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ORIGINAL ARTICLE
Year : 2016  |  Volume : 9  |  Issue : 1  |  Page : 66-71

Dexmedetomidine premedication with three different dosages to attenuate the adverse hemodynamic responses of direct laryngoscopy and intubation: a comparative evaluation


1 Department of Anaesthesiology & Critical Care, Imaging & Interventional Radiology, N.S.C.B. Subharti Medical College, Swami Vivekananda Subharti University, Subhartipuram, Meerut, Uttar Pradesh, India
2 Department of Radiodiagnosis, Imaging & Interventional Radiology, N.S.C.B. Subharti Medical College, Swami Vivekananda Subharti University, Subhartipuram, Meerut, Uttar Pradesh, India

Date of Submission20-Dec-2014
Date of Acceptance04-May-2015
Date of Web Publication17-Mar-2016

Correspondence Address:
Kumkum Gupta
DA, 108, Chanakyapuri, Shastri Nagar, Meerut 250004, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1687-7934.178882

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  Abstract 

Background
Direct laryngoscopy and tracheal intubation predictably lead to transient and variable hemodynamic responses, which can be attenuated by α2-receptor agonists. The present study aimed to evaluate comparatively the three different dosages of dexmedetomidine (0.5, 0.8, and 1 μg/kg) as premedication for the attenuation of these hemodynamic responses of direct laryngoscopy and intubation.
Participants and methods
Ninety adult consented patients of ASA grades I and II of either sex were randomized into three equal groups of 30 patients each in a double-blind manner. Dexmedetomidine in dosages of 0.5 μg/kg (group I), 0.8 μg/kg (group II), and 1 μg/kg (group III) was infused over 10 min as premedication before propofol induction. The hemodynamic changes during infusion, after induction, and after laryngoscopy and intubation were recorded for statistical analysis.
Results
Patients with a comparable demographic profile showed a decrease in heart rate and blood pressure after dexmedetomidine infusion in a dose-dependent manner. Further decrease in heart rate and blood pressure after propofol induction showed a statistically significant (P < 0.05) difference among groups. After laryngoscopy and intubation, the increase in heart rate and blood pressure was more evident in patients in whom low dosages of dexmedetomidine was infused with a statistically significant (P < 0.05) difference among the groups.
Conclusion
Premedication with dexmedetomidine at a dosage of 1 μg/kg attenuated the adverse hemodynamic responses of laryngoscopy and intubation adequately.

Keywords: adverse hemodynamic responses, dexmedetomidine, laryngoscopy and intubation, propofol


How to cite this article:
Gupta K, Bansal M, Gupta PK, Singh M, Agarwal S, Tiwari V. Dexmedetomidine premedication with three different dosages to attenuate the adverse hemodynamic responses of direct laryngoscopy and intubation: a comparative evaluation . Ain-Shams J Anaesthesiol 2016;9:66-71

How to cite this URL:
Gupta K, Bansal M, Gupta PK, Singh M, Agarwal S, Tiwari V. Dexmedetomidine premedication with three different dosages to attenuate the adverse hemodynamic responses of direct laryngoscopy and intubation: a comparative evaluation . Ain-Shams J Anaesthesiol [serial online] 2016 [cited 2019 Sep 18];9:66-71. Available from: http://www.asja.eg.net/text.asp?2016/9/1/66/178882


  Introduction Top


Direct laryngoscopy and endotracheal intubation are the most frequently performed procedures, but their clinical benefits are not without a few undesirable effects due to afferent vagal stimulation and an efferent sympathoadrenal response. These transient and variable hemodynamic changes of tachyarrhythmia and hypertension may lead to life-threatening complications in high-risk patients [1] .

Various pharmacological methods such as lidocaine, opioid analgesics, β-blockers, calcium channel blockers, angiotensin-converting-enzyme inhibitors, vasodilators, and topical anesthetics have been evaluated to attenuate these adverse hemodynamic responses, but none of them has proven to be ideal; hence, the search of an ideal agent is still continuing [2],[3] .

Dexmedetomidine is a highly selective α2-adrenergic receptor agonist and possesses the potential benefits of sedation, sympatholysis, analgesia, and cardiovascular stability. Its hemodynamic effects are predictable and dose-dependent. Dexmedetomidine, at clinically effective dosages, does not depress respiration, and therefore does not interfere with extubation. This pharmacological profile renders it suitable for premedication for general anesthesia in intravenous doses varying from 0.25 to 1 μg/kg for the attenuation of intubation responses, but the optimal dose is not yet established [4],[5],[6],[7],[8] .

The present prospective double-blind randomized study was designed to evaluate comparatively the efficacy and the safety of three different dosages of dexmedetomidine (0.5, 0.8, or 1 μg/kg) as premedication for the attenuation of the adverse hemodynamic response of laryngoscopy and intubation after propofol induction. The selection of dosages of dexmedetomidine for the present study was in accordance with the study conducted by Saoyroolu et al. [9] .


  Participants and methods Top


After Institutional Ethical Committee approval and informed consent were obtained, the present prospective randomized double-blind comparative study was carried out on 90 patients of ASA grades I and II, aged 18-58 years, of either sex, scheduled for elective surgical procedure under general anesthesia. The study was conducted from September 2012 to February 2014 at CSS Hospital associated with Subharti Medical College, Swami Vivekanand Subharti University, Meerut. All patients underwent preanesthetic examination, and patients with a history of systemic hypertension, cardiac dysfunction, hepatic, renal, endocrine, or metabolic disorder, morbid obesity, an expected difficult direct laryngoscopy or intubation (Mallampati grade III/IV), and patients who required more than one attempt for intubation were excluded from the study.

Ninety enrolled patients were divided into three equal groups of 30 patients each according to a computer-generated random number table. Patients received dexmedetomidine in dosages of 0.5 μg/kg (group I), 0.8 μg/kg (group II), and 1 μg/kg (group III), diluted in 10 ml normal saline and infused over 10 min as intravenous premedication. The study medication was prepared by an anesthesiologist who was blinded to the randomization schedule and was not involved for recording the hemodynamic changes of laryngoscopy and intubation.

All patients were admitted a day before the surgery, and fasting for 8 h was ensured. In the preoperative room, they were premedicated with injection glycopyrrolate 0.2 mg intramuscularly, 30 min before the induction of anesthesia. On arrival to the operation theater, standard monitoring of the heart rate, noninvasive blood pressure, ECG, and peripheral oxygen saturation were commenced, and administration of lactate Ringer's was started at a rate of 4-6 ml/kg. After dexmedetomidine infusion, they were given ondansetron 4 mg, midazolam 2 mg, and tramadol 100 mg intravenously. Anesthesia was induced with 1% propofol at a dosage of 2 mg/kg and intubation was facilitated with vecuronium bromide (0.1 mg/kg). Laryngoscopy was performed with a Macintosh laryngoscope with an adequate-sized blade, and the trachea was intubated with an appropriate-sized cuffed endotracheal tube. Anesthesia was maintained with nitrous oxide 60% in oxygen and isoflurane using a closed circuit. Patients were mechanically ventilated and normocapnia (EtCO 2 between 35-40 mmHg) was maintained.

The blood pressure, the heart rate, ECG, and oxygen saturation were recorded at baseline, during and after dexmedetomidine infusion, and after induction and intubation at 1-min intervals until 10 min after induction. After that, monitoring was continued at 5-min intervals till 30 min, and then at every 15 min till the end of the surgery and extubation. At the end of the surgery, the residual neuromuscular blockade was antagonized, and extubation was performed when respiration was adequate and the patient was able to obey simple verbal commands.

Hemodynamic changes occurring during the study period, that is, till 10 min after induction, were not treated unless these changes were compromising patient safety, and a record of each such event was maintained. For the present study, hypotension was defined as systolic blood pressure (SBP) less than 20% of the baseline value or less than 90 mmHg, whichever was lower; hypertension was defined as SBP more than 20% of the baseline value or more than140 mmHg, whichever was higher. Tachycardia was defined as heart rate more than 100 beats/min, and bradycardia was defined as heart rate less than 60 beats/min.

Patients were transferred to the postanesthesia care unit for further monitoring of any hemodynamic changes, shivering, respiratory depression, and postoperative nausea and vomiting, which were managed accordingly.

Study population size calculation

The preliminary sample size was decided in consultation with a statistician and was based on the initial pilot observation, which indicated that ~20 to 23 patients should be included in each group to ensure a power of 0.80 for detecting a clinically meaningful reduction by 20% in the heart rate and the mean arterial blood pressure during laryngoscopy and endotracheal intubation. Assuming a 5% dropout rate, the final size was set at 90 patients.

The data obtained in the study are presented in a tabulated manner and represented as mean ± SD. A statistical analysis was performed through the SPSS, 11.5 version software (SPSS Inc., Chicago USA). For intergroup comparison of hemodynamic changes, one-way analysis of variance was used. For qualitative data, the χ2 -test was applied. A P-value of less than 0.05 was considered as statistically significant.


  Results Top


The present study was completed successfully, and all patients were included for data analysis. The demographic profile of age, weight, BMI, sex, and ASA physical status was comparable among the groups [Table 1].
Table 1 The demographic profile of patients

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Changes in the heart rate among groups

Baseline mean heart rates were comparable in all the three groups, but showed a statistically significant difference from induction to 10 min. Multiple comparisons between groups showed that the heart rate in patients of group III was significantly less than that in patients of group I at all times. The mean difference in the heart rate was maximal at 5 min from induction. The comparison of group I with group II and group II with group III was not statistically significant [Table 2] and [Table 3].
Table 2 Changes in the mean heart rate among the groups

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Table 3 Multiple comparison of the mean heart rate among groups

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Changes in the systolic blood pressure among groups

The mean SBP at baseline was comparable among all the groups. The minimum SBP was observed at induction in all groups. After induction, the mean SBP was lower in group III as compared with group I at all times, with a statistically significant difference among the groups [Table 4].
Table 4 Changes in the systolic blood pressure among the groups

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Multiple comparisons among the groups showed a statistically significant difference, with the maximum mean difference at induction, which decreased with the increase in time between groups I and III. The comparison among groups was not always significantly different during the study period [Table 5].
Table 5 Multiple comparison of the systolic blood pressure among the groups

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Changes in the diastolic blood pressure among groups

The mean diastolic blood pressure (DBP) was comparable at baseline. There was a statistically significant difference among the groups from induction to 10 min. The mean DBP in group III was always lower as compared with groups I and II, and showed a decreasing trend from 1 to 10 min [Table 6].
Table 6 Changes in the diastolic blood pressure among the groups

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Multiple comparisons of the mean DBP among the groups showed that the mean difference between groups I and III has an increasing trend from induction to 3 min initially, and then decreases consistently. At 3 min, the maximum mean difference in the DBP was observed. Patients of group III differed significantly from group I at all time intervals [Table 7].
Table 7 Multiple comparison of the diastolic blood pressure among the groups

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Changes in the mean arterial pressure among groups

There was no significant difference in the mean arterial pressure (MAP) among the three groups at baseline. A decrease in the MAP after induction was observed in all patients, but the decrease in the mean arterial blood pressure was more profound in patients of group III, with a highly significant difference (P < 0.001). All the groups differed significantly at different time intervals during the study period [Table 8].
Table 8 Changes in the mean arterial pressure among the groups

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Multiple comparison of the mean arterial blood pressure showed that it was always low in group III as compared with groups I and II at every time interval. The maximum mean difference between groups I and III was seen at 3 min after induction [Table 9].
Table 9 Multiple comparison of the mean arterial pressure among the groups

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  Discussion Top


Protective airway reflexes of the patient are obtund after the induction of general anesthesia, but the cuffed endotracheal intubation provides excellent protection of the airway from aspiration. Direct vision laryngoscopy is a gold standard for endotracheal intubation, but it stimulates the pharyngeal tissues to cause a marked increase in the arterial blood pressure and the heart rate, occasional dysrhythmias, cough reflex, and increased intracranial pressure and intraocular pressure. Although these hemodynamic changes are transient, they are undesirable in patients with pre-exiting myocardial or cerebral insufficiency. If no specific measures are taken to attenuate these adverse hemodynamic responses, the postoperative outcome of the patient may be affected [1] .

Many strategies have been evolved to attenuate these adverse hemodynamic responses of laryngoscopy and endotracheal intubation, but choosing the ideal agent is still a controversial issue. Dexmedetomidine, the highly selective α2-adrenergic agonist, has a unique mode of action with inherit benefits of sedation, sympatholysis, analgesia, and cardiovascular stability without respiratory depression. This pharmacological profile renders it suitable for premedication for general anesthesia. Dexmedetomidine has been used in intravenous doses varying from 0.25 to 1 μg/kg for attenuating intubation responses, but the optimal dose is not yet established [8] .

In the present study, three different dosages (0.5, 0.8, and 1 μg/kg) of dexmedetomidine were studied to evaluate the effective and safe intravenous dose of dexmedetomidine to attenuate these adverse hemodynamic responses of laryngoscopy and endotracheal intubation.

The recent study by Saoyroolu and colleagues compared the clinical effects of two different dosages of dexmedetomidine (1.0 and 0.5 μg/kg) on the hemodynamic response to tracheal intubation and the quality of intubation. They concluded that dexmedetomidine at a dosage of 1 μg/kg was more effective than dexmedetomidine 0.5 μg/kg in controlling the hemodynamic pressor responses to tracheal intubation [9] . In the present study, the three different dosages of dexmedetomidine (0.5, 0.8, and 1 μg/kg) were infused before propofol induction, and the results of our study are in concurrence with their study.

Presynaptic and postsynaptic effects of α2 agonists diminish norepinephrine release and inhibit the central sympathetic outflow. In the present study, there was a significant decrease in the heart rate in all patients after induction, but it was more marked in patients who received dexmedetomidine at dosage of 1 μg/kg as premedication. The primary action of dexmedetomidine on the heart is a negative chronotropic effect by blocking the cardioaccelerator nerves and by augmenting the vagal nerve. The decrease in heart rate can be attributed to a reflex response for transient hypertension during the initial part of infusion and subsequently due to a decrease in the central sympathetic outflow [10] .

An increase in the heart rate after intubation was observed in all patients in our study, but the increase was more in patients who received dexmedetomidine in lower dosages. The difference was statistically highly significant among the groups till 5 min after intubation.

Yildiz et al. [11] and Keniya et al. [12] studied the effect of dexmedetomidine on the hemodynamic responses to laryngoscopy and intubation and on the intraoperative anesthetic requirement. They concluded that the increase in blood pressure and heart rate was significantly lower in the dexmedetomidine group than in the placebo group. Another study conducted by Sulaiman et al. [13] also found a statistically significant difference in the SBP, the DBP, and the MAPs at the first, the third, and the fifth minutes after intubation between the dexmedetomidine group and the control group.

In the present study, the hemodynamic responses were significantly attenuated in patients who received dexmedetomidine in higher dosages of 1 μg/kg, and our results are in accordance with many other previous clinical studies that concluded that dexmedetomidine is effective for hemodynamic stability during laryngoscopy and intubation as well as intraoperatively [14],[15],[16],[17] .

Scheinin et al. [18] concluded from their study that dexmedetomidine not only attenuates sympathoadrenal responses to intubation but also reduces the need for thiopentone and preoperative fentanyl. Tanskanen et al. [19] conducted a double-blind study to observe the efficacy of dexmedetomidine as an anesthetic adjuvant in patients undergoing intracranial tumor surgery and concluded that dexmedetomidine increased the perioperative hemodynamic stability, and extubation was faster without respiratory depression.

Hypotension and bradycardia (heart rate<60 beats/min) were not observed in any patient during the study period; hence, intravenous atropine or vasopressor was not used. This may be because of the adequate preanesthetic plasma volume expansion and the injection of glycopyrrolate in the premedication.

A possible limitation of our study was in assessing the intraoperative and the postoperative complications because our study was restricted till 10 min after induction and many patients were given intraoperative intravenous fentanyl for analgesia.


  Conclusion Top


Premedication with dexmedetomidine at a dosage of 1 μg/kg attenuated the adverse hemodynamic response of laryngoscopy and intubation adequately. It exhibited linear hemodynamic pharmacokinetics in the dosage range of 0.5 to 1 μg/kg.


  Acknowledgements Top


Conflicts of interest

There are no conflicts of interest.

 
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  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9]



 

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