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 Table of Contents  
Year : 2017  |  Volume : 12  |  Issue : 2  |  Page : 118-120

Comparison between magnesium sulfate (50 mg/kg) and lignocaine (2 mg/kg) for attenuation of intubation response in hypertensive patients

Department of Anesthesiology, Jawaharlal Nehru Medical College, DMIMS (DU), Wardha, Maharashtra, India

Date of Web Publication8-Sep-2017

Correspondence Address:
Nikhil S Bhalerao
Department of Anesthesiology, Jawaharlal Nehru Medical College, DMIMS (DU), Sawangi (Meghe), Wardha, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jdmimsu.jdmimsu_58_17

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Aims and Objective: The aim and objective of this study was to compare between magnesium sulfate and lignocaine for attenuation of intubation response in hypertensive patients. Materials and Methods: This prospective, randomized, double-blinded study was conducted in an operating room of Jawaharlal Nehru Medical College Institute, in which 60 adult American Society of Anesthesiologists 1 and 2 controlled hypertensive patients undergoing elective surgery under general anesthesia and requiring endotracheal intubation were selected. Patients were randomized into two groups: Group I with thirty patients who received MgSO4 50 mg/kg half an hour before induction of anesthesia and Group II with thirty patients who received lignocaine 2 mg/kg intravenous bolus. Laryngoscopy and intubation were performed to see response in both the groups. Heart rate (HR) and blood pressure (BP) were recorded before, during, and after endotracheal intubation for 10 min. Results: The changes in the HR and mean arterial pressure (MAP) were compared, and the results showed that Group I patients had minimal response to any changes after intubation while Group II patients showed changes in HR and MAP toward baseline after laryngoscopy and endotracheal intubation. Discussion: Magnesium sulfate developed hypotension at various points, though it is associated with good control of adrenergic response during intubation, while lignocaine developed rate pressure changes which were not so good, also showing cardiac instability. Conclusion: Magnesium sulfate 50 mg/kg has a better control of BP during intubation in hypertensive patients with some incidence of hypotension when compared with lignocaine 2 mg/kg.

Keywords: Hypertensive patients, laryngoscopy, lignocaine

How to cite this article:
Bhalerao NS, Modak A, Belekar V. Comparison between magnesium sulfate (50 mg/kg) and lignocaine (2 mg/kg) for attenuation of intubation response in hypertensive patients. J Datta Meghe Inst Med Sci Univ 2017;12:118-20

How to cite this URL:
Bhalerao NS, Modak A, Belekar V. Comparison between magnesium sulfate (50 mg/kg) and lignocaine (2 mg/kg) for attenuation of intubation response in hypertensive patients. J Datta Meghe Inst Med Sci Univ [serial online] 2017 [cited 2021 Nov 28];12:118-20. Available from: http://www.journaldmims.com/text.asp?2017/12/2/118/214195

  Introduction Top

Laryngoscopy and tracheal intubation stimulate somatic and visceral nociceptive afferents of the epiglottis, hypopharynx, peritracheal area, and vocal cords which augment cervical sympathetic activity. Hypertensive patients are more prone to exaggerated cardiovascular response to laryngoscopy and tracheal intubation than normotensive patients and hence they are more dangerous in those with hypertension as they may lead to myocardial ischemia, arrhythmias, and intracranial hemorrhage. Therefore, prevention of cardiovascular stimulation following tracheal intubation is of particular importance.

Magnesium sulfate inhibits the relapse of catecholamine from adrenal medulla and is effective in attenuating the blood pressure (BP) response to tracheal intubation.[1]

Intravenous (IV) lignocaine is popular because of its advantages of suppressing cough reflex,[2] preventing increase in intracranial pressure,[3] and attenuating circulatory response,[4] and because of its antiarrhythmic properties.[5] This prospective, randomized double-blinded study was planned to find which drug is more efficient in suppressing adverse hemodynamic response to tracheal intubation.

  Materials and Methods Top

After obtaining approval from the Ethical Committee of Jawaharlal Nehru Medical College and written informed consent, sixty adult hypertensive patients who had controlled hypertension (BP <140/90 mmHg) and were receiving medication for a minimum of 2 weeks were included in the study. They were posted for elective surgery under general anesthesia requiring anesthesia endotracheal intubation.

Exclusion criteria

Patients with a history of coronary artery disease (CAD), cardiac arrhythmias, hypomagnesaemia, neuromuscular disease, and increased intracranial pressure, patients with anticipated difficult intubation, and patients with the American Society of Anesthesiologists (ASA) physical status III or high were excluded from the study.

Inclusion criteria

Patients with ASA physical status I and II, those aged 18–60 years, and Mallampati Grade I and II patients were included and fasted 6 h before the surgery. They received oral diazepam 0.1 mg/kg and ranitidine 150 mg along with antihypertensive drugs in the morning of surgery.

The study included magnesium sulfate 50 mg/kg added to 100 ml of normal saline (NS) given over half an hour before the induction of anesthesia 3 cc NS given 90s before intubation in Group I and 2 mg/kg lignocaine given 90 s before intubation after giving 100 ml NS over half an hour before induction in Group II. Patients were allocated randomly to one of the two groups by sealed envelope assignment and a computer-generated sequence of random number offered just before the start of the study. Anesthesia was induced with propofol 2 mg/kg and Scoline 2 mg/kg was also given. Patients were ventilated by a face mask using 40% oxygen and 60% nitrous oxide. Contents of the test syringe (NS in Group I and lignocaine in Group II) were injected approximately 90 s before laryngoscopy and intubation was carried out 1 min after the administration of Scoline.

HR, BP (mean arterial pressure [MAP], systolic BP [SBP], and diastolic BP [DBP]), and SpO2 were recorded at baseline (i.e., before starting infusion of NS with or without magnesium sulfate), at the end of infusion (just before induction of anesthesia), at 2-min interval after prescribing propofol and Scoline immediately after laryngoscopy and intubation, and at 2-min intervals for 10 min. Just after intubation was done, vecuronium bolus was prescribed with 0.08–0.12 mg/kg. Patients and anesthesiologist present during the induction of anesthesia and collection of data were blinded to the study.

Statistical analysis was performed using SPSS 15.0 software (SPSS, Chicago IL, USA). Quantitative data were described as means ± standard deviation and compared among both the study groups using one-way analysis of variance test. Pearson's correlation coefficients were also calculated between different quantitative variables, and comparison of both groups was carried out for various categorical variations using Chi-square test. P < 0.05 was considered statistically significant.

  Results Top

Patients in both the groups were comparable with age, weight, and duration of hypotension before surgery. Beta-blockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, and diuretics were the drugs used for hypertension. All the patients were intubated on the first attempt and no patient was excluded from the study.

Baseline HR and BP were comparable among the groups. Heart rate (HR) tended to decrease after induction with a brief increase after intubation in both the groups. The difference in HR was not statistically significant between the groups throughout the study period. SBP, DBP, and MAP decreased after induction of anesthesia, with an increase toward baseline immediately after intubation in both the groups.

There was no significant increase in BP after laryngoscopy and intubation in any group of patients when compared with baseline in Group I patients. MAP decreased after intubation and remained lower after tracheal intubation compared with baseline and other groups. Patients in Group II showed a significant decrease in MAP as compared with baseline 4 and 6 min after intubation which continued until the end of study period.

Patients pretreated with magnesium sulfate (50 mg/kg) required interventions to manage hypotension and Group II patients required no interventions as no episode of hypotension was recorded. No interventions were required to treat hypertension in any group [Figure 1] and [Figure 2].
Figure 1: Median heart rate in each group from baseline to 10 minutes after intubation (postintubation) MR = Muscle relaxant

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Figure 2: Mean arterial pressure in each group from baseline to 10 minutes after intubation (postintubation) MR = Muscle relaxant

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Group I patients received magnesium sulfate (50 mg/kg) before intubation and Group II patients received lignocaine bolus 50 s before intubation [Table 1].
Table 1: Patient characteristics

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  Discussion Top

Among the therapeutic regimens useful in suppressing the hormonal stress response to tracheal intubation, magnesium sulfate may be the forerunner as it not only has direct vasodilator properties,[6] but also significantly suppresses the release of catecholamine.[7]

In the present study, magnesium sulfate attenuated the pressor response to laryngoscopy and intubation administered before the induction of anesthesia. There was no significant increase in HR or BP as compared with baseline values after laryngoscopy and intubation in any group of patients. However, patients who received magnesium sulfate developed hypotension at various points; magnesium sulfate pretreatment is associated with a good control of adrenergic response with antiadrenergic agents during intubation. Allen et al.[8] compared magnesium sulfate (40 mg/kg) with lidocaine and alfentanil in moderate-to-severe hypertensive parturient and observed optimal control of BP in the magnesium sulfate group.

In another study, 30 mg/kg of magnesium sulfate with alfentanil was superior to 40 mg/kg of magnesium sulfate alone in hypertensive lower segment cesarean section patients.[9]

Alan et al. reported that there was no increase in HR, and BP was better maintained in patients receiving magnesium sulfate than those receiving clonidine 3 μg/kg (more hypotension). Magnesium sulfate is an α-adrenergic antagonist and may lead to a transient decrease in BP associated with peripheral vasodilation. However, despite its vasodilatation properties, magnesium sulfate does not generally produce significant hypotension in normotensive patients because of a concomitant increase in cardiac output. When this increase does not occur, marked hypotension may result.

Puri et al.[10] reported that administration of magnesium sulfate was associated with a significant decrease in MAP (P< 0.001) and systemic vascular resistance (P< 0.001) in patients with CAD. They also observed that, in spite of the significant decrease in MAP, none of the patients in the magnesium sulfate group developed ST changes, while in lignocaine group, few patients had significant ST depression. The absence of significant ST segment changes in magnesium sulfate group may have both the result of a decrease in after blood and coronary vasodilatation produced by magnesium. We also observed cardiac instability in patients who received IV lignocaine.

We observed that magnesium sulfate at a dose of 50 mg/kg prevents hypertensive response to laryngoscopy and tracheal intubation in hypertensive patients. It maintains cardiac stability better than pretreatment with lignocaine 2 mg/kg, but can cause few episodes of hypotension which is not seen with IV lignocaine – we included only controlled hypertensive patients in our study.

Further studies are needed to observe the effect of magnesium sulfate in controlled hypertensive patients with associated cardiac disease.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Dubé L, Granry JC. The therapeutic use of magnesium in anesthesiology, intensive care and emergency medicine: A review. Can J Anaesth 2003;50:732-46.  Back to cited text no. 1
Steinhaus JE, Gaskin L. A study of intravenous lidocaine as a suppressant of cough reflex. Anesthesiology 1963;24:285-90.  Back to cited text no. 2
Donegan MF, Bedford RF. Intravenously administered lidocaine prevents intracranial hypertension during endotracheal suctioning. Anesthesiology 1980;52:516-8.  Back to cited text no. 3
Hamill JF, Bedford RF, Weaver DC, Colohan AR. Lidocaine before endotracheal intubation: Intravenous or laryngotracheal? Anesthesiology 1981;55:578-81.  Back to cited text no. 4
Collinsworth KA, Kalman SM, Harrison DC. The clinical pharmacology of lidocaine as an antiarrhythmic drug. Circulation 1974;50:1217-30.  Back to cited text no. 5
Altura BM, Altura BT. Magnesium and contraction of arterial smooth muscle. Microvasc Res 1974;7:145-55.  Back to cited text no. 6
James MF, Beer RE, Esser JD. Intravenous magnesium sulfate inhibits catecholamine release associated with tracheal intubation. Anesth Analg 1989;68:772-6.  Back to cited text no. 7
Allen RW, James MF, Uys PC. Attenuation of the pressor response to tracheal intubation in hypertensive proteinuric pregnant patients by lignocaine, alfentanil and magnesium sulphate. Br J Anaesth 1991;66:216-23.  Back to cited text no. 8
Ashton WB, James MF, Janicki P, Uys PC. Attenuation of the pressor response to tracheal intubation by magnesium sulphate with and without alfentanil in hypertensive proteinuric patients undergoing caesarean section. Br J Anaesth 1991;67:741-7.  Back to cited text no. 9
Puri GD, Marudhachalam KS, Chari P, Suri RK. The effect of magnesium sulphate on hemodynamics and its efficacy in attenuating the response to endotracheal intubation in patients with coronary artery disease. Anesth Analg 1998;87:808-11.  Back to cited text no. 10


  [Figure 1], [Figure 2]

  [Table 1]

This article has been cited by
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