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Propedeutics · Additional topics

Acute vascular failure

Insufficientia vascularis acuta

Acute vascular insufficiency is a syndrome that occurs when the circulating blood volume (CBV) fails to match the capacity of the vascular bed. This leads to a drop in blood pressure, impaired tissue blood supply, and the development of organ hypoxia (primarily affecting the brain).

Core conceptMismatch between circulating blood volume and vascular bed capacity.
DangerAcute cerebral hypoxia and ischemia.
FormsFainting (syncope), collapse, shock.
First aidRestoring venous return (elevating the legs).
3 min readFor medical studentsUpdated 10.10.2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesPending instructor review

Main clinical forms

The syndrome of acute vascular insufficiency manifests in three main forms, which share a common pathogenesis (decreased blood filling and organ hypoperfusion) but differ in severity:

  • Syncope (fainting) is the mildest and most short-lived form. It is characterized by rapid, reversible loss of consciousness due to transient cerebral ischemia resulting from a sharp drop in blood pressure or vascular tone.
  • Collapse is a more severe condition characterized by rapid pooling of blood in internal organs. It is accompanied by profound and persistent vascular insufficiency. In typical cases, consciousness is preserved, and multiorgan dysfunction does not develop.
  • Shock is the extreme degree of vascular insufficiency. It presents as a generalized circulatory disorder, involving all body systems and the development of multiple organ dysfunction syndrome.

Classification of collapse

Depending on the primary mechanism of development, collapse is divided into three groups:

  1. Cardiogenic — associated with a sharp drop in the heart's pumping function and a decrease in cardiac output.
  2. Vasodilatory (vascular) — occurs due to a rapid decrease in blood vessel tone.
  3. Hypovolemic — caused by a critical reduction in circulating blood volume.

By etiology, infectious (toxic), orthostatic, hypoxic, pancreatic, and poisoning-induced collapses are also distinguished. All of them fit into one of the three aforementioned pathogenetic mechanisms.

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Emergency care for syncope

When a syncopal state (or presyncope) develops, it is important to quickly restore cerebral blood flow:

  • During an attack: lay the person flat on their back, elevate their legs to increase venous return to the heart, and loosen tight clothing around the neck and chest.
  • For stimulation: splash cold water on the face, apply a cold compress, or let them inhale ammonia fumes.
  • In a presyncopal state (e.g., in a treatment room or at the dentist's): urgently move the patient to a horizontal position or, if sitting, forcefully bend their head and torso down between their knees.
  • After an attack: the patient needs to lie down for at least 10–15 minutes.

Further management depends on the cause of the syncope. For neurogenic causes, triggering factors are avoided; for orthostatic causes, patients are advised to avoid abrupt standing and to drink more fluids (2–3 liters per day). Cardiogenic syncope may require resuscitation (defibrillation, cardiac pacing) and cardiological treatment. For transient ischemic attacks, stroke prevention is carried out.

Principles of collapse treatment

Collapse therapy is based on restoring normal hemodynamics while obligatorily accounting for the underlying cause of the condition:

  • Elimination of the etiological factor: cessation of bleeding, detoxification therapy, administration of antibiotics (in infectious collapse).
  • Positioning: horizontal position with elevated lower extremities.
  • Restoration of CBV: infusion therapy using colloidal and crystalloid solutions.
  • Medication support: administration of vasopressors (e.g., norepinephrine or phenylephrine) to increase vascular tone, if necessary.
  • Additionally: oxygen therapy, strict monitoring of blood pressure, heart rate, and urine output.

Unlike shock, multiorgan dysfunction is not corrected in collapse because it does not have time to develop.

Class and exam questions

What do syncope, collapse, and shock have in common?

All these conditions share a single pathogenetic mechanism — a mismatch between the circulating blood volume and the capacity of the vascular bed, leading to a drop in blood flow and tissue hypoperfusion.

What is the main difference between collapse and shock?

In collapse, consciousness is generally not lost in typical cases, and multiple organ dysfunction does not develop. Shock is a more severe condition involving all body systems.

What to do if a patient feels they are about to faint?

They must be immediately laid on their back, or, if sitting, have their head and torso bent downward to improve blood flow to the brain.

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What else to study on this topic

  • Pathogenesis of leading symptoms in various forms of acute vascular insufficiency
  • Specific clinical picture of cardiogenic, vasodilatory, and hypovolemic collapse
  • Detailed algorithms for drug therapy (drugs, dosages, routes of administration) in shock and collapse
  • Differential diagnosis of the causes of syncopal states (cardiogenic, neurogenic, orthostatic)
  • The relationship between acute vascular insufficiency and transient ischemic attacks

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