Compounds that cause a loss of consciousness in humans or a loss of righting reflex in animals. The medical concepts also include an induced coma, appropriate for facilitating surgical applications in clinical and veterinary practices which causes a lack of awareness of painful stimuli. Furthermore, the basic definition of general anesthesia is not scientifically accepted.
Definition of General Anesthesia
A variety of medications could be administered to ensure unconsciousness, amnesia, analgesia, loss of reflexes of the autonomic nervous system and, in certain cases, muscle paralysis, with concomitant stability of the autonomic, cardiovascular, respiratory, and thermoregulatory systems. General anesthetic generates distinct EEG patterns, the most common of which is the progressive growth in low-frequency, high-amplitude activity as general anesthesia increases. clinical signs and EEG patterns of general anesthesia-induced inconscience can be identified in three periods: induction, maintenance and emergence.
Induction Period; The patient has a normal active EEG prior to induction with prominent alpha (10 Hz) activity when the eyes are closed. Administration of a small dose of hypnotic pharmaceuticals, including propofol and barbiturate, that all work on receptors for GABAA, lead to a sedation condition in which the patient is peacefully and easily excited and the eyes are generally closed. With the dose increasing slowly this will lead to increase EEG beta (13 to 25 Hz) activity The medication intended to cause unconsciousness induces excitement instead. This state is called a paradoxical state.
Maintenance Period; A combination of hypnotic agents, inhalants, opioids, muscle relaxants, cardiovascular sedatives and supportive ventilatory and thermal regulations maintain general anesthesia. Changes in heart rate and blood pressure are clinical indications of the level of general anesthesia during maintenance.
The phases of the maintenance period are defined in four EEG patterns (Figure 1). Phase 1 is characterized by decreasing EEG beta (13 to 30 Hz) and increased EEG alpha activity (8 to 12 Hz) and delta activity (0 to 4 Hz) in general anesthesia. During phase 2, the intermediate state, beta activity decreases and alpha and delta activity increases, with so-called anteriorization, the rise in activity in anterior EEG in alpha and delta is comparable concerning the posterior of leads.
The EEG in phase 2 is identical to the EEG in phase 3, non-REM (or slow- wave) sleeping. Phase 3 is a deeper phase in which the EEG is characterized by flat intervals of alpha or beta activity cycles, which is referred to as burst suppression. The time from the phases of alpha activity is increased as the general anesthesia deepens and the amplitudes of Alpha and Beta activity are reduced. The EEG is isoelectric (totally flat) in phase 4, the deepest state in general anesthesia. The administration of a barbiturate or propofol will induce an isoelectric EEG intended for protecting the brain during neurosurgery or avoid widespread seizures.
Emergence Period; General anesthesia emergence depends on the amount of drugs administered; their places of action, power and pharmacokinetics; the physiological characteristics of the patient; and the type and duration of the operation. Typical of the first medical indications when neuromuscular peripheral blockade has reduced, the return of spontaneous breathing. With the restoration of skeletal muscle tone the patient starts to grimace, choke, gag and cough, and make defensive motions, for example, reaching for the endotracheal or nasogastric duct.
As a patient emerges from general anesthesia, EEG patterns proceed from phases 2 or 3 of the maintenance to an active and fully awake EEG in approximately the reverse order (Figure 1). The patient goes through a minimally conscious state between extubation and release from the post-anesthesia care unit.
Mechanisms of General Anesthesia
In order to induce unconsciousness, anesthetics have myriad action sites and have an effect on the central nervous system (CNS) at many levels. The biochemical mechanism of general anesthetics is not well understood. Common areas of the central nervous system whose functions are interrupted or changed during general anesthesia include the cerebral cortex, thalamus, reticular activating system, and spinal cord. Current anesthetic theories not only identify target sites in the CNS but also neural networks and loops whose interruption is associated with unconsciousness. GABA, glutamate receptor, voltage-gated ion channel, glycine and serotonin receptor are potential targets of general anesthetics.
Brain cells communicate with each other through a wide range of chemical neurotransmitters. These neurotransmitters react to electric signals, are released into the synapse. The excitatory neurotransmitters and inhibitory neurotransmitters are classified according to their respective roles. Glutamate and acetylcholine, for example, cause depolarization (excitatory neurotransmitters). On the other hand, post-synaptic functions are decreased by inhibitory neurotransmitters like GABA and glycine.
Free neurotransmitters link to receptors of the ion channel to control ion flow. Control of electrical activity through ion channels is strongly connected with anesthetic physiology and the different patterns of behavioral reaction. GABAA, glycine, acetylcholine nicotinic, and NMDA receptors have general anesthetic sensitivities. Some of the volatile anesthetics also act on potassium channels and voltage-gated channels (sodium, calcium)