JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS
AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
A&A International Anesthesia Research Society
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a colleague
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (10)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Meissner, A.
Right arrow Articles by Rolf, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Meissner, A.
Right arrow Articles by Rolf, N.
Anesth Analg 1999;89:1378
© 1999 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

Limited Upper Thoracic Epidural Block and Splanchnic Perfusion in Dogs

A. Meissner, MD, T. P. Weber, MD, H. Van Aken, MD, PhD, and N. Rolf, MD, PhD

Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin der Westfälischen Wilhelms-Universität Münster, Münster, Germany

Address correspondence and reprint requests to Professor Dr. med. H. Van Aken, Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin der Westfälischen Wilhelms-Universität Münster, Albert-Schweitzer-Str. 33, D-48149 Münster, Germany.


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Epidural blockade leads to a sympathetic block in affected segments and an increase of sympathetic outflow 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.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Thoracic epidural anesthesia (TEA) is used as an adjunct to general anesthesia and for postoperative analgesia during and after major thoracic, cardiac, and abdominal surgery (1). During abdominal procedures, the level of TEA includes the preganglionic sympathetic fibers to the splanchnic organs. This leads to improved splanchnic perfusion (2), effectively decreasing recovery time from surgery (3). For cardiac surgery, TEA is limited to the upper thoracic segments resulting in improved hemodynamic stability with less cardiac ischemia and improved lung function (4,5). However, patients after cardiac surgery are prone to gastrointestinal ischemic injury that is associated with a high mortality (6). Segmental sympatholysis is accompanied by an increase of sympathetic activity in segments not affected by the block (7). As splanchnic blood flow is modulated by sympathetic fibers originating from T8-L1, a sympatholysis restricted to T1-5 could be accompanied by an increased sympathetic activity in the lower segments resulting in impaired splanchnic blood flow.

Aside from reports by Taniguchi et al. (7), who used a direct measurement of sympathetic activity in cats, there are several clinical and experimental studies demonstrating increased sympathetic activity in the unblocked regions. For lumbar epidural anesthesia, an increase in lower extremity and abdominal capacitance vessels was followed by increased sympathetic outflow marked by decreased skin temperature in the upper extremity (8) or decreased SpO2 values recorded from the hand (9). An impairment of myocardial function after lumbar epidural anesthesia has been demonstrated in cats (10) and humans (11).

We hypothesize that, in dogs, a limited upper thoracic sympatholysis decreases splanchnic perfusions due a compensatory increase outflow in the gastrointestinal efferences.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
The experimental protocol was approved by the District Government of Münster. After overnight fasting, 13 mongrel dogs (either sex, weight 20–26 kg) were premedicated intramuscularly with 15 mg piritramide and 5 mg/kg ketamine. The animals were anesthetized IV with 5 mg/kg propofol. After tracheal intubation, anesthesia was maintained with isoflurane in a mixture of oxygen in room air. Perioperative antibiotic prophylaxis was administered using 30 mg/kg cefamandole.

A left thoracotomy in the fifth intercostal space was performed under aseptic conditions. Eighteen-gauge catheters (Tygon®, Serpi-Erpac S.A., Wilsele, Belgium) were inserted into the descending aorta and the left atrium for measurement of pressures, injection of microspheres, and withdrawal of blood. After the instrumentation phase, the animals were trained daily to get accustomed to the experimental environment and to lie quietly in a cage when connected to the data acquisition system.

Aortic and left atrial pressures were measured by disposable pressure transducers (PVB Medizintechnik, Kirchseeon). Pressure was processed by a two-channel system (Baylor College of Medicine, Houston, TX).

Insertion of the epidural catheter was performed after the cardiac instrumentation on a separate day 24 h before the experiment under isoflurane anesthesia with endotracheal intubation. After lumbar puncture of the epidural space at the level of L4/L5 with the loss-of-resistance technique, an 18-gauge catheter (Arrow Deutschland GmbH, Erding, Germany) was advanced epidurally to the T2 level. Correct position of the catheter was verified by radioscopy. Spread of the local anesthetic was determined immediately after insertion of the epidural catheter, and its correct position was verified by injecting contrast solution in a volume equivalent to the calculated volume of 2% lidocaine (0.2 mL/kg). A distribution of contrast solution that included all thoracic segments above the T7 level was considered adequate. The catheter was then tunneled subcutaneously to be exteriorized in the vicinity of the aortic and left atrial catheters and secured.

After at least seven days after thoracotomy, the experiments were performed only after complete recovery from the instrumentation and when normal blood gas values and hemodynamic variables were achieved.

We studied in seven dogs the effects of limited upper thoracic epidural block (LUTEB) on splanchnic blood flow in the waking state and in six dogs during propofol anesthesia. In the awake group, measurement of splanchnic blood flow was performed without LUTEB and during fully effective LUTEB. In the propofol group, measurements were performed prior to propofol anesthesia, during steady-state propofol anesthesia, and during steady-state propofol anesthesia and fully effective LUTEB.

In all dogs, the onset of LUTEB was verified by the occurrence of a Horner’s syndrome, the loss of motility in the front legs and bradycardia. Regional abdominal blood flow was measured with colored microspheres (Triton Technology, San Diego, CA). For each determination, a total of 9 x 106 microspheres suspended in a volume of 3 mL was injected into the left atrium. The reference blood sample was withdrawn from the aortic catheter at a rate of 10 mL/min. After the animals had been killed, the abdominal organs were dissected and tissue samples were obtained. Measurement of microspheres in the tissue samples from the same region of each organ was performed as described previously (12).

Data were analyzed using repeated-measures two-way analysis of variance, followed by Bonferroni-corrected Student’s t-test whenever appropriate. P < 0.05 was considered significant. Data are presented as the means ± SEM.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Induction of LUTEB in awake animals did not change heart rate, mean arterial pressure (MAP) or left atrial pressure (Table 1).


View this table:
[in this window]
[in a new window]
  		Table 1. Hemodynamic Variables in Awake and Propofol-Anesthetized Dogs Before and After Induction of Thoracic Epidural Anesthesia
 
Propofol anesthesia did not change MAP or left atrial pressure, but led to a significant increase of heart rate, compared with baseline that was abolished by the induction of LUTEB. In propofol-anesthetized animals, LUTEB decreased MAP.

The results of splanchnic blood flow determinations are shown in Table 2. After induction of LUTEB in awake animals, blood flow to the stomach, spleen, pancreas, jejunum, and liver was not changed, compared with baseline. Propofol did not alter blood flow to the splanchnic organs, but led to an increase of blood flow to the liver. LUTEB did not induce further changes compared with propofol alone.


View this table:
[in this window]
[in a new window]
  		Table 2. Thoracic Epidural Anesthesia (TEA): Blood Flow (mL · g-1 · min-1) to Splanchnic Organs in Awake and Propofol-Anesthetized Dogs
 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
The combination of general anesthesia with central neuraxis blockade, such as epidural anesthesia, has increased within recent years. This combined technique offers a potent blockade of surgical stimuli and a protective effect on coronary perfusion (13,14) and cardiac workload (15). TEA has been established as an adjunct to general anesthesia in thoracic and abdominal procedures (16,17). Postoperatively, patient comfort is increased due to pain control. On the other hand, the desired beneficial effects of pain relief and sympathectomy in the blocked regions might be accompanied by a potentially harmful increase in sympathetic activity in unblocked regions (7).

The sympathetic fibers innervating abdominal organs originate from T8-L1. Sympathetic activation leads to a decrease in motility and decreased blood supply of splanchnic organs (7). The study design was chosen to determine all effects without the confounding influence of acute surgical trauma. Due to the technique used and the verification of the spread of the local anesthetic above T5, it can be assumed that LUTEB-induced sympathetic blockade of T1-5 spared most splanchnic sympathetic fibers. Thus, LUTEB in our study could be expected to lead to an increase of splanchnic sympathetic activity.

Aside from direct measurement of sympathetic activity in cats during lumbar and thoracic epidural anesthesia (7), the effect of an increase in sympathetic activity has been shown for forearm vascular tone in humans during lumbar epidural anesthesia (19). Due to compensatory vasoconstriction, pulse oximetry during lumbar anesthesia delivers falsely low SpO2 readings due to reduced flow when the sensor is placed at the upper limbs (9).

The effect of "epidurally administered" local anesthetics on the autonomic nervous system is not only mediated by the effect of the blockade alone, but also by the systemic effects of local anesthetics (20). Such an effect from lidocaine is unlikely, because the bolus dose we applied was three times lower than that used by Yoneda et al. (21) to induce an attenuation of arterial baroreflex control in dogs. In further contrast to our study, their bolus was followed by a continuous infusion.

Changes of blood flow during LUTEB and TEA may be the consequence of two different effects that need to be distinguished. The first is a change in general hemodynamic status; the second is a change in the resistance of the blood vessels due to sympatholysis or sympathetic activation. Greitz et al. (22,23) demonstrated these two opposing effects on hepatic venous and arterial blood flow, which are both responsible for hepatic oxygenation. High epidural anesthesia leading to a complete sympathetic block reduces mainly liver venous blood flow (22), which was restored by the application of ephedrine (23). In this context, two opposite effects exert their influence. The hemodynamic effect leads to decreased blood flow counteracted by a decreased resistance, increasing blood flow. Hepatic oxygen uptake is decreased and despite this, oxygen extraction is increased. If vascular perfusion pressure remains constant, epidural anesthesia involving splanchnic innervation leads to an increase of intestinal blood flow (2). On the other hand, positive end-expiratory pressure ventilation lowering blood pressure aggravates the effects of TEA (24). The splanchnic perfusion is not only determined by the extent of the drop in blood pressure, but also by the composition of the local anesthetic. Kennedy et al. (25) found a decrease of splanchnic perfusion to the same extent using either lidocaine-adrenaline or plain lidocaine.

In patients undergoing various types of large bowel epidural anesthesia at lower thoracic segments or high lumbar segments, this lead to an increase in intestinal blood flow due to sympathetic nerve blockade (26).

In our study, however, where blood pressure remained unchanged, blood flow to the splanchnic organs was unaltered. This is in contrast to the studies cited herein in which the block extended to a larger number of segments. It can be postulated that sympathetic blockade of the upper thoracic segments did not affect the splanchnic circulation in this experimental model and that high TEA might not jeopardize the perfusion of splanchnic organs.

LUTEB was also investigated in propofol-anesthetized dogs, because propofol is often used as a hypnotic drug during anesthesia or for sedation in intensive care settings. Propofol was administered to achieve a plasma-level suppressing movement after skin incision, which is 6 µg/mL in dogs and humans (27,28). The rate of infusion in dogs is 30 mg · kg-1 · h-1, higher than in humans due to different pharmacokinetic properties (28). Propofol does not affect splanchnic blood flow in normal rats (29) or dogs (30). This is in accordance with our findings. The main influence is exerted on the liver. Carmichael et al. (29) found an increase in liver oxygen consumption that was fully compensated by an increase in oxygen delivery. In our setting, propofol increased liver blood flow. This increase was achieved despite a significantly lower MAP after LUTEB in propofol-anesthetized animals. Nor was any further effect seen after induction of LUTEB in the other splanchnic organs.

This study in awake and anesthetized dogs shows no adverse effects of LUTEB on the splanchnic circulation. Further studies are needed to investigate effects in humans, for instance by using measurements of intramucosal PCO2 (31).


   Acknowledgments
 
We appreciate the editorial assistance of Henry Querfurth (Boston, MA) in the preparation of this manuscript.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Liu S, Carpenter RL, Neal JM. Epidural anesthesia and analgesia. Their role in postoperative outcome. Anesthesiology 1995;82:1474–506.[Web of Science][Medline]
  2. Lundberg J, Biber B, Delbro D, et al. Effects of dopamine on intestinal hemodynamics and motility during epidural analgesia in the cat. Acta Anaesthesiol Scand 1989;33:487–93.[Web of Science][Medline]
  3. Brodner G, Pogatzki E, Van Aken H, et al. A multimodal approach to control postoperative pathophysiology and rehabilitation in patients undergoing abdominothoracic esophagectomy. Anesth Analg 1998;86:228–34.[Abstract]
  4. Liem TH, Booij LH, Hasenbos MA, et al. Coronary artery bypass grafting using two different anesthetic techniques. Part I. Hemodynamic results. J Cardiothorac Vasc Anesth 1992;6:148–55.[Medline]
  5. Loick HM, Schmidt C, Van Aken H, et al. High thoracic epidural anesthesia but not clonidine attenuates the perioperative stress response via sympatholysis and reduces the release of troponin T in patients undergoing CABG. Anesth Analg 1999;88:701–9.[Abstract/Free Full Text]
  6. Perugini RA, Orr RK, Porter D, et al. Gastrointestinal complications following cardiac surgery. An analysis of 1477 cardiac surgery patients. Arch Surg 1997;132:352–7.[Abstract/Free Full Text]
  7. Taniguchi M, Kasaba T, Takasaki M. Epidural anesthesia enhances sympathetic nerve activity in the unanesthetized segments in cats. Anesth Analg 1997;84:391–7.[Abstract]
  8. Bengtsson M, Nilsson GE, Lofstrom JB. The effect of spinal analgesia on skin blood flow, evaluated by laser Doppler flowmetry. Acta Anaesthesiol Scand 1983;27:206–10.[Web of Science][Medline]
  9. Peduto VA, Tani R, Pani S. Pulse oximetry during lumbar epidural anesthesia: reliability of values measured at the hand and the foot. Analg 1994;78:921–4.[Abstract/Free Full Text]
  10. Saada M, Duval AM, Bonnet F, et al. Abnormalities in myocardial segmental wall motion during lumbar epidural anesthesia. Anesthesiology 1989;71:26–32.[Web of Science][Medline]
  11. Krantz EM, Viljoen JF, Gilbert MS. Prinzmetal’s variant angina during extradural anaesthesia. Br J Anaesth 1980;52:945–9.[Abstract/Free Full Text]
  12. Wieland W, Wouters P, Van Aken H, et al. Measurement of organ blood flow with coloured microspheres: a first time-saving improvement using automated spectrophotometry. Proc Comp Cardiol 1993;1:691–4.
  13. Blomberg S, Curelaru I, Emanuelsson H, et al. Thoracic epidural anaesthesia in patients with unstable angina pectoris. Eur Heart J 1989;10:437–44.[Abstract/Free Full Text]
  14. Blomberg S, Emanuelsson H, Kvist H, et al. Effects of thoracic epidural anesthesia on coronary arteries and arterioles in patients with coronary artery disease. Anesthesiology 1990;73:840–7.[Web of Science][Medline]
  15. Hogan Q. Cardiovascular response to sympathetic block by regional anesthesia. Reg Anesth 1997;21:26–34.
  16. Rolf N, Möllhoff T. Epidural anaesthesia for the CABG patient. Curr Opin Anaesthesiol 1997;10:17–20.
  17. Meissner A, Rolf N, Van Aken H. Thoracic epidural anesthesia and the patient with heart disease: benefits, risks, and controversies. Anesth Analg 1997;85:517–28.[Web of Science][Medline]
  18. Udassin R, Eimerl D, Schiffman J, et al. Epidural anesthesia accelerates the recovery of postischemic bowel motility in the rat. Anesthesiology 1994;80:832–6.[Web of Science][Medline]
  19. Baron JF, Payen D, Coriat P, et al. Forearm vascular tone and reactivity during lumbar epidural anesthesia. Anesth Analg 1988;67:1065–70.[Web of Science][Medline]
  20. Nishikawa K, Fukuda T, Yukioka H, et al. Effects of intravenous administration of local anesthetics on the renal sympathetic nerve activity during nitrous oxide and nitrous oxide-halothane anesthesia in the cat. Acta Anaesthesiol Scand 1990;34:231–6.[Web of Science][Medline]
  21. Yoneda I, Nishizawa M, Benson KT, et al. Attenuation of arterial baroreflex control of renal sympathetic nerve activity during lidocaine infusion in alpha-chloralose-anesthetized dogs. Anaesthesiol Scand 1994;38:70–4.
  22. Greitz T, Andreen M, Irestedt L. Haemodynamics and oxygen consumption in the dog during high epidural block with special reference to the splanchnic region. Acta Anaesthesiol Scand 1983;27:211–7.[Web of Science][Medline]
  23. Greitz T, Andreen M, Irestedt L. Effects of ephedrine on haemodynamics and oxygen consumption in the dog during high epidural block with special reference to the splanchnic region. Acta Anaesthesiol Scand 1984;28:557–62.[Web of Science][Medline]
  24. Feuk U, Jakobson S, Norlen K. Central haemodynamics and regional blood flows during thoracic epidural analgesia combined with positive pressure ventilation. An experimental study in the pig. Acta Anaesthesiol Scand 1987;31:479–86.[Web of Science][Medline]
  25. Kennedy WF Jr, Everett GB, Cobb LA, et al. Simultaneous systemic and hepatic hemodynamic measurements during high peridural anesthesia in normal man. Anesth Analg 1971;50:1069–77.[Medline]
  26. Johansson K, Ahn H, Lindhagen J, et al. Effect of epidural anaesthesia on intestinal blood flow. Br J Surg 1988;75:73–6.[Web of Science][Medline]
  27. Shafer A, Doze VA, Shafer SL, et al. Pharmacokinetics and pharmacodynamics of propofol infusions during general anesthesia. Anesthesiology 1988;69:348–56.[Web of Science][Medline]
  28. Nolan A, Reid J. Pharmacokinetics of propofol administered by infusion in dogs undergoing surgery. Br J Anaesth 1993;70:546–51.[Abstract/Free Full Text]
  29. Carmichael FJ, Crawford MW, Khayyam N, et al. Effect of propofol infusion on splanchnic hemodynamics and liver oxygen consumption in the rat. A dose-response study. Anesthesiology 1993;79:1051–60.[Web of Science][Medline]
  30. Kick O, Van Aken H, Wouters PF, et al. Vital organ blood flow during deliberate hypotension in dogs. Anesth Analg 1993;77:737–42.[Abstract/Free Full Text]
  31. Knichwitz G, Rotker J, Brüssel T, et al. A new method for continuous intramucosal PCO2 measurement in the gastrointestinal tract. Anesth Analg 1996;83:6–11.[Abstract]
Accepted for publication July 27, 1999.




This article has been cited by other articles:


Home page
 Anesth. Analg.Home page
D. A. Vagts, T. Iber, M. Puccini, B. Szabo, J. Haberstroh, F. Villinger, K. Geiger, and G. F. E. Noldge-Schomburg
The Effects of Thoracic Epidural Anesthesia on Hepatic Perfusion and Oxygenation in Healthy Pigs During General Anesthesia and Surgical Stress
Anesth. Analg., December 1, 2003; 97(6): 1824 - 1832.
[Abstract] [Full Text] [PDF]

Home page
 Br J AnaesthHome page
T. H. Gould, K. Grace, G. Thorne, and M. Thomas
Effect of thoracic epidural anaesthesia on colonic blood flow
Br. J. Anaesth., September 1, 2002; 89(3): 446 - 451.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a colleague
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (10)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Meissner, A.
Right arrow Articles by Rolf, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Meissner, A.
Right arrow Articles by Rolf, N.

Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press