Atrial fibrillation in halothane- and isoflurane-anesthetized dogs

Lisa C. Freeman From the Departments of Veterinary Clinical Sciences (Ack, Muir) and Veterinary Physiology and Pharmacology (Freeman), College of Veterinary Medicine, and the Department of Statistics, College of Arts and Sciences (Fligner), The Ohio State University, Columbus, OH 43210.

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James A. Ack From the Departments of Veterinary Clinical Sciences (Ack, Muir) and Veterinary Physiology and Pharmacology (Freeman), College of Veterinary Medicine, and the Department of Statistics, College of Arts and Sciences (Fligner), The Ohio State University, Columbus, OH 43210.

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Michael A. Fligner From the Departments of Veterinary Clinical Sciences (Ack, Muir) and Veterinary Physiology and Pharmacology (Freeman), College of Veterinary Medicine, and the Department of Statistics, College of Arts and Sciences (Fligner), The Ohio State University, Columbus, OH 43210.

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William W. Muir III From the Departments of Veterinary Clinical Sciences (Ack, Muir) and Veterinary Physiology and Pharmacology (Freeman), College of Veterinary Medicine, and the Department of Statistics, College of Arts and Sciences (Fligner), The Ohio State University, Columbus, OH 43210.

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SUMMARY

Programmed electrical stimulation techniques were used to evaluate the effects of halothane and isoflurane on induction of atrial fibrillation in anesthetized dogs. Experiments were performed in 16 dogs anesthetized with α-chloralose. Critically timed premature stimuli were applied to the right atrial appendage and Bachmann bundle to determine the atrial fibrillation threshold, defined as the minimal current required to induce rapid, irregular atrial electrical activity of at least 8 seconds' duration, Atrial fibrillation thresholds were determined at baseline (0.0% inhalational anesthetic), 0.5 minimal alveolar concentration (mac), and 1.0 mac of halothane (n = 8) and isoflurane (n = 8).

In the absence of inhalation anesthetic, it was significantly (P < 0.01) easier to induce atrial fibrillation at the Bachmann bundle vs the right atrial appendage. Atrial fibrillation threshold at the Bachmann bundle was not affected by increasing concentrations of halothane, but was increased by 1.0 mac of isoflurane (P < 0.05). It was concluded that at 1.0 mac isoflurane, but not halothane, has antifibrillatory effects in atrial tissue.

SUMMARY

Programmed electrical stimulation techniques were used to evaluate the effects of halothane and isoflurane on induction of atrial fibrillation in anesthetized dogs. Experiments were performed in 16 dogs anesthetized with α-chloralose. Critically timed premature stimuli were applied to the right atrial appendage and Bachmann bundle to determine the atrial fibrillation threshold, defined as the minimal current required to induce rapid, irregular atrial electrical activity of at least 8 seconds' duration, Atrial fibrillation thresholds were determined at baseline (0.0% inhalational anesthetic), 0.5 minimal alveolar concentration (mac), and 1.0 mac of halothane (n = 8) and isoflurane (n = 8).

In the absence of inhalation anesthetic, it was significantly (P < 0.01) easier to induce atrial fibrillation at the Bachmann bundle vs the right atrial appendage. Atrial fibrillation threshold at the Bachmann bundle was not affected by increasing concentrations of halothane, but was increased by 1.0 mac of isoflurane (P < 0.05). It was concluded that at 1.0 mac isoflurane, but not halothane, has antifibrillatory effects in atrial tissue.

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