Classification and Causes of Vascular Disorders
Peripheral blood flow pathology is divided into two broad groups depending on the caliber of the affected vessels. Medium-sized vessel disorders include arterial hyperemia (pathological form), venous hyperemia, ischemia, and stasis. At the microvascular 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 extremes, acids, alcohols, mechanical trauma).
- Endogenous: deposition of salts and calculi, accumulation of organic acids (lactic, pyruvic), or an excess of biologically active substances that decrease vascular tone (adenosine, kinins, prostaglandins).
Arterial Hyperemia: Mechanisms and Consequences
An increased arterial blood inflow is often neurogenic in origin. Three main developmental mechanisms are distinguished:
- Neurotonic — dominance of parasympathetic nerve influences over sympathetic ones.
- Neuroparalytic — loss or sharp decrease of sympathetic influences (e.g., in mechanical trauma to nerve trunks, neuritis, or ganglion removal).
- Neuromioparalytic — 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 in inflammation, delivering oxygen, phagocytes, and Ig) or pathological. The latter has no adaptive value and is dangerous due to microvessel overstretching, micro-ruptures 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 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 to-and-fro (pendulum-like) movements. Meanwhile, the axial stream of formed elements widens, while the peripheral plasma layer narrows.
The extreme degree of disorder is stasis — complete cessation of blood flow. It is caused by severe ischemia (due to lack of inflow), venous congestion (due to lack of outflow), or primary excessive accumulation of pro-aggregants in the blood.
Embolism and the Role of Collateral Circulation
The vessel lumen can be occluded from within by various substrates. The most significant are:
- Thromboembolists (fragments of detached thrombi).
- Fatty emboli (in bone and adipose tissue trauma).
- Gas emboli (with 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 marked ischemia does not develop. However, in organs with absolutely insufficient collaterals, occlusion of a major artery inevitably leads to severe ischemia and tissue infarction.