Comparative effects of dexmedetomidine versus labetalol on hemodynamic stress response to laryngoscopy and tracheal intubation: A systematic review and meta-analysis of randomized controlled trials

Endotracheal intubation and laryngoscopy are major components of airway management across a wide range of clinical settings. However, these procedures are associated with marked sympathetic response stress response, often leading to tachycardia and hypertension. Although these effects tend to be brief, these hemodynamic changes can pose negative consequences to high-risk patients, particularly those with cardiovascular or cerebrovascular disease, possibly leading to myocardial ischemia, arrhythmias, heart failure, intracerebral hemorrhage, and increased intracranial pressure [1]. A variety of pharmacological agents have been investigated to reduce this stress response. Still, many are limited by adverse effects, underscoring the need for an optimal intervention that balances safety and efficacy [2].

Dexmedetomidine is a highly selective α2 receptor agonist that reduces sympathetic tone through inhibition of norepinephrine release and decreased sympathetic outflow, primarily via central α2-receptor activation in the locus coeruleus. This mechanism leads to bradycardia and hypotension under standard dosing conditions. When administered intravenously, its onset of action occurs within 2–5 min, with peak effect typically reached by 10–15 min. However, at higher doses or with rapid intravenous administration, peripheral α2-receptor stimulation may paradoxically induce transient vasoconstriction and hypertension, followed by reflex bradycardia through baroreceptor-mediated vagal activation. In addition to its hemodynamic effects, dexmedetomidine provides anxiolytic, sedative, and analgesic properties while preserving respiratory function [3,4]. Labetalol is a combined selective α1 and non-selective β-adrenergic receptor antagonist. The α1 blockade reduces peripheral vascular resistance, while β1 antagonism decreases myocardial contractility and heart rate, thereby blunting the sympathetic surge associated with airway instrumentation. Following intravenous administration, labetalol has an onset of action within 2–5 min, with peak antihypertensive effects typically occurring between 5 and 15 min. It has been reported to preserve cardiac output and cerebral perfusion in normovolemic patients, though these effects may vary with dose and underlying hemodynamic status [5,6].

Given their pharmacodynamic profile, both dexmedetomidine and labetalol suggest that these drugs may be suitable for mitigating the hemodynamic stress response to laryngoscopy and tracheal intubation. However, direct comparative evidence between these two drugs remains scarce, and clinical consensus on the preferred agent is lacking. To address this gap, we performed a systematic review and meta-analysis to evaluate and compare the efficacy of dexmedetomidine and labetalol on reducing the hemodynamic stress response associated with laryngoscopy and tracheal intubation.

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