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Anesth Analg 2000;91:828-833
© 2000 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

The Effect of Clonidine Premedication on Hemodynamic Responses to Microlaryngoscopy and Rigid Bronchoscopy

Idit Matot, MD*, J. Y. Sichel, MD{dagger}, Valeri Yofe, MD*, and Yaacov Gozal, MD*

Departments of *Anesthesia and Critical Care Medicine, and {dagger}Ear Nose and Throat, Hadassah University School of Medicine, Jerusalem, Israel

Address correspondence and reprint requests to Idit Matot, MD, Department of Anesthesia and Critical Care Medicine, Hadassah University Medical Center, POB 12000, Jerusalem 91120, Israel. Address e-mail to matoth{at}cc.huji.ac.il


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
The usual hemodynamic response to laryngoscopy and bronchoscopy is an increase in heart rate and arterial blood pressure. Previous work has reported that 10%–18% of the patients develop ischemic ST segment changes during the procedure. Therefore, we performed a prospective, randomized, double-blinded study in 36 patients scheduled for elective microlaryngeal and bronchoscopic surgical procedures to evaluate the effects of 300-µg oral clonidine premedication (n = 18) or placebo (n = 18) on the hemodynamic alterations and the incidence of perioperative myocardial ischemic episodes. Myocardial ischemia was assessed by using continuous electrocardiographic monitoring, beginning 30 min before, and lasting until 24 h after the operation. During the procedure, patients receiving placebo exhibited a significant increase (mean ± SD) in arterial blood pressure (the systolic increasing from 137 ± 11 to 166 ± 17 mm Hg, the diastolic increasing from 80 ± 11 to 97 ± 14 mm Hg) and heart rate (increasing from 79 ± 15 to 97 ± 12 bpm) compared with the baseline and with the clonidine group. A dose of 300-µg clonidine blunted the hemodynamic response to endoscopy. Ventricular arrhythmias were more frequent in patients who were not premedicated with clonidine. Two patients in the control group, but none in the clonidine group, had evidence of myocardial ischemia. These data should encourage routine premedication with clonidine in patients undergoing microlaryngoscopic and bronchoscopic procedures.

Implications: Premedication with 300-µg oral clonidine attenuates the hemodynamic response to microlaryngoscopy and bronchoscopy. These data should encourage routine premedication with clonidine in patients undergoing microlaryngoscopic and bronchoscopic procedures.


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Although microlaryngoscopic and bronchoscopic procedures are often performed in patients with a limited pulmonary reserve, and with co-morbidities such as coronary artery disease, the morbidity and mortality are impressively low (3). Nevertheless, cardiac arrhythmias, as well as ischemic episodes, have been reported during the procedure (1–6). Manipulation of the upper and lower respiratory tract is commonly associated with an increase in heart rate and blood pressure (1–3,7). In addition, hypoxemia may occur concomitantly in the periprocedural period (3). Although these changes are of little consequence in patients with normal cardiovascular function, they may be of clinical importance in those with coronary artery disease or in elderly patients with accompanying lung disease. The increased blood pressure and heart rate and the decrease in oxygen saturation may lead to an imbalance between myocardial oxygen demand and supply, which could result in arrhythmias, myocardial ischemia, and eventual infarction (8,9).

Clonidine, a centrally acting {alpha}2-agonist, has a beneficial effect on the hyperdynamic response to endotracheal intubation (10–15). Moreover, it attenuates stress-induced sympathoadrenal responses to painful stimuli, improves the intraoperative hemodynamic stability, reduces the incidence of perioperative myocardial ischemic episodes in patients with suspected or documented coronary artery disease, and decreases anesthetic requirements during surgery (16–20). Therefore, oral clonidine seems well suited as premedication for microlaryngoscopy and rigid bronchoscopy. The objective of this placebo-controlled, prospective study was to evaluate the effects of oral clonidine premedication on the hemodynamic alterations and incidence of perioperative myocardial ischemia.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
Thirty-six ASA physical status I–III patients, age >= 50 yr, scheduled for elective microlaryngoscopic and rigid bronchoscopic procedures under general anesthesia participated in the study. The indications included diagnostic procedures (evaluation of hoarseness and lesions, and biopsies of laryngeal tumors) or therapeutic intervention (for laryngotracheal and endobronchial lesions [tumors, granulomas, and papillomatosis] and iatrogenic stenosis). Patients were excluded from the study for the following reasons: preoperative clonidine medication, heart rate (HR) < 50 bpm before premedication, atrioventricular block more than first degree, left bundle-branch block, or any gastrointestinal disturbance that would hinder enteric absorption of oral medication. A written, informed consent was obtained from each patient, and the study was approved by our institution’s ethics committee. The groups produced by randomization are presented below (Table 1).


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  		Table 1. Patient Characteristics, Type of Operation, and Duration of Anesthesia
 
Patients received a coded oral preparation containing placebo (n = 18) or 300 µg clonidine (approxi- mately 4–4.5 µg/kg) (n = 18) by the nursing staff 90 min before the procedure. All hypertensive and antianginal regimens were continued (except diuretics) up to the time of surgery. In both groups, anesthesia was induced with propofol (2.5 mg/kg) and alfentanil (15 µg/kg), administered IV, and muscle relaxation was achieved with succinylcholine (1 mg/kg). Topical anesthesia was achieved by application of 8 mL of 4% lidocaine to the oropharynx. After tracheal intubation, the lungs were ventilated with a mixture of oxygen and nitrogen via the ventilating sidearm of a rigid bronchoscope or through a microlaryngeal surgical tracheal tube to maintain an end-tidal carbon dioxide concentration of 30–35 mm Hg and oxygen saturation > 95%. Anesthesia was maintained with a four-stage decremental infusion of propofol (21,22); it was started immediately after the induction of anesthesia and consisted of 10 mg · kg-1 · h-1 for 10 min, 8 mg · kg-1 · h-1 for 10 min, 6 mg · kg-1 · h-1 for 10 min, and 4 mg · kg-1 · h-1 until the termination of the procedure. Maintenance doses of propofol were achieved by using a volumetric infusion pump. Bolus doses of propofol (40 mg) were administered during the procedure if HR or mean arterial blood pressure (BP) increased by more than 15% compared with preinduction values.

Intraoperative monitoring consisted of electrocardiogram (ECG), automated BP, pulse oximetry (SpO2), and end-tidal carbon dioxide and inspired oxygen concentrations. HR and arterial BP measurements were recorded every 2 min until the end of the procedure. Myocardial ischemia was assessed by a two-channel AM Holter ECG recorder (Series 8500; Marquette Electronics, Milwaukee, WI ), beginning 30 min before the procedure and continuing for 24 h after termination of the procedure. Two bipolar leads (leads II and V5) were used. Holter monitors were analyzed after patients were discharged by an investigator blinded to the identity of the patients and their clinical course. ECG episodes of ischemia were defined as reversible ST segment changes lasting at least 1 min and involving a shift from baseline (adjusted for positional changes) of either >=0.1mV ST depression (slope <= 0) or >=0.2mV ST increase at the J point. ST segment depression was measured 60 ms after the J point, unless the point fell within the T wave, in which case it was measured at least 40 ms after the J point. The baseline level of the ST segment was defined as its position during a stable period preceding each episode of change, and the maximal ST change from baseline was determined for each episode. The reversibility of an ischemic episode was defined by the return of the ST segment to the baseline for at least 1 min.

Hypotension was defined as an intraprocedural decrease in systolic BP of more than 30% compared with the preinduction level or absolute systolic BP < 90 mm Hg. Hypertension was defined as an increase in mean arterial BP by more than 15% compared with preinduction values or absolute systolic BP > 180 mm Hg. Bradycardia was defined as a HR < 45 bpm. Bradycardia and hypotension were treated with ephedrine.

Demographic parametric data were analyzed by using Student’s t-test, and nonparametric data were analyzed by using the {chi}2 test. Statistical comparisons between groups of interval data (hemodynamic variables) were tested by using two-way analysis of variance and the Mann-Whitney U-test. Intragroup analysis was performed on raw data by using one-way analysis of variance, followed by post hoc tests for comparison with the baseline (Scheffé method and Bonferroni’s inequality correction). Results were reported as the mean value ± SD;P < 0.05 was considered statistically significant.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Age, weight, ASA physical status, concomitant disease, type of procedure, and duration of anesthesia did not differ significantly among the groups (Table 1).

Baseline (90 min after receiving study drug) hemodynamic variables were not significantly different between the groups (Table 2). During the operation, patients receiving placebo (control group) showed a significant increase of all arterial pressure variables compared with the baseline values and compared with the clonidine group. No significant increase in BP was observed during the procedure in the clonidine group. Patients receiving clonidine, however, exhibited a significant reduction in BP during the induction of anesthesia. Specifically, maximum decrease in systolic BP compared with the baseline value ranged between 2% and 40%. Throughout the study, two patients (11%) in the clonidine group, but none in the control group, were treated for hypotension.


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  		Table 2. Blood Pressure (BP) and Heart Rate Profiles
 
HR did not differ between the groups on arrival at the operating theater and after the induction of anesthesia (Table 2). In contrast, the HR was significantly increased in the control group during intubation. During anesthesia, patients receiving clonidine exhibited a significantly lower HR than those in the control group. No patient sustained bradycardia requiring treatment.

No arrhythmias, other than occasional single supraventricular ectopic beats, were seen before anesthesia was started. The frequency of arrhythmias (all classifications) did not differ significantly among the groups (Table 3). The incidence of ventricular arrhythmias (all classifications) occurring during and after the operation was significantly higher in the control group than in the clonidine group. Ventricular couplets occurred exclusively in patients who did not receive clonidine. In addition, one patient in the control group had three short runs of ventricular tachycardia in the course of the procedure. All episodes resolved spontaneously. There was no difference in the incidence of supraventricular ectopic beats between the two groups. Supraventricular ectopics occurred in 14 (78%) and 10 (50%) patients from the control group and in 13 (72%) and 8 (44%) patients from the clonidine group, during and after the procedure, respectively.


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  		Table 3. Frequency of Arrhythmias During and After Anesthesia
 
Two patients (11%), both from the control group, developed significant ST segment changes. Although they had risk factors for coronary artery disease (smoking, hypertension, diabetes, and age >= 65 yr), both were asymptomatic for ischemic heart disease. Significant increases in BP were observed during the procedure in both patients; however, their intraoperative hemodynamics did not differ from those of the nonischemic, placebo-treated patients. In one patient, myocardial ischemia developed during the procedure and lasted for 6 h; in the other patient, ischemia developed 5 h after the procedure and lasted for 100 min. In these two patients, the HR during ischemia ranged from 40 to 85 bpm and from 90 to 132 bpm, respectively. One patient developed ventricular ectopic beats during ischemia (a total of 1553 beats), which continued, though at a slower rate, when the ischemia resolved. Because none of the patients complained of chest pain or manifested other clinical signs or symptoms of myocardial ischemia, and because Holter recordings were analyzed after patients’ discharge, cardiac enzyme levels were not assessed and 12-lead ECG was not recorded.

The requirements for intraoperative propofol were significantly reduced in patients premedicated with clonidine. The number of additional propofol boluses necessary to maintain anesthesia was reduced by 81% in the clonidine group in comparison with that in the control group: a total of 6 boluses (240 mg) versus 35 boluses (1400 mg) in the clonidine and control group, respectively (P = 0.008).

Throughout the study, clonidine-related side effects (nausea, vomiting, pruritus, or dryness of mouth) limiting the use of 300-µg oral clonidine were not observed. Time to extubation from the end of propofol infusion (12 ± 5 min and 15 ± 6 min in the placebo and clonidine groups, respectively) and to discharge from the recovery room (88 ± 22 min and 101 ± 26 min in the placebo and clonidine groups, respectively) did not differ between groups.


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
The sympathetic responses to laryngoscopy and tracheal intubation, which include hypertension, tachycardia, and tachyarrhythmias (23), are associated with an acute increase in plasma concentrations of epinephrine and norepinephrine (24). A dose of 300-µg clonidine orally or larger reduces sympathetic activity (12,14,16,25–27). Laryngoscopic and bronchoscopic procedures entail a more prolonged manipulation of the upper respiratory tract. We, therefore, hypothesized that an {alpha}2-adrenergic agonist would help to moderate the sympathetic response during these procedures. The present study shows that, in patients undergoing laryngoscopic or bronchoscopic procedures under general anesthesia, premedication with oral clonidine (4–4.5 µg/kg) attenuates hemodynamic responses. Our data confirm and extend the results of other investigators (10–15,17) who showed clonidine to be beneficial in blunting reflex tachycardia and hypertensive responses associated with intubation in both children (15) and adults, and of previous studies reporting that premedication with {alpha}2 adrenergic agonists improves cardiovascular stability during anesthesia (17–20). Thus, clonidine premedication may exert a positive effect on cardiac oxygen delivery and consumption balance.

The risk of new reversible myocardial ischemia episodes, as shown by ST segment deviation, can be reduced by oral premedication with clonidine. In patients undergoing vascular surgery, Stuhmeier et al. (19) found that premedication with oral clonidine reduced the incidence of perioperative myocardial ischemic episodes from 39% (placebo group) to 24% (clonidine group). Myocardial ischemia in the latter study was associated with hemodynamic changes in 25% of the cases. In the present study, two patients, both from the control group, had acute ischemic episodes which developed during the perioperative period. A significantly increased HR (in both patients) and BP (in one patient) accompanied these episodes. A prospective study with a larger number of patients is required, however, to determine whether the effect of clonidine on the incidence of myocardial ischemia is significant. Previous studies reported that cardiovascular events, such as atrial and ventricular arrhythmias, and myocardial ischemia, are potential complications of bronchoscopy (1–7). Indeed, ST segment changes were reported in 10%–18% (1,2) and 17% (5) of patients undergoing rigid and flexible bronchoscopy, respectively. As microlaryngoscopic and bronchoscopic surgery extends the spectrum of treatment capabilities in the bronchial tree (for example, insertion of a stent for airway stenosis), making the procedure more complicated and protracted, the complication rate may be expected to increase.

The risk of undesirable side effects is extremely important in evaluating the overall safety of preanesthetic medication. The potentially beneficial effect of {alpha}2 agonists may be negated by bradycardia (15,28) and hypotension (11,29,30). The present investigation shows that hypotension may be expected. This hypotensive effect has been reported in other studies in which clonidine was used either in its IV form (29) or as an oral dose of 4 or 5 µg/kg (11,30,31). In the present study, however, hypotension occurred only during the induction of anesthesia and might be related to the large induction dose of propofol (2.5 mg/kg) used.

Although we did not record recovery time (i.e., response to verbal command or correct recall of date of birth), clonidine premedication did not affect time to extubation from the end of propofol infusion or time spent in the recovery room. Several studies (20,22,32) using the 5-µg/kg regimen for clonidine premedication failed to detect any delay in recovery from anesthesia. Moreover, Ghignone et al. (20) and Kumar et al. (32) reported faster recovery in elderly patients undergoing intraocular surgery and premedicated with 5-µg/kg clonidine when compared with those premedicated with diazepam. Using larger doses of clonidine for premedication (8.5 µg/kg), Richards et al. (33) reported a significant delay in recovery times.

We chose a dose of 4-µg/kg clonidine in this study because previous studies reported that administration of 4-µg/kg clonidine blunted catecholamine release during intubation and surgery and that larger clonidine doses were not more effective (16). Smaller doses, however, were not sufficient to blunt the reaction to laryngoscopy (16). In addition, the maximum dose of clonidine is limited by its action on peripheral {alpha}-adrenoceptors. Larger doses might cause peripheral {alpha} stimulation, which could result in an increase in blood pressure. In most human studies, 4-µg/kg clonidine was applied without signs of peripheral {alpha} stimulation.

Our relatively small sample size may limit the interpretation of our results. Nevertheless, the results of the present study should encourage the routine use of clonidine as premedication for patients undergoing laryngoscopic or bronchoscopic procedures. By providing improved hemodynamics, clonidine may benefit a whole range of patients, particularly those with or at risk for coronary artery disease.


   Acknowledgments
 
Support was provided solely from institutional and departmental sources.


   References
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

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Accepted for publication June 9, 2000.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2000 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press