How the body defends itself: compensatory mechanisms
Posthemorrhagic hypovolemia immediately triggers a cascade of defensive reactions. Their main goal is to adjust the capacity of the vascular bed to the remaining blood volume and save vital organs.
- Centralization of blood circulation. Baro- and chemoreceptors respond to the drop in pressure by stimulating the sympathoadrenal system. A powerful spasm of veins and peripheral arterioles (skin, kidneys, liver, intestines) occurs. Meanwhile, the blood vessels of the brain, heart, and lungs remain open.
- Autohemodilution. The body attempts to make up for the volume using interstitial fluid. This blood dilution process is rapid: up to 5–7 liters of cell-free protein-free fluid can shift into the bloodstream within a couple of days.
- Organ reactions. The heart responds with tachycardia to maintain cardiac output, and the lungs respond with hyperventilation to compensate for oxygen starvation.
- Hormonal water retention. Hypovolemia triggers the release of antidiuretic hormone and aldosterone. The kidneys enhance sodium and chloride reabsorption, which clinically manifests as oliguria (decreased urine output).
Hemorrhagic shock and failure of adaptation
If the loss exceeds 20–30% of the CBV, compensatory mechanisms fail. Prolonged peripheral spasm and high vascular resistance exhaust the body's reserves.
In capillaries, due to slowed blood flow, erythrocyte aggregation ("sludging") occurs. Tissue hypoxia increases, metabolism shifts to the anaerobic pathway, and acidic metabolic products accumulate (tissue acidosis). Capillary paresis and decentralization of blood flow ensue.
If arterial hypotension lasts for more than 12 hours, multiple organ failure develops:
- Kidneys: glomerular filtration drops, anuria occurs.
- Liver: necrotic processes begin.
- Heart: myocardial contractility suffers.
- Lungs: interstitial edema ("shock lung") forms, gas exchange is impaired.
Classification and clinical presentation
The severity of the condition directly depends on the percentage of lost CBV. There are 4 degrees of blood loss:
- Grade I (mild). Loss of 500–700 ml (10–15% of CBV). No pronounced symptoms, full compensation.
- Grade II (moderate). Loss of 1000–1500 ml (15–20% of CBV). Moderate tachycardia appears (up to 100 bpm), systolic pressure drops to 90 mm Hg.
- Grade III (severe). Loss of 1500–2000 ml (20–30% of CBV). The patient is restless, covered in cold sweat. Skin is pale with cyanosis, breathing is rapid. The pulse becomes thready (up to 120 bpm), pressure drops to 70 mm Hg, and diuresis sharply decreases.
- Grade IV (massive). Loss of more than 2 liters (over 30% of CBV). Stupor and lethargy. Marked pallor with acrocyanosis. Pulse is often unmeasurable (130–140 bpm and higher), pressure is below 30 mm Hg, complete anuria sets in.
Diagnostic nuances
Assessing the loss volume solely based on complaints (thirst, weakness, dizziness, darkening in the eyes) or appearance is unreliable — with slow bleeding, clinical signs remain masked for a long time.
In the first hours, laboratory reliance on hemoglobin and hematocrit is pointless — they will change later, once autohemodilution kicks in. Determining the relative density of blood is more reliable.
The most accurate method is determining the CBV deficit. Indicators (Evans blue dye or isotopes) are injected into the bloodstream. By measuring the dilution, the plasma volume is calculated, and then, taking hematocrit into account, the total CBV is determined. The resulting figure is compared with the predicted normal value for a specific patient.
Briefly: answers to topical questions
What calculated indices are used for a rapid assessment of blood loss volume based on pulse and blood pressure?
To rapidly assess blood loss volume based on pulse and blood pressure, the shock index (Allgöwer index) is used. It is calculated as the ratio of heart rate to systolic blood pressure, provided the baseline blood pressure is over 100 mm Hg. When shock develops, this indicator becomes high.
Which groups of solutions are used for initial infusion therapy of hemorrhagic shock?
Blood-substituting fluids are used for the initial infusion therapy of hemorrhagic shock. The following groups of solutions are used at the beginning of treatment:
- Colloids — are well retained in the vascular bed (albumin, protein, medium-molecular-weight dextrans).
- Low-molecular-weight dextrans — restore volume, improve microcirculation and blood rheology.
- Crystalloids — can be used, but they rapidly leave the vascular bed (Ringer's solution, isotonic sodium chloride solution, 5% dextrose solution).
Blood products (packed red blood cells) are administered after the infusion of plasma substitutes.
What stages are distinguished in the clinical course of hemorrhagic shock?
Traditionally, three stages are distinguished in the clinical course of hemorrhagic shock:
- Compensated shock (stage of compensation or centralization of blood circulation) — characterized by pallor, small and rapid pulse, normal or slightly lowered BP, and decreased diuresis.
- Decompensated reversible shock (stage of decompensation) — manifests as cyanosis, lethargy, decreased BP and CVP, oliguria.
- Irreversible shock (stage of irreversible changes) — accompanied by loss of consciousness, unmeasurable BP, mottled skin, anuria, development of multiple organ failure and DIC syndrome.
Additionally, in obstetrics, stages are classified by severity: mild (I), moderate (II), and severe (III) shock.
What methods exist for the temporary arrest of external arterial bleeding?
The following methods are used for emergency temporary arrest of external arterial bleeding:
- Tourniquet application — the most reliable method, used mainly on limbs.
- Digital pressure on the artery — compression of the arterial trunk against underlying bone prominences proximal to the injury site (e.g., A. carotis, A. subclavia, A. brachialis).
- Pressure bandage application — used for bleeding from small arteries.
- Wound packing — tight insertion of a gauze tampon followed by fixation with a pressure bandage.
- Vessel clamping in the wound — applying a clamp to the damaged vessel.
Class and exam questions
In a complete transection, the artery reflexively contracts, and its inner lining (intima) rolls inward. This accelerates thrombus formation. If the vessel is injured tangentially, it cannot spasm, the wound gapes, and blood flows out for a long time.
In a complete transection, the artery reflexively contracts, and its inner lining (intima) rolls inward. This accelerates thrombus formation. If the vessel is injured tangentially, it cannot spasm, the wound gapes, and blood flows out for a long time.
No, you cannot. In the first few hours, the concentration of erythrocytes and hemoglobin in the remaining blood is normal. Changes will appear later (in 1.5–2 days), once extracellular fluid hemodilutes the blood.
No, you cannot. In the first hours, the concentration of red blood cells and hemoglobin in the remaining blood is normal. Changes (decreased values) will appear later, within 1.5–2 days, as tissue fluid dilutes the blood.
Women (due to physiological adaptation from menstruation) and regular donors tolerate blood loss better. Healthy individuals also compensate better, whereas in children and the elderly, adaptive reserves are extremely low.
Women (due to physiological adaptation from menstruation) and regular donors tolerate blood loss better. Healthy individuals also compensate better, whereas in children and the elderly, adaptive reserves are extremely low.
What else to study on this topic
- Changes in the relative density of blood depending on the volume of lost fluid.
- Aggravating factors (baseline anemia, starvation, coagulation disorders).
- Methodology and measurement sites for central venous pressure (CVP).
- Features of blood loss in newborns and the elderly.
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