Orina Verde asociada a Infusión de Propofol: Reporte de caso

Background/AimsIt is unclear whether continuous infusion or intermittent bolus injection of propofol is better for achieving adequate sedation in endoscopic retrograde cholangiopancreatography (ERCP). We aimed to compare the efficacy and safety of continuous infusion and intermittent bolus injection of propofol during therapeutic ERCP.MethodsIn this prospective study, we randomly assigned 232 patients undergoing therapeutic ERCP to either continuous infusion (CI group, n = 113) or intermittent bolus injection (BI group, n = 119) of propofol. The primary outcome was the quality of sedation as assessed by the endoscopist. Other sedation-related parameters included sedation induction time, total dose of propofol, recovery time, involuntary patient movement, and adverse events.ResultsOverall satisfaction with sedation by the endoscopist and monitoring nurse were significantly higher in the CI group than the BI group (mean satisfaction score, 9.66 vs. 8.0 and 9.47 vs. 7.96, respectively, p < 0.01 for both). However, patients in the CI group had a significantly longer sedation induction time (5.28 minutes vs. 4.34 minutes, p < 0.01) and received a higher dose of propofol than patients in the BI group (4.22 mg/kg vs. 2.08 mg/kg, p < 0.01). There was no significant difference in adverse events between the two groups.ConclusionsContinuous infusion of propofol during therapeutic ERCP had the advantage over intermittent bolus injection of maintaining a constant level of sedation without increasing adverse events. However, it was associated with an increased total dose of propofol and prolonged sedation induction time.

Propofol use for sedation during routine flexible bronchoscopy is expanding. However, there are concerns over propofol's reliability in targeting moderate sedation during more complex and lengthy procedures, such as endobronchial ultrasound (EBUS) bronchoscopy. Its delivery by continuous infusion, which provides a steady sedation effect, may be a practical model for achieving reliable outcomes in this setting. We tested a continuous propofol infusion protocol targeting moderate sedation for EBUS bronchoscopy. A fixed loading rate of 125 mcg/kg/min and initial maintenance rate of 75 mcg/kg/min were used. Sedation assessments were performed every 2.5 minutes. The infusion was adjusted by a nurse under the direction of the bronchoscopist to maintain moderate sedation, normal vital signs, and patient comfort. Prospectively collected data from the first 31 patients using the protocol were analyzed. A mix of EBUS types was performed in a fellowship training environment. Median procedure duration was 51 minutes (interquartile range, 41 to 75 min). Ninety-four percent of total bronchoscopy time was spent in moderate sedation, whereas only 1.9% was occupied by agitation-related delays. Average propofol dose per case was 0.07 mg/kg/min (±0.020), and infusion adjustments were required once every 8 minutes. Sampling goals were met in all patients, and diagnostic and nodal staging accuracies were 90% and 91%, respectively. All tumor specimens sent for genetics were sufficient for analysis. There were no major procedure-related complications. Bronchoscopist-directed continuous propofol infusion is effective and practical for reliably and safely targeting moderate sedation during EBUS bronchoscopy, without sacrificing the breadth and accuracy of the procedure.

Twelve buffalo calves of either sex presented to the clinic with surgical conditions like umbilical hernia, urolithiasis and fractures were utilized to study the effect of continuous intravenous infusion of propofol after premedication with medetomidine – pentazocine and midazolam – pentazocine. The animals were divided into two groups of six animals each. Medetomidine (@ 2.5 µg/kg b.wt.) – pentazocine (@ 0.5 mg/kg b.wt.) and midazolam (@ 0.25 mg/kg b.wt.) – pentazocine (@ 0.5 mg/kg b.wt.) was given intravenously in group I and II respectively. Propofol was given intravenously (@ 4 mg/kg b.wt.) after pre-medication and maintained by continuous intravenous infusion of propofol (@ 0.4 mg/kg b.wt.) in 5 % dextrose normal saline in both groups. Pulse oximetric and electrocardographic changes were recorded at 0, 5,10,15,30 and 60 min. Saturation of oxygen percentage of haemoglobin showed significant (P £ 0.05) difference in both groups but the changes were within the normal range. Electrocardiographic studies did not reveal any abnormalities except slight variations in the amplitude of P wave, T wave and QRS complex in both groups. It is concluded that both anaesthetic drug combinations can be used safely in buffaloes as they did not alter the pulse oximetry and ECG values.

In pediatric cardiac critical care, patients often require specific anesthesia and sedation considerations due to unique physiological vulnerabilities. This study assessed the incidence of propofol-related infusion syndrome (PRIS) in Pediatric Cardiac Intensive Care Unit (PCICU) patients receiving continuous propofol infusion for non-procedural sedation. We conducted a retrospective review of post-operative congenital heart disease patients < 18 years admitted to the PCICU from 1/1/2000-9/30/2024, who received continuous propofol infusions ≥ 12hours and/or ≥ 2.4mg/kg/hour. The primary outcome was the incidence of PRIS. Secondary outcomes included intensive care unit (ICU) length of stay and survival to hospital discharge. Statistical analyses included chi-square tests and the Kruskal-Wallis test, stratified by physiological complexity (single vs. double ventricle) and surgical mortality risk scores (The Society of Thoracic Surgeons-European Association for Cardio-Thoracic Surgery [STAT] score). A total of 641 patients were included. No statistically significant differences in propofol characteristics were found across physiologic or surgical risk groups. The median infusion rate was 1.2mg/kg/hour, with a median duration of 22.7hours. No cases of PRIS occurred. Survival to hospital discharge was 97%. The median ICU length of stay was 7.1 days. In this single center, retrospective study of post-operative congenital heart disease patients, continuous propofol infusion was not associated with any cases of PRIS. These findings support the cautious use of propofol in pediatric cardiac critical care. Further prospective studies are needed to evaluate safety across the heterogenous congenital heart disease population, including those with single ventricle physiology.

The aims of this study were compare the electrocardiogram (ECG) and cardiopulmonary effects of methadone or morphine, both injected intravenously (IV) in dogs anesthetized with continuous infusion of propofol. Sixteen healthy female mongrel dogs were used in this study for elective ovariohysterectomy. The animals were allocated in random order into two groups assigned GME (methadone 0.3 mg kg-1, IV) or GMO (morphine 0.3 mg kg-1, IV). Parameters were evaluated: heart rate (HR), P-wave amplitude (Ps and PmV), interval between Ps and R waves (PR), QRS duration (QRS), R-wave amplitude (R), duration the interval between the Q and T waves (QT), systolic blood pressure (SBP), rectal temperature (RT), respiratory rate (RR), end tidal of carbon dioxide (ETCO2) and periferic oxyhemoglobin saturation (SpO2). Postoperative analgesia was assessed by mechanical nociceptive stimulus based on the scale proposed by Firth and Haldane (1999) and rescue analgesia based on the visual analogue scale. HR was lower in GME in relation to GMO. The P, PmV, PR, QRS, R and QT values remained within their normality tracks, showing no clinical importance. Apnea and ETCO2 increased in both groups. There was no difference between groups of the analgesic effects. It can be concluded that methadone and morphine promote similar cardiovascular effects after IV injection during surgery in dogs anesthetized with propofol by continuous rate infusion, however, when methadone used, assisted ventilation is required. In addition, both drugs promote postoperative analgesia until six hours.

In recent years, continuous intravenous propofol infusion has been widely used in pediatric intensive care units. Several case reports have raised concerns about its safety. The objective of this study was to report our experience with continuous intravenous propofol in consecutive patients during an 18-month period. The study design was a retrospective review of a case series. Case was defined as a critically ill child who was treated with continuous intravenous propofol. The attending physician staff agreed to prescribe propofol via continuous intravenous infusion at a dose not to exceed 50 microg/kg/min. The protocol allowed for each patient to receive an additional intravenous bolus of propofol at a dose of 1 mg/kg no more than once per hour. The study entailed data collection from consecutive patients who were prescribed a continuous infusion of propofol in either the pediatric intensive care unit or bone marrow transplant unit. Data from 142 patients were analyzed. Each patient enrolled was adequately sedated. Administration of propofol via continuous intravenous infusion was not associated with metabolic acidosis or hemodynamic compromise. No patient in the study group was inadvertently extubated or had a central venous catheter accidentally discontinued. Propofol can be safely and effectively used to provide sedation to critically ill infants and children. We speculate that continuous infusion of propofol for extended periods of time should not exceed 67 microg/kg/min.

Prospective observational study on the use of continuous intravenous ketamine and propofol infusion for prolonged sedation in critical care

Continuous Upper and Lower Gastrointestinal Endoscopy Under Sedation: A Randomized Double-Blind Comparative Study Using Propofol Alone Versus Propofol Combined Midazolam

I. RECOMMENDATIONS Strength of Recommendations: Weak. Quality of Evidence: Low, from poor-quality class III studies. A. Level I There are insufficient data to support a level I recommendation for this topic. B. Level II There are insufficient data to support a level II recommendation for this topic. C. Level III* Etomidate may be considered to control severe intracranial hypertension; however, the risks resulting from adrenal suppression must be considered. Thiopental may be considered to control intracranial hypertension. *In the absence of outcome data, the specific indications, choice and dosing of analgesics, sedatives, and neuromuscular-blocking agents used in the management of infants and children with severe traumatic brain injury (TBI) should be left to the treating physician. *As stated by the Food and Drug Administration, continuous infusion of propofol for either sedation or the management of refractory intracranial hypertension in infants and children with severe TBI is not recommended. II. EVIDENCE TABLE (see Table 1)Table 1: Evidence tableIII. OVERVIEW Analgesics, sedatives, and neuromuscular-blocking agents are commonly used in the management severe pediatric TBI. Use of these agents can be divided into two major categories: 1) for emergency intubation; and 2) for management including control of elevated intracranial pressure (ICP) in the intensive care unit (ICU). This chapter evaluates these agents during ICU treatment. Analgesics and sedatives are believed to favorably treat a number of important pathophysiological derangements in severe TBI. They can facilitate necessary general aspects of patient care such as the ability to maintain the airway, vascular catheters, and other monitors. They can also facilitate patient transport for diagnostic procedures and mechanical ventilatory support. Other proposed benefits of sedatives after severe TBI include anticonvulsant and antiemetic actions, the prevention of shivering, and attenuating the long-term psychological trauma of pain and stress. Analgesics and sedatives also are believed to be useful by mitigating aspects of secondary damage. Pain and stress markedly increase cerebral metabolic demands and can pathologically increase cerebral blood volume and raise ICP. Studies in experimental models showed that a two- to threefold increase in cerebral metabolic rate for oxygen accompanies painful stimuli (1, 2). Noxious stimuli such as suctioning can also increase ICP (3–6). Painful and noxious stimuli and stress can also contribute to increases in sympathetic tone with hypertension and bleeding from operative sites (7). However, analgesic or sedative-induced reductions in arterial blood pressure can lead to cerebral ischemia as well as vasodilation and can exacerbate increases in cerebral blood volume and ICP. In the absence of advanced neuromonitoring, care must be taken to avoid this complication. The ideal sedative for patients with severe TBI has been described as one that is rapid in onset and offset, easily titrated to effect, has well-defined metabolism (preferably independent of end-organ function), neither accumulates nor has active metabolites, exhibits anticonvulsant actions, has no adverse cardiovascular or immune actions, and lacks drug–drug interactions while preserving the neurologic examination (8). Neuromuscular-blocking agents have been suggested to reduce ICP by a variety of mechanisms including a reduction in airway and intrathoracic pressure with facilitation of cerebral venous outflow and by prevention of shivering, posturing, or breathing against the ventilator (9). Reduction in metabolic demands by elimination of skeletal muscle contraction has also been suggested to represent a benefit. Risks of neuromuscular blockade include the potential devastating effect of hypoxemia secondary to inadvertent extubation, risks of masking seizures, increased incidence of nosocomial pneumonia (shown in adults with severe TBI) (9), cardiovascular side effects, immobilization stress (if neuromuscular blockade is used without adequate sedation/analgesia), and increased ICU length of stay (9, 10). Myopathy is most commonly seen with the combined use of nondepolarizing agents and corticosteroids. Incidence of this complication varies between 1% and over 30% of cases (5, 11, 12). Monitoring of the depth of neuromuscular blockade can shorten duration of its use in the ICU (13). IV. PROCESS For this update, MEDLINE was searched from 1996 through 2010 (Appendix B for search strategy), and results were supplemented with literature recommended by peers or identified from reference lists. Of 46 potentially relevant studies, two were included as evidence for this topic. V. SCIENTIFIC FOUNDATION The recommendations on the use of analgesics, sedatives, and neuromuscular-blocking agents in this chapter are for patients with a secure airway who are receiving mechanical ventilatory support yielding the desired arterial blood gas values and who have stable systemic hemodynamics and intravascular volume status. Two class III studies of the use of analgesics or sedatives met inclusion criteria for this topic and provide evidence to support the recommendations: one study about etomidate and one about thiopental. These studies only addressed ICP as the outcome (14, 15). No study addressed the most commonly used analgesics and sedatives (narcotics and benzodiazepines). Etomidate A study by Bramwell et al (14) carried out a prospective unblinded class III study of the effect of a single dose of etomidate (0.3 mg/kg, intravenously) on ICP >20 mm Hg in eight children with severe TBI. Etomidate reduced ICP vs. baseline in each 5-min interval during the 30-min study period. The patients in this study had severe intracranial hypertension and etomidate reduced ICP from 32.8 ± 6.6 mm Hg to 21.2 ± 5.2 mm Hg. An increase in cerebral perfusion pressure was also seen that was significant for the initial 25 mins after etomidate administration. Every patient in the study exhibited a reduction in ICP with treatment. No data were presented on cortisol levels in these patients. However, in the discussion section of the manuscript, the authors indicated that at 6 hrs after etomidate administration, adrenocorticotropic hormone stimulation tests were performed on each patient; four of the eight showed adrenal suppression. It is unclear if this degree of adrenal suppression is different from that normally observed in pediatric TBI (16). No patient showed clinical signs of adrenal insufficiency such as electrolyte disturbances or blood pressure lability, and no patient received steroid therapy. The availability of other sedatives and analgesics that do not suppress adrenal function, small sample size and single-dose administration in the study discussed previously, and limited safety profile in pediatric TBI limit the ability to endorse the general use of etomidate as a sedative other than as an option for single-dose administration in the setting of raised ICP. Barbiturates Barbiturates can be given as a sedative at doses lower than those required to induce or maintain barbiturate coma. No report specifically addressed their use in that capacity in pediatric TBI. One report did, however, address the effects of barbiturate administration outside of the setting of refractory raised ICP. A study by de Bray et al (15) was a prospective study of the effect of a single dose of thiopental (5 mg/kg, intravenously) on middle cerebral artery flow velocity in ten children with severe TBI and compared the findings with those seen with thiopental administration in ten children under general anesthesia for orthopedic procedures. In this small study, effects on ICP were assessed in only six of the ten children with severe TBI. In those six, thiopental reduced ICP by 48%. Flow velocity was reduced by approximately 15% to 21% in the pediatric patients with TBI. Baseline ICP was 16.5 mm Hg. Cerebral perfusion pressure was not significantly changed. At the class III level, this study supports the ability of thiopental, administered as a single dose, to reduce ICP, even when only moderately increased. The effects on flow velocity are also consistent with the reduction in cerebral blood volume that would be expected to mediate the reduction in ICP produced by thiopental. No study was identified, however, that specifically addressed barbiturate use as a sedative on any other outcome parameter. VI. INFORMATION FROM OTHER SOURCES A. Indications From the Adult Guidelines In the most recent adult guidelines, a chapter on “Anesthetics, Analgesics, and Sedatives” identified a class II study to recommend continuous infusion of propofol as the agent of choice. Only case reports or mixed adult and pediatric case series have been published supporting propofol use in pediatric TBI (17, 18). However, a number of reports (in cases not restricted to TBI) suggest that continuous infusion of propofol is associated with an unexplained increase in mortality risk in critically ill children. A syndrome of lethal metabolic acidosis (“propofol syndrome”) can occur (19–24). In light of these risks, and with alternative therapies available, continuous infusion of propofol for either sedation or management of refractory intracranial hypertension in severe pediatric TBI is not recommended. The Center for Drug Evaluation and Research Web site of the Food and Drug Administration (25) states, “Propofol is not indicated for pediatric ICU sedation as safety has not been established.” Based on the Food and Drug Administration recommendations against the continuous infusion of propofol for sedation in pediatric critical care medicine, the recommendation from the adult guidelines cannot be translated to pediatric TBI management and represents an important discontinuity between pediatric and adult TBI management. Neuromuscular-blocking agents were not addressed in the “Anesthetics, Analgesics, and Sedatives” chapter of the most recent adult guidelines. In the 2000 adult guidelines (26), the initial management section cited a study that examined 514 entries in the Traumatic Coma Data Bank and reported no beneficial effects of neuromuscular blockade and an increased incidence of nosocomial pneumonia and prolonged ICU stay associated with prophylactic neuromuscular blockade (9). It was suggested that use of neuromuscular-blocking agents be reserved for specific indications (intracranial hypertension, transport). B. Information Not Included as Evidence Ketamine exhibits neuroprotective effects in experimental models of TBI; however, concerns over its vasodilatory effects and their impact on ICP have long limited its consideration as a sedative in TBI. Recently, a study by Bar-Joseph et al (27) was carried out, which was a prospective study in 30 children with raised ICP, 24 with nonpenetrating TBI. A single dose of ketamine (1–1.5 mg/kg, intravenously) was evaluated for its ability to either 1) prevent further increases in ICP during a stressful procedure (i.e., suctioning); or 2) treat refractory intracranial hypertension. Ketamine reduced ICP in both settings. These patients had severe intracranial hypertension with an overall mean ICP of 25.8 mm Hg. The study did not meet inclusion criteria for these guidelines for two reasons. First, it fell just below the cutoff of 85% of TBI cases, and second, Glasgow Coma Scale score was not provided–although it is likely that the children had severe TBI given the ICP data. Regarding the use of etomidate in critical care, including severe TBI and multiple trauma victims (28–31), there are general concerns over adrenal suppression. As stated earlier, the availability of other sedatives and analgesics that do not suppress adrenal function, along with the small sample size and single-dose administration in the single study in the evidence table (Table 1) and limited safety profile in pediatric TBI, limit the ability to endorse the general use of etomidate as a sedative other than as an option for single-dose administration in the setting of raised ICP. VII. SUMMARY Two studies were identified that met inclusion criteria, rendering reserved class III recommendations that 1) etomidate may be considered to decrease intracranial hypertension, although the risks resulting from adrenal suppression must be considered; and 2) thiopental, given as a single dose, may be considered to control intracranial hypertension. Despite the common use of analgesics and sedatives in TBI management, there have been few studies of these drugs focused on pediatric patients with severe TBI, and studies meeting inclusion criteria for the most commonly used agents were lacking. Similarly, no studies were identified meeting inclusion criteria that addressed the use of neuromuscular blockade in pediatric patients with severe TBI. Until experimental comparisons among these agents are carried out, the choice and dosing of analgesics, sedatives, and neuromuscular-blocking agents used should be left to the treating physician. Based on recommendations of the Food and Drug Administration, continuous infusion of propofol is not recommended in the treatment of pediatric TBI. VIII. KEY ISSUES FOR FUTURE INVESTIGATION Studies are needed comparing the various sedatives and analgesics in pediatric patients with severe TBI, examining sedative and analgesic efficacy, effects on ICP, other surrogate markers, and functional outcome. Studies are needed to assess the toxicities, including hypotension, adrenal suppression, effects on long-term cognitive outcomes, and other adverse effects. Studies are needed on dosing, duration, and interaction effects with other concurrent therapies. Optimal sedation after severe TBI may differ between infants and older children and requires investigation. Specifically, given concerns over the effects of various anesthetics and sedatives on neuronal death in the developing brain (32, 33), studies of various analgesic and sedative regimens in infants with TBI are needed, including infants who are victims of abusive head trauma. The specific role of neuromuscular-blocking agents in infants and children with severe TBI needs to be defined.

The changing role of monitored anesthesia care in the ambulatory setting.

Propofol en perfusion à débit continu versus enflurane chez l'enfant opéré de strabisme. Comparaison de la qualité de l'anesthésie et du réveil

Intravenous anaesthetics such as ketamine, propofol, and thiamylal are widely used, although the direct effects of these anaesthetics on the renal blood flow (RBF) have not been well elucidated. In this study, we examined the effects of bolus and continuous administrations of ketamine, propofol, and thiamylal on cortical RBF and the effects of noradrenaline (NA) on RBF under continuous administration of these anaesthetics. We used laser Doppler flowmetry to measure the effects of bolus injection and continuous infusion of ketamine, propofol, and thiamylal on cortical RBF in male Wistar rats. We also examined the effects of the anaesthetics on mean arterial blood pressure (MAP) and heart rate (HR). Bolus injections of ketamine, propofol, or thiamylal (1–8 mg/kg each, n = 10) at clinically relevant concentrations did not affect MAP, HR, or RBF. Continuous administration of ketamine, propofol, or thiamylal (1–8 mg/kg/h each, n = 10) did not affect MAP, HR or RBF. Exogenous NA (2 µg/kg) caused an increase in MAP and a decrease in RBF and HR. In experiments with continuous infusions of propofol or thiamylal (1–8 mg/kg/h each, n = 10), similar results were observed without infusion of any anaesthetics. However, bolus injection of NA did not result in a decrease in RBF during continuous ketamine infusion (98.8 ± 6.7% of control, n = 6, p < 0.05), while ketamine did not affect the NA-induced increase in MAP. In conclusion, bolus and continuous administrations of ketamine, propofol, and thiamylal did not affect the RBF. From our present findings, ketamine would be useful for maintaining the RBF.

Nitrous oxide (N2O) and propofol exhibit directionally opposite effects on the cerebral circulation, vasodilation and vasoconstriction, respectively. The authors investigated an interaction between the two anesthetic agents on the dynamic cerebrovascular response to step changes in end-tidal pressure of carbon dioxide (PetCO2) in humans. Participants with no systemic diseases were allocated into two groups, each of which was anesthetized sequentially with two protocols. Patients in group 1 were anesthetized with 30% O2 + 70% N2O. A continuous intravenous infusion of propofol (7-10 mg x kg(-1) x h(-1)) was then added to the N2O. Patients in group 2 were anesthetized first with continuous infusion of propofol (10 mg x kg(-1) h(-1)), and then 30% O2 + 70% N2O was added to the propofol anesthesia. Using transcranial Doppler ultrasonography, blood flow velocity at the middle cerebral artery (FV(MCA)) was measured during a step increase (on-response) followed by a step decrease (off-response) in PetCO2, with PetCO2 ranging between approximately 28 and 50 mmHg. The dynamic FV(MCA)-PetCO2 relationship was analyzed using a mathematical model that was characterized with a pure time delay, and a time constant and a gain each for the on- or off-response. The addition of propofol to the N2O anesthesia increased the on-response time constant (P < 0.01), whereas the addition of N2O to the propofol anesthesia increased the time constants for on- (P < 0.01) and off-responses (P < 0.05). However, the addition of either anesthetic did not affect the gains. Propofol and N2O, when one is added to the other, produce similar dynamic FV(MCA) responses to sudden changes in PetCO2. Addition of each anesthetic slows the dynamic response and produces the response whose magnitude is proportional to the baseline FV(MCA).

To determine the effects of exogenous ramped infusions of epinephrine, norepinephrine and dopamine on arterial and effluent brain blood concentrations of propofol under steady state intravenous anesthesia. Prospective, randomized animal study. University research laboratory. Five adult female merino sheep. Induction (5 mg/kg) and continuous infusion of propofol (15 mg/min) with controlled mechanical ventilation to maintain PaCO2 40 mmHg. After 1 h of continuous anesthesia, each animal randomly received ramped infusions of epinephrine, norepinephrine (10, 20, 40 microg/min) and dopamine (10, 20, 40 microg x kg x min) in 3 x 5 min intervals followed by a 30-min washout period. Arterial and sagittal sinus whole blood for determination of propofol concentrations using high-pressure liquid chromatography. Cardiac output using a thermodilution method. Level of consciousness using an observational scale. All three drugs significantly and transiently increased cardiac output in a dose-dependent fashion to a maximum of 146-169% of baseline. Baseline arterial and sagittal sinus propofol concentrations were not statistically different prior to catecholamine infusions. All three drugs significantly reduced mean arterial propofol concentrations (95 % CI, p < 0.05): epinephrine to 41.8% of baseline (11.4-72), norepinephrine to 63 % (27-99) and dopamine to 52.9 % (18.5-87.3). There were parallel reductions of concentrations in sagittal sinus blood leaving the brain. The lowest blood concentrations were associated with emergence from anesthesia. Arterial concentrations were inversely related to the simultaneously determined cardiac output (r2 = 0.74, p < 0.0001). Comparison of the data with the predictions of a previously developed recirculatory model of propofol disposition in sheep showed the data were consistent with a mechanism based on increased first pass dilution and clearance of propofol secondary to the increased cardiac output. Catecholamines produced circulatory changes that reversed propofol anesthesia. These observations have potential clinical implications for the use of propofol in hyperdynamic circulatory conditions, either induced by exogenous catecholamine infusions or pathological states.

Introduction. Beside the traditional, intermittent bolus application of propofol, continuous propofol infusion via infusion pump is an alternative procedure for deep sedation during long-lasting interventional endoscopy. However, up to now, there are no randomized comparisons for gastrointestinal endoscopy. Methods. One hundred patients (ERCP: n = 60, EUS: n = 40) were randomly assigned to receive intermittent bolus application (“bolus group”) or continuous infusion (“perfusor group”) of propofol sedation after induction with 3 mg midazolam for deep sedation. Patients in the bolus group received an initial propofol dose according to body weight (bw <70 kg: 40 mg; bw ≥70 kg 60 mg). In the perfusor group, bw-adapted, continuous propofol infusion (6 mg/kg) via the Injectomat 2000 MC (Fresenius-Kabi) was administered after an initial bolus of 1 mg/kg. Vital signs, dose of propofol, patient cooperation (VAS 1–10), sedation depth, and the recovery time as well as the quality of recovery were evaluated. Results. Total propofol dose in the bolus group 305 ± 155 mg (100–570 mg) and in the perfusor group 343 ± 123 mg (126–590 mg, p = 0.5) were comparable. Oxygen saturation below 90% was seen in four patients of each group, with no need for assisted ventilation. Arterial blood pressure <90 mmHg was documented in two patients in the bolus group and seven patients in the perfusor group (p = 0.16). Patients' cooperation was rated as good in both groups (bolus group, 9.1 ± 0.9; perfusor group, 8.9 ± 1; p = 0.17). Recovery time was significantly shorter in the bolus group compared with the perfusor group (19 ± 5 versus 23 ± 6 min, p < 0.001) whereas the quality of recovery was nearly identical in both groups. Conclusion. Both sedation regimens allow nearly identical good controllability of propofol sedation. However, recovery time was significantly slower and hypotension was tended to occur more often in the perfusor group.