Takekazu Terai

Intravenous lidocaine as a suppressant of coughing during tracheal intubation in elderly patients

&NA; The effects of intravenously administered lidocaine on cough suppression in elderly patients over the age of 60 yr during tracheal intubation under general anesthesia were evaluated in two studies. In the first study, 100 patients received a placebo of either 0.5, 1.0, 1.5, or 2.0 mg/kg lidocaine intravenously 1 min before tracheal intubation. All visible coughs were classified as coughing. The incidence of coughing decreased as the dose of lidocaine increased. A dose of 1.5 mg/kg or more of intravenous lidocaine suppressed the cough reflex significantly (P < 0.01). In the second study, 108 patients received 2 mg/kg lidocaine intravenously or a placebo 1, 3, 5, 7, 10, or 15 min before intubation. The same criteria for determining whether a patient did or did not cough during tracheal intubation were used as in Study 1. The incidence of coughing decreased significantly (P < 0.01) when 2 mg/kg lidocaine was injected intravenously between 1 min and 3 min before attempting intubation. The cough reflex was almost entirely suppressed by plasma concentrations of lidocaine in excess of 4 μg/mL. The results suggest that intravenous administration of lidocaine is effective in suppressing the cough reflex during tracheal intubation in elderly patients under general anesthesia, but that relatively high plasma concentrations of lidocaine may be required for suppression of coughing. (Anesth Analg 1993;77:309‐12)

Administration of epidural bupivacaine combined with epidural morphine after esophageal surgery.

BACKGROUND Early tracheal extubation after esophagectomy has been postulated to reduce both morbidity rate and the cost of esophageal surgery. The purpose of this study was to determine the effect of epidural bupivacaine combined with morphine on extubation time, postoperative analgesia, respiration, and hemodynamics in patients undergoing esophagectomy. METHODS In a randomized double-blind study, twenty patients undergoing esophageal cancer surgery with a thoracoabdominal procedure were studied. All patients received epidural morphine 2 mg at T6-7 and 2 mg at L3-4 at the beginning of wound closure. Then 3 ml/hr continuous epidural administration of either 0.25% bupivacaine (group Bup, 10 patients) or normal saline solution (group NS, 10 patients) through the catheter inserted at T6-7 was continued for 16 hours, followed by low-dose epidural buprenorphine-bupivacaine. RESULTS The time from end of operation to tracheal extubation was 4.4 +/- 6.7 hours in group Bup and 13.7 +/- 7.1 hours in group NS (p < 0.05). All patients in both groups obtained moderate or adequate pain relief (visual analog scale of 21 +/- 27 mm) without serious side effects. There were no significant differences in visual analog scale, score for pain on a deep breath, blood pressure, heart rate, or respiratory rate between the two groups. CONCLUSIONS Continuous administration of epidural bupivacaine combined with morphine resulted in good analgesia without any respiratory or hemodynamic depression in patients who had undergone esophagectomy, and early extubation is related to the efficacy of continuous epidural administration of bupivacaine.

The effects of intrinsic nitric oxide on cardiac neural regulation in cats

In this study, we aimed to elucidate the effects of intrinsic nitric oxide (NO) on cardiac neural regulation.Twenty-two cats were anesthetized with 1.5% isoflurane and allocated to Group I (intact; n = 7), Group D (denervated baroreceptors and vagi; n = 8), or Group B (autonomic blockade with IV hexamethonium, propranolol, and atropine; n = 7). Cardiac sympathetic nerve activity (CSNA), mean arterial pressure (MAP), sinus heart rate (HR), and A-H and H-V intervals during pacing (150 bpm) were measured before and after IV administration of a NO synthase inhibitor, NG-nitro-L-arginine (L-NNA, 30 mg/kg) and after reversal with an excessive dose of L-arginine (300 mg/kg), before and during intermittent electrical stimulation of the posterior hypothalamus. L-NNA significantly increased MAP in Groups I and B, but not in Group D. L-NNA significantly decreased HR and lengthened A-H in Group I, but not in other groups. L-arginine further decreased HR and lengthened A-H unexpectedly. The reasons for these findings could not be determined in this study. L-NNA did not change CSNA. Hypothalamic stimulation did not potentiate L-NNA-induced changes in CSNA, hemodynamic variables, and atrioventricular conduction. In conclusion, intrinsic NO may modulate atrioventricular conduction and sinus rate through a vagal cholinergic, rather than a nonautonomic mechanism. Implications: Elucidating the roles of intrinsic nitric oxide (NO) on cardiac neural regulation is important. In intact, vagotomized, and baroreceptor-denervated or pharmacologically autonomic blockaded cats, an NO synthesis inhibitor was administered, and atrioventricular conduction and cardiac sympathetic neural discharge were measured. The results suggest a vagal cholinergic mechanism of intrinsic NO. (Anesth Analg 1998;86:1194-1200)

The Effects of Epidural Morphine on Cardiac and Renal Sympathetic Nerve Activity in α-Chloralose-anesthetized Cats

BACKGROUND Epidural morphine yields postoperative pain relief and hemodynamic stability. However, the effects of epidural morphine on sympathetic tone are unclear. This study was designed to elucidate the effects of epidural morphine on cardiac (CSNA) and renal (RSNA) sympathetic nerve activity by direct measurement in anesthetized cats. METHODS Thirty mongrel cats anesthetized with alpha-chloralose were randomly assigned to one of the following five groups: control (0.2 ml/kg thoracic epidural normal saline; n=5); thoracic epidural morphine (n=9); lumbar epidural morphine (n=6); vagotomized, sinoaortic denervated, thoracic epidural morphine (n=5); or intravenous morphine (n=5). Mean arterial pressure (MAP), heart rate (HR), CSNA, and RSNA were measured 0, 15, 30, 60, 90, and 120 min after saline or morphine (200 microg/kg) administration and 15 min after reversal with 200 microg naloxone given intravenously. RESULTS In the control group, no changes in measured variables were found after either thoracic epidural saline or intravenous naloxone. Thoracic and lumbar epidural morphine both significantly reduced MAP, HR, CSNA, and RSNA 30 through 120 min after morphine administration (P < 0.05). These changes were reversed by intravenous naloxone. Changes after thoracic epidural morphine administration in vagotomized, baroreceptor-denervated cats were similar to those in intact cats. Intravenous morphine produced no significant changes except for a decrease in MAP, which was reversed by intravenous naloxone. CONCLUSION In contrast to intravenous morphine, thoracic and lumbar epidural morphine both inhibited cardiac and renal sympathetic nerve activity and consequently reduced MAP and HR in alpha-chloralose anesthetized cats.

The effects of dobutamine and phenylephrine on atrioventricular conduction during combined use of halothane and thoracic epidural lidocaine

The purpose of this study was to measure cardiac sympathetic nerve activity (CSNA) and atrioventricular (AV) conduction and to test the effects of dobutamine (DOB) and phenylephrine (PHE) on AV conduction during 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 quadripolar 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 atrioventricular node (AV node), effective refractory period (ERP) of the atrium, atrium-His (A-H) intervals were determined just before and 10, 20, and 30 min after epidural administration of 1% lidocaine (0.2 mL/kg) in Group C. DOB 5 micro gram centered dot kg-1 centered dot min-1 (Group DOB) and PHE 0.5-1.0 micro gram centered dot kg-1 centered dot 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 epidural lidocaine during halothane anesthesia almost eliminates CSNA, and thereby attenuates sinus node automaticity and AV node function. DOB restored normal cardiac electrophysiological variables, and therefore is preferable to phenylephrine as a pressor drug. (Anesth Analg 1996;82:551-7)

Effects of intravenous lidocaine on cardiac sympathetic nerve activity and A-V conduction in halothane-anesthetized cats.

To study neural contributions to the alterations in intracardiac conduction induced by IV lidocaine, we measured cardiac sympathetic nerve activity (CSNA) simultaneously with sinus cycle length (SCL) and AV conduction time using His–bundle electrocardiography following IV lidocaine in cats. Sixteen cats were anesthetized with halothane in oxygen and mid–sternotomized. The His–bundle electrogram and CSNA were recorded from an electrode placed in the interatrial septum and from the left ventrolateral or ventromedial nerve, respectively. Atrium–His (A–H), His–Purkinje (H–V), and total intraventricular (H–S) conduction times were measured during atrial pacing conducted at a cycle length of 300 ms. In eight cats, 1 MAC, 2 MAC, and 3 MAC halothane were given during IV lidocaine (Groups H–l, H–2 and H–3). In the other eight cats, anesthesia was switched from halothane to IV alpha–chloralose (30–50 mg–kgBW‐1; Group C). A significant decrease in CSNA with IV lidocaine, 2 mg–kgBW‐1′ was recognized in Groups C and H–l, but not in Groups H–2 and H–3. Prolongations of SCL during the spontaneous cycle, A–H and H–V in the paced mode following IV lidocaine were significant in Groups C, H–l and H–2, but not significant in Group H–3. We conclude that IV lidocaine induces a significant decrease in CSNA during alpha–chloralose or 1 MAC halothane anesthesia which partly contributes to the control of intracardiac conduction.

A case of herpes zoster myelitis occurring during epidural analgesia

H erpes zoster is a viral disease characterized by skin rashes and persistent pain. Antiviral drugs, analgesics, and neural blockade have been used as treatment. Epidural analgesia is very effective in the acute stage of herpes zoster (1). Herpes zoster features various complications (2) including myelitis which is characterized by neurologic deficits such as motor neuropathy and sensory disorders (3,4). Since similar neurologic deficits may be induced accidentally by epidural analgesia, the differential diagnosis is very important when neurologic deficits develop after initiation of epidural analgesia in patients with herpes zoster. We report a case of herpes zoster myelitis which manifested after epidural analgesia.

Stellate ganglion block improved loss of visual acuity caused by retrobulbar optic neuritis after herpes zoster.

R etrobulbar optic neuritis associated with trigeminal herpes zoster is very rare (1,2). In most published cases, this condition was treated with steroids and acyclovir, but the efficacy of these treatments is controversial (3-7). We report a woman with retrobulbar optic neuritis caused by varicella-zoster virus in whom loss of visual acuity was markedly improved by stellate ganglion block (SGB) and minimally improved by aggressive administration of steroids.

Bupivacaine does not suppress cardiac sympathetic nerve activity during halothane anesthesia in the cat

Background: The finding that IV lidocaine suppresses cardiac sympathetic nerve activity during 1 MAC halothane, but not during 2 MAC or 3 MAC halothane, suggests that the neurally mediated circulatory effects of IV local anesthetics may vary with background autonomic activity. This study aimed to compare the effects of IV lidocaine and bupivacaine on cardiac sympathetic nerve activity (CSNA) during normal and high levels of CSNA.

Lumbar epidural buprenorphine for postoperative pain relief following hepatectomy

The induction of postoperative pain relief with lumbar epidural or intramuscular buprenorphine was studied in 30 patients undergoing hepatectomy. When patients first complained of pain after surgery, 0.06 mg or 0.12 mg of buprenorphine in 10 ml or 20 ml of saline was administered through an epidural catheter inserted at the L3-4 interspace, or 0.12 mg was administered intramuscularly. Two of seven patients receiving epidural buprenorphine 0.12 mg in 10 ml saline were completely pain-free, and the other five patients in this group had only slight pain. Four of eight patients receiving epidural buprenorphine 0.12 mg in 20 ml saline were completely pain-free, and the other four patients in this group had only slight pain. Epidural buprenorphine 0.06 mg in 20 ml saline and intramuscular buprenorphine 0.12 mg each yielded only incomplete analgesia. The duration of analgesia of epidural buprenorphine 0.12 mg administered at the lumbar level was about 8 h. There were no significant changes over time in circulatory or respiratory variables induced by buprenorphine. No patient had serious adverse effects. Lumbar epidural administration of buprenorphine 0.12 mg diluted to 10 or 20 ml (20 ml might be preferable) with saline is recommended for induction of postoperative analgesia following hepatectomy.