Laryngoscopy and tracheal intubation are noxious stimuli associated with a transient increase in autonomic response.This response varies with depth of anaesthesia, duration and difficulties during laryngoscopy and intubation, and certain patient factors including history of diabetes and cardiovascular disease.

The precise mechanism of the intubation response (IR) is elusive but it has been established that it has both a sympathetic and parasympathetic element. The effect is transient occurring 30 seconds after intubation and lasting for less than 10 minute. The sympathetic response is a polysynaptic pathway with the glossopharyngeal and vagus nerve forming the afferent arc to the sympathetic nervous system via the brain stem and spinal cord. This ensures a diffuse autonomic response at the efferent side including increased firing of the cardio-accelerator fibres and release of adrenergic mediators including norepinephrine, epinephrine and vasopressin.

The net effect of this autonomic surge is an increased blood pressure (BP), heart rate (HR), pulmonary artery wedge pressure and decreased ejection fraction.

The parasympathetic reflex is monosynaptic and more common in children but can occur in some adults. The reflex is mediated by increased vagal tone at the Sinoatrial node .

The haemodynamic response to laryngeal and endo- tracheal intubation  is transient and in most patients thought to be of little consequence, but in patients with coronary artery disease (CAD), hypertension, raised intra cranial pressure, it may be associated with deleterious effects like myocardial ischaemia, infarction, arrhythmias, cardiac failure, pulmonary oedema and cerebral haemorrhage.

Various drug regimens and techniques have been used from time to time for attenuating the stress response to laryngoscopy and intubation, including opioids, barbiturates, benzodiazepines, beta blockers, calcium channel blockers, vasodilators, various blades and conduits for intubations. 

Alpha-2 agonists like clonidine  and dexmedetomidine  have been used recently for attenuation of sympathoadrenal stimulation caused by tracheal intubation and surgery. Clonidine stimulates α2 adrenergic inhibitory neurons in the medullary vasomotor center. As a result there is a decrease in sympathetic nervous system outflow from central nervous system to peripheral tissues

Dexmedetomidine a selective alpha2-adrenoceptor agonist, is short acting  and has a reversal drug for its sedative effect, atipamezole which  render dexmedetomidine suitable for sedation and analgesia during the whole perioperative period. It can be administered by various routes like IV, IM, as adjuvant to local anesthetics, nasal and orally and as nebulized form. Nebulized dexmedetomidine administration may allow rapid drug absorption through nasal, respiratory, and buccal mucosa, which allow bioavailability of 65% through nasal mucosa and 82% through buccal mucosa.  Nebulized drug administration may be preferred over intranasal administration, as it avoids transient nasal irritation, cough, vocal cord irritation, or laryngospasm as seen with intranasal administration. In our study we hypothesize that nebulized dexmedetomidine also blunts the intubation response due to its rapid absorption. As dexmeditomidine also causes sedation we also contemplated entropy monitoring. ENTROPY  is a new monitor based on the analysis of the EEG signal2. The State Entropy (SE) is computed over the frequency range from 0.8 Hz to 32 Hz and primarily reflects the cortical state of the patient. The Response Entropy (RE) is computed over a frequency range from 0.8 Hz to 47 Hz, and includes both the EEG‐dominant and EMG‐dominant part of the spectrum. dexmedetomidine nebulization  in blunting the hemodynamic response to laryngoscopy and tracheal intubation.