372
P. Martínez-Vázquez et al.
sedation levels and detecting nociceptive stimuli. This limitation becomes crucial
under potential unintentional Awareness with Recall (AWR) not predicted by pharmacological models. In the last decades, there has been a significant increase in the
research and development of non-invasive neuromonitoring technologies based on
the Electroencephalogram (EEG), guiding anaesthesiologists during surgical procedures where the traditional hemodynamic and clinical signs may not be reliable. This
research and development followed a Depth of Anaesthesia-Effect site concentration
(DoA-Ce) approach, which links the Depth of Anaesthesia (DoA) to the drug effect
site concentration (Ce), the concentration at the biophase (the place where the drug
actuates), and where the EEG has the binding role. This approach allows tailoring
drug administration to each patient and surgical context, to prevent AWR events due
to underdoses [11, 36, 57] and excessive concentrations (overdoses), optimizing the
anaesthesia drug consumption [46, 50, 56], and improving patients‘ outcomes. [8,
25, 28, 44, 55].
24.2 Main EEG Patterns During Anaesthesia
The general anaesthetics, inhaled or intravenous, mediate at the neuronal level by
inhibiting or blocking excitatory neurotransmissions, acting on specific neutrotransmitters and voltage-gated ion channels. Roughly, the general anaesthetics produce a
widespread neurodepression in the central nervous system (CNS), causing multiple
behavioural responses such as unconsciousness (hypnosis), analgesia and immobility depending on which specific neurotransmitters, synaptic receptors and neuronal
pathways the drugs target to. Since the EEG reflects the activity of hundreds of
thousands of synchronized cortical pyramidal cells [23], the net inhibitory induced
changes in neural neurotransmission by GA drugs, affect the synchronization of the
pyramidal neurons, inhibiting their communication with other neurons and other
brain areas such as thalamus and hippocampus. The drug-induced changes of the
EEG wave patterns depend on multiple factors such as the intrinsic mechanism of
action of each drug, the Ce, potential drug interactions with other drugs, patients variability and many other factors that might take place during the surgical procedure.
Understanding the main qualitative changes of the EEG wave patterns is complex,
but current depth of anaesthesia monitoring technologies track quantitatively the
EEG pattern changes summarizing them into useful indexes describing the patient’s
hypnosis or sedation state.
The most widely used drugs to induce and maintain the hypnotic component
of GA are broadly divided as intravenous and inhalation agents according to their
route of administration. While intravenous agents such as propofol or barbiturates
act mainly at the GABA receptor complex systems, the mechanisms of action of
inhalation agents such as sevoflurane, desflurane or isoflurane are, additionally to a
GABA agonist mechanism, different and probably related to transient alterations of
lipid membrane of neurons. Even though, for the mentioned drugs, their surrogate
effects at the cortical level, and thus, on the EEG, are very similar.
P. Martínez-Vázquez et al.
sedation levels and detecting nociceptive stimuli. This limitation becomes crucial
under potential unintentional Awareness with Recall (AWR) not predicted by pharmacological models. In the last decades, there has been a significant increase in the
research and development of non-invasive neuromonitoring technologies based on
the Electroencephalogram (EEG), guiding anaesthesiologists during surgical procedures where the traditional hemodynamic and clinical signs may not be reliable. This
research and development followed a Depth of Anaesthesia-Effect site concentration
(DoA-Ce) approach, which links the Depth of Anaesthesia (DoA) to the drug effect
site concentration (Ce), the concentration at the biophase (the place where the drug
actuates), and where the EEG has the binding role. This approach allows tailoring
drug administration to each patient and surgical context, to prevent AWR events due
to underdoses [11, 36, 57] and excessive concentrations (overdoses), optimizing the
anaesthesia drug consumption [46, 50, 56], and improving patients‘ outcomes. [8,
25, 28, 44, 55].
24.2 Main EEG Patterns During Anaesthesia
The general anaesthetics, inhaled or intravenous, mediate at the neuronal level by
inhibiting or blocking excitatory neurotransmissions, acting on specific neutrotransmitters and voltage-gated ion channels. Roughly, the general anaesthetics produce a
widespread neurodepression in the central nervous system (CNS), causing multiple
behavioural responses such as unconsciousness (hypnosis), analgesia and immobility depending on which specific neurotransmitters, synaptic receptors and neuronal
pathways the drugs target to. Since the EEG reflects the activity of hundreds of
thousands of synchronized cortical pyramidal cells [23], the net inhibitory induced
changes in neural neurotransmission by GA drugs, affect the synchronization of the
pyramidal neurons, inhibiting their communication with other neurons and other
brain areas such as thalamus and hippocampus. The drug-induced changes of the
EEG wave patterns depend on multiple factors such as the intrinsic mechanism of
action of each drug, the Ce, potential drug interactions with other drugs, patients variability and many other factors that might take place during the surgical procedure.
Understanding the main qualitative changes of the EEG wave patterns is complex,
but current depth of anaesthesia monitoring technologies track quantitatively the
EEG pattern changes summarizing them into useful indexes describing the patient’s
hypnosis or sedation state.
The most widely used drugs to induce and maintain the hypnotic component
of GA are broadly divided as intravenous and inhalation agents according to their
route of administration. While intravenous agents such as propofol or barbiturates
act mainly at the GABA receptor complex systems, the mechanisms of action of
inhalation agents such as sevoflurane, desflurane or isoflurane are, additionally to a
GABA agonist mechanism, different and probably related to transient alterations of
lipid membrane of neurons. Even though, for the mentioned drugs, their surrogate
effects at the cortical level, and thus, on the EEG, are very similar.