Collapse

Collapse, or a collaptoid condition, is an acutely developed sharp decrease in systemic arterial pressure caused by a decrease in vascular tone and an increase in the capacity of the vascular bed. The development of collapse is accompanied by signs of cerebral hypoxia and suppression of vital functions of the body. Microcirculation and tissue blood flow suffer significantly, so the clinical picture may resemble that of cardiogenic shock. The main difference between collapsed conditions and cardiogenic shock is the absence of signs of heart failure.

What causes collapse?

The causes of collapse may be infectious diseases, allergic reactions, intoxication, adrenal insufficiency, cerebral pathology with suppression of the vasomotor center, overdose of antihypertensive drugs, etc. Among the causes of collapse, acute hypovolemia should be singled out separately, requiring special intensive care.

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 caused by a pathological increase in the capacity of the venous bed, inadequate decrease in peripheral resistance, blood sequestration, decreased venous return to the heart and acute systemic arterial hypotension. The immediate causes of these changes may be organic damage to the vessel walls, functional hypotension of the veins due to disturbances in the regulation of vascular tone, and disturbances in nervous regulation. Angiogenic collapse underlies most acute orthostatic circulatory disorders and is often accompanied by orthostatic syncope.
2. Hypovolemic collapse is caused by an absolute decrease in blood volume due to blood loss or dehydration. Compensatory reactions are unable to prevent a critical decrease in venous return in an upright body position.
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 (decrease in the contractile function of the heart, arrhythmogenic collapse). This mechanism of development of the collapse state is more correctly attributed to acute cardiovascular failure.

Basically, the mechanism of collapse development is similar to that of fainting, but unlike the latter, there are no pronounced disturbances of consciousness. In the clinic, manifestations of central hemodynamic disorders predominate, 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, chills, rigors, shortness of breath. The skin is pale. Sometimes the whole body is covered in cold sweat. Peripheral and jugular veins are collapsed. Arterial and venous pressure is low. The heart is dilated, the tones are muffled, there is no congestion in the lungs. 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 collapse state is based on the impact of endogenous toxins on the cardiovascular, respiratory and other life support systems (flu, pneumonia, sepsis, etc.). In this case, the role of toxins can be played by both natural products of the body's vital activity, presented in excess quantities, and substances that are normally absent in the biological environments of the body, but appear and accumulate in various pathological conditions.

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

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

Endotoxins are also capable of exerting a direct damaging effect on the heart, lungs, brain, liver and causing reactions of the anaphylactic type. There are pronounced disturbances in the absorption of oxygen by the body's cells due to the destruction of proteins and lipids of cells, 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 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 regulation of vegetative functions at all levels.

Anaphylaxis

The development of collapse in anaphylaxis is caused by the release of biologically active substances (histamine, bradykinins, serotonin, etc.) into the blood, resulting in impaired permeability of cell membranes, smooth muscle spasm, increased secretion of glands, etc. In the development of anaphylaxis according to the cardiovascular variant, the clinical picture is dominated by signs of cardiovascular insufficiency. Tachycardia, threadlike pulse, decreased blood pressure, and arrhythmia are observed. The skin is "marbled" due to impaired microcirculation. The electrocardiogram shows pronounced myocardial ischemia. Disorders of external respiration in this variant of anaphylactic shock are usually absent. The severity of anaphylaxis depends on the time interval - the moment the antigen enters the body before the development of signs of shock.

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Adrenal insufficiency

Collapse with uncontrolled hypotension is typical for the cardiovascular variant of acute adrenal insufficiency, which occurs as a result of a sharp decrease or complete shutdown of the adrenal cortex function and poses a huge danger to the patient's life. The development of acute adrenal insufficiency is caused by a sharp deficiency of corticosteroid hormones (gluco- and mineralocorticoids) and disturbances in water-electrolyte, carbohydrate and protein metabolism, increased capillary permeability, changes in glucose oxidation in tissues, and the release of large amounts of potassium and phosphates.

Patients often complain of sharp abdominal pain, nausea, vomiting, and severe muscle weakness. The skin is cold, often covered in cold sweat. Petechial rash and hyperpigmentation of the skin are characteristic. The pulse is rapid. Mental disorders in the form of hallucinations and delirious states are often observed. Loss of large amounts of fluid and electrolytes due to repeated vomiting and frequent loose stools is characteristic. This leads to a decrease in the content of sodium and chlorides in the blood serum against the background of an increase in the concentration of potassium. An increase in the level of residual nitrogen and urea in the blood is noted.

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Emergency care in case of collapse

Emergency care in 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 content. Transfer to artificial ventilation of the lungs is performed according to indications.

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Infusion therapy

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

• Polyglucin (400 ml) is administered after a reactogenicity test: the solution is administered at a rate of 10-15 drops/min for 1 minute, then a 3-minute break is taken to assess the patient's well-being; then the infusion is continued for 1 minute at a rate of 20-30 drops/min, followed by a 3-minute break to assess the patient's well-being; if the patient's condition does not worsen, the drug is infused at the required rate (no more than 60-80 drops/min);
• rheopolyglucin has a pronounced hemodynamic, detoxifying effect, improves microcirculation, eliminates stasis in capillaries, reduces adhesion and aggregation of platelets, which underlies its antithrombotic effect; 400-600 ml of rheopolyglucin are administered;
• administration of 400 ml of 0.9% NaCl or Ringer's solution with lactate is indicated;
• hydroxyethyl starch preparations Infucol GEC (Refortan, Stabizol) 6 and 10% solution, the average/maximum dose is 2 g/kg, which corresponds to 33 ml of 6% solution or 20 ml of 10% solution. Administered intravenously, drip. The first 10-20 ml are administered slowly (monitoring the general condition to exclude anaphylactic and anaphylactoid reactions).

Increased vascular tone

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

• adrenaline (epinephrine) stimulates both alpha- and beta-adrenergic receptors. increases myocardial contractility, dilates the bronchi, and in large doses has a vasoconstrictive effect. If it is necessary to use the drug to increase blood pressure, 1 mg of adrenaline (1 ml of 0.1% solution) is diluted in 100 ml and intravenous infusion is performed by titration to achieve the desired effect;
• norepinephrine (a natural catecholamine with a predominantly alpha-stimulating effect, has a significantly lesser effect on beta-adrenergic receptors, constricts peripheral arteries and veins, has little stimulation of the contractility of the heart, does not increase the heart rate). 1-2 ml of a 0.2% solution in 100 ml of a 5% glucose solution or saline at a rate of 30-60 drops/min (the rate of administration of the drug is gradually increased from 0.5 mcg/min until the minimum sufficient value of arterial pressure is achieved);
• Ephedrine stimulates alpha- and beta-adrenergic receptors. Its sympathomimetic action is similar to that of adrenaline, but it has a less abrupt and longer-lasting effect. It is administered intravenously by jet stream (slowly) at 0.02-0.05 g (0.4-1 ml of 5% solution) or by drip in 100-500 ml of 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-adrenergic receptor stimulant, has little effect on beta-receptors of the heart. It causes constriction of arterioles and an increase in blood pressure (with possible reflex bradycardia); compared to norepinephrine and adrenaline, it increases blood pressure less sharply, but acts longer. In case of acute decrease in blood pressure, mezaton is administered intravenously slowly in a dose of 0.1-0.3-0.5 ml of a 1% solution in 40 ml of a 5-20-40% glucose solution or isotonic sodium chloride solution; 1 ml of a 1% solution is administered dropwise in 250-500 ml of a 5% glucose solution.

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

• Dopamine is administered intravenously by drip at a rate of 5-20 mcg/kg/min, if possible reducing the dose of dopamine to the “renal” dose (2-4 mcg/kg/min).

In this mode, dopamine administration causes dilation of the coronary, cerebral, and renal arteries. The vasodilating effect is associated with stimulation of dopaminergic receptors. At an administration rate of 5.0-15.0 μg/kg/min, an optimal inotropic effect (stimulation of beta-adrenergic receptors) is achieved. At a dose exceeding 15.0 μg/kg/min, the drug has a powerful vasoconstrictor effect due to stimulation of alpha-adrenergic receptors. Usually, 800 mg of the drug (the contents of 4 ampoules 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). In case of low cardiac output, dobutamine, 5-20 μg/kg/min, is added to the dopamine or norepinephrine infusion.

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

Monitoring vital functions

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

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

In the first 6 hours after admission, it is necessary to achieve target values of central venous pressure within 8-12 mm Hg, BP greater than 65 mm Hg, diuresis of at least 0.5 ml/kg/h, hematocrit greater than 30%, and blood saturation in the superior vena cava or right atrium of at least 70%.

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

The administration of dextrans, gelatinol and hydroxyethyl starches is indicated in cases of severe circulating blood volume deficiency. The latter (with a molecular weight of 200/0.5 and 130/0.4) have a potential advantage over dextrans due to a lower risk of membrane leakage and the absence of a clinically significant effect on hemostasis. Good results are achieved with the use of protease inhibitors (combined administration of 3-5 million units of gordox and 200-250 thousand units of trasylol or 150 thousand units of contrikal per day). In some cases, high doses of glucocorticoids are indicated (dexamethasone is administered at an initial dose of 3 mg/kg, then 1 mg/kg every 4 hours). Correction of acid-base balance and water-electrolyte balance, antibacterial therapy, prevention and treatment of disseminated intravascular coagulation syndrome are necessary.

If the cause of the collapse was anaphylaxis or anaphylactoid reactions, first of all it is necessary to limit the entry of the allergen into the body (stop the administration of the drug if there is a reaction to it, apply a tourniquet proximal to the site of administration of the allergen, prevent further settlement of food, "air" and other antigens). Then it is necessary to administer 0.5 ml of 0.1% adrenaline solution subcutaneously at the site of entry of the allergen into the body and infuse 1-2 ml of 0.1% adrenaline solution in 250 ml of polyglucin (it is possible with the addition of 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, to eliminate pituitary-adrenal insufficiency, corticosteroids are used (prednisolone at a dose of 75-150 mg, dexamethasone - 4-20 mg, hydrocortisone - 150-300 mg). Antihistamines are traditionally used (2-4 ml of 2.5% pipolfen solution, 2-4 ml of 2% suprastin solution, 5 ml of 1% diphenhydramine solution), although their effectiveness is currently questionable.

In the case of bronchospasm, the administration of 5-10 ml of a 2.4% solution of euphyllin is indicated. The addition of heart failure is an indication for the administration of cardiac glycosides (corglycon 1 ml of a 0.06% solution), diuretics (lasix 40-60 mg). Infusion of anti-shock fluids (polyglucin, rheopolyglucin) and alkalization of plasma with a 4% solution of sodium bicarbonate at a rate of 3-5 ml/kg of the patient's body weight are also indicated.

In case of acute vascular insufficiency that developed against the background of or as a result of brain damage, large amounts of glucose solutions and saline should not be administered parenterally, as this may contribute to the development of edema-swelling of the brain.

If the cause of the collapse is acute adrenal insufficiency, then first of all measures are taken to normalize systemic hemodynamics (dopamine 2-5 mcg/kg per 1 minute intravenously by drip, mesaton 1-2 ml of 1% solution, 1-3 ml of 0.2% solution of norepinephrine or 0.1% solution of adrenaline, strophanthin 0.05% solution 1 ml intravenously by jet stream, cordimamine 4-6 ml). Next, it is necessary to carry out hormone replacement therapy (hydrocortisone 100-150 mg intravenously by jet stream, then - 10 mg/h up to a daily dose of 300-1000 mg, intramuscular injection of 4 ml of 0.5% deoxycorticosterone acetate solution. Fluid and sodium losses are compensated (5% glucose solution 250 ml for 1 hour, then the infusion rate is slowed down; in case of uncontrollable vomiting, 5-20 ml of 10% sodium chloride solution is administered intravenously to replenish the electrolyte deficiency, 200-600 ml of 4% sodium bicarbonate solution is indicated. The volume of infusion therapy is on average 2-3 l/day).