Thoracic epidural anesthesia attenuates hemorrhage-induced impairment of intestinal perfusion in rats

BACKGROUND: During hemorrhagic hypotension, sympathetic vasoconstriction crucially contributes to gut mucosal damage. Sympathetic blockade by thoracic epidural anesthesia has been shown to increase mucosal microvascular perfusion and to improve survival after severe hemorrhage in laboratory animals. This study investigates the effects of thoracic epidural anesthesia on intestinal microvascular perfusion during hemorrhagic hypotension in rats. METHODS: In 32 anesthetized Sprague-Dawley rats either lidocaine 2% (thoracic epidural anesthesia) or normal saline (control) was infused via thoracic epidural catheters. Hemorrhagic hypotension (mean arterial pressure 30 mmHg for 60 min) was induced by withdrawal of blood, which was subsequently retransfused for resuscitation. Functional capillary density and erythrocyte velocity in the mucosa and muscularis were determined by intravital microscopy. Leukocyte-endothelium interaction was studied in postcapillary venules and sympathetic nerve fibers of the intestinal wall were identified by immunohistochemistry. RESULTS: During hypotension functional capillary density was significantly (P < 0.001) lower in the muscularis of the control group (median [25/75 percentile]: -46.5% [-59.6/-20.8%] change from baseline) as compared with animals that received thoracic epidural anesthesia (-6.1% [-13.4/1.1%]). There were no differences in erythrocyte velocity between groups throughout the experiment. Leukocyte rolling increased significantly (P < 0.001) after resuscitation in control (12 [6/15] vs. baseline 2.5 [1/8]) but not in thoracic epidural anesthesia (4 [2.3/7] vs. baseline: 5 [3/15.5]). Sympathetic nerve fibers were identified in the muscularis and submucosa but not in the mucosa. CONCLUSIONS: During hemorrhagic hypotension and after resuscitation, thoracic epidural anesthesia has beneficial effects on intestinal microvascular perfusion. Because of blockade of sympathetic nerves, thoracic epidural anesthesia prevents perfusion impairment of the muscularis during hypotension and attenuates leukocyte rolling after resuscitation.     

High Thoracic Epidural Anesthesia Does Not Inhibit Sympathetic Nerve Activity in the Lower Extremities

Background: Sympathetic nerve activity was recorded in the leg during high thoracic epidural anesthesia with a segmental sensory blockade of the upper thoracic dermatomes to test the hypothesis that the sympathetic blockade accompanying thoracic epidural anesthesia includes caudal parts of the sympathetic nervous system.

Methods: Experiments were performed on 10 patients scheduled for thoracotomy. An epidural catheter was inserted at the T3-T4 or T4-T5 interspace. In the main protocol (seven patients), blood pressure, heart rate, and skin temperature (big toe, thumb) were continuously monitored, and multiunit postganglionic sympathetic nerve activity was recorded with a tungsten microelectrode in a muscle-innervating fascicle of the peroneal nerve. After baseline data collection, muscle sympathetic nerve activity was recorded for an additional 45-min period after epidural injection of 4-6 ml bupivacaine, 5 mg/ml. In an additional three patients, the effects of thoracic epidural anesthesia on skin-innervating sympathetic nerve activity were qualitatively assessed.

Results: Activation of thoracic epidural anesthesia caused no significant changes in peroneal muscle sympathetic nerve activity (n = 7), blood pressure, or heart rate. Skin temperature increased significantly in the hand 15 min after activation of the blockade, from 32.7 +/- 2.4[degrees]C to 34.4 +/- 1.5[degrees]C (mean +/- SD), whereas no changes were observed in foot temperature. The sensory blockade extended from T1 (C4-T2) to T8 (T6-T11).     

High thoracic epidural anesthesia does not inhibit sympathetic nerve activity in the lower extremities.

BACKGROUND: Sympathetic nerve activity was recorded in the leg during high thoracic epidural anesthesia with a segmental sensory blockade of the upper thoracic dermatomes to test the hypothesis that the sympathetic blockade accompanying thoracic epidural anesthesia includes caudal parts of the sympathetic nervous system. METHODS: Experiments were performed on 10 patients scheduled for thoracotomy. An epidural catheter was inserted at the T3-T4 or T4-T5 interspace. In the main protocol (seven patients), blood pressure, heart rate, and skin temperature (big toe, thumb) were continuously monitored, and multiunit postganglionic sympathetic nerve activity was recorded with a tungsten microelectrode in a muscle-innervating fascicle of the peroneal nerve. After baseline data collection, muscle sympathetic nerve activity was recorded for an additional 45-min period after epidural injection of 4-6 ml bupivacaine, 5 mg/ml. In an additional three patients, the effects of thoracic epidural anesthesia on skin-innervating sympathetic nerve activity were qualitatively assessed. RESULTS: Activation of thoracic epidural anesthesia caused no significant changes in peroneal muscle sympathetic nerve activity (n = 7), blood pressure, or heart rate. Skin temperature increased significantly in the hand 15 min after activation of the blockade, from 32.7 +/- 2.4 degrees C to 34.4 +/- 1.5 degrees C (mean +/- SD), whereas no changes were observed in foot temperature. The sensory blockade extended from T1 (C4-T2) to T8 (T6-T11). CONCLUSIONS: A high thoracic epidural anesthesia with adequate sensory blockade of upper thoracic dermatomes may be achieved without blockade of caudal parts of the sympathetic nervous system. This finding differs from that of earlier studies that used indirect methods to evaluate changes in sympathetic nerve activity.     

Epidural clonidine suppresses the baroreceptor-sympathetic response depending on isoflurane concentrations in cats

Epidural administration of clonidine induces hypotension and bradycardia secondary to decreased sympathetic nerve activity. In this study, we sought to elucidate the change in baroreflex response caused by epidural clonidine. Thirty-six cats were allocated to six groups (n = 6 each) and were given either thoracic epidural clonidine 4 micro g/kg or lidocaine 2 mg/kg during 0.5, 1.0, or 1.5 minimum alveolar anesthetic concentration (MAC) isoflurane anesthesia. Heart rate (HR), mean arterial blood pressure (MAP), and cardiac sympathetic nerve activity (CSNA) were measured. Depressor and pressor responses were induced by IV nitroprusside 10 micro g/kg and phenylephrine 10 micro g/kg, respectively. Baroreflex was evaluated by the change in both CSNA and HR relative to the peak change in MAP (deltaCSNA/deltaMAP and deltaHR/deltaMAP, respectively). These measurements were performed before and 30 min after epidural drug administration. Epidural clonidine and lidocaine decreased HR, MAP, and CSNA by similar extents. deltaCSNA/deltaMAP and deltaHR/deltaMAP for depressor response were suppressed with epidural lidocaine and clonidine in all groups but the clonidine 0.5 MAC isoflurane group (0.197 +/- 0.053 to 0.063 +/- 0.014 and 0.717 +/- 0.156 to 0.177 +/- 0.038, respectively, by epidural lidocaine [P < 0.05] but 0.221 +/- 0.028 to 0.164 +/- 0.041 and 0.721 +/- 0.177 to 0.945 +/- 0.239, respectively, by epidural clonidine during 0.5 MAC isoflurane). Those for pressor response were suppressed in all groups. We conclude that thoracic epidural clonidine suppresses baroreflex gain during isoflurane anesthesia >1.0 MAC but may offer certain advantages compared with epidural lidocaine during 0.5 MAC isoflurane by virtue of preserving baroreflex sensitivity when inadvertent hypotension occurs.     

Sympathetic blockade by thoracic epidural anaesthesia suppresses renin release in response to hypotension, but activates the vasopressin system.

To determine whether or not the blockade of sympathetic efferents by epidural anaesthesia blunts the normal increase in plasma renin activity in response to hypotension, we assessed the effect of hypotensive thoracic epidural anaesthesia with widespread sympathetic blockade on plasma renin activity. Plasma renin activity and vasopressin concentration, arterial pressure, and serum osmolality were measured in 17 patients before and after random epidural injection of either 6.7 ml of 0.75% bupivacaine (n = 7) or the same volume of saline (n = 10). As an indicator for efferent sympathetic drive, skin temperatures were measured on the hand and foot. A decrease in mean arterial pressure by more than 25% of baseline values was prospectively defined as hypotension requiring intervention. Thoracic epidural anaesthesia induced a decrease in mean arterial pressure of 24 mmHg (range 16-47) from 101 mmHg to 77 mmHg (P less than 0.001 vs. saline). Despite hypotension, plasma renin activity remained unchanged [medians 2.9 ng ml-1 h-1 (0-9.1) vs. 3.4 ng ml-1 h-1 (0-13.8)]. In contrast, vasopressin concentrations increased from a median of 3.8 pg ml-1 (0.5-8.2) to 6.0 pg ml-1 (4.2-33.6; P = 0.025). Both hand and foot skin temperatures increased significantly indicating widespread extent of sympathetic blockade. Serum osmolality did not change. With epidural saline, variables remained unchanged. Thus, during hypotension induced by widespread attenuation of efferent sympathetic drive through thoracic epidural anaesthesia, renin activity did not change, whilst vasopressin concentrations increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)     

Epidural Anesthesia, Hypotension, and Changes in Intravascular Volume

Background: The most common side effect of epidural or spinal anesthesia is hypotension with functional hypovolemia prompting fluid infusions or administration of vasopressors. Short-term studies (20 min) in patients undergoing lumbar epidural anesthesia suggest that plasma volume may increase when hypotension is present, which may have implications for the choice of treatment of hypotension. However, no long-term information or measurements of plasma volumes with or without hypotension after epidural anesthesia are available.

Methods: In 12 healthy volunteers, the authors assessed plasma (125I-albumin) and erythrocyte (51Cr-EDTA) volumes before and 90 min after administration of 10 ml bupivacaine, 0.5%, via a thoracic epidural catheter (T7-T10). After 90 min (t = 90), subjects were randomized to administration of fluid (7 ml/kg hydroxyethyl starch) or a vasopressor (0.2 mg/kg ephedrine), and 40 min later (t = 130), plasma and erythrocyte volumes were measured. At the same time points, mean corpuscular volume and hematocrit were measured. Systolic and diastolic blood pressure, heart rate, and hemoglobin were measured every 5 min throughout the study. Volume kinetic analysis was performed for the volunteers receiving hydroxyethyl starch.

Results: Plasma volume did not change per se after thoracic epidural anesthesia despite a decrease in blood pressure. Plasma volume increased with fluid administration but remained unchanged with vasopressors despite that both treatments had similar hemodynamic effects. Hemoglobin concentrations were not significantly altered by the epidural blockade or ephedrine administration but decreased significantly after hydroxyethyl starch administration. Volume kinetic analysis showed that the infused fluid expanded a rather small volume, approximately 1.5 l. The elimination constant was 56 ml/min.     

The effect of high thoracic epidural anesthesia on systolic and diastolic left ventricular function in patients with coronary artery disease

In patients with coronary artery disease, vasoconstriction is induced through activation of the sympathetic nervous system. Both alpha1- and alpha2-adrenergic epicardial and microvascular constriction are potent initiators of myocardial ischemia. Attenuation of ischemia has been observed when sympathetic nervous system activity is inhibited by high thoracic epidural anesthesia (HTEA). However, it is still a matter of controversy whether establishing HTEA may correspondingly translate into an improvement of left ventricular (LV) function. To clarify this issue, LV function was quantified serially before and after HTEA using a new combined systolic/diastolic variable of global LV function (myocardial performance index [MPI]) and additional variables that more specifically address systolic (e.g., fractional area change) or diastolic function (e.g., intraventricular flow propagation velocity [Vp]). High thoracic epidural catheters were inserted in 37 patients scheduled for coronary artery surgery, and HTEA was administered in the awake patients. Echocardiographic and hemodynamic measures were recorded before and after institution of HTEA. HTEA induced a significant improvement in diastolic LV function (e.g., Vp changed from 45.1 +/- 16.1 to 53.8 +/- 18.8 cm/s; P < 0.001), whereas indices of systolic function did not change. The change in the diastolic characteristics caused the MPI to improve from 0.51 +/- 0.13 to 0.35 +/- 0.13 (P < 0.001). We conclude that an improvement in cardiac function was due to improved diastolic characteristics.     

Cardiovascular Responses to the Induction of Mild Hypothermia in the Presence of Epidural Anesthesia

Background: The combining of epidural anesthesia with general anesthesia impairs central and peripheral thermoregulatory control and therefore is often accompanied by unintended intraoperative hypothermia. However, little is known about the cardiovascular response to hypothermia during combined epidural and general anesthesia. The authors assessed the effects of hypothermia during such combined anesthesia.

Methods: The authors randomly assigned 30 mongrel dogs anesthetized with isoflurane (1.0%) to three groups of 10: control, receiving general anesthesia alone; thoracic injection, additionally receiving thoracic epidural anesthesia; and lumbar injection, additionally receiving thoracolumbar epidural anesthesia. Core temperature was lowered from 38.5[degrees]C to approximately 34[degrees]C (mild hypothermia) using a femoral arteriovenous shunt in an external cool water bath. During hypothermia, the authors measured heart rate, cardiac output, and plasma catecholamine concentrations in each group. Ejection fraction was also measured using echocardiography.

Results: Compared with measurements during baseline conditions (general anesthesia alone with no epidural injection and no hypothermia) in the control, thoracic, and lumbar injection groups, the injections followed by hypothermia produced 17, 32, and 41% decreases in heart rate; 22, 32, and 47% reductions in cardiac output; 66, 85, and 92% decreases in the epinephrine concentrations; and 27, 44, and 85% decreases in the norepinephrine concentrations. In contrast, ejection fraction did not change in any group.     

Lung Function under High Thoracic Segmental Epidural Anesthesia with Ropivacaine or Bupivacaine in Patients with Severe Obstructive Pulmonary Disease Undergoing Breast Surgery

Background: Because general anesthesia with tracheal intubation can elicit life-threatening bronchospasm in patients with bronchial hyperreactivity, epidural anesthesia is often preferred. However, segmental high thoracic epidural anesthesia (sTEA) causes pulmonary sympathetic and respiratory motor blockade. Whether it can be safely used for chest wall surgery as a primary anesthetic technique in patients with chronic obstructive pulmonary disease or asthma is unclear. Furthermore, ropivacaine supposedly evokes less motor blockade than bupivacaine and might minimize side effects. To test the feasibility of the technique and the hypotheses that (1) sTEA with ropivacaine or bupivacaine does not change lung function and (2) there is no difference between sTEA with ropivacaine or bupivacaine, the authors studied 20 patients with severe chronic obstructive pulmonary disease (forced expiratory volume in 1 s [FEV1] = 52.1 +/- 17.3% of predicted [mean +/- SD]) or asthma who were undergoing breast surgery.

Methods: In a double-blind, randomized fashion, sTEA was performed with 6.6 +/- 0.5 ml of either ropivacaine, 0.75% (n = 10), or bupivacaine, 0.75% (n = 10). FEV1, vital capacity, FEV1 over vital capacity, spread of analgesia (pin prick), hand and foot skin temperatures, mean arterial pressure, heart rate, and local anesthetic plasma concentrations were measured with patients in the sitting and supine positions before and during sTEA.

Results: Segmental high thoracic epidural anesthesia (segmental spread C4-T8 [bupivacaine] and C5-T9 [ropivacaine]) significantly decreased FEV1 from 1.22 +/- 0.54 l (supine) to 1.09 +/- 0.56 l (ropivacaine) and from 1.23 +/- 0.49 l to 1.12 +/- 0.46 l (bupivacaine). In contrast, FEV1 over vital capacity increased from 64.6 +/- 13.5 to 68.2 +/- 14.5% (ropivacaine) and from 62.8 +/- 12.4 to 66.5 +/- 13.6% (bupivacaine). There was no difference between ropivacaine and bupivacaine. Skin temperatures increased significantly, whereas arterial pressure and heart rate significantly decreased indicating widespread sympathetic blockade. All 20 patients tolerated surgery well.     

Epidural anesthesia, hypotension, and changes in intravascular volume

BACKGROUND: The most common side effect of epidural or spinal anesthesia is hypotension with functional hypovolemia prompting fluid infusions or administration of vasopressors. Short-term studies (20 min) in patients undergoing lumbar epidural anesthesia suggest that plasma volume may increase when hypotension is present, which may have implications for the choice of treatment of hypotension. However, no long-term information or measurements of plasma volumes with or without hypotension after epidural anesthesia are available. METHODS: In 12 healthy volunteers, the authors assessed plasma (125I-albumin) and erythrocyte (51Cr-EDTA) volumes before and 90 min after administration of 10 ml bupivacaine, 0.5%, via a thoracic epidural catheter (T7-T10). After 90 min (t = 90), subjects were randomized to administration of fluid (7 ml/kg hydroxyethyl starch) or a vasopressor (0.2 mg/kg ephedrine), and 40 min later (t = 130), plasma and erythrocyte volumes were measured. At the same time points, mean corpuscular volume and hematocrit were measured. Systolic and diastolic blood pressure, heart rate, and hemoglobin were measured every 5 min throughout the study. Volume kinetic analysis was performed for the volunteers receiving hydroxyethyl starch. RESULTS: Plasma volume did not change per se after thoracic epidural anesthesia despite a decrease in blood pressure. Plasma volume increased with fluid administration but remained unchanged with vasopressors despite that both treatments had similar hemodynamic effects. Hemoglobin concentrations were not significantly altered by the epidural blockade or ephedrine administration but decreased significantly after hydroxyethyl starch administration. Volume kinetic analysis showed that the infused fluid expanded a rather small volume, approximately 1.5 l. The elimination constant was 56 ml/min. CONCLUSIONS: Thoracic epidural anesthesia per se does not lead to changes in blood volumes despite a reduction in blood pressure. When fluid is infused, there is a dilution, and the fluid initially seems to be located centrally. Because administration of hydroxyethyl starch and ephedrine has similar hemodynamic effects, the latter may be preferred in patients with cardiopulmonary diseases in which perioperative fluid overload is undesirable.     

Epidural anesthesia and pulmonary function

The epidural administration of local anesthetics can provide anesthesia without the need for respiratory support or mechanical ventilation. Nevertheless, because of the additional effects of epidural anesthesia on motor function and sympathetic innervation, epidural anesthesia does affect lung function. These effects, i.e., a reduction in vital capacity (VC) and forced expiratory volume in 1 s (FEV_1.0), are negligible under lumbar and low thoracic epidural anesthesia. Going higher up the vertebral column, these effects can increase up to 20% or 30% of baseline. However, compared with postoperative lung function following abdominal or thoracic surgery without epidural anesthesia, these effects are so small that the beneficial effects still lead to an improvement in postoperative lung function. These results can be explained by an improvement in pain therapy and diaphragmatic function, and by early extubation. In chronic obstructive pulmonary disease (COPD) patients, the use of thoracic epidural anesthesia has raised concerns about respiratory insufficiency due to motor blockade, and the risk of bronchial constriction due to sympathetic blockade. However, even in patients with severe asthma, thoracic epidural anesthesia leads to a decrease of about 10% in VC and FEV_1.0 and no increase in bronchial reactivity. Overall, epidural administration of local anesthetics not only provides excellent anesthesia and analgesia but also improves postoperative outcome and reduces postoperative pulmonary complications compared with anesthesia and analgesia without epidural anesthesia.     

Lung function under high thoracic segmental epidural anesthesia with ropivacaine or bupivacaine in patients with severe obstructive pulmonary disease undergoing breast surgery

BACKGROUND: Because general anesthesia with tracheal intubation can elicit life-threatening bronchospasm in patients with bronchial hyperreactivity, epidural anesthesia is often preferred. However, segmental high thoracic epidural anesthesia (sTEA) causes pulmonary sympathetic and respiratory motor blockade. Whether it can be safely used for chest wall surgery as a primary anesthetic technique in patients with chronic obstructive pulmonary disease or asthma is unclear. Furthermore, ropivacaine supposedly evokes less motor blockade than bupivacaine and might minimize side effects. To test the feasibility of the technique and the hypotheses that (1) sTEA with ropivacaine or bupivacaine does not change lung function and (2) there is no difference between sTEA with ropivacaine or bupivacaine, the authors studied 20 patients with severe chronic obstructive pulmonary disease (forced expiratory volume in 1 s [FEV1] = 52.1 +/- 17.3% of predicted [mean +/- SD]) or asthma who were undergoing breast surgery. METHODS: In a double-blind, randomized fashion, sTEA was performed with 6.6 +/- 0.5 ml of either ropivacaine, 0.75% (n = 10), or bupivacaine, 0.75% (n = 10). FEV1, vital capacity, FEV1 over vital capacity, spread of analgesia (pin prick), hand and foot skin temperatures, mean arterial pressure, heart rate, and local anesthetic plasma concentrations were measured with patients in the sitting and supine positions before and during sTEA. RESULTS: Segmental high thoracic epidural anesthesia (segmental spread C4-T8 [bupivacaine] and C5-T9 [ropivacaine]) significantly decreased FEV1 from 1.22 +/- 0.54 l (supine) to 1.09 +/- 0.56 l (ropivacaine) and from 1.23 +/- 0.49 l to 1.12 +/- 0.46 l (bupivacaine). In contrast, FEV1 over vital capacity increased from 64.6 +/- 13.5 to 68.2 +/- 14.5% (ropivacaine) and from 62.8 +/- 12.4 to 66.5 +/- 13.6% (bupivacaine). There was no difference between ropivacaine and bupivacaine. Skin temperatures increased significantly, whereas arterial pressure and heart rate significantly decreased indicating widespread sympathetic blockade. All 20 patients tolerated surgery well. CONCLUSIONS: Despite sympathetic blockade, sTEA does not increase airway obstruction and evokes only a small decrease in FEV1 as a sign of mild respiratory motor blockade with no difference between ropivacaine and bupivacaine. Therefore, sTEA can be used in patients with severe chronic obstructive pulmonary disease and asthma undergoing chest wall surgery as an alternative technique to general anesthesia.     

The effect of hypertonic saline resuscitation on responses to severe hemorrhagic shock by the skeletal muscle, intestinal, and renal microcirculation systems: seeing is believing

BACKGROUND: Decompensated hemorrhagic shock is often refractory to resuscitation, and we show here that it is associated with loss of vascular tone in skeletal muscle precapillary arterioles. We tested the hypothesis that microvascular derangements in the skeletal muscle, intestinal, and renal microcirculation systems would be reversed by initial hypertonic saline-dextran infusion. METHODS: Male Sprague-Dawley rats underwent precollicular brain stem transection without anesthesia for study. Parameters measured by in vivo videomicroscopy included cardiac output, mean arterial pressure, and microvascular responses in the skeletal muscle, ileum, and renal (i.e., the hydronephrotic kidney) microcirculation systems. Hemorrhaged was induced to a mean arterial pressure of 50 mmHg until decompensation occurred. The rats were then initially resuscitated with (1) 4 mL/kg 7.5% NaCl in 6% dextran 70, (2) 33 mL/kg .9% NaCl in 6% dextran 70, or (3) 33 mL/kg .9% NaCl. Twenty minutes later they received shed blood plus 33 mL/kg .9% NaCl to maintain mean arterial pressure at baseline levels. RESULTS: Decompensated hemorrhagic shock decreased cardiac output to between 24% and 35% of baseline values and profoundly decreased microvascular blood flow to between 10% and 19% of baseline. At the completion of resuscitation cardiac output increased to greater than baseline in all groups. Microvascular blood flow increased toward baseline transiently but then progressively deteriorated to between 36% and 69% of baseline in the 3 tissues. There was no significant difference between the three resuscitative fluids. CONCLUSIONS: Despite return of cardiac output to greater than baseline levels, muscle, intestinal, and renal microvascular blood flows remained significantly depressed. Hypertonic saline and/or dextran did not improve these deficits.     

Effects of epidural anesthesia on cardiovascular response and survival in experimental hemorrhagic shock in dogs

The purpose of the present study was to assess the effects of epidural anesthesia on cardiovascular responses and survival in experimental hemorrhagic shock in dogs. Thirty mongrel dogs were randomly assigned to one of three groups on the basis of anesthetic technique: the upper-level group (n = 10), receiving general anesthesia plus upper-level (mainly thoracic region) epidural anesthesia; the lower-level group (n = 10), receiving general anesthesia plus lower-level (mainly lumbar region) epidural anesthesia; and the control group (n = 10), receiving general anesthesia alone. After withdrawal of blood, the changes in mean arterial pressure (40 mmHg) and cardiac index were similar in all groups. In the upper-level group, a lower heart rate and systemic vascular resistance than the control group were maintained throughout in the presence of severe hypotension. A significant difference in survival was seen between the upper-level and control groups over the 100-min observation period as a whole (P less than 0.05 by the Generalized Wilcoxon test), since, at the end of the period, only two of the ten animals in the control group survived, whereas nine of ten in the upper-level group survived (P less than 0.001 by the Kaplan-Meier test). This result demonstrates that, in dogs lightly anesthetized with halothane and nitrous oxide, upper thoracic level epidural anesthesia significantly improves survival in experimental hemorrhagic shock (compared with survival in dogs with lumbar epidural or no epidural anesthesia) when the epidural is performed before hemorrhage and when the mean arterial pressure is constant.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic stability during labor and delivery with continuous epidural infusion

CONTEXT: Epidural anesthesia for labor pain is frequently complicated by maternal hypotension. OBJECTIVE: To test whether continuous epidural infusion (CEI) of local anesthetic, without bolus administration, lowers the incidence of hypotension in parturient patients. METHODS: In a single-blind clinical study, subjects were randomly assigned to CEI-only (10 mL/h of 0.2% ropivacaine hydrochloride without bolus) or control (10 mL of 0.2% ropivacaine hydrochloride per hour with 10-mL bolus) epidural dosing groups. The incidence of hypotension (20% decrease in systolic blood pressure or mean arterial pressure (MAP), systolic blood pressure lower than 100 mm Hg, or MAP lower than 65 mm Hg) was recorded for 2 hours after dosing. Statistical analysis included a 2x2 chi(2) analysis, the Fisher exact test, and paired two-tailed t tests. RESULTS: Fifty subjects were studied, with 25 randomly assigned to each study group (CEI-only vs control). Baseline blood pressure was not different between groups (CEI-only, 127 [11]/77 [8.7] mm Hg; control, 131 [14]/78 [2]). The incidence of hypotension was lower in the CEI-only group than in the control group (5 [20%] vs 15 [60%]; P=.009), with intervention required in 1 (20%) of 5 CEI-only subjects and 7 (47%) of 15 control subjects. Sensory block reached the T10 dermatome in 54.4 (18) minutes in the CEI-only group and 38 (24) minutes in the control group (P=.04). Pain scores and maternal and fetal pulse rates were not different between groups. Analgesic supplementation (250 microg of epidural fentanyl) was used more frequently in the CEI-only group (72% vs 32%; P=.01), without adverse effects. CONCLUSIONS: Continuous epidural infusion of 0.2% ropivacaine hydrochloride without bolus administration reduces the incidence of hypotension by 67% and is safer than traditional bolus dosing for routine labor. This method requires further study in high-risk patients, including those with preeclampsia and cardiovascular disease.     

Intraneural recording of muscle sympathetic activity during epidural anesthesia in humans

The extent and magnitude of sympathetic blockade during epidural anesthesia have previously been assessed only by indirect methods. In this study, direct intraneural recordings of muscle sympathetic activity (MSA) in the peroneal nerve was performed to determine the profundity of blockade of sympathetic fibers to the lower extremities during epidural anesthesia. Lumbar epidural catheters were inserted in nine volunteers. Multiunit postganglionic sympathetic activity was recorded in a muscle fascicle of the peroneal nerve before and after epidural injection of 4 mL of 2% mepivacaine followed by an additional 12-16 mL after 5 min. Apnea (30-60 s) was used to elicit transient sympathetic activation. The upper level of sensory blockade was T-3 to T-10. Muscle sympathetic activity decreased after epidural blockade with no spontaneous or apnea-induced sympathetic bursts observed later than 11 min after injection of the initial test dose. Sympathetic blockade was accompanied by increase in foot skin blood flow as well as loss of skin resistance responses to arousal. Results show that epidural anesthesia with sensory blockade above T-10 to T-11 blocks spontaneous peroneal MSA as well as the marked sympathetic activation induced by apnea.     

Lower limb wrapping prevents hypotension, but not hypothermia or shivering, after the introduction of epidural anesthesia for cesarean delivery

The decrease of arterial blood pressure and body temperature after epidural or spinal anesthesia is thought to be the result of sympathetic block, which could cause pooling and redistribution of blood into the lower extremities. Studies have demonstrated that leg wrapping with elastic bandages may reduce the incidence of hypotension after spinal anesthesia. We tried to extend these previous observations to epidural anesthesia by testing the hypothesis that leg wrapping with elastic bandages should decrease the incidence of hypotension in patients receiving epidural anesthesia. Moreover, we evaluated the effect of this maneuver as regards hypothermia and shivering. Sixty parturients were randomly allocated to receive either leg wrapping with tight elastic bandages (leg-wrapped group) or not (control group) before anesthesia. Sublingual temperature was observed at five periods: baseline, immediately after epidural anesthesia, abdominal skin disinfection, skin incision, and delivery. Hypotension and shivering during the observation periods were also recorded. The incidence of hypotension was significantly less frequent (P = 0.03) in the leg-wrapped group (23%) compared with the control group (50%). Shivering incidences were similar in both groups (70% versus 70%). Sublingual temperature decreased significantly (P < 0.001) throughout the procedure in each group. However, no differences were found between the two groups at each designated observation, even if compared by the magnitude of temperature decrease. We conclude that although leg wrapping with elastic bandages prevents maternal hypotension after epidural anesthesia, it does not reduce the incidence or magnitude of hypothermia or prevent shivering.     

Hypoxia Causes Apnea during Epidural Anesthesia in Rabbits

Background: Although pulmonary function is minimally changed by neuraxial blockade in most cases, ventilatory arrest may ensue in rare cases. The authors examined the mechanism of apnea in a rabbit model of sudden ventilatory arrest during the combination of epidural anesthesia and hypoxia.

Methods: Rabbits were studied during alpha-chloralose sedation and spontaneous ventilation through a tracheostomy tube. Heart rate and mean arterial pressure were monitored by intraarterial cannulation. Respiratory rate and tidal volume were measured by pneumotachograph. Responses were recorded during administration of oxygen at inspired oxygen concentrations of 11% for 2.5 min and 0% for 40 s, before and after either thoracolumbar epidural blockade (0.4 ml/kg lidocaine, 1.5%) or intramuscular lidocaine (15 mg/kg). In a third group of animals, epinephrine was given intravenously during epidural blockade to return mean arterial pressure to baseline values before hypoxia. In a fourth group of animals, which did not get lidocaine, sympathetic blockade and hypotension were produced with intravenously administered trimethaphan rather than epidural blockade.

Results: Thoracolumbar epidural anesthesia decreased mean arterial pressure from 76 +/- 4 mmHg (mean +/- SE) to 42 +/- 2 mmHg. Apnea during hypoxia occurred in 90% of these animals (nine of ten) but in only 11% of animals (one of nine) after intramuscularly administered lidocaine (P < 0.01). Treatment of epidural hypotension with epinephrine prevented apnea (zero of nine animals). Apnea during hypoxia occurred in 50% (three of six) of animals given trimethaphan. Apnea in all groups was sudden in onset, with no preceding decreases in respiratory rate or tidal volume.     

Racemic Ketamine Decreases Muscle Sympathetic Activity but Maintains the Neural Response to Hypotensive Challenges in Humans

Background: Cardiovascular stimulation and increased catecholamine plasma concentrations during ketamine anesthesia have been attributed to increased central sympathetic activity as well as catecholamine reuptake inhibition in various experimental models. However, direct recordings of efferent sympathetic nerve activity have not been performed in humans. The authors tested the hypothesis that racemic ketamine increases efferent muscle sympathetic activity (MSA) and maintains the muscle sympathetic response to hypotensive challenges.

Methods: Muscle sympathetic activity was recorded by microneurography in the peroneal nerve of six healthy subjects before and during anesthesia with racemic ketamine (2 mg/kg intravenously plus 30 [mu]g [middle dot] kg-1 [middle dot] min-1). Catecholamine plasma concentrations, heart rate, and blood pressure were also determined. Muscle sympathetic neural responses to a hypotensive challenge were assessed by injection of sodium nitroprusside (2-10 [mu]g/kg) before and during ketamine anesthesia. In the final step, increased arterial pressure observed during ketamine anesthesia was adjusted to preanesthetic baseline by sodium nitroprusside infusion (1-6 [mu]g [middle dot] kg-1 [middle dot] min-1).

Results: Ketamine significantly decreased MSA burst frequency (mean +/- SD, 18 +/- 9 bursts/min to 9 +/- 8 bursts/min) and burst incidence (26 +/- 11 bursts/100 heart beats to 9 +/- 6 bursts/100 heart beats). However, when increased mean arterial pressure (85 +/- 8 mmHg to 121 +/- 20 mmHg) was normalized to the awake baseline by sodium nitroprusside, MSA recovered (25 +/- 18 bursts/min; 23 +/- 14 bursts/100 heart beats). During ketamine anesthesia, both epinephrine (15 +/- 10 pg/ml to 256 +/- 193 pg/ml) and norepinephrine (250 +/- 105 pg/ml to 570 +/- 270 pg/ml) plasma concentrations significantly increased, as did heart rate (67 +/- 13 beats/min to 113 +/- 15 beats/min). Hypotensive challenges similarly increased MSA both in the awake state and during ketamine anesthesia.     

The Effects of Epidural Morphine on Cardiac and Renal Sympathetic Nerve Activity in [Greek small letter alpha]-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 [Greek small letter 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 [micro sign]g/kg) administration and 15 min after reversal with 200 [micro sign]g 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.