Abstract
Background and Aims:
Hemodynamic responses (HDR) to laryngoscopy and intubation are a significant concern for the anesthesiologist. This study aimed to compare the effects of intravenous Dexmedetomidine and nebulized Lidocaine for control of HDR to laryngoscopy and intubation when used in combination or alone.
Material and Methods:
This double-blind, parallel group, randomized clinical trial included 90 patients (30 for each group) aged 18-55 years with ASA grade 1-2. Group DL received intravenous (IV) Dexmedetomidine (1 μg kg-1) and nebulized Lidocaine 4% (3 mg kg-1) before laryngoscopy. Group D received IV Dexmedetomidine (1 μg kg-1) and group L received nebulized Lidocaine 4% (3 mg kg-1). Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) were recorded at baseline, post nebulization, and at 1, 3, 5, 7, and 10 min post-intubation. Data analysis was done by SPSS 20.0.
Results:
Post-intubation HR was better controlled in group DL than group D and group L (76.40 ± 5.61, 95.16 ± 10.60, 103.90 ± 12.98 respectively, P value <0.01). Group DL > D > L controlled SBP changes significantly (118.93 ± 7.70, 131.10 ± 9.20, 142.66 ± 19.62 respectively, P value <0.01). At 7 and 10 minutes, group D and L found similarly effective in preventing a rise in SBP. Group DL showed significantly better control of DBP than group L and D till 7 minutes (P < 0.01). Group DL also had better control of MAP post-intubation (92.86 ± 5.50) than group D (102.70 ± 6.64) and L (112.66 ± 7.66) and continued to be better till 10 minutes.
Conclusion:
We found the addition of intravenous Dexmedetomidine to nebulized Lidocaine to be superior in controlling the increase in HR and MBP post-intubation with no adverse effects.
Keywords: Blood pressure, dexmedetomidine, heart rate, intratracheal, intubation, laryngoscopy, lidocaine
Introduction
Laryngoscopy and endotracheal intubation is the most stimulating procedure leading to acute hemodynamic responses (HDR) lasting for at least 10 min.[1,2] Stretching of pharyngeal and laryngeal mucosal tissue causes sympathoadrenal response resulting in HDR such as an increase in heart rate (HR), blood pressure (BP), and even ischemic ST-segment changes caused by the release of catecholamines.[3-5] Such responses can be tolerated by young and healthy individuals but detrimental in patients with limited cardiac reserve.[2] Hence, it is vital to blunt these responses. An ideal drug should have a fast onset of action, easily administered, with minimal side effects.
Various drugs through different routes have been used in this endeavor. Increasing anesthesia depth with several medications, such as opioids, topical Lidocaine, alpha agonists, calcium channel blockers, beta-blockers, vasodilators, sodium channel blockers, and intravenous sodium nitroprusside have been tested.[6-11] But, none provide an optimal effect in attenuating the sympathoadrenal response.
Topical anesthesia has a direct inhibition of the airway reflexes and thus useful in reducing HDR at the time of laryngoscopy and endotracheal intubation.[12] Dexmedetomidine is an α2 receptor agonist with analgesic, sedative, and sympatholytic action without any respiratory depression. It acts systemically by blocking the release of norepinephrine and decreases sympathetic activity.[13] Previous research has compared intravenous (IV) Dexmedetomidine and nebulized Lignocaine with other molecules and found encouraging results.[11,14-16] Studies directly evaluating these two drugs, comparing the attenuating effect of HDR following laryngoscopy and endotracheal intubation are lacking. We expect an additive and synergistic action with these two drugs in combination than used alone because of different mechanisms of action and the effect-site.
The current study aims to compare intravenous Dexmedetomidine and nebulized Lidocaine effects when used together to reduce HDR following laryngoscopy and post-intubation than when each was given alone. The primary objective of our study was to compare heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) changes in the groups with laryngoscopy and post-intubation. The secondary objective was to find if any adverse effect is associated with the drugs when used alone or together like hypotension (MAP <60 mm Hg) and bradycardia (HR <50 beats per minute).
Material and Methods
It was a prospective, double-blind, randomized controlled trial with three parallel arms and an allocation ratio of 1, done in a tertiary care center of Eastern India. After approval from the Institutional Ethics Committee, the study was registered in the clinical trial registry (CTRI/2020/07/026918). All the procedures were conducted as per the Helsinki Declaration. Patients undergoing laparoscopic cholecystectomy under general anesthesia from August to November 2020 were recruited. Patients belonging to ASA physical status I and II with the age group between 18 to 55 years were recruited for the study. Patients with ASA physical status >II, Weight: <40 kg or >70 kg, difficult airway, cardiorespiratory comorbidity, smokers, and those taking antihypertensive were excluded from the study.
The sample size was calculated based on a previous study by Mahjoubifard et al.,[17] in which the post-intervention mean HR values at 10th min in Dexmedetomidine group and control groups were 62.03 and 73.73 and standard deviation (SD) of 5.04 and 16.87, respectively. To find the same difference with a 95 percent confidence interval and a power of 90%, a sample 24 for each group was required. One hundred and five patients were enrolled for the study considering a drop out of 20%. Ninety patients participated in the research, with 30 patients in each group due to exclusions [Figure 1].
Figure 1.
Consort diagram of patients
After obtaining the written informed consent, patients were randomly allocated to one of the three parallel groups; Group D (Intravenous dexmedetomidine group), Group L (Nebulized lidocaine 4% group), Group DL (Both intravenous Dexmedetomidine and Nebulized 4% solution of lignocaine). Randomization was done using computer-generated random numbers, which were concealed in opaque envelopes. In the preoperative area, an anesthesiologist opened the envelope and prepared the study medications according to the group allocation. He was not involved in data collection or anesthesia management of the patients.
A complete hemogram, blood urea, serum creatinine, blood sugar, urine examination, chest x-ray, and ECG were done after a pre-anesthetic checkup. Intravenous access was secured with an 18G cannula, and IV fluid Ringer lactate was started. Patients were shifted to the operation theatre, and monitors were attached, and monitoring started for noninvasive BP, HR, oxygen saturation (SpO2), and ECG.
Syringes were made of 5 ml drug solution (for nebulization) and 25 ml (for infusion) and handed over to the other anesthetist according to the patient’s group allocation based on the randomization. The patient and the anesthesiologist who monitored the patients and collected data were unaware of the group allocations.
Group D received IV Dexmedetomidine (Dexem; Themis Medicare, Uttarakhand, India) 1 μg/kg infusion (0.25 ml kg-1 for 4 μg kg-1 preparation) over 10 min before induction of anesthesia along with normal saline 0.9% (5 ml) nebulization via a face mask. Group L received nebulization with 3 mg/kg solution of 4% Lidocaine (LOX 4%; Neon, Thane, India) diluted with normal saline 0.9% to make a total volume of 5 ml, via a face mask and nebulizer with oxygen at the rate of 8 L/min in the operative room. Normal saline infusion 25 ml was given over 10 minutes before induction in the operative room (0.25 ml kg-1).
Group DL received both intravenous Dexmedetomidine and nebulized 4% solution of Lidocaine.
In the operation theatre, the drugs for nebulization (saline or lidocaine) were prepared and administered by an independent investigator. It was done using an electrical compressor nebulizer (Eco Smart, Saify Healthcare and Medi Devices, India) for 10 min. Mild side-effects of nebulized Lidocaine such as bitter taste, dysphonia and oropharyngeal numbness were noted.
Baseline (T0) HR, SBP, DBP, and MAP were recorded for all the groups in the operative room then the nebulization and infusions were started. The hemodynamic parameters (HR, SBP, DBP, and MAP) were recorded post-nebulization (T pn). After 10 minutes of administering the infusion, the patients received IV Midazolam 0.02 mg/kg and IV Fentanyl 2 μg kg-1. Anesthesia was induced with an injection of 1% Propofol 2 mg/kg. Neuromuscular blockade was achieved with IV Vecuronium 0.1 mg/kg, and the patient’s lungs were manually ventilated for over 3 minutes with 100% oxygen. Endotracheal intubation with a cuffed endotracheal tube of appropriate size was done.
Hemodynamic parameters (HR, SBP, DBP, and MAP) were noted at 1, 3, 5, 7, and 10 minutes post-intubation (PI 1, PI 3, PI 5, PI 7, PI 10). Only manipulations like painting and draping the surgical area were allowed after intubation for 10 minutes. Anesthesia maintenance was done using air and oxygen mixture (50%:50%) and Isoflurane (1 MAC). Intermittent positive pressure ventilation with a tidal volume of 6 to 8 ml/kg body weight was done to maintain end-tidal carbon-dioxide between 35 and 40 mm Hg.
Any incidences of hypotension, bradycardia during the time of the study were recorded and treated consequently. At the end of the surgery, IV Neostigmine (0.05 mg kg-1) and IV Glycopyrrolate (0.01 mgkg-1) were given to reverse the residual muscle paralysis. Post-extubation, all the patients received oxygen via a face mask during the recovery period. Any adverse effects, if they occurred, were managed accordingly.
Statistical analysis
Data were analyzed using SPSS (IBM SPSS v 20.0 licensed to the university). Mean, standard deviation were used for normally distributed descriptive data and median and interquartile range for nonparametric data. Normality distribution was determined using the Kolmogorov–Smirnov test or the Shapiro Wilk test. ANOVA for parametric data distribution or Kruskal–Wallis test for nonparametric data distribution was used to compare variables between the groups. A value of P value <0.05 was considered to be significant. Post-hoc analysis was done for pair-wise comparison between the groups.
Results
Groups were matched for their demographic data [Table 1]. A slight increase in mean HR was found in group D and L after intubation. However, group DL had shown a reduction in HR. HR changes post-intubation and till 3 mins were better controlled in group DL followed by group D and lastly group L (P < 0.01). At 5, 7, and 10 mins, group D and L were similar in action on HR but inferior to Group DL. [Table 2].
Table 1.
Demographic Profile of Patients in The Three Groups
| Variables | Group DL (n=30) | Group D (n=30) | Group L (n=30) |
|---|---|---|---|
| Age (yr), mean (SD) | 33.9 (9.49) | 38.5 (9.02) | 38.4 (8.43) |
| Gender (n) (%) | |||
| Male | 17 (56.7) | 15 (50) | 11 (36.7) |
| Female | 13 (43.3) | 15 (50) | 19 (63.3) |
| ASA grade | |||
| 1 | 20 | 21 | 18 |
| 2 | 10 | 9 | 12 |
| BMI mean (SD) | 20.6 (2.87) | 21.1 (2.59) | 20.6 (3.01) |
Table 2.
Comparison of Heart Rate in the Three Groups with Pair-Wise Comparison
| Heart rate | Group DL (n=30) | Group D (n=30) | Group L (n=30) | P | Post hoc analysis (P) | ||
|---|---|---|---|---|---|---|---|
|
| |||||||
| DL-D | DL-L | D-L | |||||
| T 0 | 85.13±8.95 | 88.0±10.45 | 81.80±11.18 | 0.064 | |||
| T pn | 85.16±8.68 | 87.76±10.7 | 82.60±11.003 | 0.152 | |||
| PI 1 | 76.40±5.61 | 95.16±10.60 | 103.90±12.98 | <0.001 | <0.001 | <0.001 | 0.004 |
| PI 3 | 74.40±5.63 | 91.16±10.64 | 98.00±10.99 | <0.001 | <0.001 | <0.001 | 0.017 |
| PI 5 | 72.50±5.77 | 86.56±8.95 | 91.03±9.44 | <0.001 | <0.001 | <0.001 | 0.095 |
| PI 7 | 71.06±4.83 | 83.03±7.31 | 81.93±919 | <0.001 | <0.001 | <0.001 | 0.831 |
| PI 10 | 70.83±4.12 | 81.26±7.20 | 77.46±7.72 | <0.001 | <0.001 | <0.001 | 0.069 |
T 0=Basal, T pn=post-nebulization, PI 3- Post-intubation at 3 min, PI 5- Post-intubation at 5 min, PI 7- Post-intubation at 7 min, PI 10- Post-intubation at 10 min
SBP changes were controlled significantly in group DL at all the time after intubation compared to the other two groups. (DL > D > L) (P value <0.01). Group D was better than group L until 5 minutes in controlling SBP rise (P = 0.046). At 7 and 10 minutes, there was no statistically significant difference between group D and L [Table 3]. Group DL showed significantly better control of DBP than group L and D till 7 minutes (P < 0.01). At 10 minutes, group DL and L were found to be similarly acting (P = 0.880). Group DL > D > L till 3 minutes and at 5 and 7 minutes Group DL > D = L and at 10-minute Group DL = L > D [Table 4].
Table 3.
Comparison of Systolic Blood Pressure in the Three Groups with Pair-Wise Comparison
| Systolic blood pressure | Group DL (n=30) | Group D (n=30) | Group L (n=30) | P | Post hoc analysis (P) | ||
|---|---|---|---|---|---|---|---|
|
| |||||||
| DL-D | DL-L | D-L | |||||
| T 0 | 119.30±8.56 | 121.53±11.079 | 121.70±8.88 | 0.564 | |||
| T pn | 120.30±8.57 | 119.90±9.711 | 123.13±7.76 | 0.299 | |||
| PI 1 | 118.93±7.70 | 131.10±9.20 | 142.66±19.62 | <0.001 | <0.001 | <0.001 | 0.004 |
| PI 3 | 116.93±5.63 | 127.66±8.53 | 136.00±8.65 | <0.001 | <0.001 | <0.001 | 0.017 |
| PI 5 | 114.50±7.51 | 124.96±8.19 | 129.03±6.80 | <0.001 | <0.001 | <0.001 | 0.046 |
| PI 7 | 111.93±7.71 | 121.93±7.59 | 123.20±6.73 | <0.001 | <0.001 | <0.001 | 0.0784 |
| PI 10 | 111.80±6.8 | 120.23±7.32 | 117.03±6.10 | <0.001 | <0.001 | <0.001 | 0.167 |
T 0=Basal, T pn=post-nebulization, PI 3- Post-intubation at 3 min, PI 5- Post-intubation at 5 min, PI 7- Post-intubation at 7 min, PI 10- Post-intubation at 10 min
Table 4.
Comparison Of Diastolic Blood Pressure In The Three Groups With Pairwise Comparison
| Diastolic blood pressure | Group DL (n=30) | Group D (n=30) | Group L (n=30) | P | Post hoc analysis (P) | ||
|---|---|---|---|---|---|---|---|
|
| |||||||
| DL-D | DL-L | D-L | |||||
| T 0 | 78.83±6.64 | 82.00±6.26 | 80.36±5.42 | 0.142 | |||
| T pn | 78.73±6.28 | 81.86±5.69 | 81.93±5.39 | 0.056 | |||
| PI 1 | 79.80±5.56 | 88.06±5.81 | 96.96±8.38 | <0.001 | <0.001 | <0.001 | <0.001 |
| PI 3 | 76.73±4.72 | 86.56±6.09 | 91.83±6.93 | <0.001 | <0.001 | <0.001 | 0.017 |
| PI 5 | 74.93±4.20 | 84.2±5.96 | 86.30±6.72 | <0.001 | <0.001 | <0.001 | 0.335 |
| PI 7 | 73.73±3.46 | 80.80±4.46 | 80.43±6.32 | <0.001 | <0.001 | <0.001 | 0.995 |
| PI 10 | 73.26±3.41 | 79.80±4.87 | 73.86±5.87 | <0.001 | <0.001 | 0.880 | <0.001 |
T 0=Basal, T pn=post-nebulization, PI 3- Post-intubation at 3 min, PI 5- Post-intubation at 5 min, PI 7- Post-intubation at 7 min, PI 10- Post-intubation at 10 min
Similar findings were noted with MAP. Group DL had better control of MAP post-intubation than group D and L and continued to be better till 10 minutes. However, at the 10th minute, there was no added advantage over group L (P value 0.221). Group D had better control on MAP than group L till 3 minutes (P value <0.001) but at the 5th and 7th-minute group, D and L were not statistically different in action (P value 0.730, 0.978). Also, at the 10th-minute, group L was better than group D in controlling MAP (P value <0.001). [Table 5]. There was no incidence of hypotension, bradycardia in any of the patients in any group. There were no other adverse effects like bitter taste, dysphonia and oropharyngeal numbness due to nebulization in any group.
Table 5.
Comparison of Mean Arterial Pressure in the Three Groups with Pairwise Comparison
| Mean arterial pressure | Group DL (n=30) | Group D (n=30) | Group L (n=30) | P | Post hoc analysis (P) | ||
|---|---|---|---|---|---|---|---|
|
| |||||||
| DL-D | DL-L | D-L | |||||
| T 0 | 92.16±6.29 | 94.46±7.31 | 93.93±6.32 | 0.380 | |||
| T pn | 92.60±5.92 | 94.56±6.34 | 95.63±5.43 | 0.137 | |||
| PI 1 | 92.86±5.50 | 102.7±6.64 | 112.66±7.66 | <0.001 | <0.001 | <0.001 | <0.001 |
| PI 3 | 90.23±4.85 | 100.20±6.62 | 106.60±7.14 | <0.001 | <0.001 | <0.001 | <0.001 |
| PI 5 | 88.06±4.67 | 97.56±6.26 | 100.90±6.49 | <0.001 | <0.001 | <0.001 | 0.730 |
| PI 7 | 86.73±3.95 | 94.4±5.21 | 94.66±5.96 | <0.001 | <0.001 | <0.001 | 0.978 |
| PI 10 | 86.03±3.91 | 93.20±5.48 | 88.20±5.48 | <0.001 | <0.001 | 0.221 | <0.001 |
T 0=Basal, T pn=post-nebulization, PI 3- Post-intubation at 3 min, PI 5- Post-intubation at 5 min, PI 7- Post-intubation at 7 min, PI 10- Post-intubation at 10 min
We had calculated our sample size assuming a power of 90 percent. On completion of our study, based on our data, power of our study was calculated and found to be 81.51 percent, considering the confidence interval of 95 percent.
Discussion
We found that the baseline and post-nebulization values of HR, SBP, DBP, and MAP among all the three groups were not significantly different. HR was controlled better with a combination of IV Dexmedetomidine and nebulized Lidocaine than when either given alone after intubation (P < .001), and this effect was consistent till 10 minutes. However, none of the patients developed bradycardia. We have selected ASA grade 1 and 2 patients as it could be unsafe to do the preliminary study on ASA grade 3 and 4 patients without establishing its safety in healthy patients.
After intubation, combined IV Dexmedetomidine and nebulized Lidocaine registered a maximum drop in SBP, DBP, and MAP followed by Dexmedetomidine and least in the Lidocaine group till 5 minutes of intubation. At 7 and 10 minutes, the Dexmedetomidine and Lidocaine group acted similarly in reducing SBP, but Lidocaine was found more effective at 10 minutes than Dexmedetomidine alone in control of DBP and MAP. We hypothesize that nebulized Lidocaine was more effective than Dexmedetomidine at 10-minute post-laryngoscopy and intubation, which could be the time taken by the nebulized Lidocaine to attain its peak systemic concentration for maximum hemodynamic effects. No maintenance infusion of Dexmedetomidine was used.
Previous studies have shown Dexmedetomidine’s effectiveness in controlling HDR to laryngoscopy and intubation.[18-20] Niyogi et al.,[18] found that Dexmedetomidine used as nasal or IV infusion over 40 min were equally effective in attenuating HR, SBP, and MAP till 10 min post-intubation. We found Dexmedetomidine to be efficient when used IV as a 10 min infusion in our study. Silpa et al.,[20] compared different doses of Dexmedetomidine and reported that 1 mg kg-1 Dexmedetomidine was more efficacious than 0.5 mg/kg in attenuating HDR to intubation in cardiac surgery.
Some studies have compared Dexmedetomidine with Fentanyl and Esmolol and concluded that Dexmedetomidine fares better in attenuating the pressor responses (11-14). Mahjoubifard and his team compared three drugs: Dexmedetomidine (1 μg kg-1), Lidocaine (1.5 mg kg-1), and Fentanyl (2 μg kg-1) given IV for recording changes in HDR with laryngoscopy and intubation in patients undergoing cardiac surgery.
The authors found that Dexmedetomidine considerably reduced HR and MBP at the 5th and 10th min post-intubation compared to the other drugs. Similar to their study, we found MBP attenuation effects of dexmedetomidine at various intervals (3, 5, 7, and 10 min). However, at the 7th and 10th min, we noted that the groups with Lidocaine (isolated and combination group) had better attenuation.[17] We have used a higher dose of nebulized Lidocaine (3 mg kg-1 at 4% concentration), which could have peaked by 7-10 minutes due to systemic absorption. In another study, Gulabani et al.,[21] found IV Dexmedetomidine (1 μg kg-1) better than IV Lidocaine (1.5 mg kg-1) in controlling the HDR to intubation for 5 min duration. We had similar responses till the same period, but the nebulized Lidocaine was more effective at 7 and 10 min than Dexmedetomidine.
Sklar and co-workers found nebulized Lidocaine (120 mg) effective till 10 min in attenuating HDR to intubation more than IV (1 mg kg-1).[16] But, Kumar et al.,[22] had shown nebulized Lidocaine (3 mg kg-1, 4%) was less effective when compared to IV Fentanyl (2 μg kg-1) in attenuating HDR to intubation. The lower MBP at 10 min noted by authors in the combination group was statistically insignificant. The authors agree with Barton et al.,[23] who have suggested that sub mucosal deep proprioceptors essential for HDR attenuation for laryngoscopy may not be blocked by topical anesthesia. But nebulized Lidocaine does anesthetize trachea and blunts the intubation responses.[24]
Moreover, we believe that it could have reached peak plasma concentration by 7-10 min and had more effect on DBP and MBP. Bruder et al.,[1] had earlier proposed that Lidocaine is particularly useful in preventing the pressor response to tracheal intubation, in any route of administration (IV or intra-tracheal), but not the increase in HR, which is also reciprocated in our study as nebulized Lidocaine was inferior in HR suppression as compared to Dexmedetomidine.
Patil et al.,[15] compared two doses of nebulized Lidocaine and observed that 4% attenuates the intubation response in a better way in comparison to 2%. We have used a higher dose (4% concentration) of nebulized Lidocaine and found it useful when used alone. However, the effect was more synchronized and better when used along with Dexmedetomidine. The response of Lidocaine used with nebulization route was more appreciated in 7th and 10th min post-intubation.
We do acknowledge certain limitations of our study. We have studied single Lignocaine and Dexmedetomidine (selected based on previous studies) in attenuating HDR. A dose-response study would be more useful. Only low ASA grade patients (who have an adequate cardiac reserve) and patients undergoing non-cardiac surgery were recruited. It would be interesting to see the changes in higher ASA grade patients with compromised cardiac reserves or cardiac surgery patients. We could not measure the plasma norepinephrine levels, which would have precisely predicted the suppression of the sympathetic response to intubation. Hence, further study can target higher ASA grade patients and with an assay of plasma concentration of Dexmedetomidine, Lidocaine, and Norepinephrine to substantiate the findings obtained from the present study.
Conclusion
We conclude that intravenous Dexmedetomidine is more effective than nebulized Lidocaine in controlling the hemodynamic response to intubation initially but had no added advantage over Lidocaine at 7 to 10 min post-intubation. However, a combination of intravenous Dexmedetomidine 1 μg kg-1 with nebulized 4% Lidocaine 3 mg kg-1 attenuates the cardiovascular responses to laryngoscopy and intubation more effectively than intravenous Dexmedetomidine and nebulized Lidocaine used alone.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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