Causes and etiology
Blood loss occurs under the influence of various factors leading to damage or dysfunction of the vascular system:
- Violation of the integrity of blood vessels and the heart — mechanical cuts or ruptures, wall arrosion by a purulent process, tumor destruction, as well as myocardial ruptures in zones of infarction and aneurysms.
- Increased vascular wall permeability — observed in the microvasculature during radiation sickness, leukemias, severe infections (sepsis, typhus), and marked vitamin C deficiency (scurvy).
- Decreased blood clotting — a significant factor contributing to prolonged bleeding.
Pathogenesis and stages of compensation
The pathogenetic process begins with a decrease in circulating blood volume (CBV), a drop in venous return, a decrease in stroke volume and cardiac output, as well as a drop in blood pressure. This leads to tissue hypoperfusion, hypoxia, acidosis, and the development of capillariotrophic insufficiency.
To eliminate the consequences, the body activates compensatory mechanisms:
- Protein compensation — protein synthesis is activated in the liver, which increases the hemostatic potential.
- Hydremic phase (days 2–3) — autohemodilution occurs (influx of tissue fluid into the bloodstream), causing a decrease in hematocrit, oligocythemia, as well as relative thrombocytopenia and leukopenia.
- Bone marrow phase (days 4–5) — erythropoietins stimulate cell proliferation in the bone marrow, leading to a reticulocyte crisis, the appearance of hypochromic and microcytic erythrocytes.
Chronic post-hemorrhagic anemia
The chronic form develops against the background of frequent and prolonged bleeding. The main causes are gastrointestinal pathologies (polyps, peptic ulcer disease, esophageal varices), kidney diseases (urolithiasis, hemorrhagic nephritis), and congenital or acquired thrombocytopathies.
The core pathogenesis involves progressive iron deficiency, which is why this pathological condition is considered a specific variant of iron deficiency anemias.
Briefly: answers to topical questions
What mechanisms provide the vascular-reflex (early) stage of compensation for acute blood loss?
The vascular-reflex stage of compensation for acute blood loss is provided by the centralization of blood circulation and stimulation of the sympathoadrenal system. The mechanisms include:
- Stimulation of the sympathoadrenal system — as a reflex response of baro- and chemoreceptors.
- Venospasm and arteriolospasm — reduction of the vascular bed volume due to increased tone of veins and peripheral arterioles.
- Increased venous tone — compensates for the loss of up to 10–15% of CBV.
- Vasoconstriction of the skin, kidneys, liver, and abdominal cavity vessels.
- Preservation of blood flow in the brain, heart, and lungs.
- Blood mobilization from depots and increased cardiac output as components of cardiovascular compensation.
What types of hypoxia develop sequentially in acute massive blood loss?
In acute massive blood loss, mixed-type hypoxia develops. The sources indicate its following components:
- Hemic hypoxia — due to a decrease in the oxygen capacity of the blood resulting from a drop in hemoglobin levels and loss of erythrocytes.
- Circulatory hypoxia — due to circulatory disorders, a drop in CBV and BP, and hemodynamic disturbances.
- Respiratory hypoxia — develops due to decreased pulmonary perfusion.
These links of mechanisms of different types of hypoxia are characterized by the mutual aggravation of processes.
What is the complete mechanism of protein compensation after acute blood loss?
The mechanism of protein compensation consists in restoring the protein composition of the blood through the activation of protein synthesis in the liver. The process has the following features:
- Activation timeline — begins several hours after blood loss; signs of increased synthesis persist for 1.5–3 weeks depending on the volume of blood loss and the reactivity of the body.
- Biological significance — the synthesis of procoagulants increases the hemostatic potential of blood.
- Result — these reactions contribute to the thrombosis of the vascular defect and the cessation of bleeding.
What is the pathogenesis of hemorrhagic shock at the microcirculation level?
The pathogenesis of hemorrhagic shock at the microcirculation level is associated with a decrease in perfusion pressure and hypoperfusion of organs and tissues. Key changes include:
- Microcirculation disorders and the development of capillariotrophic insufficiency due to reduced transport of oxygen and metabolic substrates to cells, as well as impaired removal of carbon dioxide and metabolic products.
- Erythrocyte sludging — agglutination of erythrocytes in capillaries due to their spasm and slowed blood flow.
- Blood pooling and sequestration in capillaries against the background of impaired blood rheological properties as a link in the final stage of shock.
These processes are accompanied by tissue hypoxia, the predominance of anaerobic processes, and the development of tissue acidosis.
Chronology of compensation: 2–3 days — water dilutes the blood (hydremia), 4–5 days — the bone marrow responds with reticulocytosis (erythropoiesis), and 1–2 months are required for the complete restoration of red blood cell mass.
Class and exam questions
What changes occur in peripheral blood during the hydremic phase?
Oligocythemic hypo- or normovolemia, decreased hemoglobin, erythropenia, low hematocrit, normochromia of erythrocytes, as well as thrombocytopenia and leukopenia are observed.
What are the features of the blood picture in the bone marrow phase of compensation?
Anemia becomes hypochromic, microcytic, regenerative, and normoblastic with pronounced reticulocytosis, sometimes reaching 30%.
What is the main cause of chronic post-hemorrhagic anemia?
Progressive iron deficiency in the body, arising as a result of prolonged, recurring bleeding of various etiologies.
What else to study on this topic
- Classification of blood loss by source, time, and volume
- Principles of water-electrolyte balance correction
- Correction of acid-base balance (ABB)
- Symptomatic principles of therapy for post-hemorrhagic conditions
- Mechanisms of post-hemorrhagic shock development
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