Cardiogenic shock causes emergency medical care. Cardiogenic shock in children and adults: diagnosis and treatment of left ventricular heart failure

Cardiogenic shock characterized by a sudden disruption of the heart. Since this is the main pump of human life, this situation entails serious consequences because significant heart damage occurs.

This leads to cessation of blood circulation, due to which vital organs such as the brain and kidneys do not receive the necessary nutrients.

The vessels lose their tone, therefore, in turn, they are not able to deliver oxygen and blood to these organs and even to the heart itself. This is only a superficial consideration of simple but important functions, which stop working as they should, but in reality everything happens much more complicated, so the consequences are not long in coming.

If we consider normal work our internal pump, then in one contraction it pushes out a certain amount of blood, which is described as stroke volume. The heart contracts on average 70 times per minute, that is, it pumps the minute volume. Thus, we can describe the main indicators of the pumping function of the heart muscle. Now is the time to understand what happens during certain disorders, that is, to see what the pathogenesis of cardiogenic shock is.

Causes

The whole point is that any catastrophe that happens in our body leads to a sharply increased need for oxygen, the lack of which can be compensated for with the help of an increased contraction of the heart, a higher blood pressure and rapid breathing. If an imbalance occurs and the heart or blood vessels are unable to cope with it, then stroke volume, cardiac output, or blood pressure drops. This happens because it is broken important system hearts.

It is important to remember that the heart has its own conduction system, a complete blockage of which leads to the cessation of heart function. The rhythm of excitation is disrupted, or impulses, so the cells are excited out of their rhythm, which can be described as arrhythmia.

Damage to the heart itself contributes to the disruption of full muscle contraction, and this occurs due to impaired nutrition of the heart cells or necrosis. The more necrosis, the more likely development of shock.

If the closure of the artery occurs gradually, shock may also occur with a delay. It is also important to understand that when the heart muscle ruptures, the contraction of the heart is greatly impaired. We can conclude that cardiogenic shock is a consequence of necrosis of 40% of the LV myocardium, which, by the way, is rarely compatible with life.

Role various mechanisms, responsible for the development of cardiogenic shock during MI

This big picture, allowing you to understand why and how the heart’s work goes wrong. It can be seen that all processes are interconnected and disruption of one of them can lead to shock, so there are other causes of cardiogenic shock, let’s look at some.

Myocarditis, that is, inflammation of cardiomyocytes.
Accumulation of fluid in the heart sac. Between the pericardium and myocardium there is a small space containing a certain amount of fluid, thanks to which the heart moves freely, that is, without much friction. With pericarditis, this fluid increases, and a sharp increase in volume leads to tamponade.
Embolism pulmonary artery. The flying thrombus clogs the artery of the lungs, which leads to blockage of the right heart ventricle.

Symptoms

The classification of cardiogenic shock includes five forms of this condition:

Arrhythmic shock. Arterial hypotension develops due to low cardiac output, there is a connection with tachy- or bradyarrhythmia. There is a predominant tachysystolic and bradysystolic form of arrhythmic shock.
Reflex shock. It is characterized by severe pain. The pressure drops due to the reflex effect of the affected area of the heart muscle. This form easily docked in effective ways, so some experts do not classify it as cardiogenic shock.
True cardiogenic shock. This form 100% leads to fatal outcome, because developmental mechanisms lead to irreversible disorders that are incompatible with life.
Shock due to myocardial rupture. In this case, a reflex drop in blood pressure and cardiac tamponade occurs. There is also overload of the left heart parts and a fall contractile function myocardium.
Areactive shock. This is an analogue of true shock, however, there are differences in the greater severity of pathogenetic factors, so the course is especially severe.

In this regard, the clinic of cardiogenic shock is presented as follows:

decrease in blood pressure below 80 mm Hg. Art., and if a person suffers from arterial hypertension, then below 90;
oliguria;
dyspnea;
loss of consciousness;
pallor.

The severity of a patient's condition can be determined by its duration and the person's response to pressor amines. If cardiogenic shock lasts more than five hours and cannot be stopped medicines, and also arrhythmia and pulmonary edema are observed, and areactive shock occurs.

However, it is important to understand that lowering blood pressure is relatively late sign. First, cardiac output decreases, then a reflex develops sinus tachycardia and pulse blood pressure decreases. At the same time, vasoconstriction of blood vessels in the skin, kidneys and brain develops.

Vasoconstriction may help maintain acceptable blood pressure levels. There will be a progressive deterioration in the perfusion of tissues and organs, and, of course, the myocardium. Against the background of severe vasoconstriction, it is determined by auscultation noticeable decrease Blood pressure, although intra-arterial pressure, which is determined by arterial puncture, remains normal.

This means that if invasive pressure control cannot be carried out, it is best to palpate the large arteries, that is, the femoral and carotid, as they are not so susceptible to vasoconstriction.

Diagnostics

It is very easy to identify cardiogenic shock, as this is done on a clinical basis. Considering the severity of the patient’s condition, the doctor simply does not have time to examine him in detail, so the diagnosis is based on objective data.

The skin color is marbled, pale, observed.
Reduced body temperature.
Cold, sticky sweat.
Difficulty, shallow breathing.
The pulse is frequent, thread-like, difficult to palpate, tachyarrhythmia, bradyarrhythmia.
Muffled heart sounds.
Sharply reduced systolic blood pressure, diastolic blood pressure may be less than 20.
MI on ECG.
Decreased diuresis or anuria.
Pain in the heart area.

Quick diagnosis allows you to take the necessary measures in a timely manner

However, it is important to understand that cardiogenic shock manifests itself in different ways; we have listed only the most common symptoms. Such diagnostic studies, like an ECG, coagulogram, ultrasound, and so on, are necessary in order to understand how to proceed further. They are carried out in a hospital setting, if the ambulance team managed to transport the patient to the hospital.

Treatment

Treatment of cardiogenic shock is primarily based on providing emergency care, so anyone should be familiar with the symptoms of this condition and know how to proceed. It cannot be confused with, for example, alcohol intoxication, such a turmoil can cost lives.

Myocardial infarction and subsequent shock can occur anywhere. We sometimes see a person lying on the street who may need resuscitation. Let's not pass by, because a person may be a few minutes from death.

So, if there are signs clinical death, it is necessary to immediately begin resuscitation efforts. You must also immediately call ambulance, another person can do this so as not to waste time.

Emergency care includes artificial respiration And indirect massage hearts. Take the time to explore how it's done and even practice with someone.

However, anyone can call an ambulance. In this case, the dispatcher needs to describe all the symptoms that are observed in the person.

The algorithm of action of ambulance specialists depends on how cardiogenic shock proceeds, but resuscitation measures begin immediately, that is, in the intensive care unit itself.

The patient's legs are elevated at an angle of 15 degrees.
They supply it with oxygen.
The trachea is intubated if the patient is unconscious.
Start infusion therapy if there are no contraindications such as pulmonary edema and swelling of the neck veins. This therapy is based on the use of a solution of rheopolyglucin, prednisolone, thrombolytics and anticoagulants.
Vasopressors are administered to maintain blood pressure at least at a minimum level.
They stop an attack if the rhythm is disturbed. For tachyarrhythmia, electrical pulse therapy is performed; for bradyarrhythmia, accelerating cardiac pacing is used.
Defibrillation and VF are used.
Perform indirect cardiac massage if cardiac activity stops.

Cardiogenic shock is treated not only depending on the pathogenesis, but also on the basis of symptoms. For example, if pulmonary edema is observed, diuretics, nitroglycerin, adequate pain relief are used, and alcohol is also administered. If severe pain is observed, promedol and other drugs are used.

Consequences

Even if cardiogenic shock did not last long, complications such as pulmonary infarction, rhythm disturbances, skin necrosis, and so on can rapidly develop. The condition may be of moderate severity, but mild degree there is no such thing. Even the average severity of the condition does not allow us to talk about good prognosis. Even if the body responds well to treatment, this can quickly give way to a worse picture.

Severe shock does not allow us to talk about survival. Unfortunately, in this case the patient does not respond to treatment, so about 70% of patients die in the first 24 hours, mostly within six hours. The rest die after two or three days. Only 10 people out of 100 can overcome this condition and survive, but many of them subsequently die from heart failure.

In this regard, it becomes clear how necessary it is to carefully monitor your health, starting from childhood, however, it is never too late to change your lifestyle and start all over again!

Cardiogenic shock

Protocol code: SP-010

ICD codes-10:

R57.0 Cardiogenic shock

I50.0 Congestive heart failure

I50.1 Left ventricular failure

I50.9 Heart failure, unspecified

I51.1 Rupture of chordae tendons, not elsewhere classified

I51.2 Rupture of papillary muscle, not elsewhere classified

Definition: Cardiogenic shock– extreme degree of left ventricular failure

pain, characterized by a sharp decrease in myocardial contractility (fall

shock and minute emission), which is not compensated by an increase in vascular

resistance and leads to inadequate blood supply to all organs and tissues,

First of all, vital organs. When a critical amount of myocardium is left-

the third ventricle is damaged, pump failure can be recognized clinically

as pulmonary insufficiency or as systemic hypotension, or both have minor

a hundred at the same time. With severe pumping insufficiency, pulmonary edema may develop.

to their. The combination of hypotension with pump failure and pulmonary edema is known as

cardiogenic shock. Mortality ranges from 70 to 95%.

Classification with the flow:

True cardiogenic.

lecture and arrhythmic shocks, which have a different genesis.

Risk factors:

1. Extensive transmural myocardial infarction

2. Repeated myocardial infarctions, especially heart attacks with rhythm disturbances and conduction

3. Zone of necrosis equal to or greater than 40% of the mass of the left ventricular myocardium

4. Decline in myocardial contractile function

5. Decrease in the pumping function of the heart as a result of the remodeling process,

starting in the first hours and days after the onset of acute coronary occlusion

6. Cardiac tamponade

Diagnostic criteria:

True cardiogenic shock

The patient's complaints about severe general weakness, dizziness, “fog before

eyes”, palpitations, a feeling of interruptions in the heart area, chest pain, suffocation.

1. Symptoms of peripheral circulatory failure:

Gray cyanosis or pale cyanotic, “marbled”, moist skin

Acrocyanosis

Collapsed veins

Cold hands and feet

Nail bed sample for more than 2 s (decreased peripheral blood flow velocity)

2. Impaired consciousness: lethargy, confusion, less often - agitation

3. Oliguria (decrease in diuresis less than 20 mm/hour, with severe course- anuria)

4. Decrease in systolic blood pressure to less than 90 – 80 mm Hg.

5. Decrease in pulse blood pressure to 20 mm Hg. and below.

Percussion: expansion of the left border of the heart; on auscultation, the heart sounds are deep

chie, arrhythmias, tachycardias, protodiastolic gallop rhythm (pathognomonic symptom

severe left ventricular failure).

Breathing is shallow and rapid.

The most severe course of cardiogenic shock is characterized by the development of cardiac

acute asthma and pulmonary edema. Choking appears, breathing is bubbling, coughing with

discharge of pink, frothy sputum. Percussion of the lungs reveals dullness

percussion sound in the lower sections. Here crepitus, fine tufts are also heard.

loud wheezes. As alveolar edema progresses, wheezing is heard more

more than 50% of the lung surface.

The diagnosis is based on identifying a decrease in systolic blood pressure

lower than 90 mmHg, clinical signs of hypoperfusion (oliguria, mental dullness

captivity, pallor, sweating, tachycardia) and pulmonary failure.

A . Reflex shock (pain collapse) develops in the first hours of the disease, in

a period of severe pain in the heart region due to a reflex drop in the general peripheral

ical vascular resistance.

Systolic blood pressure is about 70-80 mm Hg.

Peripheral circulatory failure - pallor, cold sweat

Bradycardia is a pathognomonic symptom of this form of shock

The duration of hypotension does not exceed 1–2 hours, the symptoms of shock disappear spontaneously.

alone or after pain relief

Develops with limited myocardial infarction of the posteroinferior sections

Characterized by extrasystoles, atrioventricular block, rhythm from the AV junction

Clinic of reflex cardiogenic shock corresponds to I degree of severity

B . Arrhythmic shock

1. Tachysystolic (tachyarrhythmic variant) cardiogenic shock

More often develops in the first hours (less often – days of illness) with paroxysmal

ventricular tachycardia, also with supraventricular tachycardia, paroxysmal

atrial fibrillation and atrial flutter. The general condition of the patient is serious.

All clinical signs of shock are expressed:

Significant hypotension

Symptoms of peripheral circulatory failure

Oligoanuria

30% of patients develop severe acute left ventricular failure

Complications - ventricular fibrillation, thromboembolism in vital organs

Relapses of paroxysmal tachycardias, expansion of the necrosis zone, development of car-

diogenic shock

2. Bradysystolic(bradyarrhythmic variant) cardiogenic shock

Develops with complete atrioventricular block with 2:1, 3:1, medical

idioventricular and nodal rhythms, Frederick's syndrome (a combination of complete

atrioventricular block with atrial fibrillation). Bradysystolic cardio-

gene shock is observed in the first hours of development of extensive and transmural infarction

that myocardium

The shock is severe

Mortality reaches 60% or more

Causes of death: severe left ventricular failure, sudden asystto-

heart failure, ventricular fibrillation

There are 3 degrees of severity of cardiogenic shock depending on the severity

clinical manifestations, hemodynamic parameters, response to ongoing

Events:

1. First degree:

Duration no more than 3-5 hours

Systolic blood pressure 90 -81 mm Hg

Pulse blood pressure 30 - 25 mm Hg

Symptoms of shock are mild

Heart failure is absent or mild

Rapid, sustained pressor response to therapeutic measures

2. Second degree:

duration 5 – 10 hours

Systolic blood pressure 80 – 61 mm Hg,

Pulse blood pressure 20 – 15 mm Hg

Symptoms of shock are severe

Severe symptoms of acute left ventricular failure

Slow, unstable pressor response to therapeutic measures

3. Third degree:

More than 10 hours

Systolic blood pressure less than 60 mm Hg, may fall to 0

Pulse blood pressure less than 15 mm Hg

The course of shock is extremely severe

Severe heart failure, severe pulmonary edema,

There is no pressor reaction to treatment, an areactive state develops

List of basic diagnostic measures:

ECG diagnostics

List of additional diagnostic measures:

CVP level measurement (for resuscitation teams)

Tactics of medical care:

For reflex shock, the main treatment measure is quick and complete

anesthesia.

In case of arrhythmic shock, cardioversion or

cardiac stimulation.

In case of shock associated with myocardial rupture, only emergency surgery is effective.

logical intervention.

Treatment program for cardiogenic shock

1.General activities

1.1. Anesthesia

1.2. Oxygen therapy

1.3. Thrombolytic therapy

1.4. Heart rate correction, hemodynamic monitoring

2. Intravenous fluid administration

3. Decrease in peripheral vascular resistance

4. Increased myocardial contractility

5. Intra-aortic balloon counterpulsation

6. Surgical treatment.

Emergency treatment is carried out in stages, quickly moving to the next stage

if the previous one is ineffective.

1. In the absence of pronounced congestion in the lungs:

Lay the patient down with the lower limbs elevated at an angle of 20 degrees;

Carry out oxygen therapy;

Pain relief – morphine 2 – 5 mg IV, again after 30 minutes or fentanyl 1-2 ml

0.005% (0.05 - 0.1 mg with droperidol 2 ml 0.25% IV diazepam 3-5 mg for psychomotor

excitement;

Thrombolytics according to indications;

Heparin 5000 units intravenously;

Correct heart rate (paroxysmal tachycardia with heart rate more than 150 per 1

min – absolute indication for cardioversion)

2. In the absence of pronounced congestion in the lungs and signs of increased central venous pressure:

200 ml 0.9; sodium chloride intravenously over 10 minutes, monitoring blood pressure, central venous pressure, respiratory rate,

auscultatory picture of the lungs and heart;

In the absence of signs of transfusion hypervolemia (CVP below 15 cm H2O.

Art.) continue infusion therapy using rheopolyglucin or dextran or 5%

glucose solution at a rate of up to 500 ml/hour, monitoring the readings every 15 minutes;

If blood pressure cannot be stabilized quickly, proceed to the next stage.

3. If in/ fluid administration is contraindicated or unsuccessful, introduce peri-

spherical vasodilators - sodium nitroprusside at a rate of 15 - 400 mcg/min or

isoket 10 mg in infusion solution intravenously.

4. Inject dopamine(dopamine) 200 mg in 400 ml of 5% glucose solution in the form of intravenous

rivinny infusion, increasing the infusion rate from 5 mcg/kg/min) until a minimum

low sufficient blood pressure;

No effect - additionally prescribe norepinephrine hydrotartrate 4 mg in 200 ml

5% glucose solution intravenously, increasing the infusion rate from 5 mcg/min to reach

reducing the minimum sufficient blood pressure

Main dangers and complications:

Inability to stabilize blood pressure;

Pulmonary edema due to increased blood pressure or intravenous administration

liquids;

Tachycardia, tachyarrhythmia, ventricular fibrillation;

Asystole;

Recurrence of anginal pain;

Acute renal failure.

List of essential medications:

1.*Morphine hydrochloride 1% 1 ml, amp

2.*Heparin 5 ml vial, with activity 5000 units in 1 ml

3.*Alteplase 50 mg powder for the preparation of infusion solution, fl

4.*Streptokinase 1,500,000 IU, powder for solution, fl

5.*Sodium chloride 0.9% 500 ml, fl

6.*Glucose 5% 500 ml, fl

7.*Reopoliglucin 400 ml, fl

8.*Dopamine 4% 5 ml, amp

List of additional medications

1.*Fentanyl 0.005% 2 ml, amp

2.*Droperidol 0.25% 10 ml, amp (fl)

3.*Diazepam 0.5% 2 ml, amp

5.*Isosorbide dinitrate (isoket) 0.1% 10 ml, amp

6.*Norepinephrine hydrotartrate 0.2% 1 ml, amp

Indicators of the effectiveness of medical care:

Relief of pain syndrome.

Relief of rhythm and conduction disturbances.

Relief of acute left ventricular failure.

Stabilization of hemodynamics.

Cardiogenic shock is a severe condition of cardio-vascular system, the mortality rate of which reaches 50–90%.

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

Simply put, this is the inability of the heart to pump blood and push it into the vessels. The vessels are not able to hold blood because they are in an expanded state, as a result of which blood pressure drops and blood does not reach the brain. The brain experiences 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. Break interventricular septum heart (IVS). The IVS is a septum that separates the right ventricle of the heart from the left.

4. Cardiac arrhythmias (heart rhythm disturbances).

5. Acute insufficiency (dilation) of heart valves.

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

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

Types of cardiogenic shock (CS)

1. Disorder of the pumping function of the heart.

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

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

The body abruptly stops its work and death occurs.

2. Severe violations heart rate

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

3. Ventricular tamponade

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

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

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

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

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

Clinical manifestations (symptoms and signs) of cardiogenic shock

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

Loss of consciousness.

Coldness of the extremities.

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

Risk factors for cardiogenic shock (CS)

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

Repeated myocardial infarction with cardiac arrhythmia.

Diabetes.

Elderly age.

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

Diagnosis of cardiogenic shock (CS)

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

Loss of consciousness.

Coldness of the extremities.

Tachycardia (increased heart rate).

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

Collapsed veins on the limbs.

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

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

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

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

Angiography is an X-ray contrast method for diagnosing vascular diseases. At the same time, in femoral artery introduce contrast agent, which, when it enters the blood, stains the vessels and outlines the defect.

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

Treatment of cardiogenic shock (CS)

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

Drug treatment of cardiogenic shock (CS)

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

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

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

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

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

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

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

Surgical treatment of cardiogenic shock (CS)

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

1. Percutaneous transluminal coronary angioplasty

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

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

2. Intra-aortic balloon counterpulsation

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

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

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

Cardiogenic shock

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

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

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

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

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

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

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

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

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

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

The sequence of treatment measures for cardiogenic shock:

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

Normalization of heart rhythm. Stabilization of hemodynamics is impossible without eliminating heart rhythm disturbances, since an acute attack of tachycardia or bradycardia in conditions of myocardial ischemia leads to sharp decline shock and minute ejection. The most effective and in a safe way Relieving tachycardia with low blood pressure is electrical pulse therapy. If the situation allows drug treatment, choice antiarrhythmic drug depends on the type of arrhythmia. In case of bradycardia, which, as a rule, is caused by acutely occurring atrioventricular block, almost the only effective means is endocardial pacing. Injections of atropine sulfate most often do not provide a significant and lasting effect.

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

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

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

Cardiogenic shock and its causes

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

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

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

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

Figure: causes of cardiogenic shock in percentage terms

Forms of cardiogenic shock

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

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

pathologies - causes of development of cardiogenic shock and their localization

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

Reduction of systolic blood pressure below permissible level 80 mmHg Art. (for those suffering arterial hypertension– below 90 mm Hg. Art.);
Diuresis less than 20 ml/h (oliguria);
Paleness of the skin;
Loss of consciousness.

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

Pathogenetic mechanisms of cardiogenic shock

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

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

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

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

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

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

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

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

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

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

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

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

Prognosis and life chances

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

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

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

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

Graph: survival after cardiogenic shock in Europe

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

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

– 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 clinical picture, ECG results, tonometry. The goal of treatment is to stabilize hemodynamics and restore heart rhythm. As part of emergency therapy, beta blockers, cardiotonics, narcotic analgesics, oxygen therapy.

Complications

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

Diagnostics

Diagnosis is carried out on the basis of physical, laboratory and instrumental examination. When examining a patient, a cardiologist or resuscitator notes external signs diseases (pallor, sweating, marbling of the skin), 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. On initial stage hypotension may be absent due to the inclusion of compensatory mechanisms. Heart sounds are muffled, moist fine rales are heard in the lungs.
Electrocardiography. A 12-lead ECG reveals characteristic features myocardial infarction: decreased amplitude of the R wave, displacement S-T segment, negative T wave. Signs of extrasystole and atrioventricular block may be observed.
Laboratory research. The concentration of troponin, electrolytes, creatinine and urea, glucose, and liver enzymes is assessed. The level of troponins I and T increases already in the first hours of AMI. 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. Absent during syncope major changes on ECG, in medical history - painful effect or psychological stress.

Treatment of cardiogenic shock

Patients with acute heart failure and signs of shock are urgently hospitalized in a cardiology hospital. The ambulance team responding to such calls must include a resuscitator. On prehospital stage Oxygen therapy is carried out, central or peripheral venous access 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 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. Appointed antiarrhythmic drugs(amiodarone), cardiotonics, narcotic analgesics, steroid hormones. 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 rate is significantly higher among patients who underwent surgical intervention, aimed at restoring the patency of damaged coronary vessels.

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

Currently, the classification of cardiogenic shock proposed by E.I. Chazov (1969) is generally accepted.

True cardiogenic shock - it is based on the death of 40 or more percent of the mass of the left ventricular myocardium.

Reflex shock - it is based on a pain syndrome, the intensity of which is often not related to the extent of myocardial damage. This type shock may be complicated by a violation of vascular tone, which is accompanied by the formation of a deficit of blood volume. Quite easily corrected with painkillers, vascular means and infusion therapy.

Arrhythmic shock - it is based on rhythm and conduction disturbances, which causes a decrease in blood pressure and the appearance of signs of shock. Treatment of cardiac arrhythmias usually relieves signs of shock.

Areactive shock can develop even against the background of a small lesion in the left ventricular myocardium. It is based on a violation of myocardial contractility caused by impaired microcirculation, gas exchange, and the addition of disseminated intravascular coagulation syndrome. Characteristic of this type of shock is the complete lack of response to the administration of pressor amines.

4§Clinical picture

Clinically, with all types of cardiogenic shocks, the following signs are noted: a typical AMI clinic with characteristic signs on the ECG, confusion, adynamia, skin grayish-pale, covered with cold, sticky sweat, acrocyanosis, shortness of breath, tachycardia, significant hypotension in combination with a decrease in pulse pressure. Oligoanuria is noted. Laboratory confirmation of AMI is the characteristic dynamics of specific enzymes (transaminases, lactate dehydrogenase “LDH”, creatine phosphokinase “CPK”, etc.).

Clinical picture of true cardiogenic shock

True cardiogenic shock usually develops in patients with extensive transmural myocardial infarction of the anterior wall of the left ventricle (often thrombosis of two or three coronary arteries is observed). The development of cardiogenic shock is also possible with extensive transmural infarctions of the posterior wall, especially with simultaneous spread of necrosis to the myocardium of the right ventricle. Cardiogenic shock often complicates the course of repeated myocardial infarctions, especially those accompanied by disturbances in heart rhythm and conduction, or in the presence of symptoms of circulatory failure even before the development of myocardial infarction.

The clinical picture of cardiogenic shock reflects severe disturbances in the blood supply to all organs, primarily vital ones (brain, kidneys, liver, myocardium), as well as signs of insufficient peripheral circulation, including in the microcirculatory system. Insufficient blood supply to the brain leads to the development of dyscirculatory encephalopathy, renal hypoperfusion leads to acute renal failure, insufficient blood supply to the liver can cause the formation of foci of necrosis in it, circulatory disorders in the gastrointestinal tract can cause acute erosions and ulcers. Hypoperfusion of peripheral tissues leads to severe trophic disorders.

The general condition of a patient with cardiogenic shock is severe. The patient is inhibited, consciousness may be darkened, complete loss of consciousness is possible, and short-term excitation is less common. The patient’s main complaints are complaints of severe general weakness, dizziness, “fog before the eyes,” palpitations, a feeling of interruptions in the heart area, and sometimes chest pain.

When examining the patient, attention is drawn to “gray cyanosis” or pale cyanotic coloration of the skin; there may be pronounced acrocyanosis. The skin is damp and cold. The distal parts of the upper and lower extremities are marble-cyanotic, the hands and feet are cold, and cyanosis of the subungual spaces is noted. The appearance of the “white spot” symptom is characteristic - an increase in the time it takes for the white spot to disappear after pressing on the nail (normally this time is less than 2 s). The above symptoms are a reflection of peripheral microcirculatory disorders, the extreme degree of which may be skin necrosis in the area of the tip of the nose, ears, distal fingers and toes.

The pulse on the radial arteries is thread-like, often arrhythmic, and often cannot be detected at all. Blood pressure is sharply reduced, always less than 90 mm. rt. Art. A decrease in pulse pressure is characteristic; according to A.V. Vinogradov (1965), it is usually below 25-20 mm. rt. Art. Percussion of the heart reveals an expansion of its left border; characteristic auscultatory signs are dullness of heart sounds, arrhythmias, low systolic murmur at the apex of the heart, protodiastolic gallop rhythm (pathognomonic symptom of severe left ventricular failure).

Breathing is usually shallow and may be rapid, especially with the development of “shock” lung. The most 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 disturbing cough with pink, frothy sputum. When percussing the lungs, a dullness of the percussion sound in the lower parts is determined; crepitus and fine bubbling rales due to alveolar edema are also heard here. If there is no alveolar edema, crepitus and moist rales are not heard or are determined in small quantities as a manifestation of congestion in the lower parts of the lungs, a small amount of dry rales may appear. With severe alveolar edema, moist rales and crepitus are heard over more than 50% of the lung surface.

When palpating the abdomen, pathology is usually not detected; in some patients, liver enlargement may be detected, which is explained by the addition of right ventricular failure. The development of acute erosions and ulcers of the stomach and duodenum is possible, which is manifested by epigastric pain, sometimes bloody vomiting, and pain on palpation of the epigastric region. However, these changes in the gastrointestinal tract are rarely observed. The most important sign of cardiogenic shock is oliguria or oligoanuria; during bladder catheterization, the amount of urine released is less than 20 ml/h.

Laboratory data

Blood chemistry. Increased bilirubin content (mainly due to the conjugated fraction); an increase in glucose levels (hyperglycemia can be 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); an increase in the level of urea and creatinine in the blood (as a manifestation of acute renal failure caused by renal hypoperfusion; an increase in the level of alanine aminotransferase (a reflection of impaired liver function).

Coagulogram. Increased blood clotting activity; platelet hyperaggregation; high content in the blood of fibrinogen and fibrin degradation products - markers of DIC syndrome;

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

Study gas composition blood. Detects a decrease in partial oxygen tension.

Severity of cardiogenic shock

Taking into account the severity of clinical manifestations, response to measures taken, and hemodynamic parameters, 3 degrees of severity of cardiogenic shock are distinguished.

Diagnosis of true cardiogenic shock

Diagnostic criteria for cardiogenic shock:

1. Symptoms of peripheral circulatory failure:

Pale cyanotic, marbled, moist skin

Acrocyanosis

Collapsed veins

Cold hands and feet

Decreased body temperature

Prolongation of time for disappearance of the white spot after pressure on the nail > 2 s (decreased peripheral blood flow velocity)

2. Impaired consciousness (lethargy, confusion, possibly unconsciousness, less often - agitation)

3. Oliguria (decreased diuresis< 20 мл/ч), при крайне тяжелом течении - анурия

4. Decrease in systolic blood pressure to< 90 мм. рт. ст (по некоторым данным менее80 мм. рт. ст), у лиц с предшествовавшей артериальной гипертензией < 100 мм. рт. ст. Длительность гипотензии >30 min

5. Decrease in pulse blood pressure to 20 mm. rt. Art. and below

6. Reduced mean arterial pressure< 60 мм. рт. ст. или при мониторировании снижение (по сравнению с исходным) среднего артериального давления >30 mm. rt. Art. for >= 30 min

7. Hemodynamic criteria:

pulmonary artery wedge pressure > 15 mm. rt. st (> 18 mm Hg, according to

Antman, Braunwald)

cardiac index< 1.8 л/мин/м2

increased total peripheral vascular resistance

increased left ventricular end-diastolic pressure

reduction in stroke and minute volumes

A clinical diagnosis of cardiogenic shock in patients with myocardial infarction can be made based on the detection of the first 6 available criteria. Determining hemodynamic criteria (point 7) for diagnosing cardiogenic shock is usually not mandatory, but is very advisable for organizing correct treatment.

Clinical picture of the reflex form of cardiogenic shock

As stated earlier, the reflex form of cardiogenic shock develops as a result of reflex effects from the focus of necrosis on the tone of peripheral vessels (the total peripheral vascular resistance does not increase, but rather decreases, probably due to a decrease in the activity of the sympathoadrenal system).

Reflex cardiogenic shock usually develops in the first hours of the disease, during severe pain in the area of the heart. The reflex form of cardiogenic shock is characterized by a drop in blood pressure (usually systolic blood pressure is about 70-80 mm Hg, less often lower) and peripheral symptoms of circulatory failure (pallor, cold sweat, cold hands and feet). The pathognomonic feature of this form of shock is bradycardia.

It should be noted that the duration of arterial hypotension most often does not exceed 1-2 hours, the symptoms of shock quickly disappear after pain relief.

The reflex form of cardiogenic shock usually develops in patients with a primary and fairly limited myocardial infarction, localized in the posteroinferior region, and is quite often accompanied by extrasystole, atrioventricular block, and a rhythm from the atrioventricular junction. In general, we can assume that the clinical picture of the reflex form of cardiogenic shock corresponds to grade I of severity.

Clinical picture of the arrhythmic form of cardiogenic shock

Tachysystolic (tachyarrhythmic) variant of cardiogenic shock

Most often develops with paroxysmal ventricular tachycardia, but can also occur with supraventricular tachycardia, paroxysmal atrial fibrillation and atrial flutter. This variant of arrhythmic cardiogenic shock develops in the first hours (less often, days) of the disease. The general condition of the patient is severe, all Clinical signs shock (significant arterial hypotension, symptoms of peripheral circulatory failure, oligoanuria). Approximately 30% of patients with the tachysystolic variant of arrhythmic cardiogenic shock develop severe left ventricular failure (cardiac asthma, pulmonary edema). The tachysystolic variant of cardiogenic shock can be complicated by life-threatening conditions - ventricular fibrillation, thromboembolism in vital organs. With this form of shock, relapses of ventricular paroxysmal tachycardia are often observed, which contributes to the expansion of the necrosis zone and then the development of true areactive cardiogenic shock.

Bradysystolic (bradyarrhythmic) variant of cardiogenic shock

It usually develops with complete atrioventricular block of the distal type with conduction 2:1, 3:1, slow idioventricular and nodal rhythms, Frederick's syndrome (a combination of complete atrioventricular block with atrial fibrillation). Bradysystolic cardiogenic shock is observed in the first hours of the development of extensive and transmural myocardial infarction. The course of shock is usually severe, with mortality reaching 60% or more. The causes of death are severe left ventricular failure, sudden cardiac asystole, and ventricular fibrillation.