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Department of Anesthesia, Akita University School of Medicine, Akita-city, Japan
Address correspondence and reprint requests to Makoto Tanaka, MD, Department of Anesthesia, Akita University School of Medicine, Akita-city 010-8543, Japan. Address e-mail to mtanaka{at}med.akita-u.ac.jp
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Abstract |
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IMPLICATIONS: Cervical epidural anesthesia with lidocaine produces depressed heart rate variability and baroreflex control of heart rate, whereas lumbar epidural anesthesia exerts minimal effects on autonomic nervous system activity in conscious humans.
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Introduction |
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Spectral analysis of HR (HR variability; HRV) using fast Fourier transformation has been applied clinically in an attempt to interpret beat-to-beat dynamic modulation of R-R intervals (RRI) by the autonomic nervous system (6). The high-frequency (HF; 0.15–0.4 Hz) component of the HRV spectrum is considered to represent predominantly cardiovagal modulation of RRI, the low-frequency (LF; 0.04–0.15 Hz) component is considered to be under the influence of the both parasympathetic and sympathetic nervous system, and the LF/HF ratio is considered to reflect sympathetic predominance (7). During inordinately high levels of neuroaxial block, catastrophic cardiovascular complications, including profound bradycardia and hypotension, may occur, possibly as a result of an imbalance between sympathetic and parasympathetic control of the heart. However, the effects of high epidural block involving cardiac sympathectomy on HRV have not been addressed. Similarly, the effects of epidural anesthesia on cardiovagal baroreflex function have been poorly understood. Cardiac sympathectomy by cervicothoracic epidural anesthesia on baroreflex control of HR produced controversial results (8,9); one study showed significant depression of the HR response to hypertensive perturbation in awake volunteers, but the other showed a depressed HR response to a hypotensive stimulus in anesthetized subjects. On the other hand, lumbar epidural anesthesia with bupivacaine enhanced baroreflex control of HR because of unloading of cardiopulmonary receptors (10).
In this study, we hypothesized that cervical epidural anesthesia would produce an imbalance of cardiac autonomic status, i.e., an increase in the vagally-mediated HF component of HRV as a result of cardiac sympathectomy, whereas lumbar epidural anesthesia would cause sympathetic predominance. We also tested the hypothesis that blockade of the efferent cardiac sympathetic nerve by cervical epidural anesthesia would not affect tonic dynamic modulation of the cardiac cycle, because the time constant of the sympathetic nervous system is too long to affect beat-to-beat alteration of HR (11), whereas lumbar epidural anesthesia would augment indices of spontaneous sequence baroreflex (SBR) sensitivity, a proposed closed-loop technique for analyzing cardiovagal baroreflex responses (12).
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Methods |
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All patients arrived at the operating room at 9:00 AM after 10-h fast without premedication. They were placed in the supine position, and a 20-gauge IV catheter was inserted, by using local anesthetic, into a peripheral vein. IV infusion of lactated Ringer’s solution was then commenced and maintained at 10 mL · kg–1 · h–1 during the insertion of the epidural catheter and was continued until the end of the determinations of baroreflex sensitivities and HRV. Fluid temperature was maintained at approximately 30°C for both epidural groups of patients. Determinations of arterial blood pressure (BP) and RRI were made from radial arterial tonometric BP (Jentow-7700TM; Nihon Colin, Aichi, Japan) and an electrocardiography (ECG) lead of the highest signal-to-noise ratio (CMS 2000TM, Hewlett Packard, Boeblingen, Germany), respectively. Respiratory rate (RR) was determined at 1-min intervals by the impedance technique from the ECG signals, and the mean value during the HRV determination period was noted. Tympanic temperature was measured in each subject. No active warming was used, but the ambient temperature was set to 25°C–30°C.
Both HRV and SBR measurements were made with patients in the supine position before the epidural catheter was placed. Cervical epidural anesthesia was performed with an 18-gauge Tuohy needle (18-gauge Epidural MinipackTM; Portex, Kent, UK), and a 22-gauge catheter was advanced 3–5 cm in the cephalad direction by using the hanging-drop technique at the C6-7 interspace with the patient in the right lateral decubitus position. By injecting 3- to 5-mL increments of plain 1.5% lidocaine through the catheter, sensory analgesia from T1 to T5 to pinprick was obtained bilaterally. A lumbar epidural catheter was placed by using the same Tuohy needle at the L3-4 interspace by using the loss-of-resistance-to-air technique, and analgesia to pinprick was confirmed bilaterally at or below T10 by injecting 3- to 5-mL increments of the same lidocaine solution. No epidural test dose containing epinephrine was used. HRV measurements and SBR sensitivities were repeated with patients in the supine position when analgesic levels, as mentioned above, were confirmed at least 20 min after the last epidural injection of lidocaine. Those with an inadequate level of analgesia, when analgesic levels differed by more than two dermatomes between the right and left sides, and those who developed hypotension (systolic BP [SBP] <70% of resting values) requiring a vasopressor drug were excluded from subsequent data analysis. Arterial blood gas analysis was performed after each session of HRV determination before and after epidural anesthesia.
To assess baroreflex sensitivities by the SBR technique, recordings of spontaneous RRI and SBP lasting for a duration of 5 min were made. During this period, patients were in the supine position and were breathing spontaneously in a quiet environment. Readings were taken before and after epidural anesthesia. Recordings of ECG for HRV analysis were made similarly. BP and RRI were determined beat to beat, digitized, stored at a sampling rate of 200 Hz in a computer, and subsequently analyzed offline. A custom program developed to process the digitized data with a 16-bit analog/digital converter (AD7120; ATM Communications, Tokyo, Japan) detected R waves to determine RRI from the ECG signals. The recordings were also observed on an oscilloscope during transfer for elimination of nonsinus or artifactual signals caused by unanticipated movement of study subjects. Digital files were thus generated, with each column consisting of SBP, diastolic BP, mean BP, and RRI values for every cardiac cycle. These files were then used for power spectral analysis of HR and calculations of baroreflex sensitivities.
The method for spectral analysis of RRI variability has previously been explained (13). For each study period of HRV examination, a time series of 512 consecutive RRI data free of artifacts were selected. A fast Fourier transformation was applied to the tachogram to calculate the amplitude of variations of RRI as a function of frequency (power spectral density: RRI power [milliseconds squared] as a function of frequency [hertz]). The RRI power was the integrated area under the power spectral density plots as an index of the frequency-specific degree of RRI variability. Spectral power was determined over the LF (0.04–0.15 Hz) and HF (0.15–0.4 Hz) ranges, and the LF/HF ratio was calculated.
Cardiovagal baroreflex gain was determined by least-square regression analysis on the linear portion between SBP and RRI, when each RRI was plotted as a function of the preceding SBP (one offset). Estimating SBR sensitivity was based on spontaneous sequences containing three or more beats relating RRI and progressively changing SBP of the same direction with linear regression analysis (12). Up-sequence and down-sequence were defined as continually increasing and decreasing sequences, respectively. Only sequences in which successive pressure pulses differed by at least 1 mm Hg were selected. Correlation coefficients (R) of SBR sensitivities more than 0.8 were accepted. In addition, the baroreflex effectiveness index was calculated as described elsewhere (14).
All statistical analyses were performed by an investigator blinded to the treatment of patients. Because no previous study was available on the effect of high epidural block on HRV, power analysis was based on a previous study demonstrating a progressive increase in log HF power by 40% as the level of analgesia reached from lumbar to high thoracic dermatomes after spinal anesthesia (15). This analysis revealed that at least nine subjects would provide a power more than 0.9 (P = 0.05) for an approximately 40% difference in temporal changes of log-transformed HF power. Hemodynamic, HRV, and baroreflex data were analyzed by paired Student’s t-test to compare data before and after epidural anesthesia. Log transformation was used for nonnormally distributed data, such as HF and LF power, before the Student’s t-test was performed. Correlations between HRV indices and SBR sensitivities were analyzed by Pearson’s correlation coefficient. All data are presented as mean ± SD, and a P value < 0.05 was considered statistically significant.
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R 0.77; P < 0.05). However, no significant correlation was seen between the LF/HF ratio versus SBR sensitivity at any interval in either epidural group. |
Discussion |
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In contrast to diminutions of both HF and LF powers by cervical epidural anesthesia, lumbar epidural anesthesia appears to exert a minimal cardiac autonomic effect, with a slightly but significantly augmented LF/HF ratio and HR, suggesting sympathetic predominance. Unchanged SBR response in our study may also be explained by unchanged tonic dynamic modulation of the cardiac cycle by vagal activity, but this is in clear contrast to a previous study by Baron et al. (10), in which epidural bupivacaine increased both the pressor and depressor test slopes. This study also showed that application of lower body negative pressure restored reflex slopes back toward preepidural levels, indicating that the enhanced baroreflex sensitivity by lumbar epidural bupivacaine was due to the unloading of cardiopulmonary receptors (18). On the basis of these considerations, unaffected SBR sensitivities by lumbar epidural anesthesia in our study may be attributed to unaltered venous return by relatively rapid IV fluid infusion; the study by Baron et al. (10) did not specify the speed of fluid infusion.
The changes in HRV by lumbar epidural anesthesia seen in our study were consistent with a previous study, in which Fleisher et al. (19) reported an increase in the LF/HF ratio due to a small decrease in HF power and an increase in LF power in spontaneously breathing patients after lumbar epidural anesthesia with bupivacaine, even though the upper level of analgesia attained in their study was higher (T3) than in ours. However, the sympathovagal effects of spinal anesthesia on HRV revealed controversial results (15,20). Kawamoto et al. (15) studied serial changes in HRV in patients undergoing spinal anesthesia and found that a high thoracic level of analgesia (T4) was associated with decreases in LF power and the LF/HF ratio with augmented HF power. In contrast, Introna et al. (20) demonstrated that analgesic levels of T3 or higher were associated with increased HF power and unchanged LF power and LF/HF ratio. These conflicting results may arise from wide subject-to-subject variations of sympathetic/sensory differential and, thus, the extent of peripheral and cardiac sympathectomy associated with neuroaxial block (21). Considerable variations of autonomic indices, as reflected by large SDs in our study after lumbar epidural anesthesia, suggest that more patients would be necessary to draw a definitive conclusion regarding the influences of lumbar epidural technique on HRV.
Before and after epidural anesthesia, SBR sensitivities correlated well with HF components of HRV in most study circumstances. In addition, the attenuation of HF power after cervical epidural anesthesia was associated with significant depressions of both up- and down-sequence baroreflex sensitivities, whereas lumbar epidural anesthesia resulted in unchanged HF power and SBR sensitivities. The magnitude of the HF component of HRV corresponds to beat-to-beat dynamic modulation of vagal efferent activity and produces short-term alterations of RRI in relation to the frequency response of the baroreceptor reflex (22). Indeed, the extent of respiratory-related sinus arrhythmia and HF power has been related to cardiovagal reflex sensitivities in humans under experimental conditions including modulated autonomic balance (23). In our study, however, cardiovagal reflex gains were determined by the SBR technique. Compared with the "Oxford" method, by which RRI was related to either increased or decreased BP by IV injections of vasoactive drugs (24), the SBR technique identifies the spontaneous sequences of three or more consecutive cardiac cycles in which SBP and RRI either progressively increase (up-sequence) or decrease (down-sequence). The regression lines relating SBP and subsequent RRI provide their correlation and regression coefficients within naturally occurring BP excursions without direct influences of vasoactive drugs on the sinus node and baroreceptor transaction. However, spontaneous indices determined by the sequence method and cross-spectral analyses have recently been shown to have limits of agreement as large as the baroreflex gain itself, as determined by the modified Oxford technique (25). Moreover, spontaneous indices correlate strongly with respiratory sinus arrhythmia, but not with carotid distensibility, suggesting that they may reflect only vagally-mediated HR oscillations and, thus, may not have utility as surrogates for baroreflex sensitivity.
A possible criticism is that we examined the autonomic modulation of the cardiac cycle in healthy subjects before surgical procedures. In addition, hemodynamic alterations without epidural anesthesia over the same time period were not examined. Changes in HRV and baroreflex responses during surgery and the recovery period would be affected not only by coexisting disorders, but also by multiple anesthetic and nonanesthetic drugs during the perioperative period (26). Second, the cervical and lumbar epidural groups had significantly different mean ages and heights. Although our protocol was constructed in an attempt to elucidate autonomic effects by each epidural technique, aging depresses both baseline vagal activity and its responses to hemodynamic perturbations. Whether older patients would have fewer cardiovagal responses to either epidural technique remains to be determined. Third, SBP changes were determined by arterial tonometry rather than by an intraarterial catheter. However, the accuracy of the tonometric SBP is to 1 mm Hg, and the SBP values corresponded well to the intraarterial SBP in normotensive subjects for the range of pressure seen in our study (27). We have no reason to question the reliability of tonometric BP in healthy individuals with no evidence of peripheral vascular abnormalities. Furthermore, arterial tonometry has been used for determinations of SBR gains in conscious humans (28). Fourth, the interpretation of our results should be confined to the spread of cervical and lumbar epidural analgesia as described and when induced by lidocaine. Finally, although respiratory variables, especially RR, would have confounded the HF power of HRV, they were not controlled in our study. However, RR and PaCO2 remained virtually unchanged by either epidural technique, suggesting that the depth of respiration was not considerably altered by epidural anesthesia. Therefore, it is unlikely that respiratory variables exerted significant confounding effects on or affected the interpretation of HRV results (29).
In conclusion, cervical epidural anesthesia attenuated the HF and LF powers of HRV and SBR sensitivities. In a separate group of younger patients, lumbar epidural anesthesia exerted no effect on HF and LF powers or SBR indices. SBR sensitivities correlated well with HF power under most of our study conditions. Our results suggest that the SBR response closely reflects beat-to-beat dynamic modulation of the cardiac cycle by the parasympathetic nervous system during epidural anesthesia.
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This article has been cited by other articles:
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  W. A. Visser, R. A. Lee, and M. J. M. Gielen Factors Affecting the Distribution of Neural Blockade by Local Anesthetics in Epidural Anesthesia and a Comparison of Lumbar Versus Thoracic Epidural Anesthesia Anesth. Analg., August 1, 2008; 107(2): 708 - 721. [Abstract] [Full Text] [PDF]
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 M. Sato, M. Tanaka, S. Umehara, and T. Nishikawa Baroreflex control of heart rate during and after propofol infusion in humans Br. J. Anaesth., May 1, 2005; 94(5): 577 - 581. [Abstract] [Full Text] [PDF]
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R. P. S. Introna, J. R. Blair, and D. C. Martin Reflex Vagal Withdrawal After Sympathetic Blockade Anesth. Analg., April 1, 2005; 100(4): 1216 - 1216. [Full Text] [PDF]
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M. Tanaka Reflex Vagal Withdrawal After Sympathetic Blockade Anesth. Analg., April 1, 2005; 100(4): 1216 - 1216. [Full Text] [PDF]
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