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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]

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]