The effects of clonidine on sensitivity to phenylephrine and nitroprusside in patients with essential hypertension recovering from surgery

Clonidine reduces postoperative circulatory instability in patients with essential hypertension. It also increases the sensitivity to vasopressors before and during anesthesia. We investigated blood pressure responses to phenylephrine and nitroprusside pre- vs postoperatively and the effect of clonidine on these responses in patients with essential hypertension. Twenty patients received clonidine 6 microg/kg orally 120 min before anesthesia and 3 microg/kg IV over the final hour of surgery or an identical placebo. During increasing bolus doses of phenylephrine and nitroprusside (30-300 microg), the maximal systolic pressure responses were recorded at baseline on the day before surgery, before the induction of anesthesia, and 1 and 3 h postoperatively. Sensitivity to phenylephrine and nitroprusside was interpolated from linear regression of the data. There was no difference between preoperative and postoperative sensitivity to phenylephrine or nitroprusside in either group. Clonidine increased sensitivity to phenylephrine versus placebo before and after surgery (response to dose of 1.5 microg/kg: 42+/-14 vs 27+/-8 mm Hg preinduction, 37+/-10 vs 26+/-8 mm Hg 3 h postoperatively; both P < 0.01), but not to nitroprusside (38+/-6 vs 37+/-10 mm Hg preinduction and 40+/-6 vs 39+/-8 mm Hg postoperatively). Clonidine increases the sensitivity to phenylephrine but not nitroprusside at baseline and postoperatively in hypertensive patients. IMPLICATIONS: Clonidine increases the sensitivity to bolus injections of the vasoconstrictor phenylephrine, but not the vasodilator sodium nitroprusside, before and after surgery in patients with preexisting hypertension. The doses of vasopressors should be reduced accordingly in hypertensive patients receiving perioperative clonidine.     

Does preoperative oral clonidine inhibit salivary secretion during general anesthesia?

Clonidine is known to inhibit salivary secretions and cause dryness of the mouth. We evaluated the effect of preoperative oral clonidine on salivary secretions before and during general anesthesia. Twenty-eight adult patients, equally divided into four groups, received the following premedication 2 hr prior to induction of anesthesia. Group 1 patients received oral ranitidine 5 mg.kg(-1) alone. Groups 2 and 3 patients received oral clonidine 1 microg.kg(-1) and 3 microg.kg(-1) respectively with oral ranitidine 5 mg.kg(-1). Group 4 patients received no premedication and served as control. The volume of salivary secretions was determined by calculating the change in weight of four cotton wool cylinders placed in the oral space 10 min before and 30, 60 and 120 min after induction of anesthesia. Salivary volume was significantly less in the clonidine treatment groups before induction of anesthesia. After induction of anesthesia, there were no significant differences in salivary secretions among the four groups. No severe hypotension or bradycardia was seen in any patient of four groups. Preoperative oral ranitidine 5 mg.kg(-1) had no effect on salivary secretion. In conclusion, clonidine did not decrease salivary secretions further over the already decreased level during general anesthesia.     

Clonidine Premedication Decreases Propofol Consumption During Bispectral Index (BIS) Monitored Propofol-Ketamine Technique for Office-Based Surgery

BACKGROUND: Propofol-ketamine anesthesia is a room air, spontaneous ventilation (RASV), dissociative intravenous (IV) sedation technique reported to have a near-zero postoperative nausea and vomiting (PONV) rate. Clonidine premedication has been reported to control blood pressure intra- and postoperatively, as well as to reduce the requirements for hypnotic agents. The bispectral index (BIS) monitor is a reproducible, objective, observer independent, quantitative measurement of the hypnotic state. OBJECTIVE: This study was designed to compare the propofol consumption rate during BIS monitored propofol-ketamine anesthesia for office-based, elective female facial rhytidectomy in patients with and without clonidine premedication. METHODS: Six patients receiving clonidine (200 microg oral premedication administered 30-60 minutes prior to induction of anesthesia were compared with a recent, historical control group of six patients who received no premedication. A BIS of 60-70 was chosen as the standard of comparison for light hypnotic state. A dilute propofol solution was used to gradually titrate anesthesia to a BIS of 60-70 prior to the administration of ketamine. RESULTS: A statistically significant reduction in propofol consumption was observed in the clonidine premedicated female elective rhytidectomy patients compared with those not receiving the clonidine. Other than modestly increased requirements for IV fluids, there were no adverse effects observed with clonidine premedication.     

Effects of oral clonidine premedication on the heart rate response to intravenous atropine during propofol anesthesia

BACKGROUND: Propofol induces suppression of the sympathetic nervous activity, and attenuates the heart rate responses to intravenous atropine. Similarly, clonidine suppresses the heart rate response to intravenous atropine under awake and enflurane-anesthetized patients. The purpose of this study is to evaluate effects of clonidine on the heart rate response to atropine under propofol anesthesia. METHODS: Thirty-two adults patients were randomly assigned to one of two groups. Clonidine group (n=16) patients received oral clonidine 5 microg x kg(-1) and famotidine 20 mg, and the control group (n=16) patients received oral famotidine alone 90 minutes before anesthesia. After tracheal intubation, anesthesia was maintained with propofol at the effect site concentration of 3 microg x ml(-1) in air and oxygen using the TCI system. All patients received incremental doses of IV atropine 5 microg x kg(-1) over 5 s at 2-min intervals until heart rate increased > 20 beats x min(-1) from baseline values or until atropine 40 microg x kg(-1) was given. RESULTS: Although heart rate response to atropine 5-25 microg kg(-1) was similar between the two groups, heart rate response to atropine 30 microg x kg(-1) in the clonidine group was smaller than that in the control group (P<0.05). When the atropine 40 microg x kg(-1) was administered, heart rate increased > 20 beats x min(-1) in all patients of the control group, but 62.5% of patients in the clonidine group (P< 0.05). CONCLUSIONS: Oral clonidine premedication attenuates the heart rate responses to IV atropine under propofol anesthesia.     

Hemodynamic responses induced by dopamine and dobutamine in anesthetized patients premedicated with clonidine.

To test the hypothesis that the pharmacological effects of dopamine (DOA) and dobutamine (DOB) are altered when there is inhibition of the release of norepinephrine from nerve endings, we examined the hemodynamic responses to DOA and DOB in anesthetized patients premedicated with oral clonidine. Seventy adult patients were assigned to one of two groups (oral premedication with clonidine 5 microg/kg or no premedication). After the induction of general anesthesia, heart rate and systemic blood pressure (BP) were measured for 10 min after each of five IV infusions (3 and 5 microg x kg(-1) x min(-1) of DOA; 0.5, 1, and 3 microg x kg(-1) x min(-1) of DOB) in a randomized, double-blind manner. In patients given clonidine, the mean BP increases induced by DOA 5 microg x kg(-1) x min(-1) were significantly attenuated (P < 0.01), whereas the mean BP increases induced by DOB-0.5, 1, or 3 microg x kg(-l) x min(-1) were significantly enhanced (P < 0.01 or 0.05). The heart rate responses to DOA and DOB did not differ between patients with or without clonidine. Premedication with clonidine alters the effects on BP to both DOA and DOB. When small doses of DOA or DOB are used in clonidine-premedicated patients, differences of pharmacological profiles need to be considered for perioperative management. IMPLICATIONS: Our randomized, double-blind study suggests that premedication with clonidine may enhance the effect on blood pressure response to a small dose of dobutamine (direct-acting) and attenuate that to a small dose of dopamine (mixed direct-and indirect-acting) in patients anesthetized with fentanyl and nitrous oxide.     

The interaction between propofol and clonidine for loss of consciousness

Clonidine premedication reduces the intraoperative requirement for opioids and volatile anesthetics. Clonidine also reduces the induction dose of IV anesthetics. There is no information, however, regarding the effect of oral clonidine premedication on the propofol blood concentrations required for loss of consciousness, and the interaction between propofol and clonidine. We randomly administered target effect-site concentrations of propofol ranging from 0.5 to 5. 0 microg/mL by using computer-assisted target-controlled infusion to 3 groups of healthy male patients: Control (n = 35), 2.5 microg/kg Clonidine (n = 36), and 5.0 microg/kg Clonidine (n = 36) groups. Nothing was administered to the Control group. Clonidine (2.5 or 5.0 microg/kg) was administered orally 90 min before the induction of anesthesia in the Clonidine groups. After equilibration between the blood and effect-site for 15 min, a verbal command to open their eyes was given two times to the patients. Arterial blood samples for analysis of the serum propofol and clonidine concentrations were taken immediately before verbal commands were given. Measured serum propofol concentrations in equilibrium with the effect-site at which 50% of the patients did not respond to verbal commands (EC50 for loss of consciousness) were determined by logistic regression. The EC50 +/- SE values in the Control, 2.5 microg/kg Clonidine, and 5.0 microg/kg Clonidine groups were 2.67 +/- 0.18, 1.31 +/- 0.12, and 0.91 +/- 0.13 microg/mL, respectively. The EC50 in the 2.5 and 5.0 microg/kg clonidine groups was significantly smaller than that in the Control group (P < 0.001). The use of a response surface modeling analysis indicated that there was an additive interaction between measured arterial propofol and clonidine concentrations in relation to loss of consciousness. These results indicate that propofol and clonidine act additively for loss of consciousness. IMPLICATIONS: Oral clonidine 2.5 and 5.0 microg/kg premedication decreases the propofol concentration required for loss of consciousness.     

Oral clonidine premedication enhances postoperative analgesia by epidural morphine

This study was designed to evaluate the effects of oral clonidine premedication on postoperative analgesia by epidural morphine in a prospective, randomized, double-blinded design. Sixty consenting patients, scheduled for total abdominal hysterectomy, were randomly assigned to one of three groups (n = 20 each); the clonidine-morphine group received oral clonidine 5 microg/kg 90 min before arriving in the operating room and epidural morphine 2 mg before induction of general anesthesia, the clonidine-placebo group received oral clonidine 5 microg/kg and no epidural morphine, and the placebo-morphine group received no clonidine and epidural morphine 2 mg. An epidural catheter was placed at the L1-2 or L2-3 interspace, and 1.5% lidocaine was used for surgical anesthesia in all patients. General anesthesia was then induced with propofol, and maintained with a continuous infusion of propofol and 67% nitrous oxide in oxygen during surgery. Four patients were subsequently withdrawn from the study. After surgery, patient-controlled analgesia using IV morphine was used to assess analgesic requirement. Morphine consumptions determined every 6 h after surgery in the clonidine-morphine and placebo-morphine groups were significantly less than the clonidine-placebo group until 12 h after surgery, whereas those of the clonidine-morphine group were significantly less than the placebo-morphine group from 13 to 42 h after surgery. Visual analog (pain) scale (VAS) scores in the clonidine-morphine group were significantly lower than the placebo-morphine group at 48 h at rest, and at 1, 24, 36, and 48 h with movement. Similarly, VAS scores in the clonidine-morphine group were significantly lower than the clonidine-placebo group at 1 and 6 h both at rest and with movement, whereas VAS scores in the clonidine-placebo group were significantly lower than the placebo-morphine group at 24, 36, and 48 h at rest and with movement. The incidence of nausea and pruritus was similar between groups. We conclude that the combination of oral clonidine and epidural morphine produces more potent and longer lasting postoperative analgesia than either drug alone without increasing the incidence of adverse effects after major gynecologic surgeries. IMPLICATIONS: A small dose of epidural morphine is often used for postoperative analgesia. We found that oral clonidine premedication 5 microg/kg improves the analgesic efficacy of epidural morphine without increasing the incidence of adverse side effects.     

Clonidine decreases stress response in patients undergoing carotid endarterectomy under regional anesthesia: a prospective, randomized, double-blinded, placebo-controlled study

Inadequate analgesia or anxiety may induce an increased stress response in patients undergoing carotid endarterectomy (CEA) under regional anesthesia (RA). Central alpha2 adrenoceptor agonists have significant sedative and analgesic properties, which may attenuate sympathoadrenal activation during CEA and improve the quality of RA. We randomly assigned 80 patients to 2 groups receiving either RA plus placebo (n = 40) or RA plus clonidine 1 microg/kg as the initial loading dose followed by 1 microg.kg(-1).h(-1) (n = 40). RA was performed as combined deep and superficial cervical plexus blockade. Hemodynamic and neurological variables were assessed before, during, and after CEA. Arterial blood samples were collected at defined time points for the determination of plasma concentrations of epinephrine, norepinephrine, cortisol, and creatinine kinase and creatinine kinase-MB. Throughout the study, all patients responded easily to neurological evaluations. Before and during clamping mean arterial blood pressure and heart rate were not different between the groups, but mean arterial blood pressure was lower in the clonidine group (P < 0.01) at skin closure and postoperatively in the intensive care unit. In the placebo group, cortisol, epinephrine, and norepinephrine plasma concentrations were increased significantly (P < 0.05) and more patients required antihypertensive treatment (P < 0.01). Postoperatively the incidence of hypertension (P < 0.001) and development of neurological deficits (P < 0.05) was significantly decreased in the clonidine group. We conclude that 1 microg.kg(-1).h(-1) clonidine suppresses the hyperadrenergic response to CEA without adverse effects on hemodynamics or clinical neurological monitoring.     

The incidence of complex regional pain syndrome after fasciectomy for Dupuytren's contracture: a prospective observational study of four anesthetic techniques

The development of complex regional pain syndrome (CRPS) is not an uncommon complication after Dupuytren's surgery. Despite increasing research interest, little is known regarding which patients are at increased risk for developing CRPS and what is the optimal perioperative treatment strategy for preventing the occurrence of this disease after surgery. We prospectively evaluated the use of four anesthetic techniques (general anesthesia, axillary block, and IV regional anesthesia [IVRA] with lidocaine with or without clonidine) for patients undergoing fasciectomy for Dupuytren's contracture. All patients were followed in the Pain Management Center at 1, 3, and 12 mo postoperatively by a blinded physician to evaluate the presence of CRPS. Significantly (P < 0.01) more patients developed postoperative CRPS in the general anesthesia group (n = 25; 24%) and the IVRA lidocaine group (n = 12; 25%) compared with either the axillary block group (n = 5; 5%) or the IVRA lidocaine and clonidine group (n = 3; 6%). We conclude that axillary block or IVRA with clonidine offers a significant advantage for decreasing the incidence of CRPS compared with either IVRA with lidocaine alone or general anesthesia for patients undergoing Dupuytren's surgery.     

Intravenous but not perineural clonidine prolongs postoperative analgesia after psoas compartment block with 0.5% levobupivacaine for hip fracture surgery

We evaluated the systemic and local effects of clonidine as an analgesic adjunct to psoas compartment block (PCB) with levobupivacaine. In a randomized, prospective, double-blind trial, 36 patients requiring hip fracture surgery received PCB and general anesthesia. Patients were randomized into three groups. Each patient received PCB with 0.4 mL/kg of levobupivacaine 0.5%. The control group (group L) received IV saline, the systemic clonidine group (group IC) received IV clonidine 1 mug/kg, and the peripheral clonidine group (group C) received IV saline and PCB with clonidine 1 microg/kg. The interval from time of completion of block injection to first supplementary analgesic administration was longer in group IC compared with group L (mean +/- sd, 13.4 +/- 6.1 versus 7.3 +/- 3.6 h; P = 0.03). There was no difference between group C and group L (10.3 +/- 5.9 versus 7.3 +/- 3.6 h; P > 0.05). The groups were similar in terms of 24 h cumulative morphine and acetaminophen consumption. There were no significant differences among groups regarding postoperative adverse effects (bradycardia, hypotension, sedation, and nausea). We conclude that IV but not perineural clonidine (1 microg/kg) prolongs analgesia after PCB without increasing the incidence of adverse effects.     

Supplemental oxygen after outpatient oral and maxillofacial surgery.

Arterial oxygen saturation (SpO2) was monitored postoperatively with pulse oximetry in 72 dental patients. Intravenous general anesthesia was employed in 57 patients. All of these patients received supplemental oxygen intraoperatively, and of these, 29 received supplemental oxygen postoperatively. Fifteen patients received only local anesthesia without supplemental oxygen and served as the control group. Continuous pulse oximetry revealed 43 episodes of arterial oxygen desaturation (SpO2 decreases greater than 3% from baseline) in patients who did not receive postanesthesia supplemental oxygen and eight episodes of desaturation in patients who did receive postanesthesia oxygen. Patients with a smoking history had more episodes of desaturation than did nonsmokers in the group that received general anesthesia and breathed room air postoperatively. The total amount of methohexital administered had no significant effect on the number of patients with desaturation episodes. These observations emphasize the need for postoperative oxygen for patients who undergo general anesthesia for outpatient oral and maxillofacial surgery.     

The awakening concentration of sevoflurane in children

Sevoflurane is frequently used as a rapidly acting drug for the induction of anesthesia. We investigated the awakening concentration (MAC-awake) of sevoflurane in ASA physical status I children (age range 2-10 yr). We also investigated the effects of two different doses of clonidine (2 and 4 microg/kg) on the MAC-awake of sevoflurane. Subjects were randomly divided into three groups and received placebo (n = 24), clonidine 2 microg/kg (n = 17), or clonidine 4 microg/kg (n = 22) orally, 100 min before the induction of anesthesia. Sedation scores were estimated, by using a five-point scale, after entry into the operating room, and anesthesia was induced and maintained with sevoflurane in oxygen and balanced nitrogen, without an additional anesthetic. After surgery, end-tidal sevoflurane was decreased stepwise by 0.2% at 15-min intervals, a standardized verbal command was played to the patients, and the MAC-awake was determined. The MAC-awake of sevoflurane alone was 0. 78% +/- 0.24% (mean +/- SD), which decreased to 0.36% +/- 0.09% and 0.36% +/- 0.16% (both P <0.0001, compared with the control group) after premedication with the small and large doses of clonidine, respectively. The lack of any dose-response relationship might be explained by a plateau effect. Implications: The awakening concentration of sevoflurane in unpremedicated children was 0.78%. Oral clonidine premedication at a dose of 2 microg/kg reduced the awakening concentration to 0.36%. However, an additional decrease in this value was not observed after the administration of the larger dose of clonidine premedication (4 microg/kg).     

The effect of spinal bupivacaine in combination with either epidural clonidine and/or 0.5% bupivacaine administered at the incision site on postoperative outcome in patients undergoing lumbar laminectomy

Spinal anesthesia has numerous advantages over general anesthesia for patients undergoing lumbar laminectomy and microdisk surgery. In this study, we evaluated the addition of epidural clonidine and/or bupivacaine, injected at the incision site, on postoperative outcome variables in patients undergoing lower spine procedures using spinal anesthesia. One hundred twenty patients having lumbar spine surgery received bupivacaine spinal anesthesia supplemented by 150 microg of epidural clonidine with or without incisional bupivacaine, epidural placebo plus incisional bupivacaine, or placebo with incisional saline. Demographic data, intraoperative hemodynamics, blood loss, pain, nausea, urinary retention, hospital discharge, and other variables were compared by using either analysis of variance or chi(2) analysis. Demographics were similar. IV fluids, blood loss, incidence of intraoperative bradycardia, and hypotension were not different among groups. Postanesthesia care unit pain scores were lower and demand for analgesics was less in patients who received both the clonidine and subcutaneous bupivacaine. Patients who received epidural clonidine also had improved postoperative hemodynamics. Hospital discharge, urinary retention, and other variables were not different. We conclude that epidural clonidine as a supplement to spinal anesthesia produced no perioperative complications and improved postoperative pain and hemodynamic stability in patients undergoing lower spine procedures. IMPLICATIONS: Spinal anesthesia with supplemental epidural clonidine in combination with incision site subcutaneous bupivacaine was evaluated both intra- and postoperatively and compared with spinal anesthesia alone for lower lumbar spine procedures. Both epidural clonidine and subcutaneous incisional bupivacaine, added to spinal anesthesia for lumbar spine surgery, improves pain relief and reduces the need for postoperative opioids with their associated side effects.     

Oral clonidine premedication reduces propofol requirement for laryngeal mask airway insertion

PURPOSE: To determine the effect of oral clonidine premedication on propofol requirement (ED(50)) for the insertion of the laryngeal mask airway (LMA) in healthy patients undergoing abdominal hysterectomy. METHODS: After ethics committee approval and informed consent, 41 patients were randomly assigned to receive 5 microg x kg(-1) clonidine po premedication 90 min before entering the operating room (n = 22), or no clonidine (n = 19). To alleviate pain associated with iv propofol, 3 ml lidocaine 2%iv were administered. General anesthesia was induced, 30 sec later, with propofol at a rate of 100 mg x min(-1) (600 ml x hr(-1)) iv. The dose of propofol at which insertion of the LMA was attempted was predetermined by modification of Dixon's up-and-down method with an initial dose of 2.5 mg x kg(-1) and 0.25 mg x kg(-1) as the step size. An LMA was inserted, without muscle relaxants or other adjuvants 90 sec after completion of the propofol injection, by an anesthesiologist blinded to the treatment of the patient. RESULTS: The ED(50) of propofol for LMA insertion in clonidine-treated patients (2.0 +/- 0.2 mg x kg(-1), 1.8-2.3 mg x kg(-1) [95% confidence interval]), was less than that in patients without clonidine (2.5 +/- 0.1 mg x kg(-1), 2.4-2.6 mg x kg(-1), P < 0.01). CONCLUSION: Oral clonidine premedication reduces propofol requirement for LMA insertion.     

Pharmacodynamics of pentamorphone during coronary artery bypass grafting in humans.

Pentamorphone is a new, highly potent opioid reported to have minimal cardiovascular effects in humans and a high therapeutic index in animals. Pentamorphone was injected intravenously (IV) as the sole anesthetic in 10 patients with left ventricular ejection fractions greater than 0.35 who were undergoing elective coronary artery bypass grafting (CABG). After premedication with lorazepam, 40 micrograms/kg, and establishment of hemodynamic monitoring, pentamorphone was infused at a rate of 2 micrograms/kg/min until unconsciousness occurred (5.1 +/- 1.6 micrograms/kg). Anesthetic induction was accompanied by an average 30% decrease in systolic, diastolic, and mean arterial pressure (MAP), a 19% decrease in heart rate (HR), but no change in cardiac output (CO) or pulmonary artery occlusion pressure. Five patients had a MAP less than 60 mm Hg after induction. Following incision, blood pressure, pulmonary artery occlusion pressure, and CO were unchanged from baseline but HR remained significantly lower. Despite additional pentamorphone (total dose 9.6 +/- 1.8 micrograms/kg), 6 patients required thiopental and/or enflurane to control hypertension intraoperatively. When pentamorphone is used as the sole IV anesthetic in lorazepam-premedicated patients with normal or mildly impaired ventricular function, there is a high incidence of hypotension during induction, and poor control of hemodynamic responses to stimulation. Pentamorphone, 10 micrograms/kg, does not seem to offer any significant advantage over opioids currently used for anesthesia in patients undergoing CABG.     

Prophylactic effects of systemic oral ephedrine in spinal anesthesia-induced hypotension during transurethral prostatectomy

OBJECTIVE: We investigated the prophylactic effects of systemic oral ephedrine in spinal anesthesia-induced hypotension during transurethral prostatectomy. MATERIAL AND METHODS: Sixty American Society of Anesthesiologists Grade II and III patients scheduled for spinal anesthesia were randomized into one of two groups. Patients in Group I (n = 30) received oral ephedrine 50 mg in addition to premedication whilst those in Group II (n = 30) received only premedication 30 min before spinal anesthesia. Pre-infusion values were measured in order to obtain baseline readings after oral ephedrine administration in Group I and after premedication in Group II. Systolic arterial pressure (SAP) and heart rate (HR) were recorded before and after infusion, during and 5 min after spinal anesthesia and intraoperatively. Hypotension was defined as SAP <100 mmHg and <20% of baseline value. Hypotension was treated with 3 mg ephedrine and bradycardia was corrected with atropine 0.5 mg, given as an i.v. bolus. RESULTS: SAP values were significantly lower in Group II during the spinal anesthesia, post-spinal and intraoperative periods (p < 0.0001). Fifteen patients received ephedrine in Group II and seven in Group I. Supplemental ephedrine was used at doses of 3.42 +/- 0.97 mg in Group I and 8.86 +/- 1.24 mg in Group II. The incidence of hypotension was halved in Group I compared to Group II (23.33% vs 50%, p = 0.003). Six patients received atropine in Group II because of severe bradycardia. Mean HR values were lower in Group II than Group I during the spinal anesthesia, post-spinal and intraoperative periods. CONCLUSIONS: We conclude that a prophylactic oral dose of ephedrine 50 mg is effective for minimizing and managing spinal anesthesia-induced hypotension during transurethral prostatectomy.     

Effects of Oral Clonidine on Heart Rate Changes after Neostigmine-Atropine Administration

Background: Clonidine reduces heart rate (HR) responses to atropine, whereas neostigmine causes bradycardia. This study was designed to determine whether clonidine premedication would reduce tachycardia after neostigmine-atropine administration.

Methods: Fifty adult patients without cardiovascular disorders who were schedule for elective surgeries were randomly assigned to receive approximately 5 [micro sign]g/kg (oral clonidine clonidine group, n = 25) or no clonidine (control group, n = 25) 90 min before induction of general anesthesia. After tracheal intubation, anesthesia was maintained with N2 O and 1-2% isoflurane in oxygen while patients were paralyzed with vecuronium and mechanically ventilated. When surgeries were completed, adequate spontaneous respiration, responses to verbal commands, and sustained tetanus by stimulating the ulnar nerve were confirmed, and patients' tracheas were extubated. Then a mixture of 0.05 mg/kg neostigmine and 0.02 mg/kg atropine was administered intravenously over 20 s under stable hemodynamic condition (systolic blood pressure and HR within +/- 5% of preceding values), and blood pressure and HR were measured noninvasively at 1-min intervals for 10 min.

Results: Increases in HR in the clonidine group were significantly less 1-4 min after neostigmine-atropine injections compared with HR values in the control group. A maximum increase in HR of the clonidine group was also significantly less than the control group (15 +/- 7 vs. 23 +/- 10 beats/min; means +/- SD), whereas absolute values of mean blood pressure were similar. Severe bradycardia (HR < 50 beats/min) developed in no patients in either group.     

The reduction in minimum alveolar concentration for tracheal extubation after clonidine premedication in children

The effects of clonidine on minimum alveolar concentration for tracheal extubation (MAC-ex) have not been elucidated. Clonidine may lead to prolonged emergence from anesthesia. We investigated the effects of oral clonidine premedication on MAC-ex and examined the emergence properties of sevoflurane in children. Sixty ASA physical status I pediatric patients, aged from 2 to 9 yr, were randomly divided into one of three groups and received placebo, clonidine 2 microg/kg, or clonidine 4 microg/kg (n = 20 each) orally, 100 min before the induction of anesthesia. The induction of anesthesia, tracheal intubation, and maintenance of anesthesia were performed with sevoflurane in air and oxygen. MAC-ex was defined according to the modification of Dixon's up-and-down method, with 0.25% as a step size. In addition, in the Control and 4 microg/kg groups, the time from tracheal extubation to spontaneous eye opening (eye-opening time) and the time from tracheal extubation to leaving the operating room (awakening time) were recorded. MAC-ex for sevoflurane (mean +/- SD) was 1.63% +/- 0.13%, 1.04% +/- 0.26%, and 0.66% +/- 0.09% respectively in the Control group, 2 microg/kg group, and 4 microg/kg group. Significant differences were observed among the three groups. The eye-opening times were 5.7 +/- 3.5 min in the Control group and 5.1 +/- 1.0 min in the 4 microg/kg group. The awakening times were 9.7 +/- 3.7 min in the Control group and 9.2 +/- 3.8 min in the 4 microg/kg group. No significant differences were observed among the groups. IMPLICATIONS: Oral clonidine premedication decreased MAC for tracheal extubation for sevoflurane dose dependency and did not prolong emergence from anesthesia.     

Preoperative and Postoperative Use of Clonidine with Neurolept Anaesthesia

The abrupt cessation of clonidine therapy can induce a withdrawal syndrome. This may also appear immediately after anaesthesia if clonidine medication is discontinued during the operation day. We studied (1) whether the withdrawal syndrome occurs postoperatively as often as otherwise when clonidine therapy is discontinued, and (2) the action of this clonidine withdrawal on the circulation as compared to patients who received clonidine without interruption during the operation day. During the recovery period in 2 out of 10 patients in whom clonidine medication was discontinued, a hypertensive crisis occurred, which was relieved by clonidine readministration. Clonidine given with premedication eliminated high rises in blood pressure during anaesthesia. During the recovery period, the regular intramuscular administration of the same dose of clonidine as the patients had used orally decreased blood pressure to almost normotensive levels. The slightly increased urinary catecholamine excretion and plasma renin activity in these patients might, however, indicate that the circulatory homeostasis was disturbed in some degree. The results suggest that it is important to give clonidine continuously, even during the operation day. The dose may be the same as, or preferably somewhat smaller than that which the patients have previously received orally.     

Clonidine prevents sevoflurane-induced agitation in children

In a double-blinded trial, 40 male children (age 2-7 yr) undergoing circumcision were randomly assigned to receive clonidine 2 microg/kg IV or placebo after anesthetic induction. For induction and maintenance of anesthesia, we used sevoflurane as the sole anesthetic. For pain treatment, a penile block was performed before surgery. After surgery the incidence and severity of agitation was measured during an observation period of 2 h. Severe agitation was treated with midazolam. In 16 placebo and 2 clonidine-treated patients agitation was observed (P < 0.001). In 6 patients of the Placebo group, agitation was graded as severe, whereas none of the patients in the Clonidine group developed severe agitation (P = 0.02). During the postoperative period heart rate and blood pressure were significantly decreased in clonidine treated patients (P < 0.05). We conclude that clonidine effectively prevents agitation after sevoflurane anesthesia. IMPLICATIONS: The recovery from sevoflurane anesthesia may be complicated by the presence of agitation in pediatric patients. Clonidine 2 microg/kg IV after anesthetic induction effectively reduces the incidence of agitation without resulting in clinically relevant bradycardia and hypotension.