To the Editor:—

We thank Dr. Magnúsdóttir et al.  1for their recent clinical investigation, which appeared in Anesthesiology. We agree with their findings of incomplete sympathetic blockade after high thoracic epidural anesthesia (TEA). As they pointed out, their results were in opposition to previous work by others 2who reported complete sympathetic blockade with the same TEA technique. We also believe that Magnúsdóttir et al.  1have correctly warned against relying solely on indirect measurement techniques to identify sympathetic activity in humans. Magnúsdóttir et al.  1instead used a microneurographic technique, which is a direct measure of sympathetic nerve (peroneal) activity, and pointed out that the conflicting work 2used an indirect thermographic measurement technique. It is interesting that these same authors, 2referred to by Magnúsdóttir et al. , 1had previously warned against our use of heart rate variability (HRV) 3–5as a measurement technique to follow sympathetic activity after spinal anesthesia. This rejection of HRV was based on their inability to show changes in low-frequency oscillations 6,7after TEA, whereas simultaneous thermographic measurements resulted in changes believed to be consistent with complete sympathetic blockade. 2At that time, we suggested that the different results of HRV versus  thermography techniques might be caused by incomplete cardiac sympathetic blockade after TEA, 5and we believe the results of Magnúsdóttir et al.  1now support this explanation.

Magnúsdóttir et al.  1suggest that much of the hemodynamic stability during thoracic epidural results from incomplete sympathetic block above and below the epidural segment. Although we agree with this concept, we disagree with the assumption by Magnúsdóttir et al.  1that TEA completely inhibits cardiac sympathetic activity. HRV measurements indicate that cardiac sympathectomy may not be as common as was once thought. 4,5Although HRV is an indirect measurement of sympathetic activity, it is a technique that is cardiac specific because it uses the heart as the end organ or effector. Because of the complexity and overlap of sympathetic afferent and efferent pathways, it is possible that some sympathetic fibers remain untouched by the epidural anesthetic and could maintain innervation to the heart. Sympathetic preganglionic fibers originate in the intermediolateral cell column of the spinal cord and exit via  the ventral nerve roots at levels from T1 to L2 or L3. Although the epidural sensory blockade of the dermatomes achieved by Magnúsdóttir et al.  1incorporates the spinal segments thought to contribute to cardiac sympathetic fibers, T1–T4, other less direct pathways to and from the heart could still remain. Sympathetic fibers above and below the segment of epidural anesthesia could travel cephalad or caudad within the sympathetic chain and, in addition to maintaining innervation outside the area of segmental block, 1could continue to innervate the heart, therefore explaining previous HRV data. 4,5 

Certainly, measurement of actual neural activity (direct technique) is superior to measurement of effector organ function (indirect techniques) when it is performed correctly. However, microneurographic techniques, as used by Magnúsdóttir et al. , 1are very difficult and invasive and have limited application in clinical research. Therefore, all the methods of measuring sympathetic nerve activity have their pitfalls. Nevertheless, we believe we are justified in saying that careful use of direct and indirect measurement techniques can provide useful information about sympathetic activity during spinal and epidural anesthesia. Finally, we believe that this article by Magnúsdóttir et al.  1correctly points out that many of the inconsistencies that are found in reports of the sympathetic effects by different anesthetic techniques are a result of the method of measuring sympathetic activity and its interpretation.

Magnúsdóttir H, Kirno K, Ricksten S-E, Elam M: High thoracic epidural anesthesia does not inhibit sympathetic nerve activity in the lower extremities. A nesthesiology 1999; 91:1299–304
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Introna R, Yodlowski E, Pruett J, Montano N, Porta A, Crumrine R: Sympathovagal effects of spinal anesthesia assessed by heart rate variability analysis. Anesth Analg 1995; 80:315–21
Hopf H-B, Skyschally A, Heusch G, Peters J: Low-frequency spectral power of heart rate variability is not a specific marker of cardiac sympathetic modulation. A nesthesiology 1995; 82:609–19
Introna RPS, Montano N, Yodlowski EH, Martin DC, Pruett JK, Crumrine RS: Low-frequency component of heart rate variability. A nesthesiology 1995; 83:884–7
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Montano N, Ruscone TG, Porta A, Lombardi F, Pegani M, Malliani A: Power spectrum analysis of heart rate variability to assess the changes in sympathovagal balance during orthostatic tilt. Circulation 1994; 90:1826–31