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Correspondence  |   July 2000
Measurement of Sympathetic Blockade: Effect of Epidural and Spinal Anesthesia
Author Notes
  • Consultant in Anesthesiology
  • Akureyri Central Hospital
  • Akureyri, Iceland
  • Director
  • klaus.kirno@medfak.gu.se
  • Professor
  • Department of Cardiothoracic Anesthesiology and Intensive Care
  • Associate Professor
  • Department of Clinical Neurophysiology
  • Sahlgrenska University Hospital
  • University of Göteborg
  • Göteborg, Sweden
Article Information
Correspondence
Correspondence   |   July 2000
Measurement of Sympathetic Blockade: Effect of Epidural and Spinal Anesthesia
Anesthesiology 7 2000, Vol.93, 302-303. doi:
Anesthesiology 7 2000, Vol.93, 302-303. doi:
In Reply:—
We appreciate the interest and comments expressed by Drs. Introna, Blair, Martin, and Yodlowski. We fully agree that indirect methods of measuring sympathetic nerve activity can provide useful, qualitative information. Quantification of sympathetic nerve activity, however, is difficult with these techniques.
The main issue raised by Introna et al.  is whether a high thoracic epidural anesthesia (TEA) completely inhibits cardiac sympathetic activity. Based on studies measuring heart rate variability, these authors are convinced that TEA with T1–T5 sensory blockade does not result in complete cardiac sympathetic blockade. However, a comparative study of heart rate variability, cardiac norepinephrine spillover, and muscle sympathetic nerve activity in humans by Kingwell et al.  1 invites some caution because it showed heart rate variability to be dependent on multiple factors in addition to cardiac sympathetic nerve activity and not directly related to cardiac norepinephrine spillover.
The degree of thoracic sympathetic blockade was not specifically addressed in our recent study, 2 which was primarily aimed at evaluating sympathetic function caudal to the TEA-induced sensory blockade and showed no sign of sympathetic blockade. However, previous microneurographic studies of lumbar epidural and spinal anesthesia have shown a fairly close relation between the extent of sensory and sympathetic blockade. 3,4 Because the nerves to internal organs are not accessible to microneurographic recording in humans, we previously used biochemical measurements of nerve transmitter release to quantify cardiac sympathetic nerve activity. 5 We used an isotope dilution technique with radiolabeled norepinephrine to demonstrate that TEA prevented the sympathetically mediated surgical stress response during coronary artery bypass surgery. Although this finding could be explained by an afferent nociceptive blockade or an efferent blockade of cardiac sympathetic nerve fibers, supportive evidence for the existence of a cardiac sympathetic blockade after TEA has been provided by Taniguchi et al.  , 6 who directly measured efferent cardiac sympathetic nerve activity after TEA in an experimental study on cats. Our recent finding 2 that vasomotor and sudomotor reflexes were abolished in the hands but remained in the feet after TEA also suggests a thoracic sympathetic blockade. Therefore, although we agree with Introna et al.  that “sympathetic fibers above and below the segment of epidural anesthesia could travel cephalad or caudad within the sympathetic chain” and “continue to innervate the heart,” we remain convinced that TEA can abolish sympathetic reflexes within thoracic segments.
References
Kingwell BA, Thompson JM, Kaye DM, McPherson GA, Jennings GL, Esler MD: Heart rate spectral analysis, cardiac norepinephrine spillover, and muscle sympathetic nerve activity during human sympathetic nervous activation and failure. Circulation 1994; 90:234–40Kingwell, BA Thompson, JM Kaye, DM McPherson, GA Jennings, GL Esler, MD
Magnúsdóttir H, Kirnö K, Ricksten S-E, Elam M: High thoracic epidural anesthesia does not inhibit sympathetic nerve activity in the lower extremities: A nesthesiology 1999; 91:1299–304Magnúsdóttir, H Kirnö, K Ricksten, S-E Elam, M
Lundin S, Kirnö K, Wallin BG, Elam M: Effects of epidural anaesthesia on sympathetic outflow to the skin. Acta Anaesthesiol Scand 1990; 34:492–7Lundin, S Kirnö, K Wallin, BG Elam, M
Kirnö K, Lundin S, Elam M: Effects of intrathecal morphine and spinal anesthesia on sympathetic nerve activity in humans. Acta Anaesthesiol Scand 1993; 37:54–9Kirnö, K Lundin, S Elam, M
Kirnö K, Friberg P, Grzegorczyk A, Milocco I, Ricksten S-E, Lundin S: Thoracic epidural anesthesia during coronary artery bypass surgery: Effects on cardiac sympathetic activity, myocardial blood flow and metabolism, and central hemodynamics. Anesth Analg 1994; 79:1075–81Kirnö, K Friberg, P Grzegorczyk, A Milocco, I Ricksten, S-E Lundin, S
Taniguchi M, Kasaba T, Takasaki M: Epidural anesthesia enhances sympathetic nerve activity in the unanesthetized segments in cats. Anesth Analg 1997; 84:391–7Taniguchi, M Kasaba, T Takasaki, M