Abstract Introduction Massive calcium-channel blocker (CCB) and beta-blocker (BB) co-ingestion can produce profound vasoplegia resistant to adrenergic vasopressors and high-dose insulin euglycemia therapy (HIET). Angiotensin II offers a non-adrenergic option to restore smooth muscle tone with increased intracellular calcium signaling via its receptor. We report a BB/CCB/angiotensin converting enzyme inhibitor/acetaminophen overdose in which angiotensin II initiation coincided with reduced norepinephrine-equivalent exposure (NEE) and insulin needs. Case A 58-year-old male with a history of hypertension and major depressive disorder ingested approximately 90 tablets each of atenolol 10 mg (900 mg), amlodipine 25 mg (2,250 mg), and lisinopril 20 mg (1,800 mg); acetaminophen co-ingestion was suspected (quantity unknown). On arrival, vitals included temperature 100 degrees Fahrenheit, heart rate of 17 beats per minute, blood pressure 57/37 mmHg, respiratory rate of 43 breaths per minute, oxygen saturation of 99%. Labs notable for K 2.9 mEq/L, CO2 17 mEq/L, pH 7.33, HCO3 16 mEq/L, and acetaminophen 159 µg/mL. Electrocardiography showed junctional bradycardia. He received charcoal, calcium, glucagon, N-acetylcysteine, HIET with dextrose and methylene blue; vasopressors were escalated with minimal response. CRRT was initiated for toxin/volume clearance. He was transferred to a quaternary care facility for possible initiation of VA-ECMO. The patient arrived critically ill on norepinephrine 1.5 µg/kg/min, epinephrine 0.5 µg/kg/min, vasopressin 0.06 U/min, and HIET 10 U/kg/hr. Angiotensin II was initiated and titrated to dose of 40ng/kg/min to maintain mean arterial pressure (MAP) 65-75 mmHg. With addition of angiotensin II, other vasopressors and insulin were subsequently de-escalated; VA-ECMO initiation was deferred. Epinephrine decreased to 0.06 mcg/kg/min by hospital day 1. Both epinephrine and HIET were tapered and discontinued by day 4; vasopressin was tapered and discontinued by day 5; norepinephrine was discontinued by day 6. Time-series visualization showed downward trends in NEE, noting angiotensin II was briefly discontinued and reinitiated (Figure 1). Angiotensin II dose and NEE were inversely associated (Pearson r = −0.35, 95% CI − 0.53 to − 0.14). Ischemic changes to the toes occurred without other macrothrombotic events. Renal function recovered back to baseline. The patient ultimately stabilized and transferred to the inpatient psychiatric unit. Conclusion This case highlights angiotensin II as a non-adrenergic adjunct for toxin-induced vasoplegia when adrenergic pathways are saturated, and renin-angiotensin-aldosterone-system signaling is suppressed. Complications (digital ischemia) underscore vigilance for ischemic risk during high-dose vasoactive therapy. The case demonstrates a consideration for early angiotensin II initiation in catecholamine-refractory toxicologic shock and provides a transparent analytic template for future reports. This abstract is funded by: University of Maryland Medical Center
Caplan et al. (Fri,) studied this question.