Treatment of arrhythmogenic cardiogenic shock. Dopamine in cardiogenic shock. What is cardiogenic shock, emergency care for the victim

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, restlessness or lethargy (blockade of the atrioventricular junction), loss of consciousness (Edams-Stokes syndrome), acrocyanosis, pallor allow one to suspect arrhythmia. skin, “marble” skin pattern. Accurate diagnosis established on the basis of ECG data.

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

Treatment arrhythmogenic shock provides for emergency restoration heart rate with a frequency that provides 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.

Version: MedElement Disease Directory

Cardiogenic shock (R57.0)

Cardiology

general information

Short description

Cardiogenic shock- This acute disorder perfusion Perfusion - 1) continuous injection of fluid (for example, blood) for therapeutic or experimental purposes in blood vessels 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 condition 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.

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 the 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 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 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.

Medical tourism

Cardiogenic shock is characterized by a sustained drop in blood pressure. The upper pressure drops below 90 mmHg. In most cases, this situation occurs as a complication of myocardial infarction and one should be prepared for its occurrence in order to help the core.

The occurrence of cardiogenic shock is facilitated (especially of the left ventricular type), in which many myocardial cells suffer. The pumping function of the heart muscle (especially the left ventricle) is impaired. As a result, problems begin in target organs.

First of all, the kidneys (the skin clearly turns pale and its humidity increases), the central nervous system, and pulmonary edema occur. Prolonged persistence of a state of shock invariably leads to the death of the core.

Due to its importance, cardiogenic shock ICD 10 is allocated to a separate section - R57.0.

Attention. True cardiogenic shock is the most dangerous manifestation of AHF (acute heart failure) of the left ventricular type, caused by severe myocardial damage. The probability of death with this condition ranges from 90 to 95%.

Cardiogenic shock - causes

More than eighty percent of all cases of cardiogenic shock are a significant decrease in blood pressure during myocardial infarction (MI) with severe damage to the left ventricle (LV). To confirm the occurrence of cardiogenic shock, more than forty percent of the LV myocardial volume must be damaged.

Much less frequently (about 20%), cardiogenic shock develops due to acute mechanical complications of MI:

• acute mitral valve insufficiency due to rupture of the papillary muscles;
• complete separation of the papillary muscles;
• myocardial ruptures with the formation of an IVS defect (interventricular septum);
• complete rupture of the IVS;
• cardiac tamponade;
• isolated right ventricular myocardial infarction;
• acute cardiac aneurysm or pseudoaneurysm;
• hypovolemia and a sharp decrease in cardiac preload.

The incidence of cardiogenic shock in patients with acute MI ranges from 5 to 8%.

Risk factors for the development of this complication are considered:

• anterior localization of the infarction,
• the patient has a history of heart attacks,
• old age of the patient,
• presence of underlying diseases:
  • diabetes,
  • chronic renal failure,
  • severe arrhythmias,
  • chronic heart failure,
  • LV systolic dysfunction (left ventricle),
  • cardiomyopathy, etc.

Types of cardiogenic shock

• true;
• reflex (development of pain collapse);
• arrhythmogenic;
• Areactive.

True cardiogenic shock. Pathogenesis of development

For the development of true cardiogenic shock, the death of more than 40% of the LV myocardial cells is necessary. In this case, the remaining 60% should start working at double load. The critical decrease in systemic blood flow that occurs immediately after a coronary attack stimulates the development of reciprocal, compensatory reactions.

Due to the activation of the sympathoadrenal system, as well as the action of glucocorticosteroid hormones and the renin-angiotensin-aldosterone system, the body tries to increase blood pressure. Thanks to this, in the first stages of cardiogenic shock, blood supply to the coronary system is maintained.

However, activation of the sympathoadrenal system leads to the appearance of tachycardia, increased contractile activity of the heart muscle, increased oxygen needs of the myocardium, spasm of microcirculatory vessels and increased cardiac afterload.

The occurrence of generalized microvascular spasm enhances blood clotting and creates a favorable background for the occurrence of DIC syndrome.

Important. Severe pain associated with severe damage to the heart muscle also aggravates existing hemodynamic disorders.

As a result of impaired blood supply, renal blood flow decreases and renal failure develops. Fluid retention by the body leads to an increase in circulating blood volume and an increase in cardiac preload.

Impaired LV relaxation in diastole contributes to a rapid increase in pressure inside the left atrium, venous congestion of the lungs and their edema.

A “vicious circle” of cardiogenic shock is formed. That is, in addition to compensatory maintenance of coronary blood flow, existing ischemia worsens and the patient’s condition worsens.

Attention. Prolonged tissue and organ hypoxia lead to disruption of the acid-base balance of the blood and the development of metabolic acidosis.

Pathogenesis of the development of reflex cardiogenic shocks

The basis for the development of this type of shock is intense pain. The severity of pain may not correspond to the true severity of damage to the heart muscle.

Unlike true cardiogenic shock, with timely medical care, the pain syndrome is quite easily relieved by the administration of analgesic and vascular drugs, as well as infusion therapy.

A complication of reflex cardiogenic shocks is a violation of vascular tone, an increase in capillary permeability and the appearance of a deficit in circulating blood volume due to the leakage of plasma from the vessel into the interstitium. This complication leads to decreased blood flow to the heart.

Attention. Infarctions with posterior localization are characterized by bradyarrhythmia (low heart rate), which increases the severity of shock and worsens the prognosis.

How does arrhythmogenic shock develop?

The most common causes of this type of shock are:

• paroxysmal tachyarrhythmia;
• ventricular tachycardia;
• atrioventricular block of the second or third degree;
• sinoatrial block;
• sick sinus syndrome.

Development of areactive cardiogenic shock

Important. Unlike true cardiogenic shock, this condition can occur even with a small area of ​​damaged LV myocardium.

The pathogenesis of areactive shock is based on the reduced ability of the heart muscle to contract. As a result, microcirculation and gas exchange are disrupted and disseminated intravascular coagulation develops.

Areactive shock is characterized by:

• high risk of death;
• complete lack of response to the introduction of pressor amines to the patient;
• the presence of paradoxical pulsation of the heart muscle (bulging, rather than contraction, of the damaged part of the myocardium during systole);
• a significant increase in the heart's need for oxygen;
• rapid increase in the ischemic zone in the myocardium;
• the emergence or increase in symptoms of pulmonary edema in response to the administration of vasoactive agents and an increase in blood pressure.

Cardiogenic shock - symptoms

The leading symptoms of cardiogenic shock are:

• pain (highly intense, widely radiating, burning, squeezing, pressing or “dagger-like” in nature). Dagger pain is most specific for slow ruptures of the heart muscle);
• decrease in blood pressure (indicative of a sharp decrease of less than 90 mmHg, and average blood pressure less than 65 and the need to use vasopressor drugs in order to maintain blood pressure. Average blood pressure is calculated based on the formula = (2 diastolic blood pressure + systolic )/3). In patients with severe arterial hypertension and initial high blood pressure, the level of systolic blood pressure during shock may be more than 90;
• severe shortness of breath;
• the appearance of a thread-like, weak pulse, tachycardia of more than one hundred beats per minute or bradyarrhythmia of less than forty beats per minute;
• disturbances of microcirculation and the development of symptoms of tissue and organ hypoperfusion: coldness of the extremities, the appearance of sticky cold sweat, pallor and marbling of the skin, renal failure with oliguria or anuria (decreased volume or complete absence of urine), disturbances in the acid-base balance of the blood and the occurrence of acidosis;
• dullness of heart sounds;
• increasing clinical symptoms of pulmonary edema (the appearance of moist rales in the lungs).

There may also be disturbances of consciousness (the appearance of psycho-motor agitation, severe retardation, stupor, loss of consciousness, coma), collapsed, unfilled peripheral veins and a positive white spot symptom (the appearance of a white, long-lasting spot on the skin of the back of the hand or foot, after light finger pressure).

Diagnostics

In the vast majority of cases, cardiogenic shock develops after acute MI. If specific clinical symptoms of cardiogenic shock occur, it is necessary to conduct additional studies in order to differentiate shock from:

• hypovolemia;
• cardiac tamponade;
• tension pneumothorax;
• pulmonary embolism;
• internal bleeding from ulcers and erosions of the esophagus, stomach or intestines.

For reference. If the data obtained indicate shock, it is necessary to determine its type (the further algorithm of actions depends on this).

It should be remembered that in elderly patients with cerebrovascular accident (cerebrovascular accident) and long-term diabetes mellitus, cardiogenic shock may occur against the background of silent ischemia.

For quick differential diagnosis, carry out:

• ECG recording (against the background of clinical symptoms of shock, there are no significant changes); pulse oximetry (quick, non-invasive assessment of blood oxygen saturation);
• blood pressure and pulse monitoring;
• assessment of the level of plasma serum lactate (the most significant factor for prognosis). True cardiogenic shock is indicated by a lactate level of more than 2 mmol/l. The higher the lactate level, the higher the risk of death).

Extremely important! Remember the half-hour rule. The patient's chances of survival increase if assistance is provided in the first half hour after the onset of shock. In this regard, all diagnostic measures should be carried out as quickly as possible.

Cardiogenic shock, emergency care. Algorithm

Attention! If cardiogenic shock does not develop in a hospital, you should immediately call an ambulance. All attempts to provide first aid on your own will only lead to loss of time and will make the patient’s chances of survival zero.

Emergency care for cardiogenic shock:

Cardiogenic shock - treatment

Treatment of cardiogenic shock consists of several stages:

• Carrying out general measures with adequate pain relief, oxygen therapy, thrombolysis, stabilization of hemodynamic parameters;
• Infusion therapy (according to indications);
• Normalization of microcirculation and reduction of peripheral vascular resistance;
• Increased contractility of the heart muscle;
• Intra-aortic balloon counterpulsation;
• Surgical intervention.

Treatment depending on the type of shock:

Drug therapy

Ataralgesia is also indicated - administration of an NSAID (ketoprofen) or a narcotic analgesic (fentanyl) in combination with diazepam.

In order to increase the contractile activity of the heart muscle, strophanthin, corglycone and glucagon are used.

To normalize blood pressure, norepinephrine, mesaton, cordiamine, and dopamine are used. If the effect of increasing blood pressure is unstable, administration of hydrocortisone or prednisolone is indicated.

When carrying out thrombolytic therapy, a combination of thrombolytics with low molecular weight heparins is administered.

In order to normalize the rheological properties of blood and eliminate hypovolemia, rheopolyglucin is administered.

Also, elimination of disturbances in the acid-base balance of the blood, repeated pain relief, correction of arrhythmia and cardiac conduction disorders are performed.

According to indications, balloon angioplasty and coronary artery bypass grafting are performed.

Prevention, complications and prognosis

Cardiogenic shock is the most severe complication of MI. Mortality with the development of true shock reaches 95%. The severity of the patient's condition is determined by severe damage to the heart muscle, tissue and organ hypoxia, the development of multiple organ failure, metabolic disorders and disseminated intravascular coagulation syndrome.

With painful and arrhythmogenic shock, the prognosis is more favorable, since patients, as a rule, respond adequately to the therapy.

For reference. There is no way to prevent shock.

After eliminating shock, the patient’s treatment corresponds to therapy for CHF (chronic heart failure). Specific rehabilitation measures are also carried out, which depend on the cause of the shock.

According to indications, extracorporeal membrane oxygenation (invasive blood saturation with O2) is performed and the patient is transferred to an expert center to decide on the need for a heart transplant.

14.01.2011 14308

Cardiogenic shock is the most serious hemodynamic complication of myocardial infarction. Characterized by an extremely high mortality rate, which reaches 80-90% with true shock, and 100% with areactive shock, this complication occurs in acute myocardial infarction in 10-25% of cases.

Cardiogenic shock is the most serious hemodynamic complication of myocardial infarction. Characterized by an extremely high mortality rate, which reaches 80-90% with true shock, and 100% with areactive shock, this complication occurs in acute myocardial infarction in 10-25% of cases.
Diagnostic criteria for cardiogenic shock on DHE:
decrease in systolic blood pressure below 80 mm Hg. (for patients with arterial hypertension 100-110 mm Hg);
low (less than 20-25 mm Hg) pulse pressure;
the presence of “peripheral microcirculatory syndrome”: pallor, cyanosis, sweating, decreased body temperature;
oliguria, anuria.
In the work of an emergency physician, the following classification of cardiogenic shock can be used:
1. Reflex cardiogenic shock or collapse.
It is characterized by a decrease in cardiac output as a result of suppression of the pumping function of the myocardium and a decrease in vascular tone by reflex influence from the damage zone. With this form of shock, a clear positive effect can be achieved with adequate pain relief (Morphine or neuroleptanalgesia). (See “Treatment of uncomplicated myocardial infarction”).


2. Arrhythmogenic tachysystolic and bradysystolic cardiogenic shock.
Elimination of the heart rhythm disturbance usually leads to the disappearance of signs of shock. Untimely or insufficient therapeutic measures for reflex shock can lead to its transformation into true shock, both in the case of arrhythmogenic and reflex shock.
3. True cardiogenic shock.
As a rule, it develops with necrosis of 40% or more of the muscle mass of the heart, as well as with repeated large-focal infarctions. Therapeutic measures include the use of non-glycoside inotropic agents (Fig. 7).


Treatment

Dopamine is administered in a dose of 200 mg in 400 ml of isotonic solution or 5% glucose. Administration rates ranging from 5 to 15 mcg/kg*min provide a positive inotropic effect without causing vasoconstriction and the risk of dangerous arrhythmias.
Dobutamine, unlike Dopamine, has a more powerful inotropic effect, has a weak effect on heart rate, and reduces wedge pressure in the pulmonary artery. It is administered at a dose of 250 mg in 500 ml of isotonic solution or 5% glucose at an initial rate of 2.5 mcg/kg*min. The maximum rate of administration is 15 mcg/kg*min.
Persistent hypotension below 60 mm Hg. against the background of the administration of inotropic drugs, it gives grounds to add Noradrenaline to therapy (the rate of administration in combination with Dopamine is no more than 8-10 mcg/min).
Experience clearly shows that the severity of cardiogenic shock depends not only on the volume of myocardial damage, but also lies in direct proportion to the duration of the period from the moment of its manifestations to the start of active therapy. Thus, the timely detection of signs of shock and the fastest possible correction of blood pressure are the primary task for the emergency physician. The most effective way to compensate for blood circulation in acute myocardial infarction (up to 6 hours, sometimes up to 12 hours) is to restore coronary blood flow, which can be achieved at the prehospital stage by systemic thrombolysis in a specialized team or intensive care team.
4. Areactive cardiogenic shock.
Clinically characterized by the lack of effect from the use of increasing doses of pressor amines.
Separately, cardiogenic shock should be considered, resulting from the spread of myocardial infarction to the right ventricle (occurs in approximately 20-25% of cases of myocardial infarction of lower localization). It develops as a result of right ventricular failure through the mechanism of hypovolemic shock and requires active plasma replacement therapy: rapid intravenous fractional (200 ml) infusion of Polyglyukin until a positive hemodynamic effect is obtained, or until signs of left ventricular failure appear.
Self-hospitalization of patients with complicated forms of myocardial infarction by linear teams is allowed only in cases of providing assistance on the street and in public places. During transportation, it is necessary to continue oxygen inhalation and drug therapy as indicated.

– 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.