Controlling deliberate hypotension in hypertensive patients undergoing spinal surgery: a comparison between remifentanil and sodium nitroprusside

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1 Anesth Pain Med 2010; 5: 38~44 Clinical Research Controlling deliberate hypotension in hypertensive patients undergoing spinal surgery: a comparison between remifentanil and sodium nitroprusside Department of Anesthesiology and Pain Medicine, *Seoul National University Bundang Hospital, Seoul National University Boramae Medical Center, Seoul National University Hospital, Seongnam, Korea Sang-Hyun Park*, Sang-Hwan Do*, Chong-Soo Kim, Young-Jin Ro, Sung-Hee Han*, Jin-Hee Kim*, and Kyoun-Ah Han Background: This study was designed to determine whether remifentanil or sodium nitroprusside (SNP) with sevoflurane anesthesia can induce safe deliberate hypotension (DH) to a target mean arterial pressure (MAP) of mmhg in patients with controlled hypertension. Methods: Thirty patients with controlled hypertension and who were scheduled for posterior lumbar interbody fusion were randomly assigned to receive remifentanil (n = 15, group R) or SNP (n = 15, group S). All the patients received a balanced anesthetic technique including vol% sevoflurane. Group R received remifentanil by target-controlled infusion. The infusion was initiated with a target concentration at 4 ng/ml and this was adjusted every 1 min by 1 ng/ml to maintain the MAP to the target level of mmhg. In group S, the infusion of SNP was initiated at 1 ug/kg/min and this was increased by 0.5 ug/kg/min. Cerebral oximetry was done and the cardiac index was measured with esophageal Doppler. Results: DH was achieved at a MAP = 60 mmhg within 5.7 min for group R and 3.7 min for group S. The intraoperative blood loss was lower in Group R than that in Group S (304 ± 103 vs 650 ± 141 ml, P < 0.05). The frequency of added ephedrine injection to control the MAP and discontinuation of the study drug due to a MAP < 60 mmhg were higher in group S than in group R (46% vs 13%, P < 0.05 and 62% vs 20%, P < 0.05, respectively). Conclusions: Compared to SNP, remifentanil with sevoflurane anesthesia induced safer DH for patients with controlled hypertension. (Anesth Pain Med 2010; 5: 38 44) Key Words: Deliberate hypotension, Remifentanil, Sodium nitroprusside. Received: September 17, Revised: 1st, September 24, 2009; 2nd, October 12, Accepted: November 9, Corresponding author: Sang-Hwan Do, M.D., Department of Anesthesiology and Pain Medicine, Seoul National University Bundang Hospital, 166, Gumi-ro, Bundang-gu, Seongnam , Korea. Tel: , Fax: , shdo@snu.ac.kr INTRODUCTION Deliberate hypotension (DH) has been used to reduce bleeding and the need for blood transfusions, and to provide a bloodless surgical field. DH is defined as a reduction of the systolic arterial pressure to mmhg or a reduction of the mean arterial pressure (MAP) to mmhg. The current rationale for setting the safe lower limit of MAP at 50 mmhg in normotensive patients is based on the belief that this range represents the lowest MAP at which autoregulation of cerebral blood flow (CBF) is still in force [1]. However, for chronically hypertensive patients, the curve for autoregulation shifts to the right, that is, the lowest arterial pressure at which autoregulation of the CBF is still in force is higher for these patients than for normotensive patients [2]. With effective antihypertensive therapy, however, the curve for autoregulation moves back to its normal position [3]. Sharrock and colleagues [4] showed that DH produced by epidural anesthesia, is a safe technique for patients with medically controlled hypertension. However, no consensus has been reached as to whether DH with general anesthesia is safe for patients with controlled hypertension. The ideal agent for induction of DH in patients with controlled hypertension must have a predictable and dose-dependent effect without suppressing the microcirculatory autoregulation of the vital organs (i.e. brain or heart). Sodium nitroprusside (SNP) is one of the most commonly used hypotensive agents and has been frequently used as a reference agent regarding hypotensive anesthesia. Recently, it was reported that remifentanil induced consistent DH with a bloodless operative field without additional potent hypotensive agents or adverse 38

2 Sang-Hyun Park, et al:remifentanil and sodium nitroprusside in controlled hypertensive patients 39 effects when combined with sevoflurane or propofol [5,6]. Accordingly, the current study was designed: a) to determine whether remifentanil and SNP with sevoflurane anesthesia can induce safe DH to a target MAP of mmhg in patients with medically controlled hypertension; and b) to determine how remifentanil and SNP affect the cardiac index measured by esophageal Doppler and brain oxygenation with cerebral oximetry during DH. MATERIALS AND METHODS This study was approved by the Institutional Review Board, and written informed consent was obtained from all participants. Patients that had a known history of hypertension and were well-controlled (systolic < 140 mmhg and diastolic < 90 mmhg) [7] that were scheduled for posterior lumbar interbody fusion were enrolled in this study. The following patients were excluded: those over 70 years of age, those with a pre-operative hematocrit (Hct) < 30%, those with a history of cerebrovascular disease, those with known or suspected neurological deficits, and those with hepatic or renal insufficiency or cardiovascular disease. The enrolled patients underwent brief neurological testing for motor, sensory and cranial nerve function and the Mini Mental State Examination (MMSE) before surgery. The patients were randomly allocated to one of two groups using a computer-generated random table: the sodium nitroprusside group (group S) or remifentanil group (group R). An attending anesthesiologist was informed of the group the patient was enrolled in, just prior to surgery. The patients received premedication with 0.04 mg/kg of midazolam intravenously before entering the operating room. Electrocardiography, non-invasive arterial pressure monitoring and pulse oximetry were continuously monitored. General anesthesia was induced with intravenous propofol 1.5 mg/kg, rocuronium 0.6 mg/kg, and alfentanil 0.6μg/kg for Group S or remifentanil 1 μg/kg for Group R, respectively. Subsequently, the lungs were ventilated with oxygen and nitrous oxide (FiO 2 0.5), and the tidal volume was adjusted to maintain an end-tidal carbon dioxide partial pressure between 30 and 35 mmhg. Anesthesia was maintained with 1.5 to 2 vol% sevoflurane. The radial artery was cannulated and the arterial pressure was monitored continuously using a standard pressure transducer kit (Pressure Monitoring Set, Edwards Lifesciences, CA, USA). Body temperature was monitored continuously via esophageal stethoscope. The near-infrared spectroscopy (NIRS) sensor (INVOS 4100, Somanetics, Troy, MI, USA) was placed at least 2 cm above the eyebrow on the forehead. The patient was placed in the prone position and the pressure transducer was placed at zero at the level of the external auditory meatus. The cardiac index (CI) was measured with an esophageal Doppler (Cardio Q, Deltex, UK). The rso 2 (regional cerebral oxygen saturation), the MAP and CI values were monitored continuously throughout surgery. The baseline data was defined as the MAP immediately prior to skin incision. DH with intravenous SNP or remifentanil was carried out at the time of the surgical incision in both groups. Due to a very limited experience with hypertensive patients in this setting, open-label drugs were used for the initial comparison. Patients assigned to group S (n = 15), according to the results of a previous investigation [8], received a continuous infusion at 1μg/kg/min, which was increased every 1 min by 0.5μg/ kg/min. Patients assigned to group R (n = 15) received remifentanil by target-controlled infusion (TCI) using an Orchestra R infusion pump system (Fresenius Kabi, Brezins, France). Infusion was initiated with a target concentration at 4 ng/ml and adjusted every 1 min by 1 ng/ml to maintain MAP to the target level of mmhg. In both groups, a maintenance dose was administered to stabilize the MAP at mmhg until muscle and skin closure were started. If the MAP fell below 50 mmhg, a protocol was followed that began with discontinuation of the study drug and administration of ephedrine 5 mg unless MAP rose above 50 mmhg within 1 min. During the operations, lactated Ringer's solution was administered at 6 ml/kg/h, and a urine output of > 0.5 ml/kg/h was maintained to prevent hypovolemia [9]. When the rso 2 value fell to 40% or was relatively decreased by more than 20% from the baseline value, Hct was checked and if Hct was < 24%, packed RBC was transfused. The packed RBC to isotonic crystalloid ratio was 1:1. If Hct was 24% or higher in those patients, hypotension was treated with the method as above. A failure of DH was defined as discontinuation of the study drug more than six times, or the need for an ephedrine bolus more than four times for maintaining the target MAP (55 65 mmhg). If systolic arterial pressure > 160 mmhg occurred after discontinuation of the study drug, it was treated in both groups with a fixed dose of intermittent nicardipine (1 mg). MAP, HR, rso 2, and CI were measured at the following time points by an anesthetic nurse who was blinded to group assignment: baseline before DH (B), 1 min (T1), 2 min (T2), 3 min (T3), 5 min (T4), 15 min (T5), 30 min (T6), 60 min

3 40 Anesth Pain Med Vol. 5, No. 1, 2010 (T7), 90 min (T8) after DH, before the discontinuation of the study drug (T9), 1 min (T10), 2 min (T11), 3 min (T12), 5 min (T13), 10 min (T14) after discontinuation of the study drug. In addition, the arterial blood gas and Hct were analyzed at B, T7 and T9. The time to reach a MAP = 60 mmhg and restore the baseline MAP after discontinuation of the hypotensive agent was recorded. The duration of DH was defined as the time from initiation to termination of the study drug. All episodes where, the rso 2 value fell to 40%, relatively decreased more than 20% from the baseline value or if a neurological abnormality was detected during follow-up were recorded. Intraoperative blood loss was calculated as the sum of sponges weighed as they were removed from the surgical field plus the difference between the irrigation and suction volumes. The amount of blood loss was replaced with one unit of packed RBC when the Hct decreased below 24%. At the postanesthesia care unit, the postoperative Hct was checked. A same surgeon performed all of the operations. The surgeon was blinded to the treatment group; however, the anesthesiologist was not. Table 1. Patient Characteristics and Procedural Summary for 28 Patients Undergoing Spinal Surgery Group S (n = 13) Group R (n = 15) Age (yr) 53.2 ± ± 6.0 Gender (M/F) 7/6 8/7 Weight (kg) 63.6 ± ± 11.0 Duration of operation (min) 310 ± ± 27 Duration of deliberate 155 ± ± 20 hypotension (min) Drug therapy at admission, (n) Calcium-channel blocker 9 11 Angiotensin II receptor 8 7 blockers Diuretics 5 3 Amount of intraoperative 2,309 ± 521 2,286 ± 629 crystalloid (ml) Temperature ( o C) 35.7 ( ) 35.6 ( ) Amount of intraoperative 406 ± ± 112 urine output (ml) Estimated blood loss (ml) 650 ± ± 103* Patients receiving blood (n) 5 2* Basal Hb (g /dl) 12.7 ± ± 2.0 Postoperative Hb (g/ dl) 9.1 ± ± 1.9* Number of levels fused 2.3 ± ± 0.5 Values are mean ± SD, medians (25% to 75%) or number of patient (n). Group S: group with sodium nitroprusside infusion, Group R: group with remifentanil infusion. *: P < 0.05 compared with group S. A sample size calculation estimated that 15 patients would be required in each group, with 80% power to detect a 10% difference in the rso 2 value between groups with a SD of 10% and an alpha level of The data were analyzed using the Statistical Package for the Social Sciences (SPSS/Windows version 15.0; SPSS Inc., Chicago, IL, USA). Comparisons of different points in time vs. baseline measures within the groups were performed using the analysis of variance for repeated measurement followed by the Dunnett's posttest. The Mann-Whitney two-sample test was used to compare patient population data and clinical data. Gender difference, number of patients receiving blood and intraoperative events between the groups were analyzed with the Chi-square test. Statistical significance was considered at a P < RESULTS Among the 30 enrolled patients, 2 patients in group S were excluded from the analysis because one patient did not get hypotensive despite high doses of SNP and the other patient maintained hypotension without SNP. Patient characteristics are summarized in Table 1. There were no significant differences between the two groups with respect to the duration of surgery and DH, the amount of crystalloid administered, body temperature and urine output. Compared to group S, the amount of intraoperative bleeding and the number of transfused patients were significantly small in group R (P < 0.05 and P < 0.05, respectively), which resulted in a significant higher Hb after operation in group R than in group S (P < 0.05, Table 1). In addition, the basal arterial blood gases and ph were similar in the two groups and did not change with hypotensive treatment (Table 2). Table 2. Changes of Arterial Blood Gas Analysis during Deliberate Hypotension Group B T7 T9 ph S 7.44 ± ± ± 0.04 R 7.46 ± ± ± 0.04 PaO 2 (mmhg) S 221 ± ± ± 38 R 219 ± ± ± 35 PaCO 2 (mmhg) S 36 ± ± ± 1.0 R 36 ± ± ± 1.1 Values are mean ± SD. Group S: group with sodium nitroprusside infusion, Group R: group with remifentanil infusion. B: baseline before deliberate hypotension (DH), 60 min (T7) after DH, before the discontinuation of hypotensive agent (T9).

4 Sang-Hyun Park, et al:remifentanil and sodium nitroprusside in controlled hypertensive patients 41 Fig. 1. Mean arterial pressure response to sodium nitroprusside or infusion. Between the groups, no significant difference was found in the arterial pressure change during the study. *P < 0.05 compared with baseline value in group S. P < 0.05 compared with baseline value in group R. B: baseline before deliberate hypotension (DH), 1 min (T1), 2 min (T2), 3 min (T3), 5 min (T4), 15 min (T5), 30 min (T6), 60 min (T7), 90 min (T8) after DH, before the discontinuation of hypotensive agent (T9), 1 min (T10), 2 min (T11), 3 min (T12), 5 min (T13), 10 min (T14) after infusion stop. Fig. 2. Heart rate response to sodium nitroprusside or infusion. *P < 0.05 compared with group S, P < 0.05 compared with baseline value. B: baseline before deliberate hypotension (DH), 1 min (T1), 2 min (T2), 3 min (T3), 5 min (T4), 15 min (T5), 30 min (T6), 60 min (T7), 90 min (T8) after DH, before the discontinuation of hypotensive agent (T9), 1 min (T10), 2 min (T11), 3 min (T12), 5 min (T13), 10 min (T14) after infusion stop. Table 3. Summary of Intraoperative Procedures Group S (n = 13) Group R (n = 15) Infusion rate (μg/ kg/ min) 1.8 ( ) 0.19 ( ) Total doses (mg) 15.8 ± ± 0.6 MAP prior to drug infusion (mmhg) ± ± 17.6 Time to reach target MAP (min) 3.7 ± ± 1.4* Time to return to 8.5 ± ± 1.9* baseline MAP (min) Ephedrine added to 46 13* control MAP (%) Drug stop due to MAP 62 20* < 60 mmhg (%) Drug increase due to MAP 31 0* > 90 mmhg (%) Failure of DH (n) 4 None Values are mean ± SD, median (range) or percentage. Target MAP: mean arterial pressure mmhg. Group S: group with sodium nitroprusside infusion, Group R: group with remifentanil infusion. *: P < 0.05 compared with group S. Failure of DH: defined as discontinuation of the study drug more than six times, or the need for an ephedrine bolus more than four times for maintaining the MAP = 60 mmhg. Between the groups, no significant difference was found in the arterial pressure change during the study (Fig. 1). Compared to the baseline value, MAP decreased significantly from T3 to T10 in group S and from T3 to T12 in group R (P < 0.05). DH to the target MAP was achieved more slowly in group R (5.7 ± 1.4 min) compared with group S (3.7 ± 0.8 min) (P < 0.05, Table 3) and returned to baseline value at T13 in group S or T14 in group R. In addition, the frequency of ephedrine used and discontinuation of the study drug due to a MAP < 50 mmhg were higher in group S than in group R (P < 0.05, Table 3). No patient had a MAP < 50 mmhg for longer than 2 min. After the discontinuation of SNP, two patients needed fixed doses of intermittent nicardipine (1 mg each) because of rebound hypertension (systolic arterial pressure > 160 mmhg). The HR was significantly increased compared to the baseline after SNP discontinuation (T11) in group S (P < 0.05, Fig. 2) and two patients in group S had tachycardia (> 110/min) during DH. By contrast, group R patients had significantly lower HR levels from T2 to T10 compared with baseline (P < 0.05, Fig. 2). Compared to group S, the HR significantly decreased from T3 to T6 and from T11 to T14 in group R (P < 0.05, Fig. 2). Group R showed significantly lower CI levels from T3 to T11 compared to group S (P < 0.05, Fig. 3). The rso 2 value kept baseline value during anesthesia in group S, but the rso 2 value significantly decreased from T4 to T11 compared to baseline value in group R (P < 0.05, Fig. 4). Compared to

5 42 Anesth Pain Med Vol. 5, No. 1, 2010 Fig. 3. Cardiac index response to sodium nitroprusside or infusion. *P < 0.05 compared with group S. B: baseline before deliberate hypotension (DH), 1 min (T1), 2 min (T2), 3 min (T3), 5 min (T4), 15 min (T5), 30 min (T6), 60 min (T7), 90 min (T8) after DH, before the discontinuation of hypotensive agent (T9), 1 min (T10), 2 min (T11), 3 min (T12), 5 min (T13), 10 min (T14) after infusion stop. Fig. 4. Cerebral oximetry changes to sodium nitroprusside or infusion. *P < 0.05 compared with group S, P < 0.05 compared with baseline value. B: baseline before deliberate hypotension (DH), 1 min (T1), 2 min (T2), 3 min (T3), 5 min (T4), 15 min (T5), 30 min (T6), 60 min (T7), 90 min (T8) after DH, before the discontinuation of hypotensive agent (T9), 1 min (T10), 2 min (T11), 3 min (T12), 5 min (T13), 10 min (T14) after infusion stop. group S, the rso 2 values were significantly low from T4 to T12 in group R (P < 0.05, Fig. 4). There was no patient in which the rso 2 value fell to 40% or fell below 20% of the baseline value. None of the patients showed an MMSE score < 24 less or any neurological abnormality during 1-week of neurological follow up. DISCUSSION The results of this study showed that remifentanil with sevoflurane anesthesia safely induced DH in patients with medically controlled hypertension. In addition, DH with remifentanil affected the CI and rso 2 in a pattern that differed from that of SNP. Moreover, the amount of blood loss was significantly less in group R than in group S. From the results of this study, SNP seems inappropriate for patients with medically controlled hypertension because it frequently causes profound hypotension (MAP < 50 mmhg) and requires more ephedrine to maintain the target MAP. Similar to our results, SNP had been shown to cause more frequent episodes of severe hypotension than nicardipine for normotensive patients [10]. In addition, Blau and colleagues [11] reported that SNP during DH was associated with more frequent deviations from the target arterial pressure than esmolol. Therefore, these unpredictable and uncontrolled cardiovascular features of SNP might suppress the microcirculatory autoregulation of the vital organs. In previous studies, continuous infusion of remifentanil induced consistent and sustained DH during surgery such as tympanoplasty and orthognathic jaw procedures [5,6,12]. Meanwhile, with continuous infusion of remifentanil, the dosage of remifentanil should be reduced by 50% in aged patients [13] and that it should be calculated on the basis of ideal weight and not on the actual weight in obese patients [14]. Therefore, TCI rather than continuous infusion in this study seems to contribute to the consistent and sustained DH for patients with medically controlled hypertension, which needs to be verified in future studies. DH is usually achieved with the use of a potent vasodilator that has predictable, easily reversible effects. SNP is often used for this purpose despite the potential disadvantages of cyanide toxicity, reflex tachycardia, and rebound hypertension. In this study, the hemodynamic effects of SNP were similar to those previously described i.e., increased CI, HR and marked vasodilatation [15,16]. After abrupt discontinuation of SNP, the HR increased in most patients of group S. Moreover, nicardipine was necessary in two patients of group S because of rebound hypertension. By contrast, in group R, the HR was significantly lower during DH and rebound hypertension was not observed. Significant differences in the amount of intraoperative blood

6 Sang-Hyun Park, et al:remifentanil and sodium nitroprusside in controlled hypertensive patients 43 loss and the number of patients receiving transfusion (packed RBC) were also noted between the two groups, which resulted in a significant difference in postoperative Hb as shown Table 1. Guay and colleagues [17] found that the intraoperative blood loss correlated only with the number of spinal levels fused and the duration of surgery. As noted in Table 1, there was no significant difference with respect to operative time or number of levels fused in this study. One possible reason for the increased blood loss with SNP in this study should be the greater hemodynamic instability with this drug, leading to more frequent episodes of severe hypotension and higher arterial pressures than with remifentanil [11]. As a combined arterial and venous vasodilator, SNP has a pronounced venous effect [18]. Thus, it is conceivable that more venous engorgement might occur and result in more blood loss in group S than group R. Moreover, avoidance of tachycardia is an essential part of DH [19] and blood loss is correlated with the left ventricular stroke work index calculated from the systemic vascular resistance, cardiac output and HR [20]. Thus, the increases in HR and cardiac output could have increased blood loss. By contrast, the HR and cardiac index were significantly lower in group R compared to group S. Similar to our results, with high-dose remifentanil, a decrease in the MAP resulted from a 25% decrease in CI, which was accompanied by a decrease in the stroke volume index and HR [21]. The advantage of remifentanil is that it lowers blood pressure by decreasing cardiac output without peripheral vasodilatation, which reduces capillary bleeding [22]. The rso 2 value kept baseline value during SNP-induced DH and decreased during remifentanil-induced DH. NIRS provides an estimation of brain tissue oxygenation by noninvasive monitoring of the oxygenation of the cerebral venous blood. Since alterations in cerebral autoregulation may lead to adverse effects on cerebral perfusion during episodes of hypotension, cerebral oximetry may be used to identify such problems [23]. In addition, Shear and colleagues [23] demonstrated the safety of DH within the recommended MAP values of mmhg by NIRS measurements. SNP is a cerebrovasodilator, thus, it might be associated with the maintenance of rso 2 baseline values, probably secondary to cerebral vasodilation. In contrast to SNP, the rso 2 value decreased during remifentanilinduced DH. However, neither fell below 40% nor decreased more than 20% from the baseline value; they were maintained within the normal range (50 80%) during DH. Recently, it was demonstrated that there was no change in intracranial pressure and cerebral blood flow velocity in response to remifentanil infusion over time [24]. The limitations of this study are the followings. First, a transcranial Doppler study was not performed to evaluate changes in cerebral hemodynamics associated with the study drug. A transcranial Doppler study might have helped explain the discrepancy between the maintained rso 2 value and impaired cerebral autoregulation with SNP by flow-metabolism uncoupling [25]. In our study, anesthesia was maintained with 1.5 to 2 vol% sevoflurane. Cerebral pressure autoregulation remains intact with sevoflurane anesthesia in humans [26]. However, higher doses of sevoflurane cause a certain degree of excessive perfusion that is indicative of impaired cerebral autoregulation [25]. Second, although anesthesia was maintained with 1.5 to 2 vol% sevoflurane and nitrous oxide in both groups, we cannot guarantee that patients in the study experienced a similar depth of anesthesia regardless of study group. Bispectral index (BIS) has been demonstrated to quantify depth of sedation-hypnosis. However, we did not place the BIS probe on the patient's forehead because of prone position and technical limitation (little space for the BIS probe). In conclusion, the results of this study demonstrated that remifentanil with sevoflurane anesthesia induced safe DH for patients with medically controlled hypertension. Considering unstable hemodynamic features in patients using SNP, remifentanil seems more appropriate than SNP as a hypotensive agent in those patients. REFERENCES 1. Slack WK, Walther WW. Cerebral circulation studies during hypotensive anaesthesia using radioactive xenon. Lancet 1963; 1: Lassen NA, Christensen MS. Physiology of cerebral blood flow. Br J Anaesth 1976; 48: Hoffman WE, Miletich DJ, Albrecht RF. The influence of antihypertensive therapy on cerebral autoregulation in aged hypertensive rats. Stroke 1982; 13: Sharrock NE, Mineo R, Urquhart B. 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