Symptoms of shock

Pathogenetic stages of central and peripheral circulatory disorders in shock have clear clinical manifestations and can be detected in shock of any etiology. However, the specific cause of shock leaves its mark on the relationship between the stages and the duration of each of them. At a certain stage, shock of any etiology passes into a phase in which a vicious circle of pathological disorders may arise, exceeding the possibilities of independent restoration of perfusion and oxygen saturation of tissues. At this stage, a chain of pathological phenomena of complex and currently insufficiently studied mechanisms of disorders in the system of regulation of the aggregate state of blood up to thrombohemorrhagic syndrome arises.

In the early compensated stage, homeostatic mechanisms function to maintain the necessary perfusion of the "central" organs. At this stage, arterial pressure, diuresis, and cardiac function remain at a relatively normal level, but there are already symptoms of inadequate tissue perfusion. In the hypotensive stage, circulatory compensation is disrupted due to ischemia, endothelial damage, and the formation of toxic metabolites. This occurs in all organs and systems. When this process causes irreversible functional losses, the terminal or irreversible stage of shock is recorded. In clinical practice, along with the true irreversibility of shock, there may be conditions in which hidden causes can stimulate irreversibility. Eliminating them may allow patients to be transferred to the category with "reversible" shock.

The most important of these reasons are the following:

• Incorrect assessment of the circulatory response to infusion therapy:
• inadequate infusion therapy;
• hypoxia due to inadequate mechanical ventilation and as a consequence of undiagnosed pneumothorax or cardiac tamponade:
• diagnosed DIC syndrome in the hypercoagulation stage;
• persistent desire to replenish the deficit in the volume of circulating red blood cells, despite their inevitable intrapulmonary aggregation and an increase in intrapulmonary shunting and hypoxia;
• unjustified treatment with protein preparations, in particular albumin, in conditions of damage to the capillary membranes of the lungs and the increase in these situations of interstitial pulmonary edema and hypoxia.

In all variants of shock conditions, the normal functioning of almost all organs is disrupted and multiple organ failure develops. The immediate circumstances that determine the severity of the observed multiple organ dysfunction are the different ability of the organs to resist hypoxia and decreased blood flow, the nature of the shock factor, and the initial functional state of the organs.

Deviation of homeostasis parameters beyond certain limits is associated with high mortality.

High mortality may be due to factors such as:

• tachycardia more than 150 per minute in children and more than 160 per minute in infants;
• systolic blood pressure less than 65 in newborns, less than 75 in infants, less than 85 in children, and less than 95 mmHg in adolescents;
• tachypnea more than 50 per minute in children and more than 60 per minute in infants;
• glycemia level less than 60 and more than 250 mg%;
• bicarbonate content less than 16 mEq/L;
• serum creatinine concentration of at least 140 μmol/l in the first 7 days of life and at the age of over 12 years; >55 from the 7th day of life to 1 year; >100 in children from 1 year to 12 years;
• prothrombin index less than 60%;
• international normalized ratio of not less than 1.4;
• cardiac index less than 2 l/min x m ² ).

A decrease in cardiac index to less than 2 l/min x ^m2 is clinically manifested by the symptom of a “pale spot” - an increase in the time of capillary filling of more than 2 s after pressing on the skin, and a cooling of the skin of the distal parts of the extremities.

Hypovolemic shock is associated with fluid loss from the body. This may occur with bleeding, trauma, burns, intestinal obstruction, peritonitis, vomiting and diarrhea due to intestinal infection, osmotic diuresis due to diabetic ketoacidosis, or due to insufficient fluid intake. Hypovolemic shock is characterized by an absolute deficit in circulating blood volume, but most often, along with the deficit in intravascular volume, a deficit in extravascular fluid also quickly develops. In hypovolemic shock, hypoxic-ischemic injury occurs at an early stage. Reperfusion changes that develop after ischemia play a critical role in tissue damage. This shock is characterized by endogenous intoxication, which occurs either immediately, under the influence of the shock factor, or at subsequent stages of shock. Anatomical and physiological characteristics of the child's body, which include reduced activity of the phagocytic reaction, low production and high consumption of immunoglobulins, high vascularization of the intestine, and insufficiency of the detoxification system, determine the rapid generalization of the infectious process. Endogenous intoxication is usually considered a universal component of septic shock, endotoxin leads to peripheral vasodilation, decreased peripheral resistance, and disruption of energy metabolism.

_{Hemorrhagic shock is manifested by} pallor, early compensatory tachycardia, increasing cardiac output, which allows maintaining oxygen delivery despite the decrease in the hemoglobin level. Compensatory tachypnea and a decrease in the partial pressure of oxygen in arterial blood (Pa02 ) _{to a level of lessthan} 60 mm Hg indicate hypoxia. A further decrease in _Pa02leads to inadequate saturation ( _Sa02 ) of hemoglobin with oxygen, and tachypnea leads to a decrease in PaCO2 and _, based on the alveolar gas equation, a proportional increase in Pa02 and, _accordingly, an increase in Pa02 _{.Ischemia inthe} early stages is manifested by tachycardia, since due to a decrease in stroke volume of the heart with hypovolemia or a decrease in myocardial contractility, cardiac output can be maintained by increasing the heart rate. Systemic vasoconstriction helps maintain blood flow to vital organs. Further reduction in cardiac output is accompanied by the development of hypotension, impaired cerebral blood supply, and impaired consciousness. At this final stage of shock, high anion gap acidosis develops, which is confirmed by laboratory tests.

Impaired glucose metabolism in shock leads to the development of acidosis with an anion gap of more than 16 mmol/l and hypoglycemia (lack of glucose as a substrate) or hyperglycemia (development of insulin resistance), or normoglycemia (a combination of glucose deficiency and insulin resistance).

Cardiogenic shock develops due to a significant decrease in myocardial contractility in congenital heart defects, myocarditis, cardiomyopathy, arrhythmia, sepsis, poisoning, myocardial infarction, and myocardial trauma.

The occurrence of an obstacle to normal blood flow in the heart or large vessels with a subsequent decrease in cardiac output leads to the development of obstructive shock. The most common causes of its development are cardiac tamponade, tension pneumothorax, massive pulmonary embolism, closure of fetal communications (oval window and arterial duct) in duct-dependent congenital heart defects. Obstructive shock manifests itself with symptoms of hypovolemic shock, quickly leads to the development of heart failure and cardiac arrest.

In distributive shocks, inadequate redistribution of circulating blood volume with insufficient organ and tissue perfusion is observed.

Septic shock develops against the background of a systemic inflammatory reaction that occurs in response to the introduction of microorganisms into the internal environment of the macroorganism. Endotoxemia and uncontrolled release of inflammation mediators - cytokines - leads to vasodilation, increased vascular permeability, DIC, and multiple organ failure.

Anaphylactic shock is a severe allergic reaction to various antigens of food, vaccines, drugs, toxins and other antigens, which causes venodilation, systemic vasodilation, increased permeability of the vascular bed and pulmonary vasoconstriction.

In anaphylactic shock, skin, respiratory and cardiovascular symptoms are combined.

The most common symptoms are:

• skin - urticarial rash;
• respiratory - obstruction of the upper and/or lower respiratory tract;
• cardiovascular - tachycardia, hypotension.

In neurogenic shock, due to damage to the brain or spinal cord above the Th ₆ level, the heart and blood vessels lose sympathetic innervation, which leads to uncontrolled vasodilation. In neurogenic shock, arterial hypotension is not accompanied by compensatory tachycardia and peripheral vasoconstriction. Clinically, neurogenic shock is manifested by arterial hypotension with a large pulse difference, bradycardia, or normal heart rate.

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