Hypovolemic shock is a critical condition of the body that occurs in the case of a sharp decrease in the effective volume of circulating blood. The name of the term "shock" comes from a French or English consonant word, which is literally means shock, shock, push. In fact, the concept of shock indicates the exceptional danger of an ongoing cascade of changes in the body.
The main pathogenetic components of the development of hypovolemic shock include small cardiac output, narrowing of peripheral vessels (vasoconstriction), disturbance of microcirculation, and subsequent respiratory failure.
The causes of a critical decrease in the volume of circulating blood can be acute blood loss (external or internal bleeding), as well as dehydration of the body that occurs during severe infections of the intestinal group (eg, cholera), and the redistribution of blood to the microcapillary part of the bloodstream (happens with pain or traumatic shock).
A sharply reduced effective volume of circulating blood causes a complex of pathological disturbances in the habitual work of the organism. This mainly affects the work of the brain and other components of the central nervous system, the cardiovascular system, the work of the lungs, and the organs of the endocrine system.
Causes of hypovolemic shock
Several factors can serve as the causes of hypovolemic shock: one-time abundant blood loss, dehydration or sudden redistribution of blood to the periphery, into the microcapillary bed.
The pathogenesis of hypovolemic shock includes a cascade of changes that are, at first, compensatory, and later evidence of depletion of compensatory mechanisms.
The triggering mechanism for further changes is small cardiac output, which as a result leads to a critical decrease in blood circulation in the tissues.
There is a sequence of changes that is directly related to the phase nature of the process. The first changes that serve as the beginning of the whole cascade are nonspecific hormonal changes.
First hypoperfusion and low pressure stimulate the release of ACTH, ADH and aldosterone. The release of the above hormones into the bloodstream affects the functioning of the kidneys and the entire excretory system. This leads to a delay in sodium and chloride, and, together with ions and water, in the body. At the same time accelerated elimination of potassium ions and a general decrease in diuresis occur. Further, the pathogenesis of hypovolemic shock includes adrenaline and norepinephrine, which contribute to peripheral vasoconstriction.
In launching the pathological cascade of changes, it is not so much the amount of blood loss that is important as the time for which it occurred.
Chronic hypovolemia , although it hurts the body's work, but does not cause such critical changes in it.
All the described changes are compensatory. While compensatory endocrine mechanisms work, the central venous pressure remains normal. These mechanisms manage to provide some time for permanent venous return, and maintain the general circulation of blood within the limits necessary for the normal functioning of all systems. But in the case when the loss of blood reaches 5-10% of the total volume, the compensatory mechanisms become insufficient to maintain the venous return, and this leads to a subsequent decrease in the central venous pressure.
The human body in any way strive to maintain homeostasis, and begins to activate subsequent mechanisms for compensation - a tachycardia begins. Thanks to this, for some time it is possible to maintain the same amount of heart at the same level. And only with the depletion and this compensatory mechanism, which usually occurs in case of a decrease in venous return to a figure of 25-30%, there is a further drop in the minute volume of the heart, which ultimately contributes to the development of the syndrome of small cardiac output.
The entire series of compensatory and adaptation mechanisms pursues a single goal - ensuring the operation of vital organs. Proper blood supply should be provided primarily to the brain, cardiac muscle, and filtration, detoxification systems - the liver and kidneys.
When the above-mentioned adaptation mechanisms cease to work, the next step, which is part of the pathogenesis of hypovolemic shock, is peripheral vasoconstriction.
Narrowing of peripheral vessels allows redistributing blood to vital organs and maintaining blood pressure at a level slightly higher than critical. Catecholamines are directly involved in this mechanism. According to some information, their content in the blood in this phase can increase by 10-30 times, in excess of the usual rate.
Centralization of blood flow, on the one hand, helps to ensure at least minimal functioning of life support systems, and on the other hand causes deep hypoxia of peripheral tissues, and along with it, acidosis . This occurs even in spite of the fact that the need for tissues in oxygen is significantly reduced.
Not the last place in the development of pathological shifts is the transition of fluid together with ions from the extracellular and vascular space inside the cells. This phenomenon is due to the weakening of the sodium-potassium pump, associated with hypoxia. Changes in the water-salt balance in hypovolemic shock, associated with the gradual loss of the tone of the precapillary sphincter, with the preserved tone of the post-capillary sphincter. Thus, over time, an increase in the concentration of endogenous catecholamines ceases to elicit an answer in the precapillary sphincter.
Subsequently, water with electrolytes continues to leave the vascular bed in connection with the increasing hydrostatic pressure and increased permeability of the walls of blood vessels. The passage of fluid into the interstitial space contributes to a further increase in the viscosity of the blood. Blood thickening leads to intravascular aggregation of erythrocytes, and multiple thrombogenesis throughout the body.
Numerous microscopic thrombi disrupt the work of all internal organs. This especially affects the work of the lungs, and plays a leading role in the development of respiratory failure accompanying shock conditions.
In addition, intravascular thrombus formation leads to a decrease in the number of platelets, the level of fibrinogen and other factors of hemocoagulation, which leads to the development of a "consumption syndrome". This reflects one of the phases of the syndrome of disseminated intravascular coagulation.
Hypercoagulation gradually leads to depletion of the hemostatic system, and inevitable hypocoagulation develops, with the development of multiple hemorrhages.
A separate important role in the development of hypovolemic shock, should be given to proteolytic enzymes, which begin to be produced inside cells in excess. Lysosomal enzymes, destroying the cell membranes, get into the bloodstream and summarily affect the internal organs. One of the effects of a group of enzymes is formed by the so-called depressant myocardial factor (MDF). The effects of this factor include a negative inotropic effect, a decrease in blood pressure, an increase in the permeability of the vascular wall, and the appearance of pain.
During the development of hypovolemic shock, a metabolic pathology also occurs, the essence of which is the activation of anaerobic pathways for energy production, in the conditions of inaccessibility of aerobic, which leads to aggravation of general acidosis.
Stages of hypovolemic shock
The hypovolemic shock clinic has a phase flow and includes three stages. It is important to record the changes in time in order to provide assistance with maximum efficiency.
♦ The first stage of hypovolemic shock - compensated shock develops in case of blood loss of 15-25% of the volume of circulating blood, which on the average is about 700-1300 ml. It is important to note that this stage is completely reversible. The main pathogenetic link of the first stage of hypovolemic shock is the syndrome of small ejection. Clinically, this syndrome is manifested by the development of moderate tachycardia, minor (sometimes absent) arterial hypotension. Venous hypotension can be recorded. There is a moderate oliguria. Peripheral vasoconstriction is manifested by cooling and blanching of the extremities.
♦ The second stage of hypovolemic shock, also called decompensated shock, develops in the event of a loss of 26-45% of the volume of circulating blood. This translates into an actual volume of blood loss, an average of 1300-1800 ml. In the second stage, tachycardia increases, the heart rate increases to 120-140 per minute. Low pulsatile arterial pressure is registered, and systolic, in turn, falls below the value of 100 mm.rt. Art. You can also record venous hypotension. Narrowing of peripheral vessels is pronounced, generalized pallor and cyanosis of integuments of the whole body are observed. Of the remaining symptoms - the appearance of cold sweat, shortness of breath, restless behavior. Significantly reduced diuresis - oliguria, less than 20 ml per hour.
♦ The third stage of hypovolemic shock is the stage of irreversible shock. At her loss of blood is more than 50% of the total volume, which is approximately 2000-2500 ml. At this stage, a critical reduction in blood pressure is noted. Figures can reach a level below 60 mm. and often blood pressure is not determined at all. Tachycardia continues to increase and reaches 140 beats per minute or more. A person in the third stage of hypovolemic shock is unconscious. Skin covers have a pronounced pale color. The skin becomes covered with a cold sweat. The whole body, especially the limbs become cold to the touch, you can observe the hypostasis. Excretory function is absent - oligouria develops.
One of the signs that indicate the irreversibility of hypovolemic shock is an increase in hematocrit, as well as a decrease in the volume of the plasma component of the blood.
Treatment of hypovolemic shock
Since the clinic of hypovolemic shock is directly related to pathogenetic changes in the body, treatment should be conducted taking into account the features of pathogenesis. The main directions in the treatment of hypovolemic shock should be selected to counteract factors that participate in the pathogenetic chain.
The first steps should be directed at eliminating the cause of hypovolemic shock, namely, the definition of the source of bleeding and its cessation.
Also it is necessary to start oxygenotherapy in the shortest possible time, using high concentrations of oxygen. This will help to counteract hypoxic changes in peripheral tissues, and aggravation of acidosis.
A necessary measure to combat hypovolemic shock is to restore the lost volume of circulating blood by transfusion of blood substitutes. Replenishment of the volume is carried out by introducing a combination of colloids and crystalloids. Often you have to resort to transfusion of blood components. This measure is aimed at maintaining hemoglobin at a level of 100 g / l.
Frozen plasma can also be used for transfusion. These measures are necessary, including to combat the "exhaustion syndrome" in the syndrome of disseminated intravascular coagulation.
Exceptionally, in the presence of the possibility of determining the pH of the blood, correction of metabolic acidosis is performed. In parallel with the conduct of transfusion, it is appropriate to monitor the parameters of sodium-potassium metabolism. In parallel with the infusion therapy, you can inject drugs that have the ability to increase the tone of blood vessels - glucocorticoids.
When it is possible to stop blood loss and restore the volume of circulating blood, the introduction of inotropic drugs is appropriate, in order to stimulate the work of the heart muscle. In the case where diuresis can not be restored, diuretic therapy is performed, even after replenishment of the lost volume.