Cardiac shock. Clinical symptoms and emergency care for cardiogenic shock. Forecasts for the development of the disease

– this 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) is an 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 often recorded in countries with high rates of cardiovascular pathology, poorly developed preventive medicine, and lack of high-tech medical care.

Causes

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, the presence of diabetes mellitus, chronic arrhythmia, hypertensive crises, and 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. The remaining 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, heart pain. At the first stage, the pathology is completely reversible.
• Decompensation. There is a comprehensive 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. It is characterized by an intensification of existing symptoms, severe coronary and cerebral ischemia, and the formation of necrosis in the 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 localization 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 disrupted, and reactions from the digestive system are noted. 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 are spider veins on the skin, vomiting “coffee grounds,” the smell of raw meat on the breath, 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. An ECG in 12 leads reveals characteristic signs of myocardial infarction: a decrease in the amplitude of the R wave, a displacement of the S-T segment, a 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. A sign of developing renal failure is an increase in the concentration 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. At the prehospital stage, oxygen therapy is provided, central or peripheral venous access is provided, and thrombolysis is performed according to indications. 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 cardiac arrhythmias, cardioversion is used, and for severe respiratory failure, mechanical ventilation is used.
• 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, lead a healthy and active lifestyle, avoid stress, and follow the principles of a healthy diet. When the first signs of a cardiac catastrophe occur, an ambulance must be called.

Version: MedElement Disease Directory

Cardiogenic shock (R57.0)

Cardiology

general information

Short description

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

Classification

To determine the severity of acute heart failure in patients with myocardial infarction, they resort to Killip 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 of clinical manifestations, response to measures taken, and hemodynamic parameters, 3 degrees of severity of cardiogenic shock are distinguished.

Indicators	Severity of cardiogenic shock
	I	II	III
Duration of shock	No more than 3-5 hours.	5-10 hours	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 mm Hg. Art.	BP sys.< 60 мм рт.ст. AD dias. may drop to 0
*Pulse blood pressure	30-25 mm. rt. Art.	20-15 mm. rt. st	< 15 мм. рт. ст.
Heart rate abbreviations	100-110 min.	110-120 min.	>120 min.
Severity of shock symptoms	Symptoms of shock are mild	Symptoms of shock are severe	Symptoms of shock are very pronounced, the course of shock is extremely severe
Severity of heart failure symptoms	Heart failure is absent or mild	Severe symptoms of acute cardiac left ventricular failure, in 20% of patients - pulmonary edema	Severe heart failure, severe pulmonary edema
Pressor reaction to therapeutic measures	Fast (30-60 min.), sustainable	Slow, unstable, peripheral signs of shock resume within 24 hours	Unstable, short-term, often absent altogether (unresponsive state)
Diuresis, ml/h	Reduced to 20	<20	0
Cardiac index value l/min/m²	Reduce to 1.8	1,8-1,5	1.5 and below
**Sealing 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
** In case of myocardial infarction of the right ventricle and hypovolemic version of shock, the wedge pressure in the pulmonary artery is reduced

Etiology and pathogenesis

The main causes of cardiogenic shock:
- cardiomyopathy;
- myocardial infarction (MI);
- myocarditis;
- severe heart defects;
- heart tumors;
- toxic myocardial damage;
- pericardial tamponade;
- severe heart rhythm disturbance;
- pulmonary embolism;
- injury.

Most often, a practicing physician encounters cardiogenic shock in patients with acute coronary syndrome (ACS), primarily with 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 dilation of peripheral vessels and a drop in blood pressure; there is no severe myocardial damage.
The occurrence of the reflex form is due to the development of the Bezold-Jarisch 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 shock, but pain collapse or pronounced arterial hypotension in a patient with MI.

True cardiogenic shock

Main pathogenetic factors:

1. Exclusion of 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 exceeds 40% of the mass of the left ventricular myocardium.

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 aortic pressure 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 impairs the systolic and diastolic functions of the myocardium.

The inability of the left ventricle to empty also 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 force of cardiac contractions. This compensatory mechanism restores stroke volume, but the 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 decreased cardiac output during cardiogenic shock, compensatory peripheral vasospasm occurs. Increasing systemic peripheral resistance is aimed at increasing blood pressure and improving blood supply to vital organs. However, because of this, the afterload increases significantly, as a result of which the myocardial oxygen demand increases, increased ischemia, a further decrease in myocardial contractility and an increase in the end-diastolic volume of the left ventricle are observed. The latter factor causes an increase in pulmonary congestion and, accordingly, hypoxia, which aggravates myocardial ischemia and a decrease in its contractility. Then the described process is repeated again.

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

Areactive form
The pathogenesis is similar to that of true cardiogenic shock, but the pathogenetic factors that act for a longer period are much more pronounced. 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 blood volume) with the listed arrhythmias and atrioventricular block. Subsequently, the inclusion of pathophysiological vicious circles described in the pathogenesis of true cardiogenic shock is observed.

Cardiogenic shock due to myocardial rupture

Main pathogenetic factors:

1. A sharply expressed reflex drop in blood pressure (collapse) as a result of irritation of the pericardial receptors by gushing blood.

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

3 Sharply expressed overload of certain parts of the heart (with internal myocardial ruptures).

4. Decline in myocardial contractile function.

Epidemiology

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

Risk factors and groups

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

Extensive infarction (MB-CPK activity in the blood more than 160 U/L);

History of diabetes mellitus;

Repeated heart attack.

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

Clinical picture

Clinical diagnostic criteria

Symptoms of peripheral circulatory failure (pale cyanotic, marbled, moist skin; acrocyanosis; collapsed veins; cold hands and feet; decreased body temperature; prolongation of the time of disappearance of the white spot after pressing on the nail for more than 2 seconds - decreased speed of peripheral blood flow); disturbance of consciousness (lethargy, confusion, possibly unconsciousness, less often - agitation); oliguria (decrease in diuresis less than 20 ml/h); in extremely severe cases - anuria; decrease in systolic blood pressure to less than 90 mm. rt. art (according to some data 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 blood pressure to 20 mm. rt. Art. and below; decrease in mean arterial pressure less than 60 mm. rt. Art. or when 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: wedge pressure in the pulmonary artery more than 15 mm. rt. Art. (more than 18 mm Hg according to Antman, Braunwald), cardiac index less than 1.8 l/min/sq.m, increased total peripheral vascular resistance, increased end-diastolic pressure of the left ventricle, decreased stroke and cardiac output

Symptoms, course

True cardiogenic shock

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

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

Main complaints:
- severe general weakness;
- heartbeat;
- feeling of interruptions in the heart area;
- dizziness, “fog before the eyes”;
- sometimes - chest pain.

According to the external examination, “gray cyanosis” or pale cyanotic coloration of the skin is revealed, severe acrocyanosis is possible Acrocyanosis - bluish discoloration of the distal parts of the body (fingers, ears, tip of the nose) due to venous stagnation, more often with right heart failure
; skin is cold and damp; 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 tint of the skin and mucous membranes caused by insufficient oxygen saturation of the blood.
subungual spaces.

A characteristic feature is the appearance "white spot" symptom- the time it takes for the white spot to disappear after pressing on the nail is longer (normally this time is less than 2 seconds).
This symptomatology reflects peripheral microcirculatory disorders, the extreme degree of which can be expressed by necrosis of the skin in the area of ​​the tip of the nose, ears, distal parts of the fingers and toes.

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

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

Heart percussion reveals an expansion of its left border. Auscultatory signs: soft systolic murmur at the apex of the heart, arrhythmias, muffled heart sounds, protodiastolic gallop rhythm (a characteristic symptom of severe left ventricular failure).

Breathing is usually shallow, possibly rapid breathing (especially with the development of “shock” lung). A particularly severe course of cardiogenic shock is characterized by the development of cardiac asthma and pulmonary edema. In this case, suffocation occurs, breathing becomes bubbling, and there is a cough with pink, frothy sputum.

At lung percussion in the lower sections, dullness of percussion sound, crepitus and fine rales due to alveolar edema are detected. In the absence of alveolar edema, crepitus and moist rales are not heard or are detected in small quantities as a manifestation of congestion in the lower parts of the lungs; a small amount of dry rales is possible. If severe 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 detected, 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 is an area of ​​the abdomen bounded above by the diaphragm and 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 is the excretion of a very small amount of urine compared to the norm.
or anuria Anuria - failure of urine to enter the bladder
, during catheterization of the bladder, the amount of urine discharged is less than 20 ml/hour.

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 heart area.
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 reduced heart rate.
(pathognomonic Pathognomonic - characteristic of a given disease (about a sign).
sign of this form).
Duration of arterial hypotension Arterial hypotension - a decrease in blood pressure by more than 20% from the initial/usual values ​​or in absolute numbers - below 90 mm Hg. Art. systolic pressure or 60 mm Hg. mean arterial pressure
usually does not exceed 1-2 hours. After pain relief, 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-inferior region and is quite often accompanied by extrasystole Extrasystole is a form of cardiac arrhythmia, characterized by the appearance of extrasystoles (a contraction of the heart or its parts that occurs earlier than the next contraction should normally occur)
, AV block Atrioventricular block (AV block) is a type of heart block that indicates a violation of the conduction of electrical impulses from the atria to the ventricles (atrioventricular conduction), often leading to disturbances in 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 grade I severity.

Arrhythmic form

1. Tachysystolic (tachyarrhythmic) variant of cardiogenic shock
It is most often observed with paroxysmal ventricular tachycardia, but can also occur with supraventricular tachycardia, paroxysmal atrial fibrillation and atrial flutter. Develops in the first hours (less often days) of the disease.
The patient is characterized by a severe general condition and significant severity of all clinical signs of shock (significant arterial hypotension, oligoanuria, symptoms of peripheral circulatory failure).
Approximately 30% of patients develop severe left ventricular failure (pulmonary edema, cardiac asthma).
Life-threatening complications such as ventricular fibrillation and thromboembolism in 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 nodal rhythms, Frederick's syndrome (a combination of complete AV block with atrial fibrillation). Bradysystolic cardiogenic shock is observed in the first hours of the development of extensive and transmural myocardial infarction.
Characterized by a severe course, the mortality rate reaches 60% or higher. 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 of contraction of ventricular myofibrils, which leads to cessation of the pumping function of the heart.
, severe left ventricular failure.

Laboratory diagnostics

1.Blood chemistry:
- increased bilirubin content (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);
- increased levels of urea and creatinine in the blood (manifestation of acute renal failure due to renal hypoperfusion);
- an increase in the level of alanine aminotransferase (a reflection of impaired liver function).

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

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

4. Blood gas study:decrease in partial oxygen tension.

Differential diagnosis

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

1. Cardiogenic shock due to aortic rupture
The clinical picture depends on factors such as the location of the rupture, the massiveness and rate of blood loss, as well as whether the blood is poured into a particular cavity or into the surrounding tissue.
Basically, the rupture 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 cardiac sac), blood flows into the pericardial cavity and causes tamponade.
Typical clinical picture:
- intense, increasing chest 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);
- expansion of the boundaries of the heart;
- dullness of heart sounds;
- embryocardia.
If cardiogenic shock worsens, patients die within a few hours. Bleeding from the aorta can occur into the pleural cavity. Then, after the onset of pain in the chest and back (often very intense), signs due to increasing anemia develop: pallor of the skin, shortness of breath, tachycardia, fainting.
Physical examination reveals signs of hemothorax. Progressive blood loss is the direct cause of the patient's death.

When the aorta ruptures with bleeding into the mediastinal tissue, severe and prolonged retrosternal pain is observed, which resembles anginal pain during myocardial infarction. Myocardial infarction can be ruled out by the absence of typical ECG changes.
The second stage of the course of cardiogenic shock with aortic ruptures is characterized by symptoms of increasing internal bleeding, which mainly determines the clinical picture of shock.

2.Cardiogenic shock in acute myocarditis

Currently, it is relatively rare (about 1% of cases). It 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 ashen-gray skin tone, the skin is moist and cold;
- pulse is weak, soft, rapid;
- blood pressure is sharply reduced (sometimes not determined);
- collapsed veins of the systemic circle;
- the boundaries of relative cardiac dullness are expanded, heart sounds are muffled, a gallop rhythm is determined;
- oliguria;
- history indicates a connection between the disease and infection (diphtheria, viral infection, pneumococcus, etc.);
An ECG reveals signs of pronounced diffuse (less often focal) changes in the myocardium, often rhythm and conduction disturbances. The prognosis is always serious.

3.Cardiogenic shock in acute myocardial dystrophies
The development of cardiogenic shock is possible in acute myocardial dystrophies, which are caused by acute cardiac overstrain, acute intoxication and other environmental influences.
Excessive physical activity, especially if performed in a painful state (for example, with a sore throat) or in violation of the regime (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 due to pericarditis

Some forms of effusion pericarditis (hemorrhagic pericarditis with scurbuta, etc.) immediately have a severe course, with symptoms of rapidly progressing circulatory failure due to cardiac tamponade.
Characteristic manifestations:
- periodic loss of consciousness;
- tachycardia;
- low filling of the pulse (an alternating or bigeminic pulse is often observed), the pulse disappears on inspiration (the so-called “paradoxical pulse”);
- blood pressure is sharply reduced;
- cold sticky sweat, cyanosis;
- pain in the heart area due to increased tamponade;
- venous stagnation (the neck and other large veins become overfilled) against the background of progressive shock.
The boundaries of the heart are expanded, the sonority of tones changes depending on the phases of breathing, and sometimes a pericardial friction noise is heard.
The ECG reveals a decrease in the voltage of the ventricular complexes, a shift in the ST segment and changes in the T wave.
X-ray and echocardiography studies help in diagnosis.
If treatment is not timely, the prognosis is unfavorable.

5. Cardiogenic shock with bacterial (infectious) endocarditis
May occur as a result of myocardial damage (diffuse myocarditis, less commonly - myocardial infarction) and destruction (destruction, separation) of heart valves; may be combined with bacterial shock (usually with gram-negative flora).
The initial clinical picture is characterized by the appearance of disturbances of consciousness, vomiting and diarrhea. Further, a decrease in the temperature of the skin of the extremities, cold sweat, a small and rapid pulse, a decrease in blood pressure, and cardiac output are observed.
An ECG reveals changes in repolarization, and rhythm disturbances are possible. EchoCG is used to assess the condition of the heart valve apparatus.

6.Cardiogenic shock due to closed heart injury
The occurrence may be associated with a rupture of the heart (external - with the 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).
When the heart is contused, pain is noted behind the sternum or in the region of the heart (often very intense), rhythm disturbances, dullness of heart sounds, gallop rhythm, systolic murmur, and hypotension are recorded.
The ECG reveals changes in the T wave, ST segment displacement, rhythm and conduction disturbances.
Traumatic myocardial infarction causes a severe anginal attack, rhythm disturbances, and is often the cause of cardiogenic shock; ECG dynamics are 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 due to electrical trauma: the most common cause of shock in such cases is rhythm and conduction disturbances.

Complications

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

Treatment abroad

Cardiogenic shock is a severe condition of the cardiovascular system, with mortality rates reaching 50–90%.

Cardiogenic shock is an extreme degree of circulatory impairment with a sharp decrease in the contractility of the heart and a significant drop in blood pressure, leading to disorders of the nervous system and kidneys.

Simply put, this is the inability of the heart to pump blood and push it into the vessels. The vessels are not able to hold blood because they are in an expanded state, as a result of which blood pressure drops and blood does not reach the brain. The brain experiences severe oxygen starvation and “turns off,” and the person loses consciousness and, in most cases, dies.

Causes of cardiogenic shock (KS)

1. Extensive (transmural) myocardial infarction (when more than 40% of the myocardium is damaged and the heart cannot adequately contract and pump blood).

2. Acute myocarditis (inflammation of the heart muscle).

3. Rupture of the interventricular septum (IVS). The IVS is a septum that separates the right ventricle of the heart from the left.

4. Cardiac arrhythmias (heart rhythm disturbances).

5. Acute insufficiency (dilation) of heart valves.

6. Acute stenosis (narrowing) of the heart valves.

7. Massive PE (pulmonary embolism) – complete occlusion of the lumen of the pulmonary artery trunk, as a result of which blood circulation is not possible.

Types of cardiogenic shock (CS)

1. Disorder of the pumping function of the heart.

This occurs against the background of an extensive myocardial infarction, when more than 40% of the area of ​​the heart muscle is damaged, which directly contracts the heart and pushes blood out of it into the vessels to ensure blood supply to other organs of the body.

With extensive damage, the myocardium loses the ability to contract, blood pressure drops and the brain does not receive nutrition (blood), as a result of which the patient loses consciousness. With low blood pressure, blood also does not flow to the kidneys, resulting in impaired production and urinary retention.

The body abruptly stops its work and death occurs.

2. Severe heart rhythm disturbances

Against the background of myocardial damage, the contractile function of the heart decreases and the coherence of the heart rhythm is disrupted - arrhythmia occurs, which leads to a decrease in blood pressure, impaired blood circulation between the heart and brain, and subsequently the same symptoms develop as in point 1.

3. Ventricular tamponade

When the interventricular septum (the wall that separates the right ventricle of the heart from the left ventricle of the heart) ruptures, the blood in the ventricles mixes and the heart, “choking” with its own blood, cannot contract and push blood out of itself into the vessels.

After this, the changes described in paragraphs 1 and 2 occur.

4. Cardiogenic shock due to massive pulmonary embolism (PE).

This is a condition when a blood clot completely blocks the lumen of the pulmonary artery trunk and blood cannot flow to the left side of the heart, so that the heart contracts and pushes blood into the vessels.

As a result, blood pressure sharply decreases, oxygen starvation of all organs increases, their work is disrupted and death occurs.

Clinical manifestations (symptoms and signs) of cardiogenic shock

A sharp decrease in blood pressure below 90/60 mm Hg. Art (usually 50/20mm Hg).

Loss of consciousness.

Coldness of the extremities.

The veins in the extremities collapse. They lose tone as a result of a sharp decrease in blood pressure.

Risk factors for cardiogenic shock (CS)

Patients with extensive and deep (transmural) myocardial infarction (infarction area more than 40% of the myocardial area).

Repeated myocardial infarction with cardiac arrhythmia.

Diabetes.

Elderly age.

Poisoning with cardiotoxic substances resulting in a decrease in myocardial contractile function.

Diagnosis of cardiogenic shock (CS)

The main sign of cardiogenic shock is a sharp decrease in systolic “upper” blood pressure below 90 mm Hg. Art (usually 50 mm Hg and below), which leads to the following clinical manifestations:

Loss of consciousness.

Coldness of the extremities.

Tachycardia (increased heart rate).

Pale (bluish, marbled, speckled) and moist skin.

Collapsed veins on the limbs.

Impaired diuresis (urine excretion), with a decrease in blood pressure below 50/0 - 30/0 mm Hg. the kidneys stop working.

If there is a question about surgical treatment aimed at eliminating the causes of shock, the following is carried out:

ECG(electrocardiogram), to determine focal changes in the myocardium (myocardial infarction). Its stage, localization (in which part of the left ventricle the infarction occurred), depth and extent.

ECHOCG (ultrasound) heart, this method allows you to evaluate the contractility of the myocardium, the ejection fraction (the amount of blood ejected by the heart into the aorta), and determine which part of the heart was more affected by a heart attack.

Angiography is an X-ray contrast method for diagnosing vascular diseases. In this case, a contrast agent is injected into the femoral artery, which, entering the blood, stains the vessels and outlines the defect.

Angiography is performed directly when it is possible to use surgical techniques aimed at eliminating the cause of cardiogenic shock and increasing myocardial contractility.

Treatment of cardiogenic shock (CS)

Treatment of cardiogenic shock is carried out in an intensive care unit. The main goal of providing assistance is to increase blood pressure to 90/60 mmHg in order to improve the contractile function of the heart and provide vital organs with blood for their further functioning.

Drug treatment of cardiogenic shock (CS)

The patient is placed horizontally with his legs elevated in order to ensure possible blood supply to the brain.

Oxygen therapy – inhalation (inhalation of oxygen using a mask). This is done in order to reduce oxygen starvation of the brain.

In case of severe pain, narcotic analgesics (morphine, promedol) are administered intravenously.

To stabilize blood pressure, a Reopoliglucin solution is administered intravenously - this drug improves blood circulation, prevents increased blood clotting and the formation of blood clots; for the same purpose, heparin solutions are administered intravenously.

A solution of glucose with insulin, potassium and magnesium is administered intravenously (drip) to improve the “nutrition” of the heart muscle.

Solutions of Adrenaline, Norepinephrine, Dopamine or Dobutamine are administered intravenously, because they can increase the force of heart contractions, increase blood pressure, dilate the renal arteries and improve blood circulation in the kidneys.

Treatment of cardiogenic shock is carried out under constant monitoring (control) of vital organs. For this, a cardiac monitor is used, blood pressure and heart rate are monitored, and a urinary catheter is installed (to control the amount of urine excreted).

Surgical treatment of cardiogenic shock (CS)

Surgical treatment is carried out in the presence of special equipment and when drug therapy for cardiogenic shock is ineffective.

1. Percutaneous transluminal coronary angioplasty

This is a procedure for restoring the patency of the coronary (heart) arteries in the first 8 hours from the onset of myocardial infarction. With its help, the heart muscle is preserved, its contractility is restored and all manifestations of cardiogenic shock are interrupted.

But! This procedure is effective only in the first 8 hours from the onset of a heart attack.

2. Intra-aortic balloon counterpulsation

This is a mechanical injection of blood into the aorta using a specially inflated balloon during diastole (relaxation of the heart). This procedure increases blood flow in the coronary (heart) vessels.

All information on the site is provided for informational purposes only and cannot be taken as a guide to self-medication.

Treatment of diseases of the cardiovascular system requires consultation with a cardiologist, a thorough examination, prescription of appropriate treatment and subsequent monitoring of the therapy.

Cardiogenic shock

Cardiogenic shock is acute left ventricular failure of extreme severity, developing during myocardial infarction. The decrease in stroke and minute blood volume during shock is so pronounced that it is not compensated by an increase in vascular resistance, as a result of which blood pressure and systemic blood flow sharply decrease, and the blood supply to all vital organs is disrupted.

Cardiogenic shock most often develops during the first hours after the onset of clinical signs of myocardial infarction and much less often in a later period.

There are three forms of cardiogenic shock: reflex, true cardiogenic and arrhythmic.

Reflex shock (collapse) is the mildest form and, as a rule, is caused not by severe myocardial damage, but by a decrease in blood pressure in response to severe pain that occurs during a heart attack. With timely relief of pain, the course of pain is benign, blood pressure rises quickly, however, in the absence of adequate treatment, a transition from reflex shock to true cardiogenic shock is possible.

True cardiogenic shock usually occurs with extensive myocardial infarction. It is caused by a sharp decrease in the pumping function of the left ventricle. If the mass of necrotic myocardium is 40 - 50% or more, then areactive cardiogenic shock develops, in which the introduction of sympathomimetic amines has no effect. Mortality in this group of patients approaches 100%.

Cardiogenic shock leads to profound disturbances in the blood supply to all organs and tissues, causing microcirculation disorders and the formation of microthrombi (DIC syndrome). As a result, brain functions are disrupted, acute renal and liver failure develop, and acute trophic ulcers can form in the digestive canal. Circulatory disorders are aggravated by poor oxygenation of blood in the lungs due to a sharp decrease in pulmonary blood flow and shunting of blood in the pulmonary circulation, and metabolic acidosis develops.

A characteristic feature of cardiogenic shock is the formation of a so-called vicious circle. It is known that when systolic pressure in the aorta is below 80 mm Hg. coronary perfusion becomes ineffective. A decrease in blood pressure sharply worsens coronary blood flow, leads to an increase in the area of ​​myocardial necrosis, further deterioration of the pumping function of the left ventricle and worsening shock.

Arrhythmic shock (collapse) develops as a result of paroxysmal tachycardia (usually ventricular) or acute bradyarrhythmia against the background of complete atrioventricular block. Hemodynamic disturbances in this form of shock are caused by changes in the frequency of ventricular contraction. After normalization of the heart rhythm, the pumping function of the left ventricle is usually quickly restored and the symptoms of shock disappear.

The generally accepted criteria on the basis of which cardiogenic shock is diagnosed during myocardial infarction are low systolic (80 mm Hg) and pulse pressure (20-25 mm Hg), oliguria (less than 20 ml). In addition, the presence of peripheral signs is very important: pallor, cold sticky sweat, cold extremities. Superficial veins collapse, the pulse on the radial arteries is threadlike, the nail beds are pale, and cyanosis of the mucous membranes is observed. Consciousness is usually confused, and the patient is not able to adequately assess the severity of his condition.

Treatment of cardiogenic shock. Cardiogenic shock is a serious complication myocardial infarction. mortality rate reaches 80% or more. Its treatment is a complex task and includes a set of measures aimed at protecting the ischemic myocardium and restoring its functions, eliminating microcirculatory disorders, and compensating for impaired functions of parenchymal organs. The effectiveness of treatment measures largely depends on the time of their initiation. Early treatment of cardiogenic shock is the key to success. The main task that needs to be solved as soon as possible is to stabilize blood pressure at a level that ensures adequate perfusion of vital organs (90-100 mmHg).

The sequence of treatment measures for cardiogenic shock:

Relief of pain syndrome. Since the intense pain syndrome that occurs during myocardial infarction. is one of the reasons for lowering blood pressure, all measures must be taken to quickly and completely relieve it. The most effective use of neuroleptanalgesia.

Normalization of heart rhythm. Stabilization of hemodynamics is impossible without eliminating cardiac arrhythmias, since an acute attack of tachycardia or bradycardia in conditions of myocardial ischemia leads to a sharp decrease in stroke and cardiac output. The most effective and safe way to relieve tachycardia with low blood pressure is electrical pulse therapy. If the situation allows for drug treatment, the choice of antiarrhythmic drug depends on the type of arrhythmia. For bradycardia, which is usually caused by acute atrioventricular block, almost the only effective remedy is endocardial pacing. Injections of atropine sulfate most often do not provide a significant and lasting effect.

Strengthening the inotronic function of the myocardium. If, after eliminating the pain syndrome and normalizing the frequency of ventricular contraction, blood pressure does not stabilize, then this indicates the development of true cardiogenic shock. In this situation, it is necessary to increase the contractile activity of the left ventricle, stimulating the remaining viable myocardium. For this purpose, sympathomimetic amines are used: dopamine (Dopamine) and dobutamine (Dobutrex), which selectively act on beta-1 adrenergic receptors of the heart. Dopamine is administered intravenously. To do this, 200 mg (1 ampoule) of the drug is diluted in 250-500 ml of 5% glucose solution. The dose in each specific case is selected empirically depending on the dynamics of blood pressure. Usually start with 2-5 mcg/kg per 1 min (5-10 drops per 1 min), gradually increasing the rate of administration until systolic blood pressure stabilizes at 100-110 mm Hg. Dobutrex is available in 25 ml bottles containing 250 mg of dobutamine hydrochloride in lyophilized form. Before use, the dry substance in the bottle is dissolved by adding 10 ml of solvent, and then diluted in 250-500 ml of 5% glucose solution. Intravenous infusion is started with a dose of 5 mcg/kg per 1 minute, increasing it until a clinical effect appears. The optimal rate of administration is selected individually. It rarely exceeds 40 mcg/kg per minute; the effect of the drug begins 1-2 minutes after administration and ceases very quickly after its completion due to its short (2 min) half-life.

Cardiogenic shock: occurrence and symptoms, diagnosis, therapy, prognosis

Perhaps the most common and serious complication of myocardial infarction (MI) is cardiogenic shock, which includes several types. A sudden serious condition ends in death in 90% of cases. The patient has the prospect of living longer only when, at the time of the development of the disease, he is in the hands of a doctor. Or better yet, an entire resuscitation team that has in its arsenal all the necessary medications, equipment and devices to return a person from the “other world.” However even with all these means, the chances of salvation are very small. But hope dies last, so doctors fight to the last for the patient’s life and in other cases achieve the desired success.

Cardiogenic shock and its causes

Cardiogenic shock, manifested acute arterial hypotension. which sometimes reaches an extreme degree, is a complex, often uncontrollable condition that develops as a result of “low cardiac output syndrome” (this is how acute failure of myocardial contractile function is characterized).

The most unpredictable period of time in terms of the occurrence of complications of acute widespread myocardial infarction is the first hours of the disease, because it is then that at any moment myocardial infarction can turn into cardiogenic shock, which usually occurs accompanied by the following clinical symptoms:

• Disorders of microcirculation and central hemodynamics;
• Acid-base imbalance;
• Shift in the water-electrolyte state of the body;
• Changes in neurohumoral and neuro-reflex regulatory mechanisms;
• Cellular metabolic disorders.

In addition to the occurrence of cardiogenic shock during myocardial infarction, there are other reasons for the development of this terrible condition, which include:

Figure: causes of cardiogenic shock in percentage terms

Forms of cardiogenic shock

The classification of cardiogenic shock is based on the identification of degrees of severity (I, II, III - depending on the clinic, heart rate, blood pressure level, diuresis, duration of shock) and types of hypotensive syndrome, which can be presented as follows:

• Reflex shock(hypotension-bradycardia syndrome), which develops against the background of severe pain, is not considered by some experts to actually be shock, since it easily docked effective methods, and the basis for the drop in blood pressure is reflex influence of the affected area of ​​the myocardium;
• Arrhythmic shock. in which arterial hypotension is caused by low cardiac output and is associated with brady- or tachyarrhythmia. Arrhythmic shock is presented in two forms: the predominant tachysystolic and especially unfavorable - bradysystolic, which occurs against the background of atrioventricular block (AV) in the early period of MI;
• True cardiogenic shock. giving a mortality rate of about 100%, since the mechanisms of its development lead to irreversible changes incompatible with life;
• Areactive shock in pathogenesis it is analogous to true cardiogenic shock, but differs somewhat in the greater severity of pathogenetic factors, and, consequently, special severity of the course ;
• Shock due to myocardial rupture. which is accompanied by a reflex drop in blood pressure, cardiac tamponade (blood pours into the pericardial cavity and creates obstacles to heart contractions), overload of the left chambers of the heart and a decrease in the contractile function of the heart muscle.

pathologies - causes of development of cardiogenic shock and their localization

Thus, we can identify the generally accepted clinical criteria for shock during myocardial infarction and present them in the following form:

1. Decrease in systolic blood pressure below the permissible level of 80 mm Hg. Art. (for those suffering from arterial hypertension – below 90 mm Hg);
2. Diuresis less than 20 ml/h (oliguria);
3. Paleness of the skin;
4. Loss of consciousness.

However, the severity of the condition of a patient who has developed cardiogenic shock can be judged more by the duration of shock and the patient's response to the administration of pressor amines than by the level of arterial hypotension. If the duration of the shock state exceeds 5-6 hours, is not relieved by medications, and the shock itself is combined with arrhythmias and pulmonary edema, such shock is called areactive .

Pathogenetic mechanisms of cardiogenic shock

The leading role in the pathogenesis of cardiogenic shock belongs to a decrease in the contractility of the heart muscle and reflex influences from the affected area. The sequence of changes in the left section can be represented as follows:

• Reduced systolic output involves a cascade of adaptive and compensatory mechanisms;
• Increased production of catecholamines leads to generalized vasoconstriction, especially arterial ones;
• Generalized spasm of arterioles, in turn, causes an increase in total peripheral resistance and promotes centralization of blood flow;
• Centralization of blood flow creates conditions for an increase in the volume of circulating blood in the pulmonary circulation and puts additional stress on the left ventricle, causing its damage;
• Increased end-diastolic pressure in the left ventricle leads to the development left ventricular heart failure .

The microcirculation pool during cardiogenic shock also undergoes significant changes due to arteriole-venous shunting:

1. The capillary bed becomes depleted;
2. Metabolic acidosis develops;
3. There are pronounced dystrophic, necrobiotic and necrotic changes in tissues and organs (necrosis in the liver and kidneys);
4. The permeability of capillaries increases, due to which there is a massive release of plasma from the bloodstream (plasmorrhagia), the volume of which in the circulating blood naturally decreases;
5. Plasmorrhages lead to an increase in hematocrit (the ratio between plasma and red blood) and a decrease in blood flow to the cardiac cavities;
6. Blood filling of the coronary arteries decreases.

Events occurring in the microcirculation zone inevitably lead to the formation of new areas of ischemia with the development of dystrophic and necrotic processes in them.

Cardiogenic shock, as a rule, has a rapid course and quickly affects the entire body. Due to disorders of erythrocyte and platelet homeostasis, microcoagulation of blood begins in other organs:

• In the kidneys with the development of anuria and acute renal failure- eventually;
• In the lungs with the formation respiratory distress syndrome(pulmonary edema);
• In the brain with its swelling and development cerebral coma .

As a result of these circumstances, fibrin begins to be consumed, which goes to the formation of microthrombi that form DIC syndrome(disseminated intravascular coagulation) and leading to bleeding (usually in the gastrointestinal tract).

Thus, the combination of pathogenetic mechanisms leads to a state of cardiogenic shock to irreversible consequences.

Treatment of cardiogenic shock should be not only pathogenetic, but also symptomatic:

• For pulmonary edema, nitroglycerin, diuretics, adequate pain relief, and alcohol are prescribed to prevent the formation of foamy fluid in the lungs;
• Severe pain is relieved with promedol, morphine, fentanyl with droperidol.

Urgent hospitalization under constant supervision in the intensive care unit, bypassing the emergency room! Of course, if it was possible to stabilize the patient’s condition (systolic pressure 90-100 mm Hg).

Prognosis and life chances

Against the background of even a short-term cardiogenic shock, other complications can rapidly develop in the form of rhythm disturbances (tachy- and bradyarrhythmias), thrombosis of large arterial vessels, infarctions of the lungs, spleen, skin necrosis, and hemorrhages.

Depending on how the blood pressure decreases, how pronounced the signs of peripheral disorders are, what reaction the patient’s body has to therapeutic measures, it is customary to distinguish between moderate and severe cardiogenic shock, which is designated in the classification as areactive. A mild degree for such a serious disease, in general, is somehow not provided for.

However even in the case of a shock of moderate severity, there is no need to delude yourself especially. Some positive response of the body to therapeutic effects and an encouraging increase in blood pressure to 80-90 mm Hg. Art. can quickly give way to the opposite picture: against the background of increasing peripheral manifestations, blood pressure begins to fall again.

Patients with severe cardiogenic shock have virtually no chance of survival. since they absolutely do not respond to therapeutic measures, therefore the vast majority (about 70%) die on the first day of the disease (usually within 4-6 hours from the moment shock occurs). Some patients can survive for 2-3 days, and then death occurs. Only 10 out of 100 patients manage to overcome this condition and survive. But only a few are destined to truly defeat this terrible disease, since some of those who return from the “other world” soon die from heart failure.

Graph: survival after cardiogenic shock in Europe

Below are statistics collected by Swiss doctors on patients who suffered a myocardial infarction with acute coronary syndrome (ACS) and cardiogenic shock. As can be seen from the graph, European doctors managed to reduce the mortality rate of patients

up to 50%. As mentioned above, in Russia and the CIS these figures are even more pessimistic.

6395 0

Cardiogenic shock is a clinical syndrome characterized by disturbances of central hemodynamics and microcirculation, pathology of water-electrolyte and acid-base composition, changes in neuro-reflex and neurohumoral regulatory mechanisms and cellular metabolism, resulting from acute failure of the 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 its muscle mass is turned off. As a result of disturbances in coronary circulation, akinesia occurs in the area of ​​myocardial infarction and hypokinesia in the peri-infarction zone, the volume of the cavity of the left ventricle increases, the tension of its wall increases and the myocardial need for oxygen increases.

The combination of a hemodynamically ineffective systole, deterioration in the elasticity of the damaged area of ​​the myocardium and a shortening of the isovolumic contraction phase 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 increased tension in the wall of the left ventricle) 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, as well as hormonal changes caused by the stress response increase the myocardial oxygen demand.

During the acute period of the disease, the pathogenesis of heart failure includes three components, the severity of which may vary: one component is associated with previous changes in the heart and is the most static; the other, depending on the mass of the muscle excluded from 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. In this case, disturbances of peripheral circulation occur at the level of arterioles, precapillaries, capillaries and venules, i.e. disturbances of the microcirculatory bed. The latter are conventionally divided into two groups: vasomotor and intravascular (rheological).

Systemic spasm of arterioles and precapillary sphincters leads to the passage 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, some of which is turned off from the blood circulation, the hydrostatic pressure in them increases, which stimulates the transudation of fluid into the surrounding tissues: the volume of circulating blood decreases.

In parallel with the described changes, disturbances in the rheological properties of blood occur. They are caused primarily by 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 cardiac output and deterioration in tissue perfusion; 2) deepening oxygen starvation of tissues due to exclusion of red blood cells from circulation; 3) mechanical microcirculatory block.

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

There are IV stages of microcirculation disorders in cardiogenic shock

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

As a result, a stage of decompensation occurs, when systemic circulation and microcirculation lose coordination, irreversible changes in general and organ circulation develop (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. Decrease in systolic pressure to 80 mm Hg. Art. is a diagnostic criterion for shock. With areactive shock, central venous pressure also decreases. Thus, in the development of cardiogenic shock in patients with acute myocardial infarction, 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 adaptation and stress reactions.

In this case, the rapid pace and progressive nature of these changes are of great importance. A decrease in blood pressure and cardiac output aggravates disturbances in coronary blood flow and microcirculation disorders, leading to oxygen starvation and irreversible changes in metabolism in the kidneys, liver, lungs, and central nervous system.

We must keep in mind the fact that cardiogenic shock can also develop with a relatively small myocardial infarction if:

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

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, the common pathogenetic factor contributing to the occurrence of shock is a sharp decrease in cardiac output.

Diagnostic criteria for cardiogenic shock

Currently, domestic and foreign authors include the following as the main criteria for cardiogenic shock.

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

Some experts admit the possibility of shock in patients with hypertension when blood pressure decreases to normal levels.

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

3. Peripheral symptoms of shock: decreased temperature and pallor of the 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) blood pressure indicators.

Classification of types of cardiogenic shock

Cardiogenic: shock can be coronarogenic (shock during myocardial infarction) and non-coronarogenic (with dissecting aortic aneurysm, cardiac tamponade of various etiologies, pulmonary embolism, closed cardiac injury, myocarditis, etc.).

There is no uniform classification of cardiogenic shock during 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 due to 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 classification of cardiogenic shock is divided into three degrees: relatively mild (I degree), moderate severity (II degree) and extremely severe (III degree).

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

Reflex shock occurs more often in patients with primary myocardial infarction localized on the posterior wall of the left ventricle (more often in men than in women). Arrhythmias (extrasystole, paroxysmal atrial fibrillation) are often observed; 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 based primarily not on a violation of the contractile function of the myocardium, but on a drop in vascular tone caused by 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. In tachysystolic shock, insufficient diastolic filling and the associated decrease in stroke and cardiac output are of greatest importance. 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 relief of tachysystole, as a rule, leads to restoration of hemodynamics and reverse development of signs of shock. However, mortality in this group of patients is higher than in uncomplicated myocardial infarction; The cause of death is usually heart failure (usually left ventricular failure). According to Echo CG, with ventricular tachycardia, the affected area is 35%, hypokinesia - 45%; with supraventricular tachyarrhythmias, the affected area is 20%, hypokinesia is 55%.

In bradysystolic shock, the drop in cardiac output is due to the fact that the increase in stroke volume does not compensate for the decrease in cardiac index associated with a decrease in the heart rate. Develops more often with repeated myocardial infarctions. The most common causes of bradysystolic shock are II-III degree atrioventricular blockades, junctional rhythm, and Frederick's syndrome.

It usually occurs 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 myocardial contractile function (with complete AV block, according to echocardiographic data, the affected area reaches 50%, and the hypokinesia zone reaches 30% of the left ventricle).

True cardiogenic shock

The diagnosis of true cardiogenic shock during myocardial infarction is established in cases where exposure to extracardiac causes of persistent hypotension and decreased cardiac output does not lead to the disappearance of signs of shock. This is the most severe, prognostically unfavorable complication of myocardial infarction (mortality reaches 75-90%). Occurs in 10-15% of patients with myocardial infarction; develops when 40-50% of the left ventricular myocardium is affected, in most cases in the first hours of the disease and less often - at a later date (after a few days).

The first clinical signs can be detected before a significant decrease in blood pressure. These are tachycardia, decreased pulse pressure, and inadequate reactions to the administration of vasoconstrictors or beta blockers. A detailed picture of true cardiogenic shock includes: persistent arterial hypotension (systolic blood pressure 80 mm Hg and below, 90 mm Hg in patients with hypertension), a decrease in pulse pressure (up to 20 mm Hg and below), tachycardia (110 beats/min or more, if there is no AV block), oliguria (30 ml/h or less), peripheral hemodynamic disorders (cold, moist, pale bluish or marbled skin), lethargy, blackout (they may be preceded by short-term excitement), dyspnea.

To assess the severity of shock, its signs are considered, such as duration, blood pressure response to the administration of vasoconstrictors (if blood pressure does not increase within 15 minutes after the administration of norepinephrine, a non-reactive course of shock is possible), the presence of oliguria and blood pressure.

Cardiogenic shock often complicates the course of repeated infarctions in elderly people.

Most patients experience a pronounced pre-infarction period: unstable angina, worsening heart failure, short-term loss of consciousness: its average duration reaches 7-8 days. The clinical picture of myocardial infarction is characterized, as a rule, by a pronounced pain syndrome and the early appearance of signs of circulatory disorders, which reflects the massiveness and rapid rate of ischemia and necrosis of the left ventricular myocardium.

Some authors have proposed dividing cardiogenic shock into three degrees of severity: relatively mild (grade I), moderate (grade II) and extremely severe (grade III). Isolating a mild form of shock is hardly justified, even if we include it as a reflex shock.

A number of experts distinguish cardiogenic shock with a slow, prolonged myocardial rupture. The following clinical features of shock during myocardial rupture are noted: 1) later appearance of signs of shock compared to true cardiogenic shock; 2) the suddenness of its development (sudden development of 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 breathing disorders, bradycardia); 3) two-stage development (the appearance of short-term hypotension at the prehospital stage, a detailed picture of shock at the hospital stage).

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

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

Internal ruptures complicate the course of myocardial infarction much less frequently than external ones.

Interventricular septal rupture 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. Localized in the muscular part of the interventricular septum, closer to the apex of the heart. The clinic is characterized by the appearance of sharp pain in the heart area, accompanied by fainting, followed by the development of a picture of cardiogenic shock.

Systolic trembling and rough systolic murmur appear with maximum intensity in the third to fifth intercostal space, on the left at the sternum; this noise spreads well to the interscapular, left axillary region, as well as to the right of the sternum, to the anterior axillary line. Then (if the patient has survived the moment of rupture), severe pain occurs in the right hypochondrium due to liver swelling, and signs of acute right ventricular failure develop.

The appearance and increase of jaundice is considered a bad prognostic sign. The ECG often shows bundle branch blocks and signs of overload in the right ventricle, right and left atria. The prognosis in most cases is unfavorable (if the patient does not undergo surgical treatment).

Rupture of the papillary muscles occurs no more often than in 1% of cases of myocardial infarction. Clinically, there is a resumption of pain, followed by pulmonary edema and cardiogenic shock. Characteristic is a rough systolic murmur (often a chordal squeak) in the apical region, spreading to the axillary region. In some cases, the chordae tendineae are torn off together with the heads of the papillary muscles; in others, a rupture of the body of the papillary muscle occurs.

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

B.G. Apanasenko, A.N. Nagnibeda

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, the 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, decreased blood pressure, loss of consciousness and serious disturbances in the blood circulation of vital organs and systems.

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

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

• acute valvular insufficiency;
• acute stenosis of heart valves;
• myxoma of the heart;
• severe forms;
• septic shock, causing dysfunction of the heart muscle;
• rupture of the interventricular septum;
• heart rhythm disturbances;
• ventricular wall rupture;
• compressive;
• 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 impairment of myocardial contractile function. 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 myocardial infarction), the heart cannot pump the required volume of blood, and this causes severe hypotension. The brain and kidneys experience hypoxia, causing the patient to lose consciousness and experience urinary retention. Cardiogenic shock can occur when 40-50% of the myocardial area is affected. Tissues, organs and systems abruptly stop functioning, DIC syndrome develops and death occurs.
2. Arrhythmic shock (tachysystolic and bradysystolic). This form of shock develops with paroxysmal tachycardia or complete atrioventricular block with acute bradycardia. Hemodynamic disturbances occur against the background of a disturbance in the frequency of ventricular contraction and a decrease in blood pressure to 80-90/20-25 mm. rt. Art.
3. Cardiogenic shock due to cardiac tamponade. This form of shock occurs when the septum between the ventricles is ruptured. The blood in the ventricles mixes and the heart loses its ability to contract. As a result, blood pressure decreases significantly, hypoxia in tissues and organs increases and leads to disruption 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’s death occurs.

Cardiologists distinguish four forms of cardiogenic shock:

1. True: accompanied by impaired contractile function of the heart muscle, microcirculatory disorders, metabolic shifts and decreased diuresis. May be complicated by severe (cardiac asthma and pulmonary edema).
2. Reflex: caused by the reflex effect of pain on myocardial function. Accompanied by a significant decrease in blood pressure, vasodilation and sinus bradycardia. There are no microcirculatory or metabolic disorders.
3. Arrhythmic: develops with severe brady- or tachyarrhythmia and is eliminated after the elimination of arrhythmic disorders.
4. Areactive: occurs quickly and severely, even intensive therapy for this condition often has no effect.

Symptoms

In the first 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 fear;
• in case of heart rhythm disturbances - interruptions in the functioning of the heart, pain in the heart area;
• with pulmonary embolism - severe shortness of breath.

As a result of a decrease in 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 scalp, 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.

The severity of cardiogenic shock can be determined by blood pressure, duration of shock, 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., mild or absent 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 shock state is about 5-10 hours, blood pressure decreases 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 – prolonged shock reaction, blood pressure drops to 20 mm. rt. Art. or not determined, signs of heart failure and peripheral shock reactions are pronounced, pulmonary edema is observed in 70% of patients.

Diagnostics

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

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

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

• Echo-CG;
• angiography.

Urgent Care

If the first signs of cardiogenic shock appear 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, legs raised and ensure peace and fresh air.

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

During drug therapy, to continuously monitor the functions of vital organs, the patient is given a urinary catheter and connected to cardiac monitors that record heart rate and blood pressure.

If it is possible to use specialized equipment and the ineffectiveness of drug therapy to provide emergency care to a patient with cardiogenic shock, the following surgical techniques may be prescribed:

• intra-aortic balloon counterpulsation: to increase coronary blood flow during diastole, blood is pumped into the aorta using a special balloon;
• percutaneous transluminal coronary angioplasty: through a 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.