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© 1999 International Anesthesia Research Society
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Abstract |
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This study was designed to determine the efficacy of heart rate (HR), systolic blood pressure (SBP), and changes in T-wave morphology in detecting intravascular injection of 15 µg of epinephrine (test dose) in sevoflurane-anesthetized adults. In addition, the testing threshold using the T-wave amplitude was derived. Ninety-six healthy patients were randomized to receive end-tidal sevoflurane 0.5%, 1%, or 2% and nitrous oxide 67% in oxygen (n = 32 for each sevoflurane concentration). Each group of patients was further randomized to receive 3 mL of 1.5% lidocaine plus 15 µg of epinephrine IV or 3 mL of saline IV (n = 16 each). HR, SBP, and T-wave amplitude were continuously monitored for 5 min after the IV injection of the study drug. None receiving IV saline and 15, 15, and 14 patients receiving the IV test dose developed HR increases
10 bpm during 0.5%, 1%, and 2% sevoflurane, respectively. No patient receiving saline and all patients receiving the test dose developed SBP increases 15 mm Hg. T-wave amplitude decreased by >0.1 mV and by >25% in all patients receiving the IV test dose, and its magnitude was similar regardless of the sevoflurane concentrations. When 0.1-mV and 25% decreases in T-wave amplitude were considered as testing thresholds, 100% sensitivities and specificities were obtained. We conclude that a peak SBP increase 15 mm Hg and a decrease in T-wave amplitude 0.1 mV and 25% are more reliable than a HR increase 10 bpm for detecting intravascular injection of epinephrine-containing test dose during sevoflurane anesthesia.
Implications: To determine whether an epidural catheter resides in a blood vessel, a standard test dose containing a local anesthetic and 15 µg of epinephrine is used. We found that, in sevoflurane-anesthetized adult patients, a systolic blood pressure increase 15 mm Hg and a decrease in T-wave amplitude 0.1 mV and 25% in lead II, but not a heart rate increase 10 bpm, are reliable indicators for detecting intravascular injection.
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Introduction |
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Continuous epidural analgesia in combination with general anesthesia is often used for postoperative analgesia. In such cases, only objective hemodynamic symptoms can indicate the intravascular migration of the epidural catheter. Inability to aspirate blood from an epidural catheter does not ensure extravascular placement, whereas the efficacy of an incremental injection of the test dose has not been substantiated in a large clinical trial (1). An inadvertent IV injection of a large amount of a local-anesthetic containing epinephrine solution could result in life-threatening cardiovascular or central nervous system complications during general anesthesia (2).
In isoflurane-anesthetized patients, a modified heart rate (HR) criterion (positive if 10 bpm increase) has been derived from the 95% confidence interval of maximal HR changes after the IV injection of the test dose (3). However, the efficacy based on the modified HR criterion depends on the concentration of isoflurane (3). In addition, HR responses and efficacy may also be influenced by the volatile anesthetic used, as seen in pediatric patients (4), because each volatile anesthetic may exert different amounts of direct depressant effects on the sinoatrial node and the baroreflex system (5,6). Meanwhile, previous reports suggested that IV epinephrine caused flattening or inversion of the T wave in adults (7) and increases in T-wave amplitude in anesthetized children (8,9), which suggests that the changes in T-wave morphology may be used as a criterion in detecting the accidental intravascular injection of the test dose. However, clinical applicability of the T-wave morphology is limited by the retrospective nature and nonuniform doses of epinephrine used in the literature.
The goals of the present study were to determine hemodynamic changes and efficacy of the epinephrine test dose in adult patients anesthetized with different concentrations of sevoflurane, to investigate whether changes in T-wave morphology could be used as a novel criterion for detecting intravascular injection and to derive a clinically appropriate testing threshold using the T-wave amplitude if it was found to be useful.
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Methods |
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The study protocol was approved by our institutional research committee, and informed consent was obtained from each patient. Ninety-six nonpregnant, ASA physical status I patients scheduled to undergo general anesthesia for elective surgeries were enrolled. None of the patients was taking ß-adrenergic blockers, calcium channel blockers, or angiotensin-converting enzyme inhibitors.
All patients arrived at the operating room after an 8 -h fast and without premedication. Preinduction blood pressure (BP) and HR were obtained noninvasively. Standard lead II electrocardiography was monitored continuously throughout the study. A radial arterial catheter was placed after local anesthetic infiltration for preinjection and subsequent BP measurements after test dose or saline injections. Lactated Ringer's solution was infused IV at a constant rate of approximately 15 mL · kg-1 · h-1 throughout the study. After the induction of general anesthesia with thiopental 5 mg/kg IV, endotracheal intubation was facilitated with vecuronium 0.1 mg/kg IV. Patients were then randomly assigned according to computer-generated random numbers to receive one of three concentrations of sevoflurane in 67% nitrous oxide in oxygen to achieve an assigned end-tidal of 0.5%, 1%, and 2% (n = 32 each). Anesthesia was maintained at the assigned end-tidal concentration of sevoflurane, and ventilation was controlled using a tidal volume of 10 mL/kg and a respiratory rate of 7–9 breaths/min to maintain end-tidal carbon dioxide tension 30–35 mm Hg. When three measurements of systolic blood pressure (SBP) and HR determined at 1 -min intervals were within 5% of the previous value, a steady end-tidal sevoflurane concentration was obtained for 5 min (end-tidal sevoflurane constantly showing 0.5%, 1%, or 2% at a constant inspiratory concentration), and when at least 20 min had elapsed after the induction of general anesthesia, each group of patients was further randomized to receive either 3 mL of isotonic sodium chloride solution IV (n = 16) or 3 mL of 1.5% lidocaine containing 15 µg of epinephrine IV (n = 16) as a simulated test dose via a peripheral IV catheter over 3 s. Continuous records (strip chart) of HR, SBP, and electrocardiography lead II (Life ScopeTM; Nihon Koden, Tokyo, Japan) were obtained after injection of the study drug, from which HR and SBP were analyzed at 20 -s intervals for 5 min. In addition, maximal HR and SBP responses were noted. The high- and low-frequency filters of electrocardiography were 0.3 and 40 Hz, respectively. The calibration of the recorder was set at 0.5 mV/cm; the chart speed was set at 25 mm/s. All measurements of T-wave amplitude were made at its maximal deflection and at 1 -min intervals for 5 min by observer blinded to the treatment group and the hemodynamic changes. The study solutions were prepared and coded by the hospital pharmacy and injected by a blinded observer (MT). On completion of the study and all data collection, these codes were broken by the author. All hemodynamic measurements were performed with patients in the supine position before the initiation of the scheduled surgery.
A power analysis based on a previous report revealed that >16 patients would provide a power >0.8 (P = 0.05) for detection of a 25% difference in paired hemodynamic responses (10). Positive HR and SBP responses to the IV test dose were prospectively defined from previous reports: HR increase 10 bpm (3) and a SBP increase 15 mm Hg within 2 min of administration (10). We determined sensitivity (true positives/[true positives + false negatives]), specificity (true negatives/[true negatives + false positives]), and positive (true positives/[true positives + false positives]) and negative predictive values (true negatives/[true negatives + false negatives]).
All values are presented as mean ± SD. Statistical analysis was performed by using two-way analysis of variance to compare changes in hemodynamic variables and T-wave amplitude (normally distributed data) among groups. When a significant difference was identified, this was followed by an unpaired Student's t-test with Bonferroni's correction. Intergroup differences in demographic data were also compared by using an unpaired Student's t-test with Bonferroni's correction or 
2 test. Changes in hemodynamic variables and T-wave amplitudes over time within each group were analyzed by using repeated-measures analysis of variance, followed by paired Student's t-test. P < 0.05 was considered the minimal level of statistical significance.
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Results |
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There were no significant differences in patients' age, weight, height, gender distribution and BP, HR, and T-wave amplitude at rest among the three groups (Table 1). After the induction of general anesthesia using sevoflurane and nitrous oxide at steady state, BP decreased significantly compared with preinduction (at rest) values in all groups, whereas HR and T-wave amplitude remained unchanged (Table 1). SBP in the sevoflurane 2% group was significantly less than that of the sevoflurane 0.5% group before injection of the study drug. There was no significant difference between patients receiving isotonic sodium chloride solution and those receiving the test dose in each group (data not shown). Oxygen saturation was
98% in all patients during the entire course of the study.
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IV injection of the test dose produced significant increases in HR between 40 and 80 s in all groups, whereas significant decreases in HR were seen 160–240, 160–240, and 160–280 s in the sevoflurane 0.5%, 1%, and 2% groups, respectively (Fig. 1). Mean maximal increases in HR in the sevoflurane 0.5%, 1%, and 2% groups were 27 ± 9, 27 ± 8, and 24 ± 9 bpm at 52 ± 7, 50 ± 11, and 48 ± 7 s after test dose injections, respectively, and showed no significant difference among groups. However, significant, monophasic increases in SBP were seen 40–200, 20–220, and 20–220 s in the sevoflurane 0.5%, 1%, and 2% groups, respectively (Fig. 2). Mean maximal increases in SBP were 57 ± 17, 51 ± 19, and 41 ± 14 mm Hg (P < 0.05 between the sevoflurane 0.5% and 2% groups) at 88 ± 16, 95 ± 23, and 84 ± 14 s after test dose injections, respectively. All patients developed decreases, but none developed increases, in T-wave amplitude within 1 min of the test dose injections. Compared with preinjection values, significant decreases in T-wave amplitudes were seen until 4, 3, and 3 min after test dose injections in the sevoflurane 0.5%, 1%, and 2% groups, respectively (Fig. 3). Mean greatest absolute decreases in T-wave amplitudes were 0.21 ± 0.08, 0.25 ± 0.14, and 0.26 ± 0.11 mV at 36 ± 9, 35 ± 12, and 35 ± 11 s in the sevoflurane 0.5%, 1, and 2% groups, respectively. The range of the greatest absolute change in T-wave amplitudes were from -0.09 to 0.11 mV in all patients receiving IV saline. However, average greatest percent decreases in T-wave amplitudes were similar among sevoflurane groups, and were 67.1% ± 20.3%, 58.0% ± 21.6%, and 71.4% ± 29.9% in the sevoflurane 0.5%, 1%, and 2% groups, respectively. The range of the greatest percent change in T-wave amplitudes after IV saline was from -16% to 14% including all patients during the entire study. Coefficients of variations of all T waves determined beat-by-beat during the first 1 min within each individual patient receiving IV saline were <4%.
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The numbers of patients who developed maximal increases in HR
10 bpm in response to the IV test doses were 15, 15, and 14 in the sevoflurane 0.5%, 1%, and 2% groups, respectively. Because no patients receiving saline developed HR increases 10 bpm regardless of the sevoflurane concentrations, the sensitivity, specificity, positive predictive value, and negative predictive value of the HR criterion were 94%, 100%, 100%, and 94% (sevoflurane 0.5%); 94%, 100%, 100%, and 94% (sevoflurane 1%); and 88%, 100%, 100%, and 89% (sevoflurane 2%), respectively. However, all patients receiving the IV test dose and none receiving IV saline developed SBP increases 15 mm Hg, maximal absolute decreases in T-wave amplitude 0.1 mV, and maximal percent decreases in T-wave amplitude 25% of preinjection values, resulting in sensitivity, specificity, positive predictive value, and negative predictive value of 100% based on the SBP and the T-wave criteria. Three patients in the sevoflurane 2% group and one each in the sevoflurane 1% and 0.5% groups developed a negative T wave, which resolved within 2 min of test dose administrations. No ventricular or supraventricular arrhythmia was observed in any patient throughout the study period.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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One of our major findings was that the HR response to a simulated IV test dose did not depend on the sevoflurane concentrations studied. More importantly, the peak HR change was not totally reliable for detecting intravascular injection even at the light level of sevoflurane anesthesia. This is in contrast to isoflurane anesthesia, during which the HR responses to the identical test dose IV were depressed in a concentration-dependent manner, and the modified HR criterion (positive if
10 bpm increase) was associated with 100% sensitivity and specificity under end-tidal isoflurane concentration 
1% (3). In vivo, HR changes due to IV epinephrine depend on the balance between direct ß1-cardiac stimulation and the degree of arterial baroreflex response. Although our study does not clarify the mechanism of differential effects of these two volatile anesthetics on the HR responses to epinephrine, one possibility would be that isoflurane and sevoflurane exert different degrees of direct depressant effects on the maximal sinus rate responses to epinephrine and/or electromechanical activities of the atrial fibers (5,11). However, baroreflex sensitivity to the increase in BP is similarly depressed between isoflurane and sevoflurane at end-tidal concentrations >1 minimum alveolar anesthetic concentration (6), but this has not been studied at subanesthetic concentrations. Therefore, another possible explanation could be that depression of the pressor test slope may be less with sevoflurane than with isoflurane at concentrations <1 minimum alveolar anesthetic concentration, resulting in greater baroreflex-mediated slowing of the HR during light levels of sevoflurane anesthesia. In this study, we also demonstrated 100% efficacy based on the changes in T-wave amplitude regardless of the sevoflurane concentration, and that 0.1 mV and a 25% decrease in the T-wave amplitude may be used as testing thresholds. T-wave morphology can be monitored noninvasively and continuously, and the magnitude of changes determined either as an absolute change or as a percent change does not depend on the wide range of sevoflurane concentrations studied, as opposed to the hemodynamic changes. These results suggest potential clinical applicability of the T-wave criteria for detecting intravascular injection of the epinephrine-containing test dose during general anesthesia. However, we did not evaluate the ability of the participating anesthesiologist to detect either 0.1 mV or 25% decrease in T-wave amplitude on the oscilloscope, which must be addressed in a blinded, prospective manner before the T-wave criteria can be considered as viable alternatives to hemodynamic criteria. Further studies are also warranted to determine the minimal effective dose of epinephrine required to demonstrate such T-wave changes and whether T-wave decreases occur with other volatile anesthetics and local anesthetics with clinically reliable efficacy.
The mechanism of the decreased T-wave amplitude due to IV epinephrine is not clear from our study. Epinephrine causes a reduction of serum potassium concentrations via ß2-adrenoceptors (12,13). However, the influence of such an effect on the transient change in the T-wave amplitude is not clear in our study because serial changes in serum potassium concentrations were not determined. In addition, flattening or inversion of the T-wave has also been reported with various physical and mental stresses in adults (7,14,15), which suggests that decreases in T-wave amplitude may also occur during surgical procedures. Because the usefulness of the criterion for detecting intravascular injection ultimately requires validation during surgery, whether simultaneous surgical stimulation produces false positivity remains to be examined.
Maximal reduction of the T-wave amplitude occurred approximately 35 s after test dose injections in our study, whereas that of HR and SBP occurred 50 and 90 s after injections, respectively. The decrease in T-wave amplitude was <20% in one patient in each group 1 min after test dose injections, whereas six, five, and five patients in the sevoflurane 0.5%, 1%, and 2% groups, respectively, developed decreases in T-wave amplitudes <20% 2 min after the test dose injections. These results indicate that the reduction of the T-wave amplitude is a transient phenomenon and occurs much earlier than the other hemodynamic alterations studied. To maximize the detectability of the test dose for intravascular injection using the T-wave criterion, a continuous record of the electrocardiography on a strip chart is highly recommended and should be started as soon as the test dose is injected.
Our results must be interpreted with some caution. First, T-wave amplitude of lead II was used in our study, whereas changes in T-wave morphology in other leads were not assessed. Whether other leads produce more reliable T-wave changes than lead II in association with the IV test dose remains to be seen. Second, increases, rather than decreases, in T-wave amplitude have been documented after a simulated IV test dose in sevoflurane-anesthetized children (16), whereas T-wave amplitudes were exclusively reduced in our study. Thus, the extent and direction of the T-wave changes due to the IV test dose may be an age-related effect; if so, determination of the cutoff age under which the T-wave criterion we describe is not applicable would be necessary. Third, preexisting T-wave abnormalities, such as those in patients taking digoxin, with ventricular hypertrophy, or with a history of myocardial infarction, precludes using the T-wave criteria for detecting intravascular injection of the test dose (17). Finally, serum potassium level, another factor known to affect the T-wave amplitude in healthy patients, was not controlled in our study population. This may explain variations of the baseline, as well as the absolute changes of the T-wave amplitudes in our study population. However, the gain of the electrocardiography waveform on the oscilloscope and the recorder can usually be adjusted to an appropriate size; hence, it may be clinically more feasible to detect the proportional change rather than the abso-lute change of the T-wave amplitude, the latter of which would require a measure.
In conclusion, a peak SBP increase 15 mm Hg, a greatest absolute decrease in T-wave amplitude 0.1 mV, and a greatest percent decrease in T-wave amplitude 25% are reliable indicators for detecting intravascular injection of an epinephrine-containing test dose, whereas a HR increase 10 bpm is an imperfect marker in adult patients anesthetized with sevoflurane and nitrous oxide.
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References |
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Matsumiya N, Dohi S, Takahashi H, et al. Cardiovascular collapse in an infant after caudal anesthesia with a lidocaine-epinephrine solution. Anesth Analg 1986;65:1074–6.
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[Abstract/Free Full Text] - Stowe DF, Dujic Z, Bosnjak ZJ, et al. Volatile anesthetics attenuate sympathomimetic actions on the guinea pig SA node. Anesthesiology 1988;68:887–94.[Web of Science][Medline]
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