Cardiovascular Effects of Convulsant and Supraconvulsant Doses of Amide Local Anesthetics

Jong, Rudolph H. de; Ronfeld, R. A.; DeRosa, Richard A.

doi:10.1097/00132586-198226040-00061

Cited by 20 publications

(45 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In healthy cats, at a dose up to 2 mg kg -1 , the bupivacaine peak plasma concentration was approximately half that reported to cause arrhythmias or convulsive EEG in cats, and about one sixth of that required to produce hypotension (Chadwick 1985, de Jong et al 1982. …”

Section: Discussionmentioning

confidence: 86%

“…Studies on bupivacaine toxicity in cats have reported different plasma concentration thresholds for toxicity (Appendix) (de Jong et al 1982;Chadwick 1985;Kasaba et al 1998). …”

Section: Resultsmentioning

confidence: 99%

“…The voltage-gated sodium channel blockade responsible for the inhibition of nerve conduction and local anesthesia may also affect the central nervous system and the cardiovascular system, and may result in toxicity. Common signs of toxicity include sedation, seizures, arrhythmias, myocardial depression, hypotension, and cardiac arrest, and the systemic toxicity appears to be related to drug absorption in by the circulation; signs correlate with plasma drug concentrations (de Jong et al 1982;Chadwick 1985).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Plasma bupivacaine concentrations following orbital injections in cats

Shilo‐Benjamini

Pypendop

Newbold

et al. 2017

Veterinary Anaesthesia and Analgesia

View full text Add to dashboard Cite

Design: Prospective, randomized, crossover, experimental trial with a two-week washout period. Animals:Six adult healthy cats weighing 4.6 ± 0.7 kg.Methods: Cats were sedated with 36 -56 µg kg -1 dexmedetomidine and received a retrobulbar injection of 0.5 % bupivacaine (0.75 mL; 3.75 mg) and iopamidol (0.25 mL), or peribulbar injection of 0.5 % bupivacaine (1.5 mL; 7.5 mg), iopamidol (0.5 mL), and 0.9 % saline (1 mL) via a dorsomedial approach. Blood was sampled (2 mL) before, and at 5, 10, 15, 22, 30, 45, 60, 120, 240, and 480 minutes after bupivacaine injection. Atipamezole was administered approximately 40 minutes after bupivacaine injection. Plasma bupivacaine and 3-hydroxybupivacaine concentrations were determined using liquid chromatography/mass spectrometry.Bupivacaine maximum plasma concentration (Cmax) and time to Cmax were determined from the data. Results:The bupivacaine median (range) Cmax, and time to Cmax were 1.4 (0.9 -2.5), and 1.7(1.0 -2.4) µg mL -1 , and 17 (4 -60), and 28 (8 -49) minutes, for retrobulbar and peribulbar injections respectively. In both treatments the 3-hydroxy-bupivacaine peak concentration was 0.05 -0.21 µg mL -1 . Conclusion:In healthy cats, at a dose up to 2 mg kg -1 , the bupivacaine peak plasma concentration was approximately half that reported to cause arrhythmias or convulsive EEG in cats, and about one sixth of that required to produce hypotension (Chadwick 1985, de Jong et al. 1982.

show abstract

Section: Discussionmentioning

confidence: 86%

“…Studies on bupivacaine toxicity in cats have reported different plasma concentration thresholds for toxicity (Appendix) (de Jong et al 1982;Chadwick 1985;Kasaba et al 1998). …”

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Plasma bupivacaine concentrations following orbital injections in cats

Shilo‐Benjamini

Pypendop

Newbold

et al. 2017

Veterinary Anaesthesia and Analgesia

View full text Add to dashboard Cite

show abstract

“…Seizure is a major CNS toxic effect of cocaine and other local anesthetics (31). Blockade of dopamine re-uptake and the resulting elevation of excitatory transmitters have been investigated (32).…”

Section: Discussionmentioning

confidence: 99%

Diazepam Protects Against the Enhanced Toxicity of Cocaine Adulterated With Atropine

et al. 2008

View full text Add to dashboard Cite

Abstract. We examined the toxicity of cocatropine (cocaine / atropine mixture) and the therapeutic potential of diazepam on some behavioral and physiological parameters in rats. Atropine (20 and 60 mg / kg) or cocaine (40 mg / kg) alone did not induce any seizure or death, but the combination significantly increased both, after both acute and binge treatment. There was a significant increase of EEG mean total spectral power in cocatropine-in comparison with cocaine-treated animals. Hyperlocomotion was observed in non-seizuring rats treated with cocaine or cocatropine. Cocaine, atropine 60, and cocatropine (40 + 20 and 40 + 60) all induced hyperthermic effects in non-seizuring rats, while cocatropine (40 + 60)-seizuring animals had hypothermia. An initial hypertensive and tachycardiac effect within 15 min was followed by a secondary fall in the cocatropine (40 + 60) group. Cocatropine toxicity was partially or fully reversed by diazepam (5 mg / kg), given intraperitoneally after the first seizure. The present findings provide, for the first time, details of a synergistic toxic effect of the cocaine / atropine mixture and of the potential of diazepam for treating cocatropine-related hospital emergencies.

show abstract

“…Cardiac resuscitation is more diffi cult after bupivacaine-induced cardiac arrest. It is important to note that patients under general anesthesia will typically present with cardiotoxicity as the fi rst sign of local anesthetic toxicity given that patients are usually not alert [ 21 ]. The very slow reversal of Na + channel blockade after a cardiac action potential, which is a hallmark of bupivacaine, is considerably faster with ropivacaine.…”

Section: Cardiovascular Systemmentioning

confidence: 99%