Effects Of Thoracic Epidural Anesthesia Research Articles

The effects of thoracic epidural anesthesia on functional recovery from myocardial stunning in propofol-anesthetized dogs.

The purpose of this investigation was to examine the effects of thoracic epidural anesthesia (TEA) on myocardial stunning during propofol anesthesia. Six dogs were chronically instrumented for measurement of left atrial, aortic, and left ventricular pressure, maximal rate of increase of left ventricular pressure, and myocardial wall-thickening fraction (WTF). Myocardial blood flow was determined with colored microspheres. Experiments were performed on separate days with 1) 10 min of left anterior descending artery (LAD) ischemia during propofol anesthesia without TEA, and 2) 10 min of LAD ischemia during propofol anesthesia with TEA. WTF was measured as baseline (BL) prior to propofol anesthesia and at predetermined time points until complete recovery from stunning. Propofol anesthesia caused a significant decrease of WTF in the LAD-perfused myocardium (LAD-WTF) compared to BL in awake animals. LAD ischemia led to a further significant decrease of LAD-WTF. There were no significant differences in LAD-WTF between the two experimental conditions at any of the time points measured. TEA did not change subendocardial blood flow in nonischemic myocardium. During ischemia neither the subendocardial/subepicardial nor the occluded/normal zone blood flow ratio were affected by TEA. After myocardial ischemia during propofol anesthesia TEA does not affect functional recovery of stunned myocardium in dogs.

The Effects of Thoracic Epidural Anesthesia on Functional Recovery from Myocardial Stunning in Propofol-Anesthetized Dogs

The Effects of Thoracic Epidural Anesthesia on Functional Recovery from Myocardial Stunning in Propofol-Anesthetized Dogs

Effects of thoracic epidural anesthesia on changes in ischemic myocardial metabolism induced by intracoronary injection of endothelin in dogs

Thoracic epidural anesthesia (TEA) has been reported to alleviate ischemic damage to the myocardium. Endothelin, an endothelium-derived peptide and a potent coronary vasoconstrictor, may contribute to poor cardiac perfusion and ischemia. The objective was to examine regional myocardial metabolism during ischemia caused by intracoronary injection of endothelin with and without TEA. The three experimental groups and three treatments were randomized. All studies were conducted in a university research laboratory. Thirty anesthetized dogs comprised the study groups. Study animals were divided into three groups of 10 animals each identified as normal saline (NS); TEA; and TEA + blood pressure controlled (TEA + BPC). The NS group had 0.5 mL/kg of normal saline injected into the T4-5 epidural space. The TEA group had 0.5 mL/kg of saline containing 1% lidocaine injected into the T4-5 space. The TEA + BPC group had blood pressure and heart rate maintained at pre-epidural injection values by partially occluding the descending aorta and by atrial pacing. Endothelin (15 pmol/kg) was bolus injected into the left anterior descending (LAD) artery of each heart. Systolic and diastolic blood pressure, heart rate, and LAD coronary blood flow (CBF) were monitored. Three minutes after injection of endothelin, myocardial tissue was sampled from the distribution of the LAD artery and from the control, left circumflex (LCx) artery. ATP, ADP, AMP, lactate, and pyruvate were measured by enzymatic methods. It was found that in each group endothelin consistently decreased LAD CBF, but the decrease was less in the TEA + BPC group. In the tissue distribution of the LAD, the levels of ATP and energy charge potential were lower, and the level of lactate was higher in the NS group than in the TEA or the TEA + BPC groups (p < 0.01). These results confirm that (1) endothelin injected into the LAD artery decreases CBF and causes selective myocardial ischemia in a fashion similar to intravascular stenosis of the LAD rather than to mechanical occlusion and (2) TEA, with or without pressure support, lessens the degree of regional ischemia induced by injection of endothelin in the LAD.

Thoracic epidural anesthesia improves functional recovery from myocardial stunning in conscious dogs.

The effects of thoracic epidural anesthesia (TEA) on the contractile performance of ischemic and postischemic myocardium have not been well investigated. The purpose of this investigation was to examine the effects of TEA on severity and duration of myocardial stunning in an experimental model for sublethal acute myocardial ischemia. Seven dogs were chronically instrumented for measurement of heart rate (HR), left atrial (LAP), aortic and left ventricular pressure (LVP), LV dP/dtmax' and myocardial wall-thickening fraction (WTF). An occluder around the left anterior descending artery (LAD) allowed induction of reversible LAD ischemia. TEA was performed with lidocaine 4 mg/kg through a chronically implanted epidural catheter at the second thoracic level. Regional myocardial blood flow was determined with colored microspheres. Two experiments were performed in a cross-over design on separate days: Experiment 1, induction of 10 min of LAD ischemia without TEA; and Experiment 2, induction of 10 min of LAD ischemia with TEA. WTF was measured at baseline (BL) and predetermined time points until complete recovery from ischemic dysfunction occurred. LAD ischemia caused a significant decrease of LAD-WTF with (-28% +/- 5.1% versus BL) and without TEA (-15.5% +/- 5.3% versus BL). After 3 h of reperfusion, WTF as percent of BL values was significantly higher with TEA (P < 0.001). BL values of WTF were reached after 24 h with TEA and after more than 48 h without TEA (P < 0.05). There were no significant differences for mean arterial pressure (MAP), heart rate (HR), LVP, LAP, and LVdP/dtmax between the groups during ischemia and reperfusion. In nonischemic myocardium TEA caused an increase of subendocardial blood flow. During ischemia neither the subendocardial/subepicardial nor the occluded/ normal zone blood flow was affected by TEA. TEA attenuates myocardial stunning in conscious dogs. This finding is consistent with data regarding a reduction of infarct size due to TEA.

The Effect of Thoracic Epidural Anesthesia on Hypoxic Pulmonary Vasoconstriction in Dogs

The aim of the present study was to examine whether hypoxic pulmonary vasoconstriction (HPV) is preserved during one-lung ventilation combined with thoracic epidural anesthesia (TEA) in dogs. Using a separately ventilated left lower lobe (LLL) in situ, the pressure-flow (P-Q) curve was obtained. The HPV response was assessed by the shift of the P-Q curve, changes in blood flow diversion rate (FDR) and decrease in PaO2 during hypoxic gas ventilation of LLL. In the control group (n = 7), the shift of P-Q curve, changes in FDR, and decrease in PaO2 remained constant during four consecutive hypoxic stimulations. In the TEA group (n = 6), the P-Q curve shifted to the left during hyperoxia, but the magnitude of the shift during hypoxia was unchanged. FDR and decrease in PaO2 were significantly reduced compared with baseline values (P < 0.05 with analysis of variance). TEA reduced heart rate, cardiac output, mean arterial pressure, mean pulmonary arterial pressure, and mixed venous oxygen tension. Our results suggest that TEA did not affect the primary pulmonary vascular tone at baseline or during lobar hypoxia, but enhanced the diversion of blood flow and arterial blood oxygenation during lobar hypoxia. This enhanced HPV response probably reflects hemodynamic changes, such as decreased cardiac output with resultant low mixed venous oxygen tension, due to sympathetic nerve activity blockade by TEA. (Anesth Analg 1996;82:1049-55)

Thoracic Epidural Anesthesia Attenuates Halothane-Induced Myocardial Sensitization to Dysrhythmogenic Effect of Epinephrine in Dogs

Background The autonomic nervous system plays a critical role in the central modulation of cardiac dysrhythmias. Because sympathetic blockade by thoracic epidural anesthesia has been documented to protect patients from various stress responses, the authors speculate that epidural anesthesia can attenuate the dysrhythmogenic interaction between halothane and epinephrine. Methods In adult mongrel dogs anesthetized with halothane, the dysrhythmogenic dose (DD) of epinephrine, defined as the smallest dose producing four or more premature ventricular contractions within a 15-s period, was determined in the presence of thoracic epidural mepivacaine or saline. To address the effect of circulating mepivacaine after epidural administration, the authors examined the DD of epinephrine in the presence of intravenous mepivacaine. They also investigated the effect of thoracic epidural anesthesia in bilaterally vagotomized dogs. Results Epidural mepivacaine significantly increased the DD of epinephrine compared with epidural saline. However, intravenous mepivacaine did not affect the DD of epinephrine, even when the plasma concentration of mepivacaine during the dysrhythmias was twice that in the epidural mepivacaine group. The beneficial effect of epidural mepivacaine was not seen in bilaterally vagotomized dogs. Conclusions Thoracic epidural anesthesia attenuated the myocardial sensitization by halothane, and vagal activity had an essential role in this action.

The Effects of Thoracic Epidural Anesthesia on Myocardial and Systemic Circulation after Coronary Artery Occlusion in Dogs

The Effects of Thoracic Epidural Anesthesia on Myocardial and Systemic Circulation after Coronary Artery Occlusion in Dogs

Thoracic Epidural Anesthesia Attenuates Halothane-induced Myocardial Sensitization to Dysrhythmogenic Effect of Epinephrine in Dogs

The autonomic nervous system plays a critical role in the central modulation of cardiac dysrhythmias. Because sympathetic blockade by thoracic epidural anesthesia has been documented to protect patients from various stress responses, the authors speculate that epidural anesthesia can attenuate the dysrhythmogenic interaction between halothane and epinephrine. In adult mongrel dogs anesthetized with halothane, the dysrhythmogenic dose (DD) of epinephrine, defined as the smallest dose producing four or more premature ventricular contractions within a 15-s period, was determined in the presence of thoracic epidural mepivacaine or saline. To address the effect of circulating mepivacaine after epidural administration, the authors examined the DD of epinephrine in the presence of intravenous mepivacaine. They also investigated the effect of thoracic epidural anesthesia in bilaterally vagotomized dogs. Epidural mepivacaine significantly increased the DD of epinephrine compared with epidural saline. However, intravenous mepivacaine did not affect the DD of epinephrine, even when the plasma concentration of mepivacaine during the dysrhythmias was twice that in the epidural mepivacaine group. The beneficial effect of epidural mepivacaine was not seen in bilaterally vagotomized dogs. Thoracic epidural anesthesia attenuated the myocardial sensitization by halothane, and vagal activity had an essential role in this action.

Effects of Thoracic Epidural Anesthesia on Pulmonary Hypertension Induced by Acute Diffuse Alveolar Hypoxia and N-nitro-L-arginine in Dogs

Effects of Thoracic Epidural Anesthesia on Pulmonary Hypertension Induced by Acute Diffuse Alveolar Hypoxia and N-nitro-L-arginine in Dogs

Effects of thoracic epidural anesthesia on coronary blood flow and cardiovascular system in dogs

Effects of thoracic epidural anesthesia on coronary blood flow and cardiovascular system in dogs

Thoracic Epidural Anesthesia Causes Rib Cage Distortion in Anesthetized, Spontaneously Breathing Dogs

The effects of thoracic epidural anesthesia on the performance of the parasternal intercostal muscles were investigated by measuring electromyographic activity and length changes of the parasternals (EMG activities and length, respectively, of the parasternals) in seven pentobarbital anesthetized, spontaneously breathing dogs. Epidural injection of 0.1 mL/kg of 2% lidocaine decreased tidal volume and minute ventilation during unstimulated breathing. These changes were accompanied by complete abolishment of EMG activities of the parasternals and passive elongation of the parasternals during inspiration. At equivalent end-tidal PCO2 values (70 and 80 mm Hg) during CO2 rebreathing, tidal volume and minute ventilation were lower after epidural block compared to the corresponding values before the block. Thoracic epidural anesthesia impaired contraction of the parasternals and conceivably other respiratory muscles in the rib cage as well and could induce a distortion of the rib cage. The authors conclude that respiratory muscles in the rib cage contribute considerably to the maintenance of ventilation in anesthetized dogs.

Beyond the lung: oxygen delivery and tissue oxygenation.

Beyond the lung: oxygen delivery and tissue oxygenation.

Effects of thoracic epidural anesthesia on myocardial pH and metabolism during ischemia

The effect of thoracic epidural anesthesia (TEA) on the ischemic myocardium was examined in open-chest dogs anesthetized intravenously. Ischemia induced by brief coronary artery occlusion caused an elevation of the ST segment in epicardial ECG and a reduction in myocardial pH and contractile force. TEA with 0.15 ml/kg of 0.4% bupivacaine solution attenuated an ischemia-induced decrease in myocardial pH and an increase of the ST segment in epicardial ECG. This attenuation was maintained even after the restoration of blood pressure and heart rate, which had been decreased significantly after TEA, to pre-TEA levels, suggesting that a beneficial effect of TEA should not be confined to its hemodynamic changes such as decreased blood pressure and heart rate. In contrast, the subendocardial contents of ATP, creatine phosphate (CP) and lactate were not affected by TEA, either in the presence or the absence of 5 min LAD occlusion. These results suggest that neither hemodynamic nor metabolic changes are responsible for the reduced myocardial ischemic acidosis induced by TEA after brief coronary artery occlusion. The acidosis-saving property of TEA is favorable for the ischemic heart.

Effects of thoracic epidural anesthesia and adrenoceptor blockade on the cardiovascular response to dopamine in the dog

The cardiovascular effects of dopamine are different before and during thoracic epidural anesthesia (TEA). To evaluate underlying adrenoceptor-mediated mechanisms, dopamine effects were investigated in nine chloralose-anesthetized dogs. The circulatory response to dopamine (0-40 micrograms.kg-1.min-1) was studied before and during TEA, and during TEA after introducing the alpha 1-antagonist prazosin (0.3 mg.kg-1), the alpha 2-antagonist rauwolscine (0.3 mg.kg-1), and the beta 1-antagonist metoprolol (0.5 mg.kg-1). TEA decreased mean arterial pressure (MAP) by 29%, cardiac output (CO) by 36%, heart rate (HR) by 27%, and the maximum rate of change of left ventricular pressure (LVdP/dt) by 52%. Systemic vascular resistance, pulmonary vascular resistance and mean pulmonary artery pressure (MPAP) remained unaltered by TEA. Dopamine-induced increases in MAP and HR were augmented by TEA. Both MAP and LVdP/dt increased above pre-TEA levels at 10 micrograms.kg-1.min-1. Prazosin attenuated the increases in MAP and MPAP by dopamine. Adding rauwolscine almost abolished the dopamine response in MAP and MPAP. Metoprolol almost eliminated the dopamine effects on CO and LVdP/dt. Only minor alterations in cardiac filling pressures were observed during the study. Plasma norepinephrine (NE) concentration was lower during than before TEA at corresponding dopamine infusion rates. NE was reduced by the beta 1-blockade. During TEA, the plasma dopamine levels were generally higher, and they were further increased by adding beta 1-blockade. In conclusion, myocardial contractility and arterial pressure were restored to pre-TEA values by dopamine at 5-10 micrograms.kg-1.min-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Thoracic Epidural Anesthesia on Coronary Arteries and Arterioles in Patients with Coronary Artery Disease

The effect of cardiac sympathetic blockade by high thoracic epidural anesthesia (TEA) (T1-T6, bupivacaine) on the luminal diameter of normal and diseased portions of epicardial coronary arteries was determined by quantitative coronary angiography in patients (n = 27) with severe coronary artery disease (CAD). In a separate group of patients (n = 9) with severe CAD, the effects of TEA on coronary arterioles (resistance vessels) were studied, by measuring total and regional myocardial blood flow and metabolism with the retrograde coronary sinus thermodilution technique. At the stenotic segments, TEA induced an increase in luminal diameter from 1.34 +/- 0.11 to 1.56 +/- 0.13 mm (P less than 0.002), but did not change the diameter of the nonstenotic segments (3.07 +/- 0.13 to 2.99 +/- 0.13 mm). In the second group of patients, TEA induced no changes in coronary perfusion pressure, total or regional myocardial blood flow, coronary venous oxygen content, coronary blood flow distribution, regional myocardial oxygen consumption, or lactate extraction or uptake. Two patients had chest pain in the control situation and had regional myocardial lactate production that was attenuated by TEA. We conclude that TEA may increase the diameter of stenotic epicardial coronary artery segments in patients with CAD without causing a dilation of coronary arterioles. These effects may be beneficial when high TEA is used to treat severe ischemic chest pain in patients at rest.

Thoracic epidural anaesthesia combined with enflurane anaesthesia reduces atrioventricular conduction in dogs

Cardiac electrophysiological variables during thoracic epidural lidocaine (TEL) were compared with those during continuous intravenous lidocaine (IVL) infusion in 14 mongrel dogs anaesthetized with enflurane in order to investigate the combined effects of thoracic epidural anaesthesia (TEA) and enflurane anaesthesia on intracardiac conduction. Thoracic epidural lidocaine suppressed intracardiac conduction. Sinus cycle length (SCL) and Atrium-His (AH) interval increased by 9 and 11 per cent respectively (P less than 0.05), 30 min after TEL. Intravenous lidocaine did not increase either SCL or AH. The functional refractory period of the atrioventricular node increased five per cent above the control value 15 min after TEL (P less than 0.05), while it was unchanged in the IVL group. The mean plasma concentrations of lidocaine ranged from 0.48 +/- 0.07 to 1.00 +/- 0.14 micrograms.ml-1 in the TEL group and from 0.98 +/- 0.13) to 1.21 +/- 0.15 micrograms.ml-1 in the IVL group. There were no significant differences in plasma concentrations of lidocaine in both groups during the observation period. Therefore, it is concluded that the depressant effects of TEA on intracardiac conduction were caused by blocking of the sympathetic efferent activity. Caution may be advised in administering TEA when cardiac conduction is already compromised.

Intestinal Hemodynamics During Laparotomy

The effects of thoracic epidural anesthesia (TEA) and dopamine infusion (4 micrograms.kg-1.min-1) on superior mesenteric artery blood flow (SMABF), the mesenteric arteriovenous oxygen difference (AVDO2), and the mesenteric venous lactate concentration were studied in nine patients before abdominal aortic reconstruction. Thoracic epidural anesthesia reduced SMABF, as measured by electromagnetic flowmetry, to 77% +/- 8% (mean +/- SEM) of control (P less than 0.05), and mean arterial pressure to 46% +/- 4% of control (P less than 0.01). The mesenteric AVDO2 increased from 27 +/- 3 to 39 +/- 6 mL/L (P less than 0.05) and superior mesenteric venous lactate from 1.03 +/- 0.11 to 1.60 +/- 0.38 mmol/kg (P less than 0.05); systemic AVDO2 and lactate did not change. Dopamine had no significant effect on SMABF and mean arterial pressure before TEA. However, dopamine increased SMABF during TEA (from 77% +/- 8% to 137% +/- 21% of control; P less than 0.01), returned mesenteric AVDO2 to 27 +/- 3 mL/L (P less than 0.05), and elevated mean arterial pressure to 62% +/- 4% of control (P less than 0.05). It is concluded that the decrease in perfusion pressure during TEA reduces SMABF with resultant evidence of intestinal reductive metabolism. The intestinal blood flow during TEA was improved by dopamine.

Effects of thoracic epidural anaesthesia on central haemodynamics compared to cardiac beta adrenoceptor blockade in conscious rats with acute myocardial infarction

The study aimed to compare the effects of thoracic epidural anaesthesia (TEA) with those of the beta-adrenoceptor blocker, metoprolol, on central haemodynamics in conscious rats with acute myocardial infarction. During methohexital anaesthesia, appropriate vascular catheters were inserted, a thoracic epidural catheter was implanted and the left coronary artery was ligated. A recovery period of 1-2 h elapsed after termination of surgery and anaesthesia. Experiments were performed on four separate groups of animals (A-D). In Group A (n = 10) mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO) were measured, and stroke volume (SV) and systemic vascular resistance (SVR) were calculated before and 10-15 min after the induction of TEA (bupivacaine 5 mg.ml-1). In Group B (n = 6) left ventricular end-diastolic pressure (LVEDP) and maximal dP/dt were recorded as in Group A. In Group C (n = 10) central haemodynamics were measured 10 min after i.v. metoprolol (0.5 mg.kg-1) and again 10-15 min after the addition of TEA. In Group D (n = 6) LVEDP and max dP/dt were measured as in Group C. The reduction in CO, SV, HR and max dP/dt was of the same magnitude with TEA and metoprolol. TEA lowered MAP by 17%, while metoprolol did not change MAP. Metoprolol caused an increase in LVEDP from 20.8 +/- 1.8 to 27.5 +/- 2.7 mmHg (2.8 +/- 0.2 to 3.7 +/- 0.4 kPa) (P less than 0.01), while TEA induced a decrease in LVEDP from 24.2 +/- 1.4 to 17.8 +/- 1.6 mmHg (3.2 +/- 0.2 to 2.4 +/- 0.2 kPa) (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Thoracic Epidural Anesthesia on Systemic Hemodynamic Function and Systemic Oxygen Supply-Demand Relationship

The effects of thoracic epidural anesthesia (TEA) on total body oxygen supply-demand ratio are complex due to potential influences on both O2 delivery (QO2) and consumption (VO2). One hundred and five patients undergoing abdominal aortic surgery were randomly assigned to one of three groups to compare the cardiovascular and metabolic responses associated with (1) thoracic epidural anesthesia plus light general anesthesia (group TEA); (2) general anesthesia with halothane (group H); and (3) neuroleptanalgesia (group NLA). Values of cardiac index (CI) and QO2 were less intraoperatively in the TEA group than in the H or NLA groups, while VO2 values were similar. VO2 during recovery was greater in both the TEA and NLA groups than in the H group. Consequently the oxygen supply-demand ratio (QO2/VO2) was less in the TEA group throughout the perioperative period and about 30% below baseline values during early recovery. At comparable VO2, CI and mixed venous O2 saturation were always less in the TEA group than in the NLA group. Heart rate was slowest intraoperatively during TEA, and stroke work was less with TEA than with NLA. As cardiac filling pressure and systemic vascular resistance did not differ among the three groups, reduced adaptation of CI to tissue O2 needs during TEA was attributed to negative inotropic and chronotropic effects of the sympathetic blockade. We conclude that in patients undergoing abdominal aortic surgery, TEA has no apparent advantage over general anesthesia.

Thoracic Epidural Anesthesia Reduces Myocardial Infarct Size after Coronary Artery Occlusion in Dogs

The effect of thoracic epidural anesthesia (TEA) with lidocaine on regional myocardial blood flow (RMBF), hemodynamic performance, and myocardial infarct size after coronary artery occlusion was assessed in 21 dogs. In seven dogs, the left anterior descending coronary artery (LAD) was temporarily occluded twice: once before TEA (control) and once during TEA. Systemic hemodynamic parameters, RMBF (using radionuclide-labeled microspheres), and epicardial electrocardiographic maps (15 sites) were obtained before and 15 min after each temporary LAD occlusion. Compared with the ischemic period before TEA, the following were decreased during ischemia with TEA: heart rate, ST segment elevation, cardiac index, the peak first time derivative of left ventricular (LV) pressure, LV tension-time index, the rate-pressure product, and LV stroke-work index. Ischemic zone endocardial RMBF was increased from a control value of 26 +/- 6% to 36 +/- 6% of normal during TEA (P less than 0.05). An additional 14 dogs randomly received either TEA (1% lidocaine, 10 ml/hr) or epidural saline plus 1% lidocaine (10 ml/hr, intramuscularly), beginning 1 hr after LAD occlusion. After 6 hr, the heart was removed and the left ventricle was sectioned parallel to the atrioventricular groove. The infarcts (tetrazolium-stained) were 46% smaller with TEA than with saline, 15.4 +/- 1.8% vs 28.7 +/- 2.3% of the left ventricle (P less than 0.05). Thus TEA reduced hemodynamic correlates of myocardial O2 consumption, improved regional (ischemic zone) endocardial perfusion, and reduced the extent of myocardial infarction.