|Year : 2018 | Volume
| Issue : 3 | Page : 265-273
Effect of dexmedetomidine on hemodynamic changes during laryngoscopy, intubation, and perioperatively in laparoscopic surgeries
Suman Gupta1, Shilpa Agarwal1, DD Jethava2, Bhanu Choudhary1
1 Department of Anesthesia, Gajra Raja Medical College, Gwalior, Madhya Pradesh, India
2 Department of Anesthesia, Mahatma Ghandhi Medical College and Hospital, Jaipur, Rajasthan, India
|Date of Web Publication||25-Sep-2018|
Dr. Shilpa Agarwal
7, Shri Ram Colony, Jhansi Road, Lashkar, Gwalior
Source of Support: None, Conflict of Interest: None
INTRODUCTION: Laryngoscopy and intubation lead to mechanical and chemical stimuli, resulting in hypertension and tachycardia. The pneumoperitineum and CO2 insufflation with positional changes result in significant hemodynamic and respiratory changes. These sudden changes may lead to myocardial ischemia, pulmonary edema, and cerebral hemorrhage. Many modalities such as propofol infusion, beta-blocker, high-dose opioid, benzodiazepine, and vasodilators have been tried to obtund these changes. Dexmedetomidine is highly selective alpha-2 agonist, has been effective in attenuating sympathomimetic response during laryngoscopy, intubation as well as during laparoscopic surgeries.
OBJECTIVE: In a randomized, prospective, double-blind, control study, we evaluate the safety and efficacy of single bolus intravenous dose followed by infusion of dexmedetomidine as compared to control group of normal saline in attenuating response to laryngoscopy, intubation, and pneumoperitoneum in laparoscopic surgeries.
MATERIALS AND METHODS: A total of 60 patients of either sex aged 18–65 years scheduled for elective laparoscopic surgeries were randomly allocated in one of the two groups of thirty patients each. Group D received injection dexmedetomidine with loading dose 1 mcg/kg before induction over 10 min followed by maintenance dose of 0.2 mcg/kg/h. Group S serve as control group received normal saline in the same dose.
RESULTS: It was observed that heart rate, systolic blood pressure, diastolic blood pressure, and mean arterial pressure were significantly less after intubation and throughout the period of pneumoperitoneum.
CONCLUSION: Dexmedetomidine is efficacious in attenuating the hemodynamic response to laryngoscopy, intubation, and pneumoperitoneum.
Keywords: Dexmedetomidine, hemodynamics, intubation, laparoscopic surgeries, laryngoscopy, pneumoperitoneum
|How to cite this article:|
Gupta S, Agarwal S, Jethava D D, Choudhary B. Effect of dexmedetomidine on hemodynamic changes during laryngoscopy, intubation, and perioperatively in laparoscopic surgeries. Indian J Health Sci Biomed Res 2018;11:265-73
|How to cite this URL:|
Gupta S, Agarwal S, Jethava D D, Choudhary B. Effect of dexmedetomidine on hemodynamic changes during laryngoscopy, intubation, and perioperatively in laparoscopic surgeries. Indian J Health Sci Biomed Res [serial online] 2018 [cited 2018 Dec 15];11:265-73. Available from: http://www.ijournalhs.org/text.asp?2018/11/3/265/242046
| Introduction|| |
The commencement of laparoscopic surgeries as an advanced technique for almost all type of surgeries performed, benefits a large number of patients with an added advantage of less pain, early mobilization, short hospital stay, better cosmetic result, a mindset in patients of less fear with laparoscopic surgeries as compared to open surgeries. Hence, it has become a most widely used technique for array of surgeries, i.e., laparoscopic cystectomy, laparoscopic hysterectomy, laparoscopic appendicectomy, and laparoscopic nephrectomy are some of these. This technique leads to pneumoperitoneum (CO2) created during surgeries, results in increased plasma levels of catecholamines and vasopressin. Elevation of intra-abdominal pressure with raised diaphragm compromises cardiac function such as decreased cardiac output, elevated abdominal pressure, increased systemic, and pulmonary vascular resistance leading to hypertension and tachycardia.
Pneumoperitoneum with CO2 insufflations combined with positional changes (reverse Trendelenburg) results in significant hemodynamic and respiratory changes which are mediated by mechanical and neurohormonal factors. Both the factors hypercapnia and pneumoperitoneum stimulates sympathetic nervous system which causes the release of catecholamines and vasopressin and also activation of rennin-angiotensin system.
There are a wide array of drugs propofol infusion, beta-blocker, high-dose opioid, benzodiazepine, vasodilators that have been studied clinically through randomized control trials and published to blunt hemodynamic response to laryngoscopy, intubation, and pneumoperitoneum.,
Dexmedetomidine is an imidazole derivative and highly specific selective alpha-2 adrenergic receptor agonist.. Alpha-2 agonists produce hyperpolarization of noradrenergic neurons and suppression of neuronal fixing on the locus cereulus leading to decreased systemic noradrenaline release resulting in attenuation of sympathoadrenal responses and hemodynamic stability during laryngoscopy and tracheal intubation. Dexmedetomidine is an alpha-2 – adrenergic agonist, which is the pharmacologically active dextro isomer of medetomidine. It has properties of analgesia, sympatholysis, and titrating sedation without major respiratory depression.,
Laryngoscopy and intubation lead to mechanical and chemical stimuli, mechanical stimuli causes reflex responses in cardiovascular and respiratory system. Laparoscopic surgeries under general anesthesia are associated with hemodynamic changes in the form of increased systemic vascular resistance, leading to hypertension, forcing the anesthesiologist to increase the depth of anesthesia, at times even requires the use of vasodilators to tackle the rising blood pressure.
Alpha-2 adrenoceptors agonist have been used as an adjuvant to anesthetic agents in perioperative period for its several beneficial action. These drugs improve hemodynamic stability during endotracheal intubation and surgical stress by its central sympatholytic action and thus reduce anesthetic and opioids requirements. Laparoscopic surgeries have added the advantage of shorter hospital stay, early ambulation, smaller scar, and less compromised post operative respiratory and gastrointestinal function. However, the procedure is not risk-free as it is associated with significant hemodynamic changes due to the creation of pneumoperitoneum, the potential for systemic absorption of CO2 and reverse Trendelenburg position.
Alpha-2 agonists such as clonidine and dexmedetomidine have been studied by some researcher for attenuation of the stress response to laryngoscopy.
In this randomized, prospective, double-blind, control study, we evaluate the safety and efficacy of single bolus intravenous dose followed by infusion of dexmedetomidine as compared to control group of normal saline in attenuating response to laryngoscopy, intubation as well as during pneumoperitoneum insufflations and release of CO2 during laparoscopic surgeries.
| Materials and Methods|| |
This prospective randomized controlled double-blind study was conducted after approval from the Institutional Ethics Committee and written informed consent from the patient. A total of sixty patients of the American Society of Anesthesiologists (ASA) Grade I and II, aged 18–65 years of either sex scheduled for elective laparoscopic surgeries, i.e., laparoscopic cholecystectomy, laparoscopic appendicectomy, laparoscopic-assisted vaginally hysterectomy, the diagnostic laparoscopic procedure under general anesthesia were included in the study, conducted in Mahatma Gandhi Medical College and Hospital Jaipur. India.
ASA Grade III and IV and patients with cardiac, hepatic, renal dysfunction, morbidly obese, and uncontrolled hypertension were excluded from the study.
Patients were randomly allocated into one of the two groups of thirty patients with the help of computer-generated table of random number as described below.
Group D (n = 30) received injection dexmedetomidine with loading dose 1 mcg/kg before induction over a period of 10 min followed by maintenance dose of 0.2 mcg/kg/h throughout the pneumoperitoneum until extubation.
Group S (n = 30) received the same dose of normal saline as loading and maintenance to serve as control group.
The study material was prepared in similar 50 ml syringe by anesthesiologist who was blinded to group randomization. Dexmedetomidine 200 mcg (2 ml) was added to 0.9% normal saline (48 ml) making a total volume of 50 ml with concentration of 4 mcg/ml. On arrival to operating room, two 18G intravenous cannula were secured, one for loading and infusion of study drug and other for induction and maintenance of general anesthesia. Routine monitor, electrocardiograph, pulse oximetry, and noninvasive blood pressure were attached and baseline parameters such as heart rate (HR), SPO2, blood pressure were recorded. Loading dose of dexmedetomidine infusion 1 mcg/kg was started and infused over a period of 10 min thereafter maintenance infusion of dexmedetomidine was given at a rate of 0.2 mcg/kg/h, whereas Group S patients received 0.9% normal saline at the same rate. All patients were premedicated with injection glycopyrolate 4 mcg/kg, injection midazolam 0.03 mg/kg and injection ondansetron 4 mg, injection fentanyl 2 mcg/kg intravenously. Patients were preoxygenated with 100% oxygen, induced 5 min after infusion of loading dose with injection Thiopentone 5 mg/kg intravenous, injection Succynylcholine 1.5 mg/kg. All the patients were intubated with appropriate size endotracheal tube, and correct position of tube was confirmed by auscultation and EtCO2 reading. Anesthesia was maintained with nitrous oxide and oxygen mixture (60:40) and isoflurane on a closed circuit. Injection vecuronium was administered for neuromuscular blockade. CO2 was insufflated into the peritoneum (at a rate of 2 L/min) to create pneumoperitoneum. Intra-abdominal pressure was maintained up to 12–14 mmHg throughout the laparoscopic procedure.
Hemodynamic changes HR, systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MAP) to laryngoscopy, intubation, and perioperatively observed and documented at baseline, during laryngoscopy, intubation, 1, 3, and 5 min after intubation, before pneumoperitoneum, 15 and 30 min after pneumoperitoneum and after extubation.
Dexmedetomidine infusion was continued until extubation of patient. Residual neuromuscular blockade was reversed by appropriate dose of neostigmine and glycopyrolate and tracheal extubation performed. Any adverse effects such as Hypotension, hypertension, bradycardia, respiratory depression, postoperative nausea vomiting were recorded. Patients were observed in the recovery room for 2 h and thereby shifted to ward.
Any hypertension (MAP >20% preoperative value) was treated by increasing isoflurane concentration to maintain SBP within 20% of preoperative value.
Hypotension (MAP <20% preoperative value) was managed with fluid bolus of normal saline 250–300 ml. If did not respond to fluid administration then injection mephentermine 5 mg intravenously was administered. Any incidence of bradycardia (HR <60/min) was treated with injection atropine 0.6 mg intravenous.
Results here presented as the mean ± standard deviation (SD) Microsoft Excel 2007 was used for statistical analysis. Chi-squared test was used for qualitative data, categorical data (age, sex, and weight ASA Grade I–II). Intragroup comparison of HR, SBP, DBP, and mean arterial pressure here compared against baseline values using paired t-test. Unpaired Student's t-test was applied for comparison of continuous variable of two groups.
Sample size of minimum of thirty patients per group have designed using(statistical software SPSS version 20.0) based on assumption of xenon of 0.05 and power of study of 80% P < 0.05 was considered statistically significant and P < 0.001 as highly significant.
| Results|| |
A total of 60 patients were enrolled in our study and was subjected to statistical analysis. Demographic profile was compared among the two groups of patients, and no significant difference (P > 0.05) were found as shown in [Table 1].
The basal HR was comparable in both the groups (P > 0.05). Mean basal HR in Group D was (95.77 ± 22.54)/min and Group S was (88.23 ± 15.83)/min as shown in [Table 2]. After administration of the study drugs, there were highly significant (P < 0.01) decrease in HR in Group D as compared to Group S at all stages of laparoscopic cholecystectomy, i.e., during laryngoscopy and intubation, 1, 3 and 5 min after intubation, before pneumoperitoneum, 15 min and 30 min after pneumoperitoneum, after release of CO2 and after extubation as shown in [Table 2]. The mean HR in Group D varied from the basal HR of (95.77 ± 22.54)/min to (83.50 ± 11.80)/min, whereas variation in HR in Group S were from (88.23 ± 15.83)/min to (113.73 ± 13.26)/min.
|Table 2: Comparison heart rate (mean±standard deviation) in both the groups during various phases intraoperatively|
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As shown in [Table 3] in Group D, there was fall in HR after the beginning of dexmedetomidine infusion up to 3 min, but it was statistically not significant. Later at 5 min after intubation, before pneumoperitoneum, 15 min after pneumoperitoneum, 30 min after pneumoperitoneum and after extubation, there was highly significant decrease in HR (P < 0,001) but clinically not apparent to need treatment for bradycardia. An average decrease of 12.6% of HR is seen from baseline to extubation in Group D.
|Table 3: Mean±standard deviation of heart rate from basal value to various intervals of Group D patients|
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As shown in [Table 4], after starting of infusion in group S there was rise in HR, which was found highly significant and it sustained till 3 min after intubation. However, it was found significant at 5 min after intubation till 15 min after pneumoperitoneum again there was highly significant rise in HR after extubation.
|Table 4: Mean change±standard deviation of heart rate from basal value to various intervals of Group S patients|
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The mean basal HR in Group S as shown in [Table 2] was (88.23 ± 15.83)/min. There was a highly significant rise in HR during laryngoscopy and intubation (115.60 ± 17.04)/min, this rise in HR continued at 1, 3, and 5 min after intubation (115.33 ± 18.47), (108.30 ± 15.49), and (100.23 ± 15.20)/min, respectively. The mean HR before pneumoperitoneum was (94.90 ± 12.59)/min. After 15 min pneumoperitoneum, there was persistent rise in HR of (95.33 ± 11.44)/min and also statistically significant as compared to basal value. At 30 min after pneumoperitoneum and after release of CO2, there was dip in mean HR i.e., (90.13 ± 12.09)/min and (83.27 ± 12.60)/min, but it was well above the basal value and found statistically significant (P < 0.05). At extubation again there was a pressor response in Group S showing HR of (113.73 ± 13.26)/min which was statistically highly significant as compared to basal HR [Figure 1] and [Table 2].
Changes in blood pressure when compared in two groups of patients have found to be statistically highly significant except the baseline value where data were comparable and not significant as shown in [Table 5]. SBP was significantly lower in Group D after induction at laryngoscopy and intubation up to 1, 3, 5 min after intubation, at pneumoperitoneum, 15 and 30 min after pneumoperitoneum, after the release of CO2 and after extubation, when statistically compared to Group S [Figure 2].
|Table 5: Comparison systolic blood pressure (mean±standard deviation) in both the groups during various phases intraoperatively|
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While analyzing DBP, after 3 and 5 min of intubation and before pneumoperitoneum there was little rise in Group S (72.60 + 12.81) mmHg and 69.77 + 11.60) mmHg but not above the basal value that rendered the intergroup comparison of DBP just before pneumoperitoneum as significant rather than highly significant as shown in [Figure 3] and [Table 6].
|Table 6: Comparison diastolic blood pressure (mean±standard deviation) in both the groups during various phases intraoperatively|
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There was rising in DBP during laryngoscopy and intubation as shown in [Table 7] which was statistically significant, thereafter the fall in DBP at 1 min after intubation was not significant. After extubation again, there was rise in DBP which was significant but remain near to basal value. Although in group S highly significant rise was found in DBP during laryngoscopy and intubation which became significant at 1 min after intubation. Thereafter, at 15 min after pneumoperitoneum and after extubation again highly significant rise in DBP was observed [Table 8].
|Table 7: Mean change±standard deviation of diastolic blood pressure from basal value to various intervals of Group D patients|
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|Table 8: Mean change±standard deviation of diastolic blood pressure from basal value to various intervals of Group S patients|
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Mean arterial pressure was statistically significantly lower in Group D as compared to Group S during all observation made right from laryngoscopy and intubation up to after extubation (P < 0.001) [Figure 4] and [Table 9].
|Table 9: Comparison mean arterial blood pressure (mean±standard deviation) in both the groups during various phases intraoperatively|
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While statistical analysis of mean + SD of intragroup of Group D reveals that in Dexmedetomidine Group D, after starting the infusion the blood pressure decreased significantly below the preoperative value. Further highly significant changes were observed after 1, 3, 5 min of intubation and 30 min after pneumoperitoneum and release of CO2 [Table 10], [Table 11], [Table 12], [Table 13].
|Table 10: Mean change±standard deviation of systolic blood pressure from basal value to various intervals of Group D patients|
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|Table 11: Mean change±standard deviation of systolic blood pressure from basal value to various intervals of Group S patients|
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|Table 12: Mean change±standard deviation of mean arterial pressure from basal value to various intervals of Group D patients|
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|Table 13: Mean change±standard deviation of mean arterial pressure from basal value to various intervals of Group S patients|
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In Group S, after starting infusion, there was a highly significant rise in mean arterial pressure at laryngoscopy intubation which was significant at 1 min, and not significant at 3 min. Again at 5 min of intubation and after extubation became highly significant depending on the stimulus of surgery, intubation, and extubation, as shown in [Table 13].
| Discussion|| |
Hemodynamic changes during laryngoscopy, intubation, and perioperatively during laparoscopic surgeries are a matter of concern and need to be obtunded by various drugs. Commonly used, i.e., lignocaine, clonidine, fentanyl, to avid hazardous effects of stress response leading to cardiovascular or neurologic complication are prevailing in practice. Various measures had been tried to obtund such reflexes. Recently, dexmedetomidine a potent alpha-2 agonist that have shown the potential to decrease this stress response. Dexmedetomidine is a highly selective alpha-2 adrenergic agonist. It acts through three types of alpha-2 receptors α-2 A1, α-2 B, α-2 C, situated in the brain and spinal cord. The resultant action is sedation, anxiolysis, analgesia, and sympatholysis. It suppresses norepinephrine release causing hypotension and bradycardia by activating α-2 A receptor in brain stem vasomotor center. Sedation is caused by stimulation of α-2 A and α-2 C in locus ceroleus. In spinal cord, activation of both α-2 A and α-2 C receptors directly reduce pain transmission by reducing release of substance P. The study reveals that laryngoscopy, intubation, pneumoperitneum and extubation do significantly increase in mean arterial pressure, and pulse rate in patients undergoing laparoscopic cholecystectomy, as seen in Group S. Furthermore, various studies supporting such observations , Dexmedetomidine attenuates this sympathoadrenal response and provides hemodynamic stability to various noxious stimuli perioperatively in laparoscopic surgeries. [Table 2] summarizes that while comparing group D with group S, a highly significant (P < 0.001) fall in mean HR was seen during laryngoscopy and intubation and remained so till after 1 min of intubation and became statistically significant (P < 0.05) after 15 min of pneumoperitoneum and throughout rest of the study. Our observations are in accordance with the findings  who studied intravenous Dexmedetomidine infusion (1 μg/kg) or saline placebo in 15 min and observed that the HR was decreased in dexmedetomidine group compared to Group S. also observed that HR was significantly lower in the dexmedetomedine group compared with other group. Bhattacharjee et al. observed that in dexmedetomedine group the HR decreased significantly after pneumoperitoneum and remained lower throughout the pneumoperitoneum as compared to placebo group. These hemodynamic effects are due to central sympatholytic and peripheral vasoconstriction effects. Dexmedetomidine causes a dose-dependent decrease in arterial blood pressure and HR associated with a decrease in serum norepinephrine concentration. It activates receptors in the medullary vasomotor center, reducing norepinephrine turnover and decreasing central sympathetic outflow resulting in attenuation in sympathetic function, thereby suppressing the hemodynamic response to intubation, extubation without any side effects such as respiratory depression and postoperative nausea and vomiting. Dexmedetomidine attenuates the sympathoadrenal response to tracheal intubation, reduces perioperative anesthetic requirement, and hemodynamic stability. [Table 5] shows that in Group D as compared to Group S, there is a highly significant (P < 0.001) decrease in systolic arterial pressure during laryngoscopy and intubation, and remained so before pneumoperitoneum and throughout the study. Our observation was well in accordance with the findings of  who observed that the maximal average increase in SBP (vs. baseline) were 1% and 21% in dexmedetomidine (0.6 μg/kg) and saline groups, respectively. Menda et al. studied intravenous dexmedetomidine infusion (1 μg/kg) and saline placebo in 15 min and observed SBP was decreased in dexmedetomidine group as compared to placebo group. Yildiz et al. also showed that SBP rate was significantly lower in the dexmedetomidine (1 μg/kg) group compared with Group S. Thus, we conclude dexmedetomidine is a highly selective alpha-2 agonist which possesses sympatholytic property. Its sympatholytic effect decreases the SBP by reducing the nor-epinephrine release.,
Similarly, [Table 6] shows that while comparing Group D with Group S, a highly significant (P < 0.001) decrease in mean DBP is seen during laryngoscopy and intubation, which is also statistically significant at 5 min after intubation but our findings before pneumoperitoneum until the release of CO2 shows insignificant differences between the two groups; however, a statistically highly significant difference was observed after extubation. The findings are in accordance with Lawrence and De Lange  who observed that dexmedetomidine (2 μg/kg) attenuates the hemodynamic response like blood pressure to tracheal intubation and extubation. Menda et al. also showed that DBP was decreased in dexmedetomidine (1 μg/kg) group compared to Group S.
Dexmedetomidine causes postsynaptic activation of alpha-2 receptor in the central nervous system inhibits sympathetic activity and thus decrease blood pressure.
[Table 9] shows that while comparing Group D with Group S, a highly significant (P < 0.001) decrease in mean arterial pressure is seen during laryngoscopy and intubation, which is also statistically significant (P < 0.05) until before pneumoperitoneum. This decrease was found to be insignificant at 15 and 30 min after pneumoperitoneum but became statistically highly significant after the release of CO2 and after extubation. The findings are in accordance with Bloor et al. which showed that after infusion of Dexmedetomidine, decrease in MAP was seen. Menda et al. also observed mean arterial pressure was decreased in dexmedetomidine group Aho et al. also observed the maximal mean arterial pressure after tracheal intubation was lower in dexmedetomidine 2.4-μg/kg and concluded that MAP values in dexmedetomidine group were lower after pneumoperitoneum and remained lower throughout the pneumoperitoneum. Thus, the change in mean HR, SBP, DBP, and mean arterial pressure was most effectively attenuated by dexmedetomidine. The efficacy of dexmedetomidine and normal saline is statistically comparable throughout the study.
In Group D, the hemodynamic effects were most effectively attenuated as compared to Group S because of predominant α-2 adrenoreceptor agonistic action of dexmedetomidine which causes decrease in HR and blood pressure. In Group S, the effects were most marked because normal saline that was being administered in this Group S, being a physiological solution is not known to cause any attenuating effect on the stress response. There were no specific complications and untoward effects noted during the study.
| Conclusion|| |
Laparoscopic surgeries are performed in various positions such as Trendelenburg, reverse Trendelenburg position. In case of reverse Trendelenburg position, there is diminished venous return. Normal heart can cope with the increase in afterload under physiologic conditions. However, patients with the compromised cardiac function may not be able to tolerate the changes in afterload produced by pneumoperitoneum, and it may have deleterious effects on their hemodynamics. Dexmedetomidine significantly reduces the release of catecholamines, especially release of norepinephrine, thereby attenuating the increase in systemic vascular resistance. Dexmedetomidine improves intraoperative and postoperative hemodynamic stability by stabilizing the changes in SBP, DBP, mean arterial pressure and HR. The present study, confirms that hemodynamic changes are attenuated by dexmedetomidine infusion during laryngoscopy, intubation, and laparoscopic surgeries. In our study, we used dexmedetomidine at an infusion rate of 0.2 μg/kg/h during laparoscopic surgeries and did not observe any significant incidence of hypotension or bradycardia. Further study with an increase in the sample size needs to be conducted to corroborate with the results and precise the role of dexmedetomidine infusion in laparoscopic surgeries.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10], [Table 11], [Table 12], [Table 13]