Classification and causes of vascular disorders
Pathology of the peripheral blood flow is divided into two major groups depending on the caliber of the affected vessels. Arterial hyperemia (pathological form), venous hyperemia, ischemia, and stasis develop in medium-sized vessels. At the microvasculature level, capillary-trophic insufficiency is distinguished.
The causes of these conditions are diverse and divided into:
- Exogenous: infectious agents (microbes and their toxins) and non-infectious factors (temperature exposure, acids, alcohols, mechanical trauma).
- Endogenous: deposition of salts and calculi, accumulation of organic acids (lactic, pyruvic), or an excess of biologically active substances that reduce vascular tone (adenosine, kinins, prostaglandins).
Arterial hyperemia: mechanisms and consequences
The increase in arterial blood inflow is often neurogenic in nature. Three main mechanisms of development are distinguished:
- Neurotonic — dominance of parasympathetic nerve influences over sympathetic ones.
- Neuroparalytic — disappearance or sharp decrease in sympathetic influences (e.g., in mechanical trauma to nerve trunks, neuritis, or ganglionectomy).
- Neuromyoparalytic — a drop in the basal tone of smooth muscle cells due to depletion of catecholamine stores in synaptic vesicles.
Hyperemia can be physiological (functional in contracting muscles or protective during inflammation, delivering oxygen, phagocytes, and Ig) and pathological. The latter carries no adaptive value and is dangerous due to microvessel overstretching, microtears of their walls, and hemorrhages.
Venous hyperemia and stasis
Impaired blood outflow leads to venous hyperemia. Externally, it manifests as cyanosis (bluish discoloration), edema, a drop in tissue area temperature, and a tendency to bleed. Inside the vessels, serious hemodynamic and rheological shifts occur: venules and capillaries dilate, and blood flow slows down to the point of pendulum-like movements. Meanwhile, the axial stream of blood cells thickens, while the peripheral plasma layer narrows.
The extreme degree of the disorder is stasis — a complete cessation of blood flow. It is caused by severe ischemia (due to insufficient inflow), venous congestion (due to a lack of outflow), or primary excessive accumulation of proaggregants in the blood.
Embolism and the role of collateral circulation
The vessel lumen can be blocked from the inside by various substrates. The most significant are:
- Thromboemboli (fragments of detached blood clots).
- Fat emboli (in bone and adipose tissue trauma).
- Gas emboli (upon a sharp drop in barometric pressure, e.g., during depressurization).
- Air emboli (in injuries to large veins).
- Tissue, microbial, and parasitic emboli.
The severity of occlusion consequences directly depends on the development of collateral pathways. In skeletal muscles, the mesentery, or the lungs, collaterals are sufficient, so severe ischemia does not occur. However, in organs with absolutely insufficient collaterals, occlusion of a major artery inevitably leads to severe ischemia and tissue infarction.
Briefly: answers to topical questions
What types of ischemia are distinguished by their mechanism of origin?
Four main types of ischemia are distinguished by their mechanism of origin.
- Angiospastic — occurs due to arterial spasm resulting from increased tone of vasoconstrictors or increased sensitivity of vascular wall smooth muscles to pressor factors.
- Obstructive — caused by partial or complete closure of the arterial lumen by a thrombus, embolus, or atherosclerotic plaque.
- Compression — develops when an artery is compressed by a scar, tumor, or tourniquet.
- Redistributive — associated with the redistribution of circulating blood volume into hyperemic zones and decreased blood inflow to other anatomical regions.
What are the causes of true capillary stasis?
The primary cause of true capillary stasis is intracapillary blood cell aggregation. This condition is triggered by the following factors:
- Changes in the vascular wall — increased capillary wall permeability, enhanced transudation, and hemoconcentration.
- Changes in blood composition — excess of coarse-dispersed proteins, increased blood viscosity, and enhanced erythrocyte aggregation.
- Intracapillary aggregation of formed elements — occurs under the action of ADP, norepinephrine, thromboxane A₂, alterations in the erythrocyte membrane properties, and the neutralization of the negative surface charge of erythrocytes due to an excess of potassium and calcium ions.
To memorize organs with absolutely insufficient collaterals, use the phrase "Heart Remembers Brain and Spleen" (Heart, Kidneys, Brain, Spleen). In these organs, vascular occlusion threatens infarction.
Class and exam questions
How does physiological arterial hyperemia differ from pathological hyperemia?
Physiological hyperemia is adequate to the stimulus and serves a protective-adaptive function (delivery of oxygen, substrates, immunoglobulins). Pathological hyperemia leads to vessel overstretching, microtears, and hemorrhages.
What microhemodynamic changes are characteristic of venous hyperemia?
Dilation of capillaries and venules, slowing of outflow up to pendulum-like blood movement, widening of the axial cell stream, and narrowing of the peripheral plasma layer are observed.
What factors cause arteriolar spasm?
Spasm occurs with the predominance of the sympathetic nervous system, as well as under the action of chemical substances (nicotine, adrenaline preparations) and biological agents (catecholamines, endothelin, toxins). At the cellular level, this is accompanied by an increase in the concentration of Ca2+ or cAMP ions in smooth muscle cells.
In what cases do gas emboli form?
They appear during a rapid transition from high barometric pressure to low. This is typical of airplane depressurization or rapid ascent of divers from great depths.
What else to study on this topic
- Detailed classification of the causes of circulatory disorders by nature (physical, chemical, biological).
- Mechanisms of development of capillary-trophic insufficiency.
- Features of the localization of arterial, venous, and lymphatic emboli.
- Pathogenesis of increased adrenoreactive properties of the vascular wall at the cellular level.
- The role of endogenous vasoconstrictors (angiotensin II, ADH, endothelin) in the development of ischemia.
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