Classification and pathogenesis
There are four main types of shock, each with a unique triggering mechanism but a common final pathway of tissue hypoxia:
- Hypovolemic shock. Occurs due to a rapid drop in circulating blood volume (CBV) by 20% or more. Main causes: acute massive blood loss, severe dehydration, profuse diarrhea or uncontrollable vomiting leading to fluid and electrolyte loss. This also includes extensive burns, where plasma massively shifts out of the microvasculature.
- Cardiogenic shock. Associated with a sharp decrease in stroke volume. This pump failure leads to a drop in blood pressure and tissue hypoperfusion, similar to hypovolemia. It occurs in extensive myocardial infarction, severe myocarditis, acute mitral or aortic regurgitation, prosthetic valve thrombosis, ventricular septal rupture, and cardiac tamponade.
- Septic (toxic-infectious) shock. Triggered by a severe infectious process. The most common culprits are gram-negative bacteria (E. coli, Proteus, Klebsiella), less often gram-positive flora (staphylococci, streptococci, pneumococci). The release of bacterial toxins (mainly endotoxins) triggers a systemic reaction: the complement, coagulation, and fibrinolysis systems are activated, along with platelets and neutrophils. A massive release of cytokines (TNF-$\alpha$, interleukins) and nitric oxide, a potent vasodilator, occurs. The result is acute circulatory failure.
- Vascular (distributive) shock. It includes two main forms: anaphylactic (generalized hypersensitivity reaction) and neurogenic (occurring in trauma, severe pain, spinal cord injury, or as a complication of anesthesia). The pathogenesis is based on pronounced vasodilation, increased capillary permeability, and arteriovenous blood shunting. Hemodynamically, this manifests as a significant decrease in systemic vascular resistance (SVR) and redistribution of intravascular volume.
Stages of development
The pathological process in shock consistently progresses through three consecutive stages:
- Non-progressive (early) stage. Characterized by an initial decrease in blood pressure and cardiac output. However, at this stage, the body actively resists: compensatory vasoconstriction occurs (primarily spasm of the skin and intestinal vessels). Due to this mechanism, a relatively normal blood supply to vital organs (the heart and brain) is maintained.
- Progressive stage. Occurs when adaptive mechanisms become exhausted. A profound collapse develops with a pronounced clinical picture. Due to increasing arterial dilation, tissue hypoperfusion of absolutely all organs occurs. Severe metabolic and circulatory disorders rapidly begin to develop.
- Irreversible stage. Characterized by severe circulatory failure at the microcirculatory level. Impairment of the vascular wall integrity occurs. Multiple organ failure (MOF) rapidly develops, which inevitably leads to a fatal outcome.
Pathomorphology of "shock organs"
At the tissue level, shock manifests as generalized dystrophic and necrotic changes. The most important morphological sign is DIC syndrome: stasis, thrombus formation, and petechial hemorrhages are observed in the microvasculature. Target organs acquire specific features:
- Shock lung: foci of atelectasis appear, serous-hemorrhagic edema develops, and fibrin strands precipitate in the alveoli, forming so-called hyaline membranes.
- Shock kidney: characterized by the development of necrotizing nephrosis, accompanied by total necrosis of the convoluted tubule epithelium.
- Liver ("shock liver"): hepatocytes undergo marked fatty degeneration; in some cases, centrilobular necrosis develops.
- Heart: macroscopically and microscopically, small (predominantly subendocardial) hemorrhages, foci of myocardial necrosis, fatty degeneration of cardiomyocytes, and signs of hypercontraction are visible.
- Brain: ischemic encephalopathy develops, accompanied by tissue edema, petechial hemorrhages, and the formation of foci of necrosis.
- Adrenal glands: a sharp decrease, up to the complete disappearance of lipids, is observed in the cortical layer. This indicates the depletion of the substrate necessary for the synthesis of steroid hormones.
- Gastrointestinal tract: multiple hemorrhages, erosions, and acute ulcers appear on the mucous membrane.
Briefly: answers to topical questions
Which mediators and biologically active substances are involved in the pathogenesis of septic shock?
A wide range of pro-inflammatory and anti-inflammatory cytokines, as well as tissue and plasma mediators, are involved in the pathogenesis of septic shock.
- Pro-inflammatory cytokines include interleukins (IL-1, IL-6, IL-8), tumor necrosis factor-alpha (TNF-α), and colony-stimulating factor (CSF).
- Anti-inflammatory cytokines include IL-4, IL-10, IL-13, and soluble TNF receptors.
- Tissue and plasma mediators include nitric oxide (NO), histamine, serotonin, kinins, and platelet-activating factor (PAF).
- Toxins are predominantly endotoxins (lipopolysaccharide) that stimulate the production of endogenous pyrogen.
Which clinical and laboratory parameters indicate the transition of shock into an irreversible stage?
The transition of shock into an irreversible stage (terminal state) is characterized by critical hemodynamic and microcirculatory disorders.
- Blood pressure is unmeasurable (during the agonal stage) or shows no pressor response to intravenous norepinephrine administration.
- Respiration becomes convulsive or ceases completely during clinical death.
- Consciousness is completely absent.
- Microcirculation — slight nail blanching upon pressure ("capillary refill sign"), which indicates peripheral vascular paresis.
In addition, multiple organ dysfunction rapidly progresses at this stage, and vascular wall integrity is compromised.
What pathogenetic mechanisms lead to the drop in blood pressure in anaphylactic shock?
The drop in blood pressure in anaphylactic shock is caused by a generalized immediate-type hypersensitivity reaction.
- Vascular reactions — pronounced vasodilation and a significant decrease in total peripheral vascular resistance (TPVR).
- Microcirculatory disorders — increased capillary permeability and arteriovenous shunting.
- Hemodynamic shifts — redistribution of intravascular blood volume.
These changes develop in the early phase of the reaction under the action of mediators released during the degranulation of mast cells and basophils after antigen binds to IgE class antibodies.
Which neurohumoral systems ensure the centralization of blood circulation during the non-progressive stage of shock?
The centralization of blood circulation in the early (non-progressive) stage of shock is primarily ensured by the activation of the sympathoadrenal system.
- The reflex response of baroreceptors and chemoreceptors triggers the release of catecholamines.
- The tone of arterioles and venules increases, which maintains systemic blood pressure and venous return to the heart.
- Compensatory vasoconstriction occurs predominantly in the vessels of the skin, intestines, kidneys, liver, and other peripheral organs, while maintaining blood flow to the brain and heart.
For quick memorization of the four main types of shock, use the mnemonic HCDC: Hypovolemic, Cardiogenic, Septic, Circulatory.
Class and exam questions
What is the main pathogenetic link in any type of shock?
The key mechanism is acute circulatory collapse, which leads to generalized tissue hypoperfusion and impaired microcirculation.
Why do vital organs not suffer from ischemia in the early stage of shock?
Compensatory vasoconstriction is triggered. The body spasms the vessels of the skin and intestines, redirecting blood to the heart and brain.
What is a «shock lung» from a morphological point of view?
This is a complex of changes including serous-hemorrhagic edema, foci of atelectasis, and the formation of hyaline membranes due to fibrin precipitation.
What does the prognosis depend on in shock?
The prognosis is determined by the type and severity of shock, the presence of complications, and the stage at which treatment was initiated.
What else to study on this topic
- Mechanisms of DIC syndrome development in shock states
- The role of gram-negative flora endotoxins in the pathogenesis of septic shock
- Differences between neurogenic and anaphylactic vascular shock
- Morphological signs of ischemic encephalopathy
- Pathogenesis of acute gastrointestinal ulcers during the centralization of blood circulation
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