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Small-Dose Bupivacaine-Sufentanil Prevents Cardiac Output Modifications After Spinal Anesthesia

Karim Asehnoune, MD*, Eric Larousse, MD*, Jean Marc Tadie , Stephane Droupy, MD, and Dan Benhamou, MD*
MD*,

Vincent Minville,

MD*,

*Service dAnesthe sie-Re animation et Unite Propre de Recherche de lEnseignement Supe rieur-Equipe dAccueil (UPRES-EA 3540) and Service dUrologie, Centre Hospitalo-Universitaire de Bice tre, AP-HP, Le Kremlin Bice tre, France

Spinal injection of small-dose (SD) bupivacaine decreases the likelihood of hypotension compared with large-dose (LD) bupivacaine. We assumed that a SD of bupivacaine could also prevent the decrease in cardiac output (CO). Patients undergoing elective urologic, lower abdominal, or lower limb surgery under spinal anesthesia were included in this prospective randomized study. Spinal injection consisted of 5 g of sufentanil and either SD (7.5 mg of hyperbaric bupivacaine with glucosemonohydrate80 mg/mL; n 19 patients) or LD (12.5 mg of hyperbaric bupivacaine with glucosemonohydrate80 mg/mL; n 19 patients). CO

(impedance cardiography), arterial blood pressure, and heart rate) were measured at 1 min before performance of spinal block and 2, 10, and 30 min after the intrathecal injection. Sensory level was also assessed at 30 min. CO was higher in the SD group as compared with the LD group from 2 min to 30 min after spinal anesthesia. Moreover, CO increased at 2 min in the SD group and decreased at 10 and 30 min in the LD group compared with baseline value. In conclusion, SD bupivacaine provides successful anesthesia and gives better CO stability than LD. (Anesth Analg 2005;101:15125)

ypotension is a common complication during spinal anesthesia (SA) (1). This complication is more hazardous in elderly patients because they may have decreased physiological reserve and compromised blood supply to various vital organs (2). Many different techniques, such as IV crystalloid and vasopressor administration, have been used to prevent this complication (2,3). However, rapid infusion of large amounts of IV fluid may be detrimental to patients with cardiac dysfunction (3,4). Moreover, ephedrine and vasopressors may lead to serious cardiac side effects (hypertension or tachycardia) (5). Ben-David et al. (6) demonstrated that a small dose (SD; 7.5 mg) of bupivacaine with fentanyl was suitable for patients undergoing ambulatory surgery. The usefulness of SD bupivacaine (10 mg) was demonstrated for motor blockade and time to recovery (7). Dose-response data on clinical anesthetic characteristics for spinal bupivacaine indicate that SD can be used for short duration surgery (6,8). SDs of bupivacaine (10 mg) decreased the likelihood of prolonged
Accepted for publication May 12, 2005. Address correspondence and reprint requests to Karim Asehnoune, MD, Service dAnesthe sie-Re animation, Ho pital de Bice tre, 94275 Le Kremlin Bice tre, France. Address e-mail to asehnounekarim@hotmail.com. DOI: 10.1213/01.ANE.0000180996.91358.CC

detrusor blockade, inability to void, and prolonged time to hospital discharge. Furthermore, Ben-David et al. (6) reported that mean arterial blood pressure (MAP) remained unchanged in 50 patients undergoing SD bupivacaine SA for ambulatory surgery. This finding is of particular interest in patients at a high risk for developing spinal-induced hypotension. Kamenik and Paver-Erzen (9), using the noninvasive impedance cardiography method, reported a decreased cardiac output (CO) after large-dose (LD; 15 mg) bupivacaine. However, the impact of SD bupivacaine on CO is not known. We hypothesized that a reduced dose of bupivacaine with sufentanil could provide successful anesthesia and stability of CO. We therefore conducted this study to compare CO changes after spinal injection of LD (12.5 mg) or SD (7.5 mg) bupivacaine.

Methods
After approval by our Human Studies Committee, written informed consent was obtained from 38 ASA physical status I and II patients undergoing elective urologic, lower abdominal, or lower limb surgery under SA. Patients with any contraindication to regional anesthesia (patients refusal, hemostasis abnormalities, or local infection), dementia, allergic reaction to
2005 by the International Anesthesia Research Society 0003-2999/05

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local anesthetics, anemia (hemoglobin 10 g/dL), and pregnant women were excluded from the study. The patients were fasted overnight, and oral fluid intake was allowed for up 6 h before the operation. Premedication consisted of oral hydroxyzine 100 mg 1 h before surgery. No IV fluid was infused before entering the study. The study was randomized and unblinded regarding the anesthesia solution. The patients received either a SD SA (SD group) or a LD SA (LD group). The SD group received 7.5 mg of hyperbaric bupivacaine with glucosemonohydrate80 mg/mL (Marcaine 0.5%; Astra, Sodertalje, Sweden) and 5 g of sufentanil; the LD group received 12.5 mg of hyperbaric bupivacaine with glucosemonohydrate80 mg/mL and 5 g of sufentanil. After arrival in the operating room, an IV catheter was placed in the patients forearm. Subarachnoid puncture was performed using a midline approach with a 25gauge Sprotte needle at the L4-5 interspace with the patient in the sitting position. The Sprotte needle aperture was oriented in a cephalad direction throughout the intrathecal injection. The injection lasted 30 s in both groups. The patients were placed supine within 10 s of the injection. CO was measured with the impedance cardiography method (ICM) (NCCOM3; BoMed Medical Manufacturing, Irvine, CA). Impedance cardiography electrodes were placed as recommended by the manufacturer just after the IV line was inserted. Slow mode data recording then started. Heart rate (HR) was continuously recorded, and noninvasive MAP, systolic blood pressure (SBP), and diastolic blood pressure (DBP) were measured by an automated blood pressure cuff every 2.5 min with an AS3 monitor (Datex-Ohmeda SAS, Champagne du Mont dOr, France). Four sets of data were recorded. Each set included HR, SBP, MAP, DBP, and CO. The first set of measurements (baseline values) took place after the insertion of the IV line and before the subarachnoid puncture (TO). The second set was performed 2 min after the end of the local anesthetic injection, and the third and fourth set were performed 10 min and 30 min after the end of the injection, respectively. A blinded observer assessed the dermatome level of sensory blockade bilaterally with an ice-cold alcoholimmersed sponge 30 min after the injection of the local anesthetic (T3). Hypotension, defined as a decrease in SBP to 100 mm Hg or 70% of baseline, was treated with IV boluses of ephedrine 6 mg repeated every 3 min. Bradycardia, defined as HR 55 bpm, was treated with atropine 1 mg. Kamenik and Paver-Erzen (9) measured CO (ICM) before and 30 min after SA (LD bupivacaine 15 mg) and noted a 25% decrease 30 min after SA (in the group of patients receiving no IV fluid therapy). Our patient population was older compared with Kamenik and Paver-Erzens patients (9); thus, we hypothesized a 30% decrease in CO in the LD group and no changes in the SD group. A power calculation for a 30% difference

in CO with a probability level of 0.05 and power of 0.80 (1-) yielded a sample size of 16 patients. Accordingly, 19 patients were enrolled in both groups. To compare demographic and surgical data, as well as patient characteristics, between groups, a 2 test or a Students t-test was used. Hemodynamic data between groups and changes from baseline were compared using variance analysis for repeated measurements, followed by paired Students t-test. P 0.05 was considered statistically significant. Data are presented as mean sd unless stated otherwise.

Results
Thirty-six patients completed the study. There were no refusals and no dropouts. The ICM device failed to monitor CO for one patient in each group. All procedures were successfully performed under SA. The two groups were similar with respect to age, sex, ASA physical status, weight, and height (Table 1). The median block level was two segments higher in the LD group as compared with the SD group (Table 1; P 0.05). No statistically significant differences were found between the groups with respect to baseline values of CO, SBP, MAP, DBP, and HR. Two patients in each group were treated for hypotension. In the LD group, one patient received 6 mg and the other received 12 mg of ephedrine. In the SD group, 2 patients received 6 mg of ephedrine. In the LD group, one patient received 1 mg of atropine. All complications were successfully treated, as described above. The exclusion of the treated patients did not modify the results. CO was significantly higher in the SD group as compared with LD group 2, 10, and 30 min after SA. In the SD group, CO significantly increased 2 min after SA (P 0.0002) and returned to baseline values (T0) after 10 and 30 min. In the LD group, CO significantly decreased 10 (P 0.001) and 30 min (P 0.0002) after SA (Fig. 1). HR and DBP were significantly lower in the LD group as compared with the SD group (at 10 and 30 min and at 30 min, respectively). SBP, MAP, and DBP significantly decreased after SA in the SD group as compared with T0, whereas HR remained unchanged. SBP, MAP, DBP, and HR significantly decreased in the LD group as compared with T0 (Table 2).

Discussion
These results demonstrate that the spinal injection of SD (7.5 mg) bupivacaine plus 5 g of sufentanil provides successful anesthesia and gives better CO stability than LD (12.5 mg) bupivacaine plus 5 g of sufentanil. The hemodynamic stability in the SD group is also reflected in the significantly higher values in HR

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Table 1. Demographic Data, and Sensory Block Level in Two Groups of Patients Demographic data Sex (M/F) ASA (I/II) Age (yr) Weight (kg) Height (cm) Sensory level # SD group (n 19) 13/6 8/11 64 16 74 12 168 8 T8 (T412) LD group (n 19) 13/6 9/10 60 20 73 18 171 9 T6 (T48) P-value NS NS NS NS NS 0.006

Data are expressed as ratio or mean sd, except #, which is the median (range). LD large dose; SD small dose; NS nonsignificant.

Figure 1. Cardiac output variations in small dose (SD) and large dose (LD) groups. Cardiac output (CO) 2, 10, and 30 min after spinal anesthesia (SA) is expressed as percent changes. The baseline value of CO (T0: before SA) represents the value 100%. **P 0.01 compared with T0 in the same group; #P 0.05 versus the LD group; ##P 0.01 versus the LD group.

and DBP observed after SD compared with LD bupivacaine. In this study, a noninvasive ICM for CO measurements was used. Although the absolute value of CO measurement is controversial, its value for monitoring the trends of CO changes has been accepted by most researchers (9,10). Comparisons with thermodilution (TD) and direct Fick methods reported that ICM measures CO accurately in different conditions (in the supine position, during head-up tilt, and after the induction of anesthesia) (11,12). Moreover, this method can be used in circumstances where there are immediate and large changes in sympathetic tone. Indeed, Sageman (13) demonstrated that accurate and reliable measurements of CO are possible in a lower body negative pressure model. An effective approach to minimizing cardiac side effects after SA is to use SDs of local anesthetics. However, whereas the use of a single shot of SD local anesthetic for SA may limit hypotension, it may not provide acceptable anesthesia. Some authors, therefore, added a lipophilic opioid for anesthetic synergy (7,14). HR and DBP were significantly lower in the LD group compared with the SD group, and only two patients in each group developed hypotension. This infrequent incidence of hypotension in the SD group is in accordance with previously published data (15,16). A reason for the infrequent incidence of hypotension

in the LD group is the low limit set in our study (17,18). Indeed, if we had operationally defined hypotension as a decrease in systemic arterial pressure 80% of baseline, seven patients (39%) in the LD group and five patients (28%) in the SD group would have developed hypotension. In the present study, CO was significantly lower in the LD group compared with the SD group. In the supine position, SA leads to blood pooling in the denervated lower extremities with a reflex vasoconstriction in the nonblocked upper extremities (19). When this vasoconstriction of the nonblocked areas remains effective, the CO is unchanged (19,20). Our results indicate that SD bupivacaine-sufentanil gives better CO stability than the LD, probably by maintaining this vasoconstriction reflex. Indeed, the sensory block level was significantly lower in the SD group compared with the LD group, although sympathetic level is very variable and may not correspond to sensory level. It has been reported that 4 mg of bupivacainefentanyl SA caused dramatically less hypotension than 10 mg of bupivacaine and nearly eliminated the need for vasopressors in the elderly (7). In this study, we showed that SD bupivacaine preserves the CO, even with 7.5 mg. This point is critical because the dose of 4 mg used by Ben-David et al. (7) in elderly patients might not be sufficient for surgeries in which the need for an intense motor block would require larger doses of local anesthetic. This preliminary study has several limitations. First, a small number of patients were studied. However, hemodynamic changes were consistently obtained, suggesting that our results can be generalized to the whole population of patients studied under similar conditions. Second, our results were obtained in a patient population 40 years of age and may not be extrapolated to other conditions such as younger patients, different operations, and varying levels of hydration. A further limitation is that the magnitude of changes might be altered by a different approach (TD or direct Fick method). Crucially, the measurement of CO might not be accurate when the patient is moving because of interference caused by changes in electrode position. Despite all this, individual patients plots of

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Table 2. Hemodynamic Changes Immediately Before Spinal Anesthesia, and 2 min, 10 min, 30 min After Spinal Anesthesia in Two Groups of Patients Hemodynamic variables Small-dose group HR (bpm) SBP (mm Hg) MAP (mm Hg) DBP (mm Hg) Large-dose group HR (bpm) SBP (mm Hg) MAP (mm Hg) DBP (mm Hg) Before SA 73 16 150 32 105 19 83 16 68 12 147 18 98 17 78 12 2 min after SA 77 11 133 31* 92 23* 76 19 67 7 130 19* 89 16 74 19 10 min after SA 74 1# 126 25** 89 16** 71 16** 62 10* 117 16** 87 18* 65 13** 30 min after SA 71 14# 132 26** 96 16* 75 15# 60 10** 124 22** 91 21 64 14**

SA spinal anesthesia; HR heart rate; SBP systolic blood pressure; MAP mean arterial blood pressure; DBP diastolic blood pressure. * P 0.05; ** P 0.01 compared with before SA value; # P 0.05 versus large-dose group.

hemodynamic changes reassured us of the validity of our results. In addition, a noninvasive technique would be highly acceptable to patients and more likely to be used routinely. In conclusion, despite limitations of ICM monitoring of CO, our study shows that a decrease in CO observed with LD bupivacaine (12.5 mg) is not associated with SD bupivacaine (7.5 mg), and the use of SD bupivacaine may prevent cardiovascular side effects.

References
1. Tarkkila PJ, Kaukinen S. Complications during spinal anesthesia: a prospective study. Reg Anesth 1991;16:101 6. 2. Lim HH, Ho KM, Choi WY, et al. The use of intravenous atropine after a saline infusion in the prevention of spinal anesthesia-induced hypotension in elderly patients. Anesth Analg 2000;91:1203 6. 3. McCrae AF, Wildsmith JAW. Prevention and treatment of hypotension during central neural block. Br J Anaesth 1993;70:672 80. 4. Buggy D, Higgins P, Moran C, et al. Prevention of spinal anesthesia-induced hypotension in the elderly: comparison between preanesthetic administration of crystalloids, colloids and no prehydration. Anesth Analg 1997;84:106 10. 5. Critchley LAH, Stuart JC, Conway F, Short TG. Hypotension during subarachnoid anaesthesia: haemodynamic effects of ephedrine. Br J Anaesth 1995;74:373 8. 6. Ben-David B, Levin H, Salomon E, et al. Spinal bupivacaine in ambulatory surgery: the effect of saline dilution. Anesth Analg 1996;83:716 20. 7. Ben-David B, Frankel R, Arzumonov T, et al. Minidose bupivacaine-fentanyl spinal anesthesia for surgical repair of hip fracture in the aged. Anesthesiology 2000;92:6 10. 8. Liu SS, Ware PD, Allen HW, et al. Dose-response characteristics of spinal bupivacaine in volunteers: clinical implications for ambulatory anesthesia. Anesthesiology 1996;85:729 36.

9. Kamenik M, Paver-Erzen V. The effects of lactated ringers solution infusion on cardiac output changes after spinal anesthesia. Anesth Analg 2001;92:710 4. 10. Critchley LAH. Electrical bioimpedance for non-invasive cardiac measurement. Crit Care Med 1998;26:1460 1. 11. Jarvela K, Honkonen SE, Jarvela T, et al. The comparison of hypertonic saline (7.5%) and normal saline (0.9%) for initial fluid administration before spinal anesthesia. Anesth Analg 2000;91:14615. 12. Koobi T, Kaukinen S, Turjanmaa VM, Uusitalo AJ. Whole-body impedance cardiography in the measurement of cardiac output. Crit Care Med 1997;25:779 85. 13. Sageman WS. Reliability and precision of a new thoracic electrical bioimpedance monitor in a lower body negative pressure model. Crit Care Med 1999;27:1986 90. 14. Tejwani GA, Rattan AK, McDonald JS. Role of spinal opioid receptor in the antinociceptive interactions between intrathecal morphine and bupivacaine. Anesth Analg 1992;74:726 34. 15. Hartmann B, Junger A, Klasen J, et al. The incidence and risk factors for hypotension after spinal anesthesia induction: an analysis with automated data collection. Anesth Analg 2002;94: 15219. 16. Vercauteren MP, Coppejans HC, Hoffmann VL, et al. Smalldose hyperbaric versus plain bupivacaine during spinal anesthesia for cesarean section. Anesth Analg 1998;86:989 93. 17. Liu SS, McDonald SB. Current issues in spinal anesthesia. Anesthesiology 2001;94:888 906. 18. Butterworth J. Physiology of spinal anesthesia: what are the implications for management? Reg Anesth Pain Med 1998;23: 370 3. 19. Arndt JO, Hock A, Stanton-Hicks M, Stuhmeier KD. Peridural anesthesia and the distribution of blood in supine humans. Anesthesiology 1985;63:616 23. 20. Larousse E, Asehnoune K, Dartayet B, et al. The hemodynamic effects of pediatric caudal anesthesia assessed by esophageal Doppler. Anesth Analg 2002;94:1165 8.

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