Shock types of shock conditions. Shock states of various origins. Monitoring of hemodynamics in the pulmonary circulation
A rapidly developing condition against the background of a severe injury, which poses a direct threat to human life, is commonly called traumatic shock. As it already becomes clear from the name itself, the cause of its development is severe mechanical damage, unbearable pain. It is necessary to act in such a situation immediately, since any delay in the provision of first aid can cost the patient's life.
Table of contents:Causes of traumatic shock
The cause may be injuries of a severe degree of development - fractures of the hip bones, gunshot or stab wounds, rupture of large blood vessels, burns, damage to internal organs. These can be injuries to the most sensitive parts of the human body, such as the neck or perineum, or vital organs. The basis of their occurrence, as a rule, are extreme situations.
note
Very often, pain shock develops when large arteries are injured, where there is a rapid loss of blood, and the body does not have time to adapt to new conditions.
Traumatic shock: pathogenesis
The principle of the development of this pathology lies in the chain reaction of traumatic conditions that have serious consequences for the patient's health and are aggravated one after another in stages.
With intense, unbearable pain and high blood loss, a signal is sent to our brain, which provokes its strong irritation. The brain abruptly releases a large amount of adrenaline, such an amount is not typical for normal human life, and this disrupts the functioning of various systems.
With severe bleeding there is a spasm of small vessels, for the first time it helps to save part of the blood. Our body cannot maintain such a state for a long time, subsequently the blood vessels expand again and blood loss increases.
In the event of a closed injury the mechanism of action is similar. Due to the secreted hormones, the vessels block the outflow of blood and this condition no longer carries a protective reaction, but, on the contrary, is the basis for the development of traumatic shock. Subsequently, a significant volume of blood is retained, there is a lack of blood supply to the heart, respiratory system, hematopoietic system, brain and others.
In the future, intoxication of the body occurs, vital systems fail one after another, and necrosis of the tissue of internal organs occurs from a lack of oxygen. In the absence of first aid, all this leads to death.
The development of traumatic shock against the background of an injury with intense blood loss is considered the most severe.
In some cases, the recovery of the body with mild and moderate pain shock can occur on its own, although such a patient should also be given first aid.
Symptoms and stages of traumatic shock
Symptoms of traumatic shock are pronounced and depend on the stage.
stage 1 - erectile
Lasts from 1 to several minutes. The resulting injury and unbearable pain provoke an atypical condition in the patient, he can cry, scream, be extremely agitated and even resist assistance. The skin becomes pale, sticky sweat appears, the rhythm of breathing and heartbeat is disturbed.
note
At this stage, it is already possible to judge the intensity of the manifested pain shock, the brighter it is, the stronger and faster the subsequent stage of shock will manifest itself.
Stage 2 - torpid
Has a rapid development. The patient's condition changes dramatically and becomes inhibited, consciousness is lost. However, the patient still feels pain, and first aid manipulations should be carried out with extreme caution.
The skin becomes even paler, cyanosis of the mucous membranes develops, the pressure drops sharply, the pulse is barely palpable. The next stage will be the development of dysfunction of internal organs.
Degrees of development of traumatic shock
Symptoms of the torpid stage can have different intensity and severity, depending on this, the degree of development of pain shock is distinguished.
1 degree
Satisfactory condition, clear consciousness, the patient clearly understands what is happening and answers questions. Hemodynamic parameters are stable. Slightly rapid breathing and pulse may occur. It often occurs with fractures of large bones. Light traumatic shock has a favorable prognosis. The patient should be assisted in accordance with the injury, give analgesics and be taken to the hospital for treatment.
2 degree
It is noted by the patient's inhibition, he can answer the question for a long time and does not immediately understand when he is being addressed. The skin is pale, the limbs may become bluish. Arterial pressure is reduced, the pulse is frequent, but weak. Lack of proper assistance can provoke the development of the next degree of shock.
3 degree
The patient is unconscious or in a state of stupor, there is practically no reaction to stimuli, pallor of the skin. A sharp drop in blood pressure, the pulse is frequent, but weakly palpable even on large vessels. The prognosis for this condition is unfavorable, especially if the ongoing procedures do not bring positive dynamics.
4 degree
Fainting, no pulse, extremely low or no blood pressure. The survival rate for this condition is minimal.
Treatment
The main principle of treatment in the development of traumatic shock is immediate action to normalize the patient's state of health.
First aid for traumatic shock should be carried out immediately, take clear and decisive action.
First aid for traumatic shock
What kind of actions are necessary is determined by the type of injury and the cause of the development of traumatic shock, the final decision comes according to the actual circumstances. If you witness the development of a pain shock in a person, it is recommended to immediately take the following actions:
A tourniquet is used for arterial bleeding (blood spouts), superimposed above the wound. It can be used continuously for no more than 40 minutes, then it should be loosened for 15 minutes. When the tourniquet is properly applied, the bleeding stops. In other cases of damage, a pressure gauze bandage or tampon is applied.
- Provide free air access. Remove or unfasten constricting clothing and accessories, remove foreign objects from the respiratory passages. The unconscious patient should be placed on their side.
- warming procedures. As we already know, traumatic shock can manifest itself in the form of blanching and coldness of the extremities, in which case the patient should be covered or additional heat should be provided.
- Painkillers. The ideal option in this case would be an intramuscular injection of analgesics.. In an extreme situation, try to give the patient an analgin tablet sublingually (under the tongue - for speedy action).
- Transportation. Depending on the injuries and their location, it is necessary to determine the method of transporting the patient. Transportation should be done only when waiting for medical attention can take a very long time.
Forbidden!
- Disturb and excite the patient, make him move!
- Transfer or move the patient from
Resuscitation and intensive care for shock.
Shock is a syndrome complex, which is based on inadequate capillary perfusion with reduced oxygenation and impaired metabolism of tissues and organs.
For various shocks, a number of pathogenetic factors are common: first of all, a small cardiac output, peripheral vasoconstriction, microcirculation disorders, and respiratory failure.
CLASSIFICATION OF SHOCKS(according to Barrett).
I - Hypovolemic shock
1 - due to blood loss
2 - due to the predominant loss of plasma (burns)
3 - general dehydration of the body (diarrhea, indomitable vomiting)
II - Cardiovascular shock
1 - acute dysfunction of the heart
2 - heart rhythm disorder
3 - mechanical blockage of large arterial trunks
4 - decrease in reverse venous blood flow
III - Septic shock
IV - Anaphylactic shock
V - Vascular peripheral shock
VI - Combined and rare forms of shock
Heatstroke
Traumatic shock.
Hypovolemic shock - acute cardiovascular insufficiency, which develops as a result of a significant deficiency of BCC. The reason for the decrease in BCC may be the loss of blood (hemorrhagic shock), plasma (burn shock). As a compensatory mechanism, the sympathetic-adrenal system is activated, the level of adrenaline and noradrenaline increases, which leads to selective vasoconstriction of the skin, muscles, kidneys, and intestines, provided that cerebral blood flow is preserved (circulation is centralized).
The pathogenesis and clinical manifestations of hemorrhagic and traumatic shock are similar in many respects. But in traumatic shock, along with blood and plasma loss, powerful streams of pain impulses come from the damaged area, intoxication of the body with decay products of injured tissues increases.
When examining the patient, the pallor of the skin, cold and moist to the touch, attracts attention. The patient's behavior is inappropriate. Despite the severity of the condition, he may be agitated or too calm. Pulse is frequent, soft. BP and CVP are reduced.
Due to compensatory reactions, even with a decrease in BCC by 15-25%, blood pressure remains within the normal range. In such cases, one should focus on other clinical symptoms: pallor, tachycardia, oliguria. The level of blood pressure can serve as an indicator only under the condition of dynamic monitoring of the patient.
The erectile and torpid phases of shock are noted.
The erectile phase of shock is characterized by a pronounced psychomotor arousal of the patient. Patients may be inadequate, they fuss, scream. Blood pressure may be normal, but tissue circulation is already impaired due to its centralization. The erectile phase is short-lived and rarely observed.
In the torpid phase, 4 degrees of severity are distinguished. In their diagnosis, the Aldgover shock index is informative - the ratio of pulse rate to systolic pressure.
In shock I degree - the patient is conscious, the skin is pale, breathing is frequent, moderate tachycardia, blood pressure - 100-90 mm Hg. Index A. almost 0.8-1. The approximate amount of blood loss does not exceed 1 liter.
With shock II Art. - the patient is lethargic, the skin is cold, pale, moist. Breathing shallow, shortness of breath. Pulse up to 130 per minute, systolic D is 85-70 mm Hg. Index A.-1-2. The approximate amount of blood loss is about 2 liters.
With shock III Art. - depression of consciousness, pupils are dilated, sluggishly react to light, pulse up to 110 per 1 min., systolic D does not exceed 70 mm Hg. Index A. - 2 and above. Approximate blood loss - about 3 liters.
With shock IU Art. - (blood loss more than 3 liters) - terminal state, consciousness is absent, pulse and blood pressure are not determined. Breathing shallow, uneven. The skin is grayish, cold, covered with sweat, the pupils are dilated, there is no reaction to light.
Treatment.
Immediate stop of external bleeding: applying a tight aseptic bandage, tight tamponade, tourniquet, applying a clamp or ligature to a bleeding vessel. With internal bleeding - cold on the damaged area
Ensuring airway patency, eliminating oxygen deficiency by inhaling oxygen through a nasal catheter or face mask, and if indicated, mechanical ventilation. In case of circulatory arrest - external heart massage.
Replenishment of DOCK. Trendelenburg position (to increase venous return). Infusion into 2-3 peripheral or 1-2 central veins at a rate of 250-500 ml per minute until bleeding stops. In order to replenish DOCC, programs of infusion-transfusion therapy are used, which allow differential use of blood components, crystalloid and colloid solutions. In our country, the blood compensation scheme according to Bryusov is used.
To eliminate the pain syndrome, intravenous administration of narcotic and non-narcotic analgesics is used.
Narcotic analgesics are not administered until the diagnosis is established in patients with TBI and damage to internal organs!
An essential component of anesthesia at the prehospital stage is adequate immobilization of the injured part of the patient's body, which is performed until the patient is transferred to a stretcher after the administration of analgesics.
In shock, accompanied by a critical deterioration in hemodynamics, large doses of glucocorticoids are used (200-300 mg of prednisolone, 30-40 mg of dexamethasone). They reduce total peripheral resistance, increase cardiac output, and stabilize lysosomal membranes.
Treatment of renal failure. Accounting for hourly diuresis in shock is mandatory. This is due to the fact that oliguria is an early sign of shock, and the restoration of diuresis (30-50 ml / h) indicates the restoration of blood flow. Stimulation of diuresis is carried out against the background of the restoration of DOCC with CVP - 10-12 cm aq. Furosemide 40 mg IV.
Correction of acid-base balance. Soda is transfused with severe metabolic acidosis (plasma pH less than 7.25. Soda 4% - 100-200 ml.
Prevention and treatment of DIC
Prevention of septic disorders
BURN SHOCK.
burns- the result of the action of thermal, chemical and radiation factors on the body.
A burn is not just a local process; if its area exceeds 10-20% for the superficial and 5-10% for the deep, then naturally there are violations of the functions of all organs and systems, the more pronounced, the more severe and extensive the lesion. That is why we should talk about burn disease, during which it is customary to single out separate periods: the period of burn shock, acute burn toxemia, septicotoxemia, convalescence.
burn shock- the first most dangerous period of burn disease. It naturally occurs when the surface of the body is damaged in an area equal to 9-10% for deep and 15-20% for superficial burns. Degree O.Sh. depends on the extent of the lesion: if the total area of the burn surface is less than 20%, mild O.Sh develops. If the lesion reaches 20-60% of the body surface, severe shock occurs, if 60% or more of the body surface is affected, extremely severe shock occurs. In children under the age of 10, O.Sh. develops when 10% of the body surface is affected. It is difficult to tolerate burns and people over 60 years old. To predict the outcome of Sh., a conditional rule is used: if the sum of the age and the total area of the burn approaches 100 or more, the prognosis is doubtful.
At the first moment, the victims are usually excited, rush about, complain of unbearable pain in the burn area. Consciousness, as a rule, is preserved, the temperature is normal or lowered. Psycho-emotional arousal can be replaced by adynamia and elements of confused consciousness. Characterized by a constant increase in heart rate (up to 120 per 1 min), which remains rhythmic, but weakened filling and labile. BP - at the level of the individual norm or slightly increased, excluding critical degrees of hypotension, characteristic of those burned in the terminal state.
With extensive deep burns, the fall in blood pressure begins after 6-20 hours. On this basis, the periodization of the OR was proposed: I stage-compensation, II - decompensation - 7-24 hours, III - stabilization - 35-48 hours. Oliguria manifests itself after 2-3 hours. Daily diuresis in the range of 100-150 ml is a poor prognostic sign, such burns are threatened with death in the first 3 days. Often there is vomiting; vomit like coffee grounds.
Toileting of burn wounds and changing of dressings should be carried out in the most gentle way, in combination with vigorous anti-shock therapy and modern methods of pain relief. Bandages are applied to the wounds with heated solutions of antiseptics or emulsions (synthomycin, Vishnevsky ointment).
Anti-shock therapy should be carried out in the following areas: pain control, BCC recovery and correction of hemodynamic disorders, prevention and treatment of acute kidney dysfunction, restoration of water and electrolyte balance, elimination of acidosis, protein deficiency, and intoxication control. The whole complex of anti-shock therapy is usually necessary to recover from shock a patient with a superficial burn area of more than 20-25% and a deep burn of more than 10-15% of the body surface; with less severe lesions, its individual elements are used.
Timely infusion-transfusion therapy is very important. The choice of solutions is determined by the time since the lesion.
In the first 24 hours, the daily amount of crystalloids = 4 ml x body weight in kg x % of the burnt body surface. In the first 8 hours, 50% of the daily amount is administered, in the second 8 hours - 25%, in the third 8 hours - 25% of the total amount. Colloidal solutions (FFP, albumin, GEKi) are administered within the fourth 8 hours, then glucose-salt solutions.
Burns of the respiratory tract are of particular severity, which, by the nature of general disorders, are equivalent to burns of 10% of the body surface. Infusion-transfusion therapy in patients with burns of the respiratory tract is carried out in accordance with general principles. Particular emphasis is placed on the need to combat ORF, which, in case of thermal damage to the DP, is primarily due to the phenomena of bronchospasm. For its elimination, it is recommended: bilateral vagosympathetic blockade according to Vishnevsky, intravenous aminophylline, as well as novodrin (izadrin), antispasmodics, glucocorticoids. Urgent tracheal intubation or tracheostomy may be necessary.
The burnt patient can be transported to the hospital only if hemodynamics is stabilized with obligatory oxygen inhalation and continued infusion during transportation. Before transportation, it is necessary to ensure proper transport immobilization: the skin of the burnt areas should be in the position of maximum physiological stretch. In the ambulance, the patient must be placed in a supine position on an uninjured part of the body.
Anaphylactic shock.
This is an allergic reaction of an immediate type, which occurs in response to the interaction of antigens of various origins with antibodies fixed on cell membranes.
More often A.Sh. cause AB, salicylic acid derivatives, local anesthetics, iodine-containing radiopaque agents, therapeutic sera and vaccines, protein hydrolysates, food products: nuts, seafood, citrus fruits; latex, plant pollen. In principle, any substance can cause an anaphylactic reaction.
Anaphylaxis can occur with any route of antigen ingestion, however, reactions occur more often and more severely with the parenteral route of antigen administration.
In the emergence of A.Sh. BAS play a special role, such as histamine, serotonin, bradykinin, as well as heparin, acetylcholine, which enter the vascular bed in large quantities. This leads to paresis of capillaries and discrepancy between the BCC and the volume of the vascular bed, which is manifested by severe arterial hypotension. Histamine and histamine-like substances often cause bronchiolospasm, which, together with increased bronchial secretion, leads to airway obstruction, asphyxia. Long A.Sh. leads to hypoxic brain damage, encephalopathy.
Clinically, there are 5 forms of A.Sh. :
Typical- discomfort, fear, nausea, vomiting, a sharp cough, tingling and itching of the skin of the face, hands, head, weakness, heaviness and tightness behind the sternum, pain in the heart area, headache
Hemodynamic- a sharp pain in the region of the heart, a significant decrease in blood pressure, deafness of tones, arrhythmia. Weakness of the pulse to the point of disappearance. Paleness, marbling of the skin
Asphyxic- clinical symptoms of ARF. Edema of the mucous membrane of the larynx (up to obstruction), bronchospasm, pulmonary edema.
cerebral- signs of dysfunction of the central nervous system (excitation, fear, convulsions, coma, epistatus)
Abdominal- clinic of "acute abdomen". Painful abdominal syndrome appears 20 minutes after the first symptoms of shock.
The most severe problem is respiratory disorders: airway edema, shortness of breath and bronchial spasm. Asphyxia is one of the most common causes of death in AS. Arterial hypotension is clinically manifested somewhat later by dizziness, fainting, impaired consciousness.
Symptoms usually appear 5-30 minutes after the onset of antigen contact in the body. The faster the onset, the more severe the reaction.
AS treatment. First of all, the cessation of the introduction of the allergen. In acute circulatory arrest, cardiopulmonary resuscitation measures are applied. When an allergen is injected into a limb, a tourniquet should be applied, the injection site should be pricked with adrenaline. When taken orally - gastric lavage (if the condition allows), take activated charcoal.
In acute AS, the following measures are taken:
Ensuring the patency of the respiratory tract (if necessary, tracheal intubation or conicotomy).
oxygen therapy
Introduction of adrenaline
fluid infusion.
Inhalation of beta-agonists.
With bronchospasm - in / in the introduction of aminophylline.
The introduction of H1- and H2-blockers (diphenhydramine -50 mg IV and ranitidine in the same dose)
Administration of corticosteroids (although not expected to have an immediate effect)
With ongoing arterial hypotension - infusion of cardiotonic and vasopressive drugs.
Adrenalin is the drug of choice for AS. Stimulation of alpha1-adrenergic receptors increases vascular tone, causes vasoconstriction and increases blood pressure, stimulation of beta-receptors has a bronchodilator effect, inhibits the release of mediators.
In the absence of a pulse in the periphery, it is necessary to administer a resuscitation dose of adrenaline - 0.25-0.5 mg. If intravenous administration is not possible in cases of severe shock, epinephrine can be administered intratracheally or, in extreme cases, sublingually or intramuscularly. Given the adverse effects of intravenous adrenaline, in the absence of critical arterial hypotension, this route of administration is not currently recommended.
With persistent arterial hypotension, intravenous dopamine infusion is used.
infusion therapy. In the treatment of AS, adequate infusion therapy is extremely important. In anaphylactic shock, hypovolemia rapidly develops due to the loss of up to 40% of fluid from the intravascular bed to the interstitial space in severe AS, which is accompanied by hemoconcentration. At the beginning of the reaction, 25-50 ml / kg of isotonic solution is administered, in cases of ongoing arterial hypotension, a solution of colloids can be added.
Ranitidine at a dose of 1 mg / kg and cimetidine - 4 mg / kg IV should be administered slowly due to the risk of hypotension.
Introduction corticosteroids does not give an immediate effect, but is useful in preventing recurrent reactions. Corticosteroids are indicated for the relief of refractory bronchospasm or hypotension. The exact dose has not been established, recommend 0.25 - 1 g of hydrocortisone or 30-35 mg / kg of methylprednisolone.
In refractory bronchiolospasm, inhaled beta-agonists may be helpful.
In the prehospital setting, patients with a severe allergic history who have already had anaphylactic reactions should self-administer epinephrine. There are special courses abroad for teaching such patients.
Toxico-infectious shock.
Toxic-infectious (bacterial, septic) shock is one of the types of shock, the trigger of which is an infection. In combination with special immune and humoral reactions of the body, the infection leads to severe hemodynamic disorders, especially microcirculation and tissue perfusion.
By frequency T-I.Sh. ranks third after traumatic and cardiogenic, and in terms of mortality -1.
TIS can be caused by a variety of microorganisms, viruses, rickettsiae, and bacteria. Gram-negative bacteria (E. coli, Proteus, etc.) lead to TIS in 75% of cases, and Gram-positive (staphylococci, streptococci, pneumococci) - in 25%.
More often TIS occurs due to infection of the urinary and biliary tract, pancreatic necrosis, peritonitis. It can occur as a result of intensive care in very debilitated patients, especially those who have been on mechanical ventilation and parenteral nutrition for a long time.
The initial symptoms of TIS are chills, a sharp rise in temperature, and a drop in blood pressure. Patients are often in a state of euphoria, do not always adequately assess their condition. Subsequently, the condition of the patients worsens. Consciousness is disturbed, the skin becomes cold, pale cyanotic. Breathing is oppressed. Oliguria develops.
Without waiting for the results of bacteriological studies (blood culture, exudate, sputum, urine, etc., determination of sensitivity to AB), antibiotic therapy is started, taking into account the alleged bacterial microflora. Patients with suspected staphylococcal infection are prescribed semi-synthetic penicillins, cephalosporins, sulfanilamide preparations, derivatives of netrofurans, antistaphylococcal plasma. In the case of the development of gram-negative sepsis - aminoglycosides, canna- and gentamicin, amikacin, and with anaerobic - metagyl.
In the event of the development of the Jarisch-Gersheimer shock reaction due to the death of bacteria and the massive intake of endotoxins into the blood, the administration of these drugs should not be stopped. To stop the reaction, additional doses of glucocorticoids are prescribed, and in severe cases, adrenomimetic drugs (fractional doses of ephedrine, mezaton, dopamine) until hemodynamics normalize.
Particular attention is paid to the adequacy of external respiration. In hypoxia, oxygen is inhaled. In the absence of effect, patients are transferred to mechanical ventilation.
Cardiac glycosides, inhibitors of proteolytic enzymes are widely used, measures are taken to prevent and treat DIC, and massive infusion therapy is carried out to maintain BCC.
POLYTRAUMA.
Trauma is the leading cause of death for young people in industrialized countries.
According to German scientists, in severe polytrauma, 85% of patients have damage to the limbs, 70% - craniocerebral injury, 35% - thoracic and 20% - abdominal.
Combined injury - an injury to 2 or more organs caused by one damaging agent.
Combined injury - damage occurs with the simultaneous impact of various types of energy.
80% of injured people die within the first 3-4 hours of injury. However, an injury incompatible with life occurs in only half of these victims. Life saving conditions:
the earliest possible provision of qualified assistance
assistance in full program, starting from the scene.
Delay in providing assistance within 15 minutes increases mortality by 30%. "Golden Hour". Adequate anesthesia must be given. Immobilization must be carried out. It is necessary to provide venous access. Immediate initiation of antishock therapy (replenishment of BCC). Diagnosis is carried out in parallel with antishock therapy.
Full treatment should begin in the full program at the pre-hospital stage, no later than 15 minutes after the injury. If treatment is started upon admission to the hospital, the injury becomes a neglected disease.
When giving first aid, remember:
with complete airway obstruction, cardiac arrest occurs only after 5-6 minutes
the duration of hemorrhagic shock for more than an hour can lead to irreversible consequences
delaying surgical care by more than 6 hours may result in limb loss or sepsis
evacuation of a victim with a combined or multiple injury later than 24 hours later or a delay in intensive medical care for 7 days leads to the development of multiple organ failure.
6 basic elements of first aid at the scene of an accident:
maintenance of airway patency (tilting the head, protruding the jaw)
IVL
stop external bleeding (bandage or tourniquet)
giving a certain position to the victim in a coma (on his side, bend one leg at the knee, pull it up to his stomach, throw the other; the patient will turn out to be littered almost on his stomach)
with signs of shock - raise your legs at an angle of 45 degrees.
the release of the victim from the ruins without causing additional injury.
For pain relief at the prehospital stage, the use of non-steroidal anti-inflammatory drugs (ketalong, ketalex, ketanov) is recommended.
If it is impossible to provide venous access: to correct hypovolemia in the absence of data for damage to the abdominal organs - up to 2 liters of fluid orally (alkaline electrolyte solutions, weakly concentrated glucose solutions). It is possible to use subcutaneous injections: 1 liter of Ringer's solution in each thigh.
Story
The state of shock was first described by Hippocrates. The term "shock" was first used in Mr. Le Dran. At the end of the 19th century, possible mechanisms for the development of the pathogenesis of shock began to be proposed, among them the following concepts became the most popular:
- paralysis of the nerves innervating the vessels;
- depletion of the vasomotor center;
- neurokinetic disorders;
- dysfunction of the endocrine glands;
- a decrease in the volume of circulating blood (BCC);
- capillary stasis with impaired vascular permeability.
The pathogenesis of shock
From a modern point of view, shock develops in accordance with G. Selye's theory of stress. According to this theory, excessive exposure to the body causes specific and non-specific reactions in it. The first depend on the nature of the impact on the body. The second - only on the strength of the impact. Nonspecific reactions under the influence of a superstrong stimulus are called the general adaptation syndrome. The general adaptation syndrome always proceeds in the same way, in three stages:
- stage compensated (reversible)
- decompensated stage (partially reversible, characterized by a general decrease in the body's resistance and even death of the body)
- terminal stage (irreversible, when no therapeutic effects can prevent death)
Thus, shock, according to Selye, is a manifestation non-specific reaction body to overexposure.
hypovolemic shock
This type of shock occurs as a result of a rapid decrease in circulating blood volume, which leads to a drop in the filling pressure of the circulatory system and a decrease in venous return of blood to the heart. As a result, a violation of the blood supply to organs and tissues and their ischemia develops.
Causes
The volume of circulating blood can quickly decrease due to the following reasons:
- blood loss;
- plasma loss (for example, with a burn, peritonitis);
- loss of fluid (for example, with diarrhea, vomiting, profuse sweating, diabetes and diabetes insipidus).
stages
Depending on the severity of hypovolemic shock, three stages are distinguished in its course, which successively replace each other. This
- The first stage is non-progressive (compensated). There are no vicious circles at this stage.
- The second stage is progressive.
- The third stage is the stage of irreversible changes. At this stage, no modern anti-shock agents can bring the patient out of this state. At this stage, medical intervention can return blood pressure and cardiac output to normal for a short period of time, but this does not stop the destructive processes in the body. Among the reasons for the irreversibility of shock at this stage, a violation of homeostasis is noted, which is accompanied by severe damage to all organs, damage to the heart is of particular importance.
vicious circles
In hypovolemic shock, many vicious circles form. Among them, the most important is the vicious circle that contributes to myocardial damage and the vicious circle that contributes to the insufficiency of the vasomotor center.
A vicious cycle that promotes myocardial damage
A decrease in the volume of circulating blood leads to a decrease in the minute volume of the heart and a drop in blood pressure. A drop in blood pressure leads to a decrease in blood circulation in the coronary arteries of the heart, which leads to a decrease in myocardial contractility. A decrease in myocardial contractility leads to an even greater decrease in cardiac output, as well as to a further drop in blood pressure. The vicious circle closes.
A vicious circle that contributes to the insufficiency of the vasomotor center
Hypovolemia is caused by a decrease in cardiac output (that is, a decrease in the volume of blood expelled from the heart in one minute) and a decrease in blood pressure. This leads to a decrease in blood flow in the brain, as well as to a disruption in the activity of the vasomotor (vasomotor) center. The latter is located in the medulla oblongata. One of the consequences of a violation in the vasomotor center is a drop in the tone of the sympathetic nervous system. As a result, the mechanisms of centralization of blood circulation are disrupted, blood pressure drops, and this, in turn, triggers a violation of cerebral circulation, which is accompanied by even greater inhibition of the vasomotor center.
shock organs
Recently, the term "shock organ" ("shock lung" and "shock kidney") has often been used. This means that the impact of a shock stimulus disrupts the function of these organs, and further violations of the state of the patient's body are closely related to changes in the "shock organs".
"Shock Lung"
Story
This term was first introduced into practice by Ashbaugh (year) when describing the syndrome of progressive acute respiratory failure. However, even in the year Burford And Burbank described a similar clinico-anatomical syndrome, calling it "wet (wet) light". After some time, it was found that the picture of the “shock lung” occurs not only in shocks, but also in craniocerebral, thoracic, abdominal injuries, with blood loss, prolonged hypotension, aspiration of acidic gastric contents, massive transfusion therapy, increasing decompensation of the heart, thromboembolism of the pulmonary artery. Currently, no relationship has been found between the duration of shock and the severity of pulmonary pathology.
Etiology and pathogenesis
The most common cause of the development of "shock lung" is hypovolemic shock. Ischemia of many tissues, as well as a massive release of catecholamines, lead to the entry of collagen, fat and other substances into the blood, which cause massive thrombosis. Because of this, microcirculation is disturbed. A large number of blood clots settle on the surface of the vessels of the lungs, which is associated with the peculiarities of the structure of the latter (long tortuous capillaries, double blood supply, shunting). Under the action of inflammatory mediators (vasoactive peptides, serotonin, histamine, kinins, prostaglandins), vascular permeability in the lungs increases, bronchospasm develops, the release of mediators leads to vasoconstriction and damage.
Clinical picture
The “shock lung” syndrome develops gradually, reaching its apogee usually after 24-48 hours, the outcome is often a massive (often bilateral) damage to the lung tissue. The process is clinically divided into three stages.
- The first stage (initial). Arterial hypoxemia (lack of oxygen in the blood) dominates, the x-ray picture of the lung is usually not changed (with rare exceptions, when an x-ray examination shows an increase in the pulmonary pattern). Cyanosis (bluish skin tone) is absent. The partial pressure of oxygen is sharply reduced. Auscultation reveals scattered dry rales.
- Second stage. In the second stage, tachycardia increases, that is, the heart rate increases, tachypnea (respiratory rate) occurs, the partial pressure of oxygen decreases even more, mental disorders increase, the partial pressure of carbon dioxide rises slightly. Auscultation reveals dry, and sometimes small bubbling rales. Cyanosis is not expressed. Radiologically, a decrease in the transparency of the lung tissue is determined, bilateral infiltrates appear, unclear shadows.
- Third stage. In the third stage, without special support, the body is not viable. cyanosis develops. X-ray reveals an increase in the number and size of focal shadows with their transition to confluent formations and total darkening of the lungs. The partial pressure of oxygen is reduced to critical figures.
"Shock Kidney"
Pathological specimen of the kidney of a patient who died from acute renal failure.
The term "shock kidney" reflects an acute impairment of kidney function. In pathogenesis, the leading role is played by the fact that during shock, compensatory shunting of arterial blood flow into the direct veins of the pyramids occurs with a sharp decrease in hemodynamic volume in the region of the cortical layer of the kidneys. This is confirmed by the results of modern pathophysiological studies.
pathological anatomy
The kidneys are somewhat enlarged, swollen, their cortical layer is anemic, pale gray in color, the pericerebral zone and pyramids, on the contrary, are dark red. Microscopically, in the first hours, anemia of the vessels of the cortical layer and a sharp hyperemia of the pericerebral zone and direct veins of the pyramids are determined. Microthromboses of capillaries of glomeruli and adductor capillaries are rare.
In the future, increasing dystrophic changes in the nephrothelium are observed, covering first the proximal and then the distal parts of the nephron.
Clinical picture
The picture of the "shock" kidney is characterized by a clinic of progressive acute renal failure. In its development, acute renal failure in shock goes through four stages:
The first stage occurs while the cause that caused acute renal failure is in effect. Clinically, there is a decrease in diuresis.
The second stage (oligoanuric). The most important clinical signs of the oligoanuric stage of acute renal failure include:
- oligoanuria (with the development of edema);
- azotemia (smell of ammonia from the mouth, itching);
- an increase in the size of the kidneys, back pain, a positive symptom of Pasternatsky (the appearance of red blood cells in the urine after tapping in the area of the projection of the kidneys);
- weakness, headache, muscle twitching;
- tachycardia, expansion of the boundaries of the heart, pericarditis;
- dyspnea, congestive rales in the lungs up to interstitial pulmonary edema;
- dry mouth, anorexia, nausea, vomiting, diarrhea, cracks in the mucous membrane of the mouth and tongue, abdominal pain, intestinal paresis;
The third stage (restoration of diuresis). Diuresis can be normalized gradually or rapidly. The clinical picture of this stage is associated with the emerging dehydration and dyselectrolytemia. The following signs develop:
- weight loss, asthenia, lethargy, lethargy, possible infection;
- normalization of nitrogen-excretory function.
Fourth stage (recovery). Homeostasis indicators, as well as kidney function, return to normal.
Literature
- Ado A.D. Pathological physiology. - M., "Triada-X", 2000. S. 54-60
- Klimiashvili A. D. Chadaev A. P. Bleeding. Blood transfusion. Blood substitutes. Shock and resuscitation. - M., "Russian State Medical University", 2006. S. 38-60
- Meyerson F. Z., Pshennikova M. G. Adaptation to stressful situations and physical loads. - M., "Triada-X", 2000. S. 54-60
- Poryadin GV Stress and pathology. - M., "Miniprint", 2002. S. 3-22
- Pods V. I. General surgery. - M., "Medicine", 1978. S. 144-157
- Sergeev ST. Surgery of shock processes. - M., "Triada-X", 2001. S. 234-338
Notes
| Emergency (urgent) conditions in endocrinology | |
|---|---|
| Impairment of consciousness Stunning Sopor Coma Glasgow Coma Scale Shakhnovich Scale Shock | |
| Emergency conditions in the clinic of endocrine diseases | |
| Hypothalamo-pituitary system |
|
| Thyroid | |
| parathyroid glands | |
In medicine, the term "shock" is used when it comes to complex (severe, pathological) conditions arising from the influence of extreme stimuli and having 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 since 1737. Now it is used to determine the body's response to external strongest stimuli.
However, shock is not a symptom or a 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 activity of internal systems.
There are only two types of shock:
- Psychological shock is a powerful reaction of the human brain, which manifests itself in response to psychological or physical trauma. This is how a person's consciousness is "protected" when it refuses to accept the reality of what happened.
- Physiological - a problem of a purely medical nature, the solution of which should be dealt with by professionals.
Among the various factors provoking the occurrence of such reactions, the following causes of shock can be distinguished:
- Injuries of a different nature (burn or other tissue disorders, electric shock, ligament rupture, etc.).
- The consequences of injury are severe hemorrhage.
- Transfusion of blood that is incompatible in the group (in large quantities).
- Severe allergic reaction.
- Necrosis that severely damaged 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 - anhydrous (due to loss of plasma), hemorrhagic (with severe blood loss). Both varieties occur against the background of acute blood insufficiency in the blood supply system, a decrease in the flow of venous blood arriving at or leaving the heart. A person can also fall into hypovolemic shock when dehydrated (dehydration).
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. Such a state of shock is accompanied by a sharp lack of oxygen in the brain, which occurs against the background of a cessation of blood supply.
There is another classification of shock, which was developed by the pathologist Selye from Canada. In accordance with it, it is possible to distinguish the main stages in the development of the pathological process, which are characteristic of each of the varieties of a serious condition described above. So, the main stages in the 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 organs of vital activity is disrupted. However, due to the fact that their work still does not stop, a very favorable prognosis is established for this stage of shock.
Stage II - partially reversible (or decompensated). At this stage, significant circulatory disorders are observed, which, provided timely and proper medical care, will not cause severe harm to the main functioning systems of the body.
Stage III - irreversible (or terminal). The most dangerous stage at which irreparable harm is done to the body, excluding the possibility of restoring functions even with timely medical intervention.
At the same time, the famous domestic surgeon Pirogov was able to identify the phases of shock, the hallmark of which is the behavior of the patient:
1. Torpid phase - a person is in a daze, passive and lethargic. Being in a state of shock, he is unable to respond to external stimuli and give answers to questions.
2. Erectile phase - the patient behaves extremely actively and excitedly, does not realize what is happening and, as a result, performs many uncontrolled actions.
How to recognize the problem
If we consider the symptoms of shock in more detail, we can identify the main signs that indicate the development of the pathological process against the background of the received shock. Its main symptoms are:
- Rapid heartbeat.
- A slight decrease in blood pressure.
- Cooling of extremities against the background of low perfusion.
- Increased perspiration on the skin.
- Drying of mucous membranes.
Unlike the symptoms of the initial stage of the problem, the 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.
- Interruptions in breathing.
- Weak, barely perceptible pulse.
- Cooling of the skin throughout the body.
- Change in skin color from normal to pale gray, marbled.
- Oligurea.
- Discoloration of the skin on the fingers - when pressed, they become pale and return to their previous color if the load is removed.
The course of shock states during dehydration is accompanied by additional symptoms: drying of the mucous membranes and a decrease in the tone of the tissues of the eyeballs. In newborns and babies up to 1-1.5 years old, a descent 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. The classification of shock conditions according to 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 per minute. A characteristic indicator of systolic pressure in a patient in this condition is 90 mm.
II degree - a person retains common sense and he can communicate, but he will speak in a muffled, slightly inhibited way. Other characteristic signs of this condition are rapid heart rate, shallow breathing, frequent inhalations and exhalations, and low blood pressure. The patient needs immediate help in the form of anti-shock procedures.
IV degree - a state of shock that occurs in severe form and is characterized by loss of consciousness, an absent response to painful stimuli, dilated pupils, convulsions, rapid breathing with sobs, cadaverous spots randomly appearing on the skin. It is difficult for a patient to check the pulse and determine blood pressure. With this form of shock, the prognosis is in most cases disappointing.
How and how to help in such situations
In such situations, you need to gradually carry out the following manipulations:
- Eliminate the initial causes that provoked shock (stop bleeding, extinguish things burning on a person), as well as weaken / eliminate objects that bind 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.
- Make artificial respiration, as well as heart massage.
- Turn the person's head to one side to prevent tongue slipping and suffocation in case of vomit.
- Check if the victim is conscious.
- If necessary, administer an anesthetic.
- Depending on the surrounding conditions, it will be necessary to either cool the person 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 the doctors establish the causes of the violation in order to properly eliminate them. Author: Elena Suvorova
The term "shock", meaning in English and French a shock, a shock, a shock, was accidentally introduced in 1743 by the now unknown translator into English of the book of the army consultant Louis XV Le Dran to describe the condition of patients after a gunshot injury. Until now, this term has been widely used to describe the emotional state of a person when exposed to unexpected, extremely strong mental factors without implying specific organ damage or physiological disorders. Applied to clinical medicine, shock means a critical condition, which is characterized by a sharp decrease in organ perfusion, hypoxia and metabolic disorders. This syndrome is manifested by arterial hypotension, acidosis and a rapidly progressive deterioration in the functions of the vital systems of the body. Without adequate treatment, shock quickly leads to death.
Acute short-term hemodynamic disturbances can be a transient episode in violation of vascular tone, reflexively caused by sudden pain, fright, blood type, stuffiness or overheating, as well as cardiac arrhythmia or orthostatic hypotension against anemia or hypotension. This episode is called collapse and in most cases resolves on its own without treatment. Due to a transient decrease in blood supply to the brain, it may develop fainting- short-term loss of consciousness, which is often preceded by neuro-vegetative symptoms: muscle weakness, sweating, dizziness, nausea, darkening of the eyes and tinnitus. Characterized by pallor, low blood pressure, brady or tachycardia. The same can develop in healthy people at high ambient temperatures, since heat stress leads to a significant expansion of skin vessels and a decrease in diastolic blood pressure. Longer hemodynamic disorders always pose a danger to the body.
Causesshock
Shock occurs when superstrong stimuli act on the body and can develop with various diseases, injuries and pathological conditions. Depending on the cause, there are hemorrhagic, traumatic, burn, cardiogenic, septic, anaphylactic, blood transfusion, neurogenic and other types of shock. There may be mixed forms of shock caused by a combination of several causes. Taking into account the pathogenesis of changes occurring in the body and requiring certain specific therapeutic measures, four main types of shock are distinguished.
hypovolemic shock occurs with a significant decrease in BCC as a result of massive bleeding or dehydration and is manifested by a sharp decrease in venous return of blood to the heart and severe peripheral vasoconstriction.
Cardiogenic shock occurs with a sharp decrease in cardiac output due to a violation of myocardial contractility or acute morphological changes in the heart valves and the interventricular septum. It develops with normal bcc and is manifested by overflow of the venous bed and the pulmonary circulation.
Redistributive shock manifested by vasodilation, a decrease in total peripheral resistance, venous return of blood to the heart and an increase in the permeability of the capillary wall.
Extracardiac obstructive shock occurs due to sudden obstruction of blood flow. Cardiac output falls sharply despite normal bcc, myocardial contractility, and vascular tone.
The pathogenesis of shock
Shock is based on generalized perfusion disorders leading to hypoxia of organs and tissues and disorders of cellular metabolism ( rice. 15.2.). Systemic circulatory disorders are the result of a decrease in cardiac output (CO) and changes in vascular resistance.
Hypovolemia, heart failure, impaired vascular tone, and obstruction of large vessels are the primary physiological disturbances that reduce effective tissue perfusion. With the acute development of these conditions, a "mediator storm" develops in the body with the activation of neurohumoral systems, the release of large amounts of hormones and pro-inflammatory cytokines into the systemic circulation, affecting vascular tone, vascular wall permeability and CO. In this case, the perfusion of organs and tissues is sharply disturbed. Acute severe hemodynamic disorders, regardless of the causes that caused them, lead to the same type of pathological picture. Serious violations of central hemodynamics, capillary circulation and a critical violation of tissue perfusion with tissue hypoxia, cell damage and organ dysfunctions develop.
Hemodynamic disorders
Low CO is an early feature of many types of shock, except for redistributive shock, in which cardiac output may even be increased in the initial stages. CO depends on the strength and frequency of myocardial contractions, venous blood return (preload) and peripheral vascular resistance (afterload). The main reasons for the decrease in CO during shock are hypovolemia, deterioration of the pumping function of the heart, and increased tone of the arterioles. The physiological characteristics of various types of shock are presented in tab. 15.2.
In response to a decrease in blood pressure, the activation of adaptive systems increases. First, there is a reflex activation of the sympathetic nervous system, and then the synthesis of catecholamines in the adrenal glands also increases. The content of norepinephrine in plasma increases by 5-10 times, and the level of adrenaline increases by 50-100 times. This enhances the contractile function of the myocardium, increases the rate of cardiac activity and causes a selective narrowing of the peripheral and visceral venous and arterial bed. The subsequent activation of the renin-angiotensin mechanism leads to even more pronounced vasoconstriction and the release of aldosterone, which retains salt and water. The release of antidiuretic hormone reduces the volume of urine and increases its concentration.
In shock, peripheral angiospasm develops unevenly and is especially pronounced in the skin, abdominal organs and kidneys, where the most pronounced decrease in blood flow occurs. Pale and cool skin observed during examination, and blanching of the intestine with a weakened pulse in the mesenteric vessels, visible during surgery, are clear signs of peripheral angiospasm.
Constriction of the vessels of the heart and brain occurs to a much lesser extent compared to other areas, and these organs are provided with blood longer than others due to a sharp restriction of the blood supply to other organs and tissues. The metabolic levels of the heart and brain are high and their stores of energy substrates are extremely low, so these organs do not tolerate prolonged ischemia. Neuroendocrine compensation of the patient in shock is primarily aimed at meeting the immediate needs of vital organs - the brain and heart. Sufficient blood flow in these organs is maintained by additional autoregulatory mechanisms, as long as blood pressure exceeds 70 mm Hg. Art.
Centralization of blood circulation- biologically expedient compensatory reaction. In the initial period, she saves the life of the patient. It is important to remember that the initial shock reactions are adaptation reactions of the body aimed at survival in critical conditions, but passing a certain limit, they begin to be pathological in nature, leading to irreversible damage to tissues and organs. The centralization of blood circulation, which persists for several hours, along with the protection of the brain and heart, is fraught with mortal danger, although more distant. This danger lies in the deterioration of microcirculation, hypoxia and metabolic disorders in organs and tissues.
Correction of central hemodynamic disorders in shock includes intensive infusion therapy aimed at increasing BCC, the use of drugs that affect vascular tone and myocardial contractility. Only in cardiogenic shock, massive infusion therapy is contraindicated.
Violations mmicrocirculation and tissue perfusion
The microvasculature (arterioles, capillaries and venules) is the most important link in the circulatory system in the pathophysiology of shock. It is at this level that nutrients and oxygen are delivered to organs and tissues, and metabolic products are removed.
The developing spasm of arterioles and precapillary sphincters in shock leads to a significant decrease in the number of functioning capillaries and slowing down the blood flow velocity in perfused capillaries, tissue ischemia and hypoxia. Further deterioration of tissue perfusion may be associated with secondary capillary pathology. The accumulation of hydrogen ions, lactate and other products of anaerobic metabolism leads to a decrease in the tone of arterioles and precapillary sphincters and an even greater decrease in systemic blood pressure. In this case, the venules remain narrowed. Under these conditions, the capillaries overflow with blood, and albumin and the liquid part of the blood intensively leave the vascular bed through the pores in the walls of the capillaries ("capillary leak syndrome"). Thickening of blood in the microcirculatory bed leads to an increase in blood viscosity, while the adhesion of activated leukocytes to endothelial cells increases, erythrocytes and other blood cells stick together and form large aggregates, kind of plugs, which further worsen microcirculation up to the development of sludge syndrome.
Vessels blocked by the accumulation of blood cells are switched off from the bloodstream. The so-called “pathological deposition” develops, which further reduces the BCC and its oxygen capacity and reduces the venous return of blood to the heart and, as a result, causes a drop in CO and a further deterioration in tissue perfusion. Acidosis, in addition, reduces the sensitivity of vessels to catecholamines, preventing their vasoconstrictive action and leads to atony of the venules. Thus, a vicious circle is closed. The change in the ratio of the tone of the precapillary sphincters and venules is considered a decisive factor in the development of the irreversible phase of shock.
An inevitable consequence of slowing capillary blood flow is the development of hypercoagulation syndrome. This leads to disseminated intravascular thrombosis, which not only enhances capillary circulation disorders, but also causes the development of focal necrosis and multiple organ failure.
Ischemic damage to vital tissues consistently leads to secondary damage that maintains and exacerbates the state of shock. The resulting vicious circle can lead to a fatal outcome.
Clinical manifestations of impaired tissue perfusion - cold, moist, pale cyanotic or marbled skin, prolongation of capillary filling time over 2 seconds, temperature gradient over 3 °C, oliguria (urination less than 25 ml/hour). To determine the capillary filling time, squeeze the tip of the nail plate or the ball of the toe or hand for 2 seconds and measure the time during which the pale area restores the pink color. In healthy people, this happens immediately. In case of deterioration of microcirculation, blanching lasts for a long time. Such microcirculation disorders are nonspecific and are a constant component of any type of shock, and their severity determines the severity and prognosis of shock. The principles of treatment of microcirculation disorders are also not specific and practically do not differ in all types of shock: elimination of vasoconstriction, hemodilution, anticoagulant therapy, antiplatelet therapy.
Metabolic disorders
Under conditions of reduced perfusion of the capillary bed, adequate delivery of nutrients to the tissues is not ensured, which leads to metabolic disorders, dysfunction of cell membranes, and cell damage. Carbohydrate, protein, fat metabolism is disturbed, the utilization of normal energy sources - glucose and fatty acids - is sharply inhibited. In this case, a pronounced catabolism of muscle protein occurs.
The most important metabolic disorders in shock are the destruction of glycogen, a decrease in glucose dephosphorylation in the cytoplasm, a decrease in energy production in mitochondria, a malfunction of the sodium-potassium pump of the cell membrane with the development of hyperkalemia, which can cause atrial fibrillation and cardiac arrest.
The increase in plasma levels of adrenaline, cortisol, glucagon and suppression of insulin secretion that develops during shock affect the metabolism in the cell by changes in the use of substrates and protein synthesis. These effects include increased metabolic rate, increased glycogenolysis and gluconeogenesis. Reduced glucose utilization by tissues is almost always accompanied by hyperglycemia. In turn, hyperglycemia can lead to a decrease in oxygen transport, disruption of water and electrolyte homeostasis, and glycosylation of protein molecules with a decrease in their functional activity. A significant additional damaging effect of stress hyperglycemia during shock contributes to the deepening of organ dysfunction and requires timely correction with the maintenance of normoglycemia.
Against the background of increasing hypoxia, the processes of oxidation in tissues are disturbed, their metabolism proceeds along the anaerobic pathway. At the same time, acidic metabolic products are formed in a significant amount, and metabolic acidosis develops. The criterion for metabolic dysfunction is the blood pH level below 7.3, base deficiency in excess of 5.0 mEq/l, and an increase in the concentration of lactic acid in the blood over 2 mEq/l.
An important role in the pathogenesis of shock belongs to a violation of calcium metabolism, which intensively penetrates into the cytoplasm of cells. Elevated intracellular calcium levels increase the inflammatory response, leading to intense synthesis of potent mediators of the systemic inflammatory response (SIR). Inflammatory mediators play a significant role in the clinical manifestations and progression of shock, as well as in the development of subsequent complications. Increased production and systemic distribution of these mediators can lead to irreversible cell damage and high mortality. The use of calcium channel blockers improves the survival of patients with various types of shock.
The action of pro-inflammatory cytokines is accompanied by the release of lysosomal enzymes and free peroxide radicals, which cause further damage - "sick cell syndrome". Hyperglycemia and an increase in the concentration of soluble products of glycolysis, lipolysis and proteolysis lead to the development of hyperosmolarity of the interstitial fluid, which causes the transition of intracellular fluid into the interstitial space, dehydration of cells and further deterioration of their functioning. Thus, cell membrane dysfunction may represent a common pathophysiological pathway for various causes of shock. And although the exact mechanisms of cell membrane dysfunction are unclear, the best way to eliminate metabolic disorders and prevent the irreversibility of shock is to quickly restore BCC.
Inflammatory mediators produced by cellular damage contribute to further disruption of perfusion, which further damages cells within the microvasculature. Thus, a vicious circle closes - a violation of perfusion leads to cell damage with the development of a systemic inflammatory response syndrome, which in turn further worsens tissue perfusion and cell metabolism. When these excessive systemic responses persist for a long time, become autonomous and cannot be reversed, the syndrome of multiple organ failure develops.
In the development of these changes, the leading role belongs to the tumor necrosis factor (TNF), interleukins (IL-1, IL-6, IL-8), platelet activating factor (PAF), leukotrienes (B4, C4, D4, E4), thromboxane A2, prostaglandins (E2, E12), prostacyclin, gamma-interferon. Simultaneous and multidirectional action of etiological factors and activated mediators in shock leads to endothelial damage, impaired vascular tone, vascular permeability, and organ dysfunction.
Persistence or progression of shock may result from either a continuing perfusion defect or cellular damage, or a combination of the two. Since oxygen is the most labile vital substrate, its inadequate delivery by the circulatory system forms the basis of the pathogenesis of shock, and timely restoration of perfusion and tissue oxygenation often completely stops the progression of shock.
Thus, the pathogenesis of shock is based on deep and progressive disorders of hemodynamics, oxygen transport, humoral regulation and metabolism. The relationship of these disorders can lead to the formation of a vicious circle with the complete depletion of the body's adaptive capabilities. Preventing the development of this vicious circle and restoring the autoregulatory mechanisms of the body is the main task of intensive care for patients with shock.
Stages of shock
Shock is a dynamic process, starting from the moment of action of the factor of aggression, which leads to systemic circulatory disorders, and with the progression of disorders ending in irreversible organ damage and death of the patient. The effectiveness of compensatory mechanisms, the degree of clinical manifestations and the reversibility of the resulting changes make it possible to distinguish a number of successive stages in the development of shock.
Preshock stage
Shock is usually preceded by a moderate decrease in systolic blood pressure, not exceeding 20 mm Hg. Art. from the norm (or 40 mm Hg if the patient has arterial hypertension), which stimulates the baroreceptors of the carotid sinus and aortic arch and activates the compensatory mechanisms of the circulatory system. Tissue perfusion is not significantly affected and cell metabolism remains aerobic. If at the same time the influence of the factor of aggression stops, then compensatory mechanisms can restore homeostasis without any therapeutic measures.
Early (reversible) stage of shock
This stage of shock is characterized by a decrease in systolic blood pressure below 90 mm Hg. Art. , severe tachycardia, shortness of breath, oliguria and cold clammy skin. At this stage, compensatory mechanisms alone are not able to maintain adequate CO and meet the oxygen needs of organs and tissues. Metabolism becomes anaerobic, tissue acidosis develops, and signs of organ dysfunction appear. An important criterion for this phase of shock is the reversibility of the resulting changes in hemodynamics, metabolism and organ functions and a fairly rapid regression of the developed disorders under the influence of adequate therapy.
Intermediate (progressive) stage of shock
This is a life-threatening emergency with systolic blood pressure below 80 mmHg. Art. and severe, but reversible dysfunction of organs with immediate intensive treatment. This requires artificial lung ventilation (ALV) and the use of adrenergic drugs to correct hemodynamic disorders and eliminate organ hypoxia. Prolonged deep hypotension leads to generalized cellular hypoxia and critical disruption of biochemical processes, which quickly become irreversible. It is from the effectiveness of therapy during the first so-called "golden hour" the patient's life depends.
Refractory (irreversible) stage of shock
This stage is characterized by severe disorders of central and peripheral hemodynamics, cell death and multiple organ failure. Intensive therapy is ineffective, even if the etiological causes are eliminated and blood pressure temporarily increases. Progressive multiple organ dysfunction usually leads to permanent organ damage and death.
Diagnostic studies and monitoring in shock
Shock does not leave time for orderly collection of information and clarification of the diagnosis before treatment. Systolic blood pressure in shock is most often below 80 mm Hg. Art. , but shock is sometimes diagnosed with higher systolic blood pressure if there are clinical signs of a sharp deterioration in organ perfusion: cold skin covered with sticky sweat, mental status change from confusion to coma, oligo- or anuria, and insufficient filling of skin capillaries. Fast breathing during shock usually indicates hypoxia, metabolic acidosis and hyperthermia, and hypoventilation - depression of the respiratory center or increased intracranial pressure.
Diagnostic studies in shock also include a clinical blood test, determination of electrolytes, creatinine, blood coagulation, blood group and Rh factor, arterial blood gases, electrocardiography, echocardiography, chest x-ray. Only carefully collected and correctly interpreted data helps to make the right decisions.
Monitoring is a system for monitoring the vital functions of the body, capable of quickly notifying about the occurrence of threatening situations. This allows you to start treatment on time and prevent the development of complications. To control the effectiveness of shock treatment, monitoring of hemodynamic parameters, activity of the heart, lungs and kidneys is indicated. The number of controlled parameters should be reasonable. Monitoring during shock should necessarily include the registration of the following indicators:
- BP, using intra-arterial measurement if necessary;
- heart rate (HR);
- intensity and depth of breathing;
- central venous pressure (CVP);
- pulmonary artery wedge pressure (PAWP) in severe shock and unclear cause of shock;
- diuresis;
- blood gases and plasma electrolytes.
For an approximate assessment of the severity of shock, you can calculate the Algover-Burri index, or, as it is also called, the shock index - the ratio of the pulse rate in 1 minute to the value of systolic blood pressure. And the higher this indicator, the greater the danger threatens the life of the patient. The inability to monitor any of these indicators makes it difficult to choose the right therapy and increases the risk of iatrogenic complications.
Central venous pressure
Low CVP is an indirect criterion for absolute or indirect hypovolemia, and its rise is above 12 cm of water. Art. indicates heart failure. Measurement of CVP with an assessment of its response to a small fluid load helps to choose an infusion therapy regimen and determine the appropriateness of inotropic support. Initially, the patient is administered a test dose of liquid for 10 minutes: 200 ml with an initial CVP below 8 cm aq. Art. ; 100 ml - with CVP within 8-10 cm aq. Art. ; 50 ml - with CVP above 10 cm aq. Art. The reaction is evaluated based on the rule “5 and 2 cm aq. Art. ": if the CVP increased by more than 5 cm, the infusion is stopped and the question of the advisability of inotropic support is decided, since such an increase indicates a breakdown in the Frank-Starling contractility regulation mechanism and indicates heart failure. If the increase in CVP is less than 2 cm of water. Art. - this indicates hypovolemia and is an indication for further intensive fluid therapy without the need for inotropic therapy. An increase in CVP in the range of 2 and 5 cm aq. Art. requires further infusion therapy under the control of hemodynamic parameters.
It must be emphasized that CVP is an unreliable indicator of left ventricular function, since it depends primarily on the state of the right ventricle, which may differ from the state of the left. More objective and broader information about the state of the heart and lungs is provided by hemodynamic monitoring in the pulmonary circulation. Without its use, in more than a third of cases, the hemodynamic profile of a patient with shock is incorrectly assessed. The main indication for pulmonary artery catheterization in shock is an increase in CVP during infusion therapy. The response to the introduction of a small volume of fluid when monitoring hemodynamics in the pulmonary circulation is assessed according to the rule “7 and 3 mm Hg. Art. ".
Monitoring of hemodynamics in the pulmonary circulation
Invasive monitoring of blood circulation in a small circle is performed using a catheter installed in the pulmonary artery. For this purpose, a catheter with a floating balloon at the end (Swan-Gans) is usually used, which allows you to measure a number of parameters:
- pressure in the right atrium, right ventricle, pulmonary artery and PAWP, which reflects the filling pressure of the left ventricle;
- SW by thermodilution method;
- partial pressure of oxygen and saturation of hemoglobin with oxygen in mixed venous blood.
The determination of these parameters greatly expands the possibilities of monitoring and evaluating the effectiveness of hemodynamic therapy. The resulting indicators allow:
- differentiate cardiogenic and non-cardiogenic pulmonary edema, detect pulmonary embolism and rupture of the mitral valve leaflets;
- evaluate BCC and the state of the cardiovascular system in cases where empirical treatment is ineffective or is associated with an increased risk;
- to adjust the volume and rate of fluid infusion, the dose of inotropic and vasodilator drugs, the value of positive end-expiratory pressure during mechanical ventilation.
Decreased venous mixed oxygen saturation is always an early indicator of cardiac output inadequacy.
Diuresis
A decrease in diuresis is the first objective sign of a decrease in BCC. Patients with shock must install a permanent urinary catheter to control the volume and rate of urination. When carrying out infusion therapy, diuresis should be at least 50 ml / hour. With alcohol intoxication, shock can occur without oliguria, since ethanol inhibits the secretion of antidiuretic hormone.
