Cardiogenic shock definition

All complications of myocardial infarction (MI) that occur in the first 2 weeks from the onset of the disease are called early. The following pathological conditions are referred to early complications:

  • acute heart failure
  • cardiogenic shock,
  • heart rhythm and conduction disturbances,
  • heart breaks, pericarditis,
  • acute papillary muscle dysfunction,
  • sudden cardiac death.

After the 2nd week, late complications of a heart attack develop, which include:

  • Dressler’s syndrome
  • thrombendocarditis,
  • chronic heart failure
  • neurological disorders.

Pulmonary edema and cardiogenic shock are some of the most adverse complications of myocardial infarction. We will talk about them in more detail. If more than 25% of the heart muscle dies during a heart attack, clinical signs and symptoms of acute heart failure appear, more than 40% of cardiogenic shock. Pulmonary edema and cardiac asthma are the main manifestations of acute heart failure.

The treatment of cardiogenic shock and pulmonary edema should begin immediately after their diagnosis, since these conditions significantly worsen the prognosis of the outcome of the disease and, in the absence of help, lead to the death of the patient. Patients with pulmonary edema and cardiogenic shock are immediately hospitalized in a hospital. Treatment is aimed at the underlying disease – myocardial infarction. His therapy aims to restore the patency of the vessel.

An important goal in the treatment of shock is to maintain the contractile function of the heart at the required level, and treatment is also aimed at reducing the amount of blood entering the heart. This allows you to reduce the load on the left ventricle, which is therefore in a very critical condition. If respiratory dysfunction is present, oxygen is included in the therapy.

Symptoms of Cardiogenic Shock

Signs indicating cardiogenic shock indicate a violation of blood circulation and externally manifest in such ways:

  • the skin turns pale, and the face and lips become grayish or bluish in color;
  • cold, sticky sweat is released;
  • pathologically low temperature is observed – hypothermia;
  • hands and feet get colder;
  • consciousness is disturbed or inhibited, and short-term excitement is possible.

In addition to external manifestations, cardiogenic shock is characterized by such clinical signs:

  • blood pressure critically decreases: in patients with severe arterial hypotension, systolic blood pressure is below 80 mm Hg. Art., and with hypertension – below 30 mm RT. st .;
  • jamming pressure of pulmonary capillaries exceeds 20 mm Hg. st .;
  • the filling of the left ventricle increases – from 18 mm RT. Art. and more;
  • cardiac output is reduced – the cardiac index does not exceed 2-2,5 m / min / m2;
  • pulse pressure drops to 30 mm RT. 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 in shock it can even rise to 1,5);
  • a drop in pressure and vasospasm leads to a small excretion of urine (less than 20 ml / h) – oliguria, and complete anuria (cessation of urine into the bladder) is possible.

Symptoms of cardiogenic shock are sinus tachycardia, decreased blood pressure, shortness of breath, cyanosis, the skin is pale, cold and wet (usually cold, sticky sweat), impaired consciousness, decreased urine output of less than 20 ml / h. It is advisable to carry out invasive hemodynamic monitoring: intra-arterial measurement Blood pressure and determination of jamming pressure in the pulmonary artery.

The classic definition of cardiogenic shock is “a decrease in systolic blood pressure of less than 90 mm Hg. Art. for 30 minutes in combination with signs of peripheral hypoperfusion. ” V. Menon JS and Hochman (2002) give the following definition: “cardiogenic shock is inadequate peripheral perfusion with an adequate intravascular volume, regardless of blood pressure.”

Hemodynamically, with cardiogenic shock, a decrease in the cardiac index of less than 2,0 l / min / m 2 (from 1,8-2,2 l / min / m 2) is observed in combination with an increase in the filling pressure of the left ventricle of more than 18 mm Hg. Art. (from 15 to 20 mm RT. Art.), if there is no concomitant hypovolemia.

Lowering Blood pressure is a relatively late sign. First, a decrease in cardiac output causes a reflex sinus tachycardia with a decrease in pulse blood pressure. At the same time, vasoconstriction begins, first of the vessels of the skin, then of the kidneys and, finally, of the brain. Due to vasoconstriction, normal blood pressure may persist. The deterioration of perfusion of all organs and tissues, including the myocardium, progressively increases.

With severe vasoconstriction (especially with the use of sympathomimetics), a marked decrease in blood pressure is often auscultatory, while intra-arterial blood pressure, determined by puncture of arteries, is within normal limits. Therefore, if invasive control is not possible, blood pressure is better guided by palpation of large arteries (carotid, femoral), less prone to vasoconstriction.

4 Diagnosis of pulmonary edema

With the death of a significant portion of the myocardium, the heart loses its ability to normal contraction. After all, such a volume of the myocardium is not enough to provide the cells with the necessary amount of oxygen. Under such conditions, the heart tries to compensate for the lack of oxygen and begins to contract faster. But the amount of blood ejected in one contraction of the left ventricle is critically small.

He is not able to push the right amount of blood into the aorta, while blood continues to flow into the ventricle. Because of this, there is a retrograde (reverse) increase in pressure in the left ventricle, left atrium and in the pulmonary vessels. In this situation, overload threatens the lungs. To protect this organ from overfilling with blood, the vessels of this organ are spasmodic (narrowing) in response to an increase in pressure.

However, in the future, in conditions of heart failure, the liquid part of the blood from the capillaries begins to sweat first in the connective tissue (interstitium), and then in the alveoli. The exit of the liquid part of the blood into the interstitium is called cardiac asthma. If heart failure progresses, and the fluid is in the alveoli, proper alveolar edema develops.

Symptoms of pulmonary edema

Interstitial edema is manifested by the following symptoms and clinical signs:

  • Sharp suffocation and a feeling of lack are the main complaints that concern a patient with cardiac asthma. There is a feeling of fear of death, breathing is frequent, superficial, inhalation is most often difficult;
  • The patient takes a forced position – one that will ease his condition a little – semi-elevated or sedentary. The behavior is restless, the air is inhaled with a wide open mouth.

This complication of a heart attack is characterized by the following symptoms:

  • Cough with foamy pink phlegm
  • Bubbling breath
  • Wheezing heard in the distance. Alveoli filled with liqu >

On the roentgenogram, the roots of the lungs acquire a peculiar shape of a “butterfly”

Diagnosis includes detailed complaints and medical history. On examination, the patient has a characteristic appearance and is in a forced position. As a rule, he seeks to take a sitting position with his legs down. The auxiliary muscles, the muscles of the upper girdle, begin to participate in breathing. Nose wings swell, intercostal spaces retract – these are signs that indicate the development of respiratory failure.

The patient swallows air with his mouth wide open. When examining a patient, the doctor reveals an expansion of the borders of the heart, heart palpitations, high blood pressure, weak pulse. Heart sounds are deaf, and wheezing is heard over the lungs. Changes appear on the electrocardiogram, indicating an overload of the left and right parts of the heart, and on the radiograph, the roots of the lungs take on a peculiar “butterfly” shape, sometimes round shadows appear over the pulmonary fields.

The main mechanism that plays a leading role in the development of cardiogenic shock is a decrease in the ability of the heart to contract. The heart muscle is so weakened that the left ventricle is not able to throw enough blood into a large circle of blood circulation. Heart failure is so pronounced that the body has to save vital organs.

This process is called centralization of blood flow, when the main blood supply goes to the brain, heart, liver and kidneys. In this case, the remaining organs and tissues, which are called peripherals, lack oxygen and begin to suffer from a lack of oxygen. In response to a decrease in cardiac contractions, vessels located on the periphery are spasmodic (narrowing) to maintain the falling pressure.

However, these processes are not enough to maintain organs and tissues for a long time in a functional state. Therefore, vital organs and those located on the periphery fall into a “starving” state. A lack of oxygen leads to a violation of their function.

How is cardiogenic shock diagnosed?

  • severe arterial hypotension (systolic blood pressure below 80 mm Hg; in patients with arterial hypertension – a decrease of more than 30 mm Hg); decrease in pulse pressure to 30 mm RT. Art. and below;
  • shock index over 0,8;

* The shock index is the ratio of heart rate to systolic blood pressure. Normally, its average value is 0,6-0,7. In shock, the index value can reach 1,5.

  • clinical signs of peripheral circulatory disorders;
  • oliguria (less than 20 ml / h);
  • retardation and confusion (there may be a short period of excitement).

The development of cardiogenic shock is also characterized by a decrease in cardiac output (cardiac index less than 2-2,5 l / min / m2) and increased filling of the left ventricle (more than 18 mmHg), the pressure of jamming of the pulmonary capillaries is more than 20 mmHg. Art.

Cardiogenic shock treatment

With a detailed picture of cardiogenic shock, the probability of survival is almost zero with any method of treatment, death usually occurs within 3-4 hours. With less pronounced hemodynamic disturbances, if drug treatment of cardiogenic shock is carried out, the probability of success is no more than 20-30%. There is evidence that thrombolytic therapy does not improve prognosis for cardiogenic shock.

Therefore, the question of the use of thrombolytics in cardiogenic shock has not been completely resolved (the pharmacokinetics and effects of these drugs in shock are unpredictable). In one study, streptokinase administration was effective in 30% of patients with cardiogenic shock – among these patients, mortality was 42%, but overall mortality remained high – about 70%. However, if there is no possibility of coronary angioplasty or coronary artery bypass grafting, thrombolytic therapy is indicated.

coronary angioplasty (CAP) or coronary artery bypass grafting (CABG). Naturally, the possibility of a complex of such events is extremely rare. During the CAP, it was possible to reduce the overall mortality to 40-60%. In one study among patients with successful recanalization of coronary arteries and restoration of coronary blood flow, mortality averaged 23% (!).

Conducting emergency CABG also reduces mortality in cardiogenic shock by up to about 50%. It is estimated that early revascularization with cardiogenic shock can save lives in 2 out of 10 treated patients under 75 years of age (SHOCK study). However, such a modern “aggressive” treatment requires early hospitalization of patients in a specialized cardiac surgery department.

With a sharp decrease in blood pressure infusion of norepinephrine to increase blood pressure above 80-90 mm RT. Art. (1-15 μg / min). After this (and with less pronounced hypotension in the first place), it is advisable to switch to the administration of dopamine. If to maintain blood pressure at about 90 mm Hg. Art. enough dopamine infusion at a rate of not more than 400 mcg / min, dopamine has a positive effect, expanding the vessels of the kidneys and organs of the abdominal cavity, as well as coronary and cerebral vessels.

If you can stabilize your blood pressure using small doses of dopamine, it is advisable to try to connect dobutamine (200-1000 mcg / min) to the treatment. Further, the rate of administration of these drugs is regulated by the reaction of blood pressure. Perhaps the additional appointment of phosphodiesterase inhibitors (milrinone, enoximon).

If there are no pronounced wheezing in the lungs, many authors recommend evaluating the response to fluid administration by the usual method: 250-500 ml for 3-5 minutes, then 50 mg every 5 minutes, until there are signs of increased stagnation in the lungs. Even with cardiogenic shock, approximately 20% of patients have relative hypovolemia.

Cardiogenic shock does not require the appointment of corticosteroid hormones. In the experiment and in some clinical studies, a positive effect was revealed from the use of glucose-insulin-potassium mixture.

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

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

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

Causes of Cardiogenic Shock
(KS)

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

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

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

4. Heart arrhythmias (cardiac arrhythmias).

5. Acute insufficiency (expansion) of heart valves.

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

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

Types of Cardiogenic Shock (KS)

1. Disorder of the pumping function of the heart.

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

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

The body abruptly stops its work and death occurs.

2. Severe heart rhythm disturbances

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

3. Tamponade of the ventricles of the heart

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

After that, the changes described in paragraph 1 and 2.

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

This is a condition when a blood clot completely blocks the lumen of the trunk of the pulmonary artery and blood cannot enter the left parts of the heart, so that, contracting, the heart pushes blood into the vessels.

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

Clinical manifestations (symptoms and signs) of cardiogenic shock

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

Veins on the limbs fall. They lose their tone, as a result of a sharp decrease in blood pressure.

Cardiogenic Shock Risk Factors (CABG)

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

Repeated myocardial infarction with heart rhythm disturbance.

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

Diagnosis of cardiogenic shock (CABG)

Tachycardia (increased heart rate).

Pale (cyanotic, marble, speckled) and wet skin.

Drooping veins on the extremities.

Violation of diuresis (urine output), with a decrease in blood pressure below 50/0 – 30 / 0mm RT. St. kidneys stop working.

ECG
(electrocardiogram), to determine focal changes in the myocardium (myocardial infarction). Its stage, localization (in which part of the left ventricle had a heart attack), depth and vastness.

ECHOKG (ultrasound)
This method allows the heart to assess myocardial contractility, the ejection fraction (the amount of blood ejected by the heart into the aorta), to determine which part of the heart is more affected by a heart attack.

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

Angiography is performed directly if surgical techniques are possible to eliminate the causes of cardiogenic shock and increase myocardial contractility.

Cardiogenic shock (CABG) treatment

Cardiogenic shock treatment is carried out in the intensive care unit. The main goal of the assistance is to increase blood pressure up to 90/60 mm Hg in order to improve the contractile function of the heart and provide vital organs with blood for their future life.

Drug treatment for cardiogenic shock (CABG)

The patient is laid horizontally with raised legs in order to provide possible blood supply to the brain.

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

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

To stabilize the blood pressure intravenously, a solution of Reopoliglukin is administered – this drug improves blood circulation, prevents increased blood clotting and blood clots, and heparin solutions are administered intravenously.

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

Solutions of Adrenaline, Norepinephrine, Dopamine or Dobutamine are injected intravenously, because they are able to increase the strength of heart contractions, increase blood pressure, expand the renal arteries and improve blood circulation in the kidneys.

Diagnostic measures

Perhaps the most common and formidable complication of myocardial infarction (MI) is cardiogenic shock, which includes several varieties. Suddenly severe condition in 90% of cases is fatal. The prospect of living with the patient appears only when, at the time of the development of the disease, he is in the hands of the doctor
.

And better – an entire resuscitation team, which has in its arsenal all the necessary medicines, equipment and devices for returning a person from the “other world”. However, even with all these means, the chances of salvation are very small.
. But hope dies last, so doctors to the last fight for the life of the patient and in other cases achieve the desired success.

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

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

  • Disorders of microcirculation and central hemodynamics;
  • Acid-base imbalance;
  • The shift of the water-electrolyte state of the body;
  • Changes in neurohumoral and neuro-reflex regulation mechanisms;
  • Disorders of cellular metabolism.

Classification of cardiogenic shock is based on the identification of degrees of severity (I, II, III – depending on the clinic, heart rate, blood pressure, urine output, duration of shock) and types of hypotensive syndrome, which can be represented as follows:

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

pathologies-causes of cardiogenic shock and their localization

Thus, the generally accepted clinical criteria for shock in myocardial infarction can be distinguished and presented in the following form:

  1. Decreased systolic blood pressure below an acceptable level of 80 mm Hg. Art. (for patients with arterial hypertension – below 90 mm Hg. Art.);
  2. Diuresis less than 20 ml / h (oliguria);
  3. Pallor of the skin;
  4. Loss of consciousness.

However, the severity of the condition of the patient who developed cardiogenic shock can be judged by the duration of the shock and the patient’s response to the administration of pressor amines than by the level of arterial hypotension. If the duration of the shock state exceeds 5-6 hours, it is not stopped by drugs, and the shock itself is combined with arrhythmias and pulmonary edema, this shock is called areactive
.

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

  • Reduced systolic ejection includes a cascade of adaptive and compensatory mechanisms;
  • Enhanced production of catecholamines leads to generalized narrowing of blood vessels, especially arterial;
  • A generalized spasm of arterioles, in turn, causes an increase in total peripheral resistance and contributes to the centralization of blood flow;
  • Centralization of blood flow creates conditions for increasing the volume of circulating blood in the pulmonary circulation and gives an additional load on the left ventricle, causing it to be damaged;
  • Increased end diastolic pressure in the left ventricle leads to the development of left ventricular heart failure
    .

The pool of microcirculation with cardiogenic shock also undergoes significant changes due to arteriovenous bypass grafting:

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

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

Cardiogenic shock, as a rule, is characterized by a rapid course and quickly captures the entire body. Due to disorders of red blood and platelet homeostasis, micro-coagulation of blood begins in other organs:

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

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

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

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

    With pulmonary edema, nitroglycerin, diuretics, adequate analgesia, and alcohol are prescribed to prevent the formation of foamy flu >Urgent hospitalization
    under constant supervision in the intensive care unit, bypassing the emergency room!
    Of course, if it was possible to stabilize the patient’s condition (systolic pressure 90-100 mm RT. Art.).

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

Depending on how the blood pressure decreases, how much signs of peripheral disturbances are expressed, what kind of reaction the patient has to treatment measures, it is customary to distinguish between moderate and severe cardiogenic shock, which is classified as reactive in the classification
. An easy degree for such a serious disease, in general, is somehow not provided for.

However, even in the case of a moderate shock, you don’t have to flatter yourself
. Some positive response of the body to therapeutic effects and an encouraging increase in blood pressure to 80-90 mm RT. Art. can quickly give way to the opposite picture: against the background of increasing peripheral manifestations, blood pressure begins to fall again.

Patients with severe cardiogenic shock have virtually no chance of survival.
. since they absolutely do not respond to therapeutic measures, so the vast majority (about 70%) die on the first day of the disease (usually within 4-6 hours from the moment of shock). Some patients can last 2-3 days, and then death occurs.

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

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

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

This condition provokes a sharp oxygen deficiency in all organs and tissues, which causes circulatory disturbance, depression of consciousness and death if emergency assistance is not provided to the victim in a timely manner.

The causes of cardiogenic shock in most cases are due to the blockage of large branches of the pulmonary artery with blood clots, which interfere with full circulation and cause severe hypoxia of organs.

This condition leads to:

  • acute myocardial infarction;
  • acute mitral valve stenosis;
  • severe hypertrophic cardiomyopathy;
  • heart rhythm disturbances;
  • hemorrhagic shock (occurs when transfusion is not appropriate for the group or rhesus blood);
  • pericarditis compressive type;
  • rupture of the septum between the ventricles;
  • septic shock, which provoked a violation of the myocardium;
  • intense pneumothorax;
  • stratified aortic aneurysm or its rupture;
  • severe pulmonary embolism;
  • tamponade of the heart.
  • Reduced systolic ejection includes a cascade of adaptive and compensatory mechanisms;
  • Enhanced production of catecholamines leads to generalized narrowing of blood vessels, especially arterial;
  • A generalized spasm of arterioles, in turn, causes an increase in total peripheral resistance and contributes to the centralization of blood flow;
  • Centralization of blood flow creates conditions for increasing the volume of circulating blood in the pulmonary circulation and gives an additional load on the left ventricle, causing it to be damaged;
  • Increased end diastolic pressure in the left ventricle leads to the development of left ventricular heart failure
    .
  1. The capillary bed is depleted;
  2. Metabolic acidosis develops;
  3. There are pronounced dystrophic, necrobiotic and necrotic changes in tissues and organs (necrosis in the liver and kidneys);
  4. The permeability of capillaries increases, due to which there is a massive exit of plasma from the bloodstream (plasmorrhagia), the volume of which in the circulating blood, naturally, decreases;
  5. Plasmorrhages lead to an increase (the ratio between plasma and red blood) and a decrease in blood flow to the heart cavities;
  6. Blood supply to the coronary arteries is reduced.
  • In the kidneys with the development of anuria and acute renal failure
    – eventually;
  • In the lungs with the formation of respiratory distress syndrome
    (pulmonary edema);
  • In the brain with edema and the development of cerebral coma
    .
  • electrocardiography to detect the location and stage of a heart attack or ischemia, as well as the extent and depth of damage;
  • echocardiography – an ultrasound of the heart, in which the ejection fraction is estimated, and the degree of decrease in the contractile ability of the myocardium is also evaluated;
  • angiography – a contrast x-ray examination of blood vessels (radiopaque method).

5 Cardiogenic shock

Cardiogenic shock is one of the earliest complications of myocardial infarction. With cardiogenic shock, the ability of the left ventricle is critically reduced. In most cases, such a formidable complication develops with extensive damage to the myocardium. However, sometimes cardiogenic shock can also complicate a small focal heart attack, if this heart attack is repeated, and the primary myocardial damage was extensive.

Pathogenetic mechanisms of cardiogenic shock

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

  1. Decreased myocardial contractility
    – when a heart attack occurs (necrosis of a certain part of the heart muscle), the heart cannot fully pump blood, which leads to a sharp decrease in blood pressure (arterial). Against this background, the brain and kidneys are the first to suffer from hypoxia, acute urinary retention develops, the victim loses consciousness. Due to respiratory depression and oxygen starvation, metabolic acidosis develops, organs and systems abruptly cease to function normally and death occurs.
  2. The development of arrhythmic shock (bradysystolic or tachysystolic)
    – This form of shock develops against a background of paroxysmal tachycardia or severe bradycardia with complete atrioventricular block. Under the influence of impaired ventricular contractility and lowering blood pressure (about 80/20 mm Hg), a severe hemodynamic change develops.
  3. Cardiac tamponade with the development of cardiogenic shock
    – diagnosed with rupture of the interventricular septum. With this pathology, the blood in the ventricles mixes, which makes it impossible to contract the heart muscle. Blood pressure drops sharply, the effects of hypoxia in vital organs increase, the patient falls into a coma and may die in the absence of adequate assistance.
  4. Massive thromboembolism, which leads to cardiogenic shock
    – This form of shock develops with complete clogging of the lumen of the pulmonary artery with blood clots. In this case, the blood ceases to flow into the left ventricle. This leads to a sharp decrease in blood pressure, increasing hypoxia and death of the patient.
Form of pathologyWhat is characterized by?
True cardiogenic shockIt is accompanied by a sharp violation of the contractile function of the myocardium, a decrease in diuresis, metabolic acidosis, hypotension and severe oxygen starvation. As a complication, cardiogenic pulmonary edema often develops, the treatment of which requires resuscitation
ReflexIt is provoked by the reflex effect of pain on myocardial contractile function. It is characterized by severe bradycardia (a decrease in heart rate below 60 beats / min), and a decrease in blood pressure. At the same time, microcirculatory disorders and metabolic acidosis do not develop
ArrhythmicIt develops against a background of severe tachycardia or bradycardia and passes after the medical elimination of arrhythmia
AreactiveIt develops suddenly, proceeds very hard and in most cases leads to death, despite all the medical measures taken

7 Clinical manifestations of cardiogenic shock

The patient’s condition is serious. Consciousness may be obscured, or its complete loss is possible. In more rare cases, there may be an excited state. If the patient is conscious, he is worried about the expressed general weakness, dizziness, “veil” in front of his eyes. From the side of the heart, the heartbeat, the sensation of interruptions in its work are disturbing, there may be chest pains.

Cardiogenic Shock Emergency Algorithm

If the patient has symptoms of cardiogenic shock, before the arrival of emergency workers, the following steps must be taken:

  1. Lay the patient on his back and raise his legs (for example, lay on a pillow) to provide the best flow of arterial blood to the heart:
  1. Call a resuscitation team, describing the patient’s condition (it is important to pay attention to all the details).
  2. Ventilate the room, free the patient from tight clothing or use an oxygen pillow. All these measures are necessary so that the patient gets free access to air.
  3. Use non-narcotic analgesics for pain relief. For example, such drugs are Ketorol, Baralgin and Tramal.
  4. Check the blood pressure of the patient, if there is a tonometer.
  5. If there are symptoms of clinical death, carry out resuscitation in the form of indirect heart massage and artificial respiration.
  6. Transfer the patient to medical personnel and describe his condition.

Further, first aid is already provided by health workers. In severe form of cardiogenic shock, transportation of a person is impossible. They are taking all measures to get him out of a critical state – they are stabilizing the heart rate and blood pressure. When the patient’s condition returns to normal, he is transported by special resuscitation machine to the intensive care unit.

Health workers can do the following:

  • introduce narcotic analgesics, which are Morphine, Promedol, Fentanyl, Droperidol;
  • intravenously administer 1% Mesatone solution and at the same time subcutaneously or intramuscularly Cordiamine, 10% caffeine solution or 5% ephedrine solution (preparations may need to be administered every 2 hours);
  • prescribe a drip intravenous infusion of a 0,2% solution of norepinephrine;
  • prescribe nitrous oxide to relieve a pain attack;
  • carry out oxygen therapy;
  • enter atropine or ephedrine in case of bradycardia or heart block;
  • inject intravenously 1% lidocaine solution in case of ventricular extrasystole;
  • conduct electrical stimulation in case of heart block, and if ventricular paroxysmal tachycardia or gastric fibrillation is diagnosed, electrical defibrillation of the heart;
  • connect the patient to a ventilator (if breathing has stopped or marked shortness of breath is noted – from 40 per minute);
  • perform surgery if the shock is caused by a wound and tamponade, while it is possible to use painkillers and cardiac glycosides (the operation is performed 4-8 hours after the onset of a heart attack, restores patency of the coronary arteries, the myocardium is preserved and the vicious cycle of shock development is interrupted).

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

When the first symptoms of cardiogenic shock appear, you should immediately call the cardiological ambulance team and begin to provide pre-medical rescue measures.

Emergency care for cardiogenic shock before the ambulance arrives is as follows:

  • reassure the patient;
  • put him to bed and raise his lower limbs just above the level of the head – this way you will prevent a rap >

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

  1. oxygen therapy – moistened oxygen is supplied to the patient through a mask. The mask is not removed before arrival at the hospital, after which the patient is connected to resuscitation devices and his condition is monitored around the clock.
  2. Narcotic analgesics – to stop a severe pain syndrome, Morphine or Promedol are administered to the patient.
  3. In order to stabilize blood pressure indicators, a solution of Reopoliglukin and plasma substitutes are administered intravenously.
  4. To dilute blood and prevent the formation of blood clots in the lumen of the coronary vessels, heparin is administered.
  5. To enhance the contractile function of the heart muscle, solutions of adrenaline, noradrenaline, sodium nitroprusside, dobutamine are administered.

Already in the hospital, the patient undergoes intensive therapy:

  • to normalize myocardial trophism, glucose solutions with insulin are infused intravenously;
  • for the course of cardiac arrhythmia, Mesatone, Lidocaine or Panangin are added to the solution of the polarizing mixture;
  • to eliminate the phenomena of acidosis against the background of severe hypoxia of organs and tissues, sodium bicarbonate solutions are intravenously dripped to the patient – this will help stabilize the acid-base balance of the blood;
  • with the development of atrioventricular blockade, Prednisolone, Ephedrine begin to be administered and an Isadrin tablet is additionally given under the tongue.

In addition to drug treatment, a urinary catheter is installed to the patient to determine the amount of urine to be excreted per day and must be connected to a cardiomonitor, which will regularly measure heart rate and blood pressure.

With the failure of drug therapy, a patient with cardiogenic shock undergoes surgical treatment:

  1. balloon intra-aortic counterpulsation – during the diastole of the heart, blood is pumped into the aorta with a special balloon, which contributes to an increase in coronary blood flow.
  2. Percutaneous coronary transluminal angioplasty – pierce an artery and through this opening restore patency of the coronary vessels. This treatment technique is effective only if no more than 7 hours have passed since the onset of signs of acute myocardial infarction.

Patients diagnosed with cardiogenic shock remain in the intensive care unit until the condition stabilizes and the crisis is resolved, after which, with a favorable prognosis, they are transferred to the cardiology department, where treatment is continued.

The development of this complication is not always a death sentence for the patient. It is very important to call an ambulance in time and stop the pain syndrome.

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

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Tatyana Jakowenko

Editor-in-chief of the Detonic online magazine, cardiologist Yakovenko-Plahotnaya Tatyana. Author of more than 950 scientific articles, including in foreign medical journals. He has been working as a cardiologist in a clinical hospital for over 12 years. He owns modern methods of diagnosis and treatment of cardiovascular diseases and implements them in his professional activities. For example, it uses methods of resuscitation of the heart, decoding of ECG, functional tests, cyclic ergometry and knows echocardiography very well.

For 10 years, she has been an active participant in numerous medical symposia and workshops for doctors - families, therapists and cardiologists. He has many publications on a healthy lifestyle, diagnosis and treatment of heart and vascular diseases.

He regularly monitors new publications of European and American cardiology journals, writes scientific articles, prepares reports at scientific conferences and participates in European cardiology congresses.

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