Cardiovascular Changes Associated with Nasotracheal Intubation inPatients under General Anaesthesia

Background: Nasotracheal intubation is frequently employed in maxillofacial, dental, and certain head‐and‐neckprocedures to optimize surgical access. Unlike orotracheal techniques, the nasal route may evoke differing sym-pathetic and nociceptive stimuli, potentially leading to distinct haemodynamic perturbations. Acute elevations inheart rate and blood pressure during intubation can increase myocardial oxygen demand and precipitate compli-cations in vulnerable patients. Despite its common use, detailed characterization of the timing, magnitude, andduration of cardiovascular responses to nasotracheal intubation remains limited. This study aimed to quantify thehaemodynamic changes occurring immediately before, during, and after nasotracheal intubation under standard-ized general anaesthesia.Methods: In this prospective observational study, 60 adult patients (ASA I–II), aged 18–65 years, scheduled forelective maxillofacial or dental surgery requiring nasotracheal intubation were enrolled. All received a uniformanaesthetic regimen: premedication with midazolam 0.05 mg/kg and fentanyl 2 μg/kg, induction with propofol 2mg/kg and vecuronium 0.1 mg/kg, and maintenance with isoflurane in oxygen/air. A well‐lubricated, appropri-ately sized nasotracheal tube was passed under direct laryngoscopy. Heart rate (HR), systolic blood pressure(SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) were recorded at baseline (pre‐induc-tion), pre‐intubation (post‐muscle relaxation), immediately after tube placement (T0), and at 1 (T1), 3 (T3), and 5minutes (T5) following intubation. Data were analysed using repeated‐measures ANOVA with Bonferroni cor-rection; p < 0.05 was deemed significant.Results: All 60 patients completed the protocol. Compared with baseline, HR increased by 18 ± 6 bpm at T0 (p< 0.001), peaked at T1 with a rise of 22 ± 7 bpm (p < 0.001), and gradually returned toward baseline by T5(increase 6 ± 4 bpm; p = 0.04). SBP rose from 122 ± 10 mm Hg at baseline to 150 ± 12 mm Hg at T0 (p < 0.001),peaked at 155 ± 14 mm Hg at T1 (p < 0.001), then declined to 130 ± 11 mm Hg by T5 (p = 0.02). DBP and MAPexhibited similar patterns, with maximal increases of 20 ± 5 mm Hg and 25 ± 6 mm Hg at T1, respectively (bothp < 0.001). No patient experienced arrhythmias or required pharmacologic intervention beyond the planned pro-tocol.Conclusions: Nasotracheal intubation under general anaesthesia elicits pronounced sympathetic responses, withheart rate and blood pressure peaking at approximately one minute post-intubation and returning toward baselineby five minutes. These transient haemodynamic surges should be anticipated and, when necessary, attenuated withtailored anaesthetic depth or short-acting vasoactive agents, especially in patients with cardiovascularcomorbidities.