{¹Associate Professor, ⁴Professor, ⁵Senior Resident, Department of Anesthesia} {^2,3Associate Professor, Department of Critical Care}

NRI Medical College, Guntur, Andhra Pradesh, INDIA.

Email: hanumanth.narni@gmail.com

Table 1: Depicts the changes in mean and SD of SBP at different time intervals in group E and group L.

From table-1: The change in mean and SD of SBP at baseline and immediately after intubation at 0 min were not statistically significant. The change in mean and SD of SBP before intubation or before the administration of the study drug is statistically significant (p<0.05) between the two groups. The change in mean and SD of SBP after intubation at 1min, 3min and 5min is statistically significant between the two groups. During the study it was observed that the SBP decreases from baseline values before the study drug administration in both the groups. But SBP increases to the highest degree at 1min (>20% from the baseline) after intubation in group L. The SBP remained above the baseline till 5 min after intubation in group L. The SBP increases to the highest value at 1 min after intubation but being less than the baseline value. The SBP remained below the baseline till 5min after intubation in group E.

Table 2: Depicts the changes in mean diastolic blood pressure at different time intervals between group E and group L.

The change in mean and SD of DBP at baseline and immediately after intubation at 0min were not statistically significant. The change in mean and SD of DBP before intubation or before the administration of the study drug is statistically significant (p<0.05) between the two groups. The change in the mean and SD of DBP after intubation at 1min, 3min and 5min is statistically highly significant between the two groups (p<0.05). During the study it was observed that in group E the DBP decreases from baseline values before the study drug administration, but there was an increase in DBP to the highest degree immediately after intubation at 0 and 3min, the increase being below the baseline values. In group L, it was observed that the DBP was near the baseline value before and after intubation at 0min, but the highest degree being at 1min and the increase in DBP remained above the baseline values till 5min after intubation in group L.

Table 3: Depicts the changes in mean arterial blood pressure at different time intervals between group E and group L.

From table-3: The mean and SD of mean arterial blood pressure at baseline and after intubation at 0 min compared between group E and L is not statistically significant. The mean and SD of mean arterial blood pressure before intubation or before the administration of the study drug is statistically highly significant (p<0.05). The mean and SD of mean arterial blood pressure after intubation at 1min, 3min and 5min after intubation is statistically significant (p<0.005). During the study it was observed that there was a decrease in MAP from baseline values in both the groups before the study drug was administered. In group E the MAP increased with a highest degree at 0 min after intubation, but the increase being less than the baseline value and it remained decreased even at 5 mins after intubation. In group L, MAP increased above the baseline value with a highest degree observed at 1 min after intubation and decreased gradually but it remained above the baseline at 5 mins after intubation.

Table 4: Depicts the comparision of changes in mean heart rate at different time intervals between group E and group L.

From table-4: The change in mean and SD of heart rate between group E and group L at base line, before the study drug administration and at 0 mins after intubation is not statistically significant. The change in mean heart rate compared between group E and group L after intubation at 1min, 3min and 5min is statistically highly significant (p<0.05). During the study the change in mean HR was observed to be decreased before the study drug administration in both the groups. In group E the mean HR remained below the baseline value even at 5min after intubation. In group L the mean HR increased >20% from the baseline value at 1 and 3 mins after intubation and remained increased even at 5 mins after intubation.

DISCUSSION

From the present study, observed a slight increase in SBP, DBP, and MAP before study drug administration or pre intubation. The change in SBP, DBP, and MAP was slightly increased in both the groups after 1min, 3min, 5min above the baseline. This might be due to intubation response. Among the two groups E and L the increase was attenuated significantly in esmolol than lignocaine. 5min after intubation HR, SBP, DBP and MAP returned to almost baseline value in esmolol group. These findings are in agreement with that of UGUR B , OGURULU M , et al.²⁷who showed attenuated hemodynamic response due to sympathetic stimulation associated with endotracheal intubation. Stanley Tam, Frances Chung, Michael Campbell ²⁸made a study for determining optimal time of injection of IV lignocaine for the attenuation of circulatory responses secondary to endotracheal intubation. Four groups received lignocaine 1.5 mg/kg IV single bolus over a period of less than 5 seconds 1, 2, 3 and 5min before intubation. Fifth group served as the control and received no IV lignocaine. They observed that cardiovascular responses were significantly above base line levels in patients given lignocaine 1min group (p < 0.05), 2min group (p < 0.05), and 5min group(p < 0.05) before intubation or in controls (p < 0.05) compared to IV lignocaine 3min before intubation group. In our study Plain preservative free Lignocaine 2%, 1.5 mg/kg IV bolus was given 3minutes prior to direct laryngoscopy. The results were in accordance to 1min, 3min and 5min group of Stanley Tam et al. study i.e, cardiovascular responses were significantly above baseline levels. Aleem et al. ²⁹compared the effects of lignocaine and fentanyl in attenuation of pressor response to laryngoscopy and tracheal intubation. After endotracheal intubation incidence of tachycardia (HR>100/min) was significantly greater in lignocaine group than in fentanyl group (p<0.05). Rise in SBP and DBP were also statistically significant in lignocaine group than in fentanyl group (p<0.05). Attenuation of pressor response is seen both with lignocaine and fentanyl. Of the two drugs fentanyl 4 microgram/kg IV bolus provides a consistent, reliable and effective attenuation as compared to lignocaine 1.5 mg/kg IV bolus. In our study Plain preservative free Lignocaine 2%, 1.5 mg/kg IV bolus was given 3min prior to direct laryngoscopy.The results were similar to that of the study conducted by Aleem et al. Abou - Modi, Keszer and Yacoub³⁰et al. who had used intravenous lignocaine in 1.5mg / kg and 0.7 mg/kg doses and found that intravenous lignocaine in 1.5mg/kg dose provided complete protection against arrhythmias, but only a borderline protection against increase in blood pressure and heart rate, while the dose 0.7mg/kg was inadequate in providing protection against arrhythmias, only preventing blood pressure elevation. They have described the possible mechanisms of action of lignocaine as – direct myocardial depressant effect, peripheral vasodilating effect and effect of synaptic transmission. Robert Stoelting³¹found that lignocaine in 1.5mg/kg intravenously can attenuate the pressor response effectively in a study conducted on 36 known heart disease patients scheduled for non – cardiac major surgeries. D.G. Clayton et al.³²studied effects of pre - treatment with intravenous lignocaine 1.5mg/kg given 1min prior to induction of anaesthesia. It was shown to reduce significantly, the incidence of dysrhythmias during dental anaesthesia and also to reduce the rise in blood pressure associated with endotracheal intubation. Gupta et al.³³compared effectiveness of intravenous esmolol and lignocaine in suppressing the cardiovascular stress response. Patients were divided into three groups of 20patients each. Group - L received lignocaine and Group – E received esmolol three minutes before intubation, Group-C did not receive any drug under study. It was found that patients given esmolol had better attenuation of stress response to laryngoscopy and intubation than patients given lignocaine. Our results were similar to that of above study.

Nooraei et al.³⁴compared the effects of intravenous administration of lignocaine and magnesium sulphate on unwanted hemodynamic responses following laryngoscopy and intubation in elective surgery candidates. This randomized doubleblind clinical trial concluded that Magnesium sulphate is more effective than lignocaine in controlling hemodynamics, although it may increase the heart rate. The results of our study were similar to that of above study. Esmolol, a water - soluble, cardioselective, and ultrashort – acting ß - adrenergic antagonist, has also been shown to be effective in controlling both the HR and BP responses to intubation, but only in patients undergoing elective surgery studied by Helfman SM³⁵Kindler CH et al.³⁶Kampine JP et al.³⁷Parnass SM et al.³⁸found in patients undergoing general anesthesia for elective surgery, that esmolol (loading dose of 500 µg/kg/min for 4 minutes, followed by a maintenance infusion of 300 µg/kg/min for 11minutes) significantly attenuated the maximum increases in HR and BP when compared with placebo. Another study found that a single bolus dose of 100 or 200 mg was able to attenuate the hypertensive and tachycardic responses to laryngoscopy and intubation (Parnass et al. Bostana and Eroglu reported that IV esmolol in dose of 1mg/kg before intubation was effective in suppressing the HR and arterial BP³⁹which are similar to the present study. Kindler et al.⁴⁰found that esmolol administration before laryngoscopy was sufficient to control HR after intubation, but it did not affect systolic arterial pressure (SAP) .In this study, esmolol 2 mg/kg was found to be quite effective in attenuating the hypertensive response (MAP) as well as the HR during laryngoscopy and tracheal intubation till 5 min. In this present study the change in mean and SD of HR, SBP, DBP, MAP during 1min, 3min and 5 min is statistically highly significant between the two groups (p<0.05). S. Sharma, et al.⁴¹ obtained similar result by comparing the ability of different bolus doses of esmolol to blunt the haemodynamic effects of laryngoscopy and tracheal intubation in treated hypertensive patients. Esmolol 100 mg given as bolus, is effective as well as safe in blunting the haemodynamic responses to laryngoscopy and tracheal intubation in treated hypertensive patient. Similar results were obtained by Bensky KP, et al.⁴²This study shows that small doses of esmolol may block the increase in heart rate and blood pressure resulting from laryngoscopy and intubation. Recently, anesthesia research has began to compare the efficacies of several drugs against each other, rather than relying on studies that isolate a single drug's effect vs a placebo intervention. The ability of esmolol vs lidocaine to attenuate the hemodynamic response to intubation was first studied by Helfman et al. in 1990. The present study compared the efficacy of IV esmolol, and IV lignocaine in determining which is best in preventing tachycardia and hypertension secondary to endotracheal intubation. The result obtained from this study found that both I.V esmolol and I.V lignocaine are effective in controlling SBP, DBP, HR, and MAP. Esmolol is more effective than I.V lignocaine in attenuating both SBP and DBP. Esmolol, at an intravenous bolus dose of 1.5mg/kg, "provided consistent and reliable protection against increases in both HR and BP accompanying laryngoscopy and Intubation. The Observations are also in close agreement with other studies who used this drug to achieve attenuation of pressor respose to direct laryngoscopy and endotracheal intubation.

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