Anesth Analg 2004;98:37-39
© 2004 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
Endoscopic Thoracic Sympathectomy Suppresses Baroreflex Control of Heart Rate in Patients with Essential Hyperhidrosis
Yurie T. Kawamata, MD*,
Tomoyuki Kawamata, MD
,
Keiichi Omote, MD,
Eiji Homma, MD*,
Tatsuo Hanzawa, MD*,
Toshifumi Kaneko, MD
, and
Akiyoshi Namiki, MD
Departments of *Anesthesiology and
Surgery, Nippon Telegraph and Telephone East Japan Sapporo Hospital, Sapporo, Japan; and
Department of Anesthesiology, Sapporo Medical University School of Medicine, Sapporo, Japan
Address correspondence and reprint requests to Tomoyuki Kawamata, MD, Department of Anesthesiology, Sapporo Medical University School of Medicine, South 1, West 16, Chuo-ku, Sapporo, Hokkaido 060-8543, Japan. Address e-mail to kawamata{at}sapmed.ac.jp
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Abstract
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Endoscopic thoracic (T2-3 or T3-4) sympathectomy (ETS) is a highly effective treatment for palmar hyperhidrosis. Because the T2-3 or T3-4 sympathetic ganglia are involved in direct sympathetic innervation of the heart, sympathectomy at this level may alter baroreflex control of heart rate. The purpose of our study was to examine the influence of ETS on baroreflex responses to pressor and depressor stimuli under small-dose sevoflurane anesthesia. We studied 40 patients with palmar or axillary hyperhidrosis who were scheduled to receive ETS. In the ETS procedure, the sympathetic trunk was identified by using thoracic endoscopy and was transected. Before and after ETS, the pressor or depressor test was performed by using an IV infusion of phenylephrine or nitroglycerin, respectively, under small-dose general anesthesia. Baroreflex sensitivity was calculated from R-R intervals and systolic blood pressure. ETS did not change heart rate and systemic blood pressure at rest, although ETS significantly altered baroreflex in both pressor and depressor tests in all patients. Baroreflex was completely suppressed in 1 of 19 patients in the pressor test and in 9 of 21 patients in the depressor test. We conclude that baroreflex responses are suppressed in patients who receive ETS.
IMPLICATIONS: Endoscopic thoracic sympathectomy suppressed the baroreflex control of heart rate during pressor and depressor tests in patients with palmar or axillary hyperhidrosis.
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Introduction
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Primary palmar or axillary hyperhidrosis, which is characterized by an overfunction of the sympathetic nervous system (1) and complex autonomic dysfunction (2), has serious consequences for the social and professional life of an affected person. It is estimated that 0.6%–1.0% of the population has primary hyperhidrosis (3). Conventional medical therapies with anticholinergic drugs or topical aluminum chloride hexahydrate are inconvenient, unpleasant, and only temporarily effective (4). Bilateral endoscopic thoracic sympathectomy (ETS) is an effective and safe method with a high success rate for treating palmar or axillary hyperhidrosis, and most treated patients are satisfied with the long-term curative effect (3–5).
Because postganglionic sympathetic fibers originating from cell bodies residing in the cervicothoracic and upper thoracic ganglia participate in baroreflex regulation of the heart, it is possible that ETS suppresses baroreflex control of heart rate (HR), which is an important neuronal control system for the maintenance of cardiovascular stability in humans. There have been a few studies on the influences of ETS on exercise or postural changes in HR and its variability (1,6–8). In the perioperative setting, particularly during anesthetic management, it is important to understand the baroreflex control of HR with sudden increases or decreases in blood pressure in the patient undergoing ETS. The purpose of our study was to determine the influence of ETS on baroreflex control of HR to pressor or depressor stimuli in patients with palmar or axillary hyperhidrosis.
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Methods
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The study protocol was approved by our institution’s ethics committee, and we obtained written, informed consent from each patient. Forty patients with palmar or axillary hyperhidrosis (ASA physical status I) who were scheduled to undergo ETS under general anesthesia were enrolled in this study. None of the patients had cardiac disease or was taking any drug known to influence the cardiovascular or neuroendocrine systems. Each patient was premedicated with IM midazolam 3.0 mg 30 min before entering the operating room. Anesthesia was induced with IV propofol 2.0 mg/kg. Muscle relaxation was achieved with vecuronium 0.1–0.2 mg/kg, and the trachea was intubated with a double-lumen tracheal tube. Anesthesia was maintained with 1.5%–2.5% sevoflurane and 100% oxygen. Before the ETS procedure, 1.5–2.0 mL of 1% lidocaine with epinephrine (1:100,000) was injected into each incisional site. A small stab incision was then made in the third intercostal space below the axilla, and a cannula was introduced into the thoracic cavity. Approximately 0.7 L of carbon dioxide was insufflated through the cannula. Because of the elevated upper part of the body, the pneumothorax was located in the upper thoracic cavity. An electroresectoscope was then introduced through the same stab incision. After the sympathetic ganglia were identified at the second, third, and fourth dorsal rib heads, the T2-3 or T3-4 sympathetic ganglia were electrocoagulated for the treatment of palmar or axillary hyperhidrosis, respectively. The electrocoagulation of sympathetic ganglia was also performed on the contralateral side. All ETS procedures were performed by the same surgeon. Patients were randomized to either a pressor test group (n = 19) or a depressor test group (n = 21). Each test was performed before and after the bilateral ETS procedure. In the pressor and depressor tests, phenylephrine (1.6 mg/h) and nitroglycerin (4 mg/h), respectively, were infused IV to change systolic blood pressure (SBP) by 20–30 mm Hg. Each drug was diluted with 5% glucose solution (50 mL of 5% glucose containing 0.2 mg of phenylephrine or 0.5 mg of nitroglycerin). Before the baroreflex test, a resting period of at least 20 min after the induction of anesthesia and the end of surgery was allowed for stabilization of blood pressure and HR. During the baroreflex tests, end-tidal sevoflurane concentration was maintained at approximately 1.0% with use of a gas analyzer. Mechanical ventilation was adjusted to maintain the end-tidal carbon dioxide concentration at 35 mm Hg.
Values of the R-R intervals were obtained from electrocardiography (lead II), and SBP was measured through a radial arterial catheter. R-R intervals were plotted against the preceding arterial pulse, and the data from the pressor and depressor tests were analyzed by using least-squares linear regression. Baroreflex sensitivity was expressed as the slope of the regression line between the R-R interval and SBP. Only individual regression slopes with correlation coefficients of >0.8 were statistically analyzed. Fisher’s exact test and paired Student’s t-tests were used to analyze demographics, hemodynamic data, and baroreflex sensitivities. All values were expressed as means ± SD. A P value <0.05 was considered significant.
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Results
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The mean age, height, and weight of study participants were 23 yr, 162 cm, and 53 kg, respectively. Six of 19 in the pressor test group and 8 of 21 in the depressor group were male. There were no significant differences in age, body weight, height, or sex between the two groups of patients. Two patients in each group received T3-4 sympathectomy, and the remaining patients received T2-3 sympathectomy. The time to perform the ETS procedure was less than 30 min. Table 1 shows SBP and HR at rest and baroreflex sensitivity before and after ETS. In each group, there were no significant differences in SBP or HR at rest between before and after ETS.
In the pressor test, ETS significantly decreased baroreflex sensitivity in all patients (P < 0.0001). In 1 of 19 patients, phenylephrine did not show any changes in the R-R interval after ETS; that is, it showed a complete inhibition of baroreflex. In the depressor test, the ETS also significantly decreased baroreflex sensitivity in all patients (P = 0.0075). Nitroglycerin did not change the R-R interval at all in 9 of 21 patients after ETS; that is, it showed a complete inhibition of baroreflex. The number of patients in whom baroreflex was completely suppressed was more in the depressor test (nine patients) than in the pressor test (one patient) (P = 0.0094). All of the patients in whom the R-R interval was unchanged in each test had received T2-3 sympathectomy. They were excluded from least-squares linear regression analysis because correlation coefficients could not be calculated. After ETS, all patients showed the increases in skin temperatures of both palms and arms on thermography and showed the disappearance of sweating, indicating that sympathectomy was successful.
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Discussion
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Our results show that ETS suppressed baroreflex control of HR in both the pressor and depressor tests in patients with palmar or axillary hyperhidrosis under small-dose sevoflurane anesthesia. Because the baroreflex test was performed during anesthesia, several factors could have affected the results. We used midazolam, propofol, and sevoflurane, drugs that suppress baroreflex control of HR, for anesthetic management (9–11). Because these drugs are short-acting, we believe that midazolam and propofol would affect the baroreflex test before, rather than after, the ETS. Therefore, it is possible that the suppressive effects of ETS on the baroreflex were underestimated in our study. It has been reported that 2.0% sevoflurane suppresses baroreflex control of HR. Although the sevoflurane concentration was maintained at 1.0% during each test in our study, it is possible that baroreflex control of HR had already been suppressed to some degree before each test. In addition, noxious stimuli due to surgery may also modify baroreceptor-mediated circulatory responses (12). It seems that the effect of surgical stimuli was minimal in our study, because the ETS procedure is minimally invasive and because local anesthetic solution was injected at the incisional sites. Moreover, there were no significant differences in SBP and HR at rest before and after ETS.
In this study, baroreflex control of HR was completely inhibited in 9 of 21 patients in the depressor test but in only 1 of 19 patients in the pressor test. All patients who showed complete inhibition had received bilateral T2-3 sympathectomy. Responses to decreased blood pressure are mediated by the sympathetic nervous system, whereas responses to increased blood pressure predominantly involve vagal compensation (13). Therefore, it seems that the effects of sympathetic denervation were most prominent in the depressor test after ETS.
The suppression of baroreflex function can be detrimental during anesthetic management. In particular, a poorly preserved baroreflex response to decreasing blood pressure may exaggerate hemodynamic perturbation after a sudden loss of circulating blood volume. In addition, it is possible that patients who have received ETS will show unexpected HR responses after the administration of a vasopressor or vasodilator. We conclude that baroreflex response as a compensatory function for hemodynamic changes is suppressed in patients who receive ETS. Because several investigators have indicated that ETS produces long-term sympathetic denervation effects, it is possible that ETS suppresses the baroreflex control of HR to a sudden increase or decrease in blood pressure for the long-term. Conversely, it has been reported that an initial sympathovagal imbalance with a parasympathetic predominance after ETS is restored on a long-term basis (1). Therefore, further study on the long-term effect of ETS on baroreflex control of HR is necessary.
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References
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Accepted for publication August 21, 2003.
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Abstract
Introduction
