Shock(from the French choc - blow, push) is an acute hemodynamic disorder, as a result of which tissue hypoperfusion develops. A more complete definition may be as follows: shock is a severe pathological process, accompanied by the depletion of the vital functions of the body and bringing it to the brink of life and death due to a critical decrease in capillary blood flow in the affected organs. In general, the concept of “shock” until now is not one of the precisely determined ones. Deslauriers famous statement on this matter: “Shock is easier to recognize than to describe, and easier to describe than to define it.”
The initial pathogenetic mechanism of shock, as a rule, is a massive flow of biologically negative afferentation entering the central nervous system from the area of influence of the damaging factor.
Initially, an idea arose about the nature of shock as a result of intolerable painful irritation associated with trauma, causing widespread overexcitation of the central nervous system with subsequent depletion.
Today, the number of conditions that various authors attribute to shock has expanded enormously and currently amounts to dozens in some sources. For example, hemolytic, painful, obstetric, spinal, toxic, hemorrhagic, cardiogenic shock, etc. The inclusion of such a significant number of pathological processes in the concept of shock is often apparently due to the fact that it is not differentiated from collapse and coma. Indeed, shock and collapse have common pathogenetic links: vascular insufficiency, respiratory failure, hypoxia, compensatory reactions.
However, there are also significant differences, for example, with collapse, the process begins precisely with systemic hemodynamic disorders; In case of shock, changes in blood circulation occur secondarily. Other differences are shown in the table (according to A.I. Volozhin, G.V. Poryadin, 1999).
Stages, manifestations and basic mechanisms of shock development. Any shock is characterized by a two-phase change in the activity of the central nervous system: initial widespread excitation of neurons (“erectile stage” or compensation stage); subsequently widespread inhibition of their activity (“torpid stage” or stage of decompensation). Consciousness is usually maintained during both phases of shock. It can be significantly reduced and changed (especially in the torpid phase of shock), but is not completely lost. Reflex reactions to external stimuli of various modalities are also preserved, although significantly weakened.
Sometimes there is a third stage of shock - the so-called terminal stage, in which consciousness is completely absent. This stage is essentially a comatose state with all its characteristic signs.
The erectile stage (compensation) of shock is characterized by increased sympathoadrenal and pituitary-adrenal influences, which increase the activity of most physiological systems. At the beginning of the torpid phase of shock, the level of catecholamines and corticosteroids usually remains elevated, but the effectiveness of their action on various organs is reduced. Subsequently, there is a decrease in the activity of the sympathoadrenal, pituitary-adrenal systems and the content of corresponding hormones in the blood. Therefore, during the first stage of shock, the functions of the circulatory system are activated and, as a result, tachycardia, arterial hypertension, and redistribution of blood flow occur; in addition, there is an increase in breathing rate and an increase in alveolar ventilation; Erythrocytosis may occur due to the release of blood from the depot.
In the second stage of shock, central hemodynamics are weakened: blood pressure decreases, the deposited blood fraction increases, blood volume and pulse pressure decrease, and a “thread-like” pulse is often noted. With mild shock, blood pressure drops to 90–100 mmHg. Art., with moderate severity - up to 70-80, with severe - up to 40-60. Alveolar ventilation decreases, and pathological forms of breathing may appear. In the stage of decompensation, increasing circulatory and respiratory failure leads to the development of severe hypoxia, and it is this that subsequently determines the severity of the shock state.
Characteristics of shock are microcirculation disorders. They can occur already at the first stage due to the redistribution of blood flow and its reduction in a number of organs (kidneys, liver, intestines, etc.). As we move into the torpid phase, microcirculatory disorders become increasingly widespread, manifesting not only as a decrease in microvascular perfusion, but also as a deterioration in the rheological properties of blood, increased permeability of capillary walls, aggregation of formed elements, and perivascular edema.
An obligatory pathogenetic factor in shocks of various etiologies is endotoxemia. Numerous biologically active substances that enter the internal environment of the body in excess (histamine, serotonin, kinins, catecholamines, etc.) have a toxic effect during shock. Denatured proteins and their breakdown products, lysosomal enzymes, toxic intestinal products, microbes and their toxins may appear in the blood. Of significant importance in the development of toxemia are metabolites that are intensively formed in cells due to metabolic disorders: lactic and pyruvic acids, keto acids, potassium, etc. Dysfunctions of the liver and kidneys that arise as a result of hypoxia and microcirculation disorders lead to even greater changes in blood composition: acidosis, ionic and protein imbalance, shifts in osmotic and oncotic pressure in various environments of the body.
The above changes in the body leave an imprint on biochemical processes in the cell (“shock” cell). Cellular disorders are characterized by the well-known triad of hypoxia: ATP deficiency, acidosis, damage to biomembranes.
It is very important that during the development of shock, so-called “vicious circles” often arise. In this case, the initial disorders of the activity of organs and systems can be potentiated, and the shock tends to “deepen itself.” For example, disorders of the central circulation and microcirculation lead to dysfunction of the liver and kidneys, and the resulting unfavorable changes in the composition of the blood aggravate circulatory disorders. At a certain stage of the torpid stage of shock, hemodynamic disturbances can reach such a degree that secondary collapse develops, which quite often joins shock with its unfavorable development and sharply worsens the patient’s condition.
So, I have outlined, in very general terms, modern ideas about the pathogenesis of shock states. It is clear that the nature, severity and specific significance of each of the pathogenetic factors can vary widely depending on the type of shock, its stage and severity, as well as the reactive properties of the body.
Let me once again emphasize the complexity of the problem of classifying various types of shock states. There is still a lot of discussion around this issue, since there is no single classification. However, most authors, taking into account the main etiological factors and pathogenetic mechanisms, identify the following forms of shock: primary hypovolemic; cardiogenic; vascular-peripheral; traumatic. Examples and brief descriptions of these forms of shock are given in textbooks. It seems to us that shock states are most successfully classified by V.A. Frolov (see diagram).
Previously, we considered the main points of the pathogenesis of anaphylactic and burn shock. Therefore, we will focus only on traumatic, blood transfusion and cardiogenic shock.
Traumatic shock. The cause is usually widespread injuries to bones, muscles, internal organs, accompanied by damage and severe irritation of nerve endings, trunks and plexuses. Traumatic shock is often accompanied or aggravated by blood loss and wound infection.
Here I will dwell on the following point. Views on the mechanism of shock development have undergone significant changes over time. If the neurogenic theory of shock, which was especially popular in the 30-40s. XX century in our country, primarily explained the development of shock as a reflex change in the state of the body in response to pain impulses that arose at the time of injury, then the theory of blood and plasma loss put forward by Blelok (1934) practically did not take into account pain impulses as a significant factor in its development. Currently, most pathophysiologists and clinicians believe that traumatic shock develops as a result of the influence of several pathological factors on the body. First of all, these are pain impulses, blood and plasma loss, and toxemia.
And two more points that you should pay attention to. Firstly, despite the fact that blood loss is one of the significant causes of the development of traumatic shock, it would be wrong to identify changes in blood circulation, including microcirculation, only with a deficiency of bcc. Indeed, in the development of pure blood loss and traumatic shock there are common pathogenetic factors - a state of stress, hypotension accompanied by hypoxia, inadequate afferent impulses from injured tissues during shock or from baro- and chemoreceptors of blood vessels during blood loss. However, disturbances in nervous activity during traumatic shock occur earlier and are more severe than during blood loss. Stimulation of the HPA axis during shock is accompanied by a sharp decrease in the ability of tissues to absorb corticosteroids, which entails the development of extra-adrenal corticosteroid insufficiency. With blood loss, on the contrary, the level of tissue consumption of corticosteroids increases.
Secondly, the activation of defense mechanisms in response to severe injury is accompanied by the activation of antinociceptive defense (see the chapter on the pathophysiology of pain). But here it should be noted that an increase in the content of endogenous opiates, which should have a protective nature in the event of severe trauma, in fact often turns into an irreparable disaster for the body. The fact is that excessive stimulation of all parts of the HPA axis, which always accompanies severe injury, leads to the release of large amounts of enkephalins and endorphins, which, in addition to blocking opiate receptors, perform a number of other functions in the body. First of all, it is involved in the regulation of blood circulation and respiration. It is now known that endorphins can disrupt the regulation of blood circulation and contribute to the development of uncontrollable hypotension.
Thus, efferent manifestations of pain, leading to excessive stimulation of the HPA axis, not only do not protect the body from injury, but, on the contrary, contribute to the development of deep damage to the body’s most important life support systems and the development of traumatic shock.
During the erectile stage, the patient experiences speech and motor agitation: he rushes about, reacts sharply even to ordinary touch; the skin is pale due to spasm of skin microvessels; the pupils are dilated due to activation of the sympathoadrenal system; indicators of central circulation and respiration are increased.
The first stage is replaced by the second - torpid. Its classic clinical picture was described by N.I. Pirogov (1865): “With an arm or leg torn off, such a numb person lies motionless at the dressing station; he does not shout, does not complain, does not take part in anything and does not demand anything; his body is cold, his face is pale; the gaze is motionless and turned into the distance, the pulse is like a thread, barely noticeable under the finger. The numb person either does not answer questions at all, or only to himself, in a barely audible whisper; breathing is also barely noticeable. The wound and skin are almost completely insensitive... The numb man has not completely lost consciousness, not only is he not at all aware of his suffering.”
Typically, patients with severe traumatic shock die from progressive circulatory disorders, respiratory or renal failure. Microperfusion disturbances occur in the lungs, blood shunting increases, and the diffusion properties of alveolar-capillary membranes deteriorate due to their swelling and the development of interstitial edema. Disturbances in the gas exchange function of the lungs during traumatic shock are a very dangerous phenomenon that requires emergency intervention (“shock lung”).
Reduction of blood circulation and microcirculatory disorders in the kidneys lead to kidney failure, manifested by oliguria (or anuria), azotemia and other disorders. In the later stages of shock in the kidneys, along with severe microcirculation disorders, blockade of the tubular apparatus is possible due to the formation of hyaline and myoglobin casts (“shock kidney”). In severe cases of traumatic shock, intestinal autointoxication develops.
Note that the course of shock in childhood has its own characteristics. The most characteristic feature of traumatic shock at an early age is the ability of the child’s body to maintain a normal blood pressure level for a long time even after a severe injury. Long-term and persistent centralization of blood circulation in the absence of treatment is suddenly replaced by hemodynamic decompensation. Therefore, the younger the child, the more unfavorable a prognostic sign for shock is arterial hypotension.
Blood transfusion shock. The direct cause of transfusion shock may be incompatibility of the blood of the donor and recipient with respect to group ABO factors, Rh factor or individual antigens. Shock can develop, and its course will worsen significantly in cases where low-quality blood is used (with hemolysis, protein denaturation, bacterial contamination, etc.).
The first signs of shock may appear already during transfusion (in case of group incompatibility) or in the next few hours (in case of Rh incompatibility or incompatibility with individual antigens).
In the occurrence of blood transfusion shock due to group or Rh incompatibility, the main pathogenetic factor is massive agglutination and the formation of erythrocyte conglomerates followed by their hemolysis. As a result, the physicochemical properties of blood change dramatically. It is believed that these changes serve as a trigger for shock as a result of extreme irritation of the wide receptive field of the vascular bed. Significant intravascular hemolysis leads to a sharp deterioration in the oxygen transport functions of the blood and the development of hemic hypoxia, the severity of which subsequently increases as a result of circulatory disorders.
Manifestations. During the erectile stage, motor excitement occurs, rapid breathing with difficulty exhaling, a feeling of heat, and pain in different parts of the body (especially in the kidney area) are noted. Systemic blood pressure may increase and tachycardia may occur.
The first stage is quickly replaced by the second (torpid). General weakness occurs, redness of the skin gives way to severe pallor, and nausea and vomiting often occur. Against the background of general physical inactivity, convulsions may develop, and blood pressure drops. This type of shock is characterized (to a large extent determine the severity of the condition) by impaired renal function (the so-called blood transfusion nephrosis). The appearance of oliguria or anuria during transfusion shock is always a sign of a dangerous deterioration in the patient's condition.
Cardiogenic shock is a critical condition that develops as a result of acute arterial hypotension caused by a sharp drop in the pumping function of the left ventricle. The primary link in the pathogenesis of cardiogenic shock is a rapid decrease in stroke volume of the left ventricle, which leads to arterial hypotension, despite compensatory spasm of resistive vessels and an increase in total peripheral vascular resistance aimed at restoring blood pressure.
Arterial hypotension and decreased blood flow through the exchange capillaries due to spasm of the smallest arteries, arterioles and precapillary sphincters disrupt blood flow in the organs in the periphery and cause the main symptoms of cardiogenic shock. Namely: disturbances of consciousness; pale skin, cold and damp extremities; oliguria (<20 мл/ч); артериальная гипотензия (систолическое АД < 90 мм рт.ст.).
Cardiogenic shock occurs, according to many authors, in 12–15% of cases of myocardial infarction. The occurrence of cardiogenic shock depends on the size of the area of myocardial damage, its initial state, central circulation, as well as on the functional characteristics of the nociceptive and antinociceptive system and other factors that determine the reactivity of the body.
When 50–65% of the myocardial mass is affected, either cardiac fibrillation or acute circulatory failure occurs. In this case, shock may not occur. Cardiogenic shock often develops when a smaller mass of the myocardium is affected (up to 50%) against the background of sharp pain, accompanied by chaotic excitation of various autonomic centers and disorders of the neuroendocrine regulation of blood circulation and other physiological systems.
I would like to draw attention to this fundamental distinctive feature of the pathogenesis of this type of shock. Arterial hypotension, which occurs due to traumatic shock, is not the leading link in the pathogenesis of this pathological condition, but a consequence of the failure of compensation for traumatic shock, in which pathological changes in organs and tissues form long before the decrease in blood pressure. In cardiogenic shock, on the contrary, arterial hypotension immediately begins to act as one of the main links in pathogenesis.
Compensatory reactions in response to arterial hypotension and circulatory hypoxia in cardiogenic shock are almost identical to those in patients in a state of traumatic or hypovolemic shock. In particular they include:
Predominantly neurogenic spasm of veins as a result of increased sympathetic vasoconstrictor influences;
Activation of the renin-angiotensin-aldosterone mechanism, including as a result of systemic adrenergic stimulation;
Compensatory autohemodilution, i.e. mobilization of fluid from the interstitial sector to the vascular sector due to changes at the systemic level in the relationship between pre- and postcapillary vascular resistance.
The biological purpose of such compensatory reactions is clear - maintaining IOC and blood pressure through an increase in total venous return, retention of sodium and water in the body, an increase in the intravascular fluid sector and an increase in peripheral vascular resistance. In cardiogenic shock, these protective reactions increase pre- and afterload, and therefore increase the utilization of free energy by cardiomyocytes. The increase in the work of contractile myocardial cells increases the discrepancy between the heart's need for oxygen and the delivery of O 2 to it. As a result, the mass of the hypoxic and hibernating myocardium increases, and its contractility decreases even more.
From the above it follows: the main pathophysiological feature of cardiogenic shock is that compensatory reactions initially have the properties of pathogenesis links, the action of which determines the progression of shock and its acquisition of an irreversible character. In addition, in cardiogenic shock, the main effector of compensatory reactions aimed at maintaining minute volume of blood circulation, the heart, is affected.
Shock can be caused by a condition in the body when blood circulation is dangerously reduced, for example, with cardiovascular disease (heart attack or failure), with large loss of blood (severe bleeding), with dehydration, with severe allergic reactions or blood poisoning (sepsis).
Shock classification includes:
Shock is a life-threatening condition and requires immediate medical treatment; emergency care is not excluded. The patient's condition in shock can quickly deteriorate; be prepared for initial resuscitation efforts.
Symptoms
Symptoms of shock may include feelings of fear or agitation, bluish lips and nails, chest pain, confusion, cold clammy skin, decreased or stopped urination, fainting, low blood pressure, pallor, excessive sweating, rapid pulse, shallow breathing, unconsciousness, weakness .
What can you do
First aid for shock
Check the victim's airway and perform artificial respiration if necessary.
If the patient is conscious and has no limbs or back, lay him on his back, with his legs raised 30 cm; don't raise your head. If the patient has suffered an injury in which raised legs cause pain, then there is no need to raise them. If the patient has received severe damage to the spine, leave him in the position in which you found him, without turning him over, and provide first aid by treating wounds and cuts (if any).
The person should stay warm, loosen tight clothing, and do not give the patient anything to eat or drink. If the patient is drooling or drooling, turn his head to the side to ensure the drainage of vomit (only if there is no suspicion of spinal injury). If there is still a suspicion of spinal injury and the patient is vomiting, it is necessary to turn him over, fixing his neck and back.
Call an ambulance and continue to monitor vital signs (temperature, pulse, respiratory rate, blood pressure) until help arrives.
Preventive measures
Preventing shock is easier than treating it. Prompt and timely treatment of the underlying cause will reduce the risk of developing severe shock. First aid will help control the state of shock.
shock) - the body’s reaction to the influence of extreme irritants, characterized by the development in a person of severe circulatory, respiratory, and metabolic disorders (ed.). Blood pressure drops sharply, the patient's skin becomes covered with cold sweat and turns pale, the pulse weakens and quickens, there is a dry mouth, dilated pupils, and urination is significantly reduced. Shock can develop as a result of a significant decrease in blood volume resulting from severe internal or external bleeding, burns, dehydration, and severe vomiting or diarrhea. It may be caused by a disorder of the heart, for example, due to coronary thrombosis, myocardial infarction or pulmonary embolism. Shock may be a consequence of the expansion of a large number of veins, as a result of which they are insufficiently filled with blood. Shock may also be caused by the presence of bacteria in the bloodstream (bacteraemic or toxic shock), a severe allergic reaction (anaphylactic shock; see Anaphylaxis), an overdose of narcotic drugs or barbiturates, or severe emotional distress. shock (neurogenic shock). In some cases (for example, with peritonitis), shock may develop as a result of a combination of several of the above factors. Treatment for shock depends on the cause of its development.
SHOCK
1. Clinical syndrome associated with impaired oxygen supply to tissues, especially to brain tissue. Shock, to some degree, accompanies every trauma, although it is usually only detected when there is a major trauma, such as a serious injury, surgery, an overdose of certain drugs, an extremely strong emotional experience, etc. 2. The result of the passage of electric current through the body. Severe shock (2) can cause shock (1). See shock therapy.
SHOCK
from fr. choc - blow, push) - a life-threatening condition that arises in connection with the body's reaction to injury, burn, surgery (traumatic, burn, surgical Sh.), with transfusion of incompatible blood (hemolytic Sh.), disruption of the heart during myocardial infarction (cardiogenic Sh.), etc. Characterized by progressive weakness, a sharp drop in blood pressure, central nervous system depression, metabolic disorders, etc. Emergency medical care is required. Sh. is also observed in animals. Psychogenic Sh. (emotional paralysis) is a type of reactive psychosis.
Shock (shocked)
fr. choc "blow") - numbness due to severe mental shock. Shock can be a consequence of rudeness, injustice, shamelessness, cynicism. Can be combined with surprise and indignation. Wed. the expression is unpleasant to hit.
He stopped in the middle of the street, rooted to the spot. A terrible suspicion stirred in him: “Is she really...” This means that all the other jewelry is also a gift from [her lovers]! It seemed to him that the earth was shaking... He waved his hands and fell unconscious (H. Maupassant, Jewels).
Henry saw Doris looking at him with horror. She was apparently shocked and shocked (A. Wolfert, Thacker's Gang).
SHOCK
observed in various pathological conditions and is characterized by insufficient blood supply to tissues (decreased tissue perfusion) with impaired function of vital organs. Impaired blood supply to tissues and organs and their functions arise as a result of collapse - acute vascular insufficiency with a drop in vascular tone, a decrease in the contractile function of the heart and a decrease in the volume of circulating blood; a number of researchers do not make a distinction at all between the concepts of “shock” and “collapse”. Depending on the cause that caused the shock, they are distinguished: painful shock, hemorrhagic (after blood loss), hemolytic (after transfusion of a different blood group), cardiogenic (due to myocardial damage), traumatic (after severe injuries), burn shock (after extensive burns), infectious- toxic, anaphylactic shock, etc.
The clinical picture of shock is due to a critical decrease in capillary blood flow in the affected organs. Upon examination, the patient’s face is characteristically in a state of shock. It was described by Hippocrates (Hippocratic mask): “...The nose is sharp, the eyes are sunken, the temples are depressed, the ears are cold and tight, the earlobes are turned away, the skin on the forehead is hard, tense and dry, the color of the whole face is green, black or pale, or leaden.” . Along with the noted signs (haggard, sallow face, sunken eyes, pallor or cyanosis), attention is drawn to the low position of the patient in bed, immobility and indifference to the environment, barely audible, “reluctant” answers to questions. Consciousness may be preserved, but confused, apathy and drowsiness are noted. Patients complain of severe weakness, dizziness, chilliness, blurred vision, tinnitus, and sometimes a feeling of melancholy and fear. Drops of cold sweat often appear on the skin, the limbs are cold to the touch, with a cyanotic tint to the skin (the so-called peripheral signs of shock). Breathing is usually rapid and shallow; when the function of the respiratory center is depressed due to increasing hypoxia of the brain, apnea is possible. Oliguria (less than 20 ml of urine per hour) or anuria is noted.
The greatest changes are observed in the cardiovascular system: the pulse is very frequent, weak filling and tension (“thread-like”), in severe cases it cannot be felt. The most important diagnostic sign and the most accurate indicator of the severity of the patient’s condition is a drop in blood pressure. The maximum, minimum, and pulse pressure decreases. Shock can be considered when systolic pressure drops below 90 mm Hg. Art. (later it decreases to 50 - 40 mm Hg or is not even detected); diastolic blood pressure decreases to 40 mm Hg. Art. and below. In persons with pre-existing arterial hypertension, the picture of shock can be observed at higher blood pressure levels. A steady increase in blood pressure with repeated measurements indicates the effectiveness of the therapy.
In hypovolemic and cardiogenic shock, all the described signs are quite pronounced. In hypovolemic shock, unlike cardiogenic shock, there are no swollen, pulsating neck veins. On the contrary, the veins are empty, collapsed, and it is difficult and sometimes impossible to obtain blood through puncture of the ulnar vein. If you raise the patient’s hand, you can see how the saphenous veins immediately fall off. If you then lower your arm so that it hangs down from the bed, the veins fill very slowly. In cardiogenic shock, the neck veins are filled with blood, and signs of pulmonary congestion are revealed. In infectious-toxic shock, the clinical features are fever with tremendous chills, warm, dry skin, and in advanced cases, strictly defined necrosis of the skin with its rejection in the form of blisters, petechial hemorrhages and pronounced marbling of the skin. In anaphylactic shock, in addition to circulatory symptoms, other manifestations of anaphylaxis are noted, in particular skin and respiratory symptoms (itching, erythema, urticarial rash, Quincke's edema, bronchospasm, stridor), abdominal pain.
Differential diagnosis is made with acute heart failure. As distinguishing signs, one can note the patient's position in bed (low in shock and semi-sitting in heart failure), his appearance (in shock, Hippocratic mask, pallor, marbling of the skin or gray cyanosis; in heart failure - more often a bluish, puffy face, swollen pulsating veins , acrocyanosis), breathing (in shock it is rapid, superficial, in heart failure - rapid and intense, often difficult), expansion of the boundaries of cardiac dullness and signs of cardiac congestion (moist rales in the lungs, enlargement and tenderness of the liver) in heart failure and a sharp fall Blood pressure in shock.
Treatment of shock must meet the requirements of emergency therapy, i.e., it is necessary to immediately use drugs that give an effect immediately after their administration. Delay in treating such a patient can lead to the development of severe microcirculation disorders, the appearance of irreversible changes in tissues and be a direct cause of death. Since a decrease in vascular tone and a decrease in blood flow to the heart play an important role in the mechanism of shock development, therapeutic measures should primarily be aimed at increasing venous and arterial tone and increasing the volume of fluid in the bloodstream.
First of all, the patient is placed horizontally, that is, without a high pillow (sometimes with his legs elevated) and oxygen therapy is provided. The head should be turned to the side to avoid aspiration of vomit in case of vomiting; Taking medications by mouth is naturally contraindicated. In case of shock, only intravenous infusion of drugs can be of benefit, since a disorder of tissue circulation impairs the absorption of drugs administered subcutaneously or intramuscularly, as well as taken orally. Rapid infusion of fluids that increase the volume of circulating blood is indicated: colloidal (for example, polyglucin) and saline solutions in order to increase blood pressure to 100 mm Hg. Art. Isotonic sodium chloride solution is quite suitable as initial emergency treatment, but if very large volumes are transfused, pulmonary edema may develop. In the absence of signs of heart failure, the first portion of the solution (400 ml) is administered as a stream. If shock is caused by acute blood loss, if possible, blood is transfused or blood substitutes are administered.
In case of cardiogenic shock, due to the risk of pulmonary edema, preference is given to cardiotonic and vasopressor drugs - pressor amines and digitalis preparations. For anaphylactic shock and shock resistant to fluid administration, therapy with pressor amines is also indicated.
Norepinephrine acts not only on blood vessels, but also on the heart - it strengthens and speeds up heart contractions. Norepinephrine is administered intravenously at a rate of 1–8 mcg/kg/min. In the absence of a dispenser, proceed as follows: pour 150–200 ml of a 5% glucose solution or an isotonic sodium chloride solution with 1–2 ml of a 0.2% norepinephrine solution into the dropper and install the clamp so that the injection rate is 16–20 drops per minute. Monitoring blood pressure every 10 - 15 minutes, if necessary, double the rate of administration. If stopping the administration of the drug for 2 - 3 minutes (using a clamp) does not cause a repeated drop in pressure, you can finish the infusion while continuing to monitor the pressure.
Dopamine has selective vascular effects. It causes vasoconstriction of the skin and muscles, but dilates the blood vessels of the kidneys and internal organs. Dopamine is administered intravenously at an initial rate of 200 mcg/min. In the absence of a dispenser, the following scheme can be used: 200 mg of dopamine is diluted in 400 ml of saline, the initial rate of administration is 10 drops per minute, if there is no effect, the rate of administration is gradually increased to 30 drops per minute under the control of blood pressure and diuresis.
Since shock can be caused by various causes, along with the administration of fluids and vasoconstrictors, measures are needed to prevent further exposure to these causative factors and the development of pathogenetic mechanisms of collapse. For tachyarrhythmias, the treatment of choice is electrical pulse therapy; for bradycardia, electrical stimulation of the heart is the treatment of choice. In hemorrhagic shock, measures aimed at stopping bleeding (tourniquet, tight bandage, tamponade, etc.) come to the fore. In the case of obstructive shock, pathogenetic treatment is thrombolysis for pulmonary embolism, drainage of the pleural cavity for tension pneumothorax, pericardiocentesis for cardiac tamponade. Pericardial puncture can be complicated by myocardial damage with the development of hemopericardium and fatal rhythm disturbances, therefore, if there are absolute indications, this procedure can only be performed by a qualified specialist in a hospital setting.
In case of traumatic shock, local anesthesia (novocaine blockade of the injury site) is indicated. In case of traumatic, burn shock, when adrenal insufficiency occurs due to stress, it is necessary to use prednisolone and hydrocortisone. For infectious-toxic shock, antibiotics are prescribed. In case of anaphylactic shock, the volume of circulating blood is also replenished with saline solutions or colloid solutions (500 - 1000 ml), but the main treatment is adrenaline in a dose of 0.3 - 0.5 mg subcutaneously with repeated injections every 20 minutes, antihistamines are additionally used, glucocorticoids (hydrocortisone 125 mg intravenously every 6 hours).
All therapeutic measures are carried out against the background of absolute peace for the patient. The patient is not transportable. Hospitalization is possible only after the patient has been brought out of shock or (if the therapy started on site is ineffective) by a specialized ambulance, in which all necessary treatment measures are continued. In case of severe shock, you should immediately begin active therapy and at the same time call the intensive care team “to take care of you.” The patient is subject to emergency hospitalization in the intensive care unit of a multidisciplinary hospital or a specialized department.
Until misfortune touches us, we tend to live in the illusion that the world around us is safe and we are in control of our lives. But the real world easily destroys our fantasies, and its impact can traumatize both our body and psyche. In psychology, there is a special type of psychotrauma – shock trauma.
The shock reaction occurs when a person is faced with an event that he experiences as a threat to his life (or the lives of others - observer trauma). Events that can lead to shock trauma include: natural disasters, catastrophes, violence (robbery, rape, etc.), military operations, sudden loss of loved ones, surgeries, many medical interventions, severe incurable diseases, sudden loss social status (divorce, job loss, bankruptcy, etc.). All these events occur suddenly and cause a strong feeling of fear and helplessness in a person. In this case, a special condition arises - shock (which is why the injury is called shock). Shock trauma becomes a turning point in a person’s life, dividing life into “before” and “after” the injury.
Consequences of shock trauma
The effects of trauma can have a very strong and destructive impact on the individual. This may be suicidal tendencies and addiction, psychosomatic illnesses, split personality, and the development of post-traumatic stress disorder (PTSD). All these disorders do not appear immediately; they can only appear several years after the traumatic event, so it is not always possible to understand their cause. For example, manifestations of PTSD are characterized by anxiety, unreasonable fears, a feeling of “frozenness” (lack of feelings), avoidance of communication, problems falling asleep, sudden outbursts of irritability, etc.
Mechanism of action of shock trauma
During shock trauma, physiological response mechanisms are activated - flight, fight or freezing (numbness). When there is no way to avoid or overcome danger, the body gets into a “dead end” and the body freezes, “freezes”. The mouse caught by the cat freezes at this moment. We can see the same process in people in a state of shock. This is an unconscious, physiological protective reaction that we cannot control. Its goal is to protect us from too strong painful sensations and feelings that cannot be experienced, a kind of “pain relief”, anesthesia. Animals, as soon as the threat passes, come out of this frozen state - they shake themselves and tremble violently, thus releasing bound energy, and can continue their normal lives. People have lost the skill of natural recovery from a frozen state, so we cannot completely return from a traumatic state without special help. Part of the energy remains “bound” in the nervous system, so the person continues to live as if the traumatic situation had not yet ended.
Retraumatization
After a shocking traumatic event, which was not fully humanly reacted at the bodily level and rethought, he finds himself in a vicious circle. On the one hand, there is fear and avoidance of both memories of what happened and similar situations reminiscent of the event, and on the other, the body feels the need to release bound energy. Therefore, situations that repeat the events of trauma are often unconsciously attracted; it is as if the person himself attracts dangerous situations. But at the same time, he cannot react differently, the freezing reaction turns on earlier than the flight/fight reactions, repeated trauma occurs, and the “passive” freezing reaction becomes more and more consolidated with each subsequent stressful situation. Traumatic situations accumulate and a trauma funnel is formed.
The Trauma Funnel and the Healing Funnel
The Trauma Funnel is a metaphor for the defensive state of a traumatized person when faced with any threatening situation. The traumatic funnel is a whirlpool that absorbs unrealized fight-flight energy. When a person is in the vortex of trauma, he experiences fear, dizziness, depression, compression, loss of strength, cold, heaviness, stiffness, while striving for self-suppression, self-restraint and self-destruction. The state of the trauma vortex begins to arise over time in situations that do not objectively threaten a person’s life, therefore, often for others, the behavior of a person in the trauma vortex is incomprehensible and inexplicable, as well as for himself. Because instinctual mechanisms operate during traumatic events, conscious control—our normal “I”—is partially or completely absent. We lose control over the situation and over our reactions (many people cannot remember at all what exactly happened at the moment of shock trauma). Such a repeated experience of “losing oneself” gives rise to a feeling of helplessness, self-doubt, a person feels like a victim, experiences enormous fear, guilt, shame and self-hatred.
However, by working with our bodily sensations, we can avoid falling into the vortex of trauma by consciously attracting the vortex of healing, when we intentionally shift our attention, look for opposite sensations in our bodily experience - stretching, a feeling of warmth, a feeling of waves of energy, relaxation, calmness, a feeling of lightness, a sense of present time, etc.
Only by being in a resource-safe state of the healing funnel can you gradually discharge the frozen energy of the trauma funnel.
How to help someone who has experienced trauma
One of the most common mistakes is to try to forget as quickly as possible, to ignore the event, not to talk about it, to erase it from memory. Thus, we fuel the state of shock and do not give the opportunity to complete the situation on a physical and emotional level. Therefore, immediately after the event that caused the shock reaction, as soon as possible, the injured person needs to:
- place him in a safe place where his body can relax;
- There must be people around him whom he can trust, safe people who are ready to listen to everything that comes up, accept and help him survive the natural bodily reactions and strong feelings that arise.
There is not enough support for relatives because they too are partly affected by the impact of the trauma. It is important to immediately involve a psychologist. It’s good when there is also a system of people you can turn to - friends, neighbors, acquaintances, distant relatives, colleagues at work. The most important thing is not to lose contact with other people, to prevent isolation and withdrawal. It is important to speak out, to speak out what has accumulated, and not to keep it to yourself. This is the only way to avoid long-term effects of injury.
How to overcome the long-term effects of injury
If help was not provided on time and the person is already suffering from post-traumatic disorder, only professional psychological help is needed. Methods of psychotherapy that help get rid of the consequences of trauma - behavioral therapy, bodynamics, EMDR, existential therapy. In such a situation, there is a difficult task - to restore trust in oneself and trust in people, confidence that a person can control both his body and his life.
If you understand that the cause of your problems is the consequences of trauma, your personal activity in recovery is very important. Here are the basic principles to follow:
- communication with other people;
- contribution to society (feeling needed);
- working on personal relationships;
- refusal of alcohol and other “painkillers”;
The effects of trauma can only be overcome when you experience it physically, emotionally, and understand the impact it had on you. At the moment when your life was in danger, you lost control of the situation. But something greater than your personality took control of the situation, and it was only thanks to this force that you survived. It doesn’t matter what name you give it - God, the unconscious, the higher mind, or instinctive nature, but recognition and trust in this force eliminates fear, allows you to believe in yourself, gives a new look at your life and the place of trauma in it, hope for recovery and gaining wholeness.
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In medicine, the term “shock” is used in cases when it comes to complex (severe, pathological) conditions that arise due to the influence of extreme irritants and have certain consequences.
In everyday life, the same term is used by people to define a strong nervous shock, although there are many different situations that can cause a state of shock. So what is shock and what emergency care should be provided in such situations?
Terminology and classifications
The first mention of shock as a pathological process appeared more than 2000 years ago, although in medical practice this term became official only in 1737. Now it is used to determine the body’s response to strong external stimuli.
However, shock is not a symptom or diagnosis. And this is not even a disease, although its definition indicates an acute pathological process developing in the body, which causes severe disturbances in the functioning of internal systems.
There are only two types of shock:
- Psychological shock is a powerful reaction of the human brain that occurs in response to psychological or physical trauma. This is how a person’s consciousness “defends itself” when it refuses to accept the reality of what happened.
- Physiological is a problem of a purely medical nature, the solution of which should be dealt with by professionals.
Among the various factors that provoke the occurrence of such reactions, the following causes of shock can be identified:
- Injuries of various types (burn or other tissue damage, electric shock, ligament rupture, etc.).
- The consequences of injury are severe hemorrhage.
- Transfusion of group-incompatible blood (in large quantities).
- Severe allergic reaction.
- Necrosis, severely damaging the cells of the liver, kidneys, intestines and heart.
- Ischemia accompanied by circulatory disorders.
1. Vascular is a shock, the cause of which is a decrease in vascular tone. It can be anaphylactic, septic and neurogenic.
2. Hypovolemic shock. Types of shock - anhydremic (due to loss of plasma), hemorrhagic (with severe blood loss). Both types occur against the background of acute blood insufficiency in the circulatory system, a decrease in the flow of venous blood arriving at or leaving the heart. A person may also go into hypovolemic shock if they become dehydrated.
3. Cardiogenic – an acute pathological condition that causes disturbances in the functioning of the cardiovascular system, which in 49-89% of cases leads to death. This state of shock is accompanied by a sharp lack of oxygen in the brain, which occurs due to the cessation of blood supply.
There is another classification of shock, which was developed by pathologist Selye from Canada. In accordance with it, we can distinguish the main stages of development of the pathological process, which are characteristic of each of the types of serious condition described above. So, the main stages of development of deviations:
Stage I – reversible (or compensated). At the initial stage of development of the body's response to an aggressive stimulus, the functioning of the main systems and vital organs is disrupted. However, due to the fact that their work does not stop, a very favorable prognosis is established for this stage of shock.
Stage II – partially reversible (or decompensated). At this stage, significant disturbances in the blood supply are observed, which, provided timely and proper medical care is provided, will not cause severe harm to the main functioning systems of the body.
Stage III – irreversible (or terminal). The most dangerous stage, in which irreparable harm is caused to the body, eliminating the possibility of restoration of functions even with timely medical intervention.
At the same time, the famous Russian surgeon Pirogov was able to identify the phases of shock, the distinctive feature of which is the patient’s behavior:
1. Torpid phase - the person is in a daze, passive and lethargic. Being in a state of shock, he is unable to react to external stimuli and give answers to questions.
2. Erectile phase - the patient behaves extremely actively and excitedly, is not aware of what is happening and, as a result, commits many uncontrolled actions.
What are the signs to recognize a problem?
If we consider the symptoms of shock in more detail, we can identify the main signs that indicate the development of a pathological process against the background of the resulting shock. Its main symptoms are:
- Increased heart rate.
- Slight decrease in blood pressure.
- Cooling of the extremities due to low perfusion.
- Increased sweat production on the skin.
- Drying of mucous membranes.
Unlike the symptoms of the initial stage of the problem, signs of shock in the third stage (terminal) are more pronounced and require an immediate response from health workers. This:
- Tachycardia.
- A sharp drop in blood pressure to a level below critical.
- Trouble breathing.
- Weak, barely palpable pulse.
- Cooling of the skin throughout the body.
- Change in skin color from normal to pale gray, marbled.
- Oligurea.
- Change in skin color on the fingers - when pressure is applied, they become pale and return to their previous color if the pressure is removed.
The occurrence of shock conditions during dehydration is accompanied by additional symptoms: drying out of the mucous membranes and a decrease in the tone of the tissues of the eyeballs. In newborns and children up to 1-1.5 years old, prolapse of the fontanel may be observed.
If we consider this problem from the point of view of the clinical picture, then three degrees of shock can be distinguished. Classification of shock states by severity allows you to correctly assess the patient’s well-being. The following degrees of the pathological process should be distinguished:
I degree - the patient remains conscious and can even maintain an adequate conversation, although he may experience inhibited reactions. In such situations, the victim’s pulse can vary between 90-100 beats/min. The typical systolic pressure in a patient in this condition is 90 mm.
II degree - the person retains his sanity and can communicate, but he will speak in a muffled, slightly inhibited manner. Other characteristic signs of this condition are rapid pulse, shallow breathing, frequent inhalations and exhalations, and low blood pressure. The patient requires immediate assistance in the form of anti-shock procedures.
IV degree - a shock state that occurs in a severe form and is characterized by loss of consciousness, absent reaction to painful stimuli, dilated pupils, convulsions, rapid breathing with sobs, and cadaverous spots randomly appearing on the skin. It is difficult to check the patient's pulse and determine blood pressure. With this form of shock, the prognosis in most cases is disappointing.
How and how to help in such situations
In such situations, you need to carry out the following manipulations step by step:
- Eliminate the initial causes that provoked shock (stop bleeding, extinguish things burning on a person), as well as loosen/remove objects that bind the limbs.
- Inspect the oral cavity and nasal sinuses for the presence of foreign bodies, which will subsequently need to be removed.
- Check if the victim is breathing and has a pulse.
- Perform artificial respiration and cardiac massage.
- Turn the person's head to the side to prevent the tongue from sticking in and suffocation if vomit comes out.
- Check whether the victim is conscious.
- If necessary, administer an anesthetic.
- Depending on the surrounding conditions, it will be necessary to either cool the person down or warm him up.
A victim in a state of shock should never be left alone. Having provided him with first aid, you should wait with him for the arrival of the ambulance team to help doctors determine the causes of the violation so that they can be properly eliminated. Author: Elena Suvorova
