Causes of Microcirculation Failure
Microcirculatory disorders are triggered by three main groups of causes. First, central and regional hemodynamic disorders (heart failure, ischemia, venous hyperemia). Second, direct damage to microvessel walls in atherosclerosis, vasculitis, or tumor growth. Third, changes in the properties of the blood itself—its concentration (hemoconcentration) during dehydration, dilution, or disseminated intravascular coagulation (DIC).
The basic pathogenesis scenario looks as follows: etiological factors increase the levels of proaggregants, cations, and macromolecular proteins in the blood. This inevitably leads to adhesion, aggregation, and agglutination of blood cells (erythrocytes, platelets, leukocytes). As a result, blood and lymph flow slows down to a complete halt, leading to stasis.
Intravascular Disorders and the Sludge Phenomenon
The intravascular group includes slowed blood flow, turbulence, and pathological blood shunting. Excessive extracapillary flow poses a particular danger: during severe stress or catecholamine release (e.g., in pheochromocytoma), arterioles spasm, and blood bypasses the capillary network through arteriovenous shunts. The capillary network is shut down, and the tissue suffers from severe ischemia.
A striking example of intravascular pathology is the sludge phenomenon (sludge). This is the separation of blood into liquid plasma and dense conglomerates of clumped cells. Sludge can act both as a primary cause of microcirculation disorders and as a secondary complication. The mechanism of sludge relies on two factors:
- Chemical: release of proaggregants (thromboxane A2, ADP, catecholamines). They cause cells to clump together, disintegrate, and release new portions of active substances, closing a vicious circle.
- Electrostatic: normally, erythrocytes are negatively charged and repel each other. During tissue damage, potassium, calcium, and sodium cations enter the blood, which 'recharges' cell membranes, turning them into magnets for each other. Adhesion to the vessel wall is achieved through the fixation of protein micelles.
Transmural Disorders
These disorders are associated with alterations in the barrier function of microvessels.
Increased permeability occurs due to acidosis (non-enzymatic hydrolysis of the basement membrane), activation of hydrolases, and rounding of endothelial cells, which widens interendothelial gaps. Fluid rapidly leaves the vascular bed due to the hyperactivation of basic mechanisms: filtration, energy-dependent transcytosis, diffusion, and osmosis. The result is the migration of cells into tissues, microhemorrhages, and the formation of hemorrhagic exudate. This picture is typical for severe sepsis, plague, and measles.
Decreased permeability is observed with thickening and sclerosis of vessel walls, as well as a deficit of energy for intracellular transport. This blocks plasma escape and critically reduces leukocyte migration into the focus of damage.
Extravascular Disorders and Final Outcome
Extravascular disorders are pathological changes in the volume of interstitial fluid. Its excess against the background of slowed drainage leads to edema (in inflammation, allergy, venous congestion).
A decrease in interstitial fluid volume (during hypohydration) is no less dangerous: it triggers a concentration mechanism. The concentration of toxic metabolic products, cytokines, and ions sharply increases in tissues. This disrupts the membrane potential of cells, worsens their damage, and blocks oxygen and carbon dioxide transport.
Prolonged progression of any of these forms leads to capillariotrophic insufficiency. This is a complex failure where blood and lymph circulation stops, transepithelial transport and metabolism cease. Tissues undergo severe dystrophy, and reparative processes are completely blocked.