Version: MedElement Disease Directory

Cardiogenic shock (R57.0)

Cardiology

General information

Brief description

Cardiogenic shock- This acute disorder perfusion 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 clinical manifestations, response to ongoing activities, hemodynamic parameters, there are 3 degrees of severity of cardiogenic shock.

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 acute cardiac left ventricular failure, in 20% of patients - pulmonary edema	Severe course heart failure, rapid pulmonary edema
Pressor reaction to therapeutic measures	Fast (30-60 min.), sustainable	Slow, unstable, peripheral signs shocks recur within 24 hours	Unstable, short-term, often absent altogether (unresponsive state)
Diuresis, ml/h	Reduced to 20	<20	0
Magnitude cardiac index l/min/m²	Reduce to 1.8	1,8-1,5	1.5 and below
**Sealing pressure V pulmonary artery, mmHg 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 violation heart rate;
- 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 with 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 cardiogenic shock most often develops due to paroxysmal ventricular tachycardia, paroxysm of 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./m2, 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 arterial hypotensionArterial 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 cupping pain syndrome, 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.Biochemical blood test:
- 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 in pleural cavity. Then, after the onset of chest and back pain (often very intense), signs develop due to increasing anemia: pale 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 scurvature, 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 heart rupture (external - with clinical picture 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.

Medical tourism

Emergency care for arrhythmogenic shock

Arrhythmogenic shock

Arrhythmogenic shock is a type of circulatory disorder in which adequate blood supply to organs and tissues is impaired due to an imbalance in the heart rate. Most often, arrhythmogenic shock can develop against the background of ventricular tachycardia, bradyarrhythmia (complete SA or AV block).

Clinical signs arrhythmogenic shock:

· decrease in blood pressure (systolic blood pressure - GARDEN below 90 mmHg Art.) lasting for at least 30 minutes

· cold damp skin, cold sweat – (caused by a sharp spasm of skin vessels, a positive symptom of a “pale spot” for more than 2 seconds)

· lethargy, lethargy (due to cerebral hypoxia)

· oliguria (decreased diuresis) – less than 20 ml/h (associated with impaired renal blood flow)

create a lying position, ensure peace

· inhalation of humidified oxygen

Peripheral vein catheterization

· specific treatment:

A) with SBP< 90 мм рт. ст, ЧСС >150 per minute

ü EIT (cm. electropulse therapy )

B)with SBP< 90 мм рт. ст., ЧСС < 50 в минуту

ü atropine 0.1%, 1-6 ml per 10 ml saline. solution (total dose of atropine 3 mg)

ü in the absence of effect - aminophylline 2.4% 10 ml per 10 ml saline. IV solution

ü in the absence of effect - inotropic support: intravenous drip dopamine 200 mg per 200 ml saline. solution at a speed of 8-10 drops per minute or adrenalin 0.1% 1 ml per 200 ml saline. solution intravenously drip

· hospitalization in a specialized cardiac surgery hospital, cardiac intensive care unit with continued respiratory support during transportation.

Characterized by the occurrence seizures sudden loss consciousness with convulsions, pallor, alternating with cyanosis and breathing problems. During an attack, blood pressure is not determined and heart sounds are usually not audible. MAS attacks occur as a result of cerebral ischemia with a sudden decrease in cardiac output caused by cardiac arrhythmias or a decrease in heart rate.

Most often it is caused various forms atrioventricular blockades. In most cases, a seizure occurs when heart rate becomes less than 30 beats per minute. The cause of a seizure can be not only excessively rare, but also excessively rapid rate of contractions of the ventricles of the heart, usually more than 200 beats per minute. Arrhythmias with such a high heart rate usually occur when the patient has additional pathways between the atria and ventricles (syndromeWРW) . Finally, sometimes the development of an attack results from the complete loss of contractile function of the ventricles of the heart due to their fibrillation or asystole.

The attack comes suddenly. The patient experiences severe dizziness, darkening of the eyes, and weakness; he turns pale and after a few seconds loses consciousness. After about half a minute, generalized epileptiform convulsions appear, and involuntary urination and defecation often occur. After about another half a minute, breathing usually stops, which may be preceded by respiratory arrhythmia, and severe cyanosis develops. The pulse during an attack is usually not detected. It is not possible to measure blood pressure. After the pumping function of the heart is restored, the patient quickly regains consciousness, but most often he does not remember the attack and the sensations that preceded it (retrograde amnesia).

When the syndrome is first identified, even if this diagnosis is presumptive, hospitalization is indicated. medical institution cardiological profile to clarify the diagnosis and select therapy.

Arrhythmogenic shock is a type of circulatory disorder in which adequate blood supply to organs and tissues is impaired due to an imbalance in the heart rate. Arrhythmia can be primary and secondary. Primary disorders include rhythm and conduction disorders caused by abnormalities in the development of the conduction system. Secondary arrhythmia is associated with cardiomyopathy, fibroslastosis, organic lesions and myocardial metabolic disorders, electrolyte disturbances. Based on the location of the pathological pacemaker, supraventricular (atrial and nodal) and ventricular arrhythmias are distinguished. There are also tachy- and bradyarrhythmia. Main pathogenetic mechanism tachyarrhythmic shock is a shortening of the diastolic filling time of the heart and a decrease in stroke output against the background of a reduction in the diastolic period of coronary blood flow.

In bradyarrhythmic shock, a decrease in cardiac output cannot be compensated by an increase in stroke output, since the volume of diastolic filling of the ventricles is limited by the ability of the myocardial wall to mechanical stretch.

A preliminary diagnosis of rhythm disturbance is established based on palpation of the pulse in the femoral or carotid arteries, cardiac auscultation and the presence of hypertension. Symptoms such as a sudden change in the child’s condition, anxiety or lethargy (blockade of the atrioventricular junction), loss of consciousness (Edams-Stokes syndrome), acrocyanosis, pallor of the skin, and “marbled” skin pattern can suggest arrhythmia. Accurate diagnosis established on the basis of ECG data.

Arrhythmogenic shock can develop against the background of excessive sinus, atrial and ventricular tachycardia, ventricular fibrillation, bradyarrhythmia (idioventricular rhythm, atrioventricular block II - III degree), ventricular extrasystoles.

Treatment of arrhythmogenic shock provides for emergency restoration of heart rhythm at a frequency that ensures adequate cardiac output. Required condition in the treatment of tachy- and bradyarrhythmic shock is the elimination of arrhythmogenic factors: negative influence vagus nerve, hypoxia, acidosis, alkalosis, electrolyte disturbances. Use antiarrhythmic drugs should be preceded by correction of hypo- and hypervolemia, anemia, hypoglycemia and mandatory atropinization at the rate of 0.01-0.03 mg/kg body weight. Priority remedy emergency therapy tachyarrhythmic shock is electrical depolarization (2 W/s per 1 kg of body weight), which allows you to gain time and select the optimal antiarrhythmic pharmacological agent. For supraventricular tachyarrhythmia, it is preferable to administer isoptin - 0.1 mg/kg over 1 minute. The same dose can be prescribed again at 15-minute intervals. Lidocaine is prescribed at a dose of 1 mg/kg and administered over 10 minutes. Mexitil is effective for ventricular tachyarrhythmia and extrasystole. The drug is administered at a dose of 5 mg/kg over 15 minutes, a maintenance dose of 5 - 20 mcg/kg per minute.

In case of bradyarrhythmic shock and there is no effect from the administration of atropine sulfate, the drug of choice is Isuprel (isoproterenol, isadrin, novodrin). If there is no effect from drug therapy, cardiac pacing is indicated.

All children are able arrhythmogenic shock hospitalized in the intensive care unit.

During development arrhythmogenic cardiogenic shock therapy is aimed at stopping rhythm disturbances and maintaining adequate blood pressure levels. For this purpose, a vein is punctured and sympathomimetics are started intravenously. The maximum adequate SBP is 110 mm Hg. Art. ( greater increase leads to an increase in the load on the myocardium, and a decrease in SBP to 100 mm Hg. Art. and below leads to a violation of the MCC).

With a purpose quick recovery rhythm in the presence of tachyarrhythmias that threaten the patient’s life, EIT is performed. It is dangerous to use AAP in this case, since they themselves sometimes lead to a decrease in myocardial contractility. If CABG is associated with cardiac arrhythmia, then, as a rule, within the next hour after the rhythm is restored, blood pressure itself returns to a satisfactory level. In case of arrhythmogenic CABG, the main task is to timely assess the threat of rhythm disturbance and promptly stop it.

During development true cardiogenic shock(as a result of impaired myocardial contractility) and a decrease in SVR, there is always a compensatory reaction from the vessels, leading to spasm. In CABG this reaction is so pronounced that it leads to disruption of the MCB. The introduction of vasopressors (dopamine, norepinephrine), which increase vascular tone, in this case is often unsuccessful: such therapy disrupts the MCB to a greater extent, which further increases the load on the myocardium. The main emphasis in the treatment of true CABG is on improving cardiac output and blood flow.

Because true cardiogenic shock develops in 99% of cases with MI, then the first thing to do is to relieve pain and restore normal blood flow through the blocked coronary artery(restore the function of the “hibernating” myocardium) through early systemic thrombolysis or PCCA. Thrombolysis relatively rarely leads to complete elimination of the thrombus that caused MI, but the administration of a fibrinolytic additionally leads to a decrease in the total thrombogenic potential of the blood, improvement in blood fluidity, MCB and the state of the intact myocardium.

With the prevalence in clinical picture of cardiogenic shock signs of pulmonary circulation overload (pulmonary artery wedge pressure more than 18 mm Hg and mean blood pressure less than 65 mm Hg) dopamine, dobutamine (which has similar inotropic, but weak chronotropic effects, can reduce afterload) is administered as initial therapy and norepinephrine. The choice of vasopressor depends on the severity of the MI and the patient's response. Thus, dopamine is usually used initially, which has little effect on heart rate (tachycardia may be useful for patients with bradycardia, but unfavorable for patients with MI).

Dopamine(having inotropic and vasoactive effects) increases cardiac output and blood pressure (with minimal magnification afterload) to an adequate level (average blood pressure should exceed 70 mm Hg) by reducing systemic hypotension through stimulation of adrenergic receptors - beta 1 (cardiac, increasing the contractility of the intact myocardium) and beta 2 (vasodilating and reducing OPS). Dopamine in small doses can increase renal blood flow.

Dopamine(40 ml of a 1% solution in 400 ml of rheopolyglucin) is first administered intravenously at a rate of 2.5-5-10 mcg/kg-min, necessary to control blood pressure and depending on which symptoms predominate: renal hypoperfusion or pulmonary congestion. If no effect is obtained (no increase in blood pressure), norepinephrine is administered intravenously (1-2 ml of 0.2% solution in 200-400 ml of 5% glucose solution) at an initial rate of 2 mcg/kg-min, then increasing it to 10- 20 mcg/kg-min to achieve a mean blood pressure of 70 mm Hg. Art.

For the same purpose you can use anticholinesterase medicines (amrinone, milrinone at an initial dose of 50 mcg/kg for 10 minutes, then at a rate of 0.375-0.75 mcg/kg-min), which quickly and significantly increase the contractility of the heart. When blood pressure rises to normal level(or subnormal), a combination of dopamine with peripheral vasodilators is justified, which further increases stroke volume and reduces LV filling pressure.

All vasopressors in large doses can cause ischemic vasoconstriction. The gastrointestinal mucosa and liver are especially sensitive to it (renal vasoconstriction appears only with very large doses of vasopressors). Severe hypotension (SBP less than 50 mm Hg) is associated with decreased pressure-dependent blood flow in the heart and brain (with subsequent myocardial depression and cerebral ischemia).

When dopamine, norepinephrine and rapid fluid infusion turned out to be ineffective in restoring perfusion, adrenaline (the drug of last choice) is used. If it does not give a positive effect (the patient is resistant to standard therapy), then they prescribe large doses GKS ( required component complex therapy KS).

Positive action of glucocorticosteroids is associated with an improvement in MCB, stabilization of lysosomal membranes, a decrease in the effect of catecholamines on vascular smooth muscle (reduction of OPS), and peripheral vasodilation. Prednisolone is administered (intravenous bolus at a dose of 90-150 mg) or solumedrol (30 mg/kg body weight, repeating injections every 4-6 hours for 48 hours), which can enhance the effect of catecholamines. GCS can also be useful in cases of the often concomitant complication of CABG - the development of adrenal insufficiency.

One of the most frequent and dangerous complications Myocardial infarction is cardiogenic shock. This complex condition patient, which in 90% of cases ends in death. To avoid this, it is important to correctly diagnose the condition and provide emergency assistance.

What is it and how often is it observed?

Extreme phase acute failure blood circulation is called cardiogenic shock. In this condition, the patient's heart does not perform main function– does not supply all organs and systems of the body with blood. Typically this is extremely dangerous result acute heart attack myocardium. At the same time, experts provide the following statistics:

• at 50% state of shock develops on days 1-2 of myocardial infarction, in 10% - at the prehospital stage, and in 90% - in the hospital;
• if myocardial infarction with a Q wave or ST segment elevation, a shock state is observed in 7% of cases, and after 5 hours from the onset of symptoms of the disease;
• if myocardial infarction is without a Q wave, a shock state develops in up to 3% of cases, and after 75 hours.

To reduce the likelihood of developing a shock state, thrombolytic therapy is performed, in which blood flow in the vessels is restored due to the lysis of the blood clot inside the vascular bed. Despite this, unfortunately, the probability of death is high - in-hospital mortality is observed in 58-73% of cases.

Reasons

There are two groups of causes that can lead to cardiogenic shock: internal (problems inside the heart) or external (problems in the vessels and membranes that envelop the heart). Let's look at each group separately:

Domestic

The following external causes can provoke cardiogenic shock:

• acute form myocardial infarction of the left stomach, which is characterized by long-term unrelieved pain and a large area of ​​necrosis, provoking the development of heart weakness;

If the ischemia extends to the right stomach, it leads to a significant worsening of shock.

• arrhythmia of paroxysmal types, which is characterized by high frequency impulses during gastric myocardial fibrillation;
• blockage of the heart due to the inability to conduct impulses that the sinus node should send to the stomach.

External

Row external reasons leading to cardiogenic shock looks like as follows:

• the pericardial sac (the cavity where the heart is located) is damaged or inflamed, which leads to compression of the heart muscle as a result of the accumulation of blood or inflammatory exudate;
• the lungs rupture and air enters the pleural cavity, which is called pneumothorax and leads to compression of the pericardial sac, and the consequences are the same as in the previously cited case;
• thromboembolism of the large trunk of the pulmonary artery develops, which leads to impaired circulation through the pulmonary artery, blockage of the right stomach and tissue oxygen deficiency.

Symptoms of cardiogenic shock

Signs indicating cardiogenic shock indicate impaired blood circulation and are externally manifested in the following ways:

• the skin turns pale, and the face and lips become grayish or bluish;
• cold, sticky sweat is released;
• observed pathologically low temperature– hypothermia;
• hands and feet become cold;
• Consciousness is disrupted or inhibited, and short-term excitation is possible.

Besides external manifestations, cardiogenic shock is characterized by the following clinical signs:

• Blood pressure decreases critically: in patients with severe arterial hypotension, systolic pressure is below 80 mmHg. Art., and with hypertension - below 30 mm Hg. Art.;
• pulmonary capillary wedge pressure exceeds 20 mmHg. Art.;
• left ventricular filling increases - from 18 mm Hg. Art. and more;
• cardiac output decreases - the cardiac index does not exceed 2-2.5 m/min/m2;
• pulse pressure drops to 30 mmHg. Art. and below;
• the shock index exceeds 0.8 (this is an indicator of the ratio of heart rate and systolic pressure, which is normally 0.6-0.7, and with shock it can even rise to 1.5);
• a drop in pressure and vascular spasms lead to low urine output (less than 20 ml/h) - oliguria, and complete anuria is possible (cessation of urine flow into the bladder).

Classification and types

The state of shock is classified into various types, the main ones being the following:

Reflex

The following phenomena occur:

1. The physiological balance between the tone of two parts of the autonomic nervous system – sympathetic and parasympathetic – is disrupted.
2. Central nervous system receives nociceptive impulses.

As a result of such phenomena, there arises stressful situation, which leads to an insufficient compensatory increase in vascular resistance - reflex cardiogenic shock.

This form is characterized by the development of collapse or severe arterial hypotension if the patient has suffered a myocardial infarction with unrelieved pain syndrome. Collaptoid state manifests itself vivid symptoms:

• pale skin;
• excessive sweating;
• low blood pressure;
• increased heart rate;
• low pulse filling.

Reflex shock is short-lived and, thanks to adequate pain relief, is quickly relieved. To restore central hemodynamics, small vasopressor drugs are administered.

Arrhythmic

Paroxysmal tachyarrhythmia or bradycardia develops, which leads to hemodynamic disturbances and cardiogenic shock. There are disturbances in the heart rhythm or its conductivity, which becomes the cause of a pronounced disorder of central hemodynamics.

Symptoms of shock will disappear after the disturbances are stopped, and sinus rhythm– restored, since this will lead to rapid normalization of the cardiac function.

True

Extensive myocardial damage occurs - necrosis affects 40% of the myocardial mass of the left stomach. This is the reason sharp decline pumping function of the heart. Often such patients suffer from a hypokinetic type of hemodynamics, in which symptoms of pulmonary edema often appear.

The exact signs depend on the pulmonary capillary wedge pressure:

• 18 mmHg Art. – congestion in the lungs;
• from 18 to 25 mm Hg. Art. – moderate manifestations of pulmonary edema;
• from 25 to 30 mm Hg. Art. – pronounced clinical manifestations;
• from 30 mm Hg Art. – the whole complex of clinical manifestations of pulmonary edema.

As a rule, signs of true cardiogenic shock are detected 2-3 hours after myocardial infarction occurs.

Areactive

This form of shock is similar to the true form, with the exception that it is accompanied by more pronounced pathogenetic factors that are long-lasting. With such a shock, the body is not affected by any therapeutic measures, which is why it is called non-reactive.

Myocardial rupture

Myocardial infarction is accompanied by internal and external myocardial ruptures, which is accompanied by the following clinical picture:

• the pouring blood irritates the pericardial receptors, which leads to a sharp reflex drop in blood pressure (collapse);
• if an external rupture occurs, cardiac tamponade prevents heart contraction;
• if it happened internal break, certain parts of the heart receive a pronounced overload;
• the contractile function of the myocardium decreases.

Diagnostic measures

The complication is recognized by clinical signs, including the shock index. In addition, there may be following methods examinations:

• electrocardiography to identify the location and stage of infarction or ischemia, as well as the extent and depth of damage;
• echocardiography - ultrasound of the heart, which evaluates the ejection fraction, and also evaluates the degree of decrease in myocardial contractility;
• angiography – contrast X-ray examination blood vessels(X-ray contrast method).

Emergency care algorithm for cardiogenic shock

If the patient has symptoms of cardiogenic shock, it is necessary to carry out next steps:

1. Place the patient on their back and elevate their legs (for example, on a pillow) to ensure better flow arterial blood to the heart:

1. Call the resuscitation team, describing the patient’s condition (it is important to pay attention to all details).
2. Ventilate the room, free the patient from tight clothes or use an oxygen blanket. All these measures are necessary to ensure that the patient has free access to air.
3. Use Not narcotic analgesics for pain relief. For example, such drugs are Ketorol, Baralgin and Tramal.
4. Check the patient's blood pressure if there is a tonometer.
5. If symptoms are present clinical death, carry out resuscitation measures in the form of indirect massage hearts and artificial respiration.
6. Transfer the patient medical workers and describe his condition.

Next, first emergency aid is provided by health workers. In severe cases of cardiogenic shock, transportation of a person is impossible. They are taking all measures to bring him out of critical condition - stabilizing his heart rate and blood pressure. When the patient’s condition returns to normal, he is transported in a special resuscitation machine to the intensive care unit.

Health care providers can do the following:

• introduce narcotic analgesics, such as Morphine, Promedol, Fentanyl, Droperidol;
• inject intravenously a 1% solution of Mezaton and at the same time subcutaneously or intramuscularly Cordiamine, a 10% solution of caffeine or a 5% solution of ephedrine (the drugs may need to be administered every 2 hours);
• prescribe a drip intravenous infusion of 0.2% norepinephrine solution;
• prescribe nitrous oxide to relieve pain;
• administer oxygen therapy;
• administer Atropine or Ephedrine in case of bradycardia or heart block;
• administer intravenously 1% lidocaine solution in case of ventricular extrasystole;
• conduct electrical stimulation in case of heart block, and if ventricular block is diagnosed paroxysmal tachycardia or gastric fibrillation - electrical defibrillation of the heart;
• connect the patient to the device artificial ventilation lungs (if breathing has stopped or there is severe shortness of breath - from 40 per minute);
• carry out surgery, if shock is caused by injury and tamponade, it is possible to use painkillers and cardiac glycosides (the operation is performed 4-8 hours after the onset of a heart attack, restores the patency of the coronary arteries, preserves the myocardium and interrupts the vicious circle of shock development).

The patient’s life depends on the prompt provision of first aid aimed at relieving the pain syndrome that causes shock.

Further treatment is determined depending on the cause of shock and is carried out under the supervision of a resuscitator. If everything is in order, the patient is transferred to the general ward.

Preventive measures

To prevent the development of cardiogenic shock, you must follow these tips:

• timely and adequately treat any cardiovascular diseases - myocardium, myocardial infarction, etc.
• eat right;
• follow the pattern of work and rest;
• give up bad habits;
• engage in moderate physical activity;
• fight stressful conditions.

Cardiogenic shock in children

This form of shock is not typical in childhood, but can be observed in connection with impaired contractile function of the myocardium. As a rule, this condition is accompanied by signs of insufficiency of the right or left stomach, since children are more likely to develop heart failure with congenital defect heart or myocardium.

In this condition, the child has a decrease in voltage on the ECG and a change in the ST interval and T wave, as well as signs of cardiomegaly on chest according to the results of radiography.

To save the patient, you need to perform emergency procedures according to the previously given algorithm for adults. Next, health workers provide therapy to increase myocardial contractility, for which inotropic drugs are administered.

So, a frequent continuation of myocardial infarction is cardiogenic shock. This condition can lead to fatal outcome, therefore, the patient needs to be provided with proper emergency care to normalize his heart rhythm and enhance myocardial contractility.