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Canadian Journal of Anesthesia 51:189 (2004)
© Canadian Anesthesiologists' Society, 2004

Correspondence

The early detection of bupivacaine toxicity in dogs

Marc Freysz, MD PhD and François Lenfant, MD PhD

Dijon, France

To the Editor:

We read with interest the article of Kim et al.1 ««Continuous mixed venous oxygen saturation, not mean blood pressure, is associated with early bupivacaine cardiotoxicity in dogs»». In 1988, we conducted similar work,2 also showing that cardiac output appeared to be the first and the most affected hemodynamic variable, whereas mean systemic blood pressure remained unchanged because of the compensatory increase in systemic vascular resistance.

In fact, bupivacaine iv primarily impairs cardiac intraventricular conduction3,4 enhancing QRS duration, as noted in Kim et al.’s Table and Figure 2.1 Contractile deficiency occurs only later.

References

1 Kim JT, Rhee KY, Bahk JH, et al. Continuous mixed venous oxygen saturation, not mean blood pressure, is associated with early bupivacaine cardiotoxicity in dogs. Can J Anesth 2003; 50: 376–81.[Abstract/Free Full Text]

2 Beal JL, Freysz M, Timour Q, Bertrix L, Lang J, Faucon G. Haemodynamic effects of high plasma concentrations of bupivacaine in the dog. Eur J Anaesthesiol 1988; 5: 251–60.[Medline]

3 Freysz M, Timour Q, Mazze RI, et al. Potentiation by mild hypothermia of ventricular conduction disturbances and reentrant arrhythmias induced by bupivacaine in dogs. Anesthesiology 1989; 70: 799–804.[Medline]

4 de La Coussaye JE, Brugada J, Allessie MA. Electrophysiologic and arrhythmogenic effects of bupivacaine. A study with high-resolution ventricular epicardial mapping in rabbit hearts. Anesthesiology 1992; 77: 132–41.[Medline]


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REPLY
Jin-Tae Kim and Kook-Hyun Lee
CJA 2004 51: 189-190. [Full Text]  




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