All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Hemorrhagic shock - Causes and pathogenesis
Medical expert of the article
Last reviewed: 04.07.2025
The causes of bleeding leading to shock in gynecological patients may be: ruptured ectopic pregnancy, ovarian rupture, spontaneous and artificial abortion, missed abortion, hydatidiform mole, dysfunctional uterine bleeding, submucous uterine fibroids, and genital trauma.
Whatever the cause of massive bleeding, the leading link in the pathogenesis of hemorrhagic shock is the disproportion between the reduced BCC and the capacity of the vascular bed, which first manifests itself as a disruption of macrocirculation, i.e. systemic circulation, then microcirculatory disorders appear and, as a consequence of them, progressive disorganization of metabolism, enzymatic shifts and proteolysis develop.
The macrocirculation system is formed by arteries, veins and the heart. The microcirculation system includes arterioles, venules, capillaries and arteriovenous anastomoses. As is known, about 70 % of the total circulating blood volume is in the veins, 15% in the arteries, 12% in the capillaries, and 3 % in the heart chambers.
When blood loss does not exceed 500-700 ml, i.e. about 10 % of the BCC, compensation occurs due to an increase in the tone of the venous vessels, the receptors of which are most sensitive to hypovolemia. In this case, there is no significant change in arterial tone, heart rate, and tissue perfusion does not change.
Blood loss exceeding these figures leads to significant hypovolemia, which is a strong stress factor. To maintain hemodynamics of vital organs (primarily the brain and heart), powerful compensatory mechanisms are activated: the tone of the sympathetic nervous system increases, the release of catecholamines, aldosterone, ACTH, antidiuretic hormone, glucocorticoids increases, 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 attraction to the bloodstream from tissues, a 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 arterial pressure. However, the centralization of blood circulation cannot ensure long-term vital activity of the woman's body, because it is carried out due to a violation of peripheral blood flow.
Continued bleeding leads to exhaustion of compensatory mechanisms and aggravation of microcirculatory disorders due to the release of the liquid part of the blood into the interstitial space, thickening of the blood, a sharp slowdown in blood flow with the development of sludge syndrome, which leads to deep tissue hypoxia. 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 an increase in osmotic pressure, hydration and cell damage. Weakening of tissue perfusion, accumulation of vasoactive metabolites contribute to blood stasis in the microcirculation system and disruption of coagulation processes with the formation of thrombi. Blood sequestration occurs, leading to a further decrease in the BCC. A sharp deficit of the BCC disrupts the blood supply to vital organs. Coronary blood flow decreases, heart failure develops. Such pathophysiological changes (including impaired blood clotting with the development of DIC syndrome) indicate the severity of hemorrhagic shock.
The degree and duration of action of compensatory mechanisms, the severity of pathophysiological consequences of massive blood loss depend on many factors, including the rate of blood loss and the initial state of the woman's body. Slowly developing hypovolemia, even significant, does not cause catastrophic hemodynamic disorders, although it represents a potential danger of an irreversible condition. Minor recurrent bleeding can be compensated by the body for a long time. However, a violation of compensation extremely quickly leads to profound and irreversible changes in tissues and organs.
[