Cardiac arrest after spinal anesthesia in a patient with neurally mediated syncope

We present the case of cardiac arrest in a patient with neurally mediated syncope (NMS). A 66-year-old male patient was scheduled to undergo right inguinal hernioplasty. He had a history of syncope, which occurred a few times a year in childhood and once a year recently. One minute after the second spinal injection, cardiac arrest (asystole) developed. Sinus rhythm was restored by cardiac massage and intravenous administration of atropine and ephedrine. The operation was cancelled. The patient was diagnosed as NMS by a cardiologist. Four months later, right inguinal hernioplasty was performed, uneventfully, under general anesthesia. High sympathetic blockade due to spinal anesthesia and transient withdrawal of sympathetic tone and increase in vagal discharge due to NMS could be the main causes of the cardiac arrest. If the patient has any possibility of NMS, anesthesiologists should consider the possibility of cardiac arrest after spinal anesthesia.     

Open cholecystectomy under thoracic epidural anesthesia in diffuse interstitial lung disease

Two patients, aged 73 and 58 years, with diffuse pulmonary fibrosis underwent emergency open cholecystectomies (subcostal approach) under thoracic epidural anesthesia with 0.5% ropivacaine and fentanyl in spontaneous ventilation. Pulmonary fibrosis was due to amiodarone administration in the first patient and of unknowon cause in the second. Both developed arterial hypotension without bradycardia in spite of optimal preloading. Inotropoic support with low doses of norepinephrine was requiered for recovery in both cases with no adverse events after reversion of the sympathetic blocks. Postoperative epidural analgesia was very satisfactory. Thoracic epidural anesthesia is a useful alternative to general anesthesia for subcostal cholecystectomy in patients with diffuse interstitial lung disease in advanced stages.     

Limited upper thoracic epidural block and splanchnic perfusion in dogs

Epidural blockade leads to a sympathetic block in affected segments and an increase of sympathetic out-flow from various unblocked segments. A limited upper thoracic epidural block (LUTEB) is used during coronary artery surgery affecting the cardiac sympathetic fibers cephalad to the fifth thoracic segment. This block does not extend to the sympathetic fibers innervating the gastrointestinal organs. A LUTEB may lead to an increase of sympathetic activity in the unaffected splanchnic sympathetic segments and the decrease in splanchnic blood flow may contribute to gastrointestinal ischemia after cardiac surgery. We tested the hypothesis that a LUTEB decreases splanchnic perfusion in anesthetized dogs. Thirteen dogs were chronically instrumented with aortic and left atrial catheters, which were used for pressure measurement, as well as injection and withdrawal of reference samples. Thoracic epidural catheters were placed under general anesthesia the day before the experiment. Splanchnic blood flow was determined by using colored microspheres. Induction of a LUTEB did not change general hemodynamics in awake dogs. Propofol anesthesia induced an increase in heart rate that was abolished after LUTEB. LUTEB also decreased mean arterial pressure during propofol anesthesia. We conclude that thoracic epidural anesthesia had no effect on splanchnic blood flow. In propofol anesthetized animals, liver blood flow was increased compared with awake animals; however, it did not change after induction of LUTEB. IMPLICATIONS: A sympathetic block in certain segments leads to increased sympathetic output in unblocked segments. For an upper thoracic epidural block, this might lead to impaired splanchnic perfusion. In awake and propofol-anesthetized, chronically instrumented dogs, however, a limited upper thoracic epidural blockade had no compromising effect on gastrointestinal perfusion.     

Vigilance of hemodynamic changes immediately after transferring patients is crucial

Purpose

A decrease in blood pressure is sometimes observed when a postsurgical patient is transferred to another bed after recovering from anesthesia. However, the mechanism behind this hypotension has not been completely elucidated. The purpose of this study was to investigate and compare changes in hemodynamic properties for possible causes of hypotension before and after transfer to another bed of postsurgical patients receiving general anesthesia, combined epidural and general anesthesia, or combined spinal and general anesthesia.

Methods

We studied 69 patients undergoing elective surgery who were randomized to receive anesthesia by one of the three methods. After surgery, the tracheal tube was removed, and each patient was transferred to another bed. Hemodynamic data recorded immediately before and after transfer of the patient to another bed were compared.

Results

After transfer of patients receiving general anesthesia or combined epidural and general anesthesia, systolic arterial pressure (SAP), diastolic arterial pressure (DAP), and cardiac output (CO) decreased; heart rate (HR) and systemic vascular resistance (SVR) did not change. However, after transfer of patients receiving combined spinal and general anesthesia, SAP, DAP, HR, and CO decreased, but SVR did not change.

Conclusion

The decrease in blood pressure observed after transfer of a postsurgical patient to another bed after general, combined epidural and general, and combined spinal and general anesthesia was associated with a decrease in CO and no change in SVR, but HR decreased after combined spinal and general anesthesia, whereas it was unchanged after general and combined epidural and general anesthesia. The decrease in blood pressure is assumed to be caused by a decrease in venous return, and several reflexes might participate in this decrease of blood pressure, especially after combined spinal and general anesthesia.     

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.     

Comparison of epidural anesthesia and general anesthesia for patients with bronchial asthma

We prospectively investigated the incidence of asthmatic attacks in 94 patients (1.5%) who were diagnosed as definite asthma. We separated the patients into three groups: epidural anesthesia (n = 10) including combined spinal/epidural anesthesia (n = 7), combined epidural and general anesthesia (n = 23), and general anesthesia (n = 54). General anesthesia was induced with propofol or midazolam and maintained with N2O and O2 with sevoflurane in adults. Patients who underwent epidural anesthesia and combined spinal and epidural anesthesia showed no asthmatic attacks. The incidence of bronchospasm with combined epidural and general anesthesia was 2/23. The incidence of bronchospasm with general anesthesia was 4/54. Bronchoconstriction occurred after tracheal intubation in 5 patients except in one patient, in whom it occurred after induction of anesthesia with midazolam. All episodes of bronchospasm in the operative period were treated successfully. The frequency of bronchospasm did not depend on the severity of asthmatic symptoms or the chronic use of bronchodilators before operation. These findings suggest that tracheal intubation, not the choice of anesthetic, plays an important role in the pathogenesis of bronchospasm.     

The effects of epidural and general anesthesia on tissue oxygenation

The risk of wound infections is inversely related to subcutaneous tissue oxygen tension. General anesthesia increases local blood flow by direct vasodilation and central inhibition of thermoregulatory vasoconstriction. Epidural anesthesia can increase perfusion in blocked regions by decreasing sympathetic tone. We therefore tested the hypothesis that epidural anesthesia increases tissue oxygen tension in awake and anesthetized subjects. Fifteen healthy volunteers underwent epidural, general, and combined epidural and general anesthesia. Subcutaneous tissue oxygen tension was measured using tonometers in the lateral upper arm and the lateral thigh. Epidural anesthesia to a T10 level was maintained with 0.75% mepivacaine. General anesthesia was maintained with 1.5% sevoflurane in 30% oxygen; 30% inspired oxygen was given via a sealed facemask during baseline and epidural anesthesia. Baseline subcutaneous tissue oxygen tensions for arm and thigh were 57 +/- 11 and 54 +/- 8 mm Hg, respectively. Epidural anesthesia significantly increased tissue oxygenation in the thigh by 9 mm Hg, to 63 +/- 7 mm Hg, without increasing arm oxygenation. Tissue oxygenation in the arm and thigh were similar during general anesthesia alone, 58 +/- 11 and 63 +/- 12 mm Hg. Arm oxygenation remained unchanged with the addition of epidural anesthesia; however, thigh subcutaneous oxygen partial pressure increased 8 +/- 3 mm Hg, from 63 +/- 12 to 71 +/- 9 mm Hg. Although epidural anesthesia increased tissue oxygenation significantly with and without general anesthesia, the magnitude of this increase might be of marginal clinical importance in regard to surgical wound infections. IMPLICATIONS: Epidural anesthesia significantly increased subcutaneous tissue oxygenation in the thigh both with and without general anesthesia. Although each increase was statistically significant, previous work suggests that the magnitude of these changes is unlikely to markedly reduce the risk of surgical wound infection.     

Does Spinal Anesthesia Result in a More Complete Sympathetic Block Than That from Epidural Anesthesia?

Background: Spinal and epidural injection of local anesthetics are used to produce sympathetic block to diagnose and treat certain chronic pain syndromes. It is not clear whether either form of regional anesthesia produces a complete sympathetic block. Spinal anesthesia using tetracaine has been reported to produce a decrease in plasma catecholamine concentrations. This has not been demonstrated for epidural anesthesia in humans with level of anesthesia below C8. One possible explanation is that spinal anesthesia results in a more complete sympathetic block than epidural anesthesia. To examine this question, a cross-over study was performed in young, healthy volunteers.

Methods: Ten subjects underwent both spinal and epidural anesthesia with lidocaine (plain) on the same day with complete recovery between blocks. By random assignment, spinal anesthesia and epidural anesthesia were induced via lumbar injection. Before and 30 min after local anesthetic injection, a cold pressor test (CPT) was performed. Blood was obtained to determine epinephrine and norepinephrine plasma concentrations at four stages: (1) 20 min after placing peripheral catheters, (2) at the end of a 2-min CPT (before conduction block), (3) 30 min after injection of epidural or spinal lidocaine, and (4) at the end of a second CPT (during anesthesia). Mean arterial pressure, heart rate, noninvasive cardiac index, and analgesia to pin-prick were monitored.

Results: Neither spinal nor epidural anesthesia changed baseline resting values of catecholamines or any hemodynamic variable, except heart rate, which was slightly decreased during spinal anesthesia. Median level of analgesia was T4 during spinal and T3 during epidural anesthesia. CPT before conduction block reliably increased heart rate, mean arterial pressure, cardiac index, epinephrine, and norepinephrine. Conduction block attenuated the increase in response to CPT only in mean arterial pressure (spinal and epidural) and cardiac index (spinal only). Neither technique blocked the increase in heart rate, norepinephrine, or epinephrine to CPT.     

Effects of epidural and spinal anesthesia on blood rheology.

This study was designed to compare the influence of epidural and spinal anesthesia on blood viscosity. We studied 22 patients, ASA classification I, who underwent elective knee or ankle arthroscopy and received epidural (n = 11) or spinal (n = 11) anesthesia with plain bupivacaine, and 10 control volunteers, who did not undergo surgery or receive anesthesia. There were significant decreases in hematocrit, plasma viscosity, and whole-blood viscosity at high (70 s-1), medium (0.5 s-1), and low (0.05 s-1) shear rates. The magnitude of changes was similar in all groups but occurred earlier in the control group (between 10 and 30 min) and after spinal administration (between 10 and 30 min) rather than after epidural administration (between 30 and 60 min) of bupivacaine. Only spinal anesthesia was associated with a decrease in erythrocyte deformability. The observed rheologic changes are attributed to hemodilution from the intravenous administration of fluids and the redistribution of fluid in the intravascular and extravascular compartments after sympathetic blockade and to postural changes rather than the effect of bupivacaine on blood elements.     

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.     

Low-frequency Spectral Power of Heart Rate Variability Is Not a Specific Marker of Cardiac Sympathetic Modulation

Background: Heart rate variability in the frequency domain has been proposed to reflect cardiac autonomic control. Therefore, measurement of heart rate variability may be useful to assess the effect of epidural anesthesia on cardiac autonomic tone. Accordingly, the effects of preganglionic cardiac sympathetic blockade by segmental epidural anesthesia were evaluated in humans on spectral power of heart rate variability. Specifically, the hypothesis that cardiac sympathetic blockade attenuates low-frequency spectral power, assumed to reflect cardiac sympathetic modulation, was tested.

Methods: Ten subjects were studied while supine and during a 15-min 40- degrees head-up tilt both before and after cardiac sympathetic blockade by segmental thoracic epidural anesthesia (sensory block: C6-T6). ECG, arterial pressure, and respiratory excursion (Whitney gauge) were recorded, and a fast-Fourier-transformation was applied to 512-s data segments of heart rate derived from the digitized ECG at the end of each intervention.

Results: With cardiac sympathetic blockade alone and the subjects supine, both low-frequency (LF, 0.06-0.15 Hz) and high-frequency (HF, 0.15-0.80 Hz) spectral power remained unchanged. During tilt, epidural anesthesia attenuated the evoked increase in heart rate (+11 *symbol* min sup -1 + 7 SD vs. +6 + 7, P - 0.024). However, while during tilt cardiac sympathetic blockade significantly decreased the LF/HF ratio (3.68 plus/minus 2.52 vs. 2.83 plus/minus 2.15, P = 0.041 vs. tilt before sympathetic blockade), a presumed marker of sympathovagal interaction, absolute and fractional LF and HF power did not change.     

Hemodynamic effects of a combination of general and peridural anesthesia during anesthesia induction in geriatric patients

For major operative procedures in the lower abdomen and many orthopedic procedures such as total hip replacement, a combination of general and epidural anesthesia is used. In order to investigate the hemodynamic effects of such a combination in 14 geriatric patients aged 63-80 years who were undergoing total hip replacement, cardiovascular monitoring was established by an arterial line and a pulmonary artery catheter. The epidural anesthesia was achieved with bupivacaine 0.5% in a dose calculated to obtain a block up to Th 6. General anesthesia was then induced and maintained with midazolam, fentanyl, pancuronium bromide, and a 2:1 nitrous oxide-oxygen mixture. Hemodynamic measurements were established before and 30 min after induction of the epidural anesthesia and 20 min after the induction of general anesthesia. After bupivacaine was injected the loss of sympathetic tone produced a systolic arterial blood pressure decrease from 174 +/- 22 to 136 +/- 28 mmHg (p less than 0.05) and a decrease in heart rate from 73 +/- 12 to 66 +/- 10 min-1 (p less than 0.05). The cardiac index did not change, but the peripheral vascular resistance decreased significantly. Because intravenous fluids were given simultaneously, preload could be maintained. Oxygen delivery and oxygen extraction did not change. During general anesthesia a significant drop in cardiac output was observed from 3.0 +/- 0.6 l/min.m2 to 2.3 +/- 0.4 l/min.m2 (p less than 0.05). The systolic arterial blood pressure decreased to as low as 95 +/- 17 mmHg (p less than 0.05) and oxygen delivery decreased from 500 +/- 125 ml/min.m2 to 323 +/- 84 ml/min.m2 (p less than 0.05).     

The effects of combined epidural and general anesthesia on the autonomic nervous system and bioavailability of nitric oxide in patients undergoing laparoscopic pelvic surgery

Background

Pneumoperitoneum during laparoscopic surgery is known to affect visceral blood flow and result in oxidative stress. Whether epidural anesthesia will effectively reduce visceral ischemia and oxidative stress by blocking the sympathetic nervous system (SNS) during laparoscopic surgery has not been proven.

Methods

Forty-five patients who were to undergo robot-assisted laparoscopic prostatectomy were randomly assigned to the combined general–epidural anesthesia group (group GE, n = 22) or to the general anesthesia group (group G, n = 23). Blood pressure, heart rate, and the balance between sympathetic and parasympathetic nervous system activity as measured by heart rate variability were recorded at 10 min after induction of anesthesia (T1), 60 (T2) and 120 (T3) min after intra-abdominal CO₂ insufflation, and 10 min after returning the patient to the supine position following CO₂ exsufflation (T4). Arterial blood gas analysis and blood sampling for measurements of nitrite (NO^2?) and malondialdehyde (MDA) were performed at all time points.

Results

Intraoperative mean blood pressure was significantly lower in group GE compared with group G. The low-frequency to high-frequency ratio was significantly increased after induction of pneumoperitoneum in group G but was unchanged in group GE. Plasma levels of nitrite decreased after pneumoperitoneum induction in group G while there was no change in group GE. A significant increase in MDA levels was seen in group G after pneumoperitoneum induction and were higher than group GE at T3 and T4. The 24-h urine output was higher in group GE than in group G on POD 1. The 24-h CrCl was higher in group GE on POD 1 but was not different between groups on POD 2.

Conclusions

Combined epidural and general anesthesia effectively blocks SNS stimulation during laparoscopic surgery and reduces NO inactivation and oxidative stress.     

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.     

Anesthetic management of a pediatric patient with severe Williams-Campbell syndrome undergoing surgery for giant ovarian tumor

We performed anesthetic management for a patient with severe Williams-Campbell syndrome, which is a congenital deficiency of cartilage in the subsegmental bronchial tree. An 11-year-old girl with this syndrome had labored breathing because of abdominal distension caused by a giant ovarian tumor, and removal of the tumor was scheduled. Because she had been receiving home oxygen therapy for 10 years due to hypoxia, it was possible that positive-pressure ventilation may have increased the risk of perioperative pulmonary complications. So we selected combined spinal and epidural anesthesia with general anesthesia, using a ProSeal (Laryngeal Mask Company, Henley on Thames, UK) laryngeal mask airway. We placed an epidural catheter and induced spinal anesthesia blockade under general anesthesia as the main analgesia technique, in order to maintain spontaneous breathing. The surgery was completed uneventfully and the patient emerged from anesthesia without dyspnea. She had an uneventful recovery and was discharged home.     

The autonomic nervous activities in man under thoracic epidural anesthesia assessed by heart rate fluctuation analysis

The R-R intervals of an electrocardiogram, the coefficient variation of R-R intervals (CV-RR), and the power spectrum of heart rate fluctuation were studied just before surgical operations in a group of 10 patients who underwent high thoracic epidural anesthesia (TEA), and before anesthesia in a control group of 10 patients who were scheduled for general anesthesia without TEA. When TEA was performed, the CV-RR increased significantly (P less than 0.05). An increasing tendency (P less than 0.1) was also observed in the R-R intervals and the spectral analysis of the peak amplitude of the low frequency component (LFC) of 0.05 to 0.15 Hz. This tendency was found, too, in the band areas of the LFC and the high frequency component (HFC) of 0.15 to 0.4 Hz. These data indicate that the sympathetic innervation of the heart might have been interrupted by TEA and the vagal tone might have become dominant. Subsequent intravenous administration of atropine 0.5 mg reduced the R-R intervals, the CV-RR, the peak amplitude and the band areas of the LFC and HFC (P less than 0.01), as were seen in the control group. These evidences will show that the heart rate regulation of man in a supine position is dominantly influenced by the vagal tone, and it will become more prominent under TEA by blocking the cardiac sympathetic innervation at spinal level. Present study also suggests that a contribution of the cardiac sympathetic nerve on heart rate fluctuation, even on LFC, is only slight.(ABSTRACT TRUNCATED AT 250 WORDS)     

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).     

Hématome péridural chez une parturiente au décours ďun choc hémorragique

PURPOSE: Epidural hematoma is a rare but serious complication of epidural anesthesia. We report a case of epidural hematoma, occurring in an obstetric patient after the epidural catheter had been withdrawn accidentally after an episode of hemorrhagic shock leading to a hypocoagulable state. CLINICAL FEATURES: A patient had the epidural catheter inserted during labour when coagulation was normal. She had a postpartum hemorrhage with alteration of coagulation (platelets 16 x 10(-9) x L(-1), thrombin time: 85 sec. Vital signs returned to normal after a general anesthetic, transfusion of blood products, volume repletion and ligation of hypogastric arteries. It was then noticed that the epidural catheter had been withdrawn inadvertently while the patient was hypocoagulable. The patient then developed neurological signs consistent with spinal cord compression due to an epidural hematoma. A hematoma extending from T3 to L5 was diagnosed by magnetic resonance imaging. Because the cord had minimal compression, no specific action was undertaken, other than clinical and radiological follow-up. There were no long-term sequelae. CONCLUSION: In the presence of an epidural hematoma, surgery for emergency cord decompression is usually required. Another option that receives increasing attention is to monitor neurological function, but the indications for this expectant treatment are not well defined.     

The effects of cervical and lumbar epidural anesthesia on heart rate variability and spontaneous sequence baroreflex sensitivity

A high level of neuroaxial block may produce profound bradycardia and hypotension, possibly as a result of an imbalance between sympathetic and parasympathetic control of heart rate. We designed this study to test the hypothesis that cervical epidural anesthesia would increase the high-frequency (HF) component of heart rate variability (HRV) as a result of cardiac sympathectomy, whereas lumbar epidural anesthesia would cause sympathetic predominance. HRV and spontaneous baroreflex (SBR) sensitivity were assessed before and after cervical and lumbar epidural anesthesia by using plain 1.5% lidocaine (median upper/lower sensory block: C3/T8 for cervical and T11/L5 for lumbar) in healthy patients (n = 10 each). Electrocardiogram and noninvasive beat-to-beat arterial blood pressure were monitored. HRV was analyzed by using fast Fourier transformation. Least-square regression analysis relating R-R interval and systolic blood pressure during spontaneous fluctuation was performed to obtain SBR sensitivities. Cervical epidural group patients were significantly older (P < 0.01) and taller (P < 0.01). Cervical epidural anesthesia attenuated HF (0.15-0.4 Hz) and low-frequency (0.04-0.15 Hz) power of HRV with concomitant reductions in up- and down-sequence SBR sensitivities, suggesting decreased vagal modulation of heart rate. Lumbar epidural anesthesia resulted in a significant increase in the low-frequency/HF ratio of HRV and unchanged SBR indices, suggesting sympathetic predominance. HF power correlated well with SBR sensitivities under most of our study conditions. Respiratory rates and Paco(2) were unchanged by either epidural technique. Our results indicate that cervical, but not lumbar, epidural anesthesia depresses phasic and tonic dynamic modulation of the cardiac cycle by the vagal nerve in conscious humans.     

Coronary artery spasm with ventricular tachycardia after administration of methoxamine during cervical epidural anesthesia - a case report

Coronary artery spasm occurred during thoracotomy under cervical epidural anesthesia in a 60-year-old male patient who had no prior history of myocardial ischemia. It is most likely that the administration of methoxamine induced the spasm. Hypotension and venodilatation induced by the epidural anesthesia and increased vagal tone might also contribute to the spasm.