Collapse

Collapse, or collapoid state - sharply developed sharp decrease in systemic arterial pressure, caused by a decrease in vascular tone and increased capacity of the vascular bed. The development of collapse is accompanied by signs of hypoxia of the brain and suppression of vital body functions. To a large extent, the imicrocirculation and tissue blood flow suffer, so the clinical picture may resemble that in cardiogenic shock. The main difference of collaptoid states from cardiogenic shock in the absence of signs of heart failure.

What causes collapse?

Causes of collapse may be infectious diseases, allergic reactions, intoxications, adrenal insufficiency, cerebral pathology with depression of the vasomotor center, overdose of antihypertensive drugs, etc. From the causes of the collapse - separately should be allocated acute hypovolemia, requiring special intensive therapy.

Depending on the leading mechanism of development, it is customary to distinguish three hemodynamic variants of acute vascular insufficiency:

1. Angiogenic collapse is a classic example of vascular insufficiency. Its development is due to a pathological increase in the capacity of the venous bed, inadequate reduction of peripheral resistance, blood sequestration, a decrease in venous return to the heart, and acute systemic arterial hypotension. The immediate causes of these changes can be organic lesion of the walls of blood vessels, functional hypotension of the veins due to disturbances in the regulation of vascular tone, disturbance of nervous regulation. Angiogenic collapse is the basis of most acute orthostatic circulatory disorders and is often accompanied by orthostatic syncope.
2. Hypovolemic collapse is due to an absolute decrease in blood volume due to blood loss or dehydration of the body. Compensatory reactions are not able to prevent a critical decrease in venous return in the vertical position of the body.
3. Cardiogenic collapse. Its occurrence is associated with a sharp decrease in the pumping function of the heart and a drop in the minute volume of blood circulation (a decrease in the contractile function of the heart, arrhythmogenic collapse). This mechanism of development of the collapoid state is more correctly attributed to acute cardiovascular insufficiency.

Basically, the mechanism of development of collapse is similar to that of fainting, but unlike the latter, there are no marked disturbances of consciousness. In the clinic, the prevalence of disorders of central hemodynamics, rather than cerebral circulation.

Symptoms of collapse

Symptoms of collapse are characterized by a sudden deterioration in the general condition. Consciousness is preserved, but the patient is inhibited and indifferent to the environment. Complains of general weakness, dizziness, chilliness, chills, dyspnea. The skin is pale. Sometimes the whole body is covered with a cold sweat. Peripheral and cervical veins asleep. Arterial and venous pressure is decreased. The heart is enlarged, tones are deaf, stagnation in the lungs is not observed. Diuresis is reduced. The prognosis of collapse is determined by the degree of hemodynamic disorders and the cause that caused its development.

Infectious-toxic collapse

In some cases, the basis of the collapoid state is the effect of endogenous toxins on the cardiovascular, respiratory and other life support systems (influenza, pneumonia, sepsis, etc.). In this case, the role of toxins can be both natural products of the body's vital activity, presented in excess quantities, and substances that are normal in the biological media of the organism, but appear and accumulate under various pathological conditions.

Toxins exert direct neuro-, cardio- and myotropic damage; cause metabolic disorders and the effects of vasopressor and vasodepressor agents; lead to disorders of the mechanisms of regulation of vascular tone and cardiac activity. Endotoxins primarily affect the microcirculation system, leading to the disclosure of arteriovenous anastomoses, disruption of transcapillary and transmembrane exchange.

These changes are accompanied by pronounced disturbances in the rheological state of the blood and the regulation of the tone of the peripheral vessels.

Endotoxins are also able to have a direct damaging effect on the heart, lungs, brain, liver and cause reactions of the type anaphylactic. Observed pronounced violations of oxygen absorption by the cells of the body due to the destruction of proteins and cell lipids, blockade of synthetic and oxidative processes, which leads to the development of histotoxic hypoxia.

In the mechanism of development of infectious-toxic collapse, hypovolemia, caused by the loss of fluid and salts, is of great importance. Collapse in this case is only part of the manifestations of shock, characterized by total disorganization of the regulation of vegetative functions at all levels.

Anaphylaxis

The development of collapse in anaphylaxis is due to the release into the blood of biologically active substances (histamine, bradykinin, serotonin, etc.), resulting in impaired permeability of cell membranes, spasm of smooth muscles, increased secretion of glands, and the like. With the development of anaphylaxis in the cardiovascular variant, the signs of cardiovascular insufficiency prevail in the clinical picture. Tachycardia, filiform pulse, decrease in arterial pressure, arrhythmias are observed. Skin "marble" due to microcirculation disorders. On the electrocardiogram sharply expressed ischemia of a myocardium is marked. Disorders of external respiration with this variant of anaphylactic shock, as a rule, are absent. The severity of anaphylaxis depends on the time interval - the moment the antigen enters the body before the development of signs of shock.

[1], [2], [3], [4], [5], [6], [7], [8], [9],

Adrenal insufficiency

Collapse with uncontrolled hypotension is characteristic for the cardiovascular variant of acute adrenal insufficiency, which results from a sharp decrease or complete exclusion of the function of the adrenal cortex and poses a huge danger to the life of the patient. The development of acute adrenal insufficiency is caused by a sharp deficit of corticosteroid hormones (gluco- and mineralocorticoids) and by disturbances in water-electrolyte, carbohydrate and protein metabolism, increased permeability of capillaries, changes in glucose oxidation in tissues, and the release of large amounts of potassium and phosphates.

Patients often complain of abdominal pain, nausea, vomiting, severe muscle weakness. Skin covers are cold, often covered with cold sweat. Characteristic of the occurrence of petechial rash and hyperpigmentation of the skin. The pulse is rapid. Often observed disturbances of the psyche in the form of hallucinations, delirious state. Characterized by the loss of large amounts of fluid and electrolytes due to repeated vomiting and frequent loose stools. This leads to a decrease in the content of sodium and chloride in the serum on the background of an increase in the concentration of potassium. There is an increase in the level of residual nitrogen and urea in the blood.

[10], [11], [12], [13],

Emergency help in case of collapse

Emergency help in case of collapse is aimed at maintaining vital functions and eliminating the discrepancy between the capacity of the vascular bed and the volume of circulating blood. They include the following basic elements.

Oxygen therapy by inhaling gas mixtures with high partial oxygen holding. According to the indications, a transfer to artificial ventilation is carried out.

[14], [15], [16]

Infusion therapy

In order to increase the volume of circulating blood, the introduction of plasma-substituting solutions is shown:

• polyglukin (400 ml) is injected after the sample for reactogenicity: for 1 minute, a solution is injected at a rate of 10-15 cap / min, then a 3-minute break is made to assess the patient's well-being; further within a minute continue infusion at a rate of 20-30 cap / min followed by a break for 3 minutes to assess the patient's well-being; in the absence of deterioration of the patient's condition, infusion of the drug at the required rate (no more than 60-80 cap / min);
• reopolyglucinum has pronounced hemodynamic, detoxifying effects, improves microcirculation, eliminates stasis in capillaries, reduces adhesion and aggregation of platelets, which is the basis of its antithrombotic effect; 400-600 ml of rheopolyglucin are administered;
• injection of 400 ml of 0.9% NaCl or Ringer's solution with lactate;
• preparations hydroxyethyl starch infusor HEK (refortan, stabilazole) 6 and 10% solution, the average / maximum dose is 2 g / kg, which corresponds to 33 ml of a 6% solution or 20 ml of a 10% solution. Enter intravenously, drip. The first 10-20 ml is injected slowly (control of the general condition to exclude anaphylactic and anaphylactoid reactions).

Increased vascular tone

To this end, use drugs that increase the tone of the walls of resistive and capacitive vessels. The most commonly used are:

• adrenaline (epinephrine) stimulates both alpha- and beta-adrenoreceptors. Increases the contractility of the myocardium, expands the bronchi, in large doses has a vasoconstrictive effect. If you need to use the drug to increase blood pressure, 1 mg of epinephrine (1 ml of 0.1% solution) is diluted in 100 ml and intravenous infusion is performed by titration to achieve the desired effect;
• norepinephrine (natural catecholamine with a predominant alpha-stimulating effect, beta-adrenergic receptors affects significantly less, narrows peripheral arteries and veins, little stimulates the contractility of the heart, does not increase the heart rate). 1-2 ml of 0.2% solution in 100 ml of a 5% solution of glucose or saline at a rate of 30-60 cap / min (the rate of administration of the drug is gradually increased from 0.5 μg / min until a minimum sufficient blood pressure value is reached) ;
• Ephedrine stimulates alpha and beta-adrenergic receptors. By sympathomimetic action is close to adrenaline, but it has a less dramatic and more prolonged effect. Intravenous injection (slowly) of 0.02-0.05 g (0.4-1 ml of a 5% solution) or intravenous injection into 100-500 ml isotonic sodium chloride solution or 5% glucose solution in a total dose of up to 0.08 g (80 mg);
• mezaton, a synthetic adrenomimetic drug, an alpha-adrenoreceptor stimulant, has little effect on the cardiac beta-receptors. It causes a narrowing of arterioles and an increase in blood pressure (with possible reflex bradycardia), in comparison with norepinephrine and adrenaline increases blood pressure less sharply, but it lasts longer. With acute lowering of arterial pressure, mezaton is administered intravenously slowly in a dose of 0.1-0.3-0.5 ml of 1% solution in 40 ml of 5-20-40% glucose solution or isotonic sodium chloride solution; 1 ml of a 1% solution in 250-500 ml of a 5% solution of glucose is injected dropwise.

Vasopressors are administered under constant control of blood pressure, as in some neurological diseases they can cause an unpredictable increase in cerebral blood flow:

• dopamine is injected intravenously at a rate of 5-20 μg / kg / min, possibly reducing the dose of dopamine to "renal" (2-4 μg / kg / min).

In this mode, the introduction of dopamine causes the expansion of the coronary, cerebral and renal arteries. The vasodilating effect is associated with the stimulation of dopaminergic receptors. At an injection rate of 5.0-15.0 μg / kg / min, an optimal inotropic effect is provided (beta-adrenoceptor stimulation). In a dose exceeding 15.0 μg / kg / min, the drug has a potent vasoconstrictive effect due to stimulation of alpha-adrenergic receptors. Usually 800 mg of the drug (the contents of 4 ampules of dopamine 200 mg each) is dissolved in 500 ml of 5% glucose solution (1 ml of this mixture contains 1.6 mg of the drug). At a low cardiac output, dobutamine is added to the infusion of dopamine or norepinephrine, 5-20 μg / kg / min.

• Glucocorticoids. A good effect is achieved by the administration of corticosteroids (90-120 mg prednisolone, 125-250 mg hydrocortisone).

Monitoring of vital functions

Hourly measurement of the volume of excreted urine allows you to monitor the level of blood flow in internal organs and the degree of their perfusion.

The tactics of further treatment depend on the cause that caused the collapoid state. Collapse in septic states and endotoxicosis requires correction of respiratory disorders, normalization of blood circulation, restoration of adequate tissue perfusion, normalization of cellular metabolism, correction of homeostatic disorders, decrease in the concentration of mediators of the septic cascade and toxic metabolites.

In the first 6 hours after admission, it is necessary to reach the target values of central venous pressure within 8-12 mm Hg. St, ADS more than 65 mm Hg. Diuresis not less than 0.5 ml / kg / h, hematocrit - more than 30%, blood saturation in the superior vena cava or atrial right of at least 70%.

The qualitative composition of the infusion therapy is determined by the degree of hypovolemia, the phase of the disease, the presence of peripheral edema, the level of albumin blood, the severity of acute pulmonary injury.

The introduction of dextrans, gelatin and hydroxyethyl starches is indicated in the presence of a pronounced deficiency in the volume of circulating blood. The latter (with a molecular weight of 200 / 0.5 and 130 / 0.4) have a potential advantage over dextran because of the lower risk of leakage through the membrane and the absence of a clinically significant effect on hemostasis. Good results are obtained using protease inhibitors (combined administration of 3-5 million units of Gordoks and 200-250 thousand units of ED trasilol or 150 thousand units of ED per day). In some cases, the appointment of large doses of glucocorticoids (dexamethasone is then administered in the initial dose at a rate of 3 mg / kg, then every 4 hours at 1 mg / kg). Correction of acid-base equilibrium and water-electrolyte balance is necessary, antibacterial therapy, prevention and management of disseminated intravascular coagulation syndrome.

If the cause of the collapse was anaphylaxis or anaphylactoid reactions, first of all it is necessary to limit the intake of the allergen (stop the drug administration in response to it, apply a tourniquet proximal to the site of the allergen injection, prevent further settling of food, "air", etc. Antigens). Then you need to inject 0.5 ml of a 0.1% solution of epinephrine subcutaneously at the site of the allergen into the body and infuse 1-2 ml of a 0.1% solution of epinephrine in 250 ml of polyglucin (can be added with 5 ml of dopamine). In this case, adrenaline, in addition to normalizing central hemodynamics, has antagonistic properties to many humoral factors that cause the development of allergic reactions. To neutralize biologically active antigen-antibody complexes, corticosteroids (prednisolone 75-150 mg, dexamethasone 4-20 mg, hydrocotisone 150-300 mg) are used to eliminate pituitary-adrenal insufficiency. Traditionally, antihistamines are used (2-4 ml of a 2.5% solution of pipolpene, 2-4 ml of a 2% solution of suprastin, 5 ml of a 1% solution of dimedrol), although their effectiveness is currently in doubt.

With the development of bronchospasm, 5-10 ml of a 2.4% solution of euphyllin is indicated. The admission of heart failure serves as an indication for the introduction of cardiac glycosides (1 ml of 0.05% solution of korglikon), diuretics (lasix 40-60 mg). Infusion of anti-shock liquids (polyglucin, reopolyglucin) and alkalization of plasma with 4% sodium bicarbonate solution are also shown at the rate of 3-5 ml / kg of body weight of the patient.

In acute vascular insufficiency, which has developed against the background or due to brain lesions, it is not necessary to administer parenterally a large number of solutions of glucose and saline, since this can contribute to the onset of edema-swelling of the brain.

If the cause of collapse was acute adrenal insufficiency, then primarily measures are taken to normalize systemic hemodynamics (dopamine 2-5 μg / kg per 1 minute intravenously drip, mezaton 1-2 ml 1% solution, 1-3 ml 0.2% noradrenaline solution or 0.1% solution of epinephrine, strophanthin 0.05% solution of 1 ml intravenously struino, cordimamine 4-6 ml). Further, hormone replacement therapy is necessary (hydrocortisone 100-150 mg intravenously, then 10 mg / h to a daily dose of 300-1000 mg, intramuscular injection of 4 ml of a 0.5% solution of deoxycorticosterone acetate.) Liquid and sodium losses are compensated glucose 5% solution 250 ml for 1 hour, then the infusion rate slows down, with indigestible vomiting, to fill the deficiency of electrolytes, 5-20 ml of 10% sodium chloride solution is intravenously injected, 200-600 ml of 4% sodium hydrogen carbonate solution is injected. FIPA average of 2-3 liters / day).