alexa A Study of the Efficacy of Cardiac Antidysrhythmic Drugs in Attenuating Haemodynamic Responses to Laryngoscopy and Endotracheal Intubation in the Black Population
ISSN: 2155-6148
Journal of Anesthesia & Clinical Research

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A Study of the Efficacy of Cardiac Antidysrhythmic Drugs in Attenuating Haemodynamic Responses to Laryngoscopy and Endotracheal Intubation in the Black Population

Sanjeev Singh1,4*, Edwin Ferguson Laing2 , William Kwame Boakye Ansah Owiredu2 , Arti Singh3 and Anbarasu Annamalai4

1Department of Anaesthesia and Intensive Care, College of Health Sciences, Ghana, West Africa

2Molecular Medicine, School of Medical Sciences, College of Health Sciences, Ghana, West Africa

3University Health Services, Kwame Nkrumah University of Science and Technology,Kumasi, Ghana, West Africa

4Department of Cardiac Anaesthesia, NHIMS, Bangalore, Karnataka, India

*Corresponding Author:
Sanjeev Singh
Department of Anaesthesia and Intensive Care
Department of Cardiac Anaesthesia
NHIMS, Bangalore, Karnataka, India
E-mail: [email protected]

Received date: June 07, 2013; Accepted date: June 18, 2013; Published date: June 20, 2013

Citation: Singh S, Laing EF, Ansah Owiredu WKB, Singh A, Annamalai A (2013) A Study of the Efficacy of Cardiac Antidysrhythmic Drugs in Attenuating Haemodynamic Responses to Laryngoscopy and Endotracheal Intubation in the Black Population. J Anesthe Clinic Res 4:326. doi: 10.4172/2155-6148.1000326

Copyright: © 2013 Singh S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Abstract

Background: Laryngeal, tracheal and bronchial receptors are stimulated by mechanical and chemical irritants during laryngoscopy and endotracheal intubation. That almost always triggers powerful cardiovascular responses. Various attempts have been made to attenuate these responses. The aim of this study was to compare the efficacy and safety of cardiac antidysrhythmic drugs lidocaine, diltiazem and esmolol in the attenuation of cardiovascular responses to endotracheal intubation in the Black normotensive population.

Patients and Methods: A randomized controlled trial was conducted in 160 adult patients of ASA physical status I or II undergoing various elective surgeries. The patients were randomly divided into four groups of 40 patients in each group - C, L, D, and E. Group - “C” received no drug (control) as placebo, group -“L” received 1.5 mg kg-1 preservative free lidocaine, group -“D” received 0.2 mg kg-1 diltiazem, and group-“E” received 2mg kg-1 esmolol IV. Group “C”, “D” and “E”, “L” one and two minutes before intubation. Changes in Heart Rate (HR), Systolic Blood Pressure (SBP), Diastolic Blood Pressure (DBP), and Mean Arterial Pressure (MAP) were measured and then compared within and between groups. Rate Pressure Product (RPP) was calculated and evaluated as well. Patients were also observed for any complications.

Result: There was a significant increase in SBP, DBP, HR, MAP and RPP from the base line in control group “C” at 1 minute with onward decreases at 3 and 5 minutes respectively after intubation. Percentage change in haemodynamic variables in groups C, L, D and E at 1 minute are as follows: SBP=23.58%, 11.84%, 9.64% and 9.9%, DBP=18.73%, 18.89%, 11.93% and 10.40%, HR=30.45%, 26.00%, 7.01% and 1.50%, MAP=20.80%, 15.89%, 10.90 and 10.20%; RPP=61.44%, 40.86%, 17.26% and 11.68% respectively. Only patients receiving placebo had increased SBP, DBP, HR, MAP and RPP values after intubation compared with baseline values (p<0.05).

Conclusions: Given the difference in the pharmacological mechanisms of these drugs, the prophylactic therapy with 2 mg kg-1 esmolol is significantly more effective and safe for attenuating haemodynamic changes to laryngoscopy and tracheal intubation, without producing increased risk of hypertension in the Black population.

Keywords

Blood pressure; Diltiazem; Esmolol; Heart rate; Intubation; Laryngoscopy; Lidocaine

Introduction

Direct laryngoscopy and endotracheal intubation frequently induces a cardiovascular stress response characterized by hypertension and tachycardia due to reflex sympathetic simulation [1]. This increase in blood pressure and heart rate are usually transitory variable and unpredictable lasting for less than 10 minutes [2]. It may be well tolerated in healthy people, but may be hazardous in patients with tachycardia, hypertension, myocardial infarction, cerebrovascular disease and other complications [3,4]. Various pharmacological approaches have been used to attenuate the pressure responses to laryngoscopy and tracheal intubation [4-7].

Hypertension is known to occur more frequently in the Black population and is associated with a higher incidence of cerebrovascular and renal complications. According to Gibbs et al. Strokes have been found to be more common in the Black hypertensives and hypertension associated end-stage renal failure occurs up to 20 times more commonly inthe Black patients compared to non-Blacks [8] .

Various pharmacological approaches considered to attenuate haemodynamic changes in Caucasians during endotracheal intubation as it reduces heart rate as well as blood pressure. Specific racial differences need to be considered before treatment in view of a report that African-Americans respond much less to beta-adrenergic receptor blocking drugs than Caucasians [9]. Beta-blockers tend to be less effective in the Black hypertensives as a result of the tendency towards a low-renin state and increased peripheral resistance and thus higher doses are required to achieve target blood pressure [8].

Several studies have looked at the efficacy of intravenous diltiazem, esmolol, lidocaine and their combination as an agent to blunt the haemodynamic response to laryngoscopy and intubation in Caucasians with different opinions; but no study available in Ghanaian population [6-8]. Efforts are being made to practice safe anaesthesia in Ghana in an attempt to reduce intraoperative complications and mortality during anaesthesia. The purpose of this study was, therefore, to determine the efficacy and safety of intravenous diltiazem, esmolol and lidocaine in attenuating haemodynamic response to laryngoscopy and intubation in the Black population.

Patients and Methods

This study was undertaken after an institutional approval by the Committee on Human Research Publications and Ethics was obtained. The study was conducted from November 2011 to May 2012. Informed consent was obtained from 160 patients. The study population consisted of American Society of Anesthesiologists (ASA) physical status I or II; male and female adults between the ages of 18-65 years scheduled for various elective surgical procedures under general anesthesia.

Study design

This study was a prospective; randomized and double-blinded clinical comparison in the Black population. The Sample size for the study was 160 generated using a sample size calculator. The study Participants were randomly divided into four groups by a computer generated randomization table. A study nurse (Person A) who was not involved in the randomisation process prepared the study drugs; all of which were diluted to 10 millilitres. All drugs were coded to enhance blinding. Person B monitored the Heart Rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), Mean Arterial Pressure (MAP) with respect to time whilst Person C was responsible for intubation of the patients. Person A and C were kept constant throughout the study. Person B, C and the patient were unaware of the drug injected to enable double-blinding.

Inclusion criteria for the study were ASA class I or II; age range 18–65, oropharyngeal anatomy of Mallampati class I and any operation other than cardiac surgery performed under general anesthesia with endotracheal intubation.

Exclusion criteria for the study included patients who were morbidly obese; patients with cardiovascular disease; Heart rate <60 beats per minute (bpm), basal SBP<100 mmHg and other conditions such as bronchial asthma, patients showing stressful features during induction and laryngoscopy (bucking, coughing, vomiting). Patients undergoing emergency surgery, diabetes mellitus, pregnant, drug allergies, difficult intubations and intubations in, which total duration of laryngoscopy exceeded 15 seconds were excluded from the study.

Pre-surgical protocol

The day prior to surgery all patients underwent a preanesthetic evaluation with special consideration to elicit a history of hypertension, dyspnoea, chest pain, cough, wheezing, convulsions and diabetes mellitus, as well as previous anesthetic history and drug sensitivity. Information collected included weight, nutritional status, airway assessment by the Mallampatti scoring system; a detailed examination of the respiratory; cardiovascular and central nervous system. A preoperative routine investigations such as haemoglobin, haematocrit, total lymphocyte count, differential lymphocyte count, serum electrolytes, blood group/Rh typing, blood urea nitrogen, serum creatinine, fasting blood sugar, chest radiography and electrocardiogram in all patients. Patients were advised to fast the night prior to surgery.

Surgical protocol

After patient identification a short preoperative history was taken; clinical examination and routine investigations were rechecked in all patients. Study objective and procedure were explained to the participants and a written informed consent was obtained from each participant.

Intravenous access was secured and infusion of Ringer’s lactate solution started. The patients were premedicated with 0.008 mg kg-1 glycopyrrolate-bromide intramuscularly 30 minutes prior to surgery. Patients were then shifted to the operating room after which routine non-invasive monitor was applied and vital signs monitored. Midazolam 0.04 mg kg-1 was administered intravenously over 30 seconds as premedication and patients were preoxygenated with four to five breaths of 100% oxygen. The patients were induced with 6mg kg-1 IV thiopentone sodium in incremental doses until loss of eyelash reflex occurred; 0.12 mg kg-1 IV vecuronium bromide was given over 20 seconds; followed up by administering the study drugs as per study protocol before laryngoscopy and intubation.

The study drug was randomly allocated to patients in a double blinded manner. Patients were ventilated with oxygen and 1% halothane using IPPV with a fresh gas flow of 6 litres min-1 by Bain circuit until intubation. About 2 minutes after IV vecuronium; laryngoscopy was performed with a Macintosh laryngoscope blade and trachea intubated with an appropriate size cuffed endotracheal tube. After confirmation of correct placement of ET tube; anaesthesia was then maintained with O2 and halothane.

HR, SBP, DBP, MAP, RPP (rate pressure product), SpO2 (oxygen saturation) and ECG (electrocardiogram) changes were recorded before induction (Basal) and after tracheal intubation at 1, 3 and 5 minutes for the purpose of this study. No manipulation like painting and draping the area of operation was allowed till 10 minutes after intubation. Injection fentanyl 2 micrograms kg-1 was given before surgery.

Parameters and statistical analysis

Summary statistics of patient demographic and anthropometric characteristics for all the groups were reported as means ± Standard Error of the Mean (SEM). HR, SBP, DBP and MAP were recorded before induction (Baseline), after endotracheal intubation at 1, 3 and 5 minutes. From the data RPP was calculated by multiplying heart rate with systolic blood pressure. Patients were also observed for complications like hypotension, hypertension, arrhythmias and hypoxaemia. Statistical analysis was done by unpaired t-test whilst categorical data were compared using Fischer’s exact test and p values were calculated. Haemodynamic variables were represented by mean ± SEM. ANOVA with repeated measures was used to compare the changes in HR, MAP and RPP values. Bonferroni’s multiple comparison tests were applied to evaluate intra group comparisons. The statistical package SPSS® 17.0 and Graph pad prism 5 was used. P<0.05 P<0.001 were considered significant and highly significant respectively for the study.

Results

All the demographic and anthropometric profiles in the control, case and total group were comparable (Table 1). The male to female ratio of control group-“C” was 1:2.64 whereas lignocaine group-“L”, diltiazem group-“D” and esmolol group “E” were 1:1.22, 1:1.5 and 1:1.5 (p=0.25), respectively (Figure 1). Out of the one hundred and sixty participants enrolled in this study, the average age was 41.81 ± 1.08 years, ranging from a minimum of 18 years to a maximum of 63 years. The ages of the case and controls of this study was matched with no statistical significant difference between their mean ages (41.82 ± 1.27, 41.78 ± 2.01, p-0.9867 for case and control respectively). Averagely an individual included in this study weighed 70.54 ± 0.75 kg and measured 163.80 ± 0.41 cm high. The weight range was found to be a minimum of 48.00 kg to a maximum of 97.00 kg, the shortest participant among the population measured 147 cm, and the tallest 174 cm. The mean weight and height of the cases and controls were statistically comparable (p-0.5073, 0.4698, respectively). Averagely the body mass index of the total participants as well as those in the individual groups according to the world health organisation’s criteria could be said to be overweight (26.26 ± 0.25; 26.31 ± 0.29 and 26.11 ± 0.54 Kg/m2 for the total population; the case and control respectively). However, though majority of the participants (56.25%) were found to be overweight, 3.75% were classified as underweight, 27.50% as normal weight, and 12.50% as obese. As show no significant difference was found when both the mean body mass indices as well as the component weight classifications were compared among the case and the control participants (Table 1).

Parameters Total (n = 160) Case (n = 120) Control (n = 40) P-value
Age(yrs) 41.81± 1.08 41.82 ± 1.27 41.78 ± 2.01 0.9867
Anthropometric parameters        
Weight (Kg) 70.54 ± 0.75 70.83 ± 0.86 69.68 ± 1.55 0.5073
Height (cm) 163.80± 0.41 164.00 ± 0.49 163.30 ± 0.73 0.4698
BMI(Kg/m2) 26.26± 0.25 26.31 ± 0.29 26.11 ± 0.54 0.724
BSA (m2) 1.79± 0.01 1.79 ± 0.01 1.77 ± 0.02 0.4444
Underweight 6/160(3.75) 4/120(3.33) 2/40(5.00) 0.6403
Normal 44/160(27.50) 30/120(25.00) 14/40(35.00) 0.2267
Overweight 90/160(56.25) 71/120(59.17) 19/40(47.50) 0.2045
Obese 20/160(12.50) 15/120(12.50) 5/40(12.50) 1.000

Table 1: Demographic and Anthropometric characteristics of the study population stratified as case and control.

anesthesia-clinical-research-diltiazem-esmolol

Figure 1: Male to female ration in Control, lidocaine, diltiazem and esmolol group.

Comparison of haemodynamic variables in the control and study groups at baseline and time (1, 3 and 5 minutes) after intubation (Tables 2-8). An increase in SBP, DBP, HR, MAP and RPP from the base line and maximum at 1 minute after intubation were observed in Control group-“C”, however, in the groups-Lidocaine- “L”; Diltiazem-“D” and Esmolol-“E” there were no significant variation of SBP, DBP, HR, MAP and RPP from the base line 1 minute after laryngoscopy and intubation (Table 6). The maximum increase in SBP and DBP over the baseline values (123.9 ± 1.02, 125.8 ±1.11, 125.5 ± 1.15 and 125.10 ± 1.31) and (83.70 ± 1.06, 82.85 ± 0.90, 82.13 ± 0.80 and 81.93 ± 0.79) in the groups C, L, D and E were recorded at one minute (153.10 ± 2.02, 140.70 ± 1.57, 137.6 ± 1.37 and 137.5 ± 1.40) after intubation. The Percentage changes in SBP and DBP from baseline and 1min after intubation were (23.58%, 11.84%, 9.64% and 9.90%) and (18.73%, 18.89%, 18.89% and 10.40%) in groups-C, L, D and E respectively (Figure 2 SYS1 and DIA1).

Parameter Control Lidocaine Diltiazem Esmolol p-value
SBP (mmHg) 123.9 ± 1.023 125.8 ± 1.11 125.5 ± 1.15 125.1 ± 1.310 0.6611
DBP (mmHg) 83.70 ± 1.06 82.85 ± 0.90 82.13 ± 0.80 81.93 ± 0.79 0.4895
HR (per min) 89.00 ± 1.47 87.30 ± 1.47 86.80 ± 1.39 90.80 ± 1.36 0.1855
MAP (mmHg) 97.08 ± 0.79 97.16 ± 0.70 96.57 ± 0.62 96.33 ± 0.68 0.8024
RPP 11010 ± 189.2 10970 ± 206.2 10890 ± 197.3 11350 ± 194.4 0.3572

Table 2: Change in haemodynamic variables in the study groups at Basal.

Parameter Control Lidocaine Diltiazem Esmolol p-value
SBP (mmHg) 153.1 ± 2.025 140.7 ± 1.575 *** 137.6 ± 1.37*** 137.5 ± 1.40*** P<0.0001
DBP (mmHg) 99.38 ± 0.82 98.50 ± 0.77 91.93 ± 0.81*** 90.43 ± 0.93*** P<0.0001
HR (per min) 116.1 ± 1.20 110.0 ± 0.78*** 92.88 ± 0.99*** 92.20 ± 1.54*** P<0.0001
MAP (mmHg) 117.3 ± 0.94 112.6 ± 0.70*** 107.1 ± 0.77*** 106.1 ± 0.79*** P<0.0001
RPP 17780 ± 304.5 15460 ± 170.1 *** 12770 ± 182.4 *** 12680 ± 253.7 *** P<0.0001

Table 3: Change in haemodynamic variables in the study groups at 1 min.

Parameter Control Lidocaine Diltiazem Esmolol p-value
SBP (mmHg) 145.0 ± 2.04 136.7 ± 1.29** 133.1 ± 1.29*** 131.9 ± 1.39*** P<0.0001
DBP (mmHg) 94.28 ± 0.802 91.80 ± 0.88 85.15 ± 0.85*** 82.63 ± 0.83*** P<0.0001
HR (per min) 109.5 ± 1.16 101.1 ± 1.31*** 89.90 ± 1.08*** 91.40 ± 1.19*** P<0.0001
MAP (mmHg) 111.2 ± 0.88 106.8 ± 0.70*** 101.1 ± 0.80*** 99.04 ± 0.65*** P<0.0001
RPP 15860 ± 267.3 13810 ± 200.5 *** 11980 ± 205.2 *** 12060 ± 213.7 *** P<0.0001

Table 4: Change in haemodynamic variables in the study groups at 3 min.

Parameter Control Lidocaine Diltiazem Esmolol p-value
SBP (mmHg) 131.6 ± 1.59 131.2 ± 1.79 128.2 ± 1.45 126.3 ± 1.37 0.0478
DBP (mmHg) 87.10 ± 0.87 86.00 ± 0.88 83.50 ± 0.73* 79.03 ± 0.93*** P<0.0001
HR (per min) 98.13 ± 1.47 97.80 ± 1.40 87.70 ± 1.41** 88.20 ± 1.39*** P<0.0001
MAP (mmHg) 101.9 ± 0.75 101.1 ± 0.76 98.38 ± 0.73** 94.77 ± 0.77*** P<0.0001
RPP 12910 ± 248.8 12840 ± 261.7 11270 ± 257.9 *** 11140 ± 221.5*** P<0.0001

Table 5: Change in haemodynamic variables in the study groups at 5 min.

Parameter Lidocaine Diltiazem Esmolol PI PII PIII PIV
SBP (mmHg) 140.7 ± 1.575 137.6 ± 1.37 137.5 ± 1.40 0.2068 0.1381 0.1301 0.9594
DBP (mmHg) 98.50 ± 0.77 91.93 ± 0.81 90.43 ± 0.93 P<0.0001 P<0.0001 P<0.0001 0.2277
HR (per min) 110.0 ± 0.78 92.88 ± 0.99 92.20 ± 1.54 P<0.0001 P<0.0001 P<0.0001 0.7131
MAP (mmHg) 112.6 ± 0.70 107.1 ± 0.77 106.1 ± 0.79 P<0.0001 P<0.0001 P<0.0001 0.3493
RPP 15460 ± 170.1 12770 ± 182.4 12680 ± 253.7 P<0.0001 P<0.0001 P<0.0001 0.7690

Table 6: Change in haemodynamic variables in the study groups at 1 min with intragroup comparison.

Parameter Lidocaine Diltiazem Esmolol PI PII PIII PIV
SBP (mmHg) 136.7 ± 1.29 133.1 ± 1.29 131.9 ± 1.39 0.0293 0.0487 0.0125 0.5291
DBP (mmHg) 91.80 ± 0.88 85.15 ± 0.85 82.63 ± 0.83 P<0.0001 P<0.0001 P<0.0001 0.0367
HR (per min) 101.1 ± 1.31 89.90 ± 1.08 91.40 ± 1.19 P<0.0001 P<0.0001 P<0.0001 0.3529
MAP (mmHg) 106.8 ± 0.70 101.1 ± 0.80 99.04 ± 0.65 P<0.0001 P<0.0001 P<0.0001 0.0473
RPP 13810 ± 200.5 11980 ± 205.2 12060 ± 213.7 P<0.0001 P<0.0001 P<0.0001 0.7704

Table 7: Change in haemodynamic variables in the study groups at 3 min with intragroup comparison.

Parameter Lidocaine Diltiazem Esmolol PI PII PIII PIV
SBP (mmHg) 131.2 ± 1.79 128.2 ± 1.45 126.3 ± 1.37 0.0758 0.1853 0.0302 0.3428
DBP (mmHg) 86.00 ± 0.88 83.50 ± 0.73 79.03 ± 0.93 P<0.0001 0.0318 P<0.0001 0.0003
HR (per min) 97.80 ± 1.40 87.70 ± 1.41 88.20 ± 1.39 P<0.0001 P<0.0001 P<0.0001 0.8013
MAP (mmHg) 101.1 ± 0.76 98.38 ± 0.73 94.77 ± 0.77 P<0.0001 0.0124 P<0.0001 0.001
RPP 12840 ± 261.7 11270 ± 257.9 11140 ± 221.5 P<0.0001 P<0.0001 P<0.0001 0.713

Table 8: Change in haemodynamic variables in the study groups at 5 min with intragroup comparison

anesthesia-clinical-research-study-population

Figure 2: Percentage change was calculated as follows: [(Variable estimate for time after intubation–Basal estimate for variable)/Basal estimate for variable] X 100%, RPP=Rate pressure product Percentage changes in haemodynamic variables from baseline and one minute after intubation in the study population stratified by treatment.

In groups C, L, D and E maximum increase in mean heart rate over the baseline values were 89.00 ± 1.47, 87.30 ± 1.47, 86.80 ± 1.39 and 90.80 ± 1.36 respectively and at one minute were 116.10 ± 1.20, 110.00 ± 0.78, 92.88 ± 0.99 and 92.20 ± 1.54 after intubation respectively. The Percentage changes in HR from baseline and 1min after intubation were 30.45%, 26.00%, 7.01% and 1.50% in groups-C, L, D and E respectively (Figure 2 HR1).

The MAP was increased in group-C as compared to groups-L, D and E following laryngoscopy and endotracheal intubation. The maximum increase in MAP over the baseline values (97.08 ± 0.79, 97.16 ± 0.70, 96.57 ± 0.62 and 96.33 ± 0.68) in the groups C, L, D and E were recorded at one minute (117.3 ± 0.94, 112.6 ± 0.70, 107.1 ± 0.77 and 106.10 ± 0.79) after intubation. The Percentage changes in MAP from baseline and 1min after intubation were 20.83%, 15.89%, 10.90% and 10.20% in groups-C, L, D and E respectively (Figure 2 MAP1).

There was marked elevation of rate pressure product in group-C as compared to groups-L, D and E after laryngoscopy and intubation with baseline values 11010 ± 189.2, 10970 ± 206.2, 10890 ± 197.3 and 11350 ± 194.4, respectively. One-minute values of groups-C, L, D and E were 17780 ± 304.5, 15460 ± 170.1, 12770 ± 182.4 and 12680 ± 253.7, respectively. The Percentage changes in RPP from baseline and 1min after intubation were 61.49%, 40.93%, 17.26% and 11.68% in groups-C, L, D and E respectively (Figure 2 RPP1).

In all four groups the vitals remained attenuated for 3 minutes after intubation; however the vitals returned to baseline values after five minutes. Control group patients undergoing laryngoscopy and intubation showed an incidence of 8% ventricular ectopics and 5% dropped beats however no such findings were recorded in the lignocaine, diltiazem and esmolol groups.

Discussion

In designing this experiment; our primary objective was to study the efficacy and safety of cardiac antidysrhythmic beta; calcium and sodium channel blockers on haemodynamic changes due to endotracheal intubation in normotensive Black patients. The precise mechanism that leads to the haemodynamic response to laryngoscopy and intubation probably involves intense sympathetic discharges and release of catecholamine [8]. As visible in the control group; markedly high cardiovascular changes occurred within few seconds following laryngoscopy and intubation. It was also determined that intravenous administration of lidocaine; considerably attenuated unwanted pressor response to laryngoscopy and tracheal intubation when given two minutes before laryngoscopy. The results of various studies, in the last decade, on the effect of haemodynamic responses to tracheal induction have varied considerably. Many studies have reported beneficial effect;while others showed no effect in Caucasians [10-13]. The difference in the results of various studies involving lidocaine; to some extent; can be explained by differences in study designs including variations in dose and timing of drug administration in relation to intubation [14]. Lidocaine attenuate haemodynamic response to laryngoscopy and intubation by one or combination of following mechanisms: lidocaine acts mainly by inhibiting sodium influx in the voltage gated sodium channels. When the influx of sodium is interrupted; signal conduction is inhibited. It also acts by decreasing the sensitivity to heart muscle to electrical pulses. This will in turn slow down conduction of electrical signals in the heart muscles; and therefore helps to restore a regular heart beat rhythm [15]. The beneficial effect of lidocaine on the haemodynamic changes may also due to its direct cardiac depression and peripheral vasodilatation properties, its ability to suppress airway reflexes elicited by irritation of tracheal mucosa, and its analgesic as well as antiarrythmia properties[16].

In our study, 0.2 mg kg-1 diltiazem given at one minute before intubation sufficiently reduced the circulatory responses in normotensive Black patients. Diltiazem prevents/blocks the release of catecholamines, which reduces sympathetic nervous system reactions [17]. By slowing conduction of normal electrical impulse through the AV node, diltiazem increases the time needed for each beat, normally resulting in reduced myocardium oxygen consumption [18]. Our results are in agreement with previous reports in Caucasians that deltiazem can, in fact, attenuate hypertension associated with tracheal intubation [19]. Surprisingly, Lee et al. (2002) found, when diltiazem alone was administered it did not attenuate heart rate [20]. This might be explained by dosage differences and timing of administration of drugs. In that study, drug was given 90 seconds before laryngoscopy as opposed to the 60 seconds in the current study. The use of calcium blockers can be best utilized when their peak effects corresponds to that of pressor responses. It has been reported before that, MAP begins to increase about 15 seconds after laryngoscopy and reaches peak value around 45 seconds, if no treatment is administered to patients [20]. That’s why, in our study, diltiazem was administered 1 minute before laryngoscopy. Manjunath et al. found diltiazem 0.2 mg.kg-1 one minute before laryngoscopy and intubatin blunts unwanted haemodynamic responses in Asian population.

Esmolol significantly reduced the circulatory responses in this cohort of normotensive Black patients. ß-blockers minimize the increase in heart rate and blood pressure by attenuating positive chronotropic and ionotropic effects of the increase in adrenergic activity. Esmolol possesses several properties which makes it a valuable agent to obtund the cardiovascular response. It is a cardio selective agent; has ultra-short duration of action (9 minutes) and has not been reported to have significant drug interaction with commonly used anaesthetic drugs [21]. Bostana and Eroglu reported that IV esmolol in doses of 1 mg kg-1 before intubation was effective in suppressing heart rate and arterial blood pressure in Caucasians [22]. Kumar et al. have reported optimal results while using higher doses of esmolol (2 mg kg-1) in an Asian population, without any incidence of unplanned hypotension or bradycardia [23]. In this normotensive cohort of Black population;esmolol, at a dose of 2 mg kg-1 effectively decreased HR, SBP, DBP, MAP and RPP without any incidence of hypotension or bradycardia. This study further observed a reduction in DBP less than that in SBP resulting in a better control of the MAP in the study population. Gupta et al.there has been no consensus regarding the optimum dose and timing of esmolol delivery in Caucasian population [2].

Studies have shown when intraoperative heart rate is more than110 beats min-1 there is increased myocardial oxygen requirement and incidence of Myocardial infarction. In our study none of the patients in study groups showed heart rate >110 beats min-1. RPP as calculated by multiplying heart rate with systolic blood pressure. The RPP levels close to 20,000 are normally associated with angina and myocardial ischemia [1]. RPP at 1 min after intubation remained less than 20,000 in study drug groups. These finding confirms the cardioprotective effect of study drugs during laryngoscopy and endotracheal intubation.

Conclusions

Intravenous lidocaine (1.5 mg kg-1);diltiazem (0.20 mg kg-1) and esmolol (2 mg kg-1) are effective agents in suppressing the hemodynamic response to laryngoscopy and intubation without any deleterious effect. Given the difference in the pharmacological mechanisms of these drugs; the prophylactic therapy with 2 mg kg-1 esmolol appears to be significantly more effective and safe for attenuating haemodynamic changes to laryngoscopy and tracheal intubation. Esmolol should be viewed as potential treatment strategy for attenuating hemodynamic changes during induction of anesthesiain the Black populations.

Comments

Further studies needs to be done in high-risk patients; using longer duration infusions to investigate the safety and efficacy of esmolol in reducing the frequency of myocardial ischaemia after non-cardiac and cardiac surgery in the Black populations.

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Anna Melissa

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David Gorantl

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Stephanie Skinner

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Nimmi Anna

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Nathan T

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Ann Jose

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Steve Harry

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