|
Findthedoctors.info gives the information about Anethesiologist who is near to you Anaesthesia may be described as a reversible loss of consciousness produced by a drug, from which arousal does not take place even with painful stimuli such as setting a fracture or surgical operation. In this latter respect it differs from sleep or the change in consciousness following sensory deprivation, and it is this that made it so revolutionary a discovery, opening the gateway to modern surgery and safer childbirth. The name is not quite exact, since loss of consciousness is not the same as loss of feeling, and a good anaesthetic in clinical practice should exert other actions, such as some analgesia (to diminish reflex responses to what would be very painful stimuli) and muscular relaxation (to facilitate the surgeon's work). When an anaesthetic such as ether or chloroform is given, there is a characteristic progression of effects, first described by Guedel in 1937: first analgesia, some loss of memory, and perhaps euphoria; then consciousness is lost, but the patient may struggle, breathe irregularly, is sweating and flushed; in the third stage, the patient becomes quieter with regular breathing, but the eyeballs move rhythmically and a good many reflexes are still present. As anaesthesia deepens, and the patient passes through the successive planes of the third stage, various reflexes progressively fall away, the breathing becomes shallower, and eventually death may ensue (the fourth stage). In modern practice anaesthesia is induced with a suitable barbiturate (such as thiopentone) injected intravenously: the patient then passes through the early stages within seconds; once 'under', anaesthesia is usually maintained by some other substance. How do anaesthetics work? It is paradoxical that more is known at the molecular level than at any other. A remarkable feature is the astonishing range of substances that can produce anaesthesia: in addition to the classical anaesthetics and the barbiturates, nitrogen in the air (if given at high pressure) and many other gases, alcohols, dry cleaning fluids (such as trichloroethene), industrial solvents, and certain steroids can all produce typical anaesthesia. There is no common chemical structure such as would suggest a specific action on some particular part of the brain. Instead, as two pharmacologists, Overton and Meyer, pointed out over 80 years ago, anaesthetics all share the property of dissolving in fats and it is remarkable that one can predict the potency of an anaesthetic quite accurately by measuring the pressure of a gas or the concentration of a vapour that will produce a given concentration (about 0.05 moles per litre) of the substance concerned in olive oil. Modern work has revealed the significance of this: the cell membrane, which defines the cell's limits, and across which an electric potential is maintained, consists of an ordered array of fatty molecules (mostly phospholipids and cholesterol); the anaesthetic dissolves in it, and slightly expands and disorders the membrane. Since the membrane also carries large protein molecules (enzymes, ion channels, receptors, transport mechanisms) which mediate its 'traffic' with its environment and with other cells, disturbance of their normal function becomes possible. A fascinating aspect is that very high pressures (which compress and reorder the membrane) cause recovery from anaesthesia. Conversely, a suitable amount of an anaesthetic can be used to neutralize the adverse effects of high pressure. The 'high-pressure nervous syndrome', which includes tremor, bursts of 'micro-sleep', and convulsions, threatened to limit the depth to which divers could go, but the addition of nitrogen (using it as a small dose of anaesthetic) to the diver's helium–oxygen mixture has extended that limit. But if one asks, 'On what synapses, or on what cell groups of the brain, is this molecular action particularly exerted?', no satisfactory answer exists. The simple fact of surgical anaesthesia shows that higher brain functions are particularly sensitive, while respiration and simple reflexes, as well as other bodily processes like the heartbeat, are relatively resistant. Detailed analysis yields a bewildering variety of effects, with actions both pre- and post-synaptically, varying with the synapse and with the anaesthetic. A simple view is that the anaesthetic picks out any delicately poised nervous activity, and that the pattern of anaesthetic activity is simply that of reduced activity in the most vulnerable nervous pathways — particularly complex nervous functions rather than (for example) simple reflex movement. Theories include the idea of a specific effect on the 'ascending reticular activating system', in the absence of whose activity the cerebral cortex is believed to relapse into a sleeping state, or on cortical cells generally. Some recent drugs (such as ketamine), which produce the so-called 'dissociative anaesthesia', may help to throw light on the problem; these differ, both in having a specific chemical structure and in producing a rather different pattern of anaesthesia. There is an abundant literature on the effects of anaesthetics on mental function, short of anaesthesia, and Humphry Davy's description (in 1800) of the effect of nitrous oxide (laughing gas) on himself and his friends (including Southey, Coleridge, Roget, and Wedgwood) reveals the salient features recorded many times subsequently: considerable variation with the individual; excitement; euphoria or sometimes dysphoria; compulsive movements or laughter; 'thrilling' sensations in the limbs; feelings of deep significance; rush of ideas; synaesthesiae; drowsiness; warmth, rapid breathing, palpitations, giddiness; and often a strong desire to repeat the performance. This last characteristic brings the risk of addiction in its train, particularly for those (such as anaesthetists and nurses) with easy access to the drugs; and it shows itself again in 'glue-sniffing' in children, or with workers using some solvents in industry. An important feature with all these volatile substances is the speed with which effects are produced by inhalation, by which the vapour passes very quickly into the circulation. More familiar to most people will be the effect of anaesthetics such as alcohol or barbiturates taken orally, with an onset delayed by circulatory absorption, and the fact that by this route some of the more dramatic effects are lacking (although euphoria and the risk of addiction remain) suggests that these effects are largely due to especially rapid access to, and uptake by, particular parts of the brain, producing a selective action which fades as distribution of the drug becomes general. With sustained exposure to any anaesthetic, the adaptation known as 'tolerance' develops, by which an increasing dose is required to produce the effect. 'Cross-tolerance' occurs between different anaesthetics — hence the difficulty often encountered of anaesthetizing an alcoholic! When exposure stops and the drug is withdrawn, characteristic symptoms appear: for example, insomnia after a short course of any sleeping pill, or delirium tremens (DTs) after prolonged high exposure to alcohol, or convulsions after chronic barbiturate use. While some of the adaptive changes may be biochemical, some of them certainly represent a change in nerve cell function, and there are interesting indications that the composition of the cell membrane changes so as to reduce the effect of the anaesthetic. One would like to think that experience with anaesthetics would deepen our understanding of consciousness, mood, sensation, pain, memory. Yet it is still impossible to move convincingly from the subjective phenomena to physiological understanding. Perhaps it is unreasonable to expect to do so until our knowledge of normal neurophysiology is more satisfactory, or perhaps pharmacology and physiology need to proceed, collaboratively, in parallel. Some areas may be picked out as potentially fruitful. 1. The effect on sense of time. There is a puzzle here: nitrous oxide and alcohol appear to reduce 'felt' time compared with 'clock' time, whereas ketamine (like cannabis) prolongs it. With the latter drugs, one can readily suggest, as William James suggested, that 'disinhibition' in the brain, allowing a greater than normal sensory input, could give rise to an experience of more numerous mental impressions than usual per unit of 'clock' time, and hence a greater 'felt' time. But why should other anaesthetics differ? 2. The effect on pain sense. There is some evidence that enkephalins or endorphins may play a part in analgesia produced by anaesthetics. (See neuropeptides.) But there remain remarkable differences between anaesthetics, some with pronounced analgesic action, some potentiating the response to a painful stimulus. Bearing in mind its practical relevance, as well as the recent advances in our knowledge of the neuroanatomy and neurochemistry of the nociceptive pathways, and the successful application of decision theory to the study of pain, a systematic study of the action of a range of anaesthetics on pain discrimination and pain report seems well worth while. 3. The effect on sensation generally. An intriguing but neglected observation is that anaesthetics facilitate the generation of impulses in the vagal nerve fibres registering the inflation of the lung, which accounts for the ability of many anaesthetics to produce what is known as 'rapid shallow breathing'. It is an intriguing action and, exerted peripherally on the proprioceptive endings in muscles, it might account for the 'thrilling' sensation described by Davy. But more generally there might also be an important effect both on the pattern of sensory input to the brain and on subsequent processing. 4. Effect on memory. With the recent advances in our knowledge of registration, consolidation, and retrieval, systematic study of the effect of a range of anaesthetics on memory is overdue, although the problem is complicated by 'state dependence'. An old method of anaesthesia for childbirth, 'twilight sleep', exploited the effect of the drug hyoscine on memory, so that, even if pain was felt, it was not remembered. The method has been abandoned because of the effect on the baby, but the approach is still interesting. 5. The concept of disinhibition is constantly, and plausibly, invoked to account for phenomena such as the rush of ideas, synaesthesia, and electroencephalographic synchronization. The underlying idea is that the great complexity of mental activity does not merely need some neurons to be active, but also needs others to be actively 'switched off' (inhibited): if the latter process were interfered with (disinhibition), then differential activity and 'gating' of information transfer could become progressively impaired. Simple model systems exist, illustrating how depression of an inhibitory pathway can lead to release phenomena, but no serious attempt has been made to extend the idea to more complex systems. Yet if certain inhibitory mechanisms are particularly vulnerable, it should be possible, by careful choice of systems sharing common elements, to identify them more closely. 6. A tedious but necessary development is that of knowledge about the kinetics of anaesthetic distribution in the brain. Some knowledge exists of the rise and fall of the concentration of an anaesthetic during and after an exposure, for samples of brain containing thousands or millions of neurons. But this is merely a gross average, telling us nothing of local concentration in synaptic detail. Equilibrium with an anaesthetic is virtually never reached in clinical practice, and rarely in experimental work, so that (as mentioned earlier) there is ample scope for differential effects arising, not from the properties of the drug itself, but from varying access and uptake. For instance, evidence is accumulating that if any part of the brain becomes particularly active it consumes more energy, with a corresponding increase in blood flow, which would at once open the way to differential access by an anaesthetic. 7. Finally one must recall that, despite all the advances in neuroanatomy, it is only a tiny minority of nervous pathways that can be precisely and completely described in anatomical and neurochemical detail, with the specific neurons and their connections specified. But some beautiful techniques now exist for mapping out these pathways, for recording the activity of single or groups of neurons, and for neurochemical analysis (see neuroanatomical techniques): the new methods of anaesthesia that a deeper understanding will provide are not far away.
Related Articles -
Find the Anethesiologist Doctors in chennai, Best, Top, Experienced Anethesiologist Doctors in Chennai, Chennai Anethesiologist Doctors, Find the Anethes,
|
