Cardiogenic shock: pathogenesis, clinical picture, diagnosis, criteria, treatment. Emergency care for cardiogenic shock: algorithm of actions

Cardiogenic shock (CS) is a critical state of tissue microcirculation against the background of inadequate cardiac output caused by a decrease in the contractility of the heart muscle.

The main mechanisms of CABG are reduced to a decrease in cardiac output, peripheral vasospasm, a decrease in BCC - the volume of circulating blood, disruption of capillary blood flow and intravascular coagulation. Most often, CABG is a fatal complication of myocardial infarction.

In accordance with the classification of Academician E.I. Chazov, there are several types of cardiogenic shock, differing in the cause of occurrence, clinical features and treatment of the condition:

• KS true;
• KS artmic;
• CS reflex;
• KS is reactive.

Reflex form of CS occurs against the background of heightened pain and is explained by reflex paresis of blood vessels with subsequent stagnation of blood in them and leakage of plasma into the intercellular tissue space. The result of a decrease in blood flow to the heart muscle is a decrease in heart beats and a drop in pressure. This form of CABG often occurs in cases of posterior wall myocardial infarction.

True KS is based on a sharp decrease in the contractility of the left ventricle, leading to a decrease in its minute volume (MV). The most serious circulatory disorders that occur with true CABG quickly lead to changes in all organs and tissues and are accompanied by anuria.

Arrhythmic form CABG is diagnosed in cases where there is a clear connection between disturbances in peripheral microcirculation and a drop in pressure with disorders heart rate and conductivity. As a rule, with the restoration of a normal rhythm, it is possible to stop the symptoms of shock.

Areactive form CABG is confirmed by the absence of a vascular response to the administration of even large doses of norepinephrine. This form of shock is the most resistant to therapeutic effects and in most cases ends in death.

Causes

There are several etiological factors for the development of CS. The following clinical situations most often lead to it:

• disorders of intracardiac hemodynamics of mechanical origin (rupture of the valve or chordae tendineae, malformations, neoplasms);
• decreased pumping function of the heart due to left ventricular failure (sepsis, pancarditis, cardiomyopathy, myocardial infarction);
• arrhythmogenic pathology (atrioventricular blockade, brady- and tachyarrhythmias);
• insufficient filling of the heart chambers during diastole (with pericardial tamponade);
• autoimmune rejection (heart transplantation);
• postoperative complications (damage or rupture of the artificial heart valve);
• thromboembolism of the pulmonary arteries.

In 60-95% of cases, CABG aggravates the course of MI, manifesting itself against the background of a critical decline in the pumping function of the left ventricle.

Risk factors that increase the likelihood of developing shock conditions are:

• extensive MI involving more than 40% of the anterior wall surface;
• severe ischemia of the areas of the heart surrounding the necrosis zone;
• the presence of old scar changes with repeated MI;
• critical decrease in the functional capacity of the left ventricle (less than 40%);
• age of the patient (50 years or more);
• damage to the intracardiac papillary muscles due to their necrosis;
• violation of the integrity of the interventricular septum;
• right ventricular myocardial infarction;
• diabetes mellitus accompanying myocardial infarction.

Cardiogenic shock most often results from myocardial infarction. and rehabilitation measures are described in detail in the article.

Read what arrhythmogenic shock is and how to treat it.

The most dangerous complication pancreatitis is a pancreatogenic shock, which in almost half of the cases leads to the death of the patient. In this topic, we will look at the symptoms and treatment methods for this condition.

Symptoms

The specificity of complaints of patients with CABG is associated with the nature of the underlying pathology. As a rule, patients are concerned about:

• pain in the heart area (behind the breastbone);
• palpitations and interruptions in heart function;
• weakness;
• dizziness;
• dyspnea;
• decrease in the amount of urine excreted (oligo-, anuria);
• cold extremities;
• increased sweating;
• feeling of fear.

An objective examination of a patient in CABG status reveals symptoms of extreme severity of his condition. IN initial stage As a rule, psychomotor agitation is expressed, which is soon replaced by lethargy and adynamia. Consciousness gradually fades along with the loss of interest in the environment, which indicates an increase in hypoxic processes in the brain.

Skin that is cold to palpation is pale, with pronounced cyanosis, and covered with sweat. The pulsation of the radial arteries is characterized by weak filling and tension, up to a thread-like pulse or its absence. Typically, the systolic level blood pressure below 80 mmHg, but in some cases it can rise to 90 and above (mainly in the presence of anamnestic arterial hypertension).

Typical signs for CABG are a critical decrease in the pulse wave (from 30 to 10 mm Hg) and pronounced dullness of heart sounds during cardiac auscultation, gallop rhythm and systolic murmur. In terminal states, tones are not audible, so determining blood pressure by auscultation becomes impossible. On the part of the lungs, tachypnea and a shallow type of breathing are observed, which in the terminal stages acquires an aperiodic type (Cheyne-Stokes). The presence of moist rales indicates the development of pulmonary edema against the background of stagnation in the pulmonary circulation.

A prognostically unfavorable symptom in CABG is considered to be a decrease in diuresis of less than 20 ml of urine excreted per hour, indicating an extreme degree of microcirculation impairment in the kidneys.

Mechanisms of occurrence

The main pathogenetic mechanisms that trigger the chain pathological processes with CABG, are the loss of the bulk of the myocardium due to occlusion of the main arteries supplying the heart, leading to multiple organ failure, and in some cases, the death of the patient.

Against the background of hypotension, which develops as a result of necrosis of the heart muscle, a syndrome of hypoperfusion of the surviving areas of the myocardium develops, followed by a deterioration in the contractility of the ventricles of the heart.

Once the loss of non-functioning myocardial mass reaches 40% of the volume of the left ventricle, irreversible consequences of CABG develop.

Compensatory reactions from the nervous and endocrine systems in the initial stages of CABG are adaptive in nature and are aimed at increasing cardiac output. Subsequently, an increase in heart rate leads to an increase in oxygen consumption by the myocardium and reflex vascular spasm. This is accompanied by the accumulation of under-oxidized products in tissues, the development of metabolic acidosis and tissue hypoxia.

In addition, against the background of damage to the vascular endothelium, significant retention of fluid and sodium occurs in the body.

The resulting cardiac arrhythmias only worsen cardiac function and in some cases lead to the death of the patient due to multiple organ failure.

Diagnosis of cardiogenic shock

Since CS is a clinical syndrome, its diagnosis includes the presence of a set of symptoms characteristic of hypoperfusion of individual organs and the body as a whole:

• arterial hypotension (less than 80 mm Hg);
• decreased pulse pressure (less than 20 mm Hg);
• decreased urine output (anuria or oliguria less than 20 ml per hour);
• lethargy and other disturbances of consciousness;
• symptoms of microcirculation crisis (marbled, pale skin color, cold extremities, acrocyanosis);
• signs of metabolic acidosis.

The absence of specific symptoms pathognomonic for CS makes it possible to make a diagnosis of cardiogenic shock solely on the basis of a combination of several clinical symptoms. In this case, one should take into account the variability of the signs of CS in each case, depending on the main diagnosis against which the shock developed.

Acute myocardial infarction of the anterior wall of the left ventricle

Objectification of hemodynamic and other disorders during CABG is achieved using:

• radiography of organs chest;
• coronary angiography;
• direct determination of cardiac output;
• measuring pressure in the cavities of the heart;
• echocardiography;
• hemodynamic monitoring.

Emergency care for cardiogenic shock - algorithm

Successful treatment of any form of CABG begins with effective pain relief.

Taking into account the hypotensive effect of narcotic analgesics, their prescription is combined with drugs from the sympathomimetic group (mesaton).

Cardiac bradycardia is an indication for intravenous atropine.

With reflex CABG, the patient's legs are elevated to increase the volume of blood flowing to the heart. In the absence of consciousness, tracheal intubation is indicated. Lidocaine is used to prevent cardiac arrhythmias. With the help of oxygen therapy (through maxa or a catheter), they achieve improved oxygen supply to tissues. Ventricular fibrillation is a direct indication for defibrillation.

Treatment

The complex of therapeutic measures for the relief of coronary artery disease consists of:

• events general plan(analgesics, thrombolytics, oxygenation, hemodynamic monitoring);
• infusion therapy (in the absence of contraindications);
• vasodilators;
• medications with inotropic action (improving myocardial contractility);
• electropulse therapy - to eliminate heart rhythm disturbances;
• electrocardiostimulation - for conduction disorders.

In addition, instrumental methods for the treatment of CABG include balloon counterpulsation inside the aorta. For ruptures of the interventricular septum, it is indicated surgical treatment(also - with ruptures or dysfunction of the papillary muscles).

Prognosis and life chances

The prognosis for CABG is very serious and is largely determined by the degree of myocardial damage, the timeliness of diagnosis and the adequacy of treatment measures.

The areactive form of CS is considered prognostically unfavorable.

In case of an adequate response to the therapeutic effect and an increase in blood pressure, a favorable outcome is possible.

However, in some cases the clinical picture may reverse. Severe forms of CABG lead to death in 70% of cases during the first hours and days of illness.

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Arrhythmia

According to the World Health Organization, arrhythmias, irregular heartbeats, affect more than 40% of people over 50 years of age. However, they are not the only ones. This insidious disease is detected even in children and often in the first or second year of life. Why is he cunning? And because it sometimes disguises pathologies of other vital organs as heart disease. Another unpleasant feature of arrhythmia is the secrecy of its course: until the disease goes too far, you may not be aware of it...

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Heart disease

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Pressure

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Heart attack

Myocardial infarction is considered to be a disease of older men. But the greatest danger it poses is not for them, but for people of working age and women over 75 years of age. It is in these groups that mortality rates are highest. However, no one should relax: today heart attacks overtake even the young, athletic and healthy. More precisely, underexamined.

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Pulse abnormalities

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Operations

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Cases of cardiogenic shock have become more frequent in patients with a necrosis value of less than 40%, without observing congestion in the lungs and without an increase in total peripheral vascular pressure. This is influenced by systemic inflammatory reactions and ischemia.

There is also an opinion that cardiogenic shock is significantly influenced by taking ACE inhibitors, morphine, beta blockers and nitrates.

There are three types of cardiogenic shock:

Sudden drop in cardiac pumping function	Damage to almost half of the left ventricular myocardium causes true cardiogenic shock. In this case, patients experience symptoms similar to pulmonary edema and hypokinetic hemodynamics. There are several types: classic picture - pressure in the pulmonary capillaries exceeds 30 mm Hg. Art.; pronounced clinical manifestations are observed from 25 to 30 mm Hg. Art.; moderate – 18 – 25 mm Hg. Art.; congestive pulmonary edema at a pressure of 18 mm Hg. Art. As a rule, the first signs of shock can be noticed a couple of hours after a heart attack.
Paroxysmal and tachyarrhythmias	cause hemodynamic disturbances, resulting in the development of arrhythmic cardiogenic shock; its appearance is caused by disturbances in cardiac conduction and heart rhythm, which cause a disorder of central hemodynamics; the phenomena disappear when cardiac pumping function normalizes; it can be restored by renewing sinus rhythm and relief of the above violations.
Stressful situation	leads to increased vascular pressure; disrupting the balance between the parts of the nervous system (parasympathetic and sympathetic tone) and the central nervous system there is nociceptive impulse; as a result, reflex cardiogenic shock occurs.

Pain syndrome that is not stopped in time during myocardial infarction causes severe arterial hypotension and collapse. Therefore, cardiogenic shock of a reflex type manifests itself with a vivid clinical picture - low impulse filling, increased heart rate, low blood pressure, increased sweating, pale skin. The so-called collaptoid state.

The duration of reflex shock is not long. Treatment of cardiogenic shock during myocardial infarction is possible with proper pain management. Sustained resumption of hemodynamics can be achieved by administering vasopressor drugs.

Symptoms of cardiogenic shock during myocardial infarction

Symptoms include:

• decreased diuresis;
• disturbances of consciousness;
• the appearance of cold sticky sweat;
• paleness of the skin;
• cyanosis;
• dyspnea;
• low blood pressure;
• sinus tachycardia.

If these signs are detected, it is necessary to resort to invasive hemodynamic monitoring: in pulmonary artery determine wedge pressure and intra-arterial blood pressure control.

The classic definition is a decrease in systolic blood pressure below 90 mmHg over 30 minutes. st in combination with pronounced manifestations of peripheral hypoperfusion.

If concomitant hypovolemia is not observed, then with hemodynamic shock a combination of an increase in filling pressure to 20 mm Hg is observed. Art. in the left ventricle and a decrease in cardiac index to 1.8 l/min/m2.

A decrease in blood pressure is a relatively late sign. Initially, pulse arterial pressure decreases and sinus reflex tachycardia appears, caused by a decrease in cardiac output. Vasoconstriction also appears, starting from the skin vessels, kidneys and ending with the brain.

The resulting vasoconstriction may keep normal level blood pressure. The perfusion of tissues and organs, including the myocardium, deteriorates quite quickly. Against the background of sympathomimetics taken, vasoconstriction is expressed.

This allows the method of auscultation to determine a decrease in blood pressure, but the blood pressure determined by arterial puncture will remain within normal limits.

Therefore, if it is not possible to carry out invasive control, then arteries less susceptible to vasoconstriction (femoral, carotid) should be palpated.

Diagnostics

Algorithm of actions when diagnosing cardiogenic shock:

Pulse pressure drops to 30 mmHg. Art. and continues to decline	Severe hypotension of the arteries - systolic pressure crosses the line of 80 mmHg. Art., and with the diagnosis “ arterial hypertension» — 30 mm Hg. Art.
Recalculation of the shock index, over 0.8	This is the relationship between systolic blood pressure and heart rate. The average value in normal condition is 0.6 - 0.7. During shock it can exceed 1.5.
Peripheral circulation disorder	With obvious clinical signs.
Oliguria	The kidneys excrete less urine, approximately 20 ml/hour.
Confusion and retardation of consciousness	Sometimes there is short-term excitement.

Treatment

Ideally, emergency care should be aimed at performing intra-arterial balloon counterpulsation. In this way, it is possible to stabilize hemodynamics and maintain relative stabilization of the condition for a long time.

Along with counterpulsation, it is necessary to diagnose ischemic disease heart by coronography, this will determine the degree, location and nature of the narrowing of the coronary artery.

It is also necessary to revascularize the myocardium using coronary artery bypass grafting or coronary angioplasty. Unfortunately, it is extremely rare to hold the full range of events. By performing coronary angioplasty, it was possible to reduce the statistics deaths almost up to 40%.

During the studies, restoration of coronary blood flow and successful recanalization of the coronary arteries among patients reduced the mortality rate, it was 23%. Urgent coronary artery bypass surgery provides up to a 50% reduction in mortality.

Timely revascularization also provides a successful prognosis. According to the SHOCK study, among patients under 75 years of age, only 2 out of 10 people were saved. But in order to provide the above assistance, it is necessary to identify and hospitalize the patient in a specialized cardiac surgery department.

In healthcare practice, the following method is used to treat patients diagnosed with cardiogenic shock.

With a rapid decrease in blood pressure, an infusion of norepinephrine is used. Blood pressure should increase to 90 mm Hg. Art. Then dopamine must be introduced. And in cases of mild hypotension, this procedure is carried out initially.

If blood pressure is maintained at 90 mm Hg. Art. when dopamine is administered at a rate of 400 mcg/min, it has a positive effect by dilating cerebral and coronary vessels, as well as organ vessels abdominal cavity and kidneys.

If the rate of dopamine infusion is increased, then positive influence is minimized. At rates above 1000 mcg/min, dopamine promotes vasoconstriction.

In case of stabilization of blood pressure with small doses of dopamine, treatment with dobutamine should be resorted to, at a dose of 200 to 1000 mcg/min. The further rate of administration of these drugs is regulated by the behavior of blood pressure. Additionally, phosphodiesterase inhibitors (enoxymone, milrinone) may be prescribed.

If there are no pronounced wheezes in the lungs, it is recommended to check the reaction to fluid administration using the usual method. This technique consists of administering 250-500 ml of liquid over 5 minutes (at least 3), then 50 mg after 5 minutes, until the manifestation of congestion in the lungs intensifies. Even with the most cardiogenic shock, 5% of patients experience relative hypovolemia.

.

Surgery for myocardial infarction is performed in the case of large-focal hemorrhages - we will tell you more about surgical intervention in.

Corticosteroid hormones are not prescribed for cardiogenic shock. Some clinical experiments and studies have revealed the positive effect on the patient of the administration of a glucose-potassium-insulin mixture.

Cardiogenic shock is a severe complication of diseases of the cardiovascular system, accompanied by impaired contractility of the heart muscle and a drop in blood pressure. As a rule, cardiogenic shock develops in a patient against the background of severe heart failure, which is caused by untreated diseases of the heart and coronary vessels.

This condition provokes a sharp deficiency of oxygen in all organs and tissues, which causes circulatory disorders, depression of consciousness and death if the victim is not promptly provided with emergency care.

The causes of cardiogenic shock in most cases are due to blockage of large branches of the pulmonary artery by blood clots, which prevent proper blood circulation and cause severe organ hypoxia.

This condition is caused by:

• acute myocardial infarction;
• mitral valve stenosis in acute form;
• hypertrophic cardiomyopathy in severe form;
• heart rhythm disturbances;
• hemorrhagic shock (occurs when transfusion of blood that does not match the blood group or rhesus);
• pericarditis of compressive type;
• rupture of the septum between the ventricles;
• septic shock, which provoked disruption of the myocardium;
• tension pneumothorax;
• dissecting aortic aneurysm or rupture;
• severe pulmonary embolism;
• cardiac tamponade.

Heart attack - emergency care is a priority

Mechanism of development of cardiogenic shock

In order to understand what cardiogenic shock is, it is important to understand the mechanism of development of the pathology, there are several of them:

1. Decreased myocardial contractility– when a heart attack occurs (necrosis of a certain area of ​​the heart muscle), the heart cannot fully pump blood, which leads to a sharp decrease in blood pressure (arterial). Against this background, the brain and kidneys are the first to suffer from hypoxia, acute urinary retention develops, and the victim loses consciousness. Due to respiratory depression and oxygen starvation, metabolic acidosis develops, organs and systems abruptly stop functioning normally and death occurs.
2. Development of arrhythmic shock (bradysystolic or tachysystolic)– this form of shock develops against the background of paroxysmal tachycardia or severe bradycardia with complete atrioventricular block. Under the influence of impaired ventricular contractility and a decrease in blood pressure (about 80/20 mm Hg), severe changes in hemodynamics develop.
3. Cardiac tamponade with the development of cardiogenic shock– diagnosed with a rupture of the interventricular septum. With this pathology, the blood in the ventricles is mixed, which makes it impossible for the heart muscle to contract. Blood pressure drops sharply, hypoxia in vital organs increases, the patient falls into a coma and may die in the absence of adequate help.
4. Massive thromboembolism leading to cardiogenic shock– this form of shock develops when the lumen of the pulmonary artery is completely blocked by blood clots. In this case, blood stops flowing into the left ventricle. This leads to a sharp decrease in blood pressure, increasing hypoxia and death of the patient.

Classification of cardiogenic shock

The table shows 4 forms of cardiogenic shock:

Form of pathology	What is it characterized by?
True cardiogenic shock	Accompanied by a sharp impairment of myocardial contractile function, decreased diuresis, metabolic acidosis, hypotension and severe oxygen starvation. Cardiogenic pulmonary edema often develops as a complication, treatment of which requires resuscitation.
Reflex	It is provoked by the reflex effect of pain on the contractile function of the myocardium. It is characterized by severe bradycardia (heart rate decrease below 60 beats/min), decreased blood pressure. At the same time, microcirculation disorders and metabolic acidosis do not develop
Arrhythmic	Develops against the background of severe tachycardia or bradycardia and resolves after drug elimination of the arrhythmia
Areactive	Develops suddenly, is very severe and in most cases leads to death, despite all the treatment measures taken

Clinical signs of cardiogenic shock

At the initial stage, the clinical manifestations of cardiogenic shock depend on the cause of the development of this condition:

• if cardiogenic shock is caused by acute myocardial infarction, then the first symptom of this complication will be severe chest pain and panic fear of death;
• in case of heart rhythm disturbances such as tachycardia or bradycardia against the background of the development of complications, the patient will complain of pain in the heart area and noticeable interruptions in the functioning of the heart muscle (the heartbeat either slows down or sharply increases);
• when the pulmonary artery is blocked by blood clots clinical symptoms cardiogenic shock manifests itself in the form of severe shortness of breath.

Against the background of a sharp decrease in blood pressure, vascular signs of cardiogenic shock appear:

• cold sweat;
• severe pallor of the skin and blueness of the lips;
• severe anxiety, followed by sudden weakness and lethargy;
• swelling of the veins in the neck;
• dyspnea;
• strong fear of death;
• With pulmonary embolism, the patient develops marbling of the skin of the chest, neck, and head.

Important! If such symptoms appear, you should act very quickly, since the progression of the clinic leads to complete cessation of breathing, depression of consciousness and death.

A cardiologist assesses the severity of cardiogenic shock using several indicators:

• blood pressure parameters;
• duration of shock - the moment from the onset of the first symptoms of cardiogenic shock to seeking medical help;
• severity of oliguria.

In cardiology, there are 3 degrees of cardiogenic shock:

Degree of cardiogenic shock	What is it characterized by?
First	No more than 3 hours have passed since the first symptoms of shock appeared; blood pressure readings are not lower than 90/50 mm Hg. The patient has signs of heart failure in mild form. If provided in a timely manner medical care the patient responds well to drug treatment and the shock is relieved within 40-60 minutes
Second	Shock lasts more than 5 hours, blood pressure is below 80/50 mm Hg, the patient has severe signs of heart failure and responds poorly to medications
Third	Shock lasts more than 10 hours, blood pressure is 20/0 mm Hg or not determined at all, symptoms of heart failure are pronounced. Most patients develop cardiogenic pulmonary edema

Diagnostics

When severe pain behind the sternum and the patient’s fear of death, it is important to differentiate cardiogenic shock from myocardial infarction, aortic aneurysm and other pathological conditions.

The criteria for diagnosis are:

• drop in systolic pressure to 90-80 mm Hg;
• decrease in diastolic pressure to 40-20 mm Hg;
• a sharp decrease in the amount of urine excreted or complete anuria;
• strong mental agitation of the patient, which suddenly gives way to apathy and lethargy;
• the presence of signs of circulatory disorders in peripheral vessels - pale skin, bluish lips, marbling of the skin, cold sweat, cold extremities, thready pulse;
• collapse of the veins of the lower extremities.

ECG, Echo-CG, and angiography will help confirm the diagnosis and evaluate the criteria for cardiogenic shock.

Help with cardiogenic shock

When the first symptoms of cardiogenic shock appear, you should immediately call a cardiology ambulance team and begin providing pre-hospital rescue measures.

Urgent Care in case of cardiogenic shock before the ambulance arrives is as follows:

• calm the patient;
• put him in bed and raise his lower limbs slightly above the level of his head - this way you will prevent a rapid decrease in pressure;
• drink warm sweet tea;
• provide access to fresh air;
• Unfasten the buttons and get rid of clothes that are constricting your chest.

Important! The patient may be very excited, jump up, try to run, so it is extremely important not to let him walk - this predetermines the further prognosis.

First aid for cardiogenic shock upon arrival of the ambulance consists of the following:

1. Oxygen therapy – the patient is given humidified oxygen through a mask. The mask is not removed until arrival at the hospital, after which the patient is connected to intensive care units and his condition is monitored around the clock.
2. Narcotic analgesics - to relieve severe pain, the patient is administered Morphine or Promedol.
3. In order to stabilize blood pressure, a Reopoliglucin solution and plasma substitutes are administered intravenously.
4. To thin the blood and prevent the formation of blood clots in the lumen of the coronary vessels, Heparin is administered.
5. To enhance the contractile function of the heart muscle, solutions of Adrenaline, Norepinephrine, Sodium Nitroprusside, and Dobutamine are administered.

Already in the hospital, the patient undergoes intensive therapy:

• to normalize myocardial trophism, glucose solutions with insulin are infused intravenously;
• for the course of cardiac arrhythmia, Mezaton, Lidocaine or Panangin are added to the solution of the polarizing mixture;
• to eliminate the effects of acidosis against the background of severe hypoxia of organs and tissues, the patient is given intravenous drips of sodium bicarbonate solutions - this will help stabilize the acid-base balance of the blood;
• when atrioventricular block develops, they begin to administer Prednisolone, Ephedrine, and additionally give an Izadrina tablet under the tongue.

Besides drug treatment The patient is fitted with a urinary catheter to determine the amount of urine excreted per day and must be connected to a cardiac monitor, which will regularly measure pulse and blood pressure parameters.

Surgical treatment

If ineffective drug therapy A patient with cardiogenic shock undergoes surgical treatment:

1. balloon intra-aortic counterpulsation - during cardiac diastole, blood is pumped into the aorta using a special balloon, which helps to increase coronary blood flow.
2. Percutaneous coronary transluminar angioplasty - the artery is punctured and the patency of the coronary vessels is restored through this hole. This treatment method is effective only if no more than 7 hours have passed since the onset of signs of acute myocardial infarction.

Patients diagnosed with cardiogenic shock remain in the intensive care unit until their condition stabilizes and the crisis has passed, after which, if the prognosis is favorable, they are transferred to the cardiology department, where treatment continues.

The development of this complication is not always a death sentence for the patient. It is very important to call in a timely manner ambulance and relieve pain.

is an extreme degree of manifestation of acute heart failure, characterized by a critical decrease in myocardial contractility and tissue perfusion. Symptoms of shock: drop in blood pressure, tachycardia, shortness of breath, signs of centralized blood circulation (pallor, decreased skin temperature, appearance of congestive spots), impaired consciousness. The diagnosis is made based on the clinical picture, ECG results, and tonometry. The goal of treatment is to stabilize hemodynamics and restore heart rhythm. As part of emergency treatment, beta blockers, cardiotonics, narcotic analgesics, and oxygen therapy are used.

ICD-10

R57.0

General information

Cardiogenic shock (CS) – acute pathological condition, in which the cardiovascular system is unable to provide adequate blood flow. The required level of perfusion is temporarily achieved due to the depleted reserves of the body, after which the decompensation phase begins. The condition belongs to class IV heart failure (the most severe form of cardiac dysfunction), mortality reaches 60-100%. Cardiogenic shock is more common in countries with high performance cardiovascular pathology, poorly developed preventive medicine, lack of high-tech medical care.

Reasons

The development of the syndrome is based on a sharp decrease in LV contractility and a critical decrease in cardiac output, which is accompanied by circulatory failure. A sufficient amount of blood does not enter the tissue, symptoms of oxygen starvation develop, blood pressure levels decrease, and a characteristic clinical picture appears. CABG can aggravate the course of the following coronary pathologies:

• Myocardial infarction. It is the main cause of cardiogenic complications (80% of all cases). Shock develops mainly with large-focal transmural infarctions with the release of 40-50% of the heart mass from the contractile process. It does not occur in myocardial infarctions with a small volume of affected tissue, since the remaining intact cardiomyocytes compensate for the function of dead myocardial cells.
• Myocarditis. Shock, leading to the death of the patient, occurs in 1% of cases of severe infectious myocarditis caused by Coxsackie viruses, herpes, staphylococcus, pneumococcus. The pathogenetic mechanism is damage to cardiomyocytes by infectious toxins, the formation of anticardiac antibodies.
• Poisoning with cardiotoxic poisons. Such substances include clonidine, reserpine, cardiac glycosides, insecticides, and organophosphorus compounds. An overdose of these drugs causes a weakening of cardiac activity, a decrease in heart rate, and a drop in cardiac output to levels at which the heart is unable to provide the required level of blood flow.
• Massive pulmonary embolism. Blockage of large branches of the pulmonary artery by a thrombus - pulmonary embolism - is accompanied by impaired pulmonary blood flow and acute right ventricular failure. Hemodynamic disorder caused by excessive filling of the right ventricle and stagnation in it leads to the formation of vascular insufficiency.
• Cardiac tamponade. Cardiac tamponade is diagnosed with pericarditis, hemopericardium, aortic dissection, and chest injuries. The accumulation of fluid in the pericardium complicates the work of the heart - this causes disruption of blood flow and shock phenomena.

Less commonly, pathology develops with papillary muscle dysfunction, ventricular septal defects, myocardial rupture, cardiac arrhythmias and blockades. Factors that increase the likelihood of cardiovascular accidents are atherosclerosis, old age, presence of diabetes mellitus, chronic arrhythmia, hypertensive crises, excessive physical activity in patients with cardiogenic diseases.

Pathogenesis

The pathogenesis is due to a critical drop in blood pressure and a subsequent weakening of blood flow in the tissues. The determining factor is not hypotension as such, but a decrease in the volume of blood passing through the vessels over a certain time. Deterioration of perfusion causes the development of compensatory and adaptive reactions. The body's reserves are used to supply blood to vital organs: the heart and brain. Other structures (skin, limbs, skeletal muscles) experience oxygen starvation. Spasm of peripheral arteries and capillaries develops.

Against the background of the described processes, activation of neuroendocrine systems occurs, the formation of acidosis, and the retention of sodium and water ions in the body. Diuresis decreases to 0.5 ml/kg/hour or less. The patient is diagnosed with oliguria or anuria, liver function is disrupted, and multiple organ failure occurs. In later stages, acidosis and cytokine release provoke excessive vasodilation.

Classification

The disease is classified according to pathogenetic mechanisms. At the prehospital stages, it is not always possible to determine the type of CABG. In a hospital setting, the etiology of the disease plays a decisive role in the choice of treatment methods. Misdiagnosis in 70-80% of cases ends in the death of the patient. The following types of shock are distinguished:

1. Reflex– violations are caused by a severe pain attack. It is diagnosed when the volume of the lesion is small, since the severity of the pain syndrome does not always correspond to the size of the necrotic lesion.
2. True Cardiogenic– a consequence of acute MI with the formation of a voluminous necrotic focus. The contractility of the heart decreases, which reduces cardiac output. A characteristic complex of symptoms develops. The mortality rate exceeds 50%.
3. Areactive- the most dangerous variety. Similar to true CS, pathogenetic factors are more pronounced. Doesn't respond well to therapy. Mortality – 95%.
4. Arrhythmogenic– prognostically favorable. It is the result of rhythm and conduction disturbances. Occurs with paroxysmal tachycardia, AV blockade of the third and second degree, complete transverse blockade. After the rhythm is restored, the symptoms disappear within 1-2 hours.

Pathological changes develop stepwise. Cardiogenic shock has 3 stages:

• Compensation. Decreased cardiac output, moderate hypotension, weakened perfusion in the periphery. Blood supply is maintained by centralizing the circulation. The patient is usually conscious, clinical manifestations are moderate. There are complaints of dizziness, headache, pain in the heart. At the first stage, the pathology is completely reversible.
• Decompensation. There is a developed symptom complex, blood perfusion in the brain and heart is reduced. Blood pressure level is critically low. There are no irreversible changes, but there are minutes left before they develop. The patient is in stupor or unconscious. Due to the weakening of renal blood flow, urine formation is reduced.
• Irreversible changes. Cardiogenic shock enters the terminal stage. Characterized by an intensification of existing symptoms, severe coronary and cerebral ischemia, the formation of necrosis in internal organs. Disseminated intravascular coagulation syndrome develops, and a petechial rash appears on the skin. Internal bleeding occurs.

Symptoms of cardiogenic shock

In the initial stages, cardiogenic pain syndrome is expressed. The location and nature of the sensations are similar to a heart attack. The patient complains of squeezing pain behind the sternum (“as if the heart is being squeezed in the palm”), spreading to the left shoulder blade, arm, side, jaw. There is no irradiation on the right side of the body.

Complications

Cardiogenic shock is complicated by multiple organ failure (MOF). The functioning of the kidneys and liver is impaired, side effects are observed digestive system. Systemic organ failure is a consequence of untimely provision of medical care to the patient or a severe course of the disease, in which the rescue measures taken are ineffective. Symptoms of MODS – spider veins on the skin, vomiting " coffee grounds", smell of raw meat from the mouth, swelling of the jugular veins, anemia.

Diagnostics

Diagnosis is carried out on the basis of physical, laboratory and instrumental examination data. When examining a patient, a cardiologist or resuscitator notes external signs of the disease (pallor, sweating, marbling of the skin) and assesses the state of consciousness. Objective diagnostic measures include:

• Physical examination. Tonometry determines a decrease in blood pressure below 90/50 mmHg. Art., pulse rate less than 20 mm Hg. Art. At the initial stage of the disease, hypotension may be absent, which is due to the inclusion of compensatory mechanisms. Heart sounds are muffled, moist fine rales are heard in the lungs.
• Electrocardiography. A 12-lead ECG reveals characteristic features myocardial infarction: decreased amplitude of the R wave, displacement S-T segment, negative T wave. Signs of extrasystole and atrioventricular block may be observed.
• Laboratory research. The concentration of troponin, electrolytes, creatinine and urea, glucose, and liver enzymes is assessed. The level of troponins I and T increases already in the first hours of AMI. Sign of developing renal failure- increased concentrations of sodium, urea and creatinine in plasma. The activity of liver enzymes increases with the reaction of the hepatobiliary system.

When carrying out diagnostics, it is necessary to distinguish cardiogenic shock from dissecting aortic aneurysm and vasovagal syncope. With aortic dissection, the pain radiates along the spine, persists for several days, and is wave-like. With syncope, there are no serious changes on the ECG, and there is no history of pain or psychological stress.

Treatment of cardiogenic shock

Patients with acute heart failure and signs of shock are urgently hospitalized in a cardiology hospital. The ambulance team responding to such calls must include a resuscitator. On prehospital stage oxygen therapy is carried out, central or peripheral venous access, according to indications, thrombolysis is performed. In the hospital, treatment started by the emergency medical team continues, which includes:

• Drug correction of disorders. To relieve pulmonary edema, loop diuretics are administered. Nitroglycerin is used to reduce cardiac preload. Infusion therapy is carried out in the absence of pulmonary edema and CVP below 5 mm Hg. Art. The infusion volume is considered sufficient when this figure reaches 15 units. Antiarrhythmic drugs (amiodarone), cardiotonics, narcotic analgesics, and steroid hormones are prescribed. Severe hypotension is an indication for the use of norepinephrine through a perfusion syringe. For persistent heart rhythm disturbances, cardioversion is used; for severe respiratory failure– IVL.
• High-tech assistance . When treating patients with cardiogenic shock, high-tech methods such as intra-aortic balloon counterpulsation, artificial ventricle, and balloon angioplasty are used. The patient receives an acceptable chance of survival with timely hospitalization in a specialized cardiology department, where the equipment necessary for high-tech treatment is available.

Prognosis and prevention

The prognosis is unfavorable. The mortality rate is more than 50%. This indicator can be reduced in cases where first aid was provided to the patient within half an hour from the onset of the disease. The mortality rate in this case does not exceed 30-40%. Survival is significantly higher among patients who underwent surgery aimed at restoring the patency of damaged coronary vessels.

Prevention consists of preventing the development of MI, thromboembolism, severe arrhythmias, myocarditis and heart injuries. For this purpose, it is important to undergo preventive courses of treatment, maintain a healthy and active image life, avoid stress, follow the principles of healthy eating. When the first signs of a cardiac catastrophe occur, an ambulance must be called.