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1987;66: 1036-8

Intravenous Lidocaine:

Optimal Time of Injection before Tracheal Intubation

Stanley Tam,


FRCP, Frances Chung,


FRCP, and Michael Campbell,


The circulatory stimulation accompanying laryngoscopy and tracheal intubation and its attendant potential hazards are well recognized. Many methods to attenuate this stress response have been studied, among which intravenous (IV) lidocaine has been popular, probably because of its theoretical advantages of suppressing cough reflex (1,2), preventing increases in intracranial pressure (3), attenuating circulatory responses (4),and its antiarrhythmic properties (5). Abou-Madi et al. (6), in comparing two doses of intravenous lidocaine (0.75and 1.5mg/kg), found that the higher dose was more effective in attenuating circulatory responses to tracheal intubation. The time of injection of IV lidocaine for this purpose has, however, been either not clearly specified (6) or chosen on an empirical basis (7). There has been no evaluation of the optimal time of injection of IV lidocaine for the attenuation of circulatory responses secondary to tracheal intubation. We undertook this study to provide such data.

perphenazine, 0.05 mg/kg IM 1 hr before induction of anesthesia. Patients were given d-tubocurarine, 0.04 mg/kg 5 min before intubation, followed by thiopental, 4.0 mg/kg and succinylcholine, 1.5 mg/kg IV 2 min before intubation. All intubations were performed by two experienced anesthetists. Patients in whom the duration of laryngoscopy was greater than 15 sec were excluded from the study. Heart rate (HR), systolic blood pressure (SBP), mean blood pressure (MBP), and diastolic blood pressure (DBP) were monitored by an automatic blood pressure cuff (Datascope) before induction (baseline values) and then at 1-min intervals throughout induction and for 5 min after intubation. Changes in each hemodynamic variable after intubation were based on the differences between baseline values and values obtained 1min after intubation. Mean values 2 one SD are reported for each group. Differences between groups were evaluated using oneway analysis of variance followed by Duncan's multiple-range test. P < 0.05 was considered statistically significant.


Seventy adult patients, ASA class 1-11, ages 27 to 70, with no previous history of hypertension, and undergoing elective noncardiac surgery requiring intubation, were admitted to the study. Institutional approval was obtained for the study. These patients were randomly divided into five groups of 14 patients each. Groups I, 11, 111, and IV received lidocaine, 1.5 mgikg IV 1, 2, 3, and 5 min before intubation, respectively. Lidocaine was injected as a single bolus over a period of less than 5 seconds. Group V served as the control and received no IV lidocaine. All patients received morphine, 0.10 mg/kg and

From the Department of Anaesthesia, Toronto Western Hospital, Toronto, Ontario, Canada. Accepted for publication May 29, 1987. Address correspondence to Dr. Chung, University of Toronto, Toronto Western Hospital, Department of Anaesthesia, 399 Bathurst St., Toronto, Ontario, Canada, M5T 258.

(0 1987 by the International Anesthesia Research Society


There were no statistically significant differences between the five groups in age, sex, or ASA classification. Results are shown in Table 1, and Figures 1 and 2. Changes in HR and blood pressure (BP)were greatest 1 min after intubation. The 1-min postintubation values were, therefore, used to compare with the baseline values to determine if the increase was statistically significant. These values were also used to determine intergroup differences. When compared with baseline values, increases in SBP, MBP, DBP, and HR after intubation were not significantly different in patients given IV lidocaine 3 min before intubation (group III), but they were significantly above baseline levels in patients given lidocaine 1 min (group I) ( P < 0.05), 2 min (group 11) (P < 0.05), and 5 min (group IV) ( P < 0.05) before intubation or in those not given lidocaine at all (group V) ( P < 0.05). When


ANESTH ANALG 1987:66:1036-8


Table 1. Hernodynamic Data Patient groups Variables Time of lidocaine administration before intubation (min) SBP: Baseline 1 min after intubation Increase MBP: Baseline 1 min after intubation Increase DBP: Baseline 1 rnin after intubation Increase HR: Baseline 1 min after intubation Increase


1 131 2 25 163 t 34 32 i 21" 99 i 19 129 i 26 30 2 2 P 77 i 18 106 2 29 29 i 23" 72 i 14 100 20 28 2 17"


2 133 i 19 162 i 20 29 i 20' 102 i 17 129 i 17 27 i 15" 79 2 11 108 i 17 29 k 15" 75 t 13 99 ? 14 24 i 15"



V (Control)


3 137 149 12 105 116 11 86 95 9 80 92 12

t 17 t 26

t 21




128 159 31 99 126 27 80 102 22 76 98 22 13 18 20 ? 13 t 18" 2 22" i 10 k 14 i 15" ? 11 i6 2 13"

i i 2



t t


t t t

16 17 15 13 14 14 15 15 10

136 174 38 106 138 32 83 109 26 77 102 25

13 23 19" 14 i 17 i 15" i8 ? 15 i 16" i 16 5 17 i13

2 i i i

"Postintubation increase significantly different from baseline P < 0.05.






-__ I Group

Group I1 Group 111 Group I V


() I




Control Group I Group I I Group 111 Group IV



1 1 1 1 1 B-5-4-3-2-1 1

Signficantly different from baseline p<O.O5




Signilicantly difterent from baseline pc0.05


1 1

1 2

l 3





TIME ( m i d







TIME ( m i d

Figure 2. Changes in heart rate (HR). B, Baseline. Negative times represent minutes before intubation. 0, time of intubation. Positive times represent minutes after intubation.

Figure 1. Changes in systolic blood pressure (SBP). 8 , Baseline. Negative times represent minutes before intubation. 0, time of intubation. Positive times represent minutes after intubation.

the data were further compared among the five groups, the 1-min postintubation increases in group I11 were found to be significantly less than in the other groups ( P < 0.04). No side effects of lidocaine were noted.


It is well known that laryngoscopy and tracheal intubation are accompanied by increases in HR and ABP (8). In most patients these changes are well tolerated. In certain groups of patients, such as those who at risk for developing arterial hypertension (9) or myocardial ischemia (lo), such changes may be detrimen-

tal. The precise mechanism by which these changes are produced is uncertain but probably involves intense sympathetic discharge caused by stimulation of the upper respiratory tract (11,12). Lidocaine has been a popular agent for attenuating circulatory responses associated with tracheal intubation. It has been used as a lidocaine gargle for oropharyngeal anesthesia (13), as a lidocaine aerosol for intratracheal anesthesia (14), or as an intravenous bolus for systemic anesthesia (4). Intravenous lidocaine, in particular, has been found to suppress the cough reflex (1,2), to prevent increases in intracranial pressure (3), to attenuate circulatory responses (4) and to possess antiarrhythmic properties (5). The best dose of intravenous lidocaine for atten-



1987;hh: 1036-8


uation of circulatory responses to laryngoscopy and intubation has been established at 1.5 mg/kg (6). The time of injection of IV lidocaine before intubation is, however, not well documented, varying, on an empirical basis, from 1 to 3 min before intubation (6,15). Our study shows that IV lidocaine at a dose of 1.5 mg/kg given 3 min before intubation offered statistically significant attenuation of increases in all of the four hemodynamic variables. IV lidocaine given at 1, 2, and 5 min offers no statistically significant protection against increases in SBP, MBP, DBP, and HR. The attenuation of circulatory response to tracheal intubation occurred only when the IV lidocaine was given 3 min before intubation. Intravenous lidocaine may suppress circulatory responses to tracheal intubation by increasing the depth of general anesthesia. Lidocaine blood levels of 3-6 pglml are known to potentiate the effects of nitrous oxide anesthesia in humans (16). Lidocaine also has direct cardiac depressant and peripheral vasodilating effects. The blood level for these direct effects has been generally accepted to be 1.5-6 pg/ml. We did not measure lidocaine blood levels in this investigation. Ideally, it would be desirable to correlate the clinical effect of lidocaine with blood levels. However, such a correlation may not be appropriate because the mechanism by which IV lidocaine suppresses pressor responses is still unclear. Also, blood level may not necessarily reflect tissue levels. Furthermore, Patel et al. (18) have reported that lidocaine blood concentration peaked within the first minute after an IV bolus, a time interval far too early for any study to observe any clinical effect. Our assumption that blood levels do not correlate with clinical effects is further substantiated by Safwat et al. (19), who found that plasma levels of propranolol did not corf relate with its clinical effect o hemodynamic control when used before rapid sequence induction of anesthesia and tracheal intubation. We conclude that IV lidocaine at 1.5 mg/kg attenuates increases in HR and ABP only when given 3 min before intubation, and offers no protection against postintubation hemodynamic changes when given at 1, 2, or 5 min before intubation.

We thank Mr. Anthony Ayiomamitis for advice in our statistical analyses.


1. Steinhaus JE, Gaskin L. A study of intravenous lidocaine as a suppressant of cough reflex. Anesthesiology 1963;24:285-90. 2. Poulton TJ, James FM 111. Cough suppression by lidocaine. Anesthesiology 1979;50:470-2. 3. Donegan MF, Bedford RF. Intravenously administered lidocaine prevents intracranial hypertension during endotracheal suctioning. Anesthesiology 1980;52:516-8. 4. Hamill JF, Bedford RF, Weaver DC, Colohan AR. Lidocaine before endotracheal intubation: intravenous or laryngotracheal? Anesthesiology 1981;55:578-81. 5. Collinsworth KA, Kalman SM, Harrison DC. The clinical pharmacology of lidocaine as an anti-arrhythmic drug. Circulation 1974;SO:1217-30. 6. Abou-Madi MN, Keszler H, Yacoub JM. Cardiovascular reactions to laryngoscopy and tracheal intubation following small and large intravenous doses of lidocaine. Can Anaesth Soc J 1977;24:12-9. 7. Stoelting RK. Blood pressure and heart rate changes during short-duration laryngoscopy for tracheal intubation: influence o viscous or intravenous lidocaine. Anesth Analg 1978;57:197-9. f 8. Prys-Roberts C, Greene LT, Meloche R, Foex P. Studies of anaesthesia in relation to hypertension. 11. Haemodynamic consequences of induction and endotracheal intubation. Br J Anaesth 1971;43:531-46. 9. Bedford RF, Feinstein BSH. Hypertension after endotracheal intubation: correlation with the pre-operative blood pressure record. Anesth Analg 1980;59:527-8. 10. Roy WL, Edelist G, Gilbert B. Myocardial ischemia during noncardiac surgical procedures in patients with coronary artery disease. Anesthesiology 1979;51:393-7. 11. Tomori Z , Widdicombe JG. Muscular, bronchomotor and cardiovascular reflexes elicited by mechanical stimulation of the respiratory tract. J Physiol (Lond) 1969;200:25-49. 12. Russell WJ, Morris RG, Frewin DB, Drew SE. Changes in plasma catecholamine concentrations during endotracheal intubation. Br J Anaesth 1981;53:837-9. 13 Stoelting RK. Circulatory response to laryngoscopy and tracheal intubation with or without prior oropharyngeal viscous lidocaine. Anesth Analg 1977;56:618-21. 14 Denlinger JK, Ellison N, Ominsky AJ. Effects of intratracheal lidocaine on circulatory responses to tracheal intubation. Anesthesiology 1974;41:409-12. 15 Stoelting RK. Circulatory changes during direct laryngoscopy and tracheal intubation. Anesthesiology 1977;47:381-4. 16 Himes RS, DiFazio CH, Burney RG. Effects of lidocaine on the anesthetic requirements for nitrous oxide and halothane. Anesthesiology 1977;47:437-40. 17 Isselbacher KJ, Adams RD, Braunwald E, Petersdorf RG, Wilson JD, eds. In: Harrison's Principles of Internal Medicine. 9th ed. New York: McGraw-Hill, 1980:1070. 18. Patel RI, Peterson RG, Aldrete JA. Endotracheal compared with intravenous injection of 3 mgikg of lignocaine. Anaesthesia 36: 772-4. 19. Safwat AM, Fung DL, Bilton DC. The use of propranolol in rapid sequence anaesthetic induction: optimal time interval for pretreatment. Can Anaesth Soc J 1984;31:638-41.


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