The Nature and Functional Significance of Haemodynamic Disturbances in the Postreanimation Period

At present it is known that the period of restoration of heart’s activity does not always predetermine the outcome of resuscita­tion. One of the main pathological shifts underlying postreanima­tion disease and governing the development of irreversible changes in the organs and tissues is circulatory insufficiency. After regular cardiac activity has been restored, marked haemodynamic distur­bances last for a considerable time in spite of the stabilization of blood pressure at quite a high level. 

Haemodynamic disturbances have been studied in greatest detail in experiments on animals that have died from loss of blood and been subsequently resuscitated after clinical death.

It has been established that the maximum increase in cardiac minute volume and of cardiac output is observed in the first three to five minutes after resuscitation. This increase in minute volume occurs with aug­menting coronary blood flow and reduction of general peripheral resistance, or its maintenance within normal limits. Arterial blood pressure increases by 50 to 100 per cent.

The progressive rise in pressure in the left and right auricles, which occurs with increasing hypertension in the vessels of the lesser circulation, indicates maximum working of the myocardium. During this period dangerous disturbances of cardiac rhythm can develop, and even extinction of cardiac activity with pressure in the auricles continuing to mount. And it is not excluded that this process has a reflex character.

When the restoration of cardiac activity is of a favourable type, in approximately the tenth minute of resuscitation, the pressure in the right and left auricles falls on a background of still higher pressure in the aorta and the pulmonary artery, though also tending to normalize. At this time reduction of cardiac output begins, along with an increase in general peripheral resistance. Thirty or forty minutes after resuscitation the heart’s working conditions deteriorate, which is expressed mainly in a raising of general peripheral resistance with continuing hypertension in the lesser circulation.

Systemic arterial pressure falls only slightly thanks to the increase in peri­pheral resistance, despite the fact that a marked diminution of cardiac output begins at this time and a lessening of blood flow to the right heart. In animals that have been three to five minutes in clinical death due to loss of blood normalization of the central haemodynamic parameters begins toward the end of the first or beginning of the second hour of resuscitation. Left auricular pres­sure, however, remains high in this period, indicating a functional insufficiency in the left ventricle. Cardiac output and minute vo­lume remain low. With prolonged cardiac arrest as a result of ventricular fibrillation and haemorrhage, normalization of the haemodynamic parameters only begins seven to nine hours after resuscitation, independently of the measures employed.

When the outcome of resuscitation is unfavourable, the distur­bances of central haemodynamics described above progress; their mechanism still remains unclear. Some authors attribute the reduction of cardiac output to depression of the myocardium’s contractile capacity as a result of exhaustion of its energy resources and of the action of toxic substances formed in the ischaemia afflicted tissues. Others con­sider that the role of the heart itself in the regulation of cardiac output is secondary, with disturbances of peripheral circulation being the main factor.

Several authors have found that the capacitance vessels play a major role in changing the level of cardiac output. They can actively regulate the quantity of circulating blood and thus increase or reduce venous flow to the heart. The disturbances of peripheral circulation are possibly due, to a considerable extent, to impairment of the regulation of resistive and capacitance vas­cular tone, and the relation between these two parts of the blood stream. Deeper study of this question, however, is necessary.

The increase in general peripheral vascular resistance might be easily explained in cases of hypovolaemia and developing hypo­tension as an expression of the general mechanisms of circulatory compensation. In these conditions, of course, centralization of cir­culation and a redistribution of the fractions of cardiac output take place, which should ensure the necessary level of circulation in organs like the heart and brain.

Limitation of blood supply to the intestine, liver, and kidneys after circulatory arrest during clinical death can be fatal to these organs, the more so that postreanimation ischaemia of the parenchymatous organs is often much more prolonged and severe than the oxygen starvation they suffered during clinical death. In the postreanimation period, however, there is raising in the general peripheral vascular resistance even in the absence of loss of blood and fluid from the organism and in quite a normal systemic arterial pressure. The state of haemody­namics in this case is possibly a result of the same compensatory mechanisms that circumvent the latent tendency to decompensa­tion of circulation.

Disturbances of microcirculation, associated with spastic state of the arterioles and the precapillary and postcapillary sphincters, and with the diversion of blood flow and the subsequent weakening of venous tone, play a certain role in increasing peripheral vas­cular resistance. Embolism of the end vascular formations by con­glomerates of blood cells, drops of neutral fat, and filaments of fibrin also helps maintain foci of hypoxia with the subsequent development of focal necroses. Marked disturbances of various orien­tation in regional blood flow and microcirculation are observed during the restorative period in the liver, mesenteric vessels, and muscle tissue, and especially in the kidneys. The presence of the mosaic and uneven character of the restoration of tissue oxygena­tion in each of these organs has been observed by means of mul­tiple polarography.

The outcome of reanimation depends greatly on the conditions of blood supply to the brain in the early postreanimation period. It has now been established that, as circulation is restored in the organism, the volume of blood flowing through the brain increases considerably. Our own re­search indicates that the volume of cerebral blood flow increased on average by 75 per cent during the fifteenth minute of the postre­animation period, after six or seven minutes of clinical death from asphyxia or 30 minutes of compression ischaemia, and flow through the carotid artery by 210 per cent. Normalization of the volume of cerebral blood flow occurs at the end of the first hour of the postreanimation period.

During the first hour, important to note, not only is there excess perfusion but also deep disturbance of the regulation of cerebral vascular tone. Brain circulation becomes more dependent on systemic haemodynamics than is normally the case, and whereas, in normal conditions, an insufficiency develops when arterial pressure drops on average to 60 mm Hg, in the postreanimation period a level of 100 or 120 mm Hg can prove critical. In that case the favourable effect exerted by an increase of arterial blood pressure to between 150 and 180 mm Hg, or higher on the restorative period becomes obvious.

After the period of excessive perfusion, however, follows one of considerable reduction of the volume of cerebral blood flow. Our own findings are that the volume of cerebral circulation and of flow in the carotid arteries drops gradually, falling to 25 or 30 per cent of the initial value after some three to three and a half hours. Simultaneously with the reduction of blood flow, cerebral vascular resistance increases by 4.0 to 4.5 times. It is important that the reduction of cerebral blood flow occurs at a time when brain func­tions are restored energetically and there is a marked increase in oxygen consumption. In the pathogenesis of the deterioration of cerebral circulation no little role may be played by the develop­ment of interstitial oedema of the brain, spasm of its arteries, and disturbances of capillary circulation. Nevertheless further special study of this question is needed.

In spite of the marked haemodynamic shifts oxygen supply to the tissues continues to be satisfactory for a long time even when the outcome of reanimation is unfavourable. Evidence of this is the drop in the first three hours in the metabolic acidosis that develops during dying and clinical death, and the absence of a further increase in the blood level of partially oxi­dized metabolites.

During the period when cardiac minute volume and output fall, circulatory insufficiency is apparently compensated by tachycardia, an increase in general peripheral resistance, and centralization of the circulation through redistribution of regional blood flow on the one hand and on the other by increased utilization of oxygen from the blood by the tissues, which considerably reduces the oxygen content and tension in mixed venous blood. In separate organs and tissues, however, stable oxygen starvation remains for a pro­tracted period.

Thus the state of the circulation during the early postreanimation period is governed by a complex interaction of pathological and compensatory processes. Of the compensatory-adaptive reac­tions known to us that play the most important role during this period are the centralization of circulation and the extremely strenuous work of the heart. But the functional sense of the com­pensatory reactions in the states in question is not solely one.

They are rational because they enable the hypoxia of vital organs to be reduced at maximum speed; at the same time they cannot be considered perfect, since their performance makes high demands of the myocardium which is already functioning with maximum strain and the disturbed blood supply to organs and tissues during prolonged centralization of the circulation can cause severe and even irreversible changes in the parenchymatous organs. It is therefore very important to determine the physiologically permis­sible limits of the tension of the organism’s useful compensatory reactions, which may cease to be a favourable factor at certain stages of the postreanimation process and become a harmful one and a cause of the development of irreversible changes in the organism.

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