Hemodynamic and catecholamine responses to laryngoscopy with vs. without endotracheal intubation

Abstract

To study the relationship between the intensity of the stimulus exerted against the base of the tongue during direct laryngoscopy and the magnitude of associated hemodynamic and catecholamine responses, a study was conducted in 40 ASA I or II patients. Laryngoscopy lasting 40 s was performed with a size 3 Macintosh blade connected to a force-displacement transducer. The intensity of the stimulus exerted during laryngoscopy is expressed by the product of its average force (N) and duration (s) and given as impulse in Ns. Highly significant relationships were found between the impulse during laryngoscopy and the maximal hemodynamic and catecholamine responses. Also, when laryngoscopy was followed by orotracheal intubation, significant relationships were found with steeper slopes of the regression lines for systolic blood pressure, heart rate and plasma epinephrine concentrations. A more rapid regression of hemodynamic data was seen in intubated patients, whereas their plasma catecholamine concentrations regressed more slowly. The mechanisms of the responses to laryngoscopy and orotracheal intubation are proposed to be by somato-visceral reflexes. Stimulation of proprioceptors at the base of the tongue during laryngoscopy induces impulse-dependent increases of systemic blood pressure, heart rate and plasma catecholamine concentrations. Subsequent orotracheal intubation recruits additional receptors that elicit augmented hemodynamic and epinephrine responses as well as some vagal inhibition of the heart.

Dexmedetomidine Versus Oral Pregabalin to Attenuate Hemodynamic Response to Laryngoscopy and Orotracheal Intubation: A Comparative Study

“…Attenuation of the sympathoadrenal stress response is important especially in high-risk patients [12]. Various methods such as α or β adrenergic blockers, opioids, topical or systemic lignocaine are being used to attenuate hemodynamic response [13][14][15].…”

Haemodynamic effects of thoracic epidural anaesthesia during induction of anaesthesia: an investigation into the effects of tracheal intubation during target‐controlled infusion of propofol*

“…Haemodynamic changes resulting from tracheal intubation may also be decreased by epidural blockade itself that reduces sympathetic activity. The mechanism of haemodynamic changes caused by tracheal intubation is thought to be somato-visceral reflexes [14], where catecholamines are released from the adrenal gland. The efferent sympathetic nerves to the heart are from the spinal cord between T1 and T5, and those to the vascular bed from between T1 and L2, and those to the adrenal glands from between T6 and L2 [15].…”

Haemodynamic and EEG changes during rapid-sequence induction of anaesthesia

“…Another investigation concluded that stimulation of the supraglottic region by tissue tension during larygnoscopy was the major cause of the haemodynamic and catecholamine responses and that tracheal intubation contributed very little additional stimulation. 5 In contrast, Hassan et al 7 reported that orotracheal intuhation was associated with further increments of plasma epinephrine concentrations. In the present study, it was shown that thiamylal (5 mg-kg -I,/v) caused cerebral and haemodynamic depression, while cerebral activity and haemodynamic variables were increased after tracheal intubation.…”