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Canadian Journal of Anesthesia 48:732-736 (2001)
© Canadian Anesthesiologists' Society, 2001
General Anesthesia

Tracheal lidocaine attenuates the cardiovascular response to endotracheal intubation

[L'administration trachéale de lidocaïne diminue la réponse cardio-vasculaire à l'intubation endotrachéale]

Koichi Takita, MD, Yuji Morimoto, MD PhD and Osamu Kemmotsu, MD PhD

From the Department of Anesthesiology and Critical Care Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan.

Address correspondence to: Dr. Koichi Takita, Department of Anesthesiology and Critical Care Medicine, Hokkaido University Graduate School of Medicine, Kita-15, Nishi-7, Kita-ku, Sappro 060-8638, Japan. Phone: +81-11-706-7861; Fax: +81-11-706-7861; E-mail: ktakita{at}med.hokudai.ac.jp


   Abstract
TOP
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Purpose: In order to examine the efficacy of tracheal lidocaine (TL) for attenuation of the cardiovascular responses to endotracheal intubation (EI), we compared the cardiovascular responses to TL alone and EI with TL, with those to EI without TL.

Methods: Seventy-five patients (ASA I-II) were studied. Anesthesia was induced with fentanyl 2 µg•kg–1 iv, thiamylal 5 mg•kg–1 iv and sevoflurane 1.0% in oxygen. Vecuronium 0.12 mg•kg–1 was used to facilitate EI. In Group A (n=25), three minutes after induction, EI was performed. In Group B (n=25), three minutes after induction, the patients received TL (4% lidocaine, 4 mL). This was followed by immediate EI. In Group C (n=25), EI was performed two minutes after TL. Heart rate, arterial blood pressure and rate- pressure product (RPP) were measured from one minute before induction until five minutes after EI.

Results: The changes of RPP caused by TL alone in Group C (TL; +34.6 ± 29.0%, mean ± SD) were significantly (P <0.01) less than those caused by EI without TL in Group A (+77.3 ± 42.6%). EI after TL in Group C did not cause significant changes in RPP (+5.4 ± 15.2%). There were no significant differences between Groups A and B (+58.3 ± 36.6%).

Conclusion: We conclude that the cardiovascular responses to TL alone are half as great as those to EI without TL, and that TL is effective for attenuation of the cardiovascular responses to EI. EI should be performed more than two minutes after TL.


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
LARYNGOSCOPY and endotracheal intubation provoke cardiovascular responses that include hypertension, tachycardia and dysrhythmias. These hemodynamic changes may be associated with myocardial ischemia, myocardial failure and cerebral hemorrhage in critically ill patients.1,2 A number of drugs, including calcium channel blocker,3–5 beta-adrenergic blockers,6,7 iv lidocaine8 and narcotics6 have been used in an attempt to prevent the cardiovascular responses to endotracheal intubation. Intratracheal administration of lidocaine (tracheal lidocaine) is also widely used for the attenuation of those cardiovascular responses. This method may avoid unexpected or excessive hypotension that can be associated with antihypertensive drug use. The efficacy of tracheal lidocaine for attenuation of the cardiovascular responses to tracheal intubation has not been fully established and some authors have questioned its efficacy.8–10 It is unknown whether the magnitude of the cardiovascular responses to tracheal lidocaine alone is less than that of endotracheal intubation without topical anesthesia. If the magnitude of the cardiovascular responses to tracheal lidocaine alone is as great as that produced by endotracheal intubation, it would have limited usefulness as an attenuating drug.

In this study, in order to elucidate the effectiveness of tracheal lidocaine in blunting the cardiovascular responses, we compared the cardiovascular responses to endotracheal lidocaine and tracheal intubation with tracheal lidocaine in ASA class I or II patients without cardiovascular disease.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
After obtaining institutional approval and informed consent, 75 patients without cardiovascular disease (ASA physical status I-II) undergoing elective surgery under general anesthesia were studied. Patients were premedicated with diazepam 5 mg or 10 mg and ranitidine 150 mg po was given 90 min before induction of anesthesia. On arrival in the operating room an iv infusion of acetate Ringer solution was started. Routine monitoring, including arterial blood pressure (AP), an electrocardiogram (ECG) and oxygen saturation (SpO2) were introduced. The AP was measured automatically and registered with an automated non-invasive AP monitor (Jentow®, Nippon Colin, Komaki, Japan). Heart rate (HR) was monitored by ECG. Anesthesia was induced with fentanyl 2 µg•kg–1 iv, thiamylal 5 mg•kg–1 iv and sevoflurane 1.0% (inspired) in oxygen. Vecuronium 0.12 mg•kg–1 iv was used to facilitate endotracheal intubation. In the control group (Group A), three minutes after induction, direct laryngoscopy with a standard Macintosh laryngoscope blade was performed and endotracheal intubation was undertaken. In Group B, three minutes after induction, the trachea was sprayed with 4% lidocaine 4 mL under direct vision with a standard Macintosh laryngoscope through a laryngotracheal anesthesia set (LTA®, Abott Ireland, Rep. of Ireland). This was followed by immediate endotracheal intubation. In Group C, three minutes after induction, the trachea was sprayed with 4% lidocaine 4 mL. The laryngoscope was removed and, two minutes later, laryngoscopic intubation was performed. During anesthesia, ventilation was assisted or controlled and end-tidal carbon dioxide was maintained at 35–40 mmHg. All intubations and tracheal lidocaine administrations were accomplished within 30 sec.

Baseline values of mean AP (MAP) (mmHg), systolic AP (SAP) (mmHg), diastolic AP (DAP) (mmHg) and HR (beats•min–1) were measured one minute before induction of anesthesia.

In Groups A and B, subsequent measurements were taken immediately before endotracheal intubation, one minute after endotracheal intubation, thereafter every one minute until five minutes after endotracheal intubation. In Group C, subsequent measurements were taken immediately before tracheal lidocaine, one minute after tracheal lidocaine, two minutes after tracheal lidocaine (immediately before endotracheal intubation), one minute after endotracheal intubation and thereafter every one minute until five minutes after endotracheal intubation. The rate-pressure product (RPP) was calculated by multiplying SAP by HR.

Data are expressed as mean ± standard deviation (SD). One-way ANOVA for repeated measurement followed by Student's t test was used for the intragroup comparisons. The pre-induction values, the maximum and the minimum values of the hemodynamic variables during intubation and the changes in the hemodynamic variables caused by endotracheal intubation and tracheal lidocaine were analyzed with one-way factorial ANOVA with Scheffe's F post hoc test. P <0.05 was considered as statistically significant.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
The patients' demographic data are shown in Table IGo. None were taking cardioactive or antihypertensive medication.


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  		TABLE I Demographic data
 
HR, MAP and RPP increased significantly (P <0.01) following endotracheal intubation in Groups A and B in comparison with the pre-induction values (Figure 1Go). In Group C, there were no significant differences in HR, MAP and RPP one minute after tracheal lidocaine and endotracheal intubation in comparison with the pre-induction values (Figure 2Go).



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  		FIGURE 1 The hemodynamic changes during intubation period in Groups A and B. Data are mean ± standard deviation. {square}=Group A; •=Group B. HR=heart rate (beats•min–1); MAP=mean arterial pressure (mmHg); RPP=rate-pressure product; EI=endotracheal intubation. *P <0.05; **P <0.01 compared with pre-induction values.

 


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  		FIGURE 2 The hemodynamic changes during intubation period in Group C. Data are mean ± standard deviation. HR=heart rate (beats•min–1); MAP=mean arterial pressure (mmHg); RPP=rate-pressure product; TL=tracheal lidocaine; EI=endotracheal intubation. *P < 0.05; **P < 0.01 compared with pre-induction values.

 
The pre-induction values and the minimum values of HR, AP and RPP during the intubation period were comparable within the groups. The maximum values of HR, AP and RPP during the intubation period in Group C were significantly less than those in Group A while there were no significant differences between Groups A and B (Table IIGo).


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  		TABLE II Maximum and minimum values in hemodynamic variables during intubation period
 
The changes in hemodynamic variables from the pre-intubation values (or the pre-tracheal lidocaine values) one minute after intubation (or tracheal lidocaine) in all three groups are shown in Table IIIGo. Endotracheal intubation in Groups A and B, and tracheal lidocaine in Group C caused a significant increase in the measured hemodynamic variables in comparison with both the pre-intubation values and the pre-tracheal lidocaine values. However, the changes of hemodynamic variables caused by tracheal lidocaine alone in Group C were significantly less than those caused by endotracheal intubation without tracheal lidocaine in Group A while there were no significant differences between Groups A and B. Endotracheal intubation two minutes after tracheal lidocaine in Group C did not cause significant changes in hemodynamic variables.


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  		TABLE III Changes (%) in hemodynamic variables from pre-EI (or pre-TL) values 1 min after EI (or TL)
 

   Discussion
TOP
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
Several studies have examined the efficacy of tracheal lidocaine for attenuation of the cardiovascular responses to endotracheal intubation. The results of these studies have been contradictory. Denlinger et al.11 showed that a simple tracheal spray with lidocaine attenuated the hypertensive responses to endotracheal intubation when compared with saline tracheal spray. Others showed that the application of topical anesthesia to the upper airway and trachea failed to prevent the pressor responses to endotracheal intubation.8–10 In the study of Denlinger et al.,11 endotracheal intubation was performed more than two minutes after a tracheal spray with local anesthetics while endotracheal intubation was performed less than one minute after topical anesthesia in the studies that indicated the ineffectiveness of tracheal lidocaine.8–10 Our study suggests that differing intervals between tracheal lidocaine and endotracheal intubation probably caused the inconsistent conclusions reported in other investigations. Our results show that endotracheal intubation performed two minutes after tracheal lidocaine attenuates the cardiovascular responses to endotracheal intubation.

In the present study, the time point of endotracheal intubation in Group C was two to three minutes later than in Groups A and B. Since sevoflurane 1% (inspired) was started at the induction of anesthesia and continued until five minutes after endotracheal intubation, it is possible that the patients in Group C were more deeply anesthetized when their trachea was intubated, than those in Groups A and B. A previous study reported that laryngoscopic intubation under 2% end-tidal sevoflurane concentration increased SAP by 36 mmHg and HR by 36 (beats•min–1) in ASA class I or II gynecological patients.12 Therefore, it is not likely that the attenuation of the cardiovascular responses to endotracheal intubation in Group C was due to deep sevoflurane anesthesia.

Most of the previous studies designed to examine the effectiveness of tracheal lidocaine place emphasis on the cardiovascular changes after endotracheal intubation. Therefore, in these studies, the cardiovascular responses to endotracheal intubation following a tracheal spray with local anesthetic were compared with those following the topical application of saline or iv application of lidocaine.8,9,11 The present study emphasizes the cardiovascular responses to tracheal lidocaine as well as those to endotracheal intubation with or without tracheal lidocaine. Although our study demonstrates that tracheal lidocaine alone provokes a significant increase in HR and blood pressure, the magnitude of these cardiovascular responses to tracheal lidocaine was half that of tracheal intubation without topical anesthesia. Tracheal lidocaine blocked the cardiovascular responses to endotracheal intubation. In addition, the present study also shows that endotracheal intubation with tracheal lidocaine does not produce an increased risk of hypotension during induction of anesthesia. This study suggests that tracheal lidocaine can reduce the dose of narcotics required to block the cardiovascular responses to endotracheal intubation, and may be a useful strategy when combined with other drugs to decrease the risk of hypotension or delayed emergence.

We conclude that tracheal lidocaine is an effective method for attenuating the cardiovascular responses to endotracheal intubation without producing an increased risk of hypotension. Endotracheal intubation should be performed more than two minutes after tracheal lidocaine in order to attenuate the cardiovascular responses to endotracheal intubation.


   Acknowledgments
 
We thank Professor Harry G.G. Kingston, Department of Anesthesiology, Oregon Health Science University, School of Medicine, for his helpful comments.

Revision received March 28, 2001. Accepted for publication February 6, 2001.


   References
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
1 Roy WL, Edelist G, Gilbert B. Myocardial ischemia during non-cardiac surgical procedures in patients with coronary-artery disease. Anesthesiology 1979; 51: 393–7.[Medline]

2 Fox EJ, Sklar GS, Hill CH, Villanueva R, King BD. Complications related to the pressor response to endotracheal intubation. Anesthesiology 1977; 47: 524–5.[Medline]

3 Nishikawa T, Namiki A. Attenuation of the pressor response to laryngoscopy and tracheal intubation with intravenous verapamil. Acta Anaesthesiol Scand 1989; 33: 232–5.[Medline]

4 Mikawa K, Obara H, Kusunoki M. Effect of nicardipine on the cardiovascular response to tracheal intubation. Br J Anaesth 1990; 64: 240–2.[Abstract/Free Full Text]

5 Fujii Y, Saitoh Y, Takahashi S, Toyooka H. Diltiazem-lidocaine combination for the attenuation of cardiovascular responses to tracheal intubation in hypertensive patients. Can J Anaesth 1998; 45: 933–7.[Abstract/Free Full Text]

6 Korpinen R, Saarnivaara L, Siren K, Sarna S. Modification of the haemodynamic responses to induction of anaesthesia and tracheal intubation with alfentanil, esmolol and their combination. Can J Anaesth 1995; 42: 298–304.[Abstract/Free Full Text]

7 Menkhaus PG, Reves JG, Kissin I, et al. Cardiovascular effects of esmolol in anesthetized humans. Anesth Analg 1985; 64: 327–34.[Abstract/Free Full Text]

8 Hamill JF, Bedford RF, Weaver DC, Colohan AR. Lidocaine before endotracheal intubation: intravenous or laryngotracheal? Anesthesiology 1981; 55: 578–81.[Medline]

9 Derbyshire DR, Smith G, Achola KJ. Effect of topical lignocaine on the sympathodrenal responses to tracheal intubation. Br J Anaesth 1987; 59: 300–4.[Abstract/Free Full Text]

10 Mostafa SM, Murthy BVS, Barrett PJ, McHugh P. Comparison of the effects of topical lignocaine spray applied before or after induction of anaesthesia on the pressor response to direct laryngoscopy and intubation. Eur J Anesthesiol 1999; 16: 7–10.[Medline]

11 Denlinger JK, Ellison N, Ominsky AJ. Effects of intratracheal lidocaine on circulatory responses to tracheal intubation. Anesthesiology 1974; 41: 409–12.[Medline]

12 Mollestad KE, Heier T, Steen PA, Raeder JC. 1 MAC-incision sevoflurane prevents explicit awareness during surgical skin incision and tracheal intubation. Acta Anaesthesiol Scand 1998; 42: 1184–7.[Medline]




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