shock(redirected from colloidoclastic shock)
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a packed conical pile of hay or straw, usually put together where the harvesting takes place. The hay is collected from the fellings when they have a moisture content of 25 to 40 percent and is dried completely in shocks over a period of two to three days. Then the hay shocks are stacked into ricks in the open field, under an awning, or in a barn. About 0.75–2 centners are used to make a rick in areas with a damp climate, and about 2.5–4 centners in dry areas. Hay bucks and harvester-stackers are used to collect the hay into shocks. Gathering straw into a shock is done simultaneously with the combine harvesting of cereals; for this operation the combines are equipped with straw collectors.
a sudden life-threatening condition resulting from severe injury and characterized by progressive impairment of all the physiological systems of the body. The main characteristic of shock is the failure of capillary circulation in the tissues owing to impairment of cardiac output and arterial and venous tonus, capillary dysfunction, and changes in the rheological properties of blood. Shock can be brought on by an injury, burns, surgery (traumatic shock, burn shock, surgical shock), incompatible blood transfusion (hemolytic shock), anaphylaxis (anaphylactic shock), functional cardiac disorders (cardiogenic shock), ischemia of tissues and organs, and excessive loss of blood. The condition was described in detail by the French surgeon H. F. Ledran (1737) and by the Russian physician N. I. Pirogov (1870), who described the symptoms of the erectile phase (brief transient excitement) and torpid phase (subsequent sharp functional inhibition) of shock. The clinical manifestations of shock vary considerably. Progressively increasing extreme weakness and a progressive drop in blood pressure are the most characteristic.
Many aspects of the mechanisms underlying the development of shock still remain unclear. From the neuroreflex viewpoint, the various dysfunctions are due to numerous pain impulses that produce sharp excitation and subsequent inhibition of the nervous system, including the vital centers of the medulla oblongata. From the hemodynamic viewpoint, the decrease in the volume of circulating blood, which leads to peripheral circulatory insufficiency, is the principal factor. From the toxemic viewpoint, shock is caused by the entry into the blood of biologically active substances of tissue origin that interfere with the local and systemic blood flow. It is reasonable to assume that each of these factors plays a part: the primary abrupt activation of the central nervous system by extreme nerve impulses (or toxic substances) increases the amount of catecholamines released into the blood, causing a redistribution of the volume of circulating blood—spasms of the blood vessels of the skin, muscles, kidneys, and abdominal cavity accompanied by the increased flow of blood through arteriovenous anastomoses with maintenance of the circulation in the heart and brain (centralization of the circulation). This period of shock is clinically manifested by pallor and clamminess of the skin, contraction of the pupils, cold perspiration on the face, decreased urine flow, and moderately rapid breathing. The blood pressure is normal or slightly lowered.
“Centralization” of the circulation under conditions of extremely severe and prolonged injury becomes the principal mechanism of circulatory failure and further aggravation of the patient’s condition. The decreased flow of blood to the tissues leads to the accumulation of the products of anaerobic metabolism, biogenic amines, kinins, and other substances. Upon entering the bloodstream, these products, along with other humoral factors, such as increased concentration of some hormones and reduced partial pressure of oxygen, further disrupt the regulatory functions of the nervous system.
The chief factors in the pathogenesis of shock in its late stages are hypoxia, decreased vascular tonus, dysfunction of the tissue microcirculation, and gross derangement of cell metabolism, which results in injury to the cell membranes. The transfer of intravascular fluid to the tissues causes a decrease in the volume of circulating blood. This stage is marked by cyanosis, rapid pulse, lowered blood pressure, and dilatation and slow reaction of the pupils.
The subsequent stage of shock is complicated by congestion in small blood vessels, intravascular agglutination of the erythrocytes, decreased blood flow to the heart, acute cardiac insufficiency, and functional impairment of the vital organs. This stage is clinically manifested by gray cyanosis, thready pulse, abrupt drop in blood pressure, rapid, shallow breathing, dilatation of the pupils, and unconsciousness.
In cases of shock, emergency therapeutic measures are undertaken, chosen according to the cause of the shock, stage of its development, and severity of the patient’s condition. Other measures include the administration of pain relievers, keeping the patient warm, the transfusion of blood and blood substitutes, the administration of oxygen, and the injection of hormones, vitamins, and cardiovascular and other agents.
The term “shock” is also applied to persons in an unusual mental state or persons with severe emotional disturbances (mental, or emotional, shock).
REFERENCES“Problemy reaktivnosti i shoka.” Trudy 1-i Vsesoiuznoi konferentsii patofiziologov. Moscow, 1952.
Petrov, I. R., and G. Sh. Vasadze. Neobratimye izmeneniia pri shoke i krovopotere. Leningrad, 1966.
Weil, M. H., and H. Shubin. Moscow, 1971. Diagnostika i lechenie shoka. (Translated from English.)
Cannon, W. B. Traumatic Shock. New York-London, 1923.
Shires, G. T. Shock. Philadelphia, 1973.
S. A. DOLINA and T. M. OKSMAN