mg/min.
Outcome: Femoral-femoral VA-ECMO was placed uneventfully at the bedside (right common femoral vein 25Fr venous cannula, left common femoral artery 19Fr cannula, 6Fr distal reperfusion catheter) and flow was initiated at 4.5L/min, 4000RPM, with sweep of 3. Labs at cannulation revealed a serum potassium of 2.9mEq/L, so HIET was paused for aggressive potassium repletion with no further episodes of VT. Post-cannulation transesophageal echo revealed poor aortic valve opening in sinus bradycardia (HR 43-47BPM), so a microaxial flow pump (Impella CP) was placed for left ventricular venting.
Pressors were weaned off over 24 hours and he had no further arrhythmias. Afterload reduction was initiated with nitroprusside and he was uneventfully decannulated from ECMO on post-cannulation day 3, with Impella removal on post-cannulation day 4. He was restarted on goal directed therapy while inpatient with discharge TTE revealing EF of 35%. He was discharged to an inpatient care facility on post-cannulation day 13.
Conclusion: High dose insulin euglycemic therapy (HIET) is a potent treatment modality for beta-blocker toxicity but risks relative hypokalemia due to intracellular buffering. This may predispose certain populations to life-threatening arrhythmias. VA-ECMO should be considered an adjunct or alternative therapeutic modality in beta blocker toxicity in select patient populations.
