Cardiovascular responses to endotracheal intubation in patients with acute and chronic spinal cord injuries.

UNLABELLED: Endotracheal intubation usually causes transient hypertension and tachycardia. We investigated whether the cardiovascular responses to intubation change as a function of the time elapsed in patients with spinal cord injury. One-hundred-six patients with traumatic complete spinal cord injury were grouped into acute and chronic groups according to the time elapsed (less than and more than 4 wk after injury) and into those with quadriplegia and paraplegia according to the level of injury (above C7 and below T5): acute quadriplegia, n = 26; chronic quadriplegia, n = 27; acute paraplegia, n = 24; and chronic paraplegia, n = 29. Twenty-five patients with no spinal cord injury served as controls. Systolic arterial blood pressure (SAP), heart rate, and plasma concentrations of catecholamines were measured. The intubation did not affect SAP in either the acute or chronic quadriplegics, but it significantly increased SAP in both acute and chronic paraplegics. Heart rate was significantly increased in all groups; however, the magnitude of change was less in acute quadriplegics than in the other groups. Plasma concentrations of norepinephrine increased in every group but the acute quadriplegics. The magnitude of increase was attenuated in chronic quadriplegics, accentuated in acute paraplegics, and similar in chronic paraplegics when compared with controls. The incidence of arrhythmias did not differ among groups. We conclude that the cardiovascular and catecholamine responses to endotracheal intubation may change as a function of the time elapsed and the level of spinal cord injury. IMPLICATIONS: Cardiovascular and catecholamine responses to endotracheal intubation may differ according to the time elapsed and the level of injury in patients with complete spinal cord injury.

Nitrous oxide attenuates pressor but augments norepinephrine response to laryngoscopy and endotracheal intubation.

UNLABELLED: Nitrous oxide (N(2)O) exerts a sympathomimetic action. We investigated whether N(2)O modifies the cardiovascular responses to tracheal intubation during general anesthesia. One-hundred healthy patients were assigned randomly to receive one of four concentrations (0%, 25%, 50%, or 75%; n = 25 each) of N(2)O in oxygen throughout the study beginning 3 min before tracheal intubation. Anesthesia was induced with IV thiopental (5-7 mg/kg) whereas patients were ventilated with designated concentrations of N(2)O. Tracheal intubation was facilitated with IV vecuronium (0.12 mg/kg). After intubation, all received 2% sevoflurane in oxygen via a semiclosed anesthesia circuit. Systolic arterial blood pressure, heart rate and rhythm, and plasma catecholamine concentrations were measured. The intubation significantly increased arterial blood pressure and heart rate. The maximum pressure changes were 46 +/- 21 and 65 +/- 24 mm Hg in 75% N(2)O and control groups, respectively (P < 0.05), being attenuated by N(2)O without affecting the tachycardiac response. Norepinephrine concentrations were increased at 1 min after the intubation, the magnitude of which was augmented by N(2)O. N(2)O did not affect the incidence of arrhythmias. It was shown that N(2)O suppressed the pressor response to endotracheal intubation, despite the augmented increase of norepinephrine concentrations. IMPLICATIONS: We examined whether nitrous oxide modifies the cardiovascular response to endotracheal intubation because it activates the sympathetic nervous system. Nitrous oxide attenuated the pressor response, whereas it augmented the norepinephrine response to laryngoscopy and endotracheal intubation.