Shock is a life-threatening critical condition developing in response to extreme stress on body homeostasis. Its fundamental basis is acute circulatory collapse, representing a critical failure of blood perfusion. This leads to a precipitous drop in tissue perfusion, depriving cells of oxygen and triggering a cascade of irreversible cellular changes.
HypovolemiaDevelops with a rapid loss of 20% or more of the circulating blood volume.
MortalityReaches 50% and higher in severe cardiogenic or septic shock.
Shock KidneyCharacterized by epithelial necrosis of the convoluted tubules (necrotizing nephrosis).
Septic ShockMost commonly caused by gram-negative bacteria (E. coli, Proteus, Klebsiella).
Classification and Pathophysiology
There are four main types of shock, each with a unique triggering mechanism but a common endpoint of tissue hypoxia:
Hypovolemic shock. Caused by a rapid drop in circulating blood volume (CBV) by 20% or more. Main causes include acute massive blood loss, severe dehydration, profuse diarrhea, or intractable vomiting leading to fluid and electrolyte loss. Extensive burns also fall into this category, 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. Most commonly caused by gram-negative bacteria (E. coli, Proteus, Klebsiella), and less frequently by gram-positive flora (staphylococci, streptococci, pneumococci). The release of bacterial toxins (primarily endotoxins) triggers a systemic reaction: complement, coagulation, and fibrinolytic systems, as well as platelets and neutrophils, are activated. A massive release of cytokines (TNF-$\alpha$, interleukins) and nitric oxide (a potent vasodilator) occurs. The result is acute circulatory failure.
Distributive (vasogenic) shock. Includes two main forms: anaphylactic (generalized hypersensitivity reaction) and neurogenic (occurring in trauma, severe pain, spinal cord injury, or as an anesthesia complication). Pathophysiology relies on pronounced vasodilation, increased capillary permeability, and arteriovenous shunting. Hemodynamically, this manifests as a significant decrease in total peripheral vascular resistance (TPVR) and redistribution of intravascular volume.
Stages of Development
The pathological process in shock consistently progresses through three consecutive stages:
Non-progressive (compensated) stage. Characterized by an initial drop in blood pressure and cardiac output. However, at this stage, the body actively fights back: compensatory vasoconstriction occurs (primarily spasmodic constriction of skin and intestinal vessels). This mechanism preserves relatively normal blood supply to vital organs (heart and brain).
Progressive (decompensated) stage. Occurs when adaptive mechanisms become exhausted. Profound collapse develops with a prominent clinical presentation. Due to escalating arterial dilation, tissue hypoperfusion affects absolutely all organs. Severe metabolic and circulatory disorders rapidly develop.
Irreversible (refractory) stage. Characterized by severe circulatory failure at the microcirculatory level. Vascular wall integrity is compromised. Multiple organ dysfunction syndrome (MODS) rapidly escalates, inevitably leading to death.
Pathomorphology of "Shock Organs"
At the tissue level, shock manifests as generalized dystrophic and necrotic changes. A critical morphological sign is disseminated intravascular coagulation (DIC): stasis, microthrombi, 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, featuring total necrosis of the convoluted tubule epithelium.
Liver ("shock liver"): hepatocytes undergo pronounced fatty change, and centrilobular necrosis forms in individual cases.
Heart: macroscopic and microscopic examination reveals small (primarily subendocardial) hemorrhages, foci of myocardial necrosis, fatty degeneration of cardiomyocytes, and contraction band necrosis.
Brain: ischemic encephalopathy develops, accompanied by tissue edema, petechial hemorrhages, and the formation of necrotic foci.
Adrenal glands: a sharp reduction to complete disappearance of lipids is observed in the cortex, indicating depletion of the substrate necessary for steroid hormone synthesis.
Gastrointestinal tract: multiple hemorrhages, erosions, and acute ulcers appear on the mucosa.
Mnemonic
To quickly remember the four main types of shock, use the mnemonic H-C-S-D (Hypovolemic, Cardiogenic, Septic, Distributive).
Frequently asked questions
Which mediators and biologically active substances participate in the pathogenesis of septic shock?
A wide spectrum of pro-inflammatory and anti-inflammatory cytokines, as well as tissue and plasma mediators, participate in septic shock pathogenesis.
Toxins — primarily endotoxins (lipopolysaccharides), which stimulate endogenous pyrogen production.
Which clinical and laboratory indicators signal the transition of shock into the irreversible stage?
The transition of shock into the irreversible stage (terminal state) is characterized by critical hemodynamic and microcirculatory failures.
Blood pressure — unmeasurable (in agony) or lacking pressor response to intravenous norepinephrine.
Respiration — becomes gasping or ceases entirely during clinical death.
Consciousness — completely absent.
Microcirculatory stasis — sluggish capillary refill («blanching sign» of nail beds), indicating peripheral vascular paresis.
Additionally, multiple organ dysfunction syndrome rapidly progresses at this stage alongside loss of vascular wall integrity.
What pathophysiological mechanisms lead to a drop in blood pressure during anaphylactic shock?
The drop in blood pressure in anaphylactic shock is caused by a generalized type I immediate hypersensitivity reaction.
Vascular reactions — marked 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 mast cell and basophil degranulation following antigen binding to IgE antibodies.
Which neurohumoral systems ensure blood redistribution (centralization of circulation) during the non-progressive stage of shock?
Centralization of circulation during the early (non-progressive) stage of shock is primarily ensured by activation of the sympathoadrenal system.
Reflex baroreceptor and chemoreceptor stimulation triggers catecholamine release.
Arteriolar and venular tone increases, maintaining 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 preserving blood flow to the brain and heart.
What is the central mechanism of pathophysiology in any type of shock?
The key link is acute circulatory collapse, which leads to generalized tissue hypoperfusion and microcirculatory disorders.
Why do vital organs escape ischemia during the early stage of shock?
Compensatory vasoconstriction is activated. The body constricts skin and intestinal vessels, redirecting blood flow to the heart and brain.
What is a "shock lung" in morphological terms?
It is a complex of changes including serous-hemorrhagic edema, foci of atelectasis, and the formation of hyaline membranes due to fibrin precipitation.
What determines the prognosis in shock?
The prognosis is determined by the type and severity of shock, the presence of complications, and the timing of treatment initiation.
Go deeper
Mechanisms of DIC development in shock states
The role of gram-negative bacterial endotoxins in the pathogenesis of septic shock
Differences between neurogenic and anaphylactic distributive shock
Morphological signs of ischemic encephalopathy
Pathogenesis of acute GI ulcers during centralization of circulation