Clinical triad of shock
The pathophysiological essence of any shock boils down to a global impairment of internal organ perfusion. Most often, this process is triggered by a critical decrease in circulating blood volume (CBV).
Diagnosis is based on identifying the classical triad of signs:
- Arterial hypotension. This is a fundamental, but not 100% specific symptom. Pressure values drop to 80–50 mm Hg, and in severe cases can be even lower.
- Central nervous system (CNS) damage. Due to a lack of blood supply, acute tissue hypoxia of the brain develops. Clinically, this manifests as a change in the patient's consciousness: they become lethargic, unresponsive, and sluggish.
- Renal damage. Insufficient blood flow immediately affects filtration function, leading to a sharp decrease in diuresis and the development of oligoanuria.
Causes and types of shock states
The etiological classification divides shock into two large groups depending on the triggering mechanism:
- Cardiogenic shock. Develops as a direct consequence of a drop in myocardial contractility (e.g., against the background of an extensive myocardial infarction).
- Non-cardiogenic types. Include conditions associated with fluid loss, vascular collapse, or external influences. These include post-hemorrhagic, burn, traumatic, septic (infectious-toxic), and anaphylactic variants.
Arterial hypotension outside of shock
A drop in blood pressure does not always mean the development of acute circulatory failure. There are several variants of hypotension occurring without shock:
- Physiological (transitory). Recorded in absolutely healthy individuals. It can be constant or episodic (e.g., circadian blood pressure drops during night sleep).
- Orthostatic. Occurs when changing body position (from horizontal to vertical) due to a malfunction of the autonomic nervous system, leading to a transient deterioration of cerebral blood supply. Manifests as dizziness and fainting (syncope). Often iatrogenic in nature—triggered by active treatment with diuretics or antihypertensive drugs.
- Cardiac. Associated with heart pathologies itself, but without a critical drop in tissue perfusion. Found in marked rhythm disorders, conduction blocks, as well as mechanical obstacles to cardiac output—aortic stenosis or hypertrophic cardiomyopathy (subaortic stenosis).
Briefly: answers to topical questions
What stages are distinguished in the pathogenesis of shock development?
In modern classification, the course of a pathological shock state is divided into three phases. The following stages are distinguished:
- Compensated shock — the deficit in circulating blood volume is compensated by functional changes in cardiovascular activity.
- Decompensated reversible shock — high total peripheral vascular resistance no longer compensates for low cardiac output, leading to systemic hypotension and organ hypoxia.
- Decompensated irreversible shock — characterized by the absence of a pressor response to intravenous norepinephrine administration or intra-arterial blood transfusion.
At what urine output volume is oligoanuria diagnosed in shock?
To assess the decrease in diuresis in shock and acute renal failure, quantitative indicators of daily urine output are used. The classification is based on the following criteria:
- Oliguria — diagnosed when diuresis drops below 500 mL/day.
- Anuria — diagnosed when diuresis drops below 100 mL/day.
At the stage preceding shock decompensation, diuresis may decrease by 1.5–2 times, but remains at least 30 mL/h. In decompensated shock, oliguria worsens due to a drop in hydrostatic pressure.
What severity classes of acute blood loss are distinguished in hemorrhagic shock?
Based on the volume of blood loss, four classes are distinguished, which determine the presence and clinical stage of hemorrhagic shock.
| Class | Blood loss volume (mL) | Shock severity / stage |
|---|---|---|
| Class 1 | 1000 | No |
| Class 2 | 1000–1500 | Mild / I |
| Class 3 | 1500–2100 | Moderate / II |
| Class 4 | 2100 | Severe / III |
What is the main mechanism of development of septic (infectious-toxic) shock?
The main mechanism of development of infectious-toxic, or septic, shock is the action of an infectious process with the release of toxins, predominantly endotoxins.
Key roles in pathogenesis are played by:
- release of toxins, predominantly endotoxins;
- activation of complement, coagulation, and fibrinolysis systems, as well as platelets and neutrophils;
- stimulation of nitric oxide, TNF-α, and interleukin production.
Excessive release of nitric oxide leads to profound hypotension due to systemic vasodilation and promotes the development of shock. The outcome is acute circulatory failure.
The triad of shock is easily remembered by the mnemonic: BP (blood pressure / hypotension) — CNS (stupor) — Kidneys (oligoanuria).
Class and exam questions
Is arterial hypotension always a sign of shock?
No. Blood pressure can drop in healthy people during sleep, upon abrupt standing up (orthostatic variant), or against the background of heart defects and arrhythmias, without leading to critical impairment of tissue perfusion.
Why do syncopal episodes occur in orthostatic hypotension?
When transitioning to a vertical position, autonomic regulation of vascular tone fails. Because of this, cerebral blood supply temporarily decreases, causing dizziness and the risk of syncope.
What is the main difference between cardiogenic and non-cardiogenic shock?
Cardiogenic shock is primarily associated with impaired myocardial contractility (as in myocardial infarction). Non-cardiogenic forms (burn, traumatic, hemorrhagic) are more often caused by a critical drop in circulating blood volume or vascular tone.
What else to study on this topic
- Principles of therapy for hypotensive conditions
- Mechanisms of orthostatic syncope development
- Iatrogenic causes of blood pressure reduction: diuretics and antihypertensives
- Cardiogenic shock in myocardial infarction
- Features of infectious-toxic and anaphylactic shock
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