Intravenous clonidine infusion in critically ill children: dose-dependent sedative effects and cardiovascular stability.
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Clonidine is used for analgesia and sedation in paediatric anaesthesia, but there are no data on its sedative properties and side effects in critically ill children. We studied 30 ventilated children aged 10 yr and under to determine an effective i.v. dosing range and to assess its cardiovascular effects. Twenty non-paralysed, ventilated children were given a background infusion of midazolam 50 micrograms kg-1 h-1 combined with a variable clonidine infusion (0.1-2 micrograms kg-1 h-1) to maintain optimal sedation. The effects of clonidine 1 microgram kg-1 h-1 on cardiac index were measured in 10 postoperative cardiac patients using a reverse Fick method. Dose-dependent sedation was achievable (713 out of 861 h) without cardiovascular side effects, but an infusion limit of clonidine 1 microgram kg-1 h-1 was inadequate in two patients. An increased dose limit of 2 micrograms kg-1 h-1 combined with midazolam 50 micrograms kg-1 h-1 achieved satisfactory sedation scores for 602 out of a total of 672 h studied with no failures. Clonidine in combination with midazolam at 1 microgram kg-1 h-1 was not associated with significant changes in heart rate arterial pressure or cardiac index. (+info)
The effects of increasing plasma concentrations of dexmedetomidine in humans.
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BACKGROUND: This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. METHODS: Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml). RESULTS: The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged. CONCLUSIONS: Increasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed. (+info)
BACKGROUND: The objective was to investigate the effects of propofol anesthesia on the pulmonary vascular response to endothelium-dependent and -independent vasodilators, compared with the responses measured in the conscious state. METHODS: Twenty-six conditioned, male, mongrel dogs were instrumented long-term to measure the left pulmonary vascular pressure-flow relation. Pressure-flow plots were measured on separate days in conscious and propofol-anesthetized (5.0 mg/kg plus 0.5 mg. kg-1. min-1 intravenously) dogs at baseline, after preconstriction with the thromboxane mimetic U46619, and during the cumulative intravenous administration of endothelium-dependent (acetylcholine and bradykinin) and -independent (proline-nitric oxide) vasodilators. RESULTS: Propofol had no effect on the baseline pressure-flow relation compared with the conscious state. A lower (P < 0.05) dose of U46619 was necessary to achieve the same degree of preconstriction during propofol anesthesia. The pulmonary vasodilator responses to bradykinin and proline-nitric oxide were similar in the conscious and propofol-anesthetized states. In contrast, the pulmonary vasodilator response to acetylcholine was markedly attenuated (P < 0.01) during propofol anesthesia. The intralipid vehicle for propofol had no effect on the acetylcholine dose-response relation. CONCLUSION: These results suggest that propofol causes a specific defect in the signal transduction pathway for acetylcholine-induced pulmonary vasodilation. This defect involves the endothelial and not the vascular smooth muscle component of the response. (+info)
Sedation with propofol plus midazolam versus propofol alone for interventional endoscopic procedures: a prospective, randomized study.
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AIM: Adequate patient sedation is mandatory for most interventional endoscopic procedures. Recent anaesthesiologic studies indicates that propofol and midazolam act synergistically in combination and therefore may be superior to sedation with propofol alone in terms of sedation efficacy, recovery and costs (due to a presumed lower total dose of propofol needed). METHODS: A total of 239 consecutive patients undergoing therapeutic EGD or ERCP (EGD/ERCP-ratio, 1:1) randomly received either propofol alone (n=120, group A, loading dose 40-60 mg intravenously, followed by repeated doses of 20 mg) or propofol plus midazolam (n=119, group B, initial midazolam dose of 2. 5-3.5 mg intravenously, followed by repeated doses of 20 mg of propofol) for sedation. Vital signs (heart rate, blood pressure, oxygen saturation, electrocardiogram) were continuously monitored. Procedure-related parameters, the recovery time and quality (post-anaesthesia recovery score) as well as the patient's co-operation and tolerance to the procedure (visual analogue scale) were prospectively assessed. RESULTS: Patients of group A and B were well matched with respect to demographic and clinical data, endoscopic findings, and the type of associated procedures. In group A, a mean dose of 0.25 +/- 0.13 mg.min/kg propofol was used compared to 0.20 +/- 0.09 mg.min/kg of propofol in group B (P < 0.01, plus additional 2.9 +/- 0.5 mg of midazolam). Clinically relevant changes in vital signs were observed at comparable frequencies with a lowering of the systolic blood pressure < 90 mmHg in six out of 119 patients in group B and one out of 120 patients in group A (P=0.07). The sedation efficacy was rated similarly in both groups, whereas the mean recovery time (group A, 19 +/- 7 min vs. group B, 25 +/- 8 min, P < 0.05) as well as the recovery score (post-anaesthesia recovery score group A, 8.0 +/- 1.1 vs. post-anaesthesia recovery score group B, 7.3 +/- 1.2, P < 0.001) were significantly better with propofol alone than with propofol plus midazolam. CONCLUSION: During therapeutic endoscopy, sedation with propofol and midazolam requires a lower total dose of propofol, but otherwise has no superior sedation efficacy and is associated with a slower post-procedure recovery than sedation with propofol alone. (+info)
Safety of patient-maintained propofol sedation using a target-controlled system in healthy volunteers.
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We investigated the safety of a patient-maintained system that allows individuals to operate a target-controlled infusion of propofol to achieve sedation. Ten healthy volunteers were recruited and instructed to try to anaesthetize themselves with the system. A target-controlled infusion of propofol was set to deliver a target propofol concentration of 1 microgram ml-1, and the subjects allowed to increase the target in increments of 0.2 microgram ml-1 by pressing a control button twice in 1 s. There was a lockout time of 2 min and a maximum permitted target concentration of 3 micrograms ml-1. Heart rate and pulse oximetry oxygen saturation (SpO2) were monitored continuously, and non-invasive arterial pressure, ventilatory frequencies and sedation scores were measured every 5 min. Sedation was continued until the subject stopped pressing the button. A keyword was then read for the individual to remember and sedation discontinued. There were no instances of significant decrease of SpO2 or loss of airway control. Maximum target blood concentration of propofol recorded ranged from 1.4 to 3 micrograms ml-1. Two subjects became oversedated, one of whom was unrousable with loss of eyelash reflex. No subject could recall the keyword, although one recognized it from a list of 10 words. We conclude that the patient-maintained sedation system described could not be guaranteed to produce only conscious sedation in all patients, and that close clinical supervision by an anaesthetist would still be required for safe operation. (+info)
Recollection of children following intensive care.
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BACKGROUND AND AIMS: The recollections of critically ill children following discharge from the paediatric intensive care unit (PICU) have not previously been described. We have interviewed such children to establish the nature of their recollections. METHODS: Children aged 4 years and above were interviewed following discharge from the PICU at the Queens Medical Centre, Nottingham, either in hospital or at home, using a semistructured interview. Their recollections were recorded and interpreted by content analysis. RESULTS: A total of 38 interviews were carried out; 44 specific recollections were reported, the majority being neutral (60%) or positive (25%). Only 15% of recollections were negative. Negative recollections related to aspects of medical care and environmental factors. No child treated with neuromuscular blocking agents remembered any period of therapeutic paralysis. CONCLUSIONS: Children's recollections of PICU are mainly neutral or positive. Mechanically ventilated children sedated with midazolam and morphine remember little of endotracheal intubation. (+info)
Reevaluation of rectal ketamine premedication in children: comparison with rectal midazolam.
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BACKGROUND: Results of previous studies of rectal ketamine as a pediatric premedication are clouded because of lack of dose-response relation, inappropriate time of assessing sedative effects, and previous administration or coadministration of benzodiazepines. Therefore, the authors reevaluated the efficacy of rectally administered ketamine in comparison with 1 mg/kg rectal midazolam. METHODS: Sixty-six infants and children (age, 7-61 months) who were American Society of Anesthesiologists physical status I and who were undergoing minor surgeries as in-patients were randomized to receive 5 mg/kg ketamine (n = 16), 7 mg/kg ketamine (n = 16), 10 mg/kg ketamine (n = 17), or 1 mg/kg midazolam (n = 17) via rectum. A blinded observer scored sedation 45 min and 15 min after administration of ketamine and midazolam, respectively, when children were separated from parent(s) for inhalational induction. All children underwent standardized general anesthesia with sevoflurane, nitrous oxide, and oxygen with endotracheal intubation. Blood pressure, heart rate, and oxyhemoglobin saturation were determined before, during, and after anesthesia. Postoperative recovery characteristics and incidence of adverse reactions were also assessed. RESULTS: Most children (88%) who received rectally 10 mg/kg ketamine or 1 mg/kg midazolam separated easily from their parents compared with those (31%) who received 7 or 5 mg/kg rectal ketamine (P < 0.05). Similarly, more children who received 10 mg/kg ketamine or 1 mg/kg midazolam underwent mask induction without struggling or crying compared with those who received 7 or 5 mg/kg ketamine (P < 0.05). There were no clinically significant changes in blood pressure, heart rate, and oxyhemoglobin saturation after administration of either drug. Immediately after surgery, more children receiving midazolam or 5 mg/kg ketamine were agitated compared with 7 or 10 mg/kg ketamine. Ketamine, 7 and 10 mg/kg, provided postoperative analgesia, but the largest dose of ketamine was associated with delayed emergence from general anesthesia. CONCLUSIONS: The results indicate that rectally administered ketamine alone produces dose-dependent sedative effects in children, when evaluated at its predicted peak plasma concentration. Ketamine, 10 mg/kg, has a delayed onset but is as effective as 1 mg/kg midazolam for sedating healthy children before general anesthesia. However, 10 mg/kg rectal ketamine is not recommended for brief surgeries because of prolonged postoperative sedation. (+info)
Respiratory effects of dexmedetomidine in the surgical patient requiring intensive care.
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STATEMENT OF FINDINGS: The respiratory effects of dexmedetomidine were retrospectively examined in 33 postsurgical patients involved in a randomised, placebo-controlled trial after extubation in the intensive care unit (ICU). Morphine requirements were reduced by over 50% in patients receiving dexmedetomidine. There were no differences in respiratory rates, oxygen saturations, arterial pH and arterial partial carbon dioxide tension (PaCO2) between the groups. Interestingly the arterial partial oxygen tension (PaO2) : fractional inspired oxygen (FIO2) ratios were statistically significantly higher in the dexmedetomidine group. Dexmedetomidine provides important postsurgical analgesia and appears to have no clinically important adverse effects on respiration in the surgical patient who requires intensive care. (+info)