Hemorrhagic shock: causes and pathogenesis

The causes of bleeding leading to shock in gynecological patients can be: a disrupted ectopic pregnancy, an ovarian rupture, spontaneous and artificial abortion, a frozen pregnancy, a bladder skeleton, dysfunctional uterine bleeding, a submucous form of uterine fibroids, trauma to the genital organs.

Whatever the cause of massive bleeding, the leading link in the pathogenesis of hemorrhagic shock is the disproportion between reduced bcc and the capacity of the vascular bed, which initially manifests as a violation of macrocirculation, ie, systemic circulation, then microcirculatory disorders appear and, as a consequence, develop a progressive disorganization metabolism, enzymatic shifts and proteolysis.

The system of macrocirculation is formed by arteries, veins and heart. The system of microcirculation includes arterioles, venules, capillaries and arteriovenous anastomoses. As is known, about 70 % of the total BCC is in the veins, 15% in the arteries, 12% in the capillaries, and 3 % in the heart chambers.

When blood loss is not more than 500-700 ml, i.e., about 10 % of BCC, there is compensation due to an increase in the tone of the venous vessels, the receptors of which are most sensitive to hypovolemia. At the same time, there is no significant change in the arterial tone, heart rate, tissue perfusion does not change.

The blood loss, exceeding these figures, leads to significant hypovolemia, which is a strong stress factor. To maintain the hemodynamics of vital organs (primarily the brain and heart) powerful compensatory mechanisms are included: the tone of the sympathetic nervous system increases, the release of catecholamines, aldosterone, ACTH, antidiuretic hormone, glucocorticoids is increased, the renin-hypertensive system is activated. Due to these mechanisms, there is an increase in cardiac activity, a delay in the release of fluid and its involvement in the bloodstream from tissues, spasm of peripheral vessels, and the opening of arteriovenous shunts. These adaptive mechanisms, leading to the centralization of blood circulation, temporarily maintain the minute volume of the heart and blood pressure. However, the centralization of blood circulation can not ensure a long life of the body of a woman, because it is due to the violation of peripheral blood flow.

Continuing bleeding leads to depletion of compensatory mechanisms and deepening of microcirculatory disorders due to the release of the liquid part of the blood into the interstitial space, thickening of the blood, a sharp slowing of the blood flow with the development of the sludge syndrome, which leads to a profound hypoxia of the tissues. Hypoxia and metabolic acidosis cause a disruption of the sodium pump function, sodium and hydrogen ions penetrate into the cells, displacing potassium and magnesium ions, which leads to increased osmotic pressure, hydration and cell damage. The weakening of tissue perfusion, the accumulation of vasoactive metabolites promote blood stasis in the microcirculation system and the violation of clotting processes with the formation of thrombi. There is a sequestration of blood, leading to a further decrease in BCC. A sharp deficit of BCC violates the blood supply of vital organs. Coronary blood flow decreases, heart failure develops. Similar pathophysiological changes (including a disruption of blood clotting with the development of the DIC syndrome) indicate the severity of hemorrhagic shock.

The degree and duration of compensatory mechanisms, the severity of the pathophysiological consequences of massive blood loss depend on many factors, including the rate of hemorrhage and the initial state of the woman's body. Slowly developing hypovolemia, even significant, does not cause catastrophic violations of hemodynamics, although it represents a potential danger of an irreversible state. Small repeated bleeding for a long time can be compensated by the body. However, the violation of compensation extremely quickly leads to profound and irreversible changes in tissues and organs.

[1], [2], [3], [4]