Effect of hypercapnia on the arrhythmogenic dose of epinephrine in horses anesthetized with guaifenesin, thiamylal sodium, and halothane

James S. Gaynor From the Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Oil 43210.

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Richard M. Bednarski From the Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Oil 43210.

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William W. Muir III From the Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Oil 43210.

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SUMMARY

The effect of hypercapnia on the arrhythmo-genic dose of epinephrine (ADE) was investigated in 14 horses. Anesthesia was induced with guaifenesin and thiamylal sodium and was maintained at an end-tidal halothane concentration between 0.86 and 0.92%. Base-apex ECG, cardiac output, and facial artery blood pressure were measured and recorded. The ADE was determined at normocapnia (arterial partial pressure of carbon dioxide [Paco2 = 35 to 45 mm of Hg), at hypercapnia (Paco2 = 70 to 80 mm of Hg), and after return to normocapnia. Epinephrine was infused at arithmetically spaced increasing rates (initial rate = 0.25 μg/kg of body weight/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate, to the nearest 0.25 μg/kg/min, at which 4 premature ventricular complexes occurred in a 15-second period. The ADE (mean ± SD) during hypercapnia (1.04 ± 0.23 μg/kg/min) was significantly (P < 0.05) less than the ADE at normocapnia (1.35 ± 0.38 μg/kg/min), whereas the ADE after return to normocapnia (1.17 ± 0.22 μg/kg/min) was not significantly different from those during normocapnia or hypercapnia. Baseline systolic and diastolic arterial pressures and cardiac output decreased after return to normocapnia. Significant differences were not found in arterial partial pressure of O2 (PaO2) or in base excess during the experiment. Two horses developed ventricular fibrillation and died during normocapnic determinations of ADE. Hypercapnia was associated with an increased risk of developing ventricular arrhythmias in horses anesthetized with guaifenesin, thiamylal sodium, and halothane.

SUMMARY

The effect of hypercapnia on the arrhythmo-genic dose of epinephrine (ADE) was investigated in 14 horses. Anesthesia was induced with guaifenesin and thiamylal sodium and was maintained at an end-tidal halothane concentration between 0.86 and 0.92%. Base-apex ECG, cardiac output, and facial artery blood pressure were measured and recorded. The ADE was determined at normocapnia (arterial partial pressure of carbon dioxide [Paco2 = 35 to 45 mm of Hg), at hypercapnia (Paco2 = 70 to 80 mm of Hg), and after return to normocapnia. Epinephrine was infused at arithmetically spaced increasing rates (initial rate = 0.25 μg/kg of body weight/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate, to the nearest 0.25 μg/kg/min, at which 4 premature ventricular complexes occurred in a 15-second period. The ADE (mean ± SD) during hypercapnia (1.04 ± 0.23 μg/kg/min) was significantly (P < 0.05) less than the ADE at normocapnia (1.35 ± 0.38 μg/kg/min), whereas the ADE after return to normocapnia (1.17 ± 0.22 μg/kg/min) was not significantly different from those during normocapnia or hypercapnia. Baseline systolic and diastolic arterial pressures and cardiac output decreased after return to normocapnia. Significant differences were not found in arterial partial pressure of O2 (PaO2) or in base excess during the experiment. Two horses developed ventricular fibrillation and died during normocapnic determinations of ADE. Hypercapnia was associated with an increased risk of developing ventricular arrhythmias in horses anesthetized with guaifenesin, thiamylal sodium, and halothane.

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