Research and Opinion in Anesthesia & Intensive Care

: 2015  |  Volume : 2  |  Issue : 2  |  Page : 1--6

Comparison of dexmedetomidine, lidocaine, and their combination in attenuation of cardiovascular and catecholamine responses to tracheal extubation and anesthesia emergence in hypertensive patients

Ashraf MA Moustafa, Hatem Atalla, Hala M Koptan 
 Department of Anaesthesia and Intensive Care, Faculty of Medicine, Menoufiya University, Menoufiya, Egypt

Correspondence Address:
Hala M Koptan
Departement of Anesthesia and Intensive Care, Menoufiya University, Menoufia


Introduction This study was carried out to compare the effi cacy of the dexmedetomidine– lidocaine combination with each drug alone in suppressing the hemodynamic and catecholamine stress responses during tracheal extubation and emergence from general anesthesia. Patients and methods Sixty hypertensive patients (ASA II– III), defi ned as systolic blood pressure more than 160 mmHg and/or diastolic blood pressure more than 95 mmHg, undergoing elective surgery were assigned to a randomized, double-blind approach and were divided into three equal groups: group D received 0.25 mg/kg dexmedetomidine intravenously, group L received 1.0 mg/kg lidocaine intravenously, and group DL received dexmedetomidine plus lidocaine at the same doses intravenously 2 min before tracheal extubation. Changes in heart rate, mean arterial pressure, rate– pressure product, and plasma catecholamine levels were measured before and after tracheal extubation. Results It was found that heart rate, mean arterial pressure, and rate– pressure product following tracheal extubation were lower in patients receiving the dexmedetomidine– lidocaine combination than in those receiving dexmedetomidine or lidocaine as a sole drug. In addition, catecholamine concentrations increased significantly after extubation (P < 0.05) in the three groups, with no signifi cant difference between them. Also, the tracheal extubation score was lower in groups L and DL compared with group D. Conclusion Although dexmedetomidine, lidocaine, or their combination failed to suppress the catecholamine responses to tracheal extubation and emergence from anesthesia, the dexmedetomidine– lidocaine combination was superior to each drug alone in attenuating the cardiovascular changes in hypertensive patients.

How to cite this article:
Moustafa AM, Atalla H, Koptan HM. Comparison of dexmedetomidine, lidocaine, and their combination in attenuation of cardiovascular and catecholamine responses to tracheal extubation and anesthesia emergence in hypertensive patients.Res Opin Anesth Intensive Care 2015;2:1-6

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Moustafa AM, Atalla H, Koptan HM. Comparison of dexmedetomidine, lidocaine, and their combination in attenuation of cardiovascular and catecholamine responses to tracheal extubation and anesthesia emergence in hypertensive patients. Res Opin Anesth Intensive Care [serial online] 2015 [cited 2020 Feb 20 ];2:1-6
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Emergence from anesthesia and tracheal extubation may be associated with hypertension, tachycardia, and high plasma catecholamine levels [1]. These responses could lead to cardiac failure, pulmonary edema, and cerebrovascular hemorrhage, especially in hypertensive patients [2]. Therefore, the prevention of these hemodynamic changes during extubation is of particular clinical importance in these patients. Various drug regimens and techniques have been used from time to time for attenuating the stress response to laryngoscopy and intubation, including opioids, barbiturates, benzodiazepines, β-blockers, calcium channel blockers, vasodilators, or by extubation under deep anesthesia [3],[4],[5],[6],[7],[8],[9],[10]. Unfortunately, many hypotensive drugs currently used for control of perioperative hypertension have undesirable side effects. Nitroprusside, for example, can produce reflex tachycardia, as can direct vasodilators such as hydralazine [11],[12]. β-Blockers are usually avoided in patients with asthma, chronic obstructive pulmonary disease, and congestive heart failure [13]. The dose of opioids required for effective attenuation of stress response is fairly high and numerous drugs have been used as adjuncts to decrease the dose of opioids with a varied level of success, but are not absolutely free from side effects [14].

Dexmedetomidine is a new α2 agonist with eight times more affinity for α2 adrenoceptors compared with clonidine, which has shown only partial agonist activity and is known to decrease the plasma catecholamines levels and suppress the release of catecholamines [15]. Dexmedetomidine induces fewer changes in hemodynamic values during the extubation period. This drug may be useful in anesthetic management requiring smooth emergence from anesthesia [16]. The net effect of dexmedetomidine action is a significant reduction in circulating catecholamines, with a slight decrease in blood pressure and a modest reduction in heart rate (HR) [17]. Lidocaine attenuates the hemodynamic response to tracheal extubation by its direct myocardial depressant effect, central stimulant effect, peripheral vasodilatory effect, and finally, it suppresses the cough reflex, an effect on synaptic transmission [18]. As the pharmacological mechanism controlling the hemodynamic changes during extubation is different between dexmedetomidine and lidocaine, the concomitant use of these drugs may enhance the prophylactic effect of each drug alone for this purpose. Therefore, the present study was designed to compare the efficacy of dexmedetomidine plus lidocaine with each drug alone in suppressing the hemodynamic changes and catecholamine responses during extubation in hypertensive patients.

 Patients and methods


After receiving approval from the local ethics committee, an informed written consent was obtained from 60 hypertensive patients. Inclusion criteria were hypertensive patients (ASA physical status II-III), age between 25 and 68 years, of both sexes, undergoing elective orthopedic procedures under general anesthesia. According to the diagnostic criteria of the WHO, hypertension was defined as systolic blood pressure more than 160 mmHg and/or diastolic blood pressure more than 95 mmHg on the preoperative patient visit. All patients had received their last current oral antihypertensive drugs 6 h before induction of anesthesia including β-adrenergic blockers (e.g. atenolol), calcium channel antagonists (e.g. nifedipine, diltiazem), or renin-angiotensin inhibitors (e.g. captopril). The exclusion criteria were a history of myocardial infarction, arrhythmias, severe aortic stenosis, presence of an arteriovenous shunt, hepatocellular insufficiency, and dexmedetomidine or lidocaine hypersensitivity.


All patients were premedicated with 5 mg diazepam orally 1 h before induction of anesthesia. On arriving to the operating room, ECG electrodes, a noninvasive blood pressure cuff, and a pulse oximeter were attached to measure HR, blood pressure, and oxygen saturation, respectively. Also, a radial arterial catheter was inserted under local anesthesia for continuous monitoring of arterial pressure and also for blood sampling for plasma catecholamine levels. Anesthesia was induced using 2 μg/kg fentanyl, 5 mg/kg thiopental, and 0.6 mg/kg atracurium intravenously. The lungs were manually ventilated by a face mask with 100% oxygen for 3 min after an injection of atracurium; thereafter, tracheal intubation was attempted. Anesthesia was maintained with isoflurane 1-1.5%. Lungs were mechanically ventilated to maintain ETCO 2 between 30 and 35 mmHg. Muscle relaxant and fentanyl supplements were administered during the maintenance of anesthesia as required. At the end of surgery, isoflurane was discontinued. Residual neuromuscular block was antagonized with neostigmine 2.5 mg and glycopyrrolate 0.5 mg. Thereafter, the patients received, in a randomized, double-blind manner, either 0.1 μg/kg dexmedetomidine (Precedex 200 μg/2 ml; Abbott, USA) (group D), or 1.0 mg/kg lidocaine (Sigma pharmaceuticals, Menoufiya, Egypt) (group L), or 0.1 μg/kg dexmedetomidine plus 1.0 mg/kg lidocaine intravenously (group DL). Each drug dosage was diluted with saline to 10 ml in identical syringes and prepared by personnel not involved in this study, according to a randomized list. Immediately before tracheal extubation, the end-tidal concentration of isoflurane was confirmed less than O.1% and patients could breathe spontaneously (EtCO 2 <45 mmHg), open their eyes on command, and hand grip well.

Pharyngeal suction was carried out without laryngoscopy using a 1a French gauge catheter. The trachea was extubated 5 min after the administration of the study drugs. Immediately after tracheal extubation, oxygen 100% was administered through a face mask for 10 min.


HR (bpm) and the mean arterial pressure (MAP) (mmHg) were monitored using the standard monitor (Nihon Kohden, Tokyo, Japan). The rate-pressure product (RPP) in bpm×mmHg was calculated by multiplying systolic blood pressure by HR. Data were recorded at the end of surgery as baseline (T0), immediately after extubation (T1), and at 1, 2, 3, 5, and 10 min (T2-T6, respectively) after extubation.

The quality of tracheal extubation was evaluated using a five-point rating scale: 1 = very smooth, no coughing or straining, 2 = smooth, minimal coughing, 3 = moderate coughing, 4 = marked coughing or straining, and 5 = poor extubation, very uncomfortable.

Arterial blood samples were obtained, to measure plasma catecholamines levels in pg/ml, at the end of surgery as baseline and 3 min after extubation. It was performed by high liquid performance chromatography [19]. All results are expressed as mean ± SD or percentages. One-way analysis of variance was used for differences among groups. A post-hoc Tukey's test was used when a significant difference was indicated by the analysis of variance. Friedman's test was used for repeated-measures comparison within groups and the Wilcoxon signed-rank test was used to compare different variables with the baseline. A P value less than 0.05 was considered statistically significant.


The demographic data did not differ among the three groups studied [Table 1]. No differences in the baseline values of hemodynamic variables were observed between groups.{Table 1}

The HR increased significantly immediately after tracheal extubation in both D and L groups (P < 0.05), and remained increased for 1 min in group D (P < 0.05) and for 3 min in group L (P < 0.05) [Figure 1]. In group D, MAP did not increase after tracheal extubation at any point in time, but RPP increased significantly only immediately after tracheal extubation (P < 0.05). In group L, there were significant increases in both MAP and RPP immediately after tracheal extubation (P < 0.05), and remained increased for 3 min (P < 0.05) [Figure 2] and [Figure 3]. In contrast, in group DL, no significant increases were found in HR, MAP, and RPP after tracheal extubation during the study period. The suppressive effects of the study drugs on the hemodynamic responses to tracheal extubation were greater in group DL than in either group D or L (P < 0.05) [Figure 1],[Figure 2] and [Figure 3]. There were evident increases in both epinephrine and norepinephrine values after extubation compared with the baseline in the three groups, with no significant difference between them [Figure 4] and [Figure 5].{Figure 1}{Figure 2}{Figure 3}{Figure 4}{Figure 5}

No arrhythmias (e.g. premature ventricular contractions), ECG evidence of myocardial ischemia, or hypoxemia (SPO 2 <95%) were recorded.

The extubation score was recorded as 1 and 2 (no and minimal cough) in 75, 75, and 30% of patients in groups L, DL, and D, respectively. Moreover, it was recorded as 4 and 5 (severe cough and poor extubation) in 25, 5, and 5% of patients in groups D, L, and DL, respectively [Table 2]. Therefore, quality of extubation was more favorable in both groups L and DL than in group D.{Table 2}


In the current study, it was found that HR, MAP, and RPP increased temporarily after tracheal extubation in patients receiving lidocaine (group L). However, these hemodynamic changes were completely inhibited in those receiving dexmedetomidine plus lidocaine (group DL), but suppressed to some extent with dexmedetomidine alone (group D). The immediate changes in RPP after tracheal extubation compared with the baseline were less in group DL than in either group D or L (P < 0.05). Thus, more satisfactory suppression of RPP during tracheal extubation can be achieved with the combination of dexmedetomidine and lidocaine. Nevertheless, RPP after tracheal extubation was not more than 20 000 (bpm×mmHg) in any of the groups, suggesting that critical increases in RPP may be avoided by administering dexmedetomidine, lidocaine, or their combination. Levels of RPP more than 20 000 (bpm×mmHg) are commonly associated with myocardial ischemia [20],[21]. Several investigators have reported that HR and MAP increase markedly after tracheal extubation in both normotensive and hypertensive patients. They reported that MAP begins to increase immediately after tracheal extubation and reaches a maximum value within 1 min when no medication is administered [3],[9],[22]. Drugs used for control of this response should act rapidly, but in a predictable and controlled manner, with few adverse effects. Potent vasodilators, such as nitroprusside, nitroglycerin, or diltiazem, may be used. However, two main problems are linked to these potent vasodilators: severe hypotension and reflex tachycardia [23],[24]. These drawbacks may counteract the potential benefits of these drugs in acute coronary syndromes. Many studies have shown that these undesired hemodynamic effects did not occur when using dexmedetomidine [25],[26],[27]. Dexmedetomidine has become one of the frequently used drugs in the anesthetic armamentarium, along with routine anesthetic drugs, because of its hemodynamic, sedative, anxiolytic, analgesic, neuroprotective, and anesthetic sparing effects. Other claimed advantages include minimal respiratory depression with cardioprotection, neuroprotection, and renoprotection, thus making it useful in various situations including offsite procedures. The α1 to α2 ratio of 1 : 1600 makes it a highly selective α2 agonist compared with clonidine, thus reducing the unwanted side effects involving α1 receptors [28]. Because of its central sympatholytic effect, dexmedetomidine is useful in blunting hemodynamic responses in the perioperative period. It is used successfully in intravenous doses varying from 0.25 to 1 mcg/kg for attenuating intubation response. Doses in the range of 0.5 mcg/kg not only blunted the extubation response but also reduced the emergence reaction and analgesic requirement to extubation following rhinoplasty and neurosurgery [29]. Unlugenc et al. [30] administered a 1 μg/kg dose of dexmedetomidine within 10 min of induction and they found a marked decrease in HR within 10 min, whereas HR and the MAP were similar to the values obtained in the other group during surgery. In a recent study, Basar et al. [31] utilized dexmedetomidine as a single preanesthetic drug to determine the hemodynamic, cardiovascular, and recovery effects in patients undergoing elective cholecystectomy. Forty adult patients were randomly assigned to receive 0.5 μg/kg dexmedetomidine or saline solution. The main cardiovascular parameters, times for awakening, and postoperative Aldrete's recovery score were recorded. The authors observed that a single dose of dexmedetomidine administered before induction of anesthesia decreased thiopental requirements without serious hemodynamic effects or any effect on recovery time. Jain et al. [32] carried out a study on the effect of dexmedetomidine on stress response to extubation and inferred that a bolus dose of the drug administered before reversal provided hemodynamic stability that may prove beneficial for cardiac patients. Aksu and colleagues carried out a comparative study of the effects of dexmedetomidine and fentanyl on airway reflexes and hemodynamic responses to tracheal extubation during rhinoplasty and concluded that dexmedetomidine 0.5 mcg/kg body weight intravenously is more effective in attenuating reflex responses to extubation without prolonging the recovery compared with fentanyl 1 mcg/kg [33].

The valuable effect of lidocaine on the hemodynamic changes may be because of its direct cardiac depression and peripheral vasodilation as it could significantly depress all excitable membranes including the heart [34]. It may also act through inhibition of cough or strain associated with tracheal extubation that could cause hypertension and tachycardia [35]. Attenuation of the activity in afferent C fibers from the larynx may contribute toward this beneficial effect [36]. In addition, lidocaine may act centrally to increase the depth of anesthesia [37]. Wallin and colleagues observed that an intravenous infusion of lidocaine during and after surgery suppressed extubation-induced hypertension and tachycardia [38]. Bidwai and colleagues also noted that the increases in HR and blood pressure that occurred after extubation could be attenuated by a previous intravenous injection of lidocaine. However, other studies disproved the ability of lidocaine to suppress the hemodynamic response to tracheal extubation [39],[40].

In the present study, there were significant increases in plasma catecholamines levels after extubation in the three groups studied as dexmedetomidine, lidocaine, and their combination failed to suppress catecholamine release. Multiple factors may explain the cardiovascular responses during tracheal extubation including wound pain, emergence from anesthesia, and tracheal irritation, all of which could release catecholamines. Plasma concentrations of epinephrine and norepinephrine had been reported to increase during this stressful period [41],[42]. Laryngoscopy alone produces a significant pressor response, presumably because of stimulation of the supraglottic region [43]. Therefore, laryngoscopy was avoided in this study on extubation and only a soft catheter was used for clearance of secretions to examine only the changes associated with emergence and extubation. Previous workers showed that lidocaine infusion failed to inhibit the general sympathetic response to extubation as assessed by increased plasma catecholamine concentration [38].

The quality of tracheal extubation using the five point's extubation score was better in both groups L and DL than in group D. Thus, lidocaine was effective either alone or in combination in the prevention of cough or laryngeal spasm following extubation. Intravenous dexmedetomidine, however, did not effectively reduce straining or coughing associated with extubation compared with lidocaine. Previous studies showed that intravenous lidocaine 2 mg/kg 1 min before extubation suppressed cough and prevented laryngeal spasm after extubation in both children and adults [37],[44]. In the current study, none of the patients sustained bradycardia or hypotension sufficient to require pressor or sympathomimetic drugs after extubation. No arrhythmia, evidence of myocardial ischemia, or hypoxemia was observed.


The dexmedetomidine-lidocaine combination is an effective and safe prophylaxis for attenuating the cardiovascular responses to tracheal extubation in hypertensive patients and is superior to each drug alone. Also, lidocaine intravenous was more beneficial in the suppression of cough or straining that may occur with extubation. Nevertheless, dexmedetomidine, lidocaine, or their combination failed to suppress the catecholamine responses to tracheal extubation and emergence from anesthesia.


Conflicts of interest

None declared.


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