Severe bradycardia during laryngoscopy in adult neurosurgical patient.

Sir,

Hemodynamic disturbances may occur during laryngoscopy. The major manifestation of laryngoscopy in adult patients is usually hypertension and tachycardia; however, bradycardia is rarely reported.[1] Here, we have reported such an event in a neurosurgical patient and also highlighted the possible causes and their management.

An 18-year-old male patient was admitted to the Department of Neurosurgery with headache, nausea and vomiting since 7 days. The Glasgow Coma Score (GCS) was 15/15. Magnetic resonance imaging revealed homogenous mass on the suprasellar region with hydrocephalus. The patient was posted for right ventriculo–peritoneal shunt placement surgery in the supine position. All the preoperative investigations including electrocardiogram (ECG) and X-ray chest were normal. On the day of surgery, the patient was premedicated with 0.2 mg glycopyrrolate intramuscularly 1 h before the surgery. Routine monitors were attached. The baseline heart rate was 70/min and the blood pressure was 120/80 mmHg. The patient was preoxygenated with 100% O2 for 3 min. Anesthesia was induced with fentanyl 2 μg/kg, propofol 2 mg/kg and tracheal intubation facilitated with rocuronium 1 mg/kg. When the laryngoscope blade was introduced to perform tracheal intubation, sudden severe bradycardia (<35/min) was observed. At once, the laryngoscope blade was removed and the heart rate reverted back to normal. Severe bradycardia was again noted during the second attempt of laryngoscopy. Then, we gave a 30 mg bolus of propofol and hyperventilated (PaCO2 = 28 mmHg) the patient, and again tried the intubation. This time, we successfully intubated the patient with an 8.0-mm cuffed portex tube, but without much change in the heart rate (58/min). Anesthesia was maintained with sevoflurane in oxygen nitrous oxide mixture (40:60) and intermittent boluses of fentanyl and vecuronium as and when required. The remainder of the intraoperative course was uneventful. The trachea was extubated when the patient was fully conscious and following commands.

Bradycardia following intubation is commonly observed in pediatric patients, especially in patients with hypoxia. The vagus overdominance in the pediatric patient is the mechanism described for this cause. Activation of afferent parasympathetic nerve fibers during stimulation of the lower pharynx, larynx, trachea and epiglottis may result in bradycardia and asystole.[2] However, this vagal dominance can be present in adults too and, combined with raised intracranial pressure, as in this patient, can produce severe hemodynamic disturbances. Laryngoscopy further raises the intracranial pressure, which in turn increases vagotonicity.[3] The other factors that may produce bradycardia are fentanyl, high doses of propofol, hypoxia and severely raised intracranial pressure. We ruled out hypoxia and hypotension-induced bradycardia by pulse oximetry and NIBP (the oxygen saturation was 100%). Moreover, in our case, deeper plane of anesthesia combined with hyperventilation minimized this vagotonic effect of raised intracranial pressure. In conclusion, during laryngoscopy simple maneuvers like additional bolus of induction agent and hyperventilation minimize the vagotonic effect of laryngoscopy on raised ICP and vice versa. However, bradycardia associated with hypotension warrants the immediate pharmacological intervention in the form of anticholinergics.