Neuroendocrine mechanisms and CNS response
Under the influence of an extreme factor, hyperafferentation triggers a powerful generalized response. The sympathoadrenal and hypothalamic-pituitary-adrenal systems, as well as the thyroid and pancreas, are involved in this process.
- Initially, protective reactions are adaptive in nature, but as damage increases, they become excessive.
- In the CNS, consciousness is preserved, and psychomotor agitation, restlessness, and hyperreflexia are observed.
- System activation leads to hyperactivity of internal organs, tachycardia, and hypertensive reactions.
Hemodynamic shifts and centralization of blood flow
Hemodynamic disorders are caused by cardiac dysfunction, changes in vascular tone, and a drop in the total circulating blood volume (CBV). Under the influence of catecholamines, arterioles and venules constrict, which maintains perfusion pressure.
- Centralization of blood flow: blood supply is maintained in the brain and heart due to high adrenergic receptor density and metabolic vasodilation.
- Peripheral ischemia: blood flow drops sharply in the skin, muscles, kidneys, and abdominal organs, leading to ischemia in these areas.
- Rheological disorders: slowed blood flow in microvessels creates a sludge phenomenon, increased blood viscosity, and a risk of thrombosis.
Metabolic shifts and the hypoxic component
The main component of pathogenesis is circulatory hypoxia, which gradually acquires a mixed character. All types of metabolism change against the background of prevailing catabolic processes:
- Protein metabolism: protein content in tissues and blood drops, azotemia develops.
- Carbohydrate metabolism: hepatic glycogenolysis is activated, and glycogen stores drop.
- Lipid metabolism: lipolysis increases, and cell membrane phospholipids break down.
- Energy metabolism: tissue ATP levels decrease due to enhanced hydrolysis and oxygen deficiency.
Toxemia and oxidative stress
During the compensation stage, the body's intoxication increases. Damaged cells release biologically active substances, enzymes, and metabolic products, while the excretory function of the liver and kidneys decreases.
- Reduced efficiency of biological oxidation leads to the accumulation of reactive oxygen species (ROS).
- Lipid peroxidation (LPO) reactions are activated.
- Toxic products and mediators exacerbate hemodynamic disorders and damage tissues.
Briefly: answers to topical questions
Which specific receptors and mechanisms prevent the blood vessels of the heart and brain from constricting during a catecholamine surge?
During centralization of blood flow, the blood vessels of the heart and brain maintain or increase blood flow due to two mechanisms specified in the source:
- Uneven distribution of adrenergic receptors: their density is high in the vessels of muscles, skin, kidneys, and the gastrointestinal tract, whereas in the vessels of the heart and brain, it is significantly lower.
- Metabolic vasodilation: vasodilators—adenosine, prostacyclin, and NO—are produced in the myocardium and brain.
Which specific inflammatory mediators and biologically active substances cause toxemia during shock?
The toxemic component in shock is associated with the action of the etiological factor and cell damage. The source lists:
- BAS (biologically active substances) released from damaged cells: kinins, biogenic amines, adenine nucleotides, enzymes.
- Etiological factors: toxins in toxic and toxico-infectious shock, burn products, anaphylactic mediators.
- Other damage and metabolic products: products of normal and impaired metabolism, ions, denatured compounds.
What is the pathogenetic essence of the sludge phenomenon in the microvasculature during shock?
The pathogenetic essence of the sludge phenomenon is a standard disorder of the blood aggregate state. It consists of:
- blood separation into plasma and distinct conglomerates of formed elements—erythrocytes, leukocytes, and platelets;
- adhesion, aggregation, and agglutination of formed elements.
During shock, this manifests as reduced blood fluidity, multiple microvascular thrombi, and microhemocirculatory disorders.
What types of hypoxia, besides circulatory, form the "mixed character" of hypoxia as shock progresses?
As shock progresses, primary circulatory hypoxia becomes mixed due to the addition of:
- respiratory disorders;
- changes in blood properties;
- disturbances in tissue metabolism.
More specific types of hypoxia for the shock progression stage are not listed in the provided source.
Shock compensation formula: SEMS (Stress-Activation $ \rightarrow $ Endocrine $ \rightarrow $ Membranes/Metabolism $ \rightarrow $ Hypoxia/Centralization).
Class and exam questions
What is the adaptive significance of the blood flow centralization phenomenon?
Centralization of blood circulation ensures the preservation of adequate perfusion of vital organs—the brain and heart—preventing their fatal ischemia at an early stage.
Why does blood viscosity increase during the shock compensation stage?
Blood viscosity increases due to a decrease in total circulating blood volume, slowed microcirculation, impaired fluid reabsorption in venules, and activation of clotting factors.
How does carbohydrate metabolism change in this stage?
Glycogenolysis is activated in the liver and tissues, leading to a sharp decrease in glycogen stores against the background of increased energy expenditure.
What else to study on this topic
- Pathogenesis of shock decompensation and irreversible changes
- The role of the kinin and complement systems in shock states
- Impaired renal excretory function and uremia
- Cytotoxic effects of oxygen free radicals
- Comparative characteristics of cardiogenic and hypovolemic shock
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