The Experts below are selected from a list of 288 Experts worldwide ranked by ideXlab platform
Patrick Wouters - One of the best experts on this subject based on the ideXlab platform.
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Effects of Thoracic Epidural Anesthesia on Neuronal Cardiac Regulation and Cardiac Function.
Anesthesiology, 2019Co-Authors: Jeroen Wink, Bernadette Th. Veering, Leon Aarts, Patrick WoutersAbstract:Cardiac sympathetic blockade with high-thoracic Epidural Anesthesia is considered beneficial in patients undergoing major surgery because it offers protection in ischemic heart disease. Major outcome studies have failed to confirm such a benefit, however. In fact, there is growing concern about potential harm associated with the use of thoracic Epidural Anesthesia in high-risk patients, although underlying mechanisms have not been identified. Since the latest review on this subject, a number of clinical and experimental studies have provided new information on the complex interaction between thoracic Epidural Anesthesia-induced sympatholysis and cardiovascular control mechanisms. Perhaps these new insights may help identify conditions in which benefits of thoracic Epidural Anesthesia may not outweigh potential risks. For example, cardiac sympathectomy with high-thoracic Epidural Anesthesia decreases right ventricular function and attenuates its capacity to cope with increased right ventricular afterload. Although the clinical significance of this pathophysiologic interaction is unknown at present, it identifies a subgroup of patients with established or pending pulmonary hypertension for whom outcome studies are needed. Other new areas of interest include the impact of thoracic Epidural Anesthesia-induced sympatholysis on cardiovascular control in conditions associated with increased sympathetic tone, surgical stress, and hemodynamic disruption. It was considered appropriate to collect and analyze all recent scientific information on this subject to provide a comprehensive update on the cardiovascular effects of high-thoracic Epidural Anesthesia and cardiac sympathectomy in healthy and diseased patients.This review provides a comprehensive update on the cardiovascular effects of high-thoracic Epidural Anesthesia and cardiac sympathectomy in healthy and diseased patients.
Nancy J. Newman - One of the best experts on this subject based on the ideXlab platform.
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Transient Horner's syndrome after lumbar Epidural Anesthesia
Neurology, 1998Co-Authors: Valérie Biousse, Raul A. Guevara, Nancy J. NewmanAbstract:Horner9s syndrome as a complication of lumbar Epidural Anesthesia is a relatively benign and transient condition that usually does not warrant further extensive investigation. Its occurrence is unpredictable, although more frequently associated with Epidural Anesthesia performed for obstetric conditions. It may indicate high sympathetic blockade, and those patients should be monitored closely for autonomic complications. We report two new cases of iatrogenic Horner9s syndrome from lumbar Epidural Anesthesia.
T Mineo - One of the best experts on this subject based on the ideXlab platform.
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Epidural Anesthesia in awake thoracic surgery
European Journal of Cardio-Thoracic Surgery, 2007Co-Authors: T MineoAbstract:Despite the indisputable and well-known advantages of general Anesthesia in thoracic surgery, this can trigger some adverse effects including an increased risk of pneumonia, impaired cardiac performance, neuromuscular problems, mechanical ventilation-induced injuries, which include barotrauma, volotrauma, atelectrauma, and biotrauma. In order to reduce the adverse effects of general Anesthesia, thoracic Epidural Anesthesia has been recently employed to perform awake thoracic surgery procedures including coronary artery bypass, management of pneumothorax, resection of pulmonary nodules and solitary metastases, lung volume reduction surgery, and even transsternal thymectomy. The results achieved in this early series have been encouraging, although indications and many pathophysiologic aspects remain to be elucidated. In this review we have tried to provide a first-step analysis of the anecdotal reports available in the literature on this topic. We also desired to provide insights into the main physiologic effects of awake thoracic surgery with Epidural Anesthesia, with particular attention to the several issues raised by its application in patients with chronic obstructive pulmonary disease, which can represent one of the most stimulating challenges in this setting.
Jeroen Wink - One of the best experts on this subject based on the ideXlab platform.
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Effects of Thoracic Epidural Anesthesia on Neuronal Cardiac Regulation and Cardiac Function.
Anesthesiology, 2019Co-Authors: Jeroen Wink, Bernadette Th. Veering, Leon Aarts, Patrick WoutersAbstract:Cardiac sympathetic blockade with high-thoracic Epidural Anesthesia is considered beneficial in patients undergoing major surgery because it offers protection in ischemic heart disease. Major outcome studies have failed to confirm such a benefit, however. In fact, there is growing concern about potential harm associated with the use of thoracic Epidural Anesthesia in high-risk patients, although underlying mechanisms have not been identified. Since the latest review on this subject, a number of clinical and experimental studies have provided new information on the complex interaction between thoracic Epidural Anesthesia-induced sympatholysis and cardiovascular control mechanisms. Perhaps these new insights may help identify conditions in which benefits of thoracic Epidural Anesthesia may not outweigh potential risks. For example, cardiac sympathectomy with high-thoracic Epidural Anesthesia decreases right ventricular function and attenuates its capacity to cope with increased right ventricular afterload. Although the clinical significance of this pathophysiologic interaction is unknown at present, it identifies a subgroup of patients with established or pending pulmonary hypertension for whom outcome studies are needed. Other new areas of interest include the impact of thoracic Epidural Anesthesia-induced sympatholysis on cardiovascular control in conditions associated with increased sympathetic tone, surgical stress, and hemodynamic disruption. It was considered appropriate to collect and analyze all recent scientific information on this subject to provide a comprehensive update on the cardiovascular effects of high-thoracic Epidural Anesthesia and cardiac sympathectomy in healthy and diseased patients.This review provides a comprehensive update on the cardiovascular effects of high-thoracic Epidural Anesthesia and cardiac sympathectomy in healthy and diseased patients.
Daniel I. Sessler - One of the best experts on this subject based on the ideXlab platform.
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Effects of Epidural Anesthesia on thermal sensation
Regional anesthesia and pain medicine, 2001Co-Authors: Angela Rajek, Robert Greif, Daniel I. SesslerAbstract:Epidural Anesthesia decreases the core temperatures triggering vasoconstriction and shivering, presumably by increasing apparent (as opposed to actual) lower-body temperature. We therefore tested the hypothesis that Epidural Anesthesia also increases the overall perception of warmth. We studied 8 volunteers in a randomized, cross-over protocol separated by at least 48 hours. On one day, Epidural Anesthesia was induced to a T11 sensory level; the other day was a control without Anesthesia. Core temperature and upper-body skin temperatures (33 degrees C) were kept constant throughout. Lower-body skin temperature was set in a random order to 31 degrees C, 32 degrees C, 33 degrees C, 34 degrees C, 35 degrees C, and 36 degrees C and maintained by circulating water and forced air. At each temperature, the volunteers rated their thermal sensation with a visual analog scale (0 = cold, 100 = hot). Core temperature was 36.8 +/- 0.1 degrees C on the control day and 36.7 +/- 0.1 degrees C on the Epidural day. Scores for thermal sensation on the Epidural day were near 47 mm at each lower-body skin temperature. On the control day, visual analog scores at a lower-body skin temperature of 31 degrees C were 16 +/- 10 mm and increased linearly to 61 +/- 6 mm at 36 degrees C. Control thermal sensation scores thus equaled those during Epidural Anesthesia when lower-body skin temperature was near 34 degrees C. Thermal sensation with and without Epidural Anesthesia was comparable at a lower-body temperature near 34 degrees C, which is a normal leg skin temperature. This suggests that autonomic and behavioral thermoregulatory consequences of Epidural Anesthesia differ-or that the current explanation for reduced vasoconstriction and shivering thresholds during Epidural Anesthesia is incorrect.
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heat flow and distribution during Epidural Anesthesia
Anesthesiology, 1995Co-Authors: Takashi Matsukawa, Daniel I. Sessler, Richard Christensen, Makoto Ozaki, Marc SchroederAbstract:BACKGROUND Core hypothermia after induction of Epidural Anesthesia results from both an internal core-to-peripheral redistribution of body heat and a net loss of heat to the environment. However, the relative contributions of each mechanism remain unknown. The authors thus evaluated regional body heat content and the extent to which core hypothermia after induction of Anesthesia resulted from altered heat balance and internal heat redistribution. METHODS Twelve minimally clothed male volunteers were evaluated in a approximately 22 degrees C environment for 2.5 control hours before induction of Epidural Anesthesia and for 3 subsequent hours. Epidural Anesthesia produced a bilateral sympathetic block in only six volunteers, and only their results are reported. Shivering, when observed, was treated with intravenous meperidine. Overall heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Arm and leg tissue heat contents were determined from 19 intramuscular needle thermocouples, 10 skin temperatures, and "deep" foot temperature. To separate the effects of redistribution and net heat loss, we multiplied the change in overall heat balance by body weight and the specific heat of humans. The resulting change in mean body temperature was subtracted from the change in esophageal or tympanic membrane (core) temperatures, leaving the core hypothermia specifically resulting from redistribution. RESULTS Arm heat content decreased approximately 5 kcal/h after induction of Anesthesia, but leg heat content increased markedly. Most of the increase in leg heat content was in the lower legs and feet. Core temperature increased slightly during the control period but decreased 0.8 +/- 0.3 degrees C in the 1st hour of Anesthesia. Redistribution, contributing 89% to this initial decrease, required a net transfer of 20 kcal from the trunk to the extremities. During the subsequent 2 h of Anesthesia, core temperature decreased an additional 0.4 +/- 0.3 degrees C, with redistribution contributing 62%. Thus, only 7 kcal were redistributed during the 2nd and 3rd hours of Anesthesia. Redistribution therefore contributed 80% to the entire 1.2 +/- 0.3 degrees C decrease in core temperature during the 3 h of Anesthesia. CONCLUSIONS Core hypothermia during the 1st hour after induction of Epidural Anesthesia resulted largely from redistribution of body heat from the core thermal compartment to the distal legs. Even after 3 h of Anesthesia, redistribution remained the major cause of core hypothermia. Despite the greater fractional contribution of redistribution during Epidural Anesthesia, core temperature decreased only half as much as during general Anesthesia because metabolic rate was maintained and the arms remained vasoconstricted.
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Thermal balance and tremor patterns during Epidural Anesthesia.
Anesthesiology, 1991Co-Authors: James M. Hynson, Daniel I. Sessler, B Glosten, Joseph McguireAbstract:Five healthy, nonpregnant volunteers were studied before and after induction of lumbar Epidural Anesthesia to determine the cause of central hypothermia during Epidural Anesthesia. Cutaneous heat loss was measured from 10 area-weighted sites using thermal flux transducers. Oxygen consumption was measured and converted to heat production in watts (W). After a 2-h control period at approximately 20 degrees C, Epidural Anesthesia was induced by injection of 30-50 ml 3% chloroprocaine. Additional boluses were given to extend the sensory blockade to at least the T5 dermatome. Tremor during Epidural Anesthesia was compared with normal shivering induced by rapid central venous infusion of approximately 4 l iced saline in six unanesthetized volunteers. Average skin temperature and cutaneous heat loss decreased during the control period, while tympanic membrane temperature remained stable. During the 1st h of Epidural blockade, tympanic membrane temperature decreased 1.1 +/- 0.3 degrees C, and average skin temperature increased 0.9 +/- 0.5 degrees C. Cutaneous heat loss increased 16 +/- 6% (15 +/- 5 W), but metabolic heat production increased even more (and was associated with a shivering-like tremor). Tremor during Epidural Anesthesia and shivering induced by iced saline infusion had similar synchronous waxing-and-waning patterns. No abnormal EMG patterns were detected during Epidural Anesthesia. We conclude that central hypothermia during the 1st h of Epidural Anesthesia does not result from heat loss to the environment in excess of metabolic heat production, but results primarily from redistribution of body heat from central to peripheral tissues. Analysis of the tremor patterns suggests that oscillations recorded during Epidural Anesthesia in nonpregnant individuals is normal thermoregulatory shivering. Shivering occurred sooner and was more intense during iced saline infusion than during Epidural Anesthesia, despite comparable central hypothermia. The low intensity of shivering during Epidural Anesthesia, and in some individuals the delay in onset, may result from blockade of afferent cutaneous cold signals.