Already in the nineteenth century certain authors were thinking of the possibility of using perfusion apparatus in order to maintain circulation in the organism. The designing of such apparatus has continued ever since.
From the beginning of the Thirties of the 20th century, right up to the present, many different designs for artificial circulation to be used both in experiments and in clinical practice, in cases of temporary arrest of cardiac circulation, have been described, especially in connection with the use of such apparatus in cardiovascular surgery. The expedience of using it in resuscitation however, was first suggested by Bryukhonenko and Chechulin. In order to determine the efficacy of artificial circulation in treating clinical death, Bryukhonenko devised his own perfusion apparatus, which he called an autojector.
Research carried out along these lines has confirmed the possibility of restoring respiration and cardiac activity by means of extracorporeal circulation in cases of clinical death due to loss of blood, drowning, asphyxia, explosive decompression, electric shock, and prolonged hypotension. It was found that use of this method to treat clinical death ensured sufficient circulation to support the vital activity of the brain, eliminate myocardial hypoxia, and restore cardiac activity. In addition, the blood substitution that occurs during extracorporeal circulation is to some extent a means of detoxication.
Certain authors stress that the vital functions of animals can be restored by means of artificial ‘heart and lungs’ after period of clinical death longer than those that can be reversed by means of the more commonly used methods of resuscitation (arterial blood transfusion, heart massage, and artificial respiration). According to Yankovsky, the limits of clinical death within which successful reanimation is possible, when artificial circulation is used by means of apparatus providing a high volumetric rate of perfusion or by means of a donor (a kind of cross circulation), are: 16 minutes for blood loss, 19 minutes for asphyxia neonatorum, 19.5 minutes for radial acceleration, 20 minutes 51 seconds for electric shock; 23-25 minutes for drowning in salt water, and 18 minutes for severe anoxia (decompression).
According to Torskaya et al., however, in these experiments on a number of the dogs considerable disorders of higher nervous activity were observed after ten minutes of clinical death due to acute blood loss, namely: listlessness, muscular weakness, inactivity, ‘whip-like tail’ (an indirect sign of alterations in the cerebellum); and in poorly illuminated rooms there was a lack of visual reaction: the animals bumped into obstacles around them and their spatial orientation was disturbed. The author also reported that study of conditioned reflexes by means of the secretory-feeding technique revealed that food stimulation in response to a repeated unconditioned stimulus was lowered in the presence of normal secretion (in one and the same experiment).
Attempts at creating three to six minute trace conditioned reflexes by direct route led to neurosis and the development of hypnoid states. Morphologic research revealed microscopic spots of necrosis and loss of cells, ‘bald patches’, throughout the whole cortex and brain stem, where the cyto-architectonics and myeloarchitectonics were impaired and connective tissue proliferated. On the other hand Yankovsky reported that many dogs that had suffered long periods of clinical death were outwardly no different from normal animals. Comparison of these findings with those of other authors draws attention to real differences in the period of clinical death during which complete reanimation of the organism is possible.
Discovery of the causes of such great differences in determining the limiting periods of clinical death and of the factors that make it possible to revive vital functions after such long arrest of circulation in the organism is undoubtedly of great interest. Especially important is all-round study of the pathophysiological laws governing the resuscitation process in cases in which artificial circulation is employed. In this connection it is not without interest to recall the statement of Chechulin and Bryukhonenko, two of the founders of this method in this country, which stressed the need for deep all-round study of the physiology of dying and reanimation, since ‘solution of the mechanical aspect of the problem, is not enough for success in resuscitating the organism as an integrated whole’.
The problems listed above understandably have a direct practical bearing, since their object is to discover how far and in what way experience of the experimental use of perfusion apparatus can be transferred to clinical practice.
All-round study of the technique of artificial circulation for purposes of reanimation was begun in our Laboratory, the object of investigation being death from loss of blood or electric shock.
Analysis of the research carried out showed that the use of extracorporeal circulation by means of the AIK-RP-64 apparatus and of artificial respiration with the Pesty RPR respirator in experiments with massive blood loss enabled cardiac activity to be restored earlier after lengthy clinical death than the usual centripetal arterial injection of blood. The volume perfused before the blood loss was made up proved to have great influence on the time needed to restore the first effective cardiac contractions. In unanaesthetized dogs that had experienced clinical death of ten minutes, in perfusion at a volumetric rate of 142 ml/kg/min, sinusal automaticity began to be recorded after 8 to 12 seconds and cardiac activity was restored after 0.8 minute. When perfusion rate was less cardiac activity took twice as long to be restored owing to the development of ventricular fibrillation in all the dogs. Application of intra-arterial injection of blood by the ordinary method after the same period of clinical death caused cardiac contractions to appear only after 2.5 minutes and in most animals ventricular fibrillation developed.
The anaesthetization background prior to dying also had a favourable effect on the restoration of cardiac activity in the experiments employing extracorporeal circulation. In dogs anaesthetized 90 minutes before bleeding cardiac activity was restored rather earlier than in conscious animals, on average within 0.5 to 0.7 minute despite the longer clinical death, and ventricular fibrillation was observed in only a quarter of the cases examined.
There can be no doubt that the frequent occurrence of ventricular fibrillation after lengthy periods of clinical death is largely a result of the disruption of intraventricular conductivity. The ECG data of almost all the dogs that had suffered ten minutes of clinical death, independently of the resuscitation technique employed, before effective restoration of cardiac activity, showed a considerable increase in the length of the ventricular complex with sharply expressed alternation.
The length of the ventricular complex when dogs were resuscitated by injection of blood into an artery can serve to illustrate this point: 0.48—0.44—0.52—0.44—0.64—0.48—0.64—0.4—0.6—0.72—0.4—0.7 second. On the other hand, in resuscitating dogs after five minutes of clinical death, the ventricular complex lengthened much less, increasing gradually from complex to complex without alternation. As alternation of this complex occurred only after lengthy periods of clinical death and did not depend on the method of resuscitation used, there are grounds for thinking that such changes in the ECG are the result of severe disruption of intraventricular conductivity as a consequence of lengthy hypoxia.
The more frequent occurrence of ventricular fibrillation in cases with injection of blood into an artery or with extracorporeal circulation at a low volumetric rate of perfusion than with artificial circulation at high volumetric rates could be due to insufficient supply of blood in coronary vessels. When there is marked hypoxia of the myocardium, restoration of the heart’s contractile function is delayed and its cavities become gorged with blood.
The character of the restoration of electrical activity in the respiratory muscles, like cardiac activity, depends on the reanimatory measures employed.
In unanaesthetized animals resuscitated after ten minutes of clinical death by means of artificial circulation apparatus with a low volumetric rate of perfusion electrical activity was restored earlier in the inspiratory muscle than in animals that received normal centripetal injection of blood. The moment of the appearance of active exhalation was identical in both cases. Normalization of the structure of the respiratory act, i.e. the disappearance of electrical activity from the accessory respiratory muscles occurred later with extracorporeal circulation at a low volumetric rate than when arterial injection of blood was employed.
In unanaesthetized animals resuscitated by means of the artificial circulation apparatus with a high volumetric rate of perfusion activity of the inspiratory muscles and active exhalation were restored later than with arterial injection of blood. The structure of the respiratory act, however, was normalized earlier than with a lower rate of perfusion. The activity of the inspiratory muscles, active exhalation, and the structure of the respiratory act were all positively restored earlier in anaesthetized dogs with a high volumetric rate of perfusion than in those not anaesthetized.
Artificial circulation in combination with artificial respiration when employed for the purpose of reanimation, with a relatively low volumetric rate of perfusion thus enables activity of the respiratory centre to be restored earlier than when the complex method of resuscitation is employed. A high rate of perfusion delays restoration of the activity of inspiratory and expiratory centres in unanaesthetized animals, which can supposedly be due to hypocapnia. Anaesthesia and the moderate hypothermia that accompanies it enables activity of the inspiratory centre and all the parameters of normalization of the structure of the respiratory act to be restored earlier than in unanaesthetized animals that have experienced the same period of clinical death.
The moment corneal reflexes develop in unanaesthetized dogs did not depend on when respiration was restored. Restoration of their electrocorticogram was delayed and began with the appearance of individual polymorphic delta-waves of low amplitude in the thirtieth minute of resuscitation. Continuous delta-activity was only formed 50 to 60 minutes after the application of reanimatory measures began.
In anaesthetized dogs corneal reflexes reappeared earlier after ten minutes of clinical death than in unanaesthetized dogs resuscitated with the same rate of perfusion.
The initial stages of the development of electrical activity were characterized in these animals, as in unanaesthetized animals, with the appearance of individual polymorphic delta-waves during the 40th to 50th minute of resuscitation. Continuous electrical activity was established within the period of 90 minutes to two hours from the beginning of resuscitation, but the considerable delay in restoration of the ECoG in anaesthetized animals did not have a negative effect on the outcome of resuscitation. When the period of clinical death was lengthened to twelve minutes all the indices of external breathing and the corneal reflexes were restored later than in animals that had endured ten minutes of clinical death.
Study of the blood of both anaesthetized animals and those not anaesthetized, experiencing ten to twelve minutes of clinical death, made during the initial and early restorative period revealed considerable disturbances of acid-base equilibrium. There was a gradual increase in uncompensated gaseous alkalosis during perfusion and in the later hours of the restorative period, plus a sharp increase in the plasma concentration of organic acids in the first few minutes of resuscitation and their slow normalization. At the same time there was an increase in the arterial-venous oxygen difference to 10-12 vol. per cent and a decrease in the oxygen saturation of venous blood to 40 or 50 per cent, both occurring in one to three hours after resuscitation.
The minute cardiac volume determined in several of these experiments showed that this was associated with a decrease in the volumetric rate of circulation. Slowing of blood flow could apparently cause the development of secondary circulatory hypoxia. The greatest shifts in acid-base equilibrium, it should be noted, and disturbance of the gaseous composition of the blood, were observed in unanaesthetized animals. These changes were less noticeable in anaesthetized animals with the same period of clinical death; but when clinical death was extended to 12 minutes they increased.
Outwardly vital functions were completely restored with resuscitation by means of an artificial circulation machine in only two of the 12 unanaesthetized animals.