Laryngoscopy and tracheal intubation transiently increase arterial pressure, heart rate (HR), and circulating catecholamines, in part attributed to reflex sympathetic discharge. In a complete spinal cord injury, the sympathetic nervous system and hence the cardiovascular responses to the intubation may be differentially affected according to the level of injury. Patients with acute quadriplegia often have a low resting arterial pressure due to inappropriate vasodilatation and loss of cardiac inotropy. Moreover, they frequently exhibit arrhythmias, reflex bradycardia, and cardiac arrest, especially during tracheal suction. In the days to weeks after injury, however, the reflex functioning of the lower cord recovers to maintain normal vascular tone. In the chronic stage, peripheral vascular changes and a loss of descending inhibitory control result in paroxysmal hypertension.
Korean investigators KY Yoo and colleagues1 aimed to determine the effect of the level (quadriplegia vs paraplegia) and duration of spinal cord injury on haemodynamic and catecholamine responses to laryngoscopy and tracheal intubation in patients with spinal cord injury. The outcome measures were the changes in systolic arterial pressure (SAP), HR, and catecholamine levels above awake baseline values after intubation.
Patients were divided into two groups: quadriplegia (above C7) and paraplegia (below T5). Each group was divided into six subgroups according to the time elapsed after the injury: <4 weeks (acute), 4 weeks– 1 yr, 1–5, 5–10, 10–20, and >20 yr. Twenty non-disabled patients undergoing surgery requiring tracheal intubation served as controls.
Patients with high-level paraplegia (T1–T4) were excluded because they were few in number and they had previously ‘shown different haemodynamic and catecholamine responses from the other groups‘ 2 which refers to work published by the same authors, in which high-paraplegic patients had a more pronounced increase in heart rate compared with other groups. Confusingly the ‘patients who were at increased risk of hyperkalemia after succinylcholine were excluded‘ although this statement appears only in the discussion, not the methods.
Anaesthesia was induced with sodium thiopental 5 mg/kg administered i.v. over 20 s, followed by succinylcholine 1 mg/kg for 5 s, and was followed by direct laryngoscopy and tracheal intubation.
Results were as follows:
SAP decreased after the induction of anaesthesia with thiopental in all subjects including the controls (P<0.05).
SAP then increased in response to tracheal intubation in the control and paraplegics (P<0.001), whereas it remained unaltered in the quadriplegics regardless of the time since injury.
In the paraplegics, the magnitude of maximum increase from baseline values was similar within 10 yr of injury, but was higher thereafter compared with that in the controls (P<0.05).
The maximum increase in SAP from baseline values after tracheal intubation was greater in the paraplegics than in the quadriplegics (P<0.0001).
An increase in SAP.130% of preinduction baseline values or 160 mm Hg was noted in three (4.2%) of 71 quadriplegics and 94 (65.7%) of 143 paraplegics.
The incidence of hypertension was significantly lower and that of hypotension significantly higher in the quadriplegics than in the control.
HR increased after induction ofanaesthesia in all groups, but less so in the quadriplegic groups.
Although baseline bradycardia was common in the acute quadriplegics, none of them showed further slowing during induction of anaesthesia and tracheal intubation.
Tracheal intubation increased plasma norepinephrine concentrations in all subjects except the acute quadriplegics.
Epinephrine concentrations were not significantly different between before and after intubation either in the quadriplegics or in the paraplegics, nor were they different between the groups with regard to the duration of injury.
The authors summarise: The pressor response was abolished in all quadriplegics regardless of the time elapsed after the injury. In contrast, the chronotropic and catecholamine responses differed over time. The chronotropic response was attenuated and the catecholamine response abolished in the acute quadriplegics. The chronotropic and catecholamine responses were improved in the quadriplegics after 4 weeks since the injury. In the paraplegic patients, cardiovascular responses did not change in the 10 yr after injury and the pressor response was enhanced at 10 yr or more after injury.
1.Altered cardiovascular responses to tracheal intubation in patients with complete spinal cord injury: relation to time course and affected level
Br J Anaesth. 2010 Dec;105(6):753-9
2. Hemodynamic and catecholamine responses to laryngoscopy and tracheal intubation in patients with complete spinal cord injuries.
Anesthesiolgy 2001; 95: 647–51
