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TECHNOLOGY, COMPUTING, AND SIMULATION

Assessing Propofol Induction of Anesthesia Dose Using Bispectral Index Analysis

From the Department of Anesthesiology, Pamukkale University School of Medicine, Denizli, Turkey

Address correspondence and reprint requests to Ercan Gürses, MD, Atakent Mah Esnaf Sitesi, Zambak Sok No:8 20045 Yeniehir Denizli, Turkey. Address email to elgurses{at}pamukkale.edu.tr

	Abstract

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In this study we sought to determine the propofol requirement and hemodynamic effects as guided by bispectral index (BIS) analysis during induction of anesthesia. Sixty patients were enrolled in this study. Propofol, 2 mg/kg, was given to Group I for induction. Propofol was administered for induction until loss of response to verbal commands and until BIS values were around 50 to Groups II and III. After induction, the smallest BIS value was different in Group I. Decreases in total propofol dose were 36% and 43% in Groups II and III respectively as compared with Group I. The dose of propofol assessed by BIS analysis results in an important reduction of propofol requirement without side effects.

IMPLICATIONS: Hypotension during induction of anesthesia with propofol is common. This study has shown that propofol requirement assessed by bispectral index analysis during anesthesia induction may decrease the dose and side effects and provide for satisfactory depth of anesthesia.

	Introduction

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Hypotension during induction of anesthesia can increase cardiac morbidity in critically-ill patients with low cardiac output (1). There is no agreement regarding the smallest propofol dose and method of administration that minimizes the risk of hypotension. Blood concentration of propofol depends on many factors, such as age, gender, body weight, dose, infusion rate, and cardiac output (2–6). Bispectral index (BIS) analysis is a variable that tends to correlate with the magnitude of sedation and loss of consciousness (6). The BIS index has correlated well with plasma propofol concentration (7–9). BIS was developed using clinical end-points of sedation and relates monotonically to both the hypnotic component of anesthesia and to anesthetic drug concentration (10). The aim of this study was to determine the propofol requirement and hemodynamic effects as guided by BIS during induction of anesthesia.

	Methods

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After obtaining institutional approval, 60 consenting patients were enrolled in this study. The patients were aged 28–55 yr, ASA physical status I–II, scheduled for elective surgery under general anesthesia and orotracheal intubation. Exclusion criteria were a history of cardiac, pulmonary, liver or renal disease, or significant obesity (body mass index >30). Long-term user of central nervous system activator drugs, benzodiazepines and/or opiates and women who might be pregnant were excluded from the study.

Patients were unpremedicated. Before induction, a canula was inserted into a forearm vein, and lactated Ringer’s solution 10 mL/kg infused. The usual monitoring, including BIS, was used. BIS was measured at the frontal lobe of the dominant hemisphere after skin preparation with disinfectant alcohol and slight rubbing, We used a BIS monitor (Aspect Medical Systems, Cambridge, MA; BIS version 3.0 rev.0.5) and BIS sensor. BIS measurement was begun before anesthesia induction and was recorded every 15 s during induction. Patients were allocated randomly (by sealed envelope technique) to three groups according to the propofol dose at the induction. Propofol was given 2 mg/kg to Group I for induction. Propofol for induction was administered until loss of response to verbal commands, and until BIS values were around 50 for Groups II and III. Propofol was administered at the same infusion rate of 20 mg · kg^-1 · h^-1 by infusion pump in all three groups. Total propofol dose was also recorded. Depth of sedation and alertness was assessed using the Responsiveness Scores of the Modified Observer’s Assessment of Alertness/Sedation Scale (OAA/S) (Table 1) (7) every 15 s during the study by a blinded investigator (EG). The level of sedation and alertness was targeted to an OAA/S score of 2.

	Results

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There were no significant differences in patient demographics and ASA physical status (Table 2). Systolic blood pressures (SBP) was not different among groups before anesthesia induction. SBP was lower in Group I than the other groups after anesthesia induction (P < 0.001) (Fig. 1). Diastolic blood pressures were not different before and after anesthesia induction. No differences were found in heart rate and peripheral oxygen saturation values within and among groups before and after anesthesia induction. BIS values were similar in all groups before anesthesia induction. After anesthesia induction, the smallest BIS values were found 21.7 ± 12.1, 33.4 ± 11.9, and 46.5 ± 12.6 in Groups I, II, and III respectively. The smallest BIS value was significantly different in Group I (P < 0.05) (Fig. 2). The total propofol doses were 147.4 ± 12.1 mg, 95.8 ± 10.2 mg, and 84.3 ± 11.4 mg in Groups I, II, and III respectively. Group I had the largest total propofol dose (Fig. 3). Decreases in total propofol dose were 36% and 43% in Groups II and III respectively as compared with Group I.

View larger version (43K): [in this window] [in a new window]   Figure 1. Systolic blood pressures in groups.

View larger version (39K): [in this window] [in a new window]   Figure 2. Bispectral index values in groups.

View larger version (28K): [in this window] [in a new window]   Figure 3. Total propofol doses in groups.

	Discussion

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A typical anesthetic induction dose of propofol (2 mg/kg) results in an approximate 30% reduction in SBP (11). This hypotension is mainly attributable to a decrease in sympathetic activity, direct vasodilation, and direct myocardial depression (5). The propofol administration rate has a critical impact on the induction dose. The pharmacokinetics of propofol are not stationary. Induction doses of propofol are highly variable at administration rates of <20 mg · kg^-1 · h^-1. Induction dose and time are dependent on infusion rate in a complex manner, and residual dose_circulation has been a factor in overdose and hemodynamic depression (4). For this reason, we used a safe small dose of propofol (20 mg · kg^-1 · h^-1) for infusion.

In this study, a 29% reduction in SBP occurred in Group I. SBP values did not change after anesthesia induction in Groups II and III. A small dose of propofol for induction of anesthesia was used with a slow and stable infusion rate, which resulted in stable hemodynamics and sufficient depth of anesthesia.

Previous studies have found that BIS correlated well with plasma propofol concentration (12–14). However, Hoymork et al. (15) did not find any correlation between plasma propofol concentration and BIS values. BIS value was calculated every 30 s in their study. They thought that 30 s was too long for the assessment of rapid changes during anesthesia induction, as BIS changes very fast. Thus, during rapid changes in patient conditions the timing of BIS registration is very critical and difficult to standardize. In this study, BIS values were calculated by averaging the values recorded during a 15-s interval.

Target plasma concentration was used in previous studies to calculate total propofol dose. Propofol requirement was decreased by using BIS (1,2,12–19). In this study, we used the BIS value to calculate propofol requirement, and the largest reduction of propofol requirement was noticed in the BIS adjustment group (Group III). In comparison with the standard propofol dose regimen, there was a 43% reduction of propofol dose in Group III. Loss of response to verbal commands was also used for calculation of propofol requirement, which resulted in a 36% reduction of propofol requirement.

In conclusion, the induction dose of propofol assessed by BIS analysis results in an important dose reduction without side effects. We suggest that using BIS analysis for guiding the propofol dose used for inducing anesthesia may be safer, especially for critically-ill elderly patients.

	References

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