Collapse

Etiology and classification

The development of collapse is based on a sharp and significant absolute or relative decrease in the circulating blood volume (CBV) relative to the capacity of the vascular bed. Based on the initiating link of pathogenesis, three main types are distinguished:

1. Cardiogenic. Occurs due to an acute drop in cardiac output. Causes are divided into cardiac (acute heart failure against the background of valve defects, pronounced tachycardia, or bradycardia) and factors impeding blood flow to the heart (embolism, stenoses of valve orifices or pulmonary artery vessels).
2. Hypovolemic. Associated with a rapid decrease in CBV. Develops during massive blood loss, plasma loss (extensive burns), or severe dehydration (intractable vomiting, profuse diarrhea, heavy sweating, poisoning). This group also includes the redistribution of blood with its pooling in veins and capillaries during shock, intoxications, or gravitational overloads.
3. Vasodilatory. Caused by an acute drop in total peripheral vascular resistance. Vessels (arterioles and venules) lose tone due to endocrinopathies (adrenal insufficiency, hypothyroidism), drug overdoses (ganglionic blockers, sympatholytics, narcotics, calcium channel blockers), or the influence of humoral factors (hypocapnia, deep hypoxia, excess histamine, kinins, and adenosine).

In clinical practice, an etiological classification is also used, distinguishing infectious, toxic, radiation, pancreatic, posthemorrhagic, and other types. It is important to note that the rate of development of the pathology largely depends on the external environment (temperature, humidity, barometric pressure) and the reactivity of the organism itself.

Pathogenesis and impact on organs

Regardless of etiology, the general pathogenesis boils down to progressive tissue hypoperfusion. First, circulatory hypoxia occurs, which is later joined by hemic and tissue hypoxia. This triggers a cascade of multiorgan disorders:

• Cardiovascular system: stroke volume and cardiac output decrease, venous congestion, centralization of circulation, and capillarotrophic insufficiency occur. Coronary insufficiency develops.
• Nervous system: the patient becomes apathetic and lethargic, neuromuscular excitability decreases, finger tremor and convulsions are possible.
• Respiratory system: tachypnea develops (frequent shallow breathing), hypoxemia and hypercapnia are recorded in the blood flowing from the lungs.
• Kidneys: excretory function is impaired — diuresis drops (oliguria), urine becomes concentrated (hypersthenuria), and the level of nitrogenous wastes in the blood rises (hyperazotemia).
• Blood system and hemostasis: blood viscosity increases, erythrocytes and platelets undergo hyperaggregation, thrombi and sludge syndrome are formed.

In severe cases, the liver is involved in the process, leading to partial or total liver failure. To save the patient in the hypovolemic variant, emergency administration of blood components, packed red blood cells, plasma substitutes, as well as solutions with ions and buffer systems is required. The body itself tries to compensate for the loss by activating hemopoiesis.

Orthostatic collapse

Orthostatic collapse deserves special attention. It occurs when a person abruptly transitions from a lying or sitting position to a vertical one, especially after prolonged physical inactivity, as well as upon irritation of the vestibular centers.

The initiating link is systemic vasodilation — the walls of arterioles and capacitance vessels sharply lose tone due to the dominance of cholinergic influences. The key pathogenetic factor here is a decrease in the reactivity of vessel walls to vasopressors (angiotensin, catecholamines). This is often observed in adrenal insufficiency (glucocorticoid deficiency) or disorders of the function of the cardiovascular center and hypothalamus.

Difference from fainting

In the International Classification of Diseases (ICD-10), fainting and collapse are combined into a single category (R55), but clinically these are different conditions.

Fainting (syncope) is an episode of temporary loss of consciousness due to acute cerebral hypoperfusion. It begins acutely and is characterized by a rapid spontaneous regression of symptoms (after 5–25 seconds, less often a few minutes).

During collapse, consciousness is initially not lost, although the patient may be severely lethargic or confused. At the same time, it is important to remember that progressive collapse can provoke the development of a syncopal state.

Class and exam questions

What else to study on this topic

• Mechanisms of development of cardiogenic collapse in heart valve defects
• Pathogenesis of multiorgan failure against the background of mixed hypoxia
• Principles of emergency therapy for hypovolemic collapse (plasma substitutes, buffer systems)
• The role of endocrinopathies (hypothyroidism, adrenal insufficiency) in reducing vascular tone
• Sludge syndrome and blood rheology disorders in systemic hypoperfusion

Other topics in "Chapter 20. Extreme and Terminal States"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.