TERMINAL STATES

From Big Medical Encyclopedia

TERMINAL STATES (Latin terminalis relating to the end boundary) — states, boundary between life and death.

K T. pages belong the condition of dying including several stages, and the initial stages of the postresuscitatic period.

Dying represents a complex of disturbances of a homeostasis and functions of the main life support systems (blood circulation and breath), to-rye own forces of an organism, without medical aid, cannot be compensated and inevitably lead to death. T. pages during the dying include a preagonal state, agony (see) and clinical death (see). The condition of the patient perishing from an incurable disease is not considered by T. page until blood circulation and gas exchange are provided with own forces of an organism.

In emergence of T. the page plays the main role hypoxia (see), and from the beginning of dying — surely that its form, edges is connected with a circulatory unefficiency (a circulator hypoxia).

The reasons of development of a terminal circulator hypoxia can be various. It is accepted to distinguish three «a collar of death» — heart, respiratory system and a brain. Damage of heart is a proximate cause of insufficiency or the termination of blood circulation. The dysfunctions of respiratory system leading to T. pages, can be initially connected with defeat of the device of external respiration or changes of a gaseous fluid, disturbance of transport of oxygen or its utilization by fabrics. The brain becomes «gate of death» at oppression first of all of the respiratory, and then vasomotor centers. The disturbances of a hemodynamics at pathology of breath and diseases or injuries of a brain leading to T. pages, develop for the second time.

Process of dying to some extent takes all systems of an organism. At the same time processes of the progressing disturbance of functions of various systems are combined with gradually dying away processes of compensation of these disturbances. At a sudden stop of blood circulation (an electric trauma, acute coronary insufficiency) mechanisms of compensation can be realized only in small degree and generally at the fabric level in this connection duration of the preagonal period and an agony decreases. During the dying owing to an incremental hypoxia of any type (e.g., at pneumonia, peritonitis, a severe injury, blood loss, etc.) mobilization of compensatory mechanisms can be considerable that significantly extends process of dying.

At the heart of the functional changes characterizing dying generalized hypoxemic pathology of metabolism lies. Quicker and with the greatest effects for an organism of disturbance of metabolism develop in a brain. At the sudden termination of blood circulation the main substrate of energy balance — glucose — disappears from tissue of a brain within 1 min., the main stocks of a glycogen are exhausted within 5 min. Approximately in the same terms phosphocreatinine (apprx. 1 min.) and available to energy balance of ATP (3 — 5 min.) disappears. The energy potential of a brain reaches extremely low values in 7,5 min. after the termination of blood circulation. Due to the change of maintenance of adeninenucleotides there is a sharp short-term increase in maintenance of tsAMF (in bark of cerebral hemispheres by 2 — 10 times). With oppression of oxidizing metabolism anaerobic amplifies glycolysis (see) as the main fabric compensatory mechanism. At the same time the maintenance of a lactate in tissue of a brain reaches a maximum (15 — 20 mk mol/g) within 5 — 10 min. then glycolysis is slowed down owing to reduction of amount of glucose in cells. Development of glycolysis against the background of oppression of oxidizing processes leads to deep acidosis of tissue of brain.

The changes of other, volatile forms of a metabolism which were more expressed at slowly developing dying are accompanied by disturbances of power metabolism. They concern all forms of a metabolism, in particular exchange of amino acids, synthesis of protein, nucleinic exchange, synthesis and utilization of neurotransmitters, exchange of phospholipids. Along with disturbance of amino-acid structure, reduction of content of the main monoamines in tissue of a brain toxic products collect: NH 4 + , unsaturated fat to - you, and also lizosomalny enzymes. Under nek-ry conditions (long deep hypotension, the increased content in blood of glucose) the quantity of a lactate by the end of dying reaches 30 — 35 µmol/g in tissue of a brain, becoming an essential factor of endogenous intoxication. At long dying in the conditions of access of nek-ry amount of oxygen independent pathogenic value gets also free radical oxidation (see. Radicals free ).

Oppression of power metabolism is the reason of paralysis of volatile ionic pumps, depolarizations of cellular membranes with escaping of cells of K+, transition in cells of Cl-and Na + (see. Membranes biological ). At the same time there is an increase in osmolarity of the intracellular sector that together with redistribution of Na + is the reason of intracellular hypostasis, reduction of volume of the extracellular sector of a brain and increase in the electric resistance (impedance) in tissue of brain. The general wet brain at a sudden stop of blood circulation does not develop. At slowly progressing dying, especially at a combination of a hypoxia to a hypercapnia or increase in venous pressure, the wet brain which is followed by increase in its volume can develop (see. Swelled also swelling of a brain ). Due to the power deficit escaping of mitochondrions of calcium ions takes place, to-rye promote damage of membranes of these organellas.

At generalized changes of metabolism and the water and electrolytic relations in a brain of the dying organism development of irreversible structural changes happens to a big delay in relation to time of exhaustion of power reserves. It is established that dysfunction of mitochondrions of a brain happens not earlier than in 30 — 40 min. after approach of an anoxia. Nek-rye morfol. changes of ultrastructure of a brain appear rather quickly. So, since 5 min. an anoxia swelling of mitochondrions, redistribution and change of number of presynaptic bubbles, hypostasis of an astrocytic glia, swelling of an endoplasmic reticulum, disintegration of polisomalny sockets, nek-ry changes in kernels are noted. But all these changes have quite reversible character. Only 25 — 30 min. later, and on a nek-eye to data, even 1 hour after the termination of blood circulation in ultrastructure of a brain irreversible changes appear. Relative stability of ultrastructure of a brain to an anoxia is premises of a possibility of full revival.

The general nature of structural changes of tissue of brain is identical at a sudden stop of blood circulation and at long dying. However in the second case there can be bigger depth of the nek-ry metabolic disturbances (degree of a laktatsidoz, expressiveness of peroxide oxidation) stated above and other distribution of damages on structures of a brain (preferential damage of zones of adjacent blood supply by the main vessels of a brain). In this regard the brain by the time of complete cessation of blood circulation undergoes considerably big metabolic and structural changes.

The described disturbances of metabolism happen not only in a brain, but also in others, first of all parenchymatous, bodies. However they proceed much more slowly, than in a brain.

Conditions of dying differ on extent of oppression of functions of c. N of page, depth of disturbances of a hemodynamics and breath.

A preagonal state (see the Agony) — a stage of dying, in the course to-rogo gradually, in the descending order functions of corticosubcortical and verkhnestvolovy departments of a brain are broken, comes at first tachycardia (see) and tachypnea (see), and then bradycardia (see) and bradipnoe (see), the ABP progressively decreases below a critical level (80 — 60 mm of mercury.), sometimes (during the dying from asphyxia) after preliminary considerable, but short-term rise. In the beginning the general motive excitement having the reflex nature can be observed; it develops before emergence of signs of power deficit of a brain and reflects operation of protective mechanisms. It biol. the sense consists in attempt to bring an organism out of the menacing situation. Practically in the conditions of the continuing action of the main reasons for death it is excitement promotes acceleration of dying. After a phase of excitement disturbances of consciousness and a hypoxemic coma develop (see). The critical level of partial pressure of oxygen (r02) in tissue of a brain, at Krom occurs a loss of consciousness, makes apprx. 30 mm of mercury. At the time of loss of consciousness signs of power deficit usually still are absent, and disturbances of consciousness connect with changes of the synoptic, neuromediator processes having protective value.

Disturbances of consciousness correlate with natural changes of EEG. At the developing hypoxia after the eclipse period, duration to-rogo depends on speed of development of air hunger, there comes the motive excitement which is shown on EEG desynchronization of rhythms. Then after a short phase of strengthening of an alpha rhythm there is a delay of fluctuations on EEG to domination of delta fluctuations of high amplitude preferential in frontal areas. This delay, though not absolutely precisely in time, matches a loss of consciousness. In process of deepening of a coma delta activity breaks up to the separate groups divided by intervals of so-called electric silence. Duration of these intervals increases in parallel with falling of amplitude of fluctuations in groups of slow waves. Then electric activity of a brain completely disappears. In some cases, at a sudden stop of blood circulation, delta activity does not manage to develop. As shown in experiments on animals, at excessively long dying from blood loss delta activity sometimes disappears before short flashes of more frequent fluctuations. After full oppression of electric activity of a brain, hl. obr. at bystry dying, short-term generalized spasms of detsereb-ratsionny type can be observed.

Oppression of electric activity of a brain, including also evoked potentials, occurs at reduction of a brain blood-groove approximately to 15 — 16 ml / 100 g/min., before the depolarization of cellular membranes occurring at critical value of a brain blood-groove of 8 — 10 ml / 100 g/min. In an interval between these sizes of a brain blood-groove the brain does not function any more, but still keeps readiness to immediately recover the functions in case of strengthening of blood circulation. Duration of the period, during to-rogo a brain, nonfunctioning owing to ischemia, completely keeps an opportunity to recover the functions, is not determined. During the falling of a blood-groove it is lower than 6 ml / 100 of g/min. there is a progressing development patol. changes in tissue of a brain.

After a preagonal state the terminal pause — the state proceeding 1 — 4 min. develops: breath stops, bradycardia, sometimes an asystolia develops, disappear reaction of pupils to light, corneal and other trunk reflexes, pupils extend. During the dying in a condition of a deep anesthesia the terminal pause is absent.

At the termination of a terminal pause the agony develops (see) — the stage of dying, to-ry is characterized by activity of bulbar departments of a brain. One of a wedge, signs of an agony is terminal (agonal) breath with the characteristic rare, short, deep convulsive respiratory movements, sometimes with participation of skeletal muscles. The respiratory movements can be and weak, low amplitude. In both cases efficiency of external respiration is sharply reduced. The agony which is coming to the end posledshsh with a breath or the last reduction of heart passes into clinical death. At a sudden cardiac standstill agonal breaths can proceed several minutes against the background of the absent blood circulation.

Clinical death — a reversible stage of dying. In this state at external signs of death of an organism (lack of cordial reductions, independent breath and any neuroreflex reactions to external influences) potentiality of recovery of its vital signs by means of methods of resuscitation remains (see). The wedge is able, death on an ECG are registered either total disappearance of complexes, or fibrillar oscillations of gradually decreasing frequency and amplitude, mono - or bipolar complexes with lack of a differentiation between initial (teeth of QRS) and final (a tooth of T) parts.

In a wedge, practice at sudden death in the conditions of the standard temperature of a body duration of a condition of clinical death makes 3 — 5 min. Sometimes duration of clinical death is determined by term from a cardiac standstill before recovery of its activity though during this period the resuscitation events supporting blood circulation in an organism were held. If these actions were begun timely and were effective about what judge by emergence of pulse on carotid arteries, for the term of clinical death it is necessary to consider time between a stop of blood circulation and the beginning of resuscitation. According to modern data, the complete recovery of functions of an organism, including and higher nervous activity, is possible also at more long terms of clinical death on condition of a number of the influences which are carried out at the same time and even later a nek-swarm time after the main resuscitation actions. These influences (the actions undertaken for increase in the system ABP, improvement of rheological indicators of blood, artificial ventilation of the lungs, hormonal therapy, a detoxication in the form of hemosorption, a plasma exchange, washings of an organism, exchange hemotransfusion and especially donor artificial circulation and also nek-ry pharmakol. impacts on a brain) neutralize a number of postresuscitatic pathogenic factors and authentically facilitate the course of a so-called postresuscitatic disease.

In experimental conditions, carried out on a dog, duration of a condition of clinical death at an electric trauma (fibrillation of heart) and even during the drowning can reach 19 — 20, and sometimes and 27 min. at a standard temperature of a body. Though the probability of a complete recovery of functions of a brain at increase in these terms decreases, in a wedge, isolated cases of successful revival and recovery of functions of a nervous system at a stop of blood circulation for 12 — 22 min. are known to practice, including and at a myocardial infarction. It is possible to believe that for experimental animals absolute terms of clinical death (considering a possibility of a complete recovery in isolated cases) less than 1 hour, but more than 4 — 5 min. average apprx. 25 — 30 min. The question of the reasons of discrepancy of data of an experiment and clinic remains open so far. It must be kept in mind that duration of clinical death is influenced by a type of the dying, its condition and duration, age dying, extent of its excitement, body temperature during the dying, etc. By means of a preventive artificial hypothermia duration of clinical death can be increased to 2 hours; at long dying from the progressing blood loss, in particular at its combination to an injury, duration of clinical death becomes equal to zero since changes, incompatible with permanent recovery of vital signs, develop in an organism to a cardiac standstill.

After clinical death there comes biological, i.e. true death, development a cut excludes a possibility of revival.

K T. the page belongs also a condition of a brisk organism after resuscitation. T. pages of this type arose in connection with development of resuscitation (see). They have the difficult pathophysiological nature and demand from the doctor of use of a special complex to lay down. died (see. Resuscitation ).

Boundary, terminal character of a state after resuscitation is defined by two circumstances: instability of all vital signs in the period following directly recovery of the cordial activity and gas exchange connected with full disorganization of systems of maintenance of a homeostasis during dying by both very gradual and their insufficiently coordinate recovery after revival; possibility of development of new, postrea-nimatsnonny forms patol. changes in an organism. These circumstances create in the postresuscitatic period a complete dependence of preservation of viability of an organism from medical aid, without cut inevitably repeated dying and death of brisk.

Existence of a peculiar complex postresuscitatic patol. the changes covering all bodies and systems of an organism formed the basis for allocation of a so-called postresuscitatic disease (see. Resuscitation ). In its etiology the combination of the heavy hypoxemic changes arising in an organism during dying to resuming of perfusion of bodies and oxygenation of fabrics matters. In a pathogeny postresuscitatic patol. processes an important role is played by changes first of all ts.n.s., and also a liver, kidneys, intestines, the hearts which arose during dying and caused by a circulator hypoxia; disturbances of fabric metabolic balance as a result of in-coordinate recovery of all forms of a metabolism; endogenous intoxication of an organism the substances which collected in fabrics in the period of a stop of blood circulation and washed away in the general blood stream after resuming of blood circulation and the substances which are formed in fabrics as a result of their oxygenation in the conditions of the suppressed energy balance (free radicals); the generalized disturbances of organ blood circulation (microcirculation) arising in the postresuscitatic period owing to disturbance of coagulant system of blood; diskoordination of neurohumoral regulation of a homeostasis.

As a result of action of the specified etiological and pathogenetic factors in the postresuscitatic period in an organism in general and in its many bodies a row new patol develops. the phenomena which were absent during the dying. So, delayed patol. phenomena are found in a metabolism and blood circulation of a brain: hypoperfusion and a hypermetabolism (sharp increase of oxygen consumption), new waves of disturbance of exchange of neurotransmitters, sharp increase of maintenance of tsAMF, the delayed disturbances of nucleinic exchange, physical. - chemical properties of proteins, etc. Phase changes undergo water and electrolytic characteristics of a brain, at certain stages of the postresuscitatic period the probability of edematization of a brain increases. Structural changes of a brain are also implemented in the postresuscitatic period (a phenomenon of «maturing»), and manifestation of these changes occurs the quicker, than the stop of blood circulation was longer.

Can develop also new patol. changes of a hemodynamics (the delayed falling of cordial emission with secondary disturbance of regional blood circulation), coagulant systems of blood, an immunological defense system, hormonal regulation. In the postresuscitatic period after a severe injury and blood loss the heavy delayed dysfunctions of vitals (shock lungs and kidneys), acid-base equilibrium, water and electrolytic balance are possible; in connection with postresuscitatic pathology the secondary hypoxia, prevention and treatment develops the cut presents great difficulties.

Postresuscitatic recovery of functions of c. the N of page and independent breath generally repeats upside-down their fading during the dying. However in case of revival after the extended terms of clinical death during recovery there can be phenomena which were absent during the dying. Three types of recovery of structure of the respiratory act are known, in two of to-rykh jumps of ratios of activity of inspiratory, expiratory and auxiliary muscles take place. In dynamics of recovery on EEG can appear patol. phenomena in the form of convulsive potentials and rhythmic activity of alpha range, to-rye are registered against the background of a deep coma and so-called electric silence of EEG or separate slow complexes. In nevrol. the status at the beginning of the postresuscitatic period the general spasms and local or widespread myoclonias are most characteristic. Disturbances of structure of the respiratory act, convulsive phenomena and alpha-like activity not only are symptoms of damage of a brain, they actively join in a nostreanima-tsionny patol. process, interfering with recovery of function of c. N of page and organism in general.

After resuscitation in different terms processes of recovery, compensation and development new patol are differently combined. changes. Depending on their relative expressiveness a number of stages of a postresuscitatic disease, the characteristic can be allocated to-rykh it is not finished yet. However it is known that the major pathogenic factors operating in the postresuscitatic period exert the impact on an organism within the first 30 — 60 min. after resuming of blood circulation and even at the uncomplicated course of postresuscitatic process the greatest instability characterizes a condition of an organism during the first 2 — 3 days. At the complicated course of a postresuscitatic disease the unstable state of a brisk organism drags on for much bigger term. The postresuscitatic state stops being terminal only after the hemodynamics is stabilized and need of artificial ventilation of the lungs disappears. Since death of a brisk organism develops against the background of use of resuscitation actions, with the help to-rykh blood circulation and gas exchange is supported, development of a special form biol is possible. death — so-called death of a brain (see. Death of a brain ).

As in the theoretical, and practical relation the question of a heating-up period of those changes in an organism is important, to-rye at its revival are irreversible. According to the traditional point of view the destiny of an organism in general, and in particular a brain, is solved during the dying since air hunger is the main reason for irreversible changes. A conclusion shall be a consequence of such representation that listed above postresuscitatic patol. phenomena are fatal result of the postponed dying and revival only creates premises for implementation of pathology, edges is predetermined by dying. Proceeding from this representation, duration of the period the wedge, death can be increased only by means of preventive decrease in sensitivity of an organism, and first of all a brain, to a hypoxia.

Thanks to progress of experimental therapy it was established that an essential part of irreversible changes in an organism not only forms in the postresuscitatic period, but also it is predetermined by postresuscitatic pathogenic factors, among to-rykh ekstratserebralny and cerebral pathogenic factors are allocated. Development of irreversibility before - and postresuscitatic patol. processes depends also on a type of dying and duration of a stop of blood circulation. At excessively long stop of blood circulation (biological death) recovery is impossible already owing to only one preresuscitation changes. At suddenly developed stop of blood circulation of average duration (clinical death) in development of irreversibility the role before - and postresuscitatic pathology is equally important.

New data about; significantly changed a heating-up period of irreversible changes in the recovered organism and a role in this process of postresuscitatic pathology ideas of deadlines of clinical death.

The correct definition to lay down. tactics demands timely assessment of weight of the damages which arose during the dying and probability of completeness of recovery of vital signs.

The forecast at T. the village can be founded on features of dying and duration of a stop of blood circulation if these data are available, and also on indicators of recovery. The forecast for the course of recovery is more reasonable since dynamics of recovery reflects totally impact of dying, individual sensitivity of an organism and influence of the major postresuscitatic factors.

Early forecast of recovery of functions of c. the N of page at revival after clinical death can be made with a certain probability within the first minutes — hour after recovery of blood circulation and gas exchange. Rather complete recovery at this time of trunk reflexes, and, in particular, consciousness does to electric activity of a brain the forecast favorable. The delay of recovery of trunk reflexes till 1 o'clock, and does to electric activity of a brain to 2 hours the forecast very doubtful. Considerably the probability of a complete recovery of functions of a brain at preservation of a coma during more than 6 hours falls; at the deep coma proceeding more than 24 hours, this probability is very small, and at the coma lasting more than 48 hours is insignificant.



Bibliography: Negoveky V. A., at r-in and the p A. M and 3 about l about t about to r y l and N and E. S. Postresuscitatic disease, M., 1979; Fundamentals of resuscitation, under the editorship of V. A. Ne-govsky, Tashkent, 1977; Brain and heart infarct II, ed. by K. J. Ziilch a. o., B. — N. Y., 1979; Branston N.M., Symon L. Strong A. J. Reversibility of ischaemically induced changes in extracellular potassium in primate cortex, J. neurol. Sci., v. 37, p. 37, 1978; To 1 a t z about I. Pathophysiologic aspects of cerebral ischemia, in book: The nervous system, ed. by D. B. Tower, v. 1, p. 313, N. Y., 1975; S i e s j V. of K. Brain energy metabolism, N. Y., 1978.


A. M. Gurvich.

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