|Year : 2014 | Volume
| Issue : 1 | Page : 32-39
The equisedative effect of dexmedetomidine versus propofol on supraclavicular brachial plexus block and recovery profile in patients with ischemic heart disease
Rasha S Bondok1, Nirvana A El-Shalakany2
1 Department of Anesthesiology and Intensive Care, Ain-Shams University, Cairo, Egypt
2 Department of Anesthesiology and Intensive Care, 6th of October University, Cairo, Egypt
|Date of Submission||05-May-2013|
|Date of Acceptance||02-Jun-2013|
|Date of Web Publication||31-May-2014|
Rasha S Bondok
MD, Department of Anesthesiology and Intensive Care, Ain-Shams University, 33 Hassan Maamuon St, Nasr City 11391, Cairo
Source of Support: None, Conflict of Interest: None
The study investigated the effect of intraoperative equisedative doses of dexmedetomidine and propofol on supraclavicular nerve block in patients with ischemic heart disease.
Patients and methods
Patients with ischemic heart disease, American Society of Anesthesia (ASA) II-III, scheduled for upper-limb orthopedic surgery after an effective ultrasound-guided supraclavicular nerve block were included in this study. Patients were randomly allocated to receive dexmedetomidine 0.5 μg/kg or propofol 0.5 mg/kg as an initial loading dose for 10 min followed by a maintenance dose adjusted intraoperatively to a bispectral index of 70-80. In the postanesthesia care unit, the sedation score was recorded every 10 min until discharge. The degree of pain was evaluated hourly for the first 12 h and at 18 and 24 h postoperatively. Duration of analgesia and need of rescue analgesia were calculated.
During recovery, hemodynamic variables were significantly high in group P compared with group D (P < 0.001). The duration of analgesia was significantly longer in group D compared with group P (11.81 ± 3.54 vs. 7.18 ± 3.21 h, P < 0.001) and requirement for rescue analgesia was significantly lower in group D (27% compared with 81% in group P, P < 0.001).
Dexmedetomidine may prove a valuable adjuvant for sedation and analgesia in ischemic heart patients undergoing surgery under regional block.
Keywords: Block, dexmedetomidine, equisedative, heart, ischemic, supraclavicular
|How to cite this article:|
Bondok RS, El-Shalakany NA. The equisedative effect of dexmedetomidine versus propofol on supraclavicular brachial plexus block and recovery profile in patients with ischemic heart disease. Ain-Shams J Anaesthesiol 2014;7:32-9
|How to cite this URL:|
Bondok RS, El-Shalakany NA. The equisedative effect of dexmedetomidine versus propofol on supraclavicular brachial plexus block and recovery profile in patients with ischemic heart disease. Ain-Shams J Anaesthesiol [serial online] 2014 [cited 2021 Apr 19];7:32-9. Available from: http://www.asja.eg.net/text.asp?2014/7/1/32/128398
| Introduction|| |
Orthopedic surgery and general anesthesia (GA) constitute a major risk in patients with ischemic heart disease (IHD). In orthopedic surgery, regional block has become a preferred option over GA because of early patient rehabilitation and the avoidance of possible complications from GA. For the anesthetist, cardiovascular and respiratory stability, rapid postoperative recovery, and preservation of protective airway reflexes are the most important advantages of regional anesthesia . GA does not attenuate the stress response; elevations in heart rate (HR) and blood pressure increase myocardial oxygen demand and result in myocardial ischemia or infarction in individuals with IHD. Coronary vasoconstriction, as a result of an increase in circulating catecholamines, decreases coronary blood flow and myocardial oxygen delivery in IHD patients. GA may result in low blood pressure and undesirable decrease in cardiac output as well. Regional anesthetic techniques should be encouraged in order to avoid hemodynamic responses to GA as seen during laryngoscopy, intubation, and extubation . By providing dense anesthesia to the upper limb, the supraclavicular brachial plexus block is ideal for operations involving the arm and forearm down to the hand . However, even under regional anesthesia, the patient may be subjected to the stresses of the surgical procedure itself, which can have marked hemodynamic effects. Sedatives are frequently used to provide patient comfort, analgesia, and sedation. Many drugs have been used for sedation, such as propofol, benzodiazepines, and opioids, with a relative risk of oversedation or increased risk of respiratory depression and oxygen desaturation. Propofol is widely used for its short duration of action, no cumulative effect, unique recovery profile, and rapid emergence of patients from anesthesia . Even though propofol is a widely used sedative with minimal analgesic properties, it may cause some respiratory depression . Dexmedetomidine is a highly specific α2 agonist with sedative properties . In addition to its analgesic sparing properties, it has been shown to attenuate the perioperative stress response in the high-risk patient population .
The purpose of this study was to evaluate the intraoperative and postoperative equisedative dose effects of dexmedetomidine and propofol on supraclavicular brachial plexus block in IHD patients undergoing upper-limb orthopedic surgery.
| Patients and methods|| |
This study was approved by the Research Ethics Committee at the Faculty of Medicine, Ain-Shams University, Egypt. Patients with IHD scheduled for an elective upper-limb (forearm or hand) orthopedic surgery under ultrasound (US)-guided supraclavicular brachial plexus nerve block who met the enrollment criteria were included in the study. All patients of ASA physical status II-III, with a BMI less than 35 kg/m 2 , and scheduled for at least a 24-h stay in the hospital were included in the study between 2011 and 2012 after their written informed consent was obtained. Inclusion criteria included IHD with myocardial infarction more than 6 months ago, previous myocardial revascularization procedures, normal renal function, and no chronic use of medical therapy that might influence the outcome of the study (such as narcotics). Exclusion criteria included a left ventricular ejection fraction of less than 40%, associated valvular lesions, more than five premature ventricular contractions per minute, myocardial infarction within 6 months, unstable angina within 3 months, second-degree or third-degree heart block, preoperative left bundle branch block, being in receipt of α2 agonists including dexmedetomidine within 28 days before the scheduled surgery, traumatic nerve injury to the upper extremity or neck, pre-existing neurodeficit in the distribution of the block, and renal or hepatic disease. Patients with a current history of respiratory or psychiatric disorders or presently on psychotropic medications, those with a history of sleep apnea, patients with a BMI of 30 kg/m 2 or above, and those with a failed supraclavicular brachial plexus block were also excluded.
All patients underwent a routine cardiologic examination, including medical history, physical examination, resting ECG, two-dimensional echocardiography Doppler imaging examination, and chest radiography.
Clopidogrel Plavix (clopidogrel bisulphate 75 mg tablet, Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership, Bridgewater, France) was withheld 1 week before surgery, whereas aspirin was stopped 3 days before surgery. Oral medications such as β-blockers, calcium channel blockers, and nitrates were continued until the morning of surgery and restarted when possible after surgery.
In the preoperative induction room, before the start of the surgical procedure, patients were instructed on the proper use of the visual analog scale (VAS). Patients rated their pain intensity using a 0-10-cm VAS, where score 0 indicates no pain and 10 indicates the worst pain ever experienced. The Observer's Assessment of Alertness/Sedation (OAA/S) scale was used to rate the alertness of the patient, where 5 = responds readily to name spoken in normal tone (awake/alert), 4 = lethargic response to name spoken in normal tone, 3 = responds only after name spoken loudly or repeatedly, 2 = responds after mild prodding or shaking, and 1 = does not respond to mild prodding or shaking (asleep/unarousable) . Thereafter, intravenous access was established in the nonoperative limb, and an infusion of normal saline was started at a maintenance rate; patients were then given 0.5 μg/kg of fentanyl and 0.03 mg/kg of midazolam for anxiolysis and transported to the operating room (OR). A nasal prong was applied and supplemental oxygen at 4 l/min of fresh gas flow was given throughout the procedure. Standard ASA monitors were used throughout the surgery (Infinity Delta, Primus; Drδger Medical, Lübeck, Germany), and HR, noninvasive mean arterial blood pressure (MAP), respiratory rate (RR), and oxygen saturation (SpO 2 ) were documented at 5-min intervals. The US-guided supraclavicular brachial plexus block was performed by a single experienced anesthesiologist. The patient was placed in the dorsal decubitus position with the neck extended toward the contralateral side. Asepsis of the skin was achieved and a local infiltration was performed with 1 ml of 1% lidocaine. A US-guided supraclavicular brachial plexus block was provided by Mindray M5 Ultrasound (Mindray DS USA Inc., Mahwah, New Jersey, USA). A linear high-frequency probe (7.5 MHz) was used to inspect the supraclavicular fossa in a coronal oblique plane, parallel and immediately posterior to the clavicle. The brachial plexus was identified as a compact group of nerves located over the first rib, laterally and posterior to the subclavian artery. The rib and pleura were identified before needle insertion. A 22-G needle was advanced in-plane with the US beam from lateral to medial direction until the brachial plexus sheath was penetrated, and the needle tip was positioned within the sheath compartment among the nerves. After a negative aspiration, the local anesthetic solution was administered incrementally, ensuring expansion of the brachial plexus sheath. This was provided by 30 ml 2% lidocaine and 0.5% bupivacaine (1 : 1). The end of injection was considered as the time for evaluating the effectiveness of the block. Sensory and motor block was assessed every 3 min within the first 30 min following completion of drug administration. The motor block was considered successful when a Bromage score of 2 was achieved (modified Bromage scale for the upper limb: 0, normal motor function; 1, ability to move only fingers; 2, complete motor block with inability to move elbow, wrist, and fingers) . The sensory block was confirmed by pinprick sensation using a 23 G needle and by thermal sensation using an alcohol swab in all dermatomes of the brachial plexus (C5-T1). The sensory block was considered successful when there was a complete lack of pinprick and loss of cold sensation in the skin area overlying the surgical field. Established criteria for a successful brachial plexus block were a motor function of 2 and absence of both pinprick and thermal distinction in all regions that were innervated by the respective divisions when compared with the contralateral limb. Upon reaching an effective block, a tourniquet was placed at the lower half of the arm and patients were randomly allocated to one of the two study intravenous sedative drugs. Randomization was achieved by using orderly, numbered, opaque sealed envelopes containing computer-generated random allocations at a ratio of 1 : 1 in balanced blocks of 10. Group D received dexmedetomidine (Precedex 2 ml, 100 μg/ml; Abbott Laboratories, Abbott Park, Illinois, USA) at an initial loading dose of 0.5 μg/kg over a 10-min period followed by a maintenance dose of 0.2 μg/kg/h; group P received propofol (Diprivan 2%; AstraZeneca Pharmaceuticals Ltd, London, UK) at an initial loading dose of 0.5 mg/kg given over a 10-min period followed by a maintenance dose of 1.5 mg/kg/h. Adequate conscious sedation was achieved based on a bispectral EEG index score (BIS) (Infinity BISx SmartPod, Infinity Delta, Primus; Drδger Medical) of 70-80. To estimate the level of consciousness, the skin was cleaned with alcohol and left to dry. The BIS sensor was placed on the forehead and temple using a frontal-temporal assembly, pressed for 5 s, and skin-sensor connection was established. The dexmedetomidine infusion was increased and adjusted to a maximum dose of 1 μg/kg/h, whereas propofol was titrated as required to attain the target BIS. On achieving the targeted BIS, surgery was commenced, and infusion doses were adjusted intraoperatively to maintain the BIS between 70 and 80 as well as an OAA/S of 4-3. Supraclavicular brachial plexus block and sedation were performed by the same anesthesiologist, who was not blinded to the procedure. All measurements during the operation were carried out by an anesthetist who was blinded to the sedative drug used. Neither the patient nor the surgeon was aware of the study drug. During surgery, if either bradypnea (RR < 10 bpm) or SpO 2 reached 92% or less, or bradycardia (HR < 45 bpm) or hypotension (MAP < 55 mmHg) was observed, 6 l/min of supplemental oxygen was administered through a face mask, intravenous atropine or ephedrine was administered, and 0.9% saline was infused, respectively; concomitantly, the rate of drug infusion was reduced aiming to arouse the patient and enable him or her to resume normal breathing.
The following measures were assessed:
- onset of sensory and motor block (complete successful block) was defined as the time from injection of local anesthesia to complete absence of thermal distinction and pain and achievement of a modified Bromage score of 2, respectively.
- to achieve adequate sedation level was defined as time from start of infusion of the study drug until achievement of the target sedation level.
- time was defined as time from start of infusion of the study drug until its discontinuation.
- regression of the block was assessed every 30 min. The duration of motor block was defined as the time from the onset of complete motor block to achievement of a modified Bromage score of 0.
- , MAP, RR, and SpO 2 were recorded every 5 min throughout surgery and in the immediate postoperative period at 15 and 30 min; baseline measurements were obtained just before the start of the study drug.
- the postanesthesia care unit (PACU), the modified Aldrete score  was assessed every 5 min until discharge. Patients were ready for discharge upon achieving an Aldrete score greater than 9, which corresponded to the time of arrival at the PACU until discharge. Time from cessation of treatment infusion until discharge from the PACU was also recorded.
- the PACU, the OAA/S score was recorded every 10 min until discharge.
- degree of pain was evaluated during rest using the VAS for pain, hourly for the first 12 h and at 18 and 24 h postoperatively.
- Duration of analgesia was defined as the time of onset of sensory block to the first complaint of pain (pain score≥4) necessitating the need for rescue analgesia. Pain (VAS≥4) was treated with intravenous tramadol 100 mg (Tramadol Hydrochloride 100 ml/2 ml; Minapharm Company, Minapharm Pharmaceutical, Heliopolis, Cairo, Egypt) as a rescue analgesic. Tramadol therapy was given by an anesthetist who was blinded to the study group. The total 24-h tramadol consumption was calculated.
- were asked to rate their satisfaction with the sedation/analgesia received using a seven-point Likert-like verbal rating scale , where 1 = extremely dissatisfied, 2 = dissatisfied, 3 = somewhat dissatisfied, 4 = undecided, 5 = somewhat satisfied, 6 = satisfied, and 7 = extremely satisfied. This assessment of patient satisfaction was carried out 6 h after leaving the PACU.
- adverse events including bradypnea (RR < 10 bpm), SpO 2 reaching 92% or less, bradycardia (HR < 45 bpm), hypotension (MAP < 55 mmHg), and chest pain were recorded. Baseline ECG was recorded preoperatively and then every 8 h postoperatively starting before PACU discharge. Any change in ECG from baseline that detected acute myocardial injury/ischemia (as elevation in the ST-segment of 1 mm or more in two specific leads, deep T-wave inversions, ST-segment depression, new left bundle branch block, posterior myocardial ischemia) was recorded and troponin I was administered to confirm myocardial ischemia.
A sample size of 42 patients (21 in each study group) was calculated to detect a 20% reduction in MAP with a power of 80% and an α-error of 5%. It was assumed that the study dropout rate would be ∼20%, and therefore a sample of 50 patients (25 in each study group) was recruited. Data were analyzed using the statistical package for social sciences (SPSS version 20; SPSS Inc., Chicago, Illinois, USA). Normality of quantitative data distribution was tested using the Shapiro-Wilk test. Normally distributed numerical data were presented as mean ± SD, percentages, and numbers as appropriate. Within-group and between-group differences were compared parametrically using one-way analysis of variance. The Scheffé post-hoc test was used for pairwise comparisons whenever the one-way analysis of variance revealed a significant difference. Nominal data were compared with the χ2 -test (with Yates correction if needed). All reported P values are two-tailed. A P value of less than 0.05 was considered significant.
| Results|| |
Fifty patients were included in the study. Two patients were excluded because of patient refusal to complete the study; technical difficulty was encountered in three patients in performing the block because of improper visualization of the plexus and another two patients had an incomplete block. Thus, a total of 43 patients having a successful block completed the study and were analyzed: 22 in group D and 21 in group P.
Both groups were comparable as regards demographic data, surgical duration, and type of operation [Table 1]. There was significant difference in the time required to achieve adequate sedation level. Targeted sedation was achieved within 19.20 ± 2.86 min in group D compared with 9.83 ± 1.64 min in group P (P < 0.001). Infusion time was statistically shorter in group D compared with group P [43.57 ± 14.50 vs. 59.52 ± 29.19 min, 95% confidence interval (CI) 3.15-28.76, respectively, P = 0.071] [Table 1]. Seven patients (32%) in group D required discontinuation of dexmedetomidine infusion before the end of surgery to maintain the BIS between 70 and 80 as well as an OAA/S of 4-3 compared with none in group P (P < 0.001) [Table 1].
|Table 1: Demodraghic data, surgical duration, time to achieve adequate sedation level, and drug infusion time|
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As regards cardiorespiratory parameters, MAP values during sedation were significantly reduced in both groups compared with baseline levels. During recovery, MAP values in group P were significantly elevated compared with group D [Figure 1].
HR values during sedation were significantly reduced in both groups compared with baseline levels. During sedation, HR values were significantly reduced in group D compared with group P, whereas during recovery HR values were significantly lower in group D compared with baseline levels and the levels of group P [Figure 2].
RR values during sedation were significantly lower than baseline levels in both groups. During recovery, RR values were significantly lower in group D compared with baseline values of dexmedetomidine and levels of group P [Figure 3].
All patients maintained clinically normal SpO 2 . Sedation causing respiratory depression and an SpO 2 of 92% or less was not encountered in either group [Figure 4].
The onset of motor and sensory block did not differ between the groups [Table 2]. The motor block lasted significantly longer in group D (6.02 ± 1.76 vs. 4.43 ± 1.58 h in group D and group P, respectively, 95% CI 2.59-0.602, P = 0.003). In addition, the duration of analgesia was significantly longer in group D compared with group P (11.81 ± 3.54 vs. 7.18 ± 3.21 h, 95% CI 6.60-2.67, P < 0.001) [Table 2]. The requirement for tramadol rescue analgesic in the postoperative period was significantly lower in group D; in the first 12 postoperative hours, six patients (27%) from group D compared with 17 patients (81%) from group P required rescue analgesia (P < 0.001) [Table 2]. Dexmedetomidine had a significantly lower VAS for pain compared with propofol in the first 6 h postoperatively [Table 3].
During recovery, patients who received dexmedetomidine had significantly higher levels of sedation compared with patients receiving propofol [Table 4]. There was no difference between the two groups in the time to achieve an Aldrete score of 9 or above [Table 4]. Time from stopping treatment infusion until discharge from the PACU was statistically longer in the dexmedetomidine group (46.57 ± 5.50 min) compared with the propofol group (29.19 ± 4.55 min) (P = 0.034).
Patient satisfaction revealed that sedation for the surgical procedure was equally satisfactory between the groups (P = 0.167) [Table 4].
Two patients in group P compared with three patients in group D had an incidence of hypotension (MAP < 55 mmHg) that necessitated the admission of ephedrine (P = 0.262) [Table 5]. Nausea, headache, and dry mouth occurred incidentally in both groups. Nevertheless, there were no episodes of bradycardia, bradypnea, or chest pain in either group [Table 5]. There were no ECG changes from preoperative baseline ECG in either group.
| Discussion|| |
Regional block has become a preferred option over GA. GA provokes a transient, but marked, sympathetic and sympathoadrenal response, resulting in hypertension, tachycardia, and arrhythmia . Transient hypertension and tachycardia are probably of no consequence in healthy individuals but may be hazardous to those with myocardial insufficiency . However, under regional anesthesia, the patient may be subjected to the stresses of the surgical procedure itself, which can have marked hemodynamic effects. This study examined the effect of dexmedetomidine at similar sedation levels with propofol on bupivacaine-induced supraclavicular brachial plexus block in IHD patients. Our findings demonstrated that dexmedetomidine maintained the cardiorespiratory parameters throughout surgery and during the recovery period in the PACU. Dexmedetomidine increases hemodynamic stability by altering the stress-induced sympathoadrenal response. In this study dexmedetomidine showed a significant decrease in HR and MAP throughout the operative and recovery period. This change was acceptable and desirable as no bradycardia was observed in any of the patients and hypotension was observed in three patients, which was comparable to the propofol group. Several studies have shown that dexmedetomidine can lead to bradycardia and hypotension ,,. Theoretically, excessive hypotension and bradycardia induced by dexmedetomidine can limit its use in patients with IHD, which may be even contraindicated especially in those receiving β-blocker therapy. Sulaiman et al.  and Menda et al.  showed that the incidence of hypotension in IHD patients receiving dexmedetomidine was not higher than that in the placebo group and none of their patients experienced bradycardia requiring treatment, which was comparable to our findings. The authors proposed that, with the β receptors already blocked, additional sympathetic block with dexmedetomidine did not appear to decrease the HR further ,,. This suggestion appears relevant to our study as well. It is recommended to administer dexmedetomidine over a minimum period of 10 min. A biphasic cardiovascular response has been described after rapid administration of dexmedetomidine resulting in transient increase in arterial blood pressure and reflex decrease in HR in young healthy patients . This response is due to α2B receptor stimulation located on the vascular smooth muscle, which mediates vasoconstriction. With this in mind, dexmedetomidine loading dose was infused over a period of 10 min in this study.
Respiratory endpoints were equivalent between treatment groups. All patients maintained clinically normal SpO 2 . Sedation causing respiratory depression and/or an arterial SpO 2 of 92% or less were not encountered in either group. Observational studies report incidents of respiratory depression (RR < 10 bpm and or SpO 2 ≤ 92%) during propofol infusion. However, in this study, patients receiving propofol did not encounter any incidence of respiratory depression. This maintenance of respiratory function may be related to the study design. Drugs were titrated to achieve a target sedation according to both BIS 70-80 and an OAA/S 4-3. Dexmedetomidine has not been associated with depressed respiratory parameters even with profound levels of sedation ,,.
Dexmedetomidine has a half-life of 2 h. Its persistent effects in the recovery room resulted in significantly more sedation when compared with the short-acting propofol. However, patients were easily aroused, and their duration of stay in the PACU was comparable to that of the propofol group. This is due to the characteristic ability of dexmedetomidine to achieve sedation but preserve patient arousability ,.
Our study showed that intravenous sedative doses of dexmedetomidine prolonged the duration of bupivacaine-induced supraclavicular brachial plexus block and the duration of analgesia. In addition, it reduced the analgesic requirements in the postoperative period. Rutkowska et al.  also demonstrated a prolonged brachial plexus block (motor and sensory block) with the administration of systemic dexmedetomidine, which was consistent with our study. Other studies demonstrated the same effect but with local administration of dexmedetomidine concomitantly with the local anesthetic ,,. Whether the effect of dexmedetomidine on bupivacaine-induced brachial plexus block is due to a local action or a systemic mode of action still needs further studies comparing both methods of administration. Dexmedetomidine is highly specific to α2 adrenoceptors, which are widely distributed in the central nervous system and peripheral tissues including the sympathetic nerve endings, neurons, vascular smooth muscles, and platelets . Several mechanisms of action have been suggested to explain the analgesic effect on regional block, and many studies have supported the direct effect of dexmedetomidine on peripheral nerve activity ,,. Butterworth et al.  demonstrated the direct action of the α2 agonist on Aα and C fibers of the rat sciatic nerve and that the effect of prolonged motor block can be explained by Aα fiber inhibition. Brummet et al.  made obvious that dexmedetomidine did not produce a sensory block, nor a sustained motor block, when administered alone for regional block; rather, it enhanced the motor and sensory block when combined with bupivacaine in a rat model of sciatic nerve blockade. Dalle et al.  reported another mechanism of the α2 agonist on nerve block independent of the stimulation of α2 adrenergic receptors. They concluded that α2 agonists enhance the activity-dependent hyperpolarization by inhibiting the hyperpolarization-activated cation current (I h ). The I h is widely distributed in excitable cells and plays an important key role in the regulation of cellular excitability and synaptic function, especially in the firing frequency in the central and peripheral nervous system . The I h current is activated during the hyperpolarization phase of an action potential and normally acts to reset a nerve for subsequent action potential. Therefore, by blocking this current, α2 agonists were found to enhance hyperpolarization and inhibit subsequent action potentials ,.
Another proposed mechanism of dexmedetomidine was the vasoconstrictive effect around the site of injection, resulting in delay in the absorption of the local anesthetic and a resultant prolongation of the local anesthetic effect . However, this was not the case in our study as dexmedetomidine was injected intravenously and the vasoconstrictive properties of dexmedetomidine were found to be weaker than those of epinephrine .
Studies suggest that the perioperative use of dexmedetomidine may result in a decreased risk for adverse cardiac events including myocardial ischemia . Our study showed no adverse cardiac events (no chest pain and no ECG changes from baseline records) in the two groups. a-Adrenoceptor stimulation can beneficially modulate coronary blood flow during myocardial ischemia by preventing transmural redistribution of blood flow away from the ischemic endocardium, by specific epicardial vasoconstriction effects leading to improvement in endocardial perfusion, and by decreasing the HR ,.
| Conclusion|| |
Intravenous sedative doses of dexmedetomidine prolong the analgesic effect of supraclavicular brachial plexus nerve block and maintain a stable cardiorespiratory status. These properties make it an ideal adjuvant particularly in patients with IHD.
| Acknowledgements|| |
Conflicts of interest
| References|| |
|1.||Asehnoune K, Albaladejo P, Smail N, Heriche C, Sitbon P, Gueneron JP, et al. Information and anaesthesia: what does the patient desire? Ann Fr Anesth Reanim 2000; 19:577-581. |
|2.||Akthar S. Ischemic heart disease. In: Hines RL, Marschall KE, editors. Stoelting′s anesthesia and co-existing disease. 5th ed. Philadelphia: Churchill Livingstone; 2008. p. 17. |
|3.||Macfarlane A, Brull R. Ultrasound guided supraclavicular block. J N Y Sch Reg Anesth 2009; 12:6-10. |
|4.||Claeys MA, Gepts E, Camu F. Haemodynamic changes during anaesthesia induced and maintained with propofol. Br J Anaesth 1988; 60:3-9. |
|5.||Leino K, Mildh L, Lertola K, Seppala T, Kirvela O. Time course of changes in breathing pattern in morphine- and oxycodone-induced respiratory depression. Anaesthesia 1999; 54:835-840. |
|6.||Hall JE, Uhrich TD, Barney JA, Arain SR, Ebert TJ Sedative, amnestic, and analgesic properties of small-dose dexmedetomidine infusions. Anesth Analg 2000; 90:699-705. |
|7.||Talke P, Chen R, Thomas B, Aggarwall A, Gottlieb A, Thorborg P, et al. The hemodynamic and adrenergic effects of perioperative dexmedetomidine infusion after vascular surgery. Anesth Analg 2000; 90:834-839. |
|8.||Chernik DA, Gillings D, Laine H, Hendler J, Silver JM, Davidson AB, et al. Validity and reliability of the Observer′s Assessment of Alertness/Sedation scale: study with intravenous midazolam. J Clin Psychopharmacol 1990; 10:244-251. |
|9.||Rutkowska K, Knapik P, Misiolek H. The effect of dexmedetomidine sedation on brachial plexus block in patients with end-stage renal disease. Eur J Anaesthesiol 2009; 26:851-855. |
|10.||Aldrete JA. The post anesthesia recovery score revisited [letter]. J Clin Anesth 1995; 7:89-91. |
|11.||Striener DL, Norman GR. Scaling responses. In: Striener DL, Norman GR, editors. Health measurement scales. A practical guide to their development and use. Oxford: Oxford University Press; 1995. p. 28-53. |
|12.||Sulaiman S, Karthekeyan RB, Vakamudi M, Sundar AS, Ravullapalli H, Gandham R. The effects of dexmedetomidine on attenuation of stress response to endotracheal intubation in patients undergoing elective off-pump coronary artery bypass grafting. Ann Card Anaesth 2012; 15:39-43. |
|13.||Menda F, Koner O, Sayin M, Ture H, Imer P, Aykac B. Dexmedetomidine as an adjunct to anesthetic induction to attenuate hemodynamic response to endotracheal intubation in patients undergoing fast-track CABG. Ann Card Anaesth 2010; 13:16-21. |
|14.||Jalonen J, Hynynen M, Kuitunen A, Heikkilä H, Perttilä J, Salmenperä M, et al. Dexmedetomidine as an anesthetic adjunct in coronary artery bypass grafting. Anesthesiology 1997; 86:331-345. |
|15.||Martin E, Ramsay G, Mantz J, Sum-Ping ST. The role of the alpha2-adrenoceptor agonist dexmedetomidine in postsurgical sedation in the intensive care unit. J Intensive Care Med 2003; 18:29-41. |
|16.||Yildiz M, Tavlan A, Tuncer S, Reisli R, Yosunkaya A, Otelcioglu S. Effect of dexmedetomidine on haemodynamic responses to laryngoscopy and intubation: perioperative haemodynamics and anaesthetic requirements. Drugs R D 2006; 7:43-52. |
|17.||Bloor BC, Ward DS, Belleville JP, Maze M. Effects of intravenous dexmedetomidine in humans. II. Hemodynamic changes. Anesthesiology 1992; 77:1134-1142. |
|18.||Ramsay MA, Luterman DL. Dexmedetomidine as a total intravenous anesthetic agent. Anesthesiology 2004; 101:787-790. |
|19.||Arain SR, Ebert TJ. The efficacy, side effects, and recovery characteristics of dexmedetomidine versus propofol when used for intraoperative sedation. Anesth Analg 2002; 95:461-466. |
|20.||Hall JE, Uhrich TD, Barney JA, Arain SR, Ebert TJ. Sedative, amnestic, and analgesic properties of small-dose dexmedetomidine infusions. Anesth Analg 2000; 90:699-705. |
|21.||El-Hennawy AM, Abd-Elwahab AM, Abd-Elmaksoud AM, El-Ozairy HS, Boulis SR. Addition of clonidine or dexmedetomidine to bupivacaine prolongs caudal analgesia in children. Br J Anaesth 2009; 103:268-274. |
|22.||Ammar AS, Mahmoud KM. Ultrasound-guided single injection infraclavicular brachial plexus block using bupivacaine alone or combined with dexmedetomidine for pain control in upper limb surgery: a prospective randomized controlled trial. Saudi J Anaesth 2012; 6:109-114. |
|23.||Saadawy I, Boker A, Elshahawy MA, Almazrooa A, Melibary S, Abdellatif AA, et al. Effect of dexmedetomidine on the characteristics of bupivacaine in a caudal block in pediatrics. Acta Anaesthesiol Scand 2009; 53:251-256. |
|24.||Yoshitomi T, Kohjitani A, Maeda S. Dexmedetomidine enhances the local anesthetic action of lidocaine via an α-2A adrenoceptor. Anesth Analg 2008; 107:96-101. |
|25.||Brummett CM, Norat MA, Lydic JM, Perineural R. Administration of dexmedetomidine in combination with bupivacaine enhances sensory and motor blockade in sciatic nerve block without inducing neurotoxicity in the rat. Anesthesiology 2008; 109:502-511. |
|26.||Butterworth JF V, Strichartz GR. The alpha 2-adrenergic agonists clonidine and guanfacine produce tonic and phasic block of conduction in rat sciatic nerve fibers. Anesth Analg 1993; 76:295-301. |
|27.||Gaumann DM, Brunet PC, Jirounek P. Clonidine enhances the effects of lidocaine on C-fiber action potential. Anesth Analg 1992; 74:719-725. |
|28.||Dalle C, Schneider M, Clergue F, Bretton C, Jirounek P. Inhibition of the I(h) current in isolated peripheral nerve: a novel mode of peripheral antinociception? Muscle Nerve 2001; 24:254-261. |
|29.||Brummett CM, Hong EK, Janda AM, Amodeo FS, Lydic R. Perineural dexmedetomidine added to ropivacaine for sciatic nerve block in rats prolongs the duration of analgesia by blocking the hyperpolarization-activated cation current. Anesthesiology 2011; 115:836-843. |
|30.||Gaumann D, Forster A, Griessen M, Habre W, Poinsot O, Della Santa D. Comparison between clonidine and epinephrine admixture to lidocaine in brachial plexus block. Anesth Analg 1992; 75:69-74. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]