- Symptoms of Hemorrhagic shock
- Reasons of Hemorrhagic shock
- Treatment of Hemorrhagic shock
Hemorrhagic shock develops as a result of acute blood loss.
Acute blood loss is a sudden vykhozhdeniye of blood from a vascular bed. The main clinical symptoms of the reduction of OTsK (hypovolemia) which arose at the same time are pallor of integuments and visible mucous membranes, tachycardia and arterial hypotonia.
Symptoms of Hemorrhagic shock:
Stage 1 (the compensated shock) when blood loss makes 15-25% of OTsK, consciousness of the patient is kept, integuments pale, cold, is moderately reduced by the ABP, pulse of weak filling, moderate tachycardia to 90-110 beats/min.
The stage 2 (dekompensirovanny shock) is characterized by increase of cardiovascular disturbances, there is a failure of compensatory mechanisms of an organism. Blood loss makes 25-40% of OTsK, disturbance of consciousness to soporous, a Crocq's disease, extremities cold, is sharply lowered by the ABP, tachycardia of 120-140 beats/min, pulse weak, threadlike, an asthma, an oliguria to 20 ml/hour.
The stage 3 (irreversible shock) is a concept relative and in many respects depends on the applied resuscitation methods. Condition of the patient extremely heavy. Consciousness is sharply oppressed before full loss, integuments pale, skin "mramornost", systolic pressure is lower than 60 mm Hg, pulse is defined only on the main vessels, sharp tachycardia to 140-160 beats/min.
As express diagnosis of assessment of severity of shock is used a concept of a shock index – ShI – the relation of heart rate to the size of systolic pressure. At shock of 1 degree of ShI = 1 (100/100), shock 2 degrees - 1,5 (120/80), shock 3 degrees – 2 (140/70).
Hemorrhagic shock is characterized by the general serious condition of an organism, insufficient blood circulation, a hypoxia, disbolism and functions of bodies. Hypotension, hypoperfusion (decrease in gas exchange) and a hypoxia of bodies and fabrics are the cornerstone of a pathogeny of shock. The major disturbing factor is the circulator hypoxia.
Rather bystry loss of 60% of OTsK is considered for the person deadly, blood loss of 50% of OTsK leads to failure of the mechanism of compensation, blood loss of 25% of OTsK is almost completely compensated by an organism.
Ratio of size of blood loss and its clinical manifestations:
Blood loss of 10-15% of OTsK (450-500 ml), hypovolemia is not present, is not lowered by the ABP;
Blood loss of 15-25% of OTsK (700-1300 ml), easy degree of a hypovolemia, the ABP it is lowered by 10%, moderate tachycardia, pallor of integuments, a cold snap of extremities;
Blood loss of 25-35% of OTsK (1300-1800 ml), moderate severity of a hypovolemia, the ABP it is lowered to 100-90, tachycardia to 120 beats/min, pallor of integuments, cold sweat, an oliguria;
Blood loss to 50% of OTsK (2000-2500 ml), heavy degree of a hypovolemia, the ABP it is lowered to 60 mm. hg, pulse threadlike, consciousness is absent or is confused, sharp pallor, cold sweat, an anury;
Blood loss of 60% of OTsK is deadly.
Frustration of a mikrotserkulyation due to blood circulation centralization is characteristic of an initial stage of hemorrhagic shock. The mechanism of centralization of blood circulation happens because of acute shortage of OTsK owing to blood loss, venous return to heart decreases, venous return to heart decreases, the stroke output of heart decreases and the ABP falls. As a result of it activity of a sympathetic nervous system increases, there is the maximum emission of catecholamines (adrenaline and noradrenaline), heart rate increases and the general peripheric resistance of vessels to a blood-groove increases.
At an early stage of shock centralization of blood circulation provides a blood stream in coronary vessels and vessels of a brain. The functional condition of these bodies is important very much for maintenance of life activity of an organism.
If there is no completion of OTsK and simpatoadrenergichesky reaction drags on in time, then in an overall picture of shock negative sides of vasoconstriction of a microcirculator bed – reduction of perfusion and a hypoxia of peripheral fabrics due to which blood circulation centralization is reached are shown. In case of lack of such reaction the organism perishes the first minutes after blood loss from an acute circulatory unefficiency.
The main laboratory indicators at acute blood losses are hemoglobin, erythrocytes, a hematocrit (the volume of erythrocytes, norm for men of 44-48%, for women of 38-42%). Definition of OTsK in emergency situations is difficult and connected with loss of time.
The syndrome of the disseminated intravascular coagulation (DVS – a syndrome) is a heavy complication of hemorrhagic shock. Development of DVS – a syndrome is promoted by disturbance of a mikrotserkulyation as a result of massive blood loss, an injury, shock of various etiology, transfusion of large amounts of stored blood, sepsis, serious infectious diseases, etc.
The first stage of DVS – a syndrome is characterized by dominance of hypercoagulation at simultaneous activation of antikoagudyantny systems at patients with blood loss and an injury.
The second stage of hypercoagulation is shown by koagulopatichesky bleedings, a stop and which treatment presents great difficulties.
The third stage is characterized by a hypercoagulative syndrome, development of trom-botichesky complications or repeated bleedings is possible.
Both koagulopatichesky bleedings, and hypercoagulative syndrome serve as manifestation of the general process in an organism – a trombogemmoragichesky syndrome which expression in a vascular bed is DVS – a syndrome. It develops against the background of the expressed blood circulation disturbances (crisis of a mikrotserkulyation) and exchange (acidosis, accumulation of biologically active agents, a hypoxia).
Reasons of Hemorrhagic shock:
The injury, spontaneous bleeding, operation can be the cause of acute blood loss. Speed and volume of blood loss are of great importance.
At slow loss even of large volumes of blood (1000-1500 ml) compensatory mechanisms manage to turn on, hemodynamic disturbances arise gradually and happen not really serious. On the contrary, intensive bleeding with loss of smaller volume of blood leads to sharp hemodynamic disturbances and, as a result, to hemorrhagic shock.
Treatment of Hemorrhagic shock:
The principles of resuscitation and intensive care at patients with acute blood loss and in a condition of hemorrhagic shock at a pre-hospital stage consist in the following:
1. Reduction or elimination of the available phenomena of acute respiratory insufficiency (ODN) which cause aspiration of the beaten-out teeth, blood, the emetic masses, liquor can be at a fracture of base of the skull. Especially often this complication is observed at patients with about confused or absent consciousness and, as a rule, combined with retraction of a root of language.
Treatment comes down to mechanical release of a mouth and a stomatopharynx, aspiration of contents by means of a suction. Transportation can be carried out with the entered air duct or an endotracheal tube and carrying out IVL through them.
2. Performing anesthesia by the medicamentous means which are not oppressing breath and blood circulation. From the central narcotic analgetics deprived of side effects of opiates it is possible to use lexirum, fortrat, tramat. Non-narcotic analgesics (analginum, Baralginum) can be combined with antihistaminic drugs. There are options of carrying out a protoxidic and oxygen analgesia, in/in introductions of subnarcotic doses of Ketaminum (Kalipsolum, Ketalorum), but these are purely anesthesiology grants demanding presence of the anesthesiologist and the necessary equipment.
3. Reduction or elimination of hemodynamic frustration, first of all hypovolemia. The first minutes after a severe injury the main reason for a hypovolemia and hemodynamic frustration is blood loss. Prevention of a cardiac standstill and all other serious violations – immediate and greatest possible elimination of a hypovolemia. Massive and bystry infusional therapy has to be the main medical action. Certainly, the stop of outside bleeding has to precede infusional therapy.
Resuscitation in case of clinical death because of acute blood loss is carried out by the standard rules.
The main objective at acute blood loss and hemorrhagic shock at a hospital stage is a carrying out a complex of actions in a certain interrelation and the sequence. Transfusion therapy is only a part of this complex and is directed to completion of OTsK.
In carrying out an intensive care at acute blood loss reliable ensuring continuous transfusion therapy at a rational combination of the available means is necessary. It is even not less important to observe a certain staging in treatment, speed and adequacy of the help in the most difficult situation.
It is possible to give the following operations procedure as an example:
• At once at receipt to the patient measure the ABP, pulse rate and breath, catheterize a bladder and consider the emitted urine, all these data fix;
• Catheterize the central or peripheral vein, begin infusional therapy, measure TsVD. At a collapse, without waiting for catheterization, begin jet injection of Polyglucinum by a puncture of a peripheral vein;
• Jet injection of Polyglucinum recover the central blood supply, and jet injection of physical solution recover a diuresis;
• Define number of erythrocytes in blood and a hemoglobin content, a hematocrit, and also approximate size of blood loss and still possible in the next few hours, render necessary amount of donor blood;
• Define a blood group of the patient and a Rhesus factor accessory. After obtaining these data and donor blood carry out tests on individual and a Rhesus factor compatibility, a bioassey and start hemotransfusion;
• At increase in TsVD over 12 cm of a water column limit injection speed to rare drops;
• If surgical intervention is supposed, resolve an issue of a possibility of its carrying out;
• After normalization of blood circulation support a water balance and normalize indicators of hemoglobin, erythrocytes, protein, etc.;
• Stop continuous in/in injection after are proved by 3-4 hour observation: lack of developing of new bleeding, stabilization of the ABP, normal intensity of a diuresis and lack of threat of heart failure.