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

1995 ◽  
Vol 82 (4) ◽  
pp. 877-883. ◽  
Author(s):  
Rom A. Stevens ◽  
David Beardsley ◽  
J. Lee White ◽  
Tzu-Cheg Kao ◽  
Rod Gantt ◽  
...  

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. Conclusions Spinal anesthesia did not result in a more complete attenuation of the sympathetic response to a CPT than did epidural anesthesia. In response to the CPT, spinal anesthesia blocked the increase in cardiac index, and epidural anesthesia resulted in a decrease in total peripheral resistance compared to the pre-anesthesia state. The differences between the techniques are not significant and are of uncertain clinical implications.

2018 ◽  
Vol 9 (1) ◽  
pp. 1-10
Author(s):  
Elif Copuroglu ◽  
Gonul Sagiroglu ◽  
Beliz Bilgili ◽  
Sevtap Hekimogl

Purpose: Transurethral resections (TUR) are commonly performed for elderly population who have multiple comorbidities which can cause intraoperative and postoperative complications. The type of anesthesia has an impact on patient outcome. The aim of the study is to compare the effectiveness of epidural and spinal anesthesia techniques for TUR. Methods: A total of 158 elective TUR cases were evaluated. The patients were randomized into 2 groups: Epidural anesthesia was applied to Group I (n=82) and spinal anesthesia was applied to Group II (n=76). Both groups were compared for intraoperative hemodynamic parameters (mean arterial pressure, heart rate, peripheral oxygen saturations), total duration of hospital stay, perioperative complications, and satisfaction of the patients and surgeons. Results: The patients in the spinal anesthesia group experienced more frequent intraoperative hypotensive episodes during TUR (n=2 vs. n=10; p=0.026) and had lower mean arterial pressure values for the first 30 minutes of anesthesia compared to epidural anesthesia group. The postoperative duration of bed stay was longer in the spinal anesthesia group (402.96±49.61 min) than the epidural anesthesia group (205.91±28.27 min) (p<0.001). The patient satisfaction score was significantly higher in the epidural anesthesia group (2.54±0.63) than the spinal anesthesia group (2.23±1.22) (p=0.04) where as the surgeon satisfaction score were similar in both groups. Conclusion: Epidural anesthesia can be considered as an effective and safe technique for ambulatory interventions especially for elderly patients providing perioperative hemodynamic stability and postoperative early mobilization.


2001 ◽  
Vol 94 (4) ◽  
pp. 678-682 ◽  
Author(s):  
Masahiro Yoshida ◽  
Keizo Shibata ◽  
Hironori Itoh ◽  
Ken Yamamoto

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. Conclusion Mild hypothermia during combined epidural anesthesia and general anesthesia markedly reduced cardiac output in dogs, mainly by decreasing heart rate.


2008 ◽  
Vol 108 (5) ◽  
pp. 802-811 ◽  
Author(s):  
Robert A. Dyer ◽  
Jenna L. Piercy ◽  
Anthony R. Reed ◽  
Carl J. Lombard ◽  
Leann K. Schoeman ◽  
...  

Background Hemodynamic responses to spinal anesthesia (SA) for cesarean delivery in patients with severe preeclampsia are poorly understood. This study used a beat-by-beat monitor of cardiac output (CO) to characterize the response to SA. The hypothesis was that CO would decrease from baseline values by less than 20%. Methods Fifteen patients with severe preeclampsia consented to an observational study. The monitor employed used pulse wave form analysis to estimate nominal stroke volume. Calibration was by lithium dilution. CO and systemic vascular resistance were derived from the measured stroke volume, heart rate, and mean arterial pressure. In addition, the hemodynamic effects of phenylephrine, the response to delivery and oxytocin, and hemodynamics during recovery from SA were recorded. Hemodynamic values were averaged for defined time intervals before, during, and after SA. Results Cardiac output remained stable from induction of SA until the time of request for analgesia. Mean arterial pressure and systemic vascular resistance decreased significantly from the time of adoption of the supine position until the end of surgery. After oxytocin administration, systemic vascular resistance decreased and heart rate and CO increased. Phenylephrine, 50 mug, increased mean arterial pressure to above target values and did not significantly change CO. At the time of recovery from SA, there were no clinically relevant changes from baseline hemodynamic values. Conclusions Spinal anesthesia in severe preeclampsia was associated with clinically insignificant changes in CO. Phenylephrine restored mean arterial pressure but did not increase maternal CO. Oxytocin caused transient marked hypotension, tachycardia, and increases in CO.


1980 ◽  
Vol 238 (4) ◽  
pp. H539-H544 ◽  
Author(s):  
T. L. Smith ◽  
P. M. Hutchins

We studied the effects of three anesthetic agents on the central hemodynamics of spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats instrumented with chronic electromagnetic flow probes and arterial pressure catheters. Cardiovascular alterations due to ether, pentobarbital sodium (PBS; 50 mg/kg), and a 2% chloralose-7.5% urethan mixture (CU; 6 ml/kg) were determined. Ether produced significant elevations in heart rate (HR), cardiac index (CI), stroke volume (SV), and peak aortic flow velocity (PAFV) in SHRs (P less than 0.01) and elevations of HR and CI in WKYs (P less than 0.05). Ether reduced total peripheral resistance (TPR) and mean arterial pressure (MAP) in WKYs and SHRs (P less than 0.01). PBS decreased HR, CI, SV, MAP, PAFV, and minute work (MW) in both WKYs and SHRs (P less than 0.05--P less than 0.001). PBS also lowered TPR in WKYs (P less than 0.05). CU produced effects similar to those of PBS, but did not alter HR or TPR. Central hemodynamics are therefore significantly altered by these anesthetics when compared to those of conscious rats. These agents also have differential effects on the hemodynamics of SHRs and WKYs.


1996 ◽  
Vol 84 (3) ◽  
pp. 672-685 ◽  
Author(s):  
Toshiaki Nishikawa ◽  
Hiroshi Naito

Background Hypoxia or hypercapnia elicits cardiovascular responses associated with increased plasma catecholamine concentrations, whereas clonidine, an alpha(2)- adrenergic agonist, decreases plasma catecholamine concentrations. The authors examined whether systemic clonidine administration would alter the hemodynamic and catecholamine responses to hypoxia or hypercapnia in anesthetized dogs. Methods Pentobarbital-anesthetized dogs whose lungs were mechanically ventilated were instrumented for measurement of mean arterial pressure, heart rate, mean pulmonary artery pressure, right atrial pressure, cardiac output, left ventricular end-diastolic pressure, and the peak of first derivative of left ventricular pressure. The dogs were randomly assigned to receive an intravenous bolus injection of 10 microg/kg clonidine followed by continous infusion at a rate of 1 microg. kg (-1). min (-1)(clonidine-10 group, n = 7), an intravenous bolus injection of microg/kg clonidine followed by continuous infusion at a rate of 0.5 micro.kg(-).min(-1)(clonidine-5 group, n = 7), or an equivalent volume of 0.9% saline (control group = 7). Each dog underwent random challenges of hypoxia (PaO2 30, 40, and 50 mmHg) and hypercapnia (PaCO2 60, 80, and 120 mmHg). Measurements of hemodynamic and plasma norepinephrine and epinephrine concentrations were made after the loading dose of clonidine and the first and the second exposure of hypoxia or hypercapnia. Results Although significant increases from prehypoxic values in mean arterial pressure (39 +/- 10 mmHg) and plasma norepinephrine (291 +/- 66 pg/ml) and epinephrine (45 +/- 22 pg/ml) concentrations were noted during hypoxia of PaO2 30, mmHg in the control group (P&lt;0.05), such changes were absent in both clonidine groups. During hypercapnia of PaCo2 120 mmHg, changes from prehypercapnic values in mean arterial pressure, mean pulmonary artery pressure, the peak of first derivative of left ventricular pressure, and plasma norepinephrine and epinephrine concentrations in the clonidine-10 and clonidine-5 groups were significantly less than those in the control group. Plasma clonidine concentrations in the clonidine-10 and clonidine-5 groups were 16.8 +/- 1.7 and 8.9 =/- 1.0, 42.5 =/- 2.9 and 21.5 +/- 1.5, and 51.1 +/- 3.2 and 26.7 +/- 1.0 ng/ml after the loading dose of clonidine and the first and the second exposure of hypoxia or hypercapnia, respectively. Conclusions Systemic clonidine administration alter the hemodynamic changes associated with hypoxia or hypercapnia and suppresses plasma catecholamine responses in anesthetized dogs when a larger dose of clonidine is administered. catecholamines: epinephrine; norepinephrine.)


1984 ◽  
Vol 12 (1) ◽  
pp. 22-26 ◽  
Author(s):  
Mary F. Cummings ◽  
W. J. Russell ◽  
D. B. Frewin ◽  
Wendy A. Miller

Tracheal intubation can be accompanied by significant increases in arterial pressure, heart rate and the plasma levels of noradrenaline and adrenaline. The drugs used at induction can enhance or attenuate these responses. In nine patients who had received gallamine, intubation was associated with a 45% rise in mean arterial pressure, a twofold rise in plasma adrenaline and a 49% rise in plasma noradrenaline concentration. When a mixture of pancuronium and alcuronium (in a ratio of 4:10 by weight) was used in ten patients, blood pressure fell 24% after induction and rose 49% after intubation. A 24% rise in plasma noradrenaline in response to intubation was also observed. Compared with pancuronium alone, the use of the mixture attentuates the rise in blood pressure and noradrenaline concentration associated with intubation but does not abolish them. In addition, the mixture was associated with a significant fall in blood pressure between induction and intubation, whereas this was not found with gallamine.


1983 ◽  
Vol 11 (2) ◽  
pp. 103-106 ◽  
Author(s):  
M. F. Cummings ◽  
W. J. Russell ◽  
D. B. Frewin ◽  
J. R. Jonsson

Changes in mean arterial pressure (MAP) and plasma catecholamine concentrations in response to endotracheal intubation were examined in 8 patients who had received d-tubocurarine and 10 who had received suxamethonium. MAP fell after induction of anaesthesia and administration of the relaxant by a mean of 11 mmHg in those who had received suxamethonium and 19 mmHg in those who had received d-tubocurarine (p <0.05 for each). MAP rose sharply when the trachea was intubated, by a mean of 29 mmHg for the suxamethonium group, and 35 mmHg for the curare group (p <0.001 for each). A significant rise in plasma noradrenaline was also noted after intubation in each group, 51% (p <0.01) for the suxamethonium group and 28% (p <0.05) for the d-tubocurarine. The results suggest that the fall in MAP after administration of d-tubocurarine does not attenuate the pressor response associated with intubation.


1987 ◽  
Vol 252 (1) ◽  
pp. R34-R39 ◽  
Author(s):  
H. J. Lenz ◽  
A. Raedler ◽  
H. Greten ◽  
M. R. Brown

Corticotropin-releasing factor (CRF) is thought to be an endogenous mediator of adrenocorticotropic hormone release following stress. We examined if CRF initiates further biological actions that are observed in response to stressful events. Male beagle dogs (10–12 kg) were fitted with a chronic intracerebroventricular cannula, intra-arterial and intravenous catheters, as well as a gastric fistula. Synthetic human CRF was microinjected into the third cerebral ventricle in conscious animals. CRF (0.1–1.0 nmol/kg) significantly (P less than 0.01) increased plasma concentrations of epinephrine, norepinephrine, glucagon, and glucose and elevated mean arterial pressure and heart rate. Pretreatment of the animals with the ganglionic blocking agent chlorisondamine completely abolished the increases in plasma catecholamine and glucose concentrations as well as the elevations in blood pressure and heart rate. CRF significantly (P less than 0.01) inhibited gastric acid secretion, but not plasma gastrin concentrations stimulated by an 8% liquid peptone meal. The gastric inhibitory action of CRF was completely prevented by chlorisondamine and, in part, by naloxone and a vasopressin antagonist. In contrast, bilateral truncal vagotomy did not affect the gastric inhibitory action of CRF. The results of this study indicate that CRF acts within the central nervous system to increase plasma glucose and glucagon concentrations, mean arterial pressure, and heart rate by activation of the autonomic nervous system. CRF inhibits meal-stimulated gastric acid secretion by activation of the sympathetic nervous system and, in part, by opiate and vasopressin-dependent pathways and not by inhibition of gastrin release.(ABSTRACT TRUNCATED AT 250 WORDS)


2002 ◽  
Vol 96 (5) ◽  
pp. 1086-1094 ◽  
Author(s):  
James M. Bailey ◽  
Wei Lu ◽  
Jerrold H. Levy ◽  
James G. Ramsay ◽  
Linda Shore-Lesserson ◽  
...  

Background Treatment of elevated blood pressure is frequently necessary after cardiac surgery to minimize postoperative bleeding and to attenuate afterload changes associated with hypertension. The purpose of this study was to investigate the pharmacodynamics and pharmacokinetics of a short-acting calcium channel antagonist, clevidipine, in the treatment of hypertension in postoperative cardiac surgical patients. Methods Postoperative cardiac surgical patients were randomized to receive placebo or one of six doses of clevidipine. Hemodynamic parameters were recorded and blood samples were drawn for determination of clevidipine plasma concentrations during infusion and after discontinuation of clevidipine. The concentration-response relation was analyzed using logistic regression, and pharmacokinetic models were applied to the data using population analysis. Results There were significant decreases in mean arterial blood pressure and systemic vascular resistance at doses greater than or equal to 1.37 microg. kg-1. min-1. There were no changes in heart rate, central venous pressure, pulmonary artery occlusion pressure, or cardiac index with increasing doses of clevidipine. The clevidipine C50 value for a 10% or greater decrease in mean arterial pressure was 9.7 microg/l and for a 20% or greater decrease in mean arterial pressure was 26.3 microg/l. The pharmacokinetics of clevidipine were best described with a three-compartment model with a volume of distribution of 32.4 l and clearance of 4.3 l/min. The early phase of drug disposition had a half-life of 0.6 min. The context-sensitive half-time is less than 2 min for up to 12 h of administration. Conclusion Clevidipine is a calcium channel antagonist with a very short duration of action that effectively decreases systemic vascular resistance and mean arterial pressure without changing heart rate, cardiac index, or cardiac filling pressures.


2021 ◽  
Vol 8 (1) ◽  
pp. 44-50
Author(s):  
Roshan Piya ◽  
Anil Shrestha ◽  
Manisha Pradhan ◽  
Shirish Amatya ◽  
Niroj Hirachan ◽  
...  

Introduction: Hypotension and bradycardia are the most common complications during spinal anesthesia. Bradycardia decreases cardiac output, resulting in hypotension and even cardiac arrest. Glycopyrronium, an anticholinergic drug increases heart rate and prevents bradycardia during spinal anesthesia by blocking the effects of acetylcholine on the sinoatrial node. The study aims to measure the maternal hemodynamic effect of glycopyrrolate after spinal anesthesia for elective caesarean section. Method: An intervention, comparative study was conducted in Patan Hospital after approval from Ethical Committee. Eighty-two pregnant women scheduled for elective caesarean section were randomly assigned in two groups by sealed envelope method; Group I received glycopyrrolate 0.2mg intravenous,  Group II did not receive glycopyrrolate. The patient’s heart rate, blood pressure, mean arterial pressure, a total dose of ephedrine, the occurrence of nausea, vomiting, and dry mouth were recorded. Independent-T test, chi-square test were used for statistical analysis. Result: Among 82 elective caesarean sections, 41 in each group, Group II (non-glycopyrrolate) reported increased heart rate compared to Group I (glycopyrrolate), but was statistically not significant. The highest recorded diastolic blood pressure was more in Group I compared to Group II and was statistically significant. The highest recorded Mean Arterial Pressure was high in the glycopyrrolate group and was statistically significant. The total dose of ephedrine was lower in the statistically significant glycopyrrolate group. The incidence of dry mouth was more in the glycopyrrolate group and the difference was statistically significant. Conclusion: Glycopyrrolate reduces the incidence of hypotension but not bradycardia and decreases the need for vasopressor.


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