Blood loss

Blood loss always leads to hypovolemia, which is characterized by a decrease in the absolute or relative volume of blood circulating in the body. Among the potentially reversible causes of circulatory arrest, hypovolemia is in second place, and this is quite natural. It can develop with acute blood loss, diseases with accompanying vomiting, diarrhea, fluid deposition in the third space, etc. In fact, hypovolemia is present in any critical condition, regardless of its genesis. A decrease in the volume of circulating blood and a decrease in venous return leads to the development of low cardiac output syndrome. And the faster the decrease in the volume of circulating blood occurs, the faster and more pronounced these changes.

Most often, the reason for the rapid development of an emergency condition in acute blood loss is blood loss.

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Blood loss: pathophysiological changes

The human body effectively compensates for acute blood loss. Blood loss of up to 10% of the circulating blood volume is successfully covered by the body due to an increase in the tone of the venous bed. The main indicators of central hemodynamics do not suffer. With a larger volume of blood loss, the blood flow from the periphery to the pulmonary circulation decreases. Due to a decrease in venous return, the stroke volume decreases. Cardiac output is compensated by an increase in the heart rate.

A further rapid decrease in the volume of circulating blood (continued blood loss, deposition and sequestration of blood) leads to the depletion of compensatory mechanisms, which is manifested by a decrease in venous return by 20-30% of the norm, a decrease in stroke volume below the critical value and the development of low output syndrome.

To a certain extent, the body is able to compensate for the low output syndrome with tachycardia and redistribution of blood flow in favor of vital organs. The phenomenon of centralization of blood circulation develops (maintenance of blood flow in the heart, brain, liver, kidneys due to reduction of perfusion of other organs and systems).

However, if blood loss continues, acid-base and water-electrolyte balance disorders (acidosis, transition of water and electrolytes into the interstitium) develop rapidly, blood viscosity increases, stasis and coagulopathy occur. Endotoxicosis develops due to accumulation of "ischemic toxins", arteriovenous anastomoses open, transcapillary and transmembrane exchange is disrupted. Peripheral vascular tone regulation is disrupted.

In addition, endotoxins can have a direct damaging effect on the heart, lungs, brain, liver, and other organs and systems, causing anaphylactic-type reactions.

There are disturbances in oxygen absorption by the body's cells due to the destruction of proteins and lipids in cells, blockade of synthetic and oxidative processes, which leads to the development of histotoxic hypoxia. Subsequently, hypovolemic (hemorrhagic) shock develops and, if adequate therapy is not provided in a timely manner, a fatal outcome occurs.

With the same deficit of circulating blood volume in hemorrhagic shock, in contrast to true hypovolemic shock, hypoxic changes in organs and tissues are expressed to a greater extent. This is due to a decrease in the oxygen capacity of the blood and the release of myocardial depressant factor (MDF).

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Determination of blood loss

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Mild bleeding

With blood loss of up to 15% of the total circulating blood volume, the patient's condition practically does not suffer.

Moderate blood loss

Characterized by functional changes in cardiovascular activity that compensate for hypovolemia. Blood loss is 15-25% of the circulating blood volume. The patient's consciousness is preserved. The skin is pale and cold. The pulse is weak, moderate tachycardia. Arterial and central venous pressure are moderately reduced. Moderate oliguria develops.

Severe blood loss

Characterized by increasing circulatory disorders. Compensatory mechanisms fail, with decreased cardiac output. It is not compensated by increased tone of peripheral vessels and tachycardia, which leads to the development of severe arterial hypotension and impaired organ circulation. Blood loss is 25-45% of the circulating blood volume. Acrocyanosis is observed, the extremities are cold. Dyspnea increases, tachycardia up to 120-140 beats per minute. Systolic blood pressure is below 100 mm Hg. Blood viscosity increases sharply due to the formation of aggregates of erythrocytes in the capillaries, an increase in the content of large-molecular proteins in the plasma, an increase in hematocrit and a proportional increase in total peripheral resistance. Due to the fact that blood is not a Newtonian fluid with a characteristic structural viscosity, a decrease in blood pressure increases blood viscosity, and vice versa. Patients experience oliguria (less than 20 ml/h).

Extremely severe blood loss

Occurs if circulatory decompensation persists for a long time (6-12 hours or more). The patient's condition is extremely severe. A spotty pattern is observed against the background of pale skin. Pulsation is determined only on large vessels, sharp tachycardia (up to 140-160 per minute). Systolic pressure is below 60 mm Hg.

In express diagnostics of the severity of shock, the concept of shock index (SI) is used - the ratio of the heart rate to the value of systolic arterial pressure. Normally, its value is 0.5 (60/120). In case of shock of the 1st degree, SI = 1 (100/100), shock of the 2nd degree - 1.5 (120/80), shock of the 3rd degree - 2 (140/70).

Massive blood loss is a decrease in blood volume approximately equal to 7% of ideal body weight in adults and 8-9% in children within 24 hours. In terms of the rate of blood loss, massive blood loss is defined as a loss of 50% of the blood volume within 3 hours, or when the rate of loss is 150 ml/min or more. The severity of blood loss can be determined with sufficient accuracy based on clinical and laboratory examination data.

The deficit in circulating blood volume can be determined by the value of central venous pressure (normal 6-12 mm H2O).

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