K. Nishikawa et al., THE EFFECTS OF DOBUTAMINE AND PHENYLEPHRINE ON ATRIOVENTRICULAR-CONDUCTION DURING COMBINED USE OF HALOTHANE AND THORACIC EPIDURAL LIDOCAINE, Anesthesia and analgesia, 82(3), 1996, pp. 551-557
The purpose of this study was to measure cardiac sympathetic nerve act
ivity (CSNA) and atrioventricular (AV) conduction and to test the effe
cts of dobutamine (DOB) and phenylephrine (PHE) on AV conduction durin
g combined use of halothane and thoracic epidural lidocaine. Cats were
anesthetized with 1% halothane and an epidural catheter was inserted
through T-9 laminectomy. His bundle and atrial electrocardiograms were
obtained and atrial electric stimulation was performed using quadripo
lar catheter electrodes. Cats underwent left thoracotomy, and CSNA was
recorded directly from the left ventrolateral or ventromedial nerve.
In addition to sinus cycle length (SCL) measurement during spontaneous
beating, the functional refractory period (FRP) of the atrioventricul
ar node (AV node), effective refractory period (ERP) of the atrium, at
rium-His (A-H) intervals were determined just before and 10, 20, and 3
0 min after epidural administration of 1% lidocaine (0.2 mL/kg) in Gro
up C. DOB 5 mu g . kg(-1). min(-1) (Group DOB) and PHE 0.5-1.0 mu g .
kg(-1). min(-1) (Group PHE) were intravenously administered from 12 to
22 min after epidural lidocaine. CSNA and mean arterial pressure (MAP
) were markedly decreased and SCL, FRP of AV node, ERP of atrium and A
-H interval were significantly prolonged after epidural lidocaine. MAP
increased to baseline level during DOB or PHE infusion. Worsening of
cardiac electrophysiological variables was improved with DOB infusion,
but did not change with PHE infusion. We conclude that thoracic epidu
ral lidocaine during halothane anesthesia almost eliminates CSNA, and
thereby attenuates sinus node automaticity and AV node function. DOB r
estored normal cardiac electrophysiological variables, and therefore i
s preferable to phenylephrine as a pressor drug.