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Collapsus

Collapsus

For medical students2 min readUpdated 2026-10-10

Collapsus is an acute, life-threatening condition characterized by circulatory failure. Its primary feature is a critical drop in arterial blood pressure leading to severe tissue hypoxia, while consciousness typically remains intact initially.

Main CauseMismatch between circulating blood volume and vascular bed capacity
Key DistinctionConsciousness is preserved during collapse (unlike syncope)
Key SymptomSharp drop in arterial blood pressure (BP)
Primary TargetThe brain suffers from circulatory insufficiency first

Etiology and Classification

The underlying mechanism of collapse is a sudden and significant absolute or relative decrease in circulating blood volume (CBV) relative to the capacity of the vascular bed. Based on the initial pathogenic link, three main types are distinguished:

  1. Cardiogenic. Occurs due to an acute drop in cardiac output. Causes are divided into cardiac factors (acute heart failure secondary to valvular defects, severe tachycardia, or bradycardia) and factors obstructing venous return to the heart (embolism, valvular or pulmonary artery stenosis).
  2. Hypovolemic. Associated with a rapid reduction in CBV. It develops in massive hemorrhage, plasma loss (extensive burns), or severe dehydration (intractable vomiting, profuse diarrhea, excessive sweating, poisoning). This group also includes blood redistribution with pooling in veins and capillaries during shock, intoxications, or gravitational overloads.
  3. Vasodilatory. Caused by an acute drop in total peripheral vascular resistance. Blood vessels (arterioles and venules) lose tone due to endocrinopathies (adrenal insufficiency, hypothyroidism), drug overdoses (ganglionic blockers, sympatholytics, narcotics, calcium channel blockers), or humoral factors (hypocapnia, deep hypoxia, excess histamine, kinins, and adenosine).

In clinical practice, an etiological classification is also used, distinguishing infectious, toxic, radiation, pancreatic, post-hemorrhagic, and other forms. The rate of onset is heavily influenced by environmental factors (temperature, humidity, barometric pressure) and individual reactivity.

Pathogenesis and Organ Effects

Regardless of the etiology, the general pathogenesis leads to progressive tissue hypoperfusion. Initially, circulatory hypoxia occurs, followed later by hemic and tissue hypoxia. This triggers a cascade of multiorgan dysfunction:

In severe cases, the liver is involved, leading to partial or total hepatic failure. To save the patient in hypovolemic collapse, emergency administration of blood components, packed red blood cells, plasma expanders, and solutions with ions and buffer systems is required. The body attempts to compensate for the loss by activating hematopoiesis.

Orthostatic Collapse

Orthostatic collapse warrants special attention. It occurs when a person transitions rapidly from a lying or sitting position to a vertical one, especially after prolonged physical inactivity (hypodynamia) or vestibular center irritation.

The initial trigger is systemic vasodilation—the walls of arterioles and capacitance vessels abruptly lose tone due to the dominance of cholinergic influences. The key pathogenic factor here is reduced vascular wall reactivity to vasopressors (angiotensin, catecholamines). This is frequently observed in adrenal insufficiency (glucocorticoid deficiency) or dysfunction of the cardiomotor center and hypothalamus.

Distinction from Syncope

In the International Classification of Diseases (ICD-10), syncope and collapse are grouped under the same rubric (R55), yet they are clinically distinct conditions.

Syncope (fainting) is a transient loss of consciousness caused by acute cerebral hypoperfusion. It begins acutely and is characterized by rapid spontaneous recovery of symptoms (within 5–25 seconds, rarely a few minutes).

In collapse, consciousness is not initially lost, although the patient may be severely lethargic or confused. However, progressive collapse can precipitate a syncopal episode.

Mnemonic

The three main mechanisms of collapse are easily remembered by the acronym CVD: Cardiogenic (dropped cardiac output), Volume-depleted/Hypovolemic (dropped blood volume), Vasodilatory (dropped vascular tone).

Frequently asked questions

Does the patient lose consciousness during collapse?

No, in classical collapse consciousness is preserved, although lethargy and confusion may be present. Loss of consciousness is characteristic of syncope (fainting), which may develop secondary to collapse.

Which type of hypoxia develops first in collapse?

Circulatory hypoxia is always primary because blood delivery to tissues is impaired. Hemic and tissue forms join later.

How does the body attempt to compensate for hypovolemic collapse?

Emergency activation of hematopoiesis occurs to replenish lost blood volume and formed elements.

Why does orthostatic collapse occur?

Due to a rapid transition to a vertical position. Blood vessels fail to constrict promptly due to decreased responsiveness to catecholamines or the predominance of cholinergic influences, leading to systemic vasodilation.

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