Effects of Intravenous Dexmedetomidine Infusion on Stress Response to Endotracheal Intubation in Controlled Diabetic Hypertensive Patients Undergoing Abdominal Surgeries

Abstract

Laryngoscopy and endotracheal intubation is often associated with hypertension and tachycardia because of the sympathoadrenal stimulation which is usually transient and lasts for 5-10 minutes, Sympathetic response associated with laryngoscopy and endotracheal intubation is recognised as a potential cause for a number of complications especially in patients with co-existing diseases as cardiac or hypertensive patients.

Various methods have been used to attenuate these haemodynamic responses; however most of the studies are in normotensive patients, the aim of our study was to assess the effect of single bolus dose of dexmedetomidine on the stress response to laryngoscopy and intubation in patients with controlled hypertension and diabetes mellitus.

This response which is called the pressor response is due to irritation of oral, nasal, pharyngeal or laryngeal mucosa resulting in tachycardia, hypertension, respiratory and metabolic changes via three axes; first is the neural axis which is the first of all stress response axes to become activated during stress arousal. This phenomenon is based upon the fact that the structure of these pathways, from origination to target-organ innervation, is completely neural, and therefore, the quickest, it occurs through the autonomic innervations of the upper respiratory mucosa.

The second axis is called the neuro-endocrine axis which is responsible for the “fight or flight” response that thought to be a mobilization of the body to prepare for muscular activity in response to a perceived threat.

The dorsomedial amygdalar complex appears to represent the highest point of origination for the “fight or flight” response as a functionally discrete psycho-physiological axis. From that point, the downward flow of neural impulses passes to the lateral and posterior hypothalamic regions. From here, neural impulses continue to descend through the thoracic spinal cord, converging at the celiac ganglion, and then innervating the adrenal gland, or more specifically, the adrenal medulla and The hormonal output of the neuro-endocrine stress response axis is the secretion of the adrenal medullary catecholamines with the following systemic effects.

The third axis is the endocrine axis which is the last to be stimulated if the stressful condition if prolonged or frequently repeated, four well established endocrine axes have been associated with the stress response; the hypothalamic pituitary adrenocortical axis, the somatotropic axis, the thyroid axis and the posterior pituitary axis. These axes not only represent the most chronic aspects of the stress response but also require greater intensity stimulation to activate.

The aim of the endocrine response is to meet the metabolic requirements in order to face the stressful event by increase utilization of glucose, amino acids and fatty acids in hepatic and extra-hepatic tissues. Cortisol causes rapid mobilization of amino acids and fat from their cellular stores, making them immediately available both for energy and synthesis of other compounds including glucose needed by different tissues.

Alpha-2 agonists including clonidine and dexmedetomidine have been extensively used, but dexmedetomidine is the first marketed sedative to make use of highly selective alpha-2 agonist activity. Sedation with dexmedetomidine differs in several important ways from sedation with other agents. First, unlike commonly used sedatives such as propofol or midazolam, dexmedetomidine produces an “interactive” form of sedation, in which patients may be aroused easily with stimulation, and are cooperative once aroused. Second, dexmedetomidine has analgesic properties and may significantly reduce concomitant opioid use. Third, dexmedetomidine is accompanied by virtually no respiratory depression at clinically relevant doses. Finally, dexmedetomidine has predictable sympatholytic effects. The use of dexmedetomidine by infusion 10 minutes before intubation not only gave the value of minimizing the associated stress response but it also decreases the anesthetic drugs doses required during induction. That was explained by the fact that dexmedetomidine not only has sympatholytic effect but it also has sedative and anxiolytic effect which made the induction of anesthesia much easier.