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Summary: Mechanisms underlying loss of consciousness following propofol administration remain incompletely understood. The objective of this study was to compare frontal lobe electroencephalography activity and brainstem reflexes during intravenous induction of general anaesthesia, in patients receiving a typical bolus dose (fast infusion) of propofol compared with a slower infusion rate. We sought to determine whether brainstem suppression ('bottom‐up') predominates over loss of cortical function ('top‐down'). Sixteen ASA physical status‐1 patients were randomly assigned to either a fast or slow propofol infusion group. Loss of consciousness and brainstem reflexes were assessed every 30 s by a neurologist blinded to treatment allocation. We performed a multitaper spectral analysis of all electroencephalography data obtained from each participant. Brainstem reflexes were present in all eight patients in the slow infusion group, while being absent in all patients in the fast infusion group, at the moment of loss of consciousness (p = 0.010). An increase in alpha band power was observed before loss of consciousness only in participants allocated to the slow infusion group. Alpha band power emerged several minutes after the loss of consciousness in participants allocated to the fast infusion group. Our results show a predominance of 'bottom‐up' mechanisms during fast infusion rates and 'top‐down' mechanisms during slow infusion rates. The underlying mechanisms by which propofol induces loss of consciousness are potentially influenced by the speed of infusion. [ABSTRACT FROM AUTHOR]

Background: Conduct of stable inhalational anesthetic induction in children with congenital heart disease (CHD) presents special challenges. It requires in-depth understanding of the effect of congenital shunt lesions on the uptake, delivery, and equilibration of anesthetic drugs. Intracardiac shunts can alter the induction time and if delivery of anesthetic agent is not carefully titrated, can lead to overdosing and undesirable myocardial depression. Aims: To study the effect of congenital shunt lesions on the speed of inhalational induction and also the impact of inhalational induction on hemodynamics in the presence of congenital shunt lesions. Setting: Tertiary care hospital. Design: A prospective, single-center clinical study. Materials and Methods: Ninety-three pediatric patients undergoing elective surgery were segregated into three equal groups, namely, Group 1: no CHD, Group 2: acyanotic CHD, and Group 3: cyanotic CHD. General anesthesia was induced with 8% sevoflurane in 6 L/min air-oxygen. The time to induction was noted at loss of eyelash reflex and decrease in bispectral index (BIS) value below 60. End-tidal sevoflurane concentration, minimum alveolar concentration, and BIS were recorded at 15 s intervals for the 1 st min followed by 30 s interval for another 1 min during induction. Hemodynamic data were recorded before and after induction. Results: Patients in Group 3 had significantly prolonged induction time (99 ± 12.3 s; P < 0.001), almost twice that of the patients in other two groups (51 ± 11.3 s in Group 1 and 53 ± 12.0 s in Group 2). Hypotension occurred after induction in Group 1. No other adverse hemodynamic perturbations were observed. Conclusion: The time to inhalational induction of anesthesia is significantly prolonged in patients with right-to-left shunt, compared to patients without CHD or those with left-to-right shunt, in whom it is similar. Sevoflurane is safe and maintains stable hemodynamics in the presence of CHD.

Background: Conduct of stable inhalational anesthetic induction in children with congenital heart disease (CHD) presents special challenges. It requires in-depth understanding of the effect of congenital shunt lesions on the uptake, delivery, and equilibration of anesthetic drugs. Intracardiac shunts can alter the induction time and if delivery of anesthetic agent is not carefully titrated, can lead to overdosing and undesirable myocardial depression.Aims: To study the effect of congenital shunt lesions on the speed of inhalational induction and also the impact of inhalational induction on hemodynamics in the presence of congenital shunt lesions.Setting: Tertiary care hospital.Design: A prospective, single-center clinical study.Materials and Methods: Ninety-three pediatric patients undergoing elective surgery were segregated into three equal groups, namely, Group 1: no CHD, Group 2: acyanotic CHD, and Group 3: cyanotic CHD. General anesthesia was induced with 8% sevoflurane in 6 L/min air-oxygen. The time to induction was noted at loss of eyelash reflex and decrease in bispectral index (BIS) value below 60. End-tidal sevoflurane concentration, minimum alveolar concentration, and BIS were recorded at 15 s intervals for the 1 st min followed by 30 s interval for another 1 min during induction. Hemodynamic data were recorded before and after induction.Results: Patients in Group 3 had significantly prolonged induction time (99 ± 12.3 s; P < 0.001), almost twice that of the patients in other two groups (51 ± 11.3 s in Group 1 and 53 ± 12.0 s in Group 2). Hypotension occurred after induction in Group 1. No other adverse hemodynamic perturbations were observed.Conclusion: The time to inhalational induction of anesthesia is significantly prolonged in patients with right-to-left shunt, compared to patients without CHD or those with left-to-right shunt, in whom it is similar. Sevoflurane is safe and maintains stable hemodynamics in the presence of CHD. [ABSTRACT FROM AUTHOR]

Study objectives: To examine whether the speed of induction of anesthesia with sevoflurane/nitrous oxide (N2O) utilizing a 10-second vital capacity rapid inhalation induction (VCRII) followed by tidal breathing was similar or faster than cautious intravenous (IV) thiopental induction with inhaled N2O.Design: Prospective, randomized, double-blinded study.Setting: Veterans Affairs Medical Center.Patients: 50 male ASA physical status I, II, and III patients scheduled for general anesthesia.Interventions: Patients were randomized to receive either 8% sevoflurane or IV thiopental. Patients were allocated to one of two groups of 25 patients each. In both groups, the breathing circuit was initially primed for 5 minutes with (4 L/min) and O2 (2 L/min), while the Y-piece was occluded. In the sevoflurane group, the circuit was additionally primed with 8% sevoflurane. Patients were trained to perform a vital capacity breath. After maximal exhalation, the occluding plug was rapidly removed from the Y-piece and connected to the facemask. The patient then inspired to vital capacity, held his breath for 10 seconds, and then was allowed to breathe normally. At the end of the 10-second breathhold, and as the patient started normal breathing, either thiopental (thiopental group) or normal saline (sevoflurane group) was injected at a rate of 4 mL every 10 seconds.Measurements: A study-blinded observer recorded the time to induction, as defined by the time to loss of eyelash reflex, and noted the occurrence of side effects.Main results: The speed of induction was the same for both groups (p > 0.05). An average of eight breaths was required before loss of eyelash reflex. Side effects occurred in 36% of the patients in the thiopental group, and 32% in the sevoflurane group (p > 0.05); these were minor and did not affect induction.Conclusion: Sevoflurane/N2O VCRII as used in this investigation is an effective inhalation technique; it resulted in an induction time similar to that of slow IV thiopental with inhaled N2O. [Copyright &y& Elsevier]

The effects of two kinds of induction speed of sevoflurane anesthesia on the EEG pattern were compared in the same individual using medical student volunteers: a first exposure of 4% was given, followed after full recovery, by incremental doses of 1, 2 and 4% successively, each being administered for 10 min. The arterial blood level of the anesthetic was measured using gaschrornatograph. The changes of EEG pattern during fast induction with 4% were not represented by the abbreviation of those observed during the slow induction with the incremental doses. The administration of 4% induced a sudden appearance of high voltage, rhythmic slow waves of 2-3 Hz at 1-3 min when the arterial blood anesthetic level increased maximally, which was then followed by a pattern of faster activities of 10-14 Hz mixed with 5-8 Hz slow waves. In contrast, the administration of incremental doses induced an increase in frequency and amplitude of EEG activities in the light plane, followed by their decreases in deeper planes. The final EEG patterns were identical for both these methods of induction. These findings confirmed our previous hypothesis that not only the arterial blood level of anesthetics but the rate of its increase are important factors determining the EEG pattern of anesthesia. [ABSTRACT FROM AUTHOR]

Mechanisms underlying loss of consciousness following propofol administration remain incompletely understood. The objective of this study was to compare frontal lobe electroencephalography activity and brainstem reflexes during intravenous induction of general anaesthesia, in patients receiving a typical bolus dose (fast infusion) of propofol compared with a slower infusion rate. We sought to determine whether brainstem suppression ('bottom-up') predominates over loss of cortical function ('top-down'). Sixteen ASA physical status-1 patients were randomly assigned to either a fast or slow propofol infusion group. Loss of consciousness and brainstem reflexes were assessed every 30 s by a neurologist blinded to treatment allocation. We performed a multitaper spectral analysis of all electroencephalography data obtained from each participant. Brainstem reflexes were present in all eight patients in the slow infusion group, while being absent in all patients in the fast infusion group, at the moment of loss of consciousness (p = 0.010). An increase in alpha band power was observed before loss of consciousness only in participants allocated to the slow infusion group. Alpha band power emerged several minutes after the loss of consciousness in participants allocated to the fast infusion group. Our results show a predominance of 'bottom-up' mechanisms during fast infusion rates and 'top-down' mechanisms during slow infusion rates. The underlying mechanisms by which propofol induces loss of consciousness are potentially influenced by the speed of infusion. [ABSTRACT FROM AUTHOR]