Mechanisms of adaptation failure
The transition of shock into the decompensation stage is caused by the depletion of the body's protective reserves, increasing internal organ dysfunction, and the ongoing impact of the extreme factor. The main problem of this stage is the profound collapse of unified physiological and functional systems.
Neuroendocrine regulation loses its effectiveness and ceases to control tissue processes. Even if blood hormone levels and nerve impulse intensity remain high (or conversely, decrease), target cells stop responding adequately. This is due to receptor hyposensitization triggered by severe ion imbalance, increasing metabolic acidosis, and structural damage to cell membranes (primarily neuronal membranes). As a result, the body's vital activity is progressively depressed.
Hemodynamic catastrophe
Circulatory disorders acquire a crucial role in the pathogenesis of decompensation. The protective adaptive mechanism of blood flow centralization collapses: the tone of capacitance and resistance blood vessels drops totally. Concurrently, acute heart failure progresses, accompanied by severe arrhythmias and a decline in myocardial contractility.
- Critical pressure drop: Systolic blood pressure drops to threatening levels of 60–30 mmHg.
- Renal shutdown: Due to such low pressure, glomerular filtration in the kidneys stops completely, inevitably leading to uremia.
- Microcirculatory disorders: The liquid part of the blood actively passes through capillary walls into the intercellular space. The circulating blood volume (CBV) continues to plummet, and blood viscosity increases significantly.
A profound imbalance in the activity of the coagulation, anticoagulation, and fibrinolytic systems occurs in the hemostatic system. This triggers DIC syndrome (disseminated intravascular coagulation), leading to total organ hypoperfusion, multiple microthromboses, hemorrhages, and subsequently to dystrophic and necrotic changes in tissues.
Hypoxia, toxemia, and metabolic shift
Against the background of systemic vascular collapse, decreased CBV, and increasing respiratory failure, progressive mixed-type hypoxia develops. Cells are forced to switch to an anaerobic energy supply mode, causing severe uncompensated metabolic acidosis.
Metabolism changes dramatically, exacerbating organ damage:
- Catabolism dominance: Proteins, lipids, carbohydrates, and complex compounds (lipoproteins, phospholipids) undergo massive breakdown. Anabolic and plastic processes stop almost entirely.
- Cellular edema: Pronounced intracellular hyperhydration occurs.
- Destruction of cellular structures: Lipid peroxidation (LPO) is activated, enzyme systems are suppressed, cell membranes are degraded, and intercellular interactions are irreversibly disrupted.
Concurrently, severe toxemia increases. The blood is poisoned by products of aberrant metabolism (lactic, pyruvic, and fatty acids, polypeptides, biogenic amines). Cytotoxic compounds—denatured proteins, intracellular enzymes, and ions—are released into the bloodstream from destroyed necrotic cells. Due to liver and kidney failure, indoles, phenols, scatoles, uric acid, and urea rapidly accumulate in the body.
Clinical manifestations and organ damage
Decompensation is clinically manifested by the systemic failure of vital organs, described by specific "shock" phenomena.
| Organ system | Characteristic clinical manifestations and disorders |
|---|---|
| Nervous system | Confusion, lethargy, hyporeflexia, critically low efficiency of neuroendocrine regulation. |
| Heart and blood vessels | Arterial hypotension, vascular collapse, heart failure, arrhythmias, capillarotrophic insufficiency. |
| Lungs | Acute respiratory failure, formation of the "shock lung" phenomenon. |
| Blood system | Blood pooling, increased viscosity, development of thrombohemorrhagic syndrome (DIC syndrome). |
| Liver and kidneys | Acute hepatic and renal failure, "shock liver" and "shock kidney" phenomena. |
Briefly: answers to topical questions
What are the phases and stages of DIC syndrome occurring during shock decompensation?
Three or four consecutive phases (stages) are distinguished in the development of DIC syndrome.
- Stage I — hypercoagulation and thrombosis (activation of hemostatic factors, fibrin formation, and microthrombus formation).
- Stage II — progressive consumption coagulopathy (decreased platelet count and fibrinogen, depletion of procoagulants).
- Stage III — profound hypocoagulation and activation of fibrinolysis (pathological fibrinolysis of previously formed thrombi).
What does the term "shock lung" mean, and what is its pathogenesis?
The term "shock lung" refers to acute pulmonary parenchyma injury leading to acute respiratory failure (an absolute synonym for acute respiratory distress syndrome).
Main pathogenetic links:
- Vascular mechanism — hypercatecholaminemia causes angiospasm and pulmonary edema.
- Bronchial mechanism — imbalance of biologically active substances provokes bronchospasm and pulmonary atelectasis.
- Hemodynamic mechanism — intravascular blood clotting (capillary microthrombosis) leads to pulmonary shunt formation.
The primary cause of the pathology is impaired full functioning of the surfactant.
To memorize the main links of decompensation pathogenesis, use the acronym HHTM: Hemodynamics (drop in BP and microcirculation), Hypoxia (mixed, progressive), Toxemia (accumulation of toxins and metabolites), Metabolism (catabolism and acidosis).
Class and exam questions
Does the patient lose consciousness during the decompensation stage of shock?
No, consciousness is not lost at this stage. However, in severe shock, the patient exhibits marked mental and motor lethargy, as well as confusion.
Why do hormones and nerve impulses stop affecting tissues?
Cellular receptor hyposensitization develops. Its main causes are increasing metabolic acidosis, severe intra- and extracellular ion imbalance, and structural damage to cell membranes.
What happens to renal function during a critical drop in blood pressure?
A drop in systolic pressure to 60–30 mmHg leads to a complete cessation of glomerular filtration in the kidneys. This triggers acute renal failure, uremia, and the formation of the "shock kidney" phenomenon.
What else to study on this topic
- Mechanisms of capillarotrophic insufficiency development in shock.
- Pathogenesis of DIC syndrome and microhemocirculatory disorders.
- Formation of "shock lung" and "shock liver" phenomena.
- The role of lipid peroxidation (LPO) in cell membrane destruction.
- Causes of cellular receptor hyposensitization during acidosis.
Master the entire topic in the "Pathophysiology" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Decompensated shock stage" and 4,913 other subject pages
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 135 video lessons on the subject
Other topics in "Chapter 20. Extreme and Terminal States"
Free video lessons: pathophysiologyShort lessons with lecture notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.