АкушерствоАнатомияАнестезиологияВакцинопрофилактикаВалеологияВетеринарияГигиенаЗаболеванияИммунологияКардиологияНеврологияНефрологияОнкологияОториноларингологияОфтальмологияПаразитологияПедиатрияПервая помощьПсихиатрияПульмонологияРеанимацияРевматологияСтоматологияТерапияТоксикологияТравматологияУрологияФармакологияФармацевтикаФизиотерапияФтизиатрияХирургияЭндокринологияЭпидемиология

Fig. 43. Development of hemorrhagic shock (according to Solovyov and Radzivill)

After a trauma the number of catecholamines (adrenalin, norepinephrine) increases that leads to vasoconstriction of arterioles' sphincters. It leads to a decrease of blood flow in the terminal portion of vascular bed, as a result of this an oxygen supply to the tissues worsens and blood goes away through A-V shunts into veins (1-st phase of shock — centralization of circulation). Under conditions of hypoxia histamine concentration in blood increases, acidosis grows that makes precapillary sphincters to open and leads to a greater slowing down of blood flow in capillaries and increase of vascular bed volume. In connection with this even a normal VCB becomes insufficient (2-nd phase of shock — decentralization of circulation). In slow capillary blood flow a hypoxia of cells continues to grow with development of metabolic acidosis at the expense of increasing lactic acid concentration in blood. A logic consequence of acidosis in a slowed down blood flow is hemolysis of erythrocytes, release of ery-throcytic thromboplastin leading to disseminated intravascular coagulation (DIC).

An occlusion of capillaries with clots leads to a stasis of blood. The latter contributes to a further accumulation of lactic acid, progression of acidosis and inactivation of cellular enzymes with a subsequent death of cells. Vascular walls begin to pass a liquid portion of blood into tissues, at the same time, aggregation of erythrocytes leads to a decrease of VCE. The 3-rd phase advances — irreversible shock.

A severity of shock, at this period, is not defined by central mechanisms, but by changes in the periphery, injury of organs (liver, kidneys, penetration of toxins from the intestine). Thus, nonspecific changes in the organism acquire a great significance.

A neuroalgesic component of injury is not a dominant one in traumatic shock, and a pain shock is encountered in clinic extremely rare. It is another point that the pain shock may aggravate patient's condition being already in shock, and in order to avoid it different blockades and immobilization are applied.

Дата добавления: 2015-02-05 | Просмотры: 779 | Нарушение авторских прав