Arterial hypotension: classification and pathogenesis

Classification and etiological variants

Arterial hypotension is conventionally divided according to several key criteria:

By clinical course: physiological and pathological.
By origin (etiology):
Primary (centrogenic, neurogenic): represented by essential hypotension.
Secondary (symptomatic): manifest as a result of other pathological conditions, such as hypothyroidism, chronic adrenal insufficiency, neuroses, or circulatory failure.
By initial pathogenetic mechanism:
Neurogenic (subdivided into centrogenic and reflex);
Endocrine (adrenal, thyroid, pituitary);
Metabolic.

Pathogenesis of neurogenic hypotension

Neurogenic forms of hypotension develop due to disorders at the central or conducting levels of hemodynamic regulation.

Centrogenic hypotension

Functional variant (neurosis): triggered by prolonged psycho-emotional stress, which suppresses motor and emotional reactions. This leads to hyperactivation of the parasympathetic nuclei of the anterior hypothalamus and the entire parasympathetic nervous system. As a result, total peripheral vascular resistance (TPVR) drops and myocardial contractility decreases, leading to a fall in cardiac output.
Organic variant: develops in cranial trauma, cerebral ischemia or venous hyperemia, as well as degeneration of the basal nuclei, extrapyramidal system, and the dorsal motor nucleus of the vagus nerve. Concurrently, pressor sympathoadrenal influences decrease, parasympathetic tone dominates, arteriolar smooth muscle tone drops, and cardiac output declines.

Reflex (conducting) hypotension

This is based on impaired conduction of vasoconstrictor impulses from the vasomotor center of the medulla oblongata via sympathetic pathways. This mechanism is observed in syringomyelia, amyotrophic lateral sclerosis (ALS), neurosyphilis, and diabetic or toxic neuropathies. Loss of sympathetic influences leads to a persistent drop in TPVR, a decrease in circulating blood volume (CBV), and a reduction in cardiac output.

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Endocrine and metabolic forms

The development of these forms is associated with a deficiency of pressor hormones or tissue metabolites.

Adrenal hypotension: arising from trauma, hemorrhage, tuberculosis, or autoimmune adrenal damage, accompanied by a shortage of catecholamines, mineralocorticoids, and glucocorticoids. This manifests as a drop in arteriolar tone, decreased CBV, and reduced cardiac output.
Pituitary hypotension: associated with decreased effects of ACTH, ADH, TSH, and GH, which is accompanied by a drop in peripheral vascular tone, CBV, and cardiac output.
Metabolic hypotension: develops in chronic infections, intoxications, or prolonged starvation causing tissue dystrophy. Insufficient synthesis of vasoconstrictor substances (endothelin, thromboxane $A_2$, prostaglandin F, angiotensinogen) leads to relaxation of the vascular wall smooth muscles.

Briefly: answers to topical questions

What clinical symptoms are most typical for patients with arterial hypotension?

The provided sources do not contain a general list of typical symptoms for isolated hypotension, but they do describe clinical manifestations accompanying blood pressure drops in various pathologies.

Syncope and collapse — develop due to systemic circulatory insufficiency (e.g., in adrenal insufficiency).
Muscle weakness and increased fatigue — characteristic of hypotension against the background of hypoaldosteronism.
Dizziness, drowsiness, nausea, and muscle tremor — accompany acute arterial hypotension in dumping syndrome.
Consciousness disturbances and cardiac arrhythmias — may also occur during a sharp drop in blood pressure shortly after eating.

What drugs are used for the pharmacotherapy of arterial hypotension?

For the pharmacological correction of arterial hypotension, the provided sources explicitly indicate sympathomimetics: they are used in arterial hypotension to normalize renal blood flow.

If arterial hypotension is caused by hypovolemia or another reversible cause, non-glycoside inotropic drugs are not recommended until the cause of hypotension is resolved. In hypovolemia, CBV is replenished; the sources indicate the following for CBV restoration:

administration of isotonic sodium chloride solution.

How to memorize

To memorize the three main hemodynamic causes of decreased blood pressure, use the acronym R-V-C: Resistance (drop in TPVR), Volume (decrease in CBV), Cardiac output (reduction in myocardial output).

Class and exam questions

What blood pressure numerical values are considered a criterion for hypotension?

Arterial hypotension is diagnosed when systolic blood pressure drops below 90–95 mm Hg and diastolic blood pressure below 50–60 mm Hg.

How does primary hypotension differ from secondary hypotension?

Primary hypotension is an independent disease (essential hypotension), whereas secondary hypotension is merely a symptom or complication of another pathology (e.g., hypothyroidism or adrenal insufficiency).

What is the mechanism of blood pressure drop in functional neurosis?

Prolonged stress leads to the activation of the parasympathetic nuclei of the anterior hypothalamus. Enhanced parasympathetic influences reduce vascular tone (TPVR) and myocardial contractility, causing a drop in cardiac output.

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What else to study on this topic

Pathogenetic mechanisms of orthostatic collapse in catecholamine metabolism disorders
The role of mineralocorticoid and glucocorticoid deficiency in the drop of CBV and TPVR
Structural damage to the medulla oblongata and diencephalic region in organic hypotension
Comparative characteristics of pituitary hormones (ACTH, ADH, GH, TSH) in blood pressure regulation
The effect of tissue metabolites (endothelin, prostaglandin F, thromboxane A2) on arteriolar smooth muscle tone

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Arterial Hypotension