Efficacy o f Lignocaine a nd Esmolol i n Attenuating t he Cardiovascular Responses t o Laryngoscopy and Endotracheal Intubation


Assistant Professor, Department of Anesthesia, Mediciti Institute of Medical Sciences, Ghanpur, Hyderabad, Telangana, India
Professor & HOD, Department of Anesthesia, Mediciti Institute of Medical Sciences, Ghanpur, Hyderabad, Telangana, India

Abstract

Background: The present study was undertaken to compare the efficacy of lignocaine and esmolol in attenuating the cardiovascular responses to laryngoscopy and endotracheal intubation. Subjects and Methods: 60 patients undergoing elective surgery were divided into two groups of 30 each, group L (Lignocaine) and group E (Esmolol). Baseline hemodynamic parameters - heart rate (HR), systolic blood pressure (SBP), diastolic blood pressures (DBP), mean arterial pressure (MAP) and rate-pressure product (RPP) were recorded. Results: There was no statistically significant difference in heart rate among the groups before and after premedication and after induction (P value >0.05). After intubation, there was rise in heart rate in both the groups. The rise was significantly less in esmolol group as compared lignocaine groups (p value <0.05) till 5 minutes of study period. There was no statistically significant difference in systolic blood pressure among the groups before and after premedication. After induction and intubation, there was no statistically significant difference in systolic blood pressure among the groups (p value >0.05). Conclusion: Esmolol hydrochloride 1mg/kg IV bolus dose is superior to lignocaine hydrochloride 1.5mg/kg IV bolus to attenuate the haemodynamic responses to laryngoscopy and endotracheal intubation.

Keywords

Esmolol hydrochloride, Endotracheal intubation, Systolic blood pressure

Introduction

Laryngoscopy and endotracheal intubation are routine procedures of modern balanced general anaesthesia technique. Laryngoscopy and endotracheal intubation frequently induce cardiovascular stress response characterized by raised serum concentration of catecholamines; hypertension and tachycardia which may culminate in increased perioperative morbidity.[1] Haemodynamic changes are generally temporary without any sequelae. However, these changes can facilitate and accelerate the development of myocardial ischemia, cardiac arrhythmias, infarction and cerebral hemorrhage in patients with coronary artery disease, hypertension or cerebrovascular disease.[2]

The quest for effective suppression of these responses continues. Knowledge and studies on the cardiovascular response has led to the development of various techniques to modify this pressor response. Some of these include maintenance of deeper planes of anaesthesia, short duration of laryngoscopy, usage of drugs like intravenous(IV) lignocaine 1.5 mg/kg, intratracheal 4% lignocaine as topical spray, IV bolus fentanyl l1-2 µg/kg, sufentanil 0.2-0.3 µg/kg, sodium nitroprusside 1-2 µg/kg, topical nitroglycerine application, sublingual nifedepine, beta blockers like protalol, metaprolol prior to laryngoscopy and intubation are the various techniques developed for the same.[3] Esmolol, an ultra short acting cardio selective beta-blocker can be effectively used either as infusion or as bolus dose.

The ideal agent should block the haemodynamic responses to laryngoscopy and endotracheal intubation, should be short acting and should not deepen the level of anaesthesia significantly which may lead to myocardial depression, hypotension, and arrhythmias. Lignocaine hydrochloride is an antiarrhythmic agent which possesses membrane stabilizing action. It has been widely used in clinical practice to suppress sympathetic response to laryngoscopy and endotracheal intubation. [4,5] Esmolol, a cardio selective beta-blocker with a rapid onset of action and a short half life has been used by various groups of workers for the same purpose. The present study was undertaken to compare the efficacy of lignocaine and esmolol in attenuating the cardiovascular responses to laryngoscopy and endotracheal intubation.

Subjects and Methods

This clinical study was conducted in Mediciti Institute of Medical Sciences, Ghanpur, Medchal, Andhra Pradesh. After approval from the hospital ethics committee, study was conducted during the period between October 2010 and 2012. A total of 60 patients undergoing elective surgery were randomly divided into two groups of 30 each, group L (Lignocaine) and group E (Esmolol).

Thorough pre-anaesthetic evaluation was done for all the patients. Written, valid informed consent was obtained both for conduct of study as well as for surgery and anaesthesia. Patients were kept nil by mouth from night before surgery and Tab. alprazolam (0.25 mg) was administered.    In the preoperative room, all the patients were reassessed on the day of surgery. ‘Nil by mouth’ status was confirmed. Baseline haemodynamic parameters - heart rate (HR), systolic blood pressure (SBP), diastolic blood pressures (DBP), mean arterial pressure (MAP), rate-pressure product (RPP), electrocardiogram (ECG) and SpO2 were recorded. Intravenous line was secured with 18G cannula and ringer lactate solution was started.

Patients were shifted to operating theater. Anaesthesia machine, other equipments, monitors and emergency drugs were checked. Monitors are attached. Patients were premeditated with Inj. glycopyrrolate 0.005mg/kg body weight and Inj. midazolam 0.05mg/kg body weight intravenously 10 minutes before induction. Heart rate, systolic and diastolic blood pressures, mean arterial pressure, ECG (lead II) and SpO2 were recorded. Preoxygenation was done with 100% oxygen for 3 min. Group L (n=30) patients received lignocaine hydrochloride 1.5 mg/kg IV and group E (n=30) patients received esmolol hydrochloride 2 mg/kg IV.

Haemodynamic parameters (HR, SBP, DBP and MAP) and oxygen saturation were recorded during intubation and thereafter at 1 min, 3 min, 5 min, 7 min and 9 minutes. All the data were tabulated analyzed and compared. P value of less than 0.05 was considered significant.

Results

Table 1: Age wise distribution

Age (years)

Lignocaine (n=30)

Esmolol (n=30)

18-26

11 (36.66%)

12 (40%)

27-35

12 (40%)

11 (36.66%)

36-45

7 (23.33%)

7 (23.33%)

Mean ±SD

30.00±7.43

29.87±7.74

[Table 1] shows that age group 18-26 years had 11 in group lignocaine and 12 in esmolol group, 27-35 years had 12 in lignocaine and 11 in esmolol, 36-45 years had 7 in lignocaine and 7 in esmolol group.

Table 2: Gender wise distribution

Gender

Lignocaine

Esmolol

Male

17 (56.66%)

14 (46.66%)

Female

13 (43.33%)

16 (53.33%)

[Table 2] shows that there were 17 (56.66%) males and 13 (43.33%) females in lignocaine group and 14 (46.66%) males and 16 (53.33%) females in esmolol group.

https://s3-us-west-2.amazonaws.com/typeset-prod-media-server/d32e390b-3e3f-4d75-b9c6-f17e59bbcf32image1.png
Figure 1: Comparison of heart rate

[Figure 1] shows that before and after premedication and after induction, there was no statistically significant difference in heart rate among the groups (p value >0.05). After intubation, there was rise in heart rate in both the groups. The rise was significantly less in esmolol group as compared lignocaine groups (p value <0.05) till 5 minutes of study period.

Table 3: Comparison of mean systolic blood pressure between study groups

Time

Lignocaine

Esmolol

P -value

Baseline

122.37±6.04

121.83±5.56

>0.05

After premedication

123.13±5.59

122.73±4.95

>0.05

After induction

122.80±5.30

122.67±4.06

>0.05

During intubation

155.17±4.68

135.87±3.93

<0.05

After Intubation

1 Minute

143.73±4.14

131.43±4.07

<0.05

3 Minute

133.50±4.06

128.57±3.54

<0.05

5 Minute

127.90±3.96

125.97±4.40

>0.05

7 Minute

125.03±4.10

124.83±4.09

>0.05

9 Minute

124.30±4.70

124.77±4.07

>0.05

[Table 3] shows that before and after premedication, there was no statistically significant difference in systolic blood pressure among the groups (p value >0.05). After induction and intubation, there was no statistically significant difference in systolic blood pressure among the groups (p value >0.05).

Table 4: Comparison of mean diastolic blood pressure between study groups

Time

Lignocaine

Esmolol

P-value

Baseline

76.53±4.82

77.27±4.72

>0.05

After premedicaton

77.77±4.64

78.30±4.61

>0.05

After induction

77.03±5.14

77.33±4.37

>0.05

During intubation

98.93±2.29

93.70±2.44

<0.05

After Intubation

1 Minute

93.17±2.39

88.37±2.57

<0.05

3 Minute

87.10±2.32

85.80±2.66

>0.05

5 Minute

81.33±4.44

80.97±2.54

>0.05

7 Minute

79.23±4.74

79.30±3.29

>0.05

9 M inute

78.60±5.01

78.30±3.86

>0.05

[Table 5] shows that before, after premedication and after induction, there was no statistically significant difference in diastolic blood pressure among the groups (p value >0.05). After intubation: There was rise in diastolic blood pressure in both the groups. The rise was significantly less in esmolol group as compared lignocaine groups (p value <0.05) till 1 minutes of study period.

Table 5: Comparison of mean of mean arterial pressure

Time

Lignocaine

Esmolol

P -value

Baseline

91.81±4.95

92.12±4.63

>0.05

After Premedication

92.89±4.65

93.11±4.31

>0.05

After Induction

92.29±4.98

92.44±3.99

>0.05

During Intubation

116.34±2.55

107.76±2.56

<0.05

After Intubation

1 Minute

108.02±2.33

102.72±2.58

<0.05

3 Minute

102.57±2.21

100.06±2.48

<0.05

5 Minute

96.86±3.68

95.97±2.79

>0.05

7 Minute

94.50±4.11

94.48±3.25

>0.05

9 Minute

93.83±4.54

93.79±3.62

>0.05

[Table 6] shows that before, after premedication and after induction, there was no statistically significant difference in mean arterial pressure among the groups (p value >0.05). After intubation: There was rise in mean arterial pressure in both the groups. The rise was significantly less in esmolol group as compared lignocaine groups (p value <0.05) till 3 minutes of study period.

Table 6: Comparison of mean rate-pressure product

Time

Lignocaine (n=30)

Esmolol (n=30)

P-value

Baseline

9830.90±839.66

9707.27±763.23

>0.05

After Premedication

9945.07±788.97

9878.80±682.53

>0.05

After Induction

9934.57±854.15

9773.87±608.75

>0.05

During Intubation

19270.10±1078.30

12405.23±767.04

<0.05

After Intubation

1 Minute

17362.73±1024.36

11560.57±647.08

<0.05

3 Minute

13659.93±1210.21

10781.20±648.08

<0.05

5 Minute

11678.47±641.90

10352.03±639.09

<0.05

7 Minute

10480.73±673.56

10199.20±669.27

>0.05

9 Minute

10216.30±683.35

10112.93±720.22

>0.05

[Table 7] shows that before, after premedication and after induction, there was no statistically significant difference in rate pressure product among the groups (p value >0.05). After intubation: There was rise in rate pressure product in both the groups. The rise was significantly less in esmolol group as compared lignocaine groups (p value <0.05) till 5 minutes of study period.

Discussion

The sequence of induction of anaesthesia, laryngoscopy and endotracheal intubation are associated with marked haemodynamic changes and autonomic reflex activity and this may be a cause of concern in many high risk patients. [6] Laryngoscopy and intubation are associated with rise in blood pressure and heart rate occasionally cardiac arrhythmias. These potentially dangerous changes disappear within 5 minutes. [7] Although the responses of blood pressure and heart rate are short lived they may have detrimental effects in high risk patients especially those with cardiovascular diseases, increased intracranial pressure or anomalies of the cerebral vessels. [8]

Many factors affect the cardiovascular responses associated with laryngoscopy and intubation. Age, drugs, duration of procedure, depth of anaesthesia, hypoxia, hypercarbia etc., influence the haemodynamic response. Variability of heart rate decreases with increasing age. Younger patients show more extreme changes. Marked fluctuations in haemodynamic responses are often seen in geriatric patients. The age of patients in this study ranged from 18 to 45 years. [9] Antihypertensive drugs can decrease pressor response. In this study patients on antihypertensive drugs were excluded. Different drugs used for premedication, induction, and muscle relaxation influence the sympathetic response to laryngoscopy and intubation. Midazolam at a dose of 0.2mg/kg IV decreases the blood pressure, and increases the heart rate similar to thiopentone. However, premedication with 0.05 mg/kg I.V has a minimal effect. Midazolam has no effect on sympathetic response to laryngoscopy and intubation. There is increase in catecholamine levels following laryngoscopy and intubation; both nor adrenaline and adrenaline. Laryngoscopy alone may produce most of the cardiovascular responses. [10]

The most important factor influencing the cardiovascular response is found to be the duration of laryngoscopy. A linear increase in heart rate and mean arterial pressure occurs during first 45 seconds. In the present study the duration of laryngoscopy and intubation was limited to 20 seconds. Adequate care was taken to achieve required depth of anaesthesia avoiding hypoxia and hypercarbia which can influence on haemodynamic variations. [11]

Excluding hypoxia and hypercarbia, continued manifestation of anxiety concerning anaesthesia and operation, inj. glycopyrrolate premedication, reflex baroreceptor effect after thiopentone and possible effects of suxamethonium are other contributory causes of hypertension and tachycardia. They seem to be less important than laryngotracheal stimulation during laryngoscopy and intubation. [12]

Various drugs and techniques have been utilized to blunt the haemodynamic response. These drugs minimize the increase in heart rate and blood pressure by attenuating positive chronotropic and inotropic effects due to the increase in adrenergic activity. Esmolol possesses several properties which makes it a valuable agent to obtund the cardiovascular response. Firstly it is a cardio selective agent. Secondly, it has ultra short duration of action (9 minutes) and finally, significant drug interactions with commonly used anaesthetics have not been reported. Lignocaine prevents rise in heart rate, blood pressure, intracranial pressure and intraocular pressure associated with laryngotracheal stimulation. It suppresses cough related to extubation. [8] It is recommended to use at a dose of 1.5 mg/kg IV and optimal time of administration is 3 minutes before laryngoscopy and intubation. [13]

The mean age of patients in lignocaine group of the present study is comparable with those of Bharthi et.al (30±5.3). [14] Singh et al, [15] studied the effect of lignocaine, esmolol and fentanyl in elderly patients. Male: female ratio in the present study, in lignocaine and esmolol groups is comparable with Suman Shree et al. [16] In lignocaine it is comparable with Ifthikar et al. [17]

In lignocaine and esmolol groups, baseline heart rate was 80.30±4.9 beats/min and 79.67±4.77 beats/min respectively. Arti Rathore et al, [18] reported that patients of esmolol group had increased heart rate after laryngoscopy and endotracheal intubation (14% rise from baseline) as compared to control (35% rise) group.

In the present study after laryngoscopy and endotracheal intubation there was rise in the heart rate in both the groups. In lignocaine group it reached peak of 124.17±5.34 beats/min at 0 minutes of intubation (55% increase over baseline), where as in esmolol group, peak heart rate was 91.30±4.88 beats/min at 0 minutes of intubation (15% increase over baseline). Heart rate subsequently declined to 82.17±3.99 beats/min and 81.03±4.64 beats/min in lignocaine and esmolol group respectively at 9 minutes. Suman Shree et al, [16] in their study, reported that there was 22% rise in DBP in lignocaine group following laryngoscopy and endotracheal intubation, where as in esmolol group there was rise in DBP by 17% above baseline.

Conclusion

Authors concluded that that esmolol hydrochloride 1mg/kg IV bolus dose is superior to lignocaine hydrochloride 1.5mg/kg IV bolus to attenuate the haemodynamic responses to laryngoscopy and endotracheal intubation. No side effects were noted with esmolol and lignocaine hydrochloride.