D A Tanen1, A M Ruha, S C Curry, K A Graeme, C G Reagan. 1. Department of Medical Toxicology, Good Samaritan Regional Medical Center, the University of Arizona College of Medicine, Phoenix, AZ, USA. dtamen@samaritan.edu
Abstract
STUDY OBJECTIVE: This study was conducted to determine whether hypertonic sodium bicarbonate would improve the hypotension associated with severe verapamil toxicity compared with volume expansion. METHODS: The study design used a nonblinded acute animal preparation. Twenty-four anesthetized and instrumented swine were poisoned with verapamil delivered at a rate of 1 mg/kg per hour for 10 minutes followed by incremental increases of 1 mg/kg per hour every 10 minutes until the endpoint of a mean arterial blood pressure of 45% of baseline was achieved. Animals alternately received either 4 mEq/kg of hypertonic sodium bicarbonate intravenously over 4 minutes or similar volumes of 0.6% sodium chloride in 10% mannitol (control). The main outcome parameter followed was mean arterial pressure. In addition, physiologic parameters including cardiac output, heart rate, pH, PCO (2), PO (2), plasma ionized calcium, sodium, and potassium were monitored. RESULTS: Verapamil toxicity, as defined by a mean arterial pressure of 45% of baseline, was produced in all animals following an average verapamil infusion dose of 0.6+/-0.12 mg/kg. This dose produced an average plasma verapamil concentration of 728.1+/-155.4 microgram/L, with no significant difference between groups. Swine treated with hypertonic sodium bicarbonate experienced a significant increase in mean arterial pressure (>50%) and cardiac output (>30%) over the first 20 minutes that slowly equilibrated with the control group over the remainder of the experiment. As expected, plasma sodium concentrations were elevated significantly in the sodium bicarbonate group while plasma potassium concentrations were decreased significantly. Finally, there was a significant decrease in plasma ionized calcium concentration in the sodium bicarbonate-treated group compared with controls. CONCLUSION: Hypertonic sodium bicarbonate reversed the hypotension and cardiac output depression of severe verapamil toxicity in a swine model.
STUDY OBJECTIVE: This study was conducted to determine whether hypertonicsodium bicarbonate would improve the hypotension associated with severe verapamiltoxicity compared with volume expansion. METHODS: The study design used a nonblinded acute animal preparation. Twenty-four anesthetized and instrumented swine were poisoned with verapamil delivered at a rate of 1 mg/kg per hour for 10 minutes followed by incremental increases of 1 mg/kg per hour every 10 minutes until the endpoint of a mean arterial blood pressure of 45% of baseline was achieved. Animals alternately received either 4 mEq/kg of hypertonicsodium bicarbonate intravenously over 4 minutes or similar volumes of 0.6% sodium chloride in 10% mannitol (control). The main outcome parameter followed was mean arterial pressure. In addition, physiologic parameters including cardiac output, heart rate, pH, PCO (2), PO (2), plasma ionizedcalcium, sodium, and potassium were monitored. RESULTS:Verapamiltoxicity, as defined by a mean arterial pressure of 45% of baseline, was produced in all animals following an average verapamil infusion dose of 0.6+/-0.12 mg/kg. This dose produced an average plasma verapamil concentration of 728.1+/-155.4 microgram/L, with no significant difference between groups. Swine treated with hypertonicsodium bicarbonate experienced a significant increase in mean arterial pressure (>50%) and cardiac output (>30%) over the first 20 minutes that slowly equilibrated with the control group over the remainder of the experiment. As expected, plasma sodium concentrations were elevated significantly in the sodium bicarbonate group while plasma potassium concentrations were decreased significantly. Finally, there was a significant decrease in plasma ionizedcalcium concentration in the sodium bicarbonate-treated group compared with controls. CONCLUSION:Hypertonicsodium bicarbonate reversed the hypotension and cardiac output depression of severe verapamiltoxicity in a swine model.
Authors: Jouni Kurola; Heli Leppikangas; Jarkko Magga; Leena Lindgren; Vesa Kiviniemi; Juha Rutanen; Esko Ruokonen Journal: Scand J Trauma Resusc Emerg Med Date: 2010-03-11 Impact factor: 2.953
Authors: J Dave Barry; Dave Durkovich; Lee Cantrell; William Richardson; Tri Tong; Steve Offerman; Richard F Clark; David A Tanen; Saralyn Williams Journal: J Med Toxicol Date: 2005-12
Authors: M St-Onge; P-A Dubé; S Gosselin; C Guimont; J Godwin; P M Archambault; J-M Chauny; A J Frenette; M Darveau; N Le Sage; J Poitras; J Provencher; D N Juurlink; R Blais Journal: Clin Toxicol (Phila) Date: 2014-10-06 Impact factor: 4.467