Anesth Analg 1999;88:67-71
© 1999 International Anesthesia Research Society
CRITICAL CARE AND TRAUMA
The Synergistic Effect of Sympathectomy and Hyperbaric Oxygen Exposure on Transcutaneous PO2 in Healthy Volunteers
P. S. Thomas, MD,
T. S. Hakim, PhD,
L. Q. Trang, MD,
S. I. Hosain, MD, and
E. M. Camporesi, MD
Department of Anesthesiology, State University of New York Health Science Center, Syracuse, New York
Address correspondence and reprints requests to P. S. Thomas, MD, Department of Anesthesiology, SUNY Health Science Center, 750 E. Adams St., Syracuse, NY 13210. Address e-mail to hschosp .umag.thomasp.
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Abstract
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The benefit of hyperbaric oxygen (HBO2) exposure is dependent on the oxygen delivery. Such benefit may be limited by the fact that hyperoxia causes vasoconstriction and decreases blood flow. The aim of this study was to determine whether regional sympathectomy attenuates this vasoconstriction response and thus improves oxygen delivery. In a double-blinded manner, healthy volunteers were subjected to HBO2 in a monoplace chamber on two occasions separated by at least 1 wk. Transcutaneous oxygen (tcPO2) and carbon dioxide (tcPCO2) on the forearm were monitored continuously, and blood flow in the axillary artery was measured using angiodynography before and after exposure to HBO2. During one visit, each volunteer received a sympathetic block to the upper extremity by an injection of lidocaine into the brachial plexus at the axilla. During a second visit, the volunteer received a placebo injection of isotonic sodium chloride solution into the brachial plexus of the same side. Skin temperature was recorded on the back of the hand. All subjects exhibited a small but significant increase in skin temperature (2.5%) and in upper limb blood flow (23%) (P < 0.05%) after sympathectomy, but not after isotonic sodium chloride solution injection. Sympathectomy increased tcPO2 marginally while in room air. However, during HBO2, tcPO2 was substantially and significantly higher (409.8 ± 98.8 mm Hg) after sympathectomy compared with that after isotonic sodium chloride solution injection (171.3 ± 38.1 mm Hg). tcPCO2 did not change significantly after sympathectomy or during HBO2. Thus, sympathectomy presumably improved oxygen delivery by preventing vasoconstriction during hyperoxia. The results suggest that sympathectomy may be a useful adjunct to HBO2 therapy in patients in whom vascular resistance is increased because of sympathetic tone or hyperoxia.
Implications: Sympathetic nerve block of the extremities markedly enhances tissue oxygen delivery during hyperbaric oxygen treatment. Sympathectomy may be a beneficial adjunct treatment to hyperbaric oxygen in peripheral vascular insufficiency.
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Introduction
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During the past 40 yr, hyperbaric oxygen exposure (HBO2) has become a viable option for the treatment of diseases such as chronic nonhealing wounds, gas gangrene, compromised skin flaps, and reperfusion injuries (1,2). This therapy may be delivered by placing one or more patients inside a specially constructed chamber and filling the chamber with 100% oxygen at >2 atm. The efficacy of HBO2 therapy is documented by improvement of symptoms and by monitoring transcutaneous oxygen (tcPO2) (3,4). Hyperoxia, however, causes vasoconstriction (5) and may limit the delivery of oxygen to peripheral tissues. HBO2 also causes a reduction in cardiac output by 10%–20%, mainly due to bradycardia (1,5). Although volumetric blood flow may be reduced, tissue oxygen delivery is usually enhanced with consequent benefits. The vasoconstriction during HBO2 may impede the benefits and prolong treatment in some patients. Vascular tone and, hence, blood flow rate, is regulated by the continuous discharge of sympathetic nerve activity. Therefore, sympathectomy (chemical or surgical) could diminish vascular tone and improve blood flow and oxygen delivery. Indeed, sympathectomy is thought to be beneficial in the treatment of peripheral vascular diseases with increased sympathetic system activity and in arterial insufficiency, especially when limb ischemia cannot be corrected by vascular surgery (6–9).
The goal of our study was to determine whether a combination of sympathectomy and HBO2 therapy could be used to maximize oxygen delivery to the tissue. We assessed the effects of chemical sympathectomy of the upper extremity on tcPO2 tension during HBO2 therapy in healthy volunteers. Our results suggest that sympathectomy potentiates tcPO2 during HBO2 and that it therefore may be a useful adjunct to HBO2 in patients with increased vascular tone.
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Methods
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After receiving institutional review board approval, we studied 10 volunteers (2 female, 8 male) 23–40 yr old, each of whom gave informed, written consent to participate. The volunteers were all healthy and were not taking any medication for heart, arterial blood pressure, or circulatory disease. The subjects were studied while in the supine position on two separate occasions, with an interval of at least 1 wk. The subjects were asked to refrain from using any medication for 24 h before each study.
Each volunteer received one injection to the brachial plexus in the axillary region on each of the two visits. One injection was isotonic sodium chloride solution (20 mL) and the other was 1% lidocaine (20 mL). During the two visits, the same limb was studied, and the order of the two injections was randomized. Neither the subject nor the investigators were aware of which medication was being injected on each day. Every subject had an IV line placed in the contralateral limb. The injections were performed using a 22-gauge, B-bevel regional block needle directed toward the brachial plexus in the axilla. The investigator attempted to elicit paraesthesia referred to the hand. When paresthesia was elicited, the solution (isotonic sodium chloride solution or lidocaine) was injected with repeated negative aspiration to confirm the lack of bleeding. All injections were performed by one investigator (PST).
After injection of the solution, the subjects were introduced into the chamber in the supine position and exposed to HBO2 inside a monoplace lucite hyperbaric chamber. The volunteers remained in the chamber for 60 min. The chamber was pressurized slowly (15 min with 100% oxygen to a pressure of 2 atm), and then decompressed slowly (15 min to atmospheric pressure). This protocol is in accordance with the normal clinical practice at our institution for HBO2 therapy.
A series of measurements was made before each injection and after removal from the hyperbaric chamber. The skin temperature of both arms was monitored by placing thermistors on the back of both hands between the first and second knuckles (Monotherm 6500; Mallinckrodt, St Louis, MO). This allowed us to compare responses between the limb receiving the injectate and the contralateral control limb that did not receive it. The skin temperatures were recorded at 5-min intervals. tcPO2 and transcutaneous carbon dioxide (tcPCO2) tensions were monitored continuously. Data from the transcutaneous probe were also recorded at 5-min intervals. The probe was applied carefully using transparent adhesive dressings, and the temperature of the skin under the probe was set at 40°C. The tcPO2 and tcPCO2 probe was placed approximately 9 cm proximal to the wrist on the medial side of the arm being injected. Blood pressure and pulse rate were recorded continuously from the contralateral arm at 5-min intervals using an automated blood pressure machine. Recording of these measurements began just before each injection and ended after the subject was removed from the hyperbaric chamber. Regional blood flow of the extremity that was being injected was measured by angiodynography using an HDI Ultramark 9 machine (Advanced Technology Laboratory, Bothell, WA). This device uses Doppler ultrasound to measure blood flow velocity and vessel diameter. These measurements were performed at three time points outside the chamber before and after sympathectomy and after the removal from the hyperbaric chamber. Data on the subclavian, axillary, and brachial arteries were acquired. The blood velocity and vessel diameter were both measured. The product of vessel area cross-sectional area and velocity was used to calculate blood flow in the vessel. All angiodynography measurements were performed by a single operator.
Results were analyzed by using analysis of variance and a paired t-test. Because of the separation in time between the measurements, a paired Student's t-test was used primarily to test for differences before and after each intervention. A P value <0.05 was considered significant.
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Results
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All subjects exhibited evidence of sympathetic blockade after lidocaine administration into the brachial plexus. A significant (P < 0.05) increase in skin temperature from 30.7 ± 0.8°C to 31.5 ± 0.9°C (Table 1) and a 23% increase in axillary blood flow from 23.7 ± 3.9 to 29.1 ± 4.9 mL/s were observed after sympathectomy, but not after isotonic sodium chloride solution injection (Fig. 1). The increase in axillary flow was caused by a combination of moderate and nonsignificant changes in diameter and velocity. The changes in temperature and flow further confirmed the effectiveness of sympathetic blockade in the arm. The isotonic sodium chloride solution injection did not affect skin temperature; in fact, it decreased axillary blood flow from 24.2 ± 4.7 to 17.4 ± 1.8 mL/s. The flow in the axillary artery was substantially higher after sympathectomy than after isotonic sodium chloride solution injection (P < 0.05). The changes in brachial artery and in subclavian artery flow (not shown) did not reach statistical significance. tcPCO2, mean blood pressure, and heart rate did not change significantly after the administration of lidocaine (Table 1).
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Figure 1. Changes in axillary artery hemodynamics using angiodynography during baseline (BL) and after the injection of isotonic sodium chloride solution (S) or lidocaine (L). Values are mean ± SE. n = 10. *Significant difference from the value after the administration of isotonic sodium chloride solution (P < 0.05).
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After sympathectomy, tcPO2 in room air increased marginally (from 41.0 ± 5.9 to 53.7 ± 8.1 mm Hg), whereas the isotonic sodium chloride solution injection had no effect (from 46.9 ± 6.3 to 41.3 ± 4.2 mm Hg) (Fig. 2). During HBO2 exposure, there was a substantial increase in tcPO2. After isotonic sodium chloride solution injection, tcPO2 increased during HBO2 exposure (from 41.3 ± 4.2 to 171.3 ± 38.1 mm Hg) (P < 0.05), but after sympathectomy, there was a much larger increase in tcPO2 (from 53.7 ± 8.1 to 409.8 ± 98.9 mm Hg). The tcPO2 value during HBO2 was significantly higher after sympathectomy than after the isotonic sodium chloride solution injection (P < 0.05). tcPCO2 did not change significantly during HBO2 exposure. The mean blood pressure was slightly increased, and the heart rate was slightly depressed during HBO2 exposure, but neither reached statistical significance.
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Figure 2. Transcutaneous PO2 (tcPO2) during baseline (BL1 and BL2), after the injection of isotonic sodium chloride solution (S) or lidocaine (L), and during exposure to hyperbaric oxygen (HBO). Values are mean ± SE. n = 10. *Significant difference from baseline value. tcPO2 during L + HBO was significantly higher than that during S + HBO (P < 0.05).
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Discussion
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The main finding in this study is that sympathectomy and HBO2 act synergistically to improve oxygen delivery to tissues, as suggested by tcPO2. This finding is consistent with data from patients with ischemia in lower extremities secondary to arteriosclerosis or thromboangiitis obliterans (10). Our results suggest that chemical sympathectomy may be a useful adjunct to HBO2 exposure.
The tcPO2 probe was developed by Huch et al. (11,12), and its reliability has been discussed previously (13,14). This probe is a modified Clark polographic device that incorporates a heating element and a thermistor. The heating element maintains the temperature of the skin under the probe constant at a selected temperature between 40 and 44°C. The heating of the skin causes local vasodilatation of the microvascular bed and capillaries, thus enhancing oxygen diffusion through the skin. The value of the tcPO2 may be influenced by local properties of the skin location, but the changes reflect changes in blood flow or arterial oxygen tension and, hence, oxygen delivery to the tissues. To avoid the influences of skin properties, the probe was placed at the same site during the two visits, and the changes in tcPO2 were evaluated. The tcPO2 probe has been used heavily in neonatal medicine as an indicator of arterial oxygen tension (13). In adults, tcPO2 is approximately 75%–80% of PaO2 but could vary due to tissue properties. Although there may be some differences in the tcPO2 values depending on the site, there is minimal variability within the same general location (14). Our values for tcPO2 while patients breathed room air and during HBO2 are consistent with other reported values (10,13–16).
The increase in tcPO2 seen after sympathetic block reflects the vasodilation response of the limb. The response to sympathectomy was confirmed by the increases in skin temperature, blood flow, and tcPO2. Lidocaine may influence blood flow in the arm secondary to its action on the central nervous system. However, such effects were apparently minimal because the temperature in the contralateral arm was unaffected and the blood pressure and heart rate remained constant. Despite some problems, sympathectomy is beneficial in peripheral vascular diseases, especially when the disease in not amendable by vascular surgery (6–9). Sympathectomy increases blood flow and oxygen delivery to the cells and enhances diffusion of oxygen between the capillaries and the skin surface. One study (17) has shown that sympathectomy improved tcPO2 but did not improve oxygen delivery in a canine model, presumably because of the opening of arterial-venous shunt pathways. This may explain some of the negative findings with sympathectomy (18). By using angiodynography, we were able to demonstrate increases in axillary artery blood flow. In patients, sympathectomy provides overwhelming benefits, as indicated by pain level at rest, accelerated tissue recovery, and improved oxygen delivery (6–9).
The changes in tcPO2 may be somewhat confounded by the fact that heating is required to vasodilate the capillary bed and to improve oxygen diffusion. Vasodilation caused by heating would make the region under the probe less likely to further vasodilate after sympathectomy. This may be why tcPO2 changed very little after sympathectomy. Nevertheless, the increase in blood flow to the arm after sympathectomy may cause a small increase in blood flow in the region under the probe and, consequently, increase tcPO2. The effect of temperature on the oxygen dissociation curve is automatically corrected to normal body temperature of 37°C.
In the healthy subjects who were included in the present study, the blood flow and oxygen delivery would be expected to be normal. In patients with peripheral vascular diseases, sympathetic tone may be altered; thus, the synergetic effect of sympathectomy may not be similar to the present results. The findings in the present study should not be extrapolated to patients who suffer from peripheral vascular disease and other conditions that may affect vascular tone. Some patients may have increased vascular tone secondary to increased sympathetic activity, whereas others may have depressed sympathetic tone. Sympathectomy is likely to be more beneficial in the former patients. The level of sympathetic tone and its effect on blood flow and oxygen delivery should be considered when sympathectomy is offered as a treatment option.
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Acknowledgments
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The authors thank C. Woodward, RN, and S. Petroff, RN, for their valuable assistance.
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References
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Accepted for publication October 19, 1998.
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Abstract
Introduction
