P. Bruelle et al., COMPARATIVE ELECTROPHYSIOLOGIC AND HEMODYNAMIC-EFFECTS OF SEVERAL AMIDE LOCAL-ANESTHETIC DRUGS IN ANESTHETIZED DOGS, Anesthesia and analgesia, 82(3), 1996, pp. 648-656
Large and equipotent doses of several local anesthetics were administe
red in a cardiac electrophysiologic model on closed-chest dogs. Five g
roups of pentobarbital-anesthetized dogs were each given intravenously
16 mg/kg lidocaine, 12 mg/kg mepivacaine, 4 mg/kg or 8 mg/kg etidocai
ne, and 4 mg/kg bupivacaine. Lidocaine induced bradycardia, slowing of
atrioventricular node conduction (AH), and marked hemodynamic depress
ion, represented by a decrease in mean aortic pressure (MAoP), in the
peak of first derivative of left ventricular pressure (LVdP/dt(max)) a
nd by an increase in left ventricular end-diastolic pressure (LVEDP).
Atrial pacing at pacing cycle length (PCL) of 298 ms did not enhance t
he alteration of variables of ventricular conduction (His ventricle [H
V] interval and QRS duration). Mepivacaine induced slight alteration o
f electrophysiologic variables. Atrial pacing at PCL of 312 ms did not
enhance the alteration of HV and QRS duration. Mepivacaine induced tr
ansient hemodynamic depression. Etidocaine (4 mg/kg) induced electroph
ysiologic and hemodynamic alterations similar to mepivacaine but artri
al pacing at PCL of 330 ms enhanced HV lengthening and QRS widening (P
< 0.05). Etidocaine (8 mg/kg) induced marked impairment of PR, HV, QR
S, and QT(c) and dramatic hemodynamic depression represented by a decr
ease in MAoP from 123.5 +/- 16.2 at baseline to 36.5 +/- 8.3 mm Hg at
1 min (P < 0.001) and of LVdP/dt(max) from 1446 +/- 379 to 333 +/- 93
mm Hg/s (P < 0.001). Bupivacaine induced dramatic impairment of electr
ophysiologic variables. Bupivacaine also decreased LVdP/dt(max) (from
1333 +/- 347 to 617 +/- 299, P < 0.001) and increased LVEDP. We conclu
de that mepivacaine induced moderate cardiotoxicity. In contrast, lido
caine induced dramatic hemodynamic depression while etidocaine and bup
ivacaine markedly impaired both electrophysiologic and hemodynamic var
iables. This double impairment could explain the great difficulty in r
esuscitating patients who have had cardiotoxic accidents induced by et
idocaine or bupivacaine.