Symptoms of shock

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

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

The most important of these reasons are:

• incorrect assessment of the response of blood circulation to infusion therapy:
• inadequate infusion therapy;
• hypoxia due to inadequate ventilation and as a result of undiagnosed pneumothorax or cardiac tamponade:
• diagnosed DIC syndrome in the stage of hypercoagulation;
• a stubborn desire to fill the deficiency of circulating red blood cells, despite their inevitable intrapulmonary aggregation and increased intrapulmonary shunting and hypoxia;
• unreasonable treatment with protein preparations, in particular albumin, in conditions of damage to the capillary membranes of the lungs and intensification of interstitial edema of the lungs and hypoxia in these situations.

In all cases of shock conditions, normal activity of almost all organs is disrupted and multi-organ failure is developing. Immediate circumstances that determine the severity of the observed multi-organ dysfunction are the different ability of organs to withstand hypoxia and reduce blood flow, the nature of the shock factor and the initial functional state of the organs.

The deviation of homeostasis beyond certain boundaries is associated with high mortality.

High mortality can be caused by such factors 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 mm Hg. In adolescents;
• tachypnea more than 50 per minute in children and more than 60 per minute in infants;
• the level of glycemia is less than 60 and more than 250 mg%;
• the content of bicarbonate is less than 16 meq / l;
• the serum creatinine concentration is at least 140 μmol / l in the first 7 days of life and over the age of 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%;
• the international normalized ratio is not less than 1.4;
• cardiac index less than 2 l / min ² ).

Decrease in cardiac index less than 2 l / minhm ² ) clinically manifests as a "pale spot" symptom - lengthening the time of capillary filling more than 2 s after pressing on the skin, cooling the skin of the distal limbs.

Hypovolemic shock is associated with loss of fluid from the body. This is possible with bleeding, trauma, burn, intestinal obstruction, peritonitis, vomiting and diarrhea with intestinal infection, osmotic diuresis with diabetic ketoacidosis or due to insufficient intake of fluid into the body. With hypovolemic shock, an absolute deficit of BCC is observed, but most often along with a deficit of the intravascular volume, the ectvascular fluid deficiency also rapidly develops. With hypovolemic shock, hypoxic-ischemic damage 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 in subsequent stages of shock. Anatomical and physiological features of the child's organism, which include reduced activity of the phagocytic reaction, low production and high consumption of immunoglobulins, high vascularization of the intestine, inadequacy of the detoxification system, cause a rapid generalization of the infectious process. Endogenous intoxication is usually considered a universal component of septic shock, endotoxin leads to peripheral vasodilation, a decrease in peripheral resistance and a disruption of energy metabolism.

Hemorrhagic shock is manifested by pallor, early compensatory tachycardia, which increases cardiac output, which allows to maintain the delivery of oxygen, despite the reduction in hemoglobin level. Compensatory tachypnea and a decrease in partial oxygen tension in the arterial blood (P _a 0 ₂ ) to a level of less than 60 mm Hg. Indicates hypoxia. A further decrease in P _a 0 ₂ leads to an inadequate saturation (S _a 0 ₂ ) of hemoglobin with oxygen, and tachypnea to a decrease in P _a C0 ₂ and, starting from the equation of the alveolar gas, proportional to the increase of P _a 0 ₂ and, respectively, an increase of P _a 0 ₂. Ischemia in the early stages is manifested by tachycardia, since cardiac output can be maintained by increasing the heart rate because of a decrease in stroke volume in hypovolemia or a decrease in the contractility of the myocardium. At the same time, systemic vasoconstriction helps maintain blood flow in vital organs. Further reduction in cardiac output is accompanied by the development of hypotension, a violation of the blood supply to the brain and a violation of consciousness. At this final stage of shock, acidosis with a high anionic interval develops, which is confirmed by laboratory analyzes.

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

Cardiogenic shock develops due to a significant decrease in contractility of the myocardium in congenital heart diseases, myocarditis, cardiomyopathy, arrhythmia, sepsis, poisonings, myocardial infarction, myocardial trauma.

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

In distributive shocks, an inadequate redistribution of BCC with insufficient organ and tissue perfusion was noted.

Septic shock develops against a 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 inflammatory mediators - cytokines - leads to vasodilation, increased vascular permeability, internal combustion engine, multi-organ failure.

Anaphylactic shock is a severe allergic reaction to various food antigens, vaccines, drugs, toxins and other antigens, in which venodilation, systemic vasodilation develops. Increased vascular permeability and pulmonary vasoconstriction.

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

The most common symptoms are:

• cutaneous - urticaria rash;
• Respiratory - obstruction of the upper and / or lower respiratory tract;
• cardiovascular - tachycardia, hypotension.

With 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.

[1], [2], [3], [4], [5], [6]