60. Hypovolemic shock: definition, etiology, pathogenesis, pathological anatomy.

Tissue (cellular) embolism is possible when tissues are destroyed due to injury or a pathological process, which leads to the entry of pieces of tissue (cells) into the blood.

Emboli can be tumor tissue or complexes of tumor cells during its disintegration, pieces of heart valves in ulcerative endocarditis, brain tissue in head trauma. Embolism of the cerebral tissue of the vessels of the small and large circulatory circles is also possible in newborns with birth trauma. Embolism with amniotic fluid in maternity patients is also referred to as tissue embolism.

More often, tissue (cellular) embolism is observed in the vessels of the large circle, less often in the small circle of blood circulation. A special category of tissue embolism is embolism by malignant tumor cells, since it underlies the hematogenous metastasis of the tumor. Microbial embolism occurs when microbes circulating in the blood clog the capillaries. These can be lumps of glued bacteria or fungi, animal parasites, protozoa. Bacterial emboli are often formed by purulent melting of a blood clot. Bacterial embolism determines the metastasis of pus.

At the site of blockage of the vessel by bacterial emboli, metastatic ulcers are formed: with embolism of small circle vessels — in the lungs, under the pleura, with embolism of large circle vessels — in the kidneys, spleen, heart and other organs.

61. Cardiogenic shock: definition, etiology, pathogenesis, pathological anatomy.

cardiogenic shock is a pathological condition caused by a rapid decrease in the volume of circulating blood. It is manifested by a decrease in blood pressure, tachycardia, thirst, nausea, dizziness, fainting, loss of consciousness and pallor of the skin.

The basis of this type of shock is:

• decrease in blood volume as a result of bleeding (both external and internal);

• excessive fluid loss (dehydration), for example, with diarrhea, vomiting, burns, excessive sweating;

• peripheral vasodilation. Generalized dilation of small vessels leads to excessive blood deposition in peripheral vessels. Pathogenesis: There are three phases of hypovolemic shock development: deficiency of circulating blood volume, stimulation of the sympathoadrenal system and shock itself.

Phase 1 is a shortage of BCC. Due to a shortage of blood volume, venous flow to the heart decreases, central venous pressure and stroke volume of the heart decrease. The liquid that was previously in the tissues moves compensatorily into the capillaries.

Phase 2 – stimulation of the sympathoadrenal system. Irritation of baroreceptors stimulates a sharp increase in the secretion of catecholamines. The content of adrenaline in the blood increases hundreds of times, norepinephrine – dozens of times. Due to the stimulation of beta-adrenergic receptors, vascular tone, myocardial contractility and heart rate increase. The spleen, veins in skeletal muscles, skin and kidneys are contracting. Thus, the body manages to maintain arterial and central venous pressure, ensure blood circulation in the heart and brain due to the deterioration of blood supply to the skin, kidneys, muscular system and organs innervated by the vagus nerve (intestines, pancreas, liver). This mechanism is effective for a short period of time, and recovery follows with rapid recovery of the BCC. If the shortage of blood volume persists, the consequences of prolonged ischemia of organs and tissues come to the fore in the future. Spasm of peripheral vessels is replaced by paralysis, a large volume of fluid from the vessels passes into the tissues, which leads to a sharp decrease in BCC in conditions of an initial shortage of blood.

Phase 3 is actually hypovolemic shock. BCC deficiency progresses, venous return and filling of the heart decrease, blood pressure decreases. All organs, including vital ones, do not receive the necessary amount of oxygen and nutrients, and multiple organ failure occurs.