Acute respiratory insufficiency, like disturbed haemodynamics, plays an important role in the aetiology and pathogenesis of terminal states and aggravates postreanimation diseases in the postresuscitation period. Experimental research has established that, in cases of massive loss of blood and traumatic shock, disturbed respiration can become an important pathogenetic factor in the development of irreversible alterations in the various organs.
A main cause of the development of respiratory insufficiency in the early postreanimation period is hypoxia due to the sharp increase in tissue oxygen requirements, in such unfavourable conditions as disturbed haemodynamics and anaemia. The respiratory insufficiency observed in the later postreanimation period is due, as a rule, to the development of pathological processes in organs directly involved in the respiratory act.
The results of treating patients brought out of terminal states undoubtedly depend on the timely application and effectiveness of measures directed against hypoxia. But clinical signs of hypoxia are frequently not visible until there are profound, even irreversible, lesions of vital organs. Because of the involvement of compensatory mechanisms directed to eliminating oxygen starvation in the tissues the gaseous composition of the blood does not alter considerably in the early stages of the development of respiratory insufficiency. For this reason, the term ‘respiratory insufficiency’ needs to be understood not only as the changes in pulmonary ventilation that lead to the development of hypoxia and hypercapnia, but also as the maximum tension of all the compensatory reactions tending to maintain adequate gas exchange.
Functional methods of investigating the state of breathing, for purposes of earlier diagnosis of respiratory insufficiency, have attracted much attention of late. But many aspects of this important problem await much further study. The majority of the work published is devoted to the functional changes in external breathing and the treatment of respiratory insufficiency in patients who have had operations on the thoracic organs and in those suffering from diseases of the central nervous system. As concerns the features of the development and therapy of respiratory insufficiency in man in other forms of illness there are only isolated communications in the literature. At the same time, it is obvious that the character of the functional changes in breathing and the tactics of the treatment to be applied will depend on the causes of the respiratory insufficiency and will not be identical for all cases. In spite of the fact that artificial pulmonary ventilation is quite widely applied in cases of respiratory insufficiency, there are still no clear indications for its application and discontinuation.
In view of this, and keeping in mind the well known fact that pulmonary hyperventilation is a first symptom of increased tissue demand for oxygen in the tissues, the Reanimation department of our Laboratory undertook to study the alterations in pulmonary ventilation and its compensatory possibilities in patients suffering from massive loss of blood in order to refine the indications for the application of artificial respiration.
The degree of oxygen deficit was evaluated from the absorption of oxygen, the total level of organic acids in blood plasma, and from the findings of functional tests recording oxyhaemograms during breathing of oxygen with subsequent breathing of air.
Patients who had suffered massive loss of blood without complications in the form of respiratory disease in the postoperative period as a rule had no clinical symptoms of hypoxia, or only weakly expressed ones. The difference in the oxygen saturation of the blood when air was breathed compared with the previous breathing of 100 per cent oxygen, after arbitrary stopping of the oxyhaemograph pen recorder at 98 per cent, was 5.3 per cent. During subsequent breathing of oxygen this value increased by 2.1 per cent. The character of the oxyhaemogram curves indicated fairly uniform distribution of air throughout the lungs and adequate diffusion of gases through the alveolar membranes. During breathing of oxygen the plateau was reached after 80 seconds. When breathing was switched to air, an oxyhaemogram began to drop after 11.5 seconds; and when breathing of oxygen was resumed it rose in the first five seconds. But, in spite of the absence of arterial hypoxaemia, tissue hypoxia was observed, as indicated by an increase in total organic acid concentration to 21.4 mEq/litre (normally not over 12 mEq/litre).
The development of tissue hypoxia in these patients was to a considerable degree predetermined rather by the increase in tissue oxygen demand on a background of anaemia and of disorders of peripheral circulation. Progressive consolidation of the lungs, or the development of so-called shock lungs, is of great importance in the pathogenesis of respiratory insufficiency and hypoxia.
The development of hyperventilation is evidence of the increase in tissue oxygen consumption; so too is the increase in oxygen absorption in 79.4 per cent of patients, by more than 200 per cent of the normal level when breathing oxygen, and its decrease by 40 to 127 per cent during subsequent breathing of air.
The increase in the organism’s oxygen consumption is compensated, as we know, in two ways: (a) by an increase in pulmonary ventilation, and (b) by an increase in the amount of oxygen extracted from each litre of air.
In most patients who had suffered massive haemorrhage and surgical intervention an increase was observed in the amount of oxygen absorbed per litre of air. With breathing of oxygen, oxygen absorption was of 337.2 per cent, CU02 110, and MRV not above 170 per cent of the needed level. Compensation of oxygen lack through a greater increase in hyperventilation was observed in only 30 per cent of all the patients examined. In these cases oxygen absorption was considerably less with CU02 of 36.4.
A very favourable factor was the fact that the increase in pulmonary ventilation in the absence of clinical symptoms of hypoxia was a result of a reliable increase in respiratory volume with a slight increase in the frequency of inhalation.
Thus, with an MRV of 100 to 150 per cent, RV was 79.5 per cent; when the MRV was of 151 to 200 per cent, RV increased to 99.1 per cent; and with very marked pulmonary hyperventilation, RV exceeded 100 per cent and had an average value of 123.6 per cent. Simultaneously with the increase in RV a reliable increase in vital lung capacity from 17 per cent to 45 per cent, was observed, which was indirect evidence of restoration of the organism’s reserve possibilities.
The comparison of the data on pulmonary ventilation and oxygen absorption and those on the haemoglobin content of the blood showed that the compensatory possibilities of eliminating oxygen deficit depended greatly on the degree of anaemia. Thus, when haemoglobin level rose to 9.5 grams per cent as a result of daily blood transfusion, the elimination of oxygen deficit in 63.4 per cent of cases was the result of an increase in oxygen absorption per litre of air. Hyperventilation of the lungs predominated in only 36.6 per cent of cases. With marked anaemia the opposite was the case; compensation of the oxygen deficit being due in most cases to a marked increase in pulmonary ventilation, and in only 37 per cent of cases to increased oxygen absorption per litre of air.
A sharp increase in pulmonary ventilation was observed only during the postoperative period. Patients with gastro-intestinal haemorrhage, examined before operation, as a rule, showed an increase in oxygen absorption per litre, independently of the degree of anaemia. The findings obtained suggested that the development of marked pulmonary hyperventilation in the postoperative period is due to aggravation of oxygen deficit in the tissues as a result of their increased oxygen consumption.
Compensation of oxygen deficit through an increase in oxygen absorption is, of course, more physiological and more economic than an extraordinary increase in the level of pulmonary ventilation, in which the additional effort of the respiratory muscles involves considerable additional loss of energy. It cannot be excluded, moreover, that the volume of absorbed oxygen in marked pulmonary hyperventilation on a background of anaemia does not correspond to the oxygen consumption of the tissues. As mentioned above, with moderate hyperventilation of the lungs, when it would seem that tissue oxygen consumption should be less, oxygen absorption was almost double that with a considerable increase of hyperventilation.
Thus the character of the compensatory reactions to increased tissue consumption of oxygen does not depend on the anaemia alone, but also on other factors, in particular on surgical intervention.
In order to avoid severe oxygen starvation in the tissues, as a result of a considerable increase in oxygen consumption immediately after surgical intervention and the end of narcosis, it is advisable to continue controlled respiration. Artificial or auxiliary respiration is especially indicated in the early postoperative period with patients who have lost more than 3000 ml of blood. With less marked blood loss when there had been prolonged hypotension, repeated operations, or during induction of anaesthesia complications leading to aggravation of hypoxia have developed. Controlled respiration is usually continued for at least two hours, and sometimes for several days, until the fullest possible restoration of circulating blood volume has been achieved, marked anaemia has been eliminated, and serious disturbances of metabolism corrected. Subsequently inhalation of oxygen is indicated in combination with haemotransfusion and measures directed to normalizing peripheral circulation. This therapy enables the number of postoperative and postreanimation complications to be reduced.
With patients who had lost more than 2000 ml of blood, and had received such therapy, the postoperational period went smoothly.
The majority of the patients whose lungs were not artificially ventilated after narcosis, subsequently developed severe respiratory and hepato-renal insufficiency.
Where respiratory insufficiency was the result of lesions of organs directly involved in the respiratory act clinical symptoms of hypoxia were usually observed. The gravity of the patient’s condition, however, depended on the character of the pathological process.
When focal pneumonia developed in the postoperational period or after tracheostomy performed because of oedema of the subligamentary space of the larynx, the clinical symptoms corresponded to relatively weak hypoxia: namely, panting not faster than 25 inhalations per minute, slight cyanosis of the skin, a sensation of lack of air, fairly easily eliminated by inhalation of oxygen; but the total organic acid concentration of blood varied from 19.2 to 24 mEq/litre, and the difference in oxygen saturation of the blood with inhalation of oxygen and air varied from II to 16 per cent. In patients suffering from these forms of pathology, like in those who had suffered massive blood loss not complicated by respiratory disorders, hyperventilation of the lungs was determined by an increase in RV with respiratory rate, as a rule, not exceeding 24 per minute. The appropriate therapy (inhalation of oxygen, and transfusion therapy aimed at eliminating anaemia and metabolic disorders) reduced the difference in oxygen saturation of the blood with breathing of air and of oxygen to 4 or 6 per cent and the total plasma organic acid concentration to 15 mEq/litre.
With double pneumonia, pulmonary atelectasis, and obstruction of the trachea and bronchi by purulent phlegm and plugs, clinical signs of severe respiratory insufficiency developed; respiration 25 to 45 per minute often involving the cervical accessory muscles; marked cyanosis of the skin and visible mucosa; complaints of lack of air, in spite of inhalation of oxygen; delirium, hallucinations, agitation, tachycardia; and frequently a rise in blood pressure. Because of the clinical symptoms of severe respiratory insufficiency most of the patients received artificial respiration. In some, oxygen saturation of the blood dropped to 70 per cent and below when breathing air and increased to 90 per cent or more when breathing oxygen.
The indices of the functional test, with recording of an oxyhaemogram in breathing of oxygen and air, however, did not always correspond to the clinical picture of severe hypoxia. In several patients the difference in oxygen saturation with breathing of air after preliminary breathing of oxygen did not exceed 8 per cent. In contrast to the oxyhaemograms of patients suffering from massive blood loss not complicated by respiratory disorders, the patients of this group had a drop in oxygen saturation of the blood when breathing was switched from oxygen to air, which began two to four times later and lasted two or three times as long. During subsequent breathing of oxygen, the oxyhaemogram curves either did not change, or increased very slightly. This pattern was observed, as a rule, in patients with most marked lesions of the lungs (massive pneumonia, aggravation of chronic respiratory insufficiency), when uniform distribution of air within the lungs was disturbed and pulmonary circulation did not correspond to pulmonary ventilation. Measurement of the oxygen tension of arterial and venous blood gives a more exact idea of the degree of hypoxia.
Sharp hyperventilation of the lungs was observed in all patients with marked clinical signs of hypoxia, and was due mainly to an increase in the rate of respiration. When the MRV was between 150 and 180 per cent of the needed level, RV was less than 60 per cent in the overwhelming majority of cases, and the rate of respiration was 38 per minute. Where the MRV was between 180 and 250 per cent RV increased only to 78 per cent with a rate of respiration of 31 per minute, and a VLC not above 17 per cent of the needed level.
There was no possibility of determining the level of oxygen absorption of patients with severe respiratory deficiency, as they withstood even short periods of spirographic examination with difficulty. Nonetheless it was obvious that their compensation of oxygen deficit was far from complete; hyperventilation of the lungs was due either to sharp quickening of respiration or to extraordinary tension of all the compensatory mechanisms. At the same time it is well known that much more oxygen is expended on the work of the respiratory muscles with marked shortness of breath than with quiet breathing, and the other organs and tissues consequently suffer from severe oxygen starvation.
Dynamic observation of the functional state of breathing in patients with double pneumonia showed that hyperventilation increased initially through quickening of respiration and an increase in RV with a simultaneous decrease in VLC. Subsequently RV diminished and MRV either rose slightly as a result of the much higher rate of respiration or diminished. There was usually already no possibility of determining the vital volume of the lungs. Excessive ventilation on a background of decreasing VLC is, of course, dangerous, as it is evidence of maximum exhaustion of all reserves.
Carbon dioxide tension in blood taken from a finger was within normal limits for 59.4 per cent of all patients, decreased for 23.7 per cent and increased for 16.9 per cent. No strict dependence of the degree of hyperventilation on the carbon dioxide tension in the capillary blood of patients with pathological conditions of the respiratory organs developing after massive loss of blood and trauma could be established. When the MRV was 218 per cent, for example, carbon dioxide tension in most cases was within normal limits, and in individual cases even hypercapnia developed. The greater the lack of correlation between these indices, the more serious was the course of the respiratory insufficiency.
From dynamic study of the state of pulmonary ventilation, it was possible to distinguish four forms of respiratory insufficiency: (1) a gradual increase in MRV through increase in RV at a respiration rate not exceeding 25 per minute and simultaneous increase in VLC; (2) an increase of MRV through quickening of respiration with no change in RV or a slight decrease; (3) an increase in MRV through deepening of respiration, but with simultaneous decrease in VLC; (4) a decrease in pulmonary ventilation on a background of quickening of respiration with reduction of RV. Comparison of the changes in ventilation with the findings of clinical examination gives reason to think that the first form is typical of slight degree of respiratory insufficiency, the second and third of severe degree and the fourth of total decompensation.
Analysis of the clinical observations showed that artificial ventilation of the lungs did not give positive results in extreme cases of respiratory insufficiency if blood loss exceeded 2000 ml or if severe nephropathia had occurred even with small loss of blood. The main causes of a fatal outcome were then not only pneumonia, but also severe degenerative alterations in the liver and kidneys. The data of the Mobile Reanimation Centre indicate that massive blood loss not complicated by respiratory insufficiency far from always leads to grave irreversible alterations in the liver and kidneys; only one such patient in 58 died. It is quite obvious that the development of hypoxic hypoxia in such pathological states aggravates hepatorenal insufficiency. At the same time, prompt elimination of the hypoxia avoids these complications.
There is reason to believe that the outcome of reanimation greatly depends on prompt application of artificial ventilation of the lungs but, for patients with blood loss and trauma, complicated by disorders of the respiratory organs, some of the objective indications for artificial respiration do not always apply, in particular, the development of hypercapnia; decrease of VLC to 30-50 per cent in patients with disorders of the central nervous system; a 10 per cent drop in the oxygen saturation of the blood during breathing of air after oxygen in the presence of severe respiratory insufficiency.
As a result of hyperventilation during severe forms of respiratory insufficiency, the carbon dioxide tension in mixed capillary blood may be high or low, but often remains within the normal range. As regards VLC, it remains below normal in patients who have undergone laparotomy or are in a state of skeletal traction even after phenomena of respiratory insufficiency have been eliminated or reduced to insignificance.
In our opinion the most complete indications for the application of artificial ventilation are changes in the indices of pulmonary ventilation; in order to avoid the development of severe hypoxic alterations in the parenchymatous organs in combination with primary or secondary respiratory insufficiency it is advisable to begin artificial respiration when the MRV rises by more than 180 per cent as a result of quickening of respiration, with an RV less than 70 per cent, or when the MRV increases as a result of deepening of respiration, while the VLC decreases with fairly high pO2 indices of arterial blood and hypocapnia. In those cases, when for any reason it is impossible to determine the indices of pulmonary ventilation, the only indication for artificial respiration is a clinical picture of respiratory insufficiency: apnoe, serious disturbance of respiratory rhythm, clinical symptoms of severe hypoxia and hypercapnia. It must, however, be kept in mind that the evaluation of the gravity of respiratory insufficiency from the clinical symptoms may prove subjective. Moreover, as mentioned above, clinical signs of hypoxia sometimes develop when severe functional and morphologic alterations have already occurred in the organs most sensitive to oxygen starvation.
It has been established that artificial ventilation of the lungs is a most powerful and effective therapeutic measure directed to eliminating hypoxia when respiratory insufficiency develops. With marked hyperventilation on a background of disturbed haemodynamics and anaemia, artificial ventilation of the lungs allows more economical and rational utilization of oxygen by avoiding increased work of the respiratory muscles.
In the Hospital reanimation department artificial ventilation has been applied for periods from a few hours to several months in patients who have experienced a terminal state due to various causes: e. g. trauma, lesions of the central nervous system, mechanical asphyxia, pneumonia, certain forms of poisoning, etc.
In particular, in cases of severe cranio-cerebral trauma artificial ventilation with an air-oxygen mixture not only eliminates hypoxia, but has a curative and prophylactic effect on the traumatic oedema of the brain, lowering the cerebrospinal pressure by 30 per cent on average. In that connection not only is stable arterial hypoxaemia in the presence of central hyper- or hypoventilation of the lungs an indication of the need to employ artificial ventilation, but so too is high centralized hypertension, independent on the degree of oxygen saturation of the blood and of the oxygen tension.
Clinical research has established that prompt and proper adaptation of the patient to the respirator is of great importance in the initial period of artificial ventilation. Patients with functional insufficiency of the respiratory muscles were found to adapt more easily than others. In those patients who were in a comatose state, particularly in cases of trauma and brain diseases and in those in whom pathological processes were accompanied with disturbance of the ratio of ventilation and pulmonary circulation, it was much more difficult to synchronize breathing with artificial respiration.
Four types of unsynchronized respiration are distinguished: (1) complete absence of coincidence of the rhythms of spontaneous and artificial respiration; (2) spontaneous inhalations of the patient inserted between inhalations of the respirator; (3) when the patient is in advance of the respirator’s inhalation; and (4) resistance to the machine at the height of inhalation.
A main cause of lack of correspondence between the rhythm of spontaneous respiration and the machine is alveolar hypoventilation with an inadequate minute volume delivered by the respirator, and leaks in the elements of the system. The unpleasant sensation the patient feels when the machine is connected, moreover, plays a role. The patient’s adaptation also depends on the type of machine used.
To adapt the patient to artificial ventilation of the lungs the most important problems are to discover and eliminate the causes of asynchrony; in this proper choice of rhythm and of the gas mixture to be inhaled are of great importance. Hyperventilation and the creation of moderate gaseous alkalosis are usually applied and the oxygen concentration in the breathed mixture increased. At the same time attempts have been made to synchronize the patient with artificial ventilation by means of commands to inhale and exhale, and of manual ventilation using a bag connected to the artificial respiration machine. It is of great importance to decompress the gastrointestinal tract and carefully anaesthetize patients with traumatic injuries. According to our findings, depression of spontaneous respiration by means of narcotics, neuroplegic drugs or other preparations can to be resorted to with great caution and only when it is completely impossible to obtain synchronization without them in which case the possibility of adequately adjusting artificial ventilation to the needs of the patient is excluded. Special caution is needed when muscle relaxants are employed owing to their unfavourable effect on haemodynamics and to the fact that they make it difficult to diagnose complications. Among the medicaments used to synchronize respiration, sodium oxybutyrate gives good results.
Automatic ventilation of the lungs has its own special features depending on the aetiology of the terminal state and of the respiratory insufficiency. In patients suffering massive loss of blood, especially in obstetric cases, it is advisable to resort to artificial respiration with active exhalation in order to avoid haemodynamic complications.
When the terminal state is the result of severe trauma of the thoracic cage, artificial respiration of infrequent rhythm with a large respiratory volume and passive exhalation, and simultaneous, thorough anaesthesia and prophylaxis of the tensed pneumothorax are indicated.
Artificial respiration has become widely used of late in aggravated chronic respiratory insufficiency, and oedema of the lungs. But there is still no clear idea as to what methods are best to use for this purpose. Thus, for example, in treating oedema, it is sufficient, in the opinion of some investigators, to create high pressure in the lungs only during inhalation; others recommend creating resistance during exhalation in order to raise average pulmonary pressure.
Research has shown that it is most expedient in cases of oedema of the lungs, to employ artificial respiration with 100 per cent oxygen in a rhythm of 16 to 22 inhalations per minute and an RV of 700 to 800 ml. Raising pulmonary pressure to +10 to +15 cm of water column by creating resistance during exhalation was found to be a decisive factor in liquidating oedema. Cases have been observed where oedema of the lungs developed on a background of artificial respiration and was only relieved by increasing average tracheal pressure. The high efficacy of the increased tracheal pressure was due to a considerable reduction in the filling of the right ventricle and to a drop in the gradient of transcapillary pressure in the lungs. Let us cite an example.
Artificial ventilation of the lungs with resistance during exhalation or positive pressure at the end of exhalation has a favourable effect on gas exchange in the lungs. The number of ventilated alveoles increases, the difference in oxygen content between the alveoles and the arteries diminishes, as does the venous shunt in the lungs. Although the raising of intrapulmonary pressure causes a noticeable reduction of cardiac output, the positive effect of the considerable increase in oxygen partial pressure in the blood on the patient’s condition is much greater than the detrimental effect of the disturbances of haemodynamics developing from it. For that reason the technique of artificial ventilation of the lungs with resistance during exhalation is being more and more often employed to treat pneumonia or patients with ‘shock lungs’, i.e. with disorders accompanied by a decrease in pulmonary elasticity, and an increase in oxygen difference between alveoles and arteries, and in venous shunt.
With aggravation of chronic respiratory insufficiency, the most effective method is auxiliary respiration through a lip mask during the early period of aggravation of this condition. In an uncompensated attack of bronchial asthma active inhalation is excluded so as to avoid aggravation of the bronchospasm. Artificial respiration of infrequent rhythm with high RV, but with its subsequent reduction as the bronchospasm is ended, has been found to be most effective. When the respiratory tract is free and pulmonary pliancy reduced (pneumonia, pneumosclerosis, pulmonary emphysema) patients are synchronized with the respirator more easily if pulmonary ventilation was increased considerably, the rate of respiration being 26 to 28 per minute, and tracheal pressure not more than 35 cm of water column.
The considerable diminution of hypoxaemia is not the sole explanation of the high efficacy of artificial respiration in treating respiratory insufficiency compared with other measures. The more rational utilization of absorbed oxygen through reduction of its consumption by the respiratory muscles is also of importance.
During the preparations for, and application of, artificial respiration it must be kept in mind that patients brought out of a terminal state remain extremely sensitive for a long time to even temporary hypoxia, and that septic complications can easily set in in them because of their very severe immunodepression. All manipulations must therefore be carried out rapidly, in sterile conditions, and by experienced personnel. The success of treatment often depends on proper organization of the department and strict observance of asepsis.
When the course of the respiratory insufficiency is favourable, oxygen saturation of the blood increases during artificial respiration of air and subsequently during spontaneous respiration. Patients synchronize easily with the respirator when ventilation and the oxygen concentration of the inhaled mixture diminish. When the course is unfavourable, it is more difficult to synchronize patients with the respirator. An increase of ventilation using 100 per cent oxygen to 20 to 26 litres does not give positive results, and patients cannot support breathing of air even temporarily. It is not possible to determine the oxygen saturation of the blood on change of its concentration, as slight alterations in the regime of the respirator lead to asynchronization.
Several authors with great experience in employing artificial respiration warn against prolonged use of mixtures containing high concentrations of oxygen.
Even with a favourable course, it must be noted, the timeliness of discontinuance of artificial respiration has a great influence on the outcome of treatment. Research carried out in our department showed that, to explain the changes that have taken place in the process of breathing, a single examination of the state of pulmonary ventilation is not sufficient even when the difference in oxygen saturation of blood in breathing of pure oxygen and air is of not above 8 per cent. Given latent respiratory insufficiency, and more so when it is manifest, an increase in ventilation is observed as the time the patient is disconnected from the respirator lengthens. With severe forms of respiratory insufficiency an increase in pulmonary ventilation through quickening of respiration begins in the first ten minutes of spontaneous respiration. As the condition of the organs involved improves, these alterations in ventilation develop later. A good prognostic sign is an increase in ventilation through increase in RV with a simultaneous rise in VLC. We suggest that artificial respiration can be discontinued finally when the MRV does not change or increases slightly as a result of deepening of respiration over a period of six to eight hours. But with hypoventilation or hyperventilation it is premature to discontinue artificial respiration.
Evidence of latent respiratory insufficiency is an increase in oxygen absorption as the time the patient is disconnected from the respirator lengthens.
The wide use of hyperbarotherapy in the conditions of reanimation, including the restorative period, is a special problem. Its role in the treatment of states of hypoxia is exceptionally great. The physiological basis of hyperbarotherapy is the possibility of supplementary oxygen saturation of tissues through excess dissolving of oxygen in the tissues owing to the increase in its pressure in the surrounding medium. Analysis of experimental findings has shown that oxygen tension in the tissues increases regularly as pressure increases in the pressure chamber. According to Berezin’s findings, animals can breathe pure oxygen safely for 30 to 60 minutes. Indices of a toxic effect on the organism are changes in the EEQ pattern, and in the frequency of pulse and respiration. In the conditions of a pressure chamber the blood lactic acid content of animals in states of shock fell to the original level, or to half what it was in the controls.
Hyperbarotherapy is now beginning to be applied as a method of treating diseases involving the development of hypoxia, and in cases of traumatic shock, anaerobic infection, and tetanus. The indications and contraindications for its use in the conditions of reanimation departments are gradually being made precise.