Hyperemia

HYPEREMIA, hyperaemia (from Greek hyper- excessively and haima- blood), local blood congestion. A distinction is made between arterial, or active, hyperemia and venous, or passive, hyperemia. In the first case, blood flows through the arteries and capillaries of an organ in greater quantity and more rapidly than normal; in the second case, it drains from the organ through the veins more slowly than usual, sometimes to the point of complete stoppage - stasis (see). The causes of arterial hyperemia were previously divided into mechanical, chemical, thermal, and neuropathic, but now there is a tendency to classify them into 2 groups: mechanical and trophoneurotic, since chemical factors affect both the trophic state of the vascular wall and the vasoconstrictor innervation, and thermal hyperemia is now classified as mechanical. In its pure form, however, mechanical arterial hyperemia is observed only in cases of decreased pressure in a given area, atmospheric or otherwise (hyperaemia ex vacuo), for example, with dry cups, under which a rarefied space is formed, or when any effusions are released from serous cavities, similar conditions being created in the latter. Under the influence of heat, the vessels dilate, and thus the influx of arterial blood is also mechanical. - An example of chemical arterial hyperemia can be cases of hyperemia from mustard plasters. But even in the mechanism of collateral hyperemia, despite the importance of the mechanical factor here, the vasoconstrictor also plays an essential role, as is evident from Stefani's experiment: if before tying the main artery of a limb in an animal all nerves of the limb are cut, then collateral circulation does not develop properly after the ligation, and gangrene of the limb may even occur. Neuropathic hyperemia may depend either on paralysis of vasoconstrictors (then it is called neuroparalytic hyperemia) or on irritation of vasodilators (then it is called neurotonic hyperemia). As early as Claude Bernard showed that if in a rabbit the cervical portion of the sympathetic trunk is cut on one side, then the vessels of the ear on the same side dilate due to paralysis of the vasoconstrictor nerves passing in the sympathetic nerve trunk. Hyperemia based on disorders of vasoconstrictor innervation, like any nervous phenomenon, can be of both peripheral and reflex origin, as well as central. Examples of peripheral neuroparalytic hyperemia can be cases of hyperemia of half the face after various types of injuries in the neck area, fractures of the clavicle, or in the presence of pressure on the cervical sympathetic nerve (tumors, aneurysms, goiter, etc.). This also includes the so-called 'tuberculous flush' - redness of the cheeks, apparently based on decreased tone of vasoconstrictors in the cervical sympathetic trunk, created reflexly from the tuberculous focus in the lung. Central neuroparalytic hyperemia occurs when the vasomotor center is depressed [brain injuries, intracranial tumors, depressive affects (fright)]. Differentiating neuroparalytic hyperemia from neurotonic is not always easy, but in general it could be said that the latter is less prolonged compared to the former. And neurotonic hyperemia can also be of peripheral (resp. reflex - from sensory nerves) as well as central origin. An example of the first type of hyperemia can be cases of redness of half the face in toothache, and an example of the second type - the blush of shame and anger. An increased tendency to such neuropathic hyperemia constitutes the essence of many angioneuroses [dermatographism (see), erythrophobia (fear of blushing), etc.]. In the so-called erythromelalgia, consisting in the appearance, sometimes symmetrically, of red spots on the extremities, accompanied by swelling and burning pain, irritation of vasodilators also plays an essential role, however, it is apparently not only a neurosis but a more complex disorder. Symptoms of arterial hyperemia during life (after death, the latter significantly decreases due to displacement of blood into capillaries and veins) consist in redness, local increase in temperature (in the case of hyperemia of external coverings) from the influx of warmer blood from deeper parts, subjectively manifested as a sensation of local heat, and with stronger influxes of blood - to an increase in volume of the hyperemic area. On mucous membranes, increased secretion of serous fluid is often observed, due to displacement of interstitial fluid from tissue spaces, on which the therapeutic effect of arterial hyperemia, artificially induced by various therapeutic measures (hot compresses, sand baths, etc.: absorption of pathological products when circulation is revived). Prolonged arterial hyperemia, with enhanced functioning of the organ, can lead to hypertrophy of the vascular wall. The causes of venous hyperemia are of two kinds: either difficulties in the outflow of blood through veins (such as: blockage of veins; compression by tumors, pregnant uterus or ligatures; prolonged vertical position of resting extremities - professional venous stagnation of typesetters, etc.) or weakening of the propulsive force of the heart. In the latter case, venous hyperemia takes on a more general character, as also with weakening of the suction activity of the chest cavity (emphysema). But venous hyperemia can also occur based on relaxation of both the vascular walls themselves and the surrounding connective tissue, for example, under the influence of low temperature (frostbite) or alcohol ('red-blue nose' of drunkards). In general, however, the abundance of anastomoses in veins protects the body from the development of venous hyperemia when there are difficulties in outflow somewhere on the periphery. Signs of venous hyperemia: 1) greater than normal redness of the tissue with a bluish, cyanotic tint, unlike the bright redness in arterial hyperemia; with general venous stagnation - general cyanosis, especially noticeable on mucous membranes and generally in places with a thin covering (lips, ears, under nails), due to dilation of veins filled with blood rich in carbon dioxide; 2) decrease in local temperature in peripheral parts with venous hyperemia (easily freezing, relatively cold extremities in persons with weakened heart) and 3) increase in volume and swelling of the corresponding area, due to edema (along with dilation of veins), based on increased permeability of stretched veins. Under the microscope, for example in the experiment of bilateral application of ligatures to the veins of a frog's tongue, the so-called pendulum-like movement of blood (fluxus and refluxus) is first observed, then complete stoppage (stasis) and exit of red blood cells (diapedesis). Consequences of venous hyperemia. Transient hyperemias can pass without a trace; prolonged ones, in addition to a general decrease in organ function, lead to various regressive changes (degeneration, atrophy) with simultaneous proliferation of connective tissue (cyanotic induration), sometimes reaching in the skin such degrees that one speaks of elephantiasis (elephantiasis cutis). The cause of connective tissue proliferation in venous hyperemia is twofold: on the one hand, violation of tissue equilibrium (atrophy of parenchyma), on the other - the irritating effect of retained metabolic products. Sometimes the consequences of venous hyperemia are also hemorrhages from ruptured vessels (such as hemorrhoidal bleeding). But artificially induced (by applying an elastic bandage) venous hyperemia can also be used for therapeutic purposes in certain diseases of the extremities [treatment of venous hyperemia according to Viru for large joints, paronychia, etc. (see Viru method)], which perhaps can be explained by the harmful effect of accumulating CO₂ on bacteria.