EDITOR:

Laryngoscopy and tracheal intubation may cause undesirable increases in blood pressure (BP), heart rate (HR) and intraocular pressure (IOP). Esmolol, a short-acting β₁-adrenoceptor antagonist, and dexmedetomidine, a selective α₂-adrenoceptor agonist, have been used to modify the IOP increases and cardiovascular responses after laryngoscopy and tracheal intubation. However, data comparing the aforementioned effects of these drugs to each other are not available in the literature. Here we present the data comparison of the effects of a single pre-induction intravenous (i.v.) dose of dexmedetomidine vs. esmolol on IOP and haemodynamic changes due to tracheal intubation.

After obtaining Hospital Ethics Committee approval and informed written consent from the patients, we studied 60 ASA Grade I–II patients, aged 18–60 yr, who required tracheal intubation for elective non-ophthalmic surgery. Exclusion criteria included any known allergies or contraindications to the drugs used, pre-existing eye disease, predicted difficulty in intubation and pregnancy.

After routine monitoring, patients were premedicated with midazolam 0.03 mg kg⁻¹ 30 min before induction of anaesthesia. Patients were assigned randomly, in a double-blind fashion, to receive either saline as placebo (20 mL) (Group P, n = 20), esmolol (0.5 mg kg⁻¹) (Group E, n = 20) or dexmedetomidine (0.5 μg kg⁻¹) (Group D, n = 20) diluted in saline, using 20 mL syringes, 2 min before anaesthesia induction. Anaesthesia was induced with fentanyl (2 μg kg⁻¹), rocuronium (0.6 mg kg⁻¹) and propofol (titrated until the eyelash reflex was lost), and maintained with sevoflurane and nitrous oxide 50% in oxygen. HR, mean arterial pressure (MAP) and IOP values were recorded before and 2 min after the administration of the drug, 1 min after induction, and at 1, 3, 5 and 10 min after intubation.

After topical application of local anaesthetic, IOP was measured with a Tono-pen^® XL hand-held tonometer (Medtronicsolan, Jacksonville, FL, USA). Possible adverse effects during and after administration of esmolol or dexmedetomidine and during the postoperative period such as arrhythmia, bradycardia, tachycardia, hypotension or hypertension were recorded.

The decision to include 20 patients in each group was based on a power analysis (α = 0.05, β = 0.1), which revealed that at least 19 patients should be included in each group. Differences between three groups were compared with the Mann-Whitney U-test. Differences from baseline within groups were evaluated using the Wilcoxon signed rank test. Categorical variables were analysed using the χ ²-test. Statistical analysis was performed using SPSS version 10.0 for windows (SPSS, Chicago, IL, USA). Statistical significance was accepted as P < 0.05. All the 60 patients who were recruited completed the study.

Patient characteristics were comparable in all groups. The induction dose of propofol at which the eyelash reflex was lost was lower in the dexmedetomidine group (61.3 ± 10.2 mg) than in the esmolol (137.5 ± 16.3 mg) and placebo (144.0 ± 14.1 mg) groups (P < 0.001 for both groups). None of the patients needed active treatment for cardiac problems during the study period.

After administration of study drugs, IOP, MAP and HR were lower in Groups D and E when compared with Group P (IOP: P < 0.001 for Groups D and E; MAP: P < 0.001 for Group D, P = 0.028 for Group E; HR: P < 0.001 for Group D and P = 0.014 for Group E). Following induction, there were no differences in IOP values among groups but MAP was significantly decreased in Group D compared with Group P (P = 0.043), while HR was lower in Groups D and E than in Group P (P < 0.001 for both groups). The amount of reduction in HR in Group D was higher than that in Group E (P = 0.046). IOP and HR at 1, 3, 5 and 10 min after intubation were lower in Group D compared with Groups E and P (IOP: P < 0.001 for all variables; HR: P < 0.001, P < 0.001, P < 0.001 and P = 0.020 for Group E and P < 0.001, P < 0.001, P < 0.001 and P = 0.005 for Group P, respectively). Additionally, in patients receiving esmolol, decreases in IOP at time points of 1, 3 and 5 min after intubation were higher when compared with the patients in Group P (P = 0.001, P < 0.001 and P = 0.008, respectively). MAP at 1 min after intubation in Group D was significantly less than that in Groups E and P (P = 0.012 and P = 0.005, respectively) (Table 1).

Table 1 Changes in intraocular pressure, mean arterial pressure and heart rate.

IOP: intraocular pressure; MAP: mean arterial pressure; HR: heart rate.

Data are presented as mean ± SD.

^§P < 0.05 and *P < 0.001 vs. Group E; ^♯P < 0.05, ^†P < 0.01 and ^‡P < 0.001 vs. Group P.

Both esmolol and dexmedetomidine have been used for the attenuation of the adrenergic response to laryngoscopy and tracheal intubation. There is a dose-dependent risk of hypotension and bradycardia before laryngoscopy when esmolol and dexmedetomidine are combined with anaesthesia induction agents. We preferred single-bolus low doses for both drugs in our study instead of an infusion or higher dose administration in order to prevent the potential risk of bradycardia or hypotension. However, especially for esmolol, no consensus has been reached regarding the optimum dose nor the mode and timing of its delivery [Reference Figueredo and Garcia-Fuentes1]. Bensky and colleagues [Reference Bensky, Donahue-Spencer, Hertz, Anderson and James2] suggested that small doses of esmolol (0.2 or 0.4 mg kg⁻¹) may block the increases in HR and BP resulting from laryngoscopy and intubation. Nevertheless, Kovac and colleagues [Reference Kovac, Bennets, Ohara, LaGreca, Khan and Calkins3] reported that esmolol 1.5 mg kg⁻¹ given 30 s prior to induction was found to blunt the maximum increase in HR but not MAP or IOP. Regarding dexmedetomidine, Jaakola and colleagues [Reference Jaakola, Ali-Melkkila, Kanto, Kallio, Scheinin and Scheinin4] have reported attenuation of the increase in the HR and arterial pressure during intubation by a bolus injection of 0.6 μg kg⁻¹ dexmedetomidine, 10 min before anaesthesia induction, which also decreased intra-operative IOP and anaesthetic requirements for thiopentone and isoflurane. The continuous i.v. infusion of dexmedetomidine has been shown to decrease propofol requirements in volunteers and patients [Reference Dutta, Karol, Cohen, Jones and Mant5,Reference Peden, Cloote, Stratford and Prys-Roberts6]. In our study, single i.v. dose of dexmedetomidine (0.5 μg kg⁻¹) blunted the haemodynamic and IOP responses to tracheal intubation. Secondarily, the single-bolus dose administration of dexmedetomidine in contrast to the continuous i.v. infusion used in previous studies also proved to reduce the propofol requirements for induction of anaesthesia. However, esmolol, with the dose of 0.5 mg kg⁻¹ used in this study, was shown to be ineffective in the attenuation of IOP and haemodynamic responses to tracheal intubation.

In conclusion, the results of this study emphasise that dexmedetomidine is more effective than esmolol in preventing the haemodynamic and IOP responses to tracheal intubation in ASA I–II patients. In order to further evaluate the effects of esmolol, additional studies should be planned to assess the optimum dose, mode and delivery timing of this drug. Furthermore, it should be noted that this study included only healthy patients and does not reflect the effects of these drugs on patients with a history of hypertension or glaucoma.