As a result of the suffered hypoxia and of intoxication by partially oxidized metabolites the organism’s vital functions are gravely disturbed in the postreanimation period, which sometimes leads to fatal results. Moreover, the disturbances of haemodynamics and respiration developing, often in combination with anaemia, after the restoration of cardiac activity, aggravate the oxygen starvation of the tissues and create conditions highly unfavourable for the normalization of the organism’s functions.
Thus, in the postreanimation period it is characteristic that all forms of hypoxia develop, namely hypoxic, circulatory, anaemic, and tissue. For that reason the gravity of the pathological processes in the restorative period is predetermined not only by the character and duration of dying and clinical death, but also by the effectiveness of the measures applied in order to restore cardiac activity and respiration and avoid disturbances in the organism’s other functions in the later postreanimation period.
Practice has shown that too low or too high a level of arterial pressure at the beginning of resuscitation, premature discontinuation of artificial respiration, pulmonary hypoventilation or hyperventilation, the administration of substances stimulating or causing sharp inhibition of the still not wholly revived cells of the cerebral cortex in the early restorative period can all lead to death.
The gravest complications in the postreanimation period are functional disturbances of the central nervous system, oedema of the brain and lungs, and cardiac, respiratory, hepatic, and renal insufficiency.
Disturbances of metabolism and the development of serious pathological processes, it must be noted, happen not only in patients who have experienced clinical death, but also in those revived from states of agony or III or IV degree traumatic shock.
Here, in connection with the not always adequate use of the term ‘shock’ in reanimation practice, we must make a short digression.
The concept of ‘traumatic shock’, as an alarm signal for the doctor, will apparently retain its significance for some time to come, although as methods of diagnosis improve and our understanding of the pathogenesis of terminal state deepens there, the sphere in which this diagnosis is used will gradually shrink, and it will more and more often be replaced by more concrete definitions revealing the essence of the pathological process that has led to the patient’s grave state. In this connection we may perhaps cite the following example. Detailed examination in our Laboratory of the clinical forms of severe poisoning by acetic essence made it possible to clarify several of its particular phenomena and symptoms, which used all to be described by the general concept ‘intoxication and shock’.
There are grounds, apparently, for believing that the leading factors in the mechanism of the development of this state are not the neurogenic ones but many other causes, like damage to vital organs, etc. At the same time, even then, when there is no doubt about the role of the central nervous system it would be incorrect to link it exclusively to the higher sectors, and the cerebral cortex since we know that many reflexes close in the subcortical zone without ever involving the cortex.
As a rule the nervous system is involved in the development of shock but it is far from always the cause of the patient’s grave state. In the various stages of the development of shock, however, functional disturbances of the nervous system can become the main factor in its pathogenesis, and if the role of the pain factor is included, such a state can become one of true neurogenic shock.
In that connection several questions arise. Can the pain factor be ignored in shock? In no case. Can pain exhaust the organism? Undoubtedly. Does classical shock, as described by Pirogov, exist? Certainly. In our opinion the answers to these questions are not open to doubt. It must only be kept in mind that the exhaustion of the central nervous system may be due to several other factors, such as deep disturbances of haemodynamics, and not simply to the influence of pain impulses.
Another aspect of this problem needs touching on. People die not only from shock, therefore no terminal or preterminal state can be identified automatically as shock. When this term is used to emphasize the gravity of the patient’s condition, its conventional character needs to be kept in mind; in evaluating the concrete, true causes of the terminal state we cannot apply the criteria we use in evaluating true shock.
As concerns the disturbances of metabolism in patients in a terminal state, it must be noted that alterations in metabolic processes also occur in conditions of prolonged hypotension or severe respiratory insufficiency due to various causes. Earlier experimental and clinical research established that, as the period of hypotension due to loss of blood is prolonged, the prognosis deteriorates. The main causes of an unfavourable outcome after prolonged hypotension are alterations of a degenerative or necrotic nature in the parenchymatous organs.
Not so long ago, the interests of people working in the field of reanimatology were mainly focused on study of the pathophysiological laws governing the dying and resuscitation of the organism and the elaboration of a complex of reanimation methods. The progress made in this direction is well known; we now dispose of a powerful arsenal of means of resuscitation, which has become available to wide circles of general practitioners.
At the same time there is ample experimental and clinical material showing beyond any doubt that, after the first stage of reanimation, i.e. the restoration of cardiac activity and respiration, an even more complex problem arises, treatment of the results of the general hypoxia suffered. As has already been mentioned, the state in which the resuscitated organism is after a certain period of clinical death, and of the dying that preceded it, has several qualitative features, namely, specific disturbances of metabolism, characteristic alterations in the functioning of the central nervous system and the internal organs, and special features in the mechanisms sustaining homeostasis. All this allows us to speak of postreanimation disease as of a special nosological form.
In that connection it is clear that the treatment and prevention of terminal states are not the sole organic constituent of reanimatology and that it also includes treatment of the pathological states that arise in the postreanimation period, which may be called ‘disease of the reanimated organism’.