Ventilation Prevents Blood Gas Changes During Local-anesthetic-induced Convulsions in Paralyzed Cats. Issue 3 (July 1982)

• Record Type: Journal Article
• Authors: de Jong, Rudolph H.; Bonin, John D.; Gamble, Charles A.
• Is Part Of: Regional anesthesia. Volume 7:Issue 3(1982)
• Page Start: 103
• Page End: 106
• Publication Date: 1982-07
• Subjects: Acid-base equilibrium -- Acidosis -- metabolic -- Bicarbonate ion concentration -- Carbon dioxide tension -- Bupivacaine -- Lidocaine -- Complications -- acidemia -- convulsions; Conduction anesthesia -- Periodicals; Pain medicine -- Periodicals; 617.964
• DOI: 10.1136/rapm-00115550-198207030-00004
• Languages: English
• ISSNs: 0146-521X

Abstract

Abstract : Lightly anesthetized, ventilated, paralyzed cats had convulsions induced by lidocaine (n = 40) or bupivacaine (n = 45). The mean control arterial Po2 (Fio2 ⋍ 0.3) was 176 torr; the lowest Po2 anytime thereafter was never less than 120 torr. At the onset of convulsions, arterial p H was 0.04 (bupivacaine group) to 0.06 (lidocaine group) units less than control; Pco2 was 1.1 (bupivacaine group) to 2.1 (lidocaine group) torr greater than control; plasma bicarbonate ion concentration decreased 1.1 (bupivacaine group) to 1.4 mmol/L (lidocaine group). To yield long-lasting seizures, local anesthetic infusion was continued until twice the convulsant dose (bupivacaine 10.6 mg/kg, lidocaine 56.0 mg/kg) had been given. Some 15 minutes later, arterial Pco2 and p H had not changed significantly from threshold ictal values. We conclude that adequate alveolar ventilation will maintain acid-base balance and aid survival after massive overdoses of amide local anesthetics.