|Year : 2022 | Volume
| Issue : 1 | Page : 93-96
Therapeutic Efficacy of dexmedetomidine on the pressor response due to endotracheal intubation and on the induction dose of propofol for surgeries under general anesthesia
Shilpa Sarang Kore, Vazhakalayil Subha Teresa Jose, Krusha Suresh Shah
Department of Ananesthesiology, Dr. D. Y. Patil Medical College and Research Centre, Pune, Maharashtra, India
|Date of Submission||02-Jul-2021|
|Date of Decision||24-Aug-2021|
|Date of Acceptance||07-Sep-2021|
|Date of Web Publication||08-Nov-2021|
Shilpa Sarang Kore
Dr. D. Y. Patil Medical College and Research Centre, Pimpri, Pune, Maharashtra
Source of Support: None, Conflict of Interest: None
Introduction: Pressor response to laryngoscopy and endotracheal intubation has been associated with sympathetic and parasympathetic responses which can be attenuated by alpha 2 receptor agonists. Aims: The present study aimed to compare and evaluate the effectiveness of dexmedetomidine in attenuating hemodynamic response to endotracheal intubation and also on the induction dose of propofol. Materials and Methods: It was a prospective, randomized, double-blinded, parallel group, placebo-controlled study in tertiary care hospital. A total of 50 patients aged 18–60 years, American Society of Anaesthesiology 1 and 2, scheduled for elective surgeries under general anesthesia (GA). Each patient in Group 1 received a loading dose of dexmedetomidine at 0.001 mg/kg over 10 min before induction of anesthesia and Group 2 received 20 ml normal saline over 10 min. Hemodynamic parameters prior to laryngoscopy and up to 10 min after intubation were measured. The requirement of induction dose of propofol was also calculated. Results: Dexmedetomidine showed significant efficacy in suppressing pressor response during endotracheal intubation. Furthermore, lesser dose of propofol was required for induction of GA. Conclusion: Dexmedetomidine can be used as an adjuvant in GA to prevent pressor response during intubation and decrease the requirement of intravenous induction agent propofol.
Keywords: Dexmedetomidine, intubation, laryngoscopy, response
|How to cite this article:|
Kore SS, Teresa Jose VS, Shah KS. Therapeutic Efficacy of dexmedetomidine on the pressor response due to endotracheal intubation and on the induction dose of propofol for surgeries under general anesthesia. Med J DY Patil Vidyapeeth 2022;15:93-6
|How to cite this URL:|
Kore SS, Teresa Jose VS, Shah KS. Therapeutic Efficacy of dexmedetomidine on the pressor response due to endotracheal intubation and on the induction dose of propofol for surgeries under general anesthesia. Med J DY Patil Vidyapeeth [serial online] 2022 [cited 2022 May 19];15:93-6. Available from: https://www.mjdrdypv.org/text.asp?2022/15/1/93/329931
| Introduction|| |
General anesthesia (GA) is associated with a drug-induced controlled and reversible loss of consciousness during which patients are not arousable even by painful stimuli. Laryngoscopy and endotracheal intubation are necessary for effective control of airway and ventilation, but it has deleterious effects such as hypertension and bradycardia. These hemodynamic changes are due to the reflex sympathetic activity and the magnitude of response is directly proportional to the duration and strength of laryngoscopy. Several drugs and techniques have been tried to attenuate the stress response to laryngoscopy and endotracheal intubation, but none of them have proven to be ideal.,, Dexmedetomidine is a highly selective alpha 2 receptor agonist and possesses the properties of sedation, analgesia, and opioid-sparing effect., It has been shown to reduce the laryngeal stress response, reduce the requirement of intravenous (IV) anesthetics, and provides hemodynamic stability. Our study was designed to evaluate the effect of dexmedetomidine on the stress response due to laryngoscopy and induction dose of propofol during GA.
| Materials and Methods|| |
After getting approval from the institutional ethics subcommittee (research protocol no. IESC/FP/2020/23), a randomized prospective double-blind study was carried out in a tertiary referral medical college. After obtaining informed consent, the American Society of Anesthesiology (ASA) 1 and ASA 2 physical status was randomly divided into two groups of 25 each. Group 1 received dexmedetomidine 0.001 mg/kg diluted up to 20 ml of normal saline infused over 10 min. Group 2 received a placebo of 20 ml of normal saline infused over 10 min.
- ASA Grade I or II fit patients
- Ages between 18 and 60 years
- Elective surgical procedures under GA.
- Patient refusal
- ASA Grade III and IV
- Severely Hypovolemic state
- Difficult airway
- History of cardiac disease and neurological disease.
Preoperative fasting status was confirmed. A large bore vascular access was obtained after which standard monitors such as electrocardiography (ECG), blood pressure (BP), pulse oximeter, and end-tidal carbon dioxide were attached.
Baseline heart rate (HR), systolic BP (SBP), diastolic BP (DBP), and saturation (SpO2) were measured. Patients were given IV ringer's lactate. Patients were premedicated with injection glycopyrrolate 0.2 mg and injection ondensetron ½ h prior to surgery.
Later, the study drug was given as an infusion over 10 min. After 5 min of completion of drug infusion, the vital parameters were noted again and GA was initiated.
The patient was preoxygenated with 100% of oxygen (O2) for 3 min. The patient was induced with 20 mg titrated doses of propofol which was repeated every 30 s. The absence of verbal response and loss of eyelash reflex was used as the clinical sign for titration of propofol dose. This was followed by injection suxamethonium 2 mg/kg IV.
Intubation was done within 15 s with direct laryngoscopy by a senior anesthetist.
Anesthesia was maintained with oxygen, nitrous oxide, sevoflurane, and controlled ventilation using a closed circuit with vecuronium as a muscle relaxant.
Pulse rate, SBP, DBP, and mean arterial pressure (MAP) were recorded with the help of a digital monitor.
The vitals were recorded during laryngoscopy, 1 min, 2 min, 4 min, 5 min, 7 min, and 10 min after intubation. In addition, pulse, BP, and ECG, were monitored throughout the intraoperative and immediate postoperative period. Respiratory rate and depth of respiration were monitored postoperatively.
| Results|| |
All patients in both the groups were comparable according to age and sex distribution [Chart 1] and [Chart 2]. The baseline HR, SBP, DBP, and mean BP were not significantly different between both the groups, but at laryngoscopy and up to 10 min after laryngoscopy, they were significantly lower in the study group than in the control group (P < 0.05) [Table 1], [Table 2]. The total mean dose of propofol required in the study control was 91.6+/-19.7 mg versus in the control group was 104 ± 21.4 mg [Table 3]. This was statistically significant.
|Table 1: Evaluation of heart rate of patients in study and control groups at different points of time|
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|Table 3: Comparison of total propofol requirement (mg) in study and control groups|
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| Discussion|| |
GA during surgery produces a state of controlled unconsciousness during which the patient is unaware and insensitive to pain. During the unconscious state, airway is maintained by laryngoscopy and endotracheal intubation. This procedure causes an intense stress response in the form of tachycardia, hypertension, arrhythmia, raised intracranial pressure, and intraocular pressure. The hemodynamic changes brought about by laryngoscopy and intubation were first described by Reid and Brace. The response to laryngoscopy is seen within 5 s of laryngoscopy, peak being at 1–2 min and returns to normal level by 5 min. The pressor response is well tolerated by a normal patient, but this can cause deleterious effects such as myocardial infarction, arrhythmias, left ventricular failure, pulmonary edema, or cerebrovascular accident in compromised patients. Stress response can be suppressed by many drugs such as calcium channel blockers, opioids, and alpha 2 receptor agonists. The commonly used alpha 2 receptor agonists are dexmedetomidine and clonidine. These drugs act on the alpha 2 A receptors located in locus ceruleus in the upper brain stem. In the presynaptic center, alpha 2 A receptors inhibit noradrenaline release and cause sedation and hypnosis. Postsynaptic activation of alpha 2 receptors causes decreased sympathetic activity leading to bradycardia and hypotension. Thus, dexmedetomidine is a highly selective alpha 2 adrenergic agonist with benefits of sedation, sympatholysis, analgesia, and cardiovascular stability without respiratory depression. In our present study, dexmedetomidine infusion in the dose 0.001 mg/kg attenuated the hemodynamic response during preinduction and up to 10 min after laryngoscopy and intubation compared to control group. Similarly, Menda et al. demonstrated that SBP, DBP, and MAP were lower at all times when dexmedetomidine was used at a dose of 0.001 mg/kg. Sharma and Mehta in their study concluded that both the loading doses of 0.001 mg/kg and 0.0005 mg/kg were equally effective in reducing the induction dose of propofol, improving the intubating condition and blunting the hemodynamic response to laryngoscopy and intubation. Harshavardhana et al. also concluded that dexmedetomidine at 0.001 mg/kg attenuated the tachycardia response to laryngoscopy, intubation, and pneumoperitoneum. It also has a better dose sparing effect on anesthetic drugs used intraoperatively. Deepali and Arora also showed similar results in their study. De Cassai et al. concluded that patients receiving premedication with dexmedetomidine for tracheal intubation, compared with no dexmedetomidine, have a lower BP and HR. Propofol is a frequently used IV anesthetic agent for induction and maintenance during surgeries. Although known for its remarkable safety, even short-term infusion can lead to intraoperative complications which is suggested by recent literature. In our study, we also concluded that the total induction dose of propofol required was significantly less in the group where dexmedetomidine was used during preinduction. We noted a reduction in propofol dose needed for induction with a standard clinical sign (loss of verbal response and eyelash reflex) for titration of the dose drug. Sen et al. in their study concluded that administration of dexmedetomidine at a dose of 0.001 mg/kg significantly reduces the requirement of propofol during induction of GA in the spine surgery along with stable hemodynamic parameters.
Park et al. evaluated low-dose dexmedetomidine infusion 0.0003 mg/kg/h on the requirement of propofol during laparoscopic cholecystectomy. They concluded that dexmedetomidine decreased the requirement of propofol. Madhusudan et al. in their study used 0.001 mg/kg dexmedetomidine as infusion and concluded that thiopentone requirement was decreased by 50% for induction of GA. Vishwanath et al. in their study concluded that the mean requirement of propofol for induction was reduced by 26.6% in the dexmedetomidine group compared to the control group. In our study, we did not observe hypotension or bradycardia in any patient. This may be because of adequate preanesthetic plasma volume expansion and injection glycopyrrolate in the premedication.
| Conclusion|| |
Premedication with dexmedetomidine at a dose of 0.001 mg/kg compared to normal saline was more effective in attenuating hemodynamic stress of laryngoscopy and endotracheal intubation. Dexmedetomidine also significantly reduced the requirement of propofol during induction of GA.
Invasive BP monitoring was not used which would have given a better view of the hemodynamic parameters.
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Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2], [Table 3]