Sechenov School
Home › Pathophysiology › Hemorrhage

Hemorrhage

Haemorrhagia

For medical students3 min readUpdated 2026-10-10

Hemorrhage is a standard pathological process resulting from the escape of blood from blood vessels or heart chambers. The severity of the condition and prognosis depend on the volume of lost blood, the rate of bleeding, and individual reactivity.

Lethal VolumeLoss of 50% or more of the total circulating blood volume (CBV) is fatal, especially when rapid.
CentralizationTo protect the brain and heart, the body dramatically vasoconstricts the skin, skeletal muscles, and abdominal organs.
Response SpeedCardiovascular compensation triggers within seconds, whereas protein restoration takes hours.
Risk FactorsDeep anesthesia, hypothermia, and hyperthermia significantly worsen the consequences of blood loss.

Classification and Types

Bleeding can be external (into the external environment) or internal (into body cavities or the lumen of hollow organs). When escaped blood accumulates in surrounding tissues, it is termed a hemorrhage. In isolated hemorrhages, systemic hemodynamics typically remain unaffected due to the small volume of lost blood.

Types of tissue hemorrhages:

Based on the source, bleeding is classified as arterial, venous, capillary, or mixed. Based on timing, it is divided into primary (immediately after trauma) and secondary (delayed).

The severity of the condition directly correlates with the proportion of lost circulating blood volume (CBV):

  1. Mild degree: up to 20–25% CBV. Usually not life-threatening and compensated by emergency mechanisms.
  2. Moderate degree: 25–35% CBV. Causes significant central hemodynamic and microcirculatory disorders.
  3. Severe degree: greater than 35–40% CBV.

Reactivity Factors

The clinical course of the pathological process depends on individual patient characteristics. Studies show that women and adults tolerate blood loss better than men and children.

Condition of the organism also plays a critical role. Extreme temperature exposures (hypothermia or hyperthermia), as well as deep general anesthesia, depress compensatory mechanisms and exacerbate vital function disorders. Additionally, a decrease in clotting factors or hyperactivation of the fibrinolytic system increases the rate and total volume of blood loss.

Compensatory Mechanisms

To counteract hypovolemia, the body activates four groups of mechanisms. They are triggered at different times but operate concurrently, reinforcing one another.

1. Cardiovascular Stage (First Seconds) Immediate cardiac stimulation occurs: heart rate and stroke volume increase. Centralization of blood flow develops — a selective alteration in vascular tone. Arterioles in peripheral tissues (skin, muscles, kidneys) constrict, while vessels of vital organs (brain, heart) dilate. Arteriolar spasm forces pooled blood into the active circulation, maintaining CBV.

2. Hydremic Stage (First Minutes) Aiming to shift fluid from tissues into blood vessels. The reduction in CBV is detected by baroreceptors, prompting the secretion of ADH (vasopressin).

Fluid shifts down an osmotic gradient from cells into the interstitium, then into lymph and blood. By days 2–3, oligocythemic hypo- or normovolemia develops.

3. Protein Stage (After Several Hours) Protein synthesis is activated in the liver. Plasma protein composition is restored, and procoagulants are produced to thrombose the vascular defect. Signs of elevated synthesis persist for up to 1.5–3 weeks.

4. Bone Marrow Stage Triggered in response to mixed hypoxia: emic (low red blood cell count), circulatory (impaired blood flow), and respiratory (reduced pulmonary perfusion). Activation of hematopoiesis eliminates the deficit of formed elements.

Principles of Therapy

Treatment is based on two main principles:

Mnemonic

To remember the compensation stages, use the phrase: Stop Hemorrhage Prevent Collapse (Cardiovascular, Hydremic, Protein, Bone marrow/Cellular).

Frequently asked questions

What changes occur in a complete blood count (CBC) in the first hours following acute hemorrhage?

During the first hours after acute hemorrhage, total blood volume decreases while hematocrit remains within the normal range.

Subsequent blood parameter dynamics:

  • Initial stage — hematocrit remains within normal limits.
  • Days 2–3 — oligocythemic hypo- or normovolemia develops due to tissue fluid influx into the vascular bed.
  • Parameter changes — hematocrit falls below normal, and a deficit of formed elements persists, accompanied by a decrease in blood oxygen capacity.
What is the difference between a hematoma and hemorrhagic imbibition?

In a hematoma, blood dissects and destroys tissues, creating an artificial cavity. In hemorrhagic imbibition (infiltration), blood permeates between cells while preserving the original tissue structure.

Why does urine output decrease during blood loss?

The drop in blood volume triggers the release of ADH and aldosterone. These hormones compel the kidneys to maximally reabsorb water and sodium back into the circulation to maintain blood pressure, sharply reducing urine production.

What is the centralization of blood flow phenomenon?

It is a protective vasoconstriction of the skin, skeletal muscles, kidneys, and abdominal organs. This redirects remaining blood flow to vital organs—the brain and heart—whose vessels vasodilate in response.

Go deeper

More topics in Pathophysiology

Classification of HypoxiaType III Hypersensitivity ReactionsChemical CarcinogensTypes of Substance Dependence and ToxicomaniaGeneral Adaptation SyndromeExtreme StatesAngina PectorisAlveolar HypoventilationPathogenesis of Digestive System DiseasesHepatic FailureCentrogenic EndocrinopathiesClassification of Nervous System DisordersPathophysiology →