The Effects of a Single Preanesthetic dose of Dexmedetomidine on Propofol Induction, Hemodynamics, and Cardiovascular Parameters

Abstract

IntroductIonDexmedetomidine is a highly selective α-2 adrenoceptor agonist commonly used in anesthesia practice. Dexmedetomidine produces sedation, hypnosis, analgesia, anxiolysis, and sympatholysis with minimal respiratory depression. [1] The central effects are due to the activation of α-2A receptors in locus coeruleus, and cardiovascular effects are due to a dose-dependent decrease in the central sympathetic outflow. The transient hypertensive response is seen initially due to its effects on α-2B receptors present in the vascular smooth muscle until there is a decrease in the central sympathetic outflow. [2] Dexmedetomidine has been shown to reduce perioperative oxygen consumption and blunt the sympathetic response to laryngoscopy and surgical stimuli, resulting in improved cardiac outcomes. [3,4] Dexmedetomidine infusions postoperatively have been shown to reduce plasma catecholamine levels and lesser hemodynamic fluctuations. [5] Dexmedetomidine has also been shown to reduce anesthetic and analgesic requirements. [6,7] The above-stated properties make dexmedetomidine an ideal preanesthetic agent. A study demonstrated that single preanesthetic dose of dexmedetomidine decreased the thiopental dose requirement without any serious hemodynamic changes. [7] Objective: To find out the dose of propofol consumption for induction and also the variation in hemodynamics following single-dose dexmedetomidine premedication. Methods: A total of 60 American Society of Anesthesiologists Class 1 and 2 patients aged between 18 and 80 years, posted for elective surgeries were randomized into two groups: Group C -premedication with 2 mcg/kg fentanyl and Group D -premedication with 1 mcg/kg dexmedetomidine + 2 mcg/kg fentanyl. Both groups were preloaded with 10 ml/kg crystalloid solution. The parameters measured were propofol requirements, heart rate (HR), mean arterial pressure (MAP), cardiac index (CI), cardiac output (CO), and stroke volume variation (SVV). Results: Propofol requirements were 26.6% lesser in Group D (P < 0.001). In Group C, HR was significantly low at baseline (P = 0.008), induction (P = 0.006), and at intubation (P = 0.001) in Group D. Cardiovascular parameters such as MAP (P = 0.007), CI (P = 0.038), and CO (P = 0.021) were significantly lower in Group D compared to Group C only at baseline. There were no differences at any other point during the study. SVV was noted to be significantly lower (P = 0.018) in Group D only at intubation. Conclusion: Dexmedetomidine decreases the requirements of propofol for induction and also attenuates the hemodynamic response to intubation. Cardiovascular parameters such as MAP, CI, and CO were significantly lower in Group D only at baseline. Hemodynamic stability is mainly attributed to adequate preloading and less propofol requirement in the dexmedetomidine group.