Anesth Analg 2003;97:1162-1167
© 2003 International Anesthesia Research Society
NEUROSURGICAL ANESTHESIA
Cardiovascular Responses to Endotracheal Intubation in Patients with Acute and Chronic Spinal Cord Injuries
Kyung Y. Yoo, MD PhD,
Seong W. Jeong, MD PhD,
Seok J. Kim, MD,
In H. Ha, MD PhD, and
JongUn Lee, MD PhD
Department of Anesthesiology and Research Institute of Medical Sciences, Chonnam National University Medical School, Gwangju, South Korea
Address correspondence and reprint requests to Kyung Yeon Yoo, MD, PhD, Department of Anesthesiology, Chonnam National University Medical School, 8 Hak-dong, Gwangju 501-746, Korea. Address e-mail to kyyoo{at}chonnam.ac.kr
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Abstract
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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.
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Introduction
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Laryngoscopy and tracheal intubation usually result in increased blood pressure and heart rate (HR) (1). The mechanism underlying these hemodynamic responses has been, in part, attributed to a reflex sympathetic discharge (1,2). In patients with spinal cord lesions, the sympathetic nervous system may be differentially affected according to the level of the injury, whereas the parasympathetic system may remain intact.
An initial transient decrease of cardiovascular responses may occur after spinal cord injury. Indeed, patients with acute quadriplegia often show low resting blood pressure. Moreover, they frequently exhibit arrhythmias, reflex bradycardia, and cardiac arrest, especially during tracheal suction (3). In contrast, in the chronic stage, an increase of adrenoceptor function and/or a loss of descending inhibitory control results in paroxysmal hypertension (4,5). Taken together, spinal cord injury may alter cardiovascular responses to intubation as a function of both the time elapsed since injury and the level of injury. However, the effect of elapsed time after spinal cord injury on the cardiovascular response to intubation has not been established. This study examined the cardiovascular responses to laryngoscopy and endotracheal intubation in acute and chronic spinal-cord-injured patients.
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Methods
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This study was approved by the University Hospital Ethics Committee. Written, informed consent was obtained before the study. In patients who were unable to give consent because of injury, their consent was taken from the next of kin. One-hundred-six patients with traumatic clinically complete spinal cord injuries scheduled for a spinal or nonspinal surgery with general anesthesia were prospectively studied. They were divided into four groups according to the timing of injury and the most cephalic level of complete motor and sensory lesions: acute quadriplegia (time lag, <4 wk; level of injury above C7; n = 26), chronic quadriplegia (time lag, >4 wk; level of injury above C7; n = 27), acute paraplegia (time lag, <4 wk; level of injury below T5; n = 24), and chronic paraplegia (time lag, >4 wk; level of injury below T5; n = 29). Four weeks were taken to classify acute and chronic groups because life-threatening cardiovascular disturbances frequently occur during that period (3). Twenty-five age-matched, nondisabled patients served as controls.
Patient exclusion criteria were as follows: 1) history of any cardiovascular, pulmonary, or metabolic disease; 2) medications that would influence autonomic or cardiovascular response to intubation; 3) spinal shock state with or without vasopressors; 4) risk of pulmonary aspiration; and 5) anticipation of difficult ventilation with a face mask. Patients with high paraplegia (T1 to T4) were also excluded because their population was small and they showed different hemodynamic and catecholamine responses from those in the other groups.
Neurological examinations were performed by the University Hospital Spine Center according to the 1996 American Spinal Injury Association standards (6). Motor function was examined by using key muscles for levels C5 through T1 and L2 through S1, and total paralysis of motor strength was regarded as a complete lesion. Sensory level was examined by light touch and pinprick at each dermatome, and anesthesia and analgesia were regarded as a complete lesion.
All patients were premedicated with midazolam 0.1 mg/kg orally 60 min before the induction of anesthesia. Before arrival in the operating room, an IV catheter was placed to allow the administration of fluids and medications. Additionally, a 20-gauge catheter was inserted into a radial artery connected to a pressure transducer to measure blood pressure and to collect blood samples. HR was determined from electrocardiogram traces. All external stabilizing de-vices—including soft and hard collars, halo vest, and weighted tractions—were removed before anesthesia induction. For each patient, a rest period of at least 30 min was provided between the time of cannulation and the start of the study.
After baseline values were recorded, anesthesia was induced with 5–7 mg/kg of IV thiopental, followed by 0.12 mg/kg of IV vecuronium after breathing 100% oxygen. Direct laryngoscopy and endotracheal intubation were performed when neuromuscular block was achieved, and anesthesia was maintained with 50% nitrous oxide and 1 vol% isoflurane (inspired) in oxygen. Laryngoscopy and intubation were performed in all patients by an experienced faculty anesthesiologist. No effort was made to fully expose the glottis during laryngoscopy; exposure was limited to that necessary to allow passage of the endotracheal tube through the vocal cords under direct vision. In patients with unstable cervical spine fracture or high spinal cord injury, cervical immobilization was maintained manually by a member of a skilled anesthesiology team to reduce the likelihood of secondary neurological injury during the process of intubation. Lungs were mechanically ventilated with a ventilator to maintain an end-tidal CO2 tension between 35 and 40 mm Hg. Data from patients in whom intubation required longer than 15 s were excluded.
HR and arterial blood pressure were continuously monitored. Hypertension was defined as a systolic arterial blood pressure (SAP) >130% of the baseline value or >160 mm Hg, whereas hypotension was defined as SAP <70% of the baseline value or <90 mm Hg. Tachycardia and bradycardia were defined as HR more than 120 and <60 bpm, respectively. The incidences of hypertension, hypotension, tachycardia, and bradycardia were recorded throughout the study. A dysrhythmia was defined as any ventricular or supraventricular premature beat or any sustained rhythm other than sinus. The incidence of dysrhythmia after intubation was also compared among the groups.
Arterial blood samples were drawn before (baseline) and 1 min after the onset of intubation for measurement of plasma catecholamine concentrations. The samples were collected into prechilled tubes containing EDTA/Na and immediately centrifuged at 3000 rpm for 10 min at 4°C. The plasma was stored at -70°C until assayed. Plasma concentrations of epinephrine and norepinephrine were measured in duplicate by using high-pressure liquid chromatography (7). The assay sensitivity was 10 pg/mL, and the within-run precision coefficients of variation were 14.2% and 13.5% for epinephrine and norepinephrine, respectively.
All results are expressed as mean ± SD. Statistical analysis of the data for each hemodynamic variable and catecholamine was performed by a two-way analysis of variance with repeated measures. The Scheffé test was used for multiple pairwise comparisons when a significant difference was indicated with analysis of variance. Complication rates among the groups were analyzed by using the 
2 test where appropriate. A P value <0.05 was considered statistically significant.
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Results
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There were no significant differences among groups with respect to sex ratio, age, weight, or height (Table 1). All acute quadriplegic and paraplegic patients but 1 (who had hip surgery), 12 (44%) of 27 chronic quadriplegics, and 5 (17%) of 29 chronic paraplegics received anterior or/and posterior spinal fusions. Thirteen (48%) chronic quadriplegics and 19 (66%) chronic paraplegics had local flap surgery because of decubitus ulcer. Baseline SAP was lower in acute quadriplegics than in acute paraplegics. Baseline HR was also slower in acute quadriplegics than in the other groups (Figs. 1 and 2).
SAP decreased after the induction of anesthesia with thiopental in all groups. In response to tracheal intubation, however, SAP increased in controls, acute paraplegics, and chronic paraplegics, whereas it remained unaltered in acute and chronic quadriplegics. The maximum increase in SAP was noted within 30 s and persisted until 2 min after intubation. SAP then decreased to the control value or even to less than baseline values; this occurred earlier in quadriplegics than in control and paraplegic patients (Fig. 1). A SAP increase to >130% of preinduction baseline values or 160 mm Hg was noted in 44 (42%) of 106 patients studied. The incidence of hypertension was significantly less and that of hypotension was significantly more in both acute and chronic quadriplegics than in control patients (Table 2).
HR increased after anesthesia induction in all groups. In response to tracheal intubation, HR further increased; however, the peak values were smaller in acute quadriplegics than in the other groups (Fig. 2). The incidence of tachycardia was more frequent in chronic paraplegics, and that of bradycardia was more frequent in acute quadriplegics. Although basal bradycardia was common in acute quadriplegics, none of them showed further slowing of HR during anesthesia induction and endotracheal intubation. Premature ventricular contractions appeared immediately after tracheal intubation in 2 of 25 control patients and in 4 of 29 patients with chronic paraplegia. The arrhythmias disappeared spontaneously without treatment (Table 2).
Baseline norepinephrine concentrations were smallest in acute quadriplegics. Endotracheal intubation increased plasma norepinephrine concentrations in all but the acute quadriplegics. However, the magnitude of increase was attenuated in chronic quadriplegics, accentuated in acute paraplegics, and comparable to control in chronic paraplegics. No group showed significant changes in plasma epinephrine concentrations after intubation, although the baseline values of both the acute and chronic quadriplegics were smaller compared with controls (Table 3).
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Discussion
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Our results demonstrated that the cardiovascular and catecholamine responses to tracheal intubation differed according to the timing and level of injury. The pressor response was abolished both in acute and chronic quadriplegics, whereas the chronotropic and catecholamine responses differed between them. The chronotropic response was attenuated and the catecholamine response was abolished in acute quadriplegics, whereas the chronotropic response was not affected and catecholamine changes were evident in chronic quadriplegics. However, cardiovascular responses were not altered in either acute or chronic paraplegics, although catecholamine responses were exaggerated in the former and unaltered in the latter.
Laryngoscopy and endotracheal intubation usually result in hypertension and tachycardia, which depend on sympathetic efferent outflow. Sympathetic innervation to the heart originates from the spinal cord between T1 and T4, to the vascular bed from between T1 and L2, and to the adrenal medulla from between T3 and L3 (8,9). Patients with complete cervical cord injuries lose all sympathetic outflow. Consequently, the pressor response to intubation was abolished in both acute and chronic quadriplegics.
After a complete cervical cord injury, the vagal efferent pathway remains intact. Quadriplegics thus not only may fail to respond with an increase of HR, but may also exhibit bradycardia. Indeed, quadriplegic patients who have sustained recent injury frequently show bradycardia not only with changes in position, but also with Valsalva maneuvers or increased intrathoracic pressure (10). Lehmann et al. (3) observed reflex severe bradycardia and cardiac arrest in 5 (17%) of 31 individuals with acute severe cervical cord injury during tracheal suction, although no episodes were observed in 40 patients with mild cervical or thoracolumbar injuries. However, we observed an apparent tachycardia in response to intubation in acute and chronic quadriplegics. Afferent inputs from the lung and airway travel along both the vagus and the sympathetic nerves to the upper thoracic segments (11), whereas those from the pharyngolaryngeal regions traverse through the glossopharyngeal and vagus nerves to the vasomotor center (12). Such a difference may explain different HR responses between endotracheal intubation and broncho-carinal stimulation. This speculation is supported by the finding that acute sympathectomy, induced in part by cervical epidural block (C4 to T8), did not attenuate the circulatory responses to laryngoscopy and endotracheal intubation but prevented them in response to broncho-carinal stimulation (13). Endotracheal intubation may not provoke severe bradycardia or cardiac arrest even in the acute stage of quadriplegia, unlike in broncho-carinal stimulation.
In this study, however, acute quadriplegics showed a significantly lower maximal HR (79 ± 14 bpm) than the other groups. This finding suggests an altered sympathetic activity in acute quadriplegics. Because sympathetic innervation of the heart is completely interrupted in quadriplegics, autonomic activity related to heart rhythm is likely to be mediated only through the vagus. Indeed, Koh et al. (14) have found that most quadriplegic patients have a low-frequency R-R interval that is proportional to arterial pressure and is abolished by atropine. Similarly, Grimm et al. (15) examined HR in quadriplegics and paraplegics and found that the resting sympathetic and parasympathetic outflows were lower when the level and extent of injury were higher and more complete. One of the two autonomic divisions regulating the cardiovascular system may exert its homeostatic role even when the other is severely compromised. In this context, quadriplegic patients may modulate HR exclusively by modulating vagal tone. However, the chronotropic response associated with a reduced vagal activity may not be sufficient to compensate for the diminished sympathetic nervous activity, especially in the acute stage.
An increase of norepinephrine concentration associated with the tachycardiac response to intubation in chronic quadriplegics may indicate that sympathetic innervation to the heart is partly intact. However, there was only a slight increase in norepinephrine concentration (7%), with no pressor responses, in this study. Previous studies also showed that norepinephrine and epinephrine were similarly increased when the effect of physical exercise on catecholamine concentrations was examined in chronic quadriplegic patients (16). Moreover, acute quadriplegic patients did not show any changes in norepinephrine concentration, despite an apparent tachycardia in response to intubation. It is unlikely that a partially intact sympathetic pathway contributed to the tachycardiac response in the quadriplegic group.
However, the cardiovascular responses to intubation were not altered in either acute or chronic paraplegics. Acute patients showed increased basal and postintubation norepinephrine concentrations, whereas chronic patients showed catecholamine concentrations similar to those in the control group. These findings suggest different compensatory responses to preserve circulatory homeostasis in acute and chronic patients. To compensate for handicap-related disorders, such as hypotension due to abdominal or lower limb blood pooling, basal and stimulated upper thoracic sympathetic activities may be augmented in paraplegic patients, especially in the acute stage (17). However, autonomic and reflex activity may be gradually restored over time. Loss of descending inhibitory control; alterations of adrenoceptor function; or a decreased reuptake, rather than an increased release, of catecholamines may lead to an enhanced pressor responsiveness in the chronic stage (4,5).
The reported incidence of dysrhythmias during intubation has been widely variable (18). The 9%–12% incidence in this study is relatively small, probably because patients with known cardiac disorders predisposing to dysrhythmias were excluded and because the subjects were relatively young. However, the increases in SAP, particularly in chronic paraplegics, were occasionally alarming. For instance, SAP was 262 mm Hg in 1 patient and was more than 200 mm Hg in 12 (40%) of 29 patients.
In contrast, 33%–35% of either acute or chronic quadriplegics developed hypotension during induction. This transient hypertension and hypotension may be hazardous, particularly in those with limited coronary or myocardial reserve, hypertension, or cerebrovascular diseases (19). Individuals with spinal cord injuries are at a particularly increased cardiovascular risk. In fact, coronary artery disease is one of the most important causes of death in patients with spinal cord injuries (20). Moreover, because autoregulation of blood flow is lost in the injured spinal cord, especially during the acute stage, hypotension may jeopardize cord perfusion (21).
This study has several limitations. First, to standardize the technique, we did not use rapid-sequence induction with succinylcholine. Succinylcholine may be contraindicated in vulnerable cord-injured patients because of the potential for generating hyperkalemia. Instead, patients who were at increased risk for aspiration and those in whom difficult face mask ventilation was anticipated were excluded from the study. Second, we did not examine Mallampati class or laryngoscopy grade. However, we excluded data from patients in whom intubation took longer than 15 seconds. Acute quadriplegics are expected to have more prolonged intubation and more stress responses than other groups. Nevertheless, the acute quadriplegics showed fewer stress responses (i.e., less hypertension, less tachycardia, and fewer catecholamine responses) than others in our study. The diminished stress responses may be related to an interruption of sympathetic nerves to the cardiovascular system in the acute quadriplegics. Third, we examined the degree of spinal cord injury only by using American Spinal Injury Association standards (6). Spinal cord injury is not an "all or nothing" phenomenon. Therefore, it may be difficult to guarantee that all had a complete transection with no neural functioning below the level of injury in this study. It may have been better to stratify the patients before surgery by the autonomic level of dysfunction or to evaluate autonomic cardiovascular control in relation to the intensity of baroreceptor stimulation or to vagolysis. Additionally, intraoperative evaluation of the cardiac sympathovagal balance by using R-R intervals or of the cardiovascular responses by measurement of hemodynamic variables such as cardiac output or filling pressures would strengthen our study.
In conclusion, the circulatory and catecholamine responses to laryngoscopy and tracheal intubation differ according to the timing and the level of injury in complete spinal cord injury. The pressor response to tracheal intubation was abolished in both acute and chronic quadriplegics but was not affected in either acute or chronic paraplegics. Although tracheal intubation increased the HR in every group, the magnitude was attenuated in acute quadriplegics. The catecholamine response was abolished in acute quadriplegics and was attenuated in chronic quadriplegics, whereas it was exaggerated in acute paraplegics.
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Acknowledgments
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Supported by a research grant (R13-2002-013-010003-0) from the Korea Science and Engineering Foundation through the Medical Research Center for Gene Regulation.
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Accepted for publication April 16, 2003.
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Abstract
Introduction
P < 0.05 versus the control group; 
P < 0.05 versus the acute QP group.
