Pulse pressure in cardiogenic shock. Cardiogenic shock: clinic, emergency care

Description:

Cardiogenic shock (CS) is a critical, lethal condition, which is an acute decrease in contractility myocardium with impaired blood supply to vital organs.

The condition is more common in states with low level medical care, including preventive care.

Important! Mortality in patients with cardiogenic shock is 60-100%.

Causes of occurrence:

If we talk about the mechanism of development of KSh, then there are several main directions:

Violation of the contractility of the left heart;
severe arrhythmias;
- accumulation of fluid between the layers of the heart sac
(blood or inflammatory effusion);
blockage of blood vessels carrying blood to the lungs.

Now about the reasons that provoke these mechanisms:

1. Myocardial infarction is the cause of CABG in 8 out of 10 cases. The main condition for development cardiogenic shock in case of a heart attack, at least half of the volume of the heart is “turned off” from work. Massive transmural damage leads to such a serious condition.

5. pulmonary trunk.

6. Action of cardiotoxic substances. These include cardiac glycosides, reserpine, clonidine, some insecticides. As a result of exposure to these compounds, blood pressure decreases, heart rate slows down to a level that is ineffective for
blood supply to organs.

Important! At risk for CABG are people over 65 years of age, with a history of myocardial infarction, with concomitant diabetes mellitus.

Symptoms:

The symptoms of cardiogenic shock are acute, bright and affect several body systems at once. First comes to the fore. Pain of a compressive nature, localized in the center behind the sternum, radiates to left hand, shoulder blade, jaw. This is the stage sharp violation blood flow in the wall of the heart. As a result of the shutdown of the most active and important department - the left ventricle, a symptom complex occurs with pulmonary edema:

1. Respiratory disorders. Respiratory rate less than 12 per minute, blue skin and mucous membranes, participation in the act of inhalation of auxiliary muscles (wings of the nose, intercostal muscles), foam from the mouth.

2. Panic, fear of death.

3. Forced position - sitting, with the torso tilted forward, arms resting
onto a hard surface.

Due to inadequate functioning of the lungs, there is no proper gas exchange and oxygen saturation of the tissues. This leads to oxygen starvation of other body systems:

1. CNS - impaired consciousness varying degrees up to coma.
2. CCC -, arterial hypotension.
3. MVP - lack of urine.
4. Gastrointestinal tract - "coffee grounds", violation of peristalsis,

Important! In most cases of myocardial infarction, clinical manifestations of cardiogenic shock are added within 2 days.

Diagnostics:

Examination algorithm:

1. General inspection- pale (bluish) color of the skin, cold sweat, impaired consciousness (stunning or disinhibition), systolic blood pressure less than 90 mm Hg, more than 30 minutes, muffled heart sounds, cardiac murmur, noisy breathing, a mass of wet rales, with a release of pink foam.

3. BP monitoring.

4. - determination of blood oxygen saturation by percutaneous method.

5. Laboratory research- blood biochemistry, determination of markers of myocardial damage (troponin, MB-CPK, LDH), kidney waste (creatinine, urea), liver enzymes.

6. Ultrasound of the heart.

7. Emergency coronary angiography.

Treatment:

For treatment appoint:

Important! A patient with suspected CABG needs mandatory, urgent hospitalization!

On prehospital stage in cardiogenic shock urgent measures- restoration of breathing (ventilation with a bag and mask,), removal pain attack infusion of fluid into a vein.

The main directions of treatment of CS in a hospital:

1. Oxygen therapy - the mixture is supplied with spontaneous breathing through nasal catheters, a facial mask. With severe respiratory failure or in the absence of breathing, the patient is transferred to artificial oxygen-dependent ventilation.

2. Maintenance blood pressure in organs by constant infusion inotropic drugs(dopamine, dobutamine). The dose is calculated taking into account the weight of the patient and the severity of the condition.

3. Thrombolytic therapy - dissolution of blood clots with streptokinase, urokinase, tissue plasminogen activator.

4. Anesthesia with narcotic analgesics.

Important! The use of nitroglycerin preparations to reduce pain is undesirable! They have by-effect as an extension peripheral vessels and additional reduction in peripheral pressure.

Conservative therapy usually has a short duration positive effect. To normalize blood circulation in the organs, it is necessary to restore the working capacity of the heart. To correct myocardial ischemia, highly specialized procedures are used:

1. Balloon counterpulsation - injection of blood into the aorta with a special medical "pump".

2. Artificial ventricle - a device that simulates the function of the left ventricle of the heart.

3. Balloon stenting of myocardial vessels - introduction into the cavity coronary arteries a probe that expands the lumen of blood vessels.

Despite modern possibilities resuscitation and cardiac surgery, the prognosis for health and life is unfavorable. Mortality in cardiogenic shock remains critical.

Cardiogenic shock- This clinical syndrome, which is characterized by disorders of central hemodynamics and microcirculation, pathology of water-electrolyte and acid-base composition, changes in the neuro-reflex and neurohumoral mechanisms of regulation and cellular metabolism arising from acute insufficiency propulsive function of the heart.

Pathogenesis

The development of cardiogenic shock in acute myocardial infarction is based on a decrease in minute volume and tissue perfusion due to a deterioration in the pumping function of the left ventricle when 40% of it is turned off. muscle mass. As a result of violation coronary circulation there is akinesia in the area of ​​myocardial infarction and hypokinesia of the peri-infarction zone, the volume of the cavity of the left ventricle increases, the tension of its wall increases and myocardial oxygen demand increases.

The combination of hemodynamically inefficient systole, deterioration of the elasticity of the damaged area of ​​the myocardium and shortening of the phase of isovolumic contraction in favor of the isotonic phase further increases the energy deficit of the body and reduces the stroke output of the heart. This exacerbates systemic hyperfusion and reduces the systolic component of coronary blood flow. An increase in intramyocardial pressure (due to an increase in left ventricular wall tension) leads to an even greater myocardial oxygen demand due to compression of the coronary arteries.

The resulting transient increase in inotropism, tachycardia, an increasing dominant of the isotonic phase of systole, an increase in the load on the heart due to a reflex increase in peripheral vascular resistance, and also caused by a stress reaction hormonal shifts increase myocardial oxygen demand.

At acute period diseases The pathogenesis of heart failure includes three components, the severity of which may be different: one component is associated with previous changes in the heart and is the most static; the other, depending on the mass of the muscle turned off from the contraction, occurs at the very beginning of the disease at the stage of deep ischemia and reaches its maximum severity on the first day of the disease; the third, the most labile, depends on the nature and severity of the body's primary adaptive and stress reactions in response to heart damage. This, in turn, is closely related to the rate of development of the lesion and general hypoxia, the severity of the pain syndrome and the individual reactivity of the patient.

A decrease in stroke and minute volume causes widespread vasoconstriction in patients with myocardial infarction, accompanied by an increase in total peripheral resistance. This results in violations peripheral circulation at the level of arterioles, precapillaries, capillaries and venules, i.e., violations of the microvasculature. The latter are conditionally divided into two groups: vasomotor and intravascular (rheological).

Systemic spasm of arterioles and precapillary sphincters leads to the transfer of blood from arterioles to venules through anastomoses, bypassing the capillaries. This leads to impaired tissue perfusion, hypoxia and acidosis, which, in turn, leads to relaxation of the precapillary sphincters; postcapillary sphincters, less sensitive to acidosis, remain spasmodic. As a result, blood accumulates in the capillaries, part of which is turned off from the circulation, the hydrostatic pressure in them increases, which stimulates the extravasation of fluid into the surrounding tissues: the volume of circulating blood decreases.

In parallel with the described changes, there are violations rheological properties blood. They are primarily due to a sharp increase in intravascular aggregation of erythrocytes associated with a slowdown in blood flow, an increase in the concentration of high-molecular proteins, an increase in the adhesive ability of the erythrocytes themselves, and a decrease in blood pH. Along with erythrocyte aggregation, platelet aggregation induced by hypercatecholemia also occurs.

As a result of the described changes, capillary stasis develops - deposition and sequestration of blood in the capillaries, which causes: 1) a decrease in venous return of blood to the heart, which leads to a further decrease in minute volume and deterioration of tissue perfusion; 2) deepening of oxygen starvation of tissues due to the exclusion of erythrocytes from circulation; 3) mechanical microcirculatory block.

A vicious circle emerges: metabolic disorders in tissues stimulate the appearance of vasoactive substances, aggravating vascular disorders and aggregation of erythrocytes, which, in turn, deepens changes in tissue metabolism.

Allocate IV stages of microcirculation disorders in cardiogenic shock

I. Systemic vasoconstriction, slowing down capillary blood flow, decrease in the number of functioning capillaries.
II. Dilatation of the resistive sections of the microvasculature in combination with constriction of its capacitive links, increased capillary permeability, sludge syndrome.
III. Deposition and sequestration of blood in the microvasculature, a decrease in venous return.
IV. Disseminated intravascular coagulation with the formation of microthrombi and mechanical blocking of microcirculation systems.

As a result, the stage of decompensation occurs, when the systemic circulation and microcirculation lose coordination, develop irreversible changes general and organ circulation (in the myocardium, lungs, liver, kidneys, central nervous system, etc.).

Cardiogenic shock is characterized by arterial hypotension, which occurs as a result of a decrease in cardiac output, despite an increase in peripheral arterial resistance. decline systolic pressure up to 80 mm Hg. Art. is diagnostic criterion shock. At areactive shock the central venous pressure also decreases. Thus, in the development of cardiogenic shock in patients acute infarction myocardium, the most significant role is played (taking into account previous changes in the heart) by the mass of the affected myocardium and the severity of adaptive and stress reactions.

Wherein great importance are fast paced and progressive these changes. Decreased blood pressure and cardiac output exacerbates violations coronary blood flow and microcirculation disorders, leading to oxygen starvation and irreversible changes in metabolism in the kidneys, liver, lungs, central nervous system.

It must be borne in mind the fact that cardiogenic shock can also develop with a relatively small myocardial infarction if:

• repeated myocardial infarction and is combined with a large cicatricial field or left ventricular aneurysm;
• arrhythmias occur that disrupt hemodynamics (complete atrioventricular blockade).

In addition, cardiogenic shock often develops if there is damage to the papillary muscles, internal or external rupture of the heart.

In all these cases, a common pathogenetic factor contributing to the onset of shock is a sharp decline cardiac output.

Diagnostic criteria for cardiogenic shock

Currently, domestic and foreign authors refer the following to the main criteria for cardiogenic shock.

1. Critical decrease in systemic arterial pressure. systolic arterial pressure drops to 80 mm Hg. Art. and below (with the previous arterial hypertension- up to 90 mm Hg. Art.); pulse pressure - up to 20 mm Hg. Art. and below. However, one should take into account the difficulty of determining pulse pressure due to the difficulty of auscultatory assessment of diastolic pressure. It is important to emphasize the severity and duration of hypotension.

Some experts admit the possibility of shock in patients hypertension when blood pressure drops to normal level.

2. Oliguria (in severe cases, anuria) - diuresis decreases to 20 ml / h and below. Along with the filtration, the nitrogen excretion function of the kidneys is also impaired (up to the azotemichesky coma).

3. Peripheral symptoms of shock: fever and pallor skin, sweating, cyanosis, collapsed veins, dysfunction of the central nervous system(lethargy, confusion, loss of consciousness, psychosis).

4. Metabolic acidosis caused by hypoxia associated with circulatory failure.

The criteria for the severity of shock are: 1) its duration; 2) reaction to pressor drugs; 3) acid-base disorders; 4) oliguria; 5) indicators of arterial pressure.

Classification of types of cardiogenic shock

Cardiogenic: shock can be coronary (shock with myocardial infarction) and non-coronary (with dissecting aortic aneurysm, cardiac tamponade various etiologies, thromboembolism pulmonary artery, closed injury heart, myocarditis, etc.).

There is no single classification of cardiogenic shock in myocardial infarction. In 1966, I. E. Ganelina, V. N. Brikker and E. I. Volpert proposed the following classification of types of cardiogenic shock (collapse): 1) reflex; 2) arrhythmic; 3) true cardiogenic; 4) shock against the background of myocardial rupture. E. I. Chazov in 1970 identified reflex, arrhythmic and true cardiogenic shock. According to the proposal by V. N. Vinogradov. V. G. Popov and A. S. Smetnev classify cardiogenic shock into three degrees: relatively mild (I degree), moderate (II degree) and extremely severe (III degree).

Reflex shock occurs at the very beginning of the disease against the background of an anginal attack, is characterized by hypotension and peripheral symptoms(pallor, lowering the temperature of the extremities, cold sweat), and often bradycardia. The duration of hypotension usually does not exceed 1-2 hours; after the restoration of the normal level of blood pressure, hemodynamic parameters do not differ significantly from those in patients with uncomplicated myocardial infarction.

Reflex shock is more common in patients with primary myocardial infarction with localization on back wall left ventricle (in men more often than in women). Arrhythmias are often observed (extrasystole, paroxysmal atrial fibrillation); changes in the acid-base state are moderate and do not require correction. Reflex shock does not significantly affect the prognosis. The pathogenesis of this type of shock is mainly not a violation contractile function myocardium, and the fall vascular tone due to reflex mechanisms.

Arrhythmic shock

The decrease in cardiac output in this type of shock is mainly due to rhythm and conduction disturbances and, to a lesser extent, a decrease in the contractile function of the myocardium. I. E. Ganelina in 1977 identified tachysystolic and bradysystolic shock. With tachysystolic shock highest value has insufficient diastolic filling and the associated decrease in shock and minute volumes hearts. The cause of this type of shock is most often paroxysmal ventricular tachycardia, less often - supraventricular tachycardia and paroxysmal atrial fibrillation. It develops more often in the first hours of the disease.

characterized by hypotension. peripheral signs, oliguria, metabolic acidosis. Successful arrest of tachysystole, as a rule, leads to the restoration of hemodynamics and reverse development signs of shock. However, mortality in this group of patients is higher than in uncomplicated myocardial infarction; cause deaths usually is heart failure (more often - left ventricular). According to echocardiography, ventricular tachycardia affected area - 35%, hypokinesia - 45%; with supraventricular tachyarrhythmias, the affected area is 20%, hypokinesia - 55%.

In bradysystolic shock, the fall in cardiac output is due to the fact that the increase in stroke volume does not compensate for the decrease cardiac index associated with a decrease in heart rate. It develops more often with repeated myocardial infarctions. Most common causes bradysystolic shock are atrioventricular blockade II-III degree, junctional rhythm, Frederick's syndrome.

Occurs, as a rule, at the very beginning of the disease. The prognosis is often unfavorable. This is due to the fact that bradysystolic shock is observed in patients with a pronounced decrease in the contractile function of the myocardium (with complete AV blockade, according to echocardiographic data, the affected area reaches 50%, and the hypokinesia zone - 30% of the left ventricle).

True cardiogenic shock

The diagnosis of true cardiogenic shock in myocardial infarction is established in cases where exposure to extracardiac causes of persistent hypotension and a decrease in cardiac output does not lead to the disappearance of signs of shock. This is the most difficult prognostic adverse complication myocardial infarction (mortality reaches 75-90%). It occurs in 10-15% of patients with myocardial infarction; develops with damage to 40-50% of the myocardium of the left ventricle, in most cases in the first hours of the disease and less often - in more late dates(in a few days).

First Clinical signs can be determined before a significant decrease in blood pressure. This is tachycardia, a decrease in pulse pressure, inadequate reactions to the introduction of vasoconstrictors or beta-blockers. A detailed picture of true cardiogenic shock includes: persistent arterial hypotension(systolic blood pressure of 80 mm Hg and below, 90 mm Hg in hypertensive patients), a decrease in pulse pressure (up to 20 mm Hg and below), tachycardia (110 beats per minute or more, if no AV block), oliguria (30 ml/h or less), peripheral hemodynamic disturbances (cold, wet, pale cyanotic or marble skin), lethargy, blackout of consciousness (they may be preceded by short-term excitement), dyspnea.

To assess the severity of shock, consider such signs as its duration, the reaction of blood pressure to the introduction of vasoconstrictors (if blood pressure does not increase within 15 minutes after the administration of norepinephrine, an unreactive course of shock is possible), the presence of oliguria and the magnitude of blood pressure.

Cardiogenic shock often complicates the course of repeated heart attacks in the elderly.

Most patients have a pronounced pre-infarction period: unstable angina increase in heart failure, momentary loss consciousness: average duration it reaches 7-8 days. Clinical picture myocardial infarction is characterized, as a rule, by a pronounced pain syndrome And early appearance signs of circulatory disorders, which reflects the massiveness and rapid rate of ischemia and necrosis of the left ventricular myocardium.

Some authors have proposed to divide cardiogenic shock into three degrees of severity: relatively mild (I degree), moderate (II degree) and extremely severe (III degree). Selection mild form shock is hardly justified, even if reflex shock is attributed to it.

A number of specialists distinguish cardiogenic shock in slowly current, prolonged myocardial rupture. Note the following clinical features shock in myocardial rupture: 1) more late appearance signs of shock compared to true cardiogenic; 2) the suddenness of its development ( sudden development shock with a drop in blood pressure and the appearance of symptoms of insufficient blood supply to the brain - loss of consciousness, agitation or lethargy, as well as respiratory disorders, bradycardia); 3) the two-stage nature of its development (the appearance of short-term hypotension at the prehospital stage, a detailed picture of shock - at the hospital).

However, it must be borne in mind that myocardial rupture often occurs in early dates(the first 4-12 hours from the onset of the disease) and the clinic of cardiogenic shock is deployed at the same time at the prehospital stage.

For the diagnosis of early ruptures, it is important to identify cardiogenic shock, which is not amenable to medical correction either at the prehospital or at the hospital stage of treatment.

Internal ruptures are much less likely to complicate the course of myocardial infarction than external ones.

Gap interventricular septum occurs in approximately 0.5% of patients with myocardial infarction in cases where the proximal part of the left descending and right coronary arteries is occluded; occurs both in the early (first day) and late stages of the disease. It is localized in the muscular part of the interventricular septum, closer to the apex of the heart. The clinic is characterized by the appearance sharp pains in the region of the heart, accompanied by fainting, followed by a picture of cardiogenic shock.

There is systolic trembling and rough systolic murmur with maximum intensity in the third-fifth intercostal space, on the left side of the sternum; this noise propagates well into the interscapular, left axillary region, and also to the right from the sternum, to the anterior axillary line. Then (if the patient survived the moment of rupture) there are severe pain in the right hypochondrium due to swelling of the liver, signs of acute right ventricular failure develop.

A bad prognostic sign is the appearance and increase of jaundice. On the ECG, blockade of the legs of the His bundle, signs of overload of the right ventricle, right and left atria are often recorded. The prognosis in most cases is unfavorable (if the patient does not undergo surgical treatment).

Rupture of the papillary muscles occurs no more than in 1% of cases of myocardial infarction. Clinically, there is a recurrence of pain, followed by pulmonary edema and cardiogenic shock. A rough systolic murmur (often a chordal squeak) is characteristic in the apex region, spreading into the axillary region. Tendon chords in some cases come off along with the heads of the papillary muscles, in others, a rupture of the body of the papillary muscle occurs.

More often there is a lesion of the papillary muscles without their rupture, leading to acute insufficiency. mitral valve against the background of impaired contractile function of the myocardium of the left ventricle. It also leads to the development of acute left ventricular failure and cardiogenic shock.

B.G. Apanasenko, A.N. Nagnibed

Version: Directory of Diseases MedElement

Cardiogenic shock (R57.0)

Cardiology

general information

Short description

Cardiogenic shock- This acute disorder perfusion Perfusion - 1) prolonged injection of fluid (for example, blood) for therapeutic or experimental purposes in blood vessels organ, part of the body or the whole organism; 2) the natural blood supply of certain organs, such as the kidneys; 3) artificial circulation.
body tissues, caused by significant damage to the myocardium and a violation of its contractile function.

Classification

To determine the severity of acute heart failure in patients with myocardial infarction, they resort to Killip's classification(1967). According to this classification, the state of cardiogenic shock corresponds to a decrease in blood pressure< 90 мм рт. ст. и присутствие признаков периферической вазоконстрикции (цианоз, олигурия, потливость).

Taking into account the severity clinical manifestations, response to ongoing activities, hemodynamic parameters distinguish 3 degrees of severity of cardiogenic shock.

Indicators	Severity of cardiogenic shock
	I	II	III
Shock duration	No more than 3-5 hours.	5-10 o'clock	More than 10 hours (sometimes 24-72 hours)
Blood pressure level	BP sys.< 90 мм. рт. ст. (90-81 мм рт.ст.)	BP sys. 80 - 61 mmHg Art.	BP sys.< 60 мм рт.ст. AD dias. can drop to 0
*Pulse blood pressure	30-25 mm. rt. Art.	20-15 mm. rt. st	< 15 мм. рт. ст.
heart rate cuts	100-110 min.	110-120 min.	>120 min.
Severity of symptoms of shock	Symptoms of shock are mild	Signs of shock are severe	The symptoms of shock are very pronounced, the course of shock is extremely severe.
Severity of symptoms of heart failure	Heart failure is absent or mild	Severe symptoms acute cardiac left ventricular failure, in 20% of patients - pulmonary edema	Severe course heart failure, pulmonary edema
pressor response to medical measures	Fast (30-60 min.), stable	Delayed, unstable, peripheral signs of shock resume within 24 hours	Unstable, short-term, often absent altogether (areactive state)
Diuresis, ml/h	Reduced to 20	<20	0
The value of the cardiac index l / min / m²	Down to 1.8	1,8-1,5	1.5 and below
**Wedging pressure in the pulmonary artery, mm Hg. Art.	Increase to 24	24-30	above 30
Partial voltage oxygen in the blood pO 2, mm. rt. Art.	Reduction to 60 mmHg Art.	60-55 mm. rt. st	50 and below

Notes:
*Blood pressure values ​​can fluctuate significantly
** With right ventricular myocardial infarction and hypovolemic shock, wedge pressure in the pulmonary artery is reduced

Etiology and pathogenesis

The main causes of cardiogenic shock are:
- cardiomyopathy;
- myocardial infarction (MI);
- myocarditis;
- severe heart defects;
- tumors of the heart;
- toxic damage to the myocardium;
- pericardial tamponade;
- severe cardiac arrhythmias;
- pulmonary embolism;
- trauma.

Most often, the practitioner encounters cardiogenic shock in patients with acute coronary syndrome (ACS), primarily in ST-segment elevation MI. Cardiogenic shock is the main cause of death in patients with MI.

Forms of cardiogenic shock:

Reflex;
- true cardiogenic;
- areactive;
- arrhythmic;
due to myocardial rupture.

Pathogenesis

reflex form
The reflex form of cardiogenic shock is characterized by dilatation of peripheral vessels and a drop in blood pressure; there is no severe myocardial damage.
The appearance of the reflex form is due to the development of the Bezold-Jarish reflex from the receptors of the left ventricle during myocardial ischemia. The posterior wall of the left ventricle is more sensitive to irritation of these receptors, as a result of which the reflex form of shock is more often observed during the period of intense pain during myocardial infarction of the posterior wall of the left ventricle.
Taking into account the pathogenetic features, the reflex form of cardiogenic shock is considered to be not a shock, but a painful collapse or pronounced arterial hypotension in a patient with MI.

True cardiogenic shock

The main pathogenetic factors:

1. Exclusion of the necrotic myocardium from the contraction process is the main reason for the decrease in the pumping (contractile) function of the myocardium. The development of cardiogenic shock is noted when the size of the necrosis zone is equal to or greater than 40% of the mass of the myocardium of the left ventricle.

2. Development of a pathophysiological vicious circle. First, there is a sharp decrease in the systolic and diastolic function of the left ventricular myocardium due to the development of necrosis (especially extensive and transmural). A pronounced drop in stroke volume leads to a decrease in pressure in the aorta and a decrease in coronary perfusion pressure, and then to a reduction in coronary blood flow. In turn, a decrease in coronary blood flow increases myocardial ischemia, which further disrupts the systolic and diastolic functions of the myocardium.

Also, the inability of the left ventricle to empty leads to an increase in preload. An increase in preload is accompanied by an expansion of the intact, well-perfused myocardium, which, in accordance with the Frank-Starling mechanism, causes an increase in the strength of heart contractions. This compensatory mechanism restores stroke volume, but ejection fraction, which is an indicator of global myocardial contractility, decreases due to an increase in end-diastolic volume. At the same time, dilatation of the left ventricle leads to an increase in afterload (the degree of myocardial tension during systole in accordance with Laplace's law).
As a result of a decrease in cardiac output in cardiogenic shock, compensatory peripheral vasospasm occurs. An increase in systemic peripheral resistance is aimed at increasing blood pressure and improving blood supply to vital organs. However, because of this, afterload increases significantly, resulting in an increase in myocardial oxygen demand, an increase in ischemia, a further decrease in myocardial contractility and an increase in the end-diastolic volume of the left ventricle. The latter factor causes an increase in pulmonary congestion and, accordingly, hypoxia, aggravating myocardial ischemia and reducing its contractility. Further, the described process is repeated again.

3. Violations in the microcirculation system and a decrease in the volume of circulating blood.

Areactive form
The pathogenesis is similar to that in true cardiogenic shock, however, pathogenetic factors are much more pronounced, acting for a longer time. There is a lack of response to therapy.

Arrhythmic form
This form of cardiogenic shock most often develops as a result of paroxysmal ventricular tachycardia, paroxysmal atrial flutter, or distal type of complete atrioventricular block. There are bradysystolic and tachysystolic variants of the arrhythmic form of cardiogenic shock.
Arrhythmic cardiogenic shock occurs as a result of a decrease in stroke volume and cardiac output (minute volume of blood) with the listed arrhythmias and atrioventricular blockade. Further, the inclusion of the pathophysiological vicious circles described in the pathogenesis of true cardiogenic shock is observed.

Cardiogenic shock due to myocardial rupture

The main pathogenetic factors:

1. A pronounced reflex drop in blood pressure (collapse) as a result of irritation of the pericardial receptors with outflowing blood.

2. Mechanical obstacle to heart contraction in the form of cardiac tamponade (with external rupture).

3 A pronounced overload of certain parts of the heart (with internal myocardial ruptures).

4. Decreased contractile function of the myocardium.

Epidemiology

In accordance with the data of various authors, the frequency of cardiogenic shock in myocardial infarction ranges from 4.5% to 44.3%. Epidemiological studies conducted under the WHO program in a large population with standard diagnostic criteria have shown that in patients with myocardial infarction under the age of 64 years, cardiogenic shock develops in 4-5% of cases.

Factors and risk groups

- low left ventricular ejection fraction during hospitalization (less than 35%) - the most significant factor;
- age over 65;

Extensive infarction (MB-CPK activity in the blood over 160 units/l);

History of diabetes mellitus;

Re-infarction.

In the presence of three risk factors, the probability of developing cardiogenic shock is about 20%, four - 35%, five - 55%.

Clinical picture

Clinical Criteria for Diagnosis

Symptoms of peripheral circulatory insufficiency (pale cyanotic, marbled, moist skin; acrocyanosis; collapsed veins; cold hands and feet; decrease in body temperature; prolongation of the disappearance of the white spot after pressing on the nail for more than 2 seconds - a decrease in the speed of peripheral blood flow); impaired consciousness (lethargy, confusion, possibly unconsciousness, less often - agitation); oliguria (diuresis decrease less than 20 ml/h); with extremely severe course - anuria; decrease in systolic blood pressure to a value of less than 90 mm. rt. st (according to some sources, less than 80 mm Hg), in persons with previous arterial hypertension less than 100 mm. rt. Art.; duration of hypotension more than 30 minutes; decrease in pulse arterial pressure up to 20 mm. rt. Art. and below; decrease in mean arterial pressure less than 60 mm. rt. Art. or during monitoring, a decrease (compared to baseline) in mean arterial pressure of more than 30 mm. rt. Art. for a time greater than or equal to 30 minutes; hemodynamic criteria: pressure "jamming" in the pulmonary artery more than 15 mm. rt. st (more than 18 mm Hg according to Antman, Braunwald), cardiac index less than 1.8 l/min./sq.m, increase in total peripheral vascular resistance, increase in left ventricular end-diastolic pressure, decrease in stroke and minute volumes

Symptoms, course

True cardiogenic shock

It usually develops in patients with extensive transmural myocardial infarction, with repeated heart attacks, in the presence of symptoms of circulatory failure even before the development of myocardial infarction.

The general condition of the patient with cardiogenic shock is severe. There is congestion, there may be a blackout of consciousness, there is a possibility of a complete loss of consciousness, less often there is a short-term excitation.

Main complaints:
- severe general weakness;
- heartbeat;
- sensation of interruptions in the heart;
- dizziness, "fog before the eyes";
- sometimes - retrosternal pain.

According to the external examination, "gray cyanosis" or pale cyanotic coloration of the skin is revealed, pronounced acrocyanosis is possible Acrocyanosis - bluish coloration of the distal parts of the body (fingers, ears, nose tip) due to venous stasis, more often with right heart failure
; the skin is cold and moist; the distal parts of the upper and lower extremities are marble-cyanotic, the hands and feet are cold, cyanosis is noted Cyanosis is a bluish hue of the skin and mucous membranes due to insufficient oxygenation of the blood.
subungual spaces.

A characteristic feature is the appearance white spot symptom- the time for the disappearance of the white spot after pressing on the nail lengthens (normally this time is less than 2 seconds).
This symptomatology reflects peripheral microcirculatory disorders, the extreme degree of which can be expressed by skin necrosis in the region of the tip of the nose, auricles, distal fingers and toes.

The pulse on the radial arteries is threadlike, often arrhythmic, and often may not be detected at all.

Arterial pressure is sharply lowered (constantly below 90 mm Hg. Art.).
A decrease in pulse pressure is characteristic - as a rule, it is less than 25-20 mm Hg. Art.

Percussion of the heart detects an extension of its left border. Auscultatory signs: soft systolic murmur at the apex of the heart, arrhythmias, deafness of heart tones, protodiastolic gallop rhythm (a characteristic symptom of severe left ventricular failure).

Breathing, as a rule, is superficial, rapid breathing is possible (especially with the development of a "shock" lung). For a particularly severe course of cardiogenic shock, the development of cardiac asthma and pulmonary edema are characteristic. In this case, there is suffocation, breathing becomes bubbling, there is a cough with pink frothy sputum.

At lung percussion in the lower sections, dullness of percussion sound, crepitus and fine bubbling rales due to alveolar edema are revealed. In the absence of alveolar edema, crepitus and moist rales are not heard or are detected in small quantities as a manifestation of stagnation in the lower parts of the lungs, a small amount of dry rales is possible. If marked alveolar edema is observed, moist rales and crepitus are heard over more than 50% of the lung surface.

Palpation belly usually does not reveal pathology. In some patients, liver enlargement can be determined, which is explained by the addition of right ventricular failure. There is a possibility of developing acute erosions, ulcers of the stomach and duodenum, which is manifested by pain in the epigastrium Epigastrium - the region of the abdomen, bounded from above by the diaphragm, from below by a horizontal plane passing through a straight line connecting the lowest points of the tenth ribs.
, sometimes bloody vomiting, pain on palpation of the epigastric region. However, these changes in the gastrointestinal tract are rare.

The most important sign cardiogenic shock - oliguria Oliguria - the release of a very small amount of urine compared to the norm.
or anuria Anuria - failure to pass urine to the bladder
, during catheterization of the bladder, the amount of urine separated is less than 20 ml / h.

reflex form

The development of reflex cardiogenic shock usually occurs in the first hours of the disease, during a period of severe pain in the region of the heart.
Characteristic manifestations:
- drop in blood pressure (usually systolic blood pressure is about 70-80 mm Hg, less often - lower);
- peripheral symptoms of circulatory failure (pallor, cold hands and feet, cold sweat);
- bradycardia Bradycardia is a low heart rate.
(pathognomonic Pathognomonic - characteristic of a given disease (about a symptom).
sign of this form).
Duration of arterial hypotension Arterial hypotension - a decrease in blood pressure by more than 20% of the original / usual values, or in absolute terms - below 90 mm Hg. Art. systolic pressure or 60 mm Hg. mean arterial pressure
usually does not exceed 1-2 hours. After stopping the pain syndrome, the symptoms of shock quickly disappear.

The reflex form develops in patients with primary and fairly limited myocardial infarction, which is localized in the posterior-lower section and is often accompanied by extrasystole Extrasystole - a form of heart rhythm disturbance, characterized by the appearance of extrasystoles (a contraction of the heart or its departments that occurs earlier than the next contraction should normally occur)
, AV block Atrioventricular block (AV block) is a type of heart block that denotes a violation of the conduction of an electrical impulse from the atria to the ventricles (atrioventricular conduction), often leading to a violation of the heart rhythm and hemodynamics
, the rhythm of the atrioventricular connection.
In general, it is believed that the clinical picture of the reflex form of cardiogenic shock corresponds to the I degree of severity.

Arrhythmic form

1. Tachysystolic (tachyarrhythmic) variant of cardiogenic shock
Most often observed in paroxysmal ventricular tachycardia, but can also occur with supraventricular tachycardia, paroxysmal atrial fibrillation and atrial flutter. It develops in the first hours (rarely days) of the disease.
The severe general condition of the patient and the significant severity of all clinical signs of shock (significant arterial hypotension, oligoanuria, symptoms of peripheral circulatory insufficiency) are characteristic.
Approximately 30% of patients develop severe left ventricular failure (pulmonary edema, cardiac asthma).
Life-threatening complications such as ventricular fibrillation, thromboembolism to vital organs are possible.
With the tachysystolic variant of cardiogenic shock, relapses of ventricular paroxysmal tachycardia are frequent, contributing to the expansion of the necrosis zone and then the development of true areactive cardiogenic shock.

2. Bradysystolic (bradyarrhythmic) variant of cardiogenic shock

It usually develops with complete distal AV block with conduction 2:1, 3:1, slow idioventricular and junctional rhythms, Frederick's syndrome (a combination of complete AV block with atrial fibrillation). Bradysystolic cardiogenic shock is noted in the first hours of the development of extensive and transmural myocardial infarction.
Severe course is characteristic, mortality reaches 60% and above. Cause of death - sudden asystole Asystole - complete cessation of activity of all parts of the heart or one of them with no signs of bioelectrical activity
heart, ventricular fibrillation Ventricular fibrillation is a cardiac arrhythmia characterized by complete asynchrony in the contraction of ventricular myofibrils, which leads to the cessation of the pumping function of the heart.
, severe left ventricular failure.

Laboratory diagnostics

1.Blood chemistry:
- an increase in the content of bilirubin (mainly due to the conjugated fraction);
- an increase in glucose levels (hyperglycemia can be observed as a manifestation of diabetes mellitus, the manifestation of which is provoked by myocardial infarction and cardiogenic shock, or occur under the influence of activation of the sympathoadrenal system and stimulation of glycogenolysis);
- an increase in the content of urea and creatinine in the blood (manifestation of acute renal failure due to hypoperfusion of the kidneys);
- an increase in the level of alanine aminotransferase (a reflection of a violation of the functional ability of the liver).

2. Coagulogram:
- increased blood clotting activity;
- platelet hyperaggregation;
- high blood levels of fibrinogen and fibrin degradation products (markers of DIC Consumption coagulopathy (DIC) - impaired blood clotting due to massive release of thromboplastic substances from tissues
).

3. Study of indicators of acid-base balance: signs of metabolic acidosis (decrease in blood pH, deficiency of buffer bases).

4. Study of the gas composition of the blood: Decreased partial tension of oxygen.

Differential Diagnosis

In most cases, true cardiogenic shock is differentiated from its other varieties (arrhythmic, reflex, drug shock, shock with rupture of the septum or papillary muscles, shock with slow current myocardial rupture, shock with damage to the right ventricle), as well as hypovolemia, pulmonary embolism, internal bleeding and arterial hypotension without shock.

1. Cardiogenic shock in aortic rupture
The clinical picture depends on factors such as the location of the rupture, the massiveness and rate of blood loss, and also on whether blood is poured into a particular cavity or into the surrounding tissue.
Basically, the gap occurs in the thoracic (in particular - in the ascending) aorta.

If the rupture is localized in the immediate vicinity of the valves (where the aorta lies in the cavity of the heart shirt), blood flows into the pericardial cavity and causes its tamponade.
Typical clinical picture:
- intense, growing retrosternal pain;
- cyanosis;
- shortness of breath;
- swelling of the neck veins and liver;
- motor restlessness;
- small and frequent pulse;
- a sharp decrease in blood pressure (with an increase in venous pressure);
- expanding the boundaries of the heart;
- deafness of heart sounds;
- embryocardia.
In the event of an increase in the phenomena of cardiogenic shock, patients die within a few hours. Bleeding from the aorta may occur into the pleural cavity. Then, after the onset of pain in the chest and back (often very intense), signs develop due to increasing anemia: pallor of the skin, shortness of breath, tachycardia, fainting.
Physical examination reveals signs of hemothorax. Progressive blood loss is the direct cause of the death of the patient.

With a rupture of the aorta with bleeding into the tissue of the mediastinum, there is a strong and prolonged retrosternal pain, which resembles anginal pain in myocardial infarction. To exclude myocardial infarction allows the absence of typical ECG changes for it.
The second stage of the course of cardiogenic shock in aortic ruptures is characterized by symptoms of increasing internal bleeding, which basically determines the shock clinic.

2.Cardiogenic shock in acute myocarditis

Currently, it is relatively rare (about 1% of cases). Occurs against the background of extensive myocardial damage, which causes a critical decrease in cardiac output, combined with vascular insufficiency.

Characteristic manifestations:
- weakness and apathy;
- pallor with an ash-gray tint of the skin, the skin is moist and cold;
- pulse of weak filling, soft, quickened;
- arterial pressure is sharply reduced (sometimes not determined);
- collapsed veins of the large circle;
- the boundaries of relative cardiac dullness are expanded, the heart sounds are muffled, the gallop rhythm is determined;
- oliguria;
- the anamnesis indicates the connection of the disease with the infection (diphtheria, viral infection, pneumococcus, etc.);
ECG reveals signs of pronounced diffuse (rarely focal) changes in the myocardium, often - rhythm and conduction disturbances. The prognosis is always serious.

3.Cardiogenic shock in acute myocardial dystrophy
It is possible to develop cardiogenic shock in acute myocardial dystrophies, which are caused by acute overexertion of the heart, acute intoxications and other environmental influences.
Excessive physical activity, especially if performed in a painful condition (for example, with angina) or in violation of the regimen (alcohol, smoking, etc.), can cause acute heart failure, including cardiogenic shock, as a result of the development of acute myocardial dystrophy , in particular contracture.

4. Cardiogenic shock in pericarditis

Some forms of effusion pericarditis (hemorrhagic pericarditis with scurvy, etc.) immediately have a severe course, with symptoms of rapidly progressive circulatory failure due to cardiac tamponade.
Characteristic manifestations:
- periodic loss of consciousness;
- tachycardia;
- small filling of the pulse (often there is an alternating or bigeminic pulse), on inspiration the pulse disappears (the so-called "paradoxical pulse");
- arterial pressure is sharply reduced;
- cold sticky sweat, cyanosis;
- pain in the region of the heart due to increased tamponade;
- venous congestion (the neck and other large veins overflow) against the background of progressive shock.
The boundaries of the heart are expanded, the sonority of tones varies depending on the phases of respiration, sometimes a pericardial friction rub is heard.
ECG reveals a decrease in the voltage of the ventricular complexes, displacement of the ST segment and changes in the T wave.
X-ray and echocardiography studies help the diagnosis.
With untimely therapeutic measures, the prognosis is unfavorable.

5. Cardiogenic shock in bacterial (infectious) endocarditis
May occur as a result of myocardial damage (diffuse myocarditis, less often - myocardial infarction) and destruction (destruction, detachment) of the heart valves; can be combined with bacterial shock (more often with gram-negative flora).
The initial clinical picture is characterized by the appearance of impaired consciousness, vomiting and diarrhea. Further, there is a decrease in the temperature of the skin of the extremities, cold sweat, a small and frequent pulse, a decrease in blood pressure, and cardiac output.
ECG reveals changes in repolarization, rhythm disturbances are possible. Echocardiography is used to assess the state of the valvular apparatus of the heart.

6.Cardiogenic shock in closed heart injury
The occurrence may be associated with a rupture of the heart (external - with a clinical picture of hemopericardium or internal - with a rupture of the interventricular septum), as well as with massive contusions of the heart (including traumatic myocardial infarction).
With a heart contusion, pain behind the sternum or in the region of the heart (often very intense) is noted, rhythm disturbances, deafness of heart sounds, gallop rhythm, systolic murmur, hypotension are recorded.
ECG reveals changes in the T wave, ST segment displacement, rhythm and conduction disturbances.
Traumatic myocardial infarction causes a severe anginal attack, rhythm disturbance, and is often the cause of cardiogenic shock; ECG dynamics is characteristic of myocardial infarction.
Cardiogenic shock in polytrauma is combined with traumatic shock, significantly aggravating the condition of patients and complicating the provision of medical care.

7.Cardiogenic shock in electrical trauma: the most common cause of shock in such cases are rhythm and conduction disturbances.

Complications

- severe dysfunction of the left ventricle;
- acute mechanical complications: mitral insufficiency, rupture of the free wall of the left ventricle with cardiac tamponade, rupture of the interventricular septum;
- violations of rhythm and conduction;
- right ventricular infarction.

Medical tourism

Pathologies of the cardiovascular system rank first in terms of mortality among the population. In severe heart failure or complicated myocardial infarction, patients are at risk of developing such a critical condition as cardiogenic shock, which in 70-85% leads to death. What is cardiogenic shock, what are its symptoms and how to provide first aid for cardiogenic shock?

What is cardiogenic shock?

Cardiogenic shock is a critical state of the body, in which there is a sharp decrease in blood pressure, followed by a deterioration in blood circulation in all internal organs and systems. The danger of cardiogenic shock lies in the fact that during its development, the rheological property of the blood changes significantly, its viscosity increases, and microthrombi are formed in the body. With cardiogenic shock, a decrease in heart rhythms occurs, which entails the development of disorders in the whole organism. All vital organs cease to receive oxygen, as a result, hypoxia develops: necrosis of the liver, kidneys, metabolic processes are disturbed, the work of the nervous system and the whole organism worsens. Despite advances in modern cardiology and medicine, only 10% of patients who develop symptoms of cardiogenic shock can be saved.

Types of cardiogenic shock

In medicine, there are three main types of cardiogenic shock, each of which has its own severity and causes of development:

1. Reflex - a mild form of cardiogenic shock, in which extensive damage to the myocardium occurs. A decrease in blood pressure occurs against the background of a strong pain syndrome in the chest area. Timely medical care will help to stop the symptoms, improve the prognosis for further treatment.
2. Arrhythmic shock is the result of acute bradyarrhythmia. With the timely introduction of antiarrhythmic drugs, the use of a defibrillator, the acute period can be bypassed.
3. Areactive shock - may occur with repeated myocardial infarction, when there is no positive response to drug therapy. In the process of development of this disease, irreversible changes in tissues occur with a 100% fatal outcome.

Regardless of the type of cardiogenic shock and its severity, the pathogenesis is practically the same: a sharp decrease in blood pressure, severe oxygen hypoxia of internal organs and systems.

Signs and symptoms of cardiogenic shock

The clinic of cardiogenic shock is pronounced, develops within a few hours and is characterized.

• A sharp drop in blood pressure.
• The appearance of the big one changes: sharp and panicked features, pallor of the skin.
• Cold sweat breaks out.
• Breathing, rapid.
• Weak pulse.
• Loss of consciousness.

With the development of cardiogenic shock, the blood supply to the brain is disrupted, as a result of untimely assistance to the patient - 100% mortality. The only way to save a person or increase the chances of life before the arrival of the ambulance team is to provide first aid to the patient. Of course, if cardiogenic shock has developed in a hospital, the patient has a better chance of life, since doctors will be able to quickly provide emergency care for cardiogenic shock.

First aid for cardiogenic shock

Any person who is nearby should help the patient with cardiogenic shock. It is very important to "remove" the panic, gather your thoughts and realize that a person's life depends on your actions. The emergency care algorithm for cardiogenic shock, before the arrival of the resuscitation team, consists of the following actions:

• Lay the patient on his back.
• Call a team of doctors, while clearly describing to the dispatcher the symptoms of the person and his condition.
• To increase blood flow to the heart, you can slightly raise your legs.
• Provide free air to the patient, unbutton his shirt, open the windows.
• Measure blood pressure.
• If necessary, when the patient has lost consciousness, perform cardiopulmonary resuscitation.
• After the arrival of the doctors, tell them what actions you have taken and all other information about the person's health, of course, if it is familiar to you.

If a person does not have a medical education or does not know what medicines are allowed for a particular patient, it makes no sense to give heart drops or nitroglycerin, and painkillers or medicines for hypertension can harm the patient even more. Even if a person knows the cardiogenic shock algorithm and can provide all the necessary assistance to the patient, there is no 100% guarantee that the patient will live, especially in severe forms of a critical condition.

If the patient's condition is critical, it cannot be transported. Medical workers must carry out all emergency manipulations on site. Only after the pressure stabilizes, the patient can be hospitalized in the intensive care unit, where further assistance will be provided to him. It is very difficult to give a prognosis for cardiogenic shock, it all depends on the degree of damage to the heart and internal organs, as well as the age of the patient and other features of his body.

Cardiogenic shock is a severe condition caused by severe heart failure, accompanied by a significant decrease in blood pressure and a decrease in myocardial contractility. In this condition, a sharp decrease in the amount of minute and stroke volume of blood is so pronounced that it cannot be compensated by an increase in vascular resistance. Subsequently, this condition causes severe hypoxia, lowering blood pressure, loss of consciousness and serious disturbances in the circulation of vital organs and systems.

Thromboembolism of large branches of the pulmonary artery can cause cardiogenic shock in the patient.

Cardiogenic shock in almost 90% of cases can lead to the death of the patient. The reasons for its development can be:

• acute valvular insufficiency;
• acute stenosis of the heart valves;
• myxoma of the heart;
• severe forms;
• septic shock, provoking dysfunction of the heart muscle;
• rupture of the interventricular septum;
• heart rhythm disturbances;
• rupture of the wall of the ventricle;
• squeezing;
• cardiac tamponade;
• tension pneumothorax;
• hemorrhagic shock;
• rupture or dissection of an aortic aneurysm;
• coarctation of the aorta;
• massive.

Classification

Cardiogenic shock is always caused by a significant violation of the contractile function of the myocardium. There are such mechanisms for the development of this serious condition:

1. Decreased pumping function of the myocardium. With extensive necrosis of the heart muscle (during a myocardial infarction), the heart cannot pump the necessary volume of blood, and this causes severe hypotension. The brain and kidneys experience hypoxia, as a result of which the patient loses consciousness, and he has urinary retention. Cardiogenic shock can occur when 40-50% of the myocardial area is affected. Tissues, organs and systems abruptly stop functioning, DIC develops and death occurs.
2. Arrhythmic shock (tachysystolic and bradysystolic). This form of shock develops with paroxysmal tachycardia or complete atrioventricular blockade with acute bradycardia. Violation of hemodynamics occurs against the background of a violation of the frequency of contraction of the ventricles and a decrease in blood pressure to 80-90 / 20-25 mm. rt. Art.
3. Cardiogenic shock in cardiac tamponade. This form of shock is observed when the septum ruptures between the ventricles. The blood in the ventricles mixes and the heart loses its ability to contract. As a result, blood pressure is significantly reduced, hypoxia in tissues and organs increases and leads to a violation of their function and death of the patient.
4. Cardiogenic shock caused by massive pulmonary embolism. This form of shock occurs when the pulmonary artery is completely blocked by a thrombus, in which blood cannot flow into the left ventricle. As a result, blood pressure drops sharply, the heart stops pumping blood, oxygen starvation of all tissues and organs increases, and the patient dies.

Cardiologists distinguish four forms of cardiogenic shock:

1. True: accompanied by a violation of the contractile function of the heart muscle, microcirculatory disorders, a metabolic shift and a decrease in diuresis. May be complicated by severe (cardiac asthma and pulmonary edema).
2. Reflex: due to the reflex effect of pain on myocardial function. Accompanied by a significant decrease in blood pressure, vasodilation and sinus bradycardia. Microcirculation disorders and metabolic disorders are absent.
3. Arrhythmic: develops with severe brady- or tachyarrhythmia and is eliminated after the elimination of arrhythmic disorders.
4. Areactive: proceeds quickly and severely, even intensive therapy for this condition often does not work.

Symptoms

In the early stages, the main signs of cardiogenic shock largely depend on the cause of the development of this condition:

• with myocardial infarction, the main symptoms are pain and a sense of fear;
• in case of heart rhythm disturbances - interruptions in the work of the heart, pain in the region of the heart;
• with pulmonary embolism - pronounced shortness of breath.

As a result of lowering blood pressure, the patient develops vascular and autonomic reactions:

• cold sweat;
• pallor, turning into cyanosis of the lips and fingertips;
• severe weakness;
• restlessness or lethargy;
• fear of death;
• swelling of the veins in the neck;
• cyanosis and marbling of the skin of the head, chest and neck (with pulmonary embolism).

After the complete cessation of cardiac activity and respiratory arrest, the patient loses consciousness, and, in the absence of adequate assistance, death may occur.

It is possible to determine the severity of cardiogenic shock by indicators of blood pressure, the duration of shock, the severity of metabolic disorders, the body's response to drug therapy, and the severity of oliguria.

• I degree - the duration of the state of shock is about 1-3 hours, blood pressure drops to 90/50 mm. rt. Art., slight severity or absence of symptoms of heart failure, the patient quickly responds to drug therapy and relief of the shock reaction is achieved within an hour;
• II degree - the duration of the state of shock is about 5-10 hours, blood pressure drops to 80/50 mm. rt. Art., peripheral shock reactions and symptoms of heart failure are determined, the patient slowly responds to drug therapy;
• III degree - long-term shock reaction, blood pressure drops to 20 mm. rt. Art. or not determined, signs of heart failure and peripheral shock reactions are pronounced, 70% of patients have pulmonary edema.

Diagnostics

The generally accepted criteria for diagnosing cardiogenic shock are the following indicators:

1. Decrease in systolic pressure to 80-90 mm. rt. Art.
2. Decrease in pulse (diastolic pressure) up to 20-25 mm. rt. Art. and below.
3. A sharp decrease in the amount of urine (oliguria or anuria).
4. Confusion, agitation, or fainting.
5. Peripheral signs: pallor, cyanosis, marbling, cold extremities, thready pulse on the radial arteries, collapsed veins on the lower extremities.

If it is necessary to perform a surgical operation to eliminate the causes of cardiogenic shock, the following is performed:

• Echo-KG;
• angiography.

Urgent Care

If the first signs of cardiogenic shock appeared in a patient outside the hospital, then it is necessary to call a cardiological ambulance. Before her arrival, the patient must be laid on a horizontal surface, raise his legs and ensure peace and fresh air.

Emergency care for cardiogenic care begins to be performed by ambulance workers:

During drug therapy, for continuous monitoring of the functions of vital organs, a urinary catheter is installed for the patient and cardiac monitors are connected, which record heart rate and blood pressure.

With the possibility of using specialized equipment and the ineffectiveness of drug therapy for emergency care of a patient with cardiogenic shock, the following surgical techniques can be prescribed:

• intra-aortic balloon counterpulsation: to increase coronary blood flow during diastole, blood is injected into the aorta using a special balloon;
• percutaneous transluminal coronary angioplasty: through the puncture of the artery, the patency of the coronary vessels is restored, this procedure is recommended only in the first 7-8 hours after the acute period of myocardial infarction.