Pulmonary embolism

Mechanisms and agents for blood volume restoration

Effective increase in circulating blood volume (CBV) is achieved not only by the physical addition of the infused medium. An important role is played by the redistribution of one's own blood from physiological reservoirs and the recruitment of fluid from the interstitial space into the vascular bed. A properly selected infusion has a qualitative effect: it improves rheology, restores oxygen capacity, and provides a hemostatic effect.

Since an ideal fluid does not exist, clinical practice utilizes a rational combination of them:

• Crystalloid solutions: Saline solutions allow for very rapid, even jet, replacement without pronounced adverse reactions. Their main disadvantage is that only about 25% of the administered volume remains in the vascular bed.
• Colloid solutions (hemocorrectors): These are high-molecular-weight agents (e.g., gelatinol — 35,000, rheopolyglucin — 40,000, polyglucin — 70,000). They are capable of increasing CBV by 1.2–1.3 times their own volume due to the active attraction of tissue fluid.
• Blood products: Include protein fractions (albumin, protein), plasma, as well as red blood cell and platelet concentrates. They are as close as possible to natural blood in protein composition and transport properties.
• Whole blood: Although it is optimal for replacing losses, it is currently practically never transfused due to high immunological incompatibility and the colossal risk of severe post-transfusion complications.

Assessment of blood volume deficit and infusion rules

The severity of hypovolemia directly depends on the percentage of lost blood volume. A loss of up to 15% is usually compensated by the body independently and proceeds without overt clinical symptoms. A deficit of 20–25% causes moderate hypovolemia, 30–40% causes a moderately severe condition with the possible development of oliguria. A loss exceeding 40% leads to severe, life-threatening disorders.

Basic rules of therapy in acute blood loss:

1. In massive CBV deficit, the decisive factor is not the specific type of solution, but the timeliness of initiation, high administration rate, and adequate volume.
2. The total infusion volume must exceed the initial deficit by 1.5–2.0 times.
3. The optimal ratio of colloid and crystalloid media is approximately 1 : 2.
4. The proportion of transfused blood products must under no circumstances exceed the volume of the blood loss itself. In compensated shock, blood transfusion is not indicated at all.

The criterion for therapeutic success is not a mathematical calculation of blood loss, but the clinical response of the body: stabilization of blood pressure, decrease in central venous pressure (CVP), and restoration of adequate diuresis.

Hemodynamics and respiratory support

The state of pre- and post-capillary vascular resistance determines fluid exchange in tissues and the magnitude of CBV. It is important to remember the absolute rule: it is unacceptable to use vasoconstrictor drugs (adrenaline, noradrenaline) without prior restoration of CBV. Artificially increasing vascular tone against the background of empty capillaries will yield no effect and will only exacerbate tissue hypoxia.

Restoration of gas exchange begins with ensuring airway patency. In chest trauma, inhalation-exhalation mechanics are restored surgically:

• Open pneumothorax requires the application of an occlusive dressing.
• Tension pneumothorax or massive hemothorax are managed by puncture and drainage of the pleural cavity.
• Flail chest requires rib fixation or placing the patient on mechanical ventilation.

Oxygen therapy has strict indications. In respiratory failure, hypocapnia is frequently observed. Administration of oxygen during blood loss and a normal oxyhemoglobin level is dangerous — it impairs oxygen delivery to tissues and deepens hypoxia. Oxygen is indicated only in hypoxia combined with hypercapnia (in the presence of cyanosis).

Complications: tissue ischemia and embolism

After resuscitating the patient from shock, severe syndromes may develop due to prolonged ischemia. Due to the accumulation of calcium ions in the smooth muscles of blood vessels, persistent vasoconstriction persists — the no-reflow phenomenon.

In the lungs, areas of ischemic tissue lead to the pathological opening of arteriovenous shunts. Through these pathways, fat emboli are able to bypass the pulmonary filter and penetrate directly into the arterial system of the brain, causing the cerebral form of fat embolism and focal neurological deficit.

Other severe complications include:

• Stress ulcers: Develop on days 1–2 due to ischemia of the gastric wall. Mucus loses its barrier function, and acid causes superficial erosions. They do not lead to perforations, but can become a source of massive bleeding (in 5% of patients, mortality >80%). Prophylaxis with antacids and gastroprotectors is mandatory.
• Translocation phenomenon: Intestinal ischemia disrupts the barrier, allowing microflora to enter the blood, which leads to systemic infection.
• Hospital-acquired diarrhea: Develops in 50% of intensive care patients who received massive anti-shock therapy and represents a potential life threat.

Class and exam questions

What else to study on this topic

• Pathogenesis of calcium ion accumulation in vessels during hypoperfusion
• Principles of calculating oxygen debt in the post-resuscitation period
• Mechanisms of bacterial translocation in gastrointestinal ischemia
• Protocols of nutritional support and stress ulcer prevention in the ICU
• Multiple organ dysfunction syndrome as an outcome of prolonged hypovolemia

Other topics in the section "General Questions of Traumatology and Orthopedics"

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