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ORIGINAL ARTICLE
Year : 2023 | Volume
: 24
| Issue : 1 | Page : 21-28
Alleviating hemodynamic response to tracheal extubation: A comparative study between dexmedetomidine and lignocaine in surgical patients
Neha T Gaidhankar1, K Chandra Mohan1, R Arun Kumar2, Amar Nandha Kumar1
1 Department of Anaesthesiology, Kovai Medical Center and Hospital Limited, Coimbatore, Tamil Nadu, India
2 Department of Anaesthesiology, PSG Institute of Medical Sciences and Research, Coimbatore, Tamil Nadu, India
Correspondence Address:
Dr. K Chandra Mohan
Kovai Medical Center and Hospital Limited, Post Box No. 3203, Avinashi Road, Civil Aerodrome Post, Coimbatore, Tamil Nadu
India
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/TheIAForum.TheIAForum_74_22
Background: Tracheal extubation is a crucial step during general anesthesia involving the removal of artificial airway when the indication for its placement no longer exists. Airway and circulatory interferences could be due to diminished tolerance to the tracheal tube, catecholamine surge, surgical pain, and airway irritation on behalf of suctioning or change in posture of the tube. Complications are more common during extubation than that occurring during induction and intubation.
Aim: The main aim of the study was to compare the effectiveness of a single dose of dexmedetomidine and lignocaine in alleviating hemodynamic and stress responses during extubation and recovery.
Materials and Methodology: Sixty patients of the age group between 20 and 65 years belonging to ASA 1 and 2 undergoing elective surgical procedures with a minimum anticipated duration of 60 min requiring endotracheal intubation were included in the study. The patients were assigned randomly into two groups with 30 participants in each group and were called as Group D receiving dexmedetomidine 0.5 μg/kg and Group L receiving lignocaine 1.5 mg/kg.
Observation and Results: Data were statistically analyzed with the SPSS version 20.0 software. Independent t-test analysis was used, and all the statistical test was examined with P ≤ 0.05 level of significance. Hemodynamic response was noted as more significant in Group D, whereas emergence and extubation time was noted sooner in Group L.
Conclusion: We conclude that Dexmedetomidine 0.5 mcg/kg causes significant attenuation of hemodynamic stress response and deeper sedation when compared to lignocaine 1.5 mg/kg.
Keywords: Dexmedetomidine, hemodynamics, lignocaine, tracheal extubation
Tracheal extubation is a crucial step during general anesthesia[1] involving the removal of the artificial airway, such as the endotracheal tube or supraglottic airway, when the indication for its placement no longer exists.[2] Tracheal extubation stimulates an intense physiological response during emergence when there is a change from controlled to the uncontrolled awakening state of anesthesia.[3] Stress responses to tracheal extubation results in unexplained tachycardia, hypertension, bucking, coughing, agitation, sore throat, drop in saturation, impaired analgesia, bronchospasm, and laryngospasm due to inadequate analgesia.[4],[5],[6]
Literature review states that the airway and circulatory interferences could be due to diminished tolerance to the tracheal tube, catecholamine surge, surgical pain, and airway irritation on behalf of suctioning or change in posture of the tube. Complications are more common during extubation than that occurring during induction and intubation.[7] The effect of cough results in raised intraocular, intrathoracic, intracranial, and intraabdominal pressures and bucking, which causes deleterious effects to the patients.[8] Hence, all the factors which produce stimulation during extubation need to be abolished.[9]
Drugs, such as narcotic analgesics,[10],[11] inhalational agents, vasodilators, local anesthetics,[12] beta blockers, adrenoceptor blockers,[8],[13] and dexmedetomidine,[14] are used in attenuation of stress responses during extubation as a sole or combined agent. Dexmedetomidine, a highly selective α2 adrenoceptor agonist, shows theoretical effects in the suppression of hemodynamic responses and airway reflexes during extubation and lignocaine which is an amide local anesthetic agent abolishes the airway reflexes in various routes. This comparative study between these two drugs was the background in our study. The study was conceptualized to determine the efficacy of intravenous 0.5 μg/kg dexmedetomidine with 1.5 mg/kg lignocaine in alleviating hemodynamic response and maintain hemodynamic stability with maintaining airway reflexes during extubation.
Aim and objectives of the study
The main aim of the study was to compare the effectiveness of a single dose of dexmedetomidine and lignocaine in alleviating hemodynamic and airway responses during extubation and recovery. The secondary objective was to study the effects of drugs on observing the time to emergence and time to tracheal extubation and undesirable effects of the study drug.
Materials and MethodologyThe study “Alleviating haemodynamic response to tracheal extubation: A Comparative study between Dexmedetomidine and Lignocaine in surgical patients” was done after obtaining Institutional Human ethics committee clearance from the institution between January 2019 and December 2020, registered in the clinical trial registry (CTRI/2020/11/029326) and informed written consent from all the patients who participated in the study. It was a double-blinded prospective-based randomized control study, and the sample size was calculated using a 95% confidence interval, the power of the study being 80% and a sampling ratio of 1, considering the heart rate (HR) parameter from Gosai et al.[3] as the basis for the study population. The sample size was 30 in each group. Sixty patients of the age group between 20 and 65 years belonging to ASA 1 and 2 undergoing elective surgical procedures with a minimum anticipated duration of 60 min requiring endotracheal intubation were included in the study.
The patients were randomly allocated into two groups with 30 participants in each group and were called as grouped as Group D received dexmedetomidine 0.5 μg/kg and Group L received lignocaine 1.5 mg/kg. Patients were randomly allocated to one of the two groups by computer generated program assigning random table number. It was a double-blinded study, where the patient and the personnel assessing the outcome were not aware of the group they were alloted. The method of randomization used was block randomization, in which the study population was divided into block sizes of six. The randomization codes for each subject were then enclosed in a sealed envelope. Before the study, the anesthesiologist who was not involved in the study was made to pick among a lot of opaques concealed envelope, which was handed over to the anaesthesiologist involved in the concerned surgery, who would administer the study drug and observe the parameters [Figure 1].
Patients aged between 20 and 65 years belonging to ASA 1 and ASA 2 undergoing elective surgical procedures in general surgery, gynecology, and ENT surgery with a minimum anticipated duration of 60 min requiring endotracheal intubation were included in the study. Patients with cardiorespiratory, renal, and hepatic dysfunctions necessitating postoperative mechanical ventilation, metabolic disorder, bleeding disorder, severe hypovolemia, neurological deficit, emergency surgery, morbid obesity, pregnancy, difficult airway and who are on antihypertensives, antiarrhythmics, psychotropics and allergic medications to any drugs were excluded from the study.
The routine preoperative assessment was made and the patients were kept nil per oral from 10 PM the day before surgery. Informed written consent was obtained. All the patients were premedicated with the tablet of pantoprazole 40 mg, metoclopramide 10 mg, and alprazolam 0.25 mg orally the day before surgery at night and pantoprazole 40 mg with metoclopramide 10 mg at 6 AM on the morning of surgery.
In the preoperative room, an 18G intravenous cannula was inserted and a maintenance infusion of the plasma-lyte solution started. On arrival inside the operating suite, preinduction monitors such as five-lead electrocardiogram, pulse oximetry, noninvasive blood pressure, temperature, end-tidal CO2, and end-tidal anesthetic agent concentration using Philips MP50 – Intellivue multi-parameter monitor were connected and baseline values were recorded. Anesthesia workstation used for the study is GE Healthcare Avance CS2 care station® with an inbuilt gas analyzer to measure end-tidal CO2 and end-tidal anesthetic agent concentration.
All patients received intravenous premedication with glycopyrrolate 0.2 mg; analgesia was supplemented with fentanyl 2 μg/kg, induced with propofol 2 mg/kg, bag-mask ventilation done and intubated using atracurium 0.5 mg/kg to facilitate endotracheal intubation. Tube position was secured and confirmed with EtCO2. Anesthesia was maintained with sevoflurane in 60% Nitrous oxide and 40% oxygen mixture to achieve the MAC value of 0.8–1.2 and to target the EtCO2 value between 30 and 35 mmHg. Morphine 0.1 mg/kg was given to supplement further analgesia.
An incremental dose of atracurium 0.1 mg/kg was given every 30 min for muscle relaxation. 15 min before the end of the surgery, the inhalational agent and nitrous oxide were cut off gradually and after the adequate return of spontaneous respiratory attempts, patients belonging to Group D received Dexmedetomidine 0.5 μg/kg dose and Group L received lignocaine 1.5 mg/kg intravenously. The values for HR were more than 70/min, systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) were obtained just before the administration of these drugs and were considered as baseline. Over the next 60 s, neuromuscular blockade was reversed with neostigmine 0.05 mg/kg and glycopyrrolate 0.01 mg/kg and the trachea was extubated when the patient obeyed commands with no airway compromise after observing for 2 min.
The following parameters were noted:
•Hemodynamic variables were obtained at 0 (baseline), 1st, 2nd, 3rd, 4th, 5th, 10th, and 15th min from the time of administration of the study drug. The maximum rise of HR and MAP was noted during tracheal extubation in the hemodynamic chart. Emergence and extubation times were also noted with follow-up of patients in recovery for sedation score
•Extubation quality was clinically assessed using the parameter - cough at the time of extubation with a five-point extubation quality scoring system.[2] Grading of cough was noted as a measure of the quality of extubation.[2],[15]
1 – No coughing
2 – Smooth extubation, minimal coughing (1 or 2 times)
3 – Moderate coughing (3 or 4 times)
4 – Severe coughing (5–10 times) and straining
5 – Poor extubation, very uncomfortable (laryngospasm and coughing >10 times)
•Sedation in the postoperative period was rated using Ramsay's six-point sedation score.[2],[15]
1 – Anxious or agitated and restless or both
2 – Cooperative, oriented, and tranquil
3 – Drowsy but responds to commands
4 – Asleep, brisk response to light glabellar tap or loud auditory stimulus
5 – Asleep, sluggish response to light glabellar tap or loud auditory stimulus
6 – Asleep and unarousable
•Complications such as delayed emergence, bradycardia, hypotension, airway obstruction, breath holding, desaturation, laryngospasm, bronchospasm, postoperative nausea, and vomiting were noted and recorded
We defined hypotension as SBP <20% of baseline or 90 mmHg or MAP <60 mmHg whichever is lower and hypertension as SBP >20% of baseline or MAP >150 mmHg whichever is higher. In our study, we recorded bradycardia when HR <25% and tachycardia when HR >25% of baseline value and desaturation with the drop in SpO2 ≤92% was noted as the reference value. Emergence time was defined as the time interval between discontinuing of anesthetic agents and the patient following verbal commands. Extubation time was defined as the time interval between cessation of anesthetic agents and tracheal extubation. Delayed emergence was defined as a state of unresponsiveness from which the patient cannot be aroused after 60–90 min. Breath holding was defined as holding breath for 20 s or more.
Data were statistically analyzed with the statistical package for the social sciences (IBM SPSS Statistics version 20.0, Chicago, United states), and descriptive analysis such as mean, standard deviation, and the percentage is used to exhibit the clinical parameters considered in the research pro forma. Independent t-test analysis was more suitable data for this, and all the statistical test was examined with P ≤ 0.05 level of significance.
Observation and ResultsThis study was conducted on 60 patients with 30 participants in each group, where one group received dexmedetomidine (group D) and the other group with lignocaine (group L). Majority of the study participants were in the age group between 32 and 59 years with mean age of 44.37 in group D and 45.37 in group L. Other demographic parameters like sex distribution of the individual, weight, BMI, and ASA grading were comparable among both the groups [Table 1].
The administration of the reversal drug between two groups from the time of study drug proved statistical significance with P=0.000 [Table 2]. Haemodynamic parameters like HR, SBP, DBP and MAP was significant with P<0.05 at 5 mins [Table 3]. None of the patients in both the group had complications [Table 4]. With regard to the quality of extubation and extubation time, the groups were comparable with P value 0.890 and 0.471 respectively [Table 5].
Table 3: Intergroup comparison of hemodynamic profiles between two groupsIn our study, the dexmedetomidine group showed deeper scores of sedation at the 20th min and both the groups reached an acceptable sedation score, which was statistically significant P<0.05 [Table 6].
Table 6: Association of Ramsay sedation score between dexmedetomidine and lignocaine at different intervals Discussion Tracheal extubation is the most unpredictable and uncomfortable state during reversal stage from general anesthesia, which results in transient rise of heart rate and arterial blood pressure lasting for about 5-10 mins in 10-30% individuals reflecting the sympathoadrenal discharge produced by epipharyngeal and laryngopharyngeal stimulation.[7] Extubation during lighter planes of anesthesia or sedation can stimulate reflexes by laryngeal and tracheal irritation. Bucking resembles the Valsalva maneuver physiologically and can result in negative pressure pulmonary edema when the lung volumes are lesser than the vital capacity.[16]
Nonpharmacological techniques like leaving the tracheal tube or laryngeal mask airway in situ with cuff deflated can make the patient breathe around it if the tube is bitten on during emergence. A nasal endotracheal tube can be used as a nasal conduit during emergence while the tube is withdrawn till the nasopharynx. Bailey's maneuver and clearance of secretions by suctioning prior have also been used to abate tracheal extubation response.[17] Pharmacological techniques have been employed to alleviate such responses like deep extubation using inhalational agents, agents such as calcium channel blockers, narcotic agents, vasodilator agents, local anesthetics, beta-adrenoceptor blockers, and alpha-adrenoceptor agonist.[18]
Lignocaine attenuates the hemodynamic responses to tracheal extubation by its direct myocardial depressant effect, central stimulant effect, peripheral vasodilatory effect, and finally, it suppresses the cough reflex, an effect on synaptic transmission.[19] Dexmedetomidine exerts its physiological actions through the potentiation of postsynaptically situated alpha-2 adrenoceptor, thus carrying its sympatholytic, analgesic, hypnotic, sedative, and anxiolytic response which contributes to attenuating hemodynamic responses to tracheal extubation.[20] The need to avoid the exaggerated tracheal extubation response still continues though many medications were tried.
In our study, dexmedetomidine group showed a decrease in HR when compared to the lignocaine group from 2nd to 5th min, which was statistically significant. Gosai et al.[3] showed a significant decrease in HR in dexmedetomidine group (0.5 mcg/kg) as compared to lignocaine group (1.5 mg/kg) and Group P (P < 0.05) at all-time interval after extubation. Turan et al.[14] showed significant lower HR with dexmedetomidine (0.5 mcg/kg) after extubation. Luthra et al.[21] showed a significant reduction in HR just before extubation and up to 10 min postextubation in the dexmedetomidine (0.2 mcg/kg) and dexmedetomidine (0.4 mcg/kg) groups as compared to placebo. We also observed increase in HR at the 10th min in the dexmedetomidine group, which can be attributed to the use of reversal agent, but was statistically insignificant.
On assessing SBP in our study, the dexmedetomidine group showed a decreasing trend in SBP when compared to the lignocaine group after the 5th min, which was statistically significant (P < 0.05). Goyal et al.[22] showed significantly lower values of SBP, DBP, and HR in the dexmedetomidine group (0.5 mcg/kg) as compared to the control group from 3 min after drug administration to 15 min after extubation (P < 0.01) and Guler et al.[9] showed an increase in SBP at extubation in both groups, but the increase was less significant with dexmedetomidine. Aksu et al.[10] suggested that dexmedetomidine 0.5 μg/kg IV administered before extubation was significantly more effective in continuing hemodynamic stability with no change in recovery duration, compared with fentanyl 1 μg/kg IV in patients undergoing rhinoplasty. We also observed a rise in SBP at the first 2 min in the dexmedetomidine group, which can be attributed to the peripheral alpha-2 vasoconstriction effect [Figure 2].
Statistical significance was noted at the 5th and 15th min with regard to DBP showing a decreasing trend in group D when compared with group L [Figure 2]. In similar studies, Kothari et al.[12] showed a statistically significant increase in HR, SBP, and DBP in both dexmedetomidine and lignocaine groups during extubation and immediately after extubation. Tendulkar and Ninave[23] concluded that IV dexmedetomidine (0.5 mcg/kg) significantly attenuates both pressors as well as the airway responses to extubation better than IV Esmolol (1.5 mg/kg). We also observed a rise in DBP at the first 2 min in the dexmedetomidine group, which can be attributed to the peripheral alpha-2 vasoconstriction effect.
We observed dexmedetomidine group showed a statistical significance with decreasing trend in MAP when compared to the lignocaine group after the 5th and 15th min. Dutta et al.[24] showed that the rise in MAP and HR was more with the lignocaine group compared with the dexmedetomidine group (0.3 mcg/kg) during extubation proving statistical significance. In another study, Bindu et al.[2] showed a significantly attenuated hemodynamic response with dexmedetomidine (0.75 mcg/kg) than in the placebo group after extubation. In another study, Gosai et al.[3] showed a significant decrease in MAP in dexmedetomidine group (0.5 mcg/kg) as compared to lignocaine group (1.5 mg/kg). We also observed a rise in MAP at the first 2 min in the dexmedetomidine group.
With regard to the quality of extubation, there was no statistical significance and the groups were comparable. Savitha et al.[25] observed that lignocaine 1 mg/kg is superior to 0.5 mg/kg in attenuating the hemodynamic responses to tracheal extubation. Hariharan et al.[20] revealed that postextubation cough was effectively suppressed by both the infusion doses (0.2 and 0.4 μg/kg/h) of dexmedetomidine, which was significantly lower than the control group. Sharma et al.[26],[27] observed that Extubation Quality Scores were 1 in 80%, and 2 in 20% in the dexmedetomidine group; and the lignocaine group showed 1 for 55% and 2 for 45%, respectively. From this, they concluded that the diminution of airway response was better controlled in Dexmedetomidine (0.5 μg/kg) group in comparison with lignocaine (1.5 mg/kg) and the placebo group favoring a smooth simple extubation.[27] We also observed that the extubation time and emergence time were sooner in lignocaine group than dexmedetomidine group but statistically not significant.
In our study, we observed that the dexmedetomidine group showed deeper scores of sedation but at the 20th min, both the groups reached an acceptable sedation score, which was statistically significant (P < 0.05). In Kothari et al.[12] studies, dexmedetomidine (0.5 mcg/kg) showed a higher grade degree of sedation as compared with lignocaine (1.5 mg/kg) with negligible coughing and breath-holding episodes. Tendulkar and Ninave[23] concluded IV dexmedetomidine (0.5 mcg/kg) significantly showed a higher degree of sedation better than IV Esmolol (1.5 mg/kg). Mistry et al.[13] investigated the extubation response between verapamil (0.1 mg/kg) and dexmedetomidine (0.3 mcg/kg) in patients scheduled for spinal surgeries and concluded that the sedative effect of dexmedetomidine was noted to be higher than verapamil group in which most of the patients were anxious and agitated or restless.
Limitations in our study
Certain interpretations may be statistically not significant, but it will be clinically significant. Few parameters, such as emergence and extubation time, were sooner in the lignocaine group than in the dexmedetomidine group but statistically not significant. Complications were more in the dexmedetomidine group but statistically insignificantA larger sample size with statistical significance would have been clearer and more evident than the smaller sample sizeDexmedetomidine at a dosage of 0.5 mcg/kg can be recommended for attenuation of the hemodynamic response, but a careful look toward the complications is necessary. ConclusionWe conclude that dexmedetomidine (0.5 mcg/kg) causes significant attenuation of hemodynamic response and deeper sedation when compared to lignocaine (1.5 mg/kg). However, early emergence and extubation time was associated with lignocaine, and the extubation quality was comparable between both groups.
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Conflicts of interest
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