Cardiogenic shock signs of emergency care. Cardiogenic shock in children and adults: diagnosis and treatment of left ventricular heart failure
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
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 complains of 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, in severe cases - anuria)
4. Decreased systolic blood pressure 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
noah 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.
wheezing. 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 infarctions of the posterior lower sections
Characterized by extrasystoles, atrioventricular blockade, rhythm from the AV junction
The clinic of reflex cardiogenic shock corresponds to I degree of severity
B . Arrhythmic shock
1. Tachysystolic (tachyarrhythmic variant) of cardiogenic shock
More often it develops in the first hours (less often - the days of the disease) with paroxysmal
ventricular tachycardia, also with supraventricular tachycardia, paroxysmal
atrial fibrillation and atrial flutter. The general condition of the patient is severe.
All clinical signs of shock are expressed:
Significant arterial hypotension
Symptoms of peripheral circulatory insufficiency
Oligoanuria
30% of patients develop severe acute left ventricular failure
Complications - ventricular fibrillation, thromboembolism in vital or-
Relapses 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 BP 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, rapid pulmonary edema,
There is no pressor response to treatment, an areactive state develops
List of main diagnostic measures:
ECG diagnostics
List of additional diagnostic measures:
CVP level measurement (for resuscitation teams)
Tactics of rendering medical care :
With reflex shock, the main therapeutic measure is quick and complete.
anesthesia.
For life-saving arrhythmic shock, cardioversion or
cardiac stimulation.
In 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 drip.
4. Inject dopamine(dopamine) 200 mg in 400 ml of 5% glucose solution as an 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 medicines
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
Health Care Performance Indicators:
Relief of pain syndrome.
Relief of rhythm and conduction disturbances.
Relief of acute left ventricular failure.
Stabilization of hemodynamics.
Cardiogenic shock (CS) is a critical state of tissue microcirculation against the background of inadequate cardiac output caused by decreased contractility heart muscle.
The main mechanisms of CABG are reduced to a decrease in cardiac output, peripheral vasospasm, a decrease in BCC - the volume of circulating blood, disruption of capillary blood flow and intravascular coagulation. Most often, CABG is a fatal complication of myocardial infarction.
In accordance with the classification of Academician E.I. Chazov, there are several types of cardiogenic shock, differing in the cause of occurrence, clinical features and treatment of the condition:
- KSh true;
- KS artmic;
- CS reflex;
- KS is reactive.
Reflex form of CS occurs against the background of heightened pain and is explained by reflex paresis of blood vessels with subsequent stagnation of blood in them and leakage of plasma into the intercellular tissue space. The result of a decrease in blood flow to the heart muscle is a decrease in heart beats and a drop in pressure. This form of CABG often occurs in cases of posterior wall myocardial infarction.
True KSH is based on a sharp decrease in the contractility of the left ventricle, leading to a decrease in its minute volume (MV). The most serious circulatory disorders that occur with true CABG quickly lead to changes in all organs and tissues and are accompanied by anuria.
Arrhythmic form CABG is diagnosed in cases where a clear connection between the disorder is recorded peripheral microcirculation and decline in pressure with disturbances heart rate and conductivity. Typically with restoration normal rhythm manages to relieve symptoms of shock.
Areactive form CABG is confirmed by the absence of a vascular response to the administration of even large doses of norepinephrine. This form of shock is the most resistant to therapeutic effects and in most cases ends in death.
Causes
There are several etiological factors development of KSh. The following clinical situations most often lead to it:
- disorders of intracardiac hemodynamics of mechanical origin (rupture of the valve or chordae tendineae, malformations, neoplasms);
- decreased pumping function of the heart due to left ventricular failure (sepsis, pancarditis, cardiomyopathy, myocardial infarction);
- arrhythmogenic pathology (atrioventricular blockade, brady- and tachyarrhythmias);
- insufficient filling of the heart chambers during diastole (with pericardial tamponade);
- autoimmune rejection (heart transplantation);
- postoperative complications (damage or rupture of the artificial heart valve);
- thromboembolism of the pulmonary arteries.
In 60-95% of cases, CABG aggravates the course of MI, manifesting itself against the background of a critical decline in the pumping function of the left ventricle.
Risk factors that increase the likelihood of developing shock conditions are:
- extensive MI involving more than 40% of the anterior wall surface;
- severe ischemia of the areas of the heart surrounding the necrosis zone;
- the presence of old scar changes with repeated MI;
- critical decrease in the functional capacity of the left ventricle (less than 40%);
- age of the patient (50 years or more);
- damage to the intracardiac papillary muscles due to their necrosis;
- integrity violations interventricular septum;
- right ventricular myocardial infarction;
- diabetes mellitus accompanying myocardial infarction.
Cardiogenic shock most often results from myocardial infarction. And rehabilitation measures are described in detail in the article.
What's happened arrhythmogenic shock and how to treat it, read.
The most dangerous complication pancreatitis is a pancreatogenic shock, which in almost half of the cases leads to the death of the patient. In this topic, we will look at the symptoms and treatment methods for this condition.
Symptoms
The specificity of complaints of patients with CABG is associated with the nature of the underlying pathology. As a rule, patients are concerned about:
- pain in the heart area (behind the breastbone);
- palpitations and interruptions in heart function;
- weakness;
- dizziness;
- dyspnea;
- decrease in the amount of urine excreted (oligo-, anuria);
- cold extremities;
- increased sweating;
- feeling of fear.
An objective examination of a patient in CABG status reveals symptoms of extreme severity of his condition. In the initial stage, as a rule, it is expressed psychomotor agitation, which soon gives way to lethargy and adynamia. Consciousness gradually fades along with the loss of interest in the environment, which indicates an increase in hypoxic processes in the brain.
Skin that is cold to palpation is pale, with pronounced cyanosis, and covered with sweat. Ripple radial arteries characterized by weak filling and tension, up to a thread-like pulse or its absence. As a rule, the level of systolic blood pressure is below 80 mmHg, but in some cases it can rise to 90 and above (mainly in the presence of anamnestic arterial hypertension).
Typical signs for CABG are a critical decrease in the pulse wave (from 30 to 10 mm Hg) and pronounced dullness of heart sounds during cardiac auscultation, gallop rhythm and systolic murmur. IN terminal states tones are not audible, so determining blood pressure by auscultation becomes impossible. On the part of the lungs, tachypnea and a shallow type of breathing are observed, which in the terminal stages acquires an aperiodic type (Cheyne-Stokes). The presence of moist rales indicates the development of pulmonary edema against the background of stagnation in the pulmonary circulation.
Prognostically adverse symptom with CABG, a decrease in diuresis of less than 20 ml of urine excreted per hour is considered to indicate an extreme degree of microcirculation impairment in the kidneys.
Mechanisms of occurrence
The main pathogenetic mechanisms that trigger the chain pathological processes with CABG, are the loss of the bulk of the myocardium due to occlusion of the main arteries supplying the heart, leading to multiple organ failure, and in some cases, the death of the patient.
Against the background of hypotension, which develops as a result of necrosis of the heart muscle, a syndrome of hypoperfusion of the surviving areas of the myocardium develops, followed by a deterioration in the contractility of the ventricles of the heart.
Once the loss of non-functioning myocardial mass reaches 40% of the volume of the left ventricle, irreversible consequences KSH.
Compensatory reactions from the nervous and endocrine systems V initial stages CABGs are adaptive in nature and are aimed at increasing cardiac output. Subsequently, an increase in heart rate leads to an increase in oxygen consumption by the myocardium and reflex vascular spasm. This is accompanied by the accumulation of under-oxidized products in tissues, the development of metabolic acidosis and tissue hypoxia.
In addition, against the background of damage to the vascular endothelium, significant retention of fluid and sodium occurs in the body.
The resulting cardiac arrhythmias only worsen cardiac function and in some cases lead to the death of the patient due to multiple organ failure.
Diagnosis of cardiogenic shock
Since CS is a clinical syndrome, its diagnosis includes the presence of a set of symptoms characteristic of hypoperfusion individual organs and the body as a whole:
- arterial hypotension (less than 80 mm Hg);
- decrease pulse pressure(less than 20 mmHg);
- decreased urine output (anuria or oliguria less than 20 ml per hour);
- lethargy and other disturbances of consciousness;
- symptoms of microcirculation crisis (marbled, pale skin color, cold extremities, acrocyanosis);
- signs of metabolic acidosis.
The absence of specific symptoms pathognomonic for CS makes possible staging diagnosis of cardiogenic shock solely on the basis of a combination of several clinical symptoms. In this case, one should take into account the variability of the signs of CS in each case, depending on the main diagnosis against which the shock developed.
Acute myocardial infarction of the anterior wall of the left ventricle
Objectification of hemodynamic and other disorders during CABG is achieved using:
- chest radiography;
- coronary angiography;
- direct determination of cardiac output;
- measuring pressure in the cavities of the heart;
- echocardiography;
- hemodynamic monitoring.
Emergency care for cardiogenic shock - algorithm
Successful treatment of any form of CABG begins with effective pain relief.
Taking into account the hypotensive effect of narcotic analgesics, their prescription is combined with drugs from the sympathomimetic group (mesaton).
Cardiac bradycardia is an indication for intravenous atropine.
With reflex KSh, the patient's legs are raised in order to increase the volume of blood flowing to the heart. In the absence of consciousness, tracheal intubation is indicated. Lidocaine is used to prevent cardiac arrhythmias. With the help of oxygen therapy (through a maxa or a catheter), an improvement in the supply of oxygen to tissues is achieved. Ventricular fibrillation is a direct indication for defibrillation.
Treatment
The complex of therapeutic measures for the relief of CABG consists of:
- general measures (analgesics, thrombolytics, oxygenation, hemodynamic monitoring);
- infusion therapy (in the absence of contraindications);
- vasodilators;
- inotropic drugs (improvement of myocardial contractility);
- electropulse therapy - to eliminate cardiac arrhythmias;
- electrocardiostimulation - with conduction disorders.
In addition, instrumental methods for the treatment of CS include balloon counterpulsation inside the aorta. With ruptures of the interventricular septum, surgical treatment is indicated (also for ruptures or dysfunction of the papillary muscles).
Prognosis and life chances
The prognosis for CABG is very serious and is largely determined by the degree of myocardial damage, the timeliness of diagnosis and the adequacy of therapeutic measures.Prognostically unfavorable is the unreactive form of CABG.
When adequate reaction a favorable outcome is possible on the therapeutic effect and an increase in the level of blood pressure.
However, in some cases, the clinical picture may reverse. Severe forms CABG in 70% of cases lead to death during the first hours and days of illness.
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Description:
Cardiogenic shock (CS) is a critical, lethal condition, which is an acute decrease in myocardial contractility with impaired blood supply to vital organs.
The condition is more common in states with low level medical care, including preventive care.
Important! Mortality in patients with cardiogenic shock is 60-100%.
Causes:
If we talk about the mechanism of development of KSh, then there are several main directions:
Violation of the contractility of the left heart;
severe arrhythmias;
- accumulation of fluid between the leaves of the heart sac
(blood or inflammatory effusion);
blockage of blood vessels, carrying blood to the lungs.
Now about the reasons that provoke these mechanisms:
1. Myocardial infarction is the cause of CABG in 8 out of 10 cases. The main condition for the development of cardiogenic shock in a heart attack is the "shutdown" of at least half of the volume of the heart. Massive transmural damage leads to such a serious condition.
5. pulmonary trunk.
6. Effect of cardiotoxic substances. These include cardiac glycosides, reserpine, clonidine, and some insecticides. As a result of exposure to these compounds, blood pressure decreases, heart rate slows down to a level that is ineffective for
blood supply to organs.
Important! At risk for CABG are people over 65 years of age, with a history of myocardial infarction, with concomitant diabetes mellitus.
Symptoms:
The symptoms of cardiogenic shock are acute, bright and affect several body systems at once. At first it comes to the fore. The pain is of a compressive nature, localized in the center behind the sternum, radiating to left hand, shoulder blade, jaw. This is the stage sudden violation blood flow in the wall of the heart. As a result of the shutdown of the most active and important department - the left ventricle, a symptom complex occurs with pulmonary edema:
1. Respiratory disorders. Respiratory rate less than 12 per minute, blue skin and mucous membranes, participation in the act of inhalation of auxiliary muscles (nose wings, intercostal muscles), foam from the mouth.
2. Panic, fear of death.
3. Forced position - sitting, with the torso tilted forward, arms resting
on a hard surface.
Due to inadequate functioning of the lungs, proper gas exchange and oxygen saturation of tissues do not occur. It leads to oxygen starvation other body systems
1. Central nervous system - disturbance of consciousness varying degrees, up to coma.
2. CCC -, arterial hypotension.
3. MVP - absence of urine.
4. Gastrointestinal tract - "coffee grounds", violation of peristalsis,
Important! In most cases of myocardial infarction clinical manifestations cardiogenic shock join within 2 days.
Diagnostics:
Examination algorithm:
1. General inspection- pale (bluish) color of the skin, cold sweat, impaired consciousness (stupefaction or disinhibition), systolic blood pressure less than 90 mm Hg, more than 30 minutes, muffled heart sounds, cardiac murmur, noisy breathing, a mass of wet rales, with a release of pink foam.
3. Blood pressure monitoring.
4. - determination of blood oxygen saturation by percutaneous method.
5. Laboratory research- blood biochemistry, determination of markers of myocardial damage (troponin, MB-CK, LDH), kidney waste (creatinine, urea), liver enzymes.
6. Ultrasound of the heart.
7. Emergency coronary angiography.
Treatment:
For treatment the following is prescribed:
Important! A patient with suspected CABG requires mandatory, urgent hospitalization!
On prehospital stage in case of cardiogenic shock, emergency measures are taken - restoration of breathing (ventilation with a bag and mask), removal pain attack, infusion of fluid into a vein.
The main directions of treatment of CABG in a hospital setting:
1. Oxygen therapy - the mixture is supplied during spontaneous breathing through nasal catheters and a face mask. In severe respiratory failure or in the absence of breathing, the patient is transferred to artificial oxygen-dependent ventilation.
2. Maintenance blood pressure in organs using constant infusion of inotropic drugs (dopamine, dobutamine). The dose is calculated taking into account the weight of the patient and the severity of the condition.
3. Thrombolytic therapy - dissolution of blood clots with drugs streptokinase, urokinase, tissue plasminogen activator.
4. Pain relief with narcotic analgesics.
Important! The use of nitroglycerin preparations to reduce pain is undesirable! They have by-effect as an extension peripheral vessels and additional reduction in peripheral pressure.
Conservative therapy usually has a short-term positive effect. To normalize blood circulation in the organs, it is necessary to restore the functioning of the heart. To correct myocardial ischemia, highly specialized procedures are used:
1. Balloon counterpulsation - pumping blood into the aorta with a special medical “pump”.
2. Artificial ventricle - a device that simulates the function of the left ventricle of the heart.
3. Balloon stenting of myocardial vessels - insertion of a probe into the cavity of the coronary arteries, which expands the lumen of the vessels.
Despite modern capabilities intensive care and cardiac surgery, the prognosis for health and life is unfavorable. Mortality in cardiogenic shock remains critical.
One of the most severe conditions encountered in emergency medical practice is cardiogenic shock, which develops mainly as a complication of acute myocardial infarction.
Cardiogenic shock most often occurs with prolonged (several hours) anginal (painful) status. However, sometimes its development is possible even with moderate pain and even with silent myocardial infarction.
The development of cardiogenic shock is based on a decrease in cardiac output as a result of a sharp decrease in myocardial contractile function. Heart rhythm disturbances, which often occur in acute period myocardial infarction. The severity of cardiogenic shock and its prognosis are determined by the size of the necrosis focus.
Pathogenesis
With cardiogenic shock, peripheral vascular tone increases, peripheral resistance increases, and acute circulatory failure develops with a pronounced decrease in blood pressure (BP). The liquid part of the blood goes beyond the vascular bed into pathologically dilated vessels. So-called blood sequestration develops with hypovolemia and a decrease in central venous pressure (CVP). Arterial hypovolemia (decreased circulating blood volume) and hypotension lead to decreased blood flow in the various organs and tissues: kidneys, liver, heart, brain. Metabolic acidosis (accumulation of acidic metabolic products) and tissue hypoxia appear, and vascular permeability increases.
The famous Soviet cardiologist academician. B.I. Chazov identified 4 forms of cardiogenic shock. A clear knowledge of them, as well as the main links in the pathogenesis of cardiogenic shock, is necessary for average medical workers prehospital level, since only under this condition is it possible to carry out a comprehensive, rational and effective therapy aimed at saving the patient's life.
Reflex shock
With this form, the main importance is reflex influences from the focus of necrosis, which is a painful stimulus. Clinically, such shock occurs most easily, with proper and timely treatment the prognosis is more favorable.
"True" cardiogenic shock
IN in its development, the main role is played by disturbances in the contractile function of the myocardium due to profound metabolic disorders. This type of shock has a pronounced clinical picture.
Areactive shock
This is the most severe form of shock, observed in cases of complete exhaustion of the body's compensatory capabilities. Almost impossible to treat.
Arrhythmic shock
The clinical picture is dominated by arrhythmia: both an increase in the number of heart contractions (tachycardia) and a decrease in heart rate (bradycardia) up to complete atrioventricular block.
The pathogenesis in both cases is based on a decrease in cardiac output, but in the case of tachycardia this occurs due to sharp increase heart contractions, a decrease in the time of diastolic filling of the heart and systolic ejection, with bradycardia - due to a significant decrease in heart rate, which also leads to a reduction in cardiac output.
V.N. Vinogradov, V.G. Popov and A.S. Smetnev, according to the severity of the course, 3 degrees of cardiogenic shock were distinguished:
- relatively light
- moderate severity
- extremely heavy.
Cardiogenic shockI degrees The duration usually does not exceed 3 - 5 hours. Blood pressure 90/50 - 60/40 mm Hg. Art. It should be taken into account that in patients with initial hypertension, blood pressure may be within normal limits, masking the existing (compared to the initial level) hypotension. In most patients, 40 - 50 minutes after carrying out rational complex therapeutic measures, a fairly rapid and steady increase in blood pressure is observed, the disappearance of peripheral signs of shock (pallor and acrocyanosis decrease, limbs become warmer, the pulse becomes slower, its filling and tension increase).
However, in some cases, especially in elderly patients, the positive dynamics after the start of treatment may be slow, sometimes followed by a short-term decrease in blood pressure and the resumption of cardiogenic shock.
Cardiogenic shockIIdegrees differs in longer duration (up to 10 hours). Blood pressure is lower (within 80/50 - 40/20 mm Hg). Peripheral signs of shock are much more pronounced; there are often symptoms of acute left ventricular failure: shortness of breath at rest, cyanosis, acrocyanosis, congestive moist rales in the lungs, and sometimes their swelling. Reaction to introduction medicines unstable and slow; during the first day there is a multiple decrease in blood pressure and a resumption of shock.
Cardiogenic shockIIIdegrees characterized by extremely severe and long course With sharp drop, blood pressure (up to 60/40 mm Hg and below), decreased pulse pressure (the difference between systolic and diastolic blood pressure is less than 15 mm Hg), progression of disorders peripheral circulation and an increase in the symptoms of acute heart failure. In 70% of patients, alveolar pulmonary edema develops, characterized by a rapid course. The use of drugs that increase blood pressure and other components of complex therapy is usually ineffective. The duration of such areactive shock 24 - 72 hours, sometimes it becomes protracted and undulating and usually ends in death.
Main clinical symptoms cardiogenic shock are hypotension, a decrease in pulse pressure (a decrease to 20 mm Hg or less is always accompanied by peripheral signs of shock, regardless of the level of blood pressure before the disease), pallor of the skin, often with a gray-ash or cyanotic tint, cyanosis and coldness of the extremities, cold sweat, small and frequent, sometimes detectable pulse, dullness of heart sounds, cardiac arrhythmias of various types. With very severe shock, a characteristic marbled skin pattern appears, which indicates an unfavorable prognosis. Due to a drop in blood pressure, renal blood flow decreases, oliguria and anuria occur. A bad prognostic sign is diuresis less than 20 - 30 ml/day (less than 500 ml/day).
In addition to circulatory disorders, with cardiogenic shock, psychomotor agitation or adynamia, sometimes confusion or temporary loss of consciousness, and skin sensitivity disorders are observed. These phenomena are caused by cerebral hypoxia under conditions severe violation blood circulation In some cases, cardnogenic shock may be accompanied by persistent vomiting, flatulence, and intestinal paresis (the so-called gastralgic syndrome), which is associated with dysfunction of the gastrointestinal tract.
An electrocardiographic study is important in diagnosis, which should preferably be carried out at the prehospital stage. With a typical transmural infarction, the ECG shows signs of necrosis (deep and wide wave Q), damage (raised arcuate segment S - T), ischemia (invertive sharp symmetrical wave T). Diagnosis of atypical forms of myocardial infarction, as well as determination of its localization, is often very difficult and is the responsibility of a doctor in a specialized cardiology team. Determination of central venous pressure plays an important role in the diagnosis of cardiogenic shock. Its change in dynamics allows for timely correction of the therapy. Normally, CVP ranges from 60 to 120 mmHg. Art. (0.59 - 0.18 kPa). CVP less than 40 mm water. Art. - a sign of hypovolemia, especially if it is combined with hypotension. With severe hypovolemia, CVP often becomes negative.
Diagnostics
Differential diagnosis cardiogenic shock caused by acute heart attack myocardium, often has to be carried out with other conditions that have a similar clinical picture. This is a massive pulmonary embolism, dissecting aortic aneurysm, acute tamponade heart, acute internal bleeding, acute disorder cerebral circulation, diabetic acidosis, overdose antihypertensive drugs, acute adrenal insufficiency (mainly caused by hemorrhage into the adrenal cortex in patients receiving anticoagulants), acute pancreatitis. Considering the complexity of differential diagnosis of these conditions, even in specialized hospitals, one should not strive for its mandatory implementation at the prehospital stage.
Treatment
Treatment of cardiogenic shock is one of the most complex problems modern cardiology. The main requirements for it are complexity and urgency of application. The following therapy is used both for cardiogenic shock and for conditions that mimic it.
Complex therapy of cardiogenic shock is carried out in the following areas.
Relief of anginal status
Narcotic and non-narcotic analgesics, drugs that potentiate their effect (antihistamines and antipsychotic drugs). We emphasize: all medications should be used only intravenously, since subcutaneous and intramuscular injections are useless due to existing circulatory disorders - the drugs are practically not absorbed. But then, when adequate blood pressure is restored, their absorption is delayed, often in large doses(repeated unsuccessful introductions), cause side effects. The following drugs are prescribed: 1 - 2% promedol (1 - 2 ml), 1 - 2% omnopon (1 ml), 1% morphine (1 ml), 50% analgin (2 - 5 ml maximum), 2% suprastin (1 - 2 ml), 0.5% seduxen (or relanium) (2 - 4 ml), 0.25% droperidol (1 - 3 ml), 20% sodium hydroxybutyrate (10 - 20 ml). The so-called therapeutic neuroleptanalgesia is very effective: the introduction of a powerful morphine-like synthetic narcotic analgesic fentanyl (0.005%, 1 - 3 ml) mixed with the neuroleptic droperidol (0.25%, 1 - 3 ml). In case of cardiogenic shock, this ensures, along with relief of pain and psycho-emotional arousal, normalization of indicators general hemodynamics And coronary circulation. The doses of the components of neuroleptanalgesia vary: with the predominance of fentanyl, it is provided predominantly analgesic effect(indicated for severe anginal status), with the predominance of droperidol, the neuroleptic (sedative) effect is more pronounced.
It should be remembered that when using these drugs a prerequisite is a slow pace of administration due to the moderate hypotensive effect of some of them (droperidol, morphine). In this regard, these drugs are used in combination with vasopressor, cardiotonic and other drugs.
Elimination of hypovolemia by administration of plasma substitutes
Typically, 400, 600 or 800 ml (up to 1 l) of polyglucin or rheopolyglucin are administered, (preferably) intravenously at a rate of 30 - 50 ml/min (under central venous pressure control). A combination of polyglucin with rheopolyglucin is also possible. The first has a high osmotic pressure and circulates in the blood for a long time, promoting fluid retention in the vascular bed, and the second improves microcirculation and causes the movement of fluid from tissues into the vascular bed.
Restoring the rhythm and conductivity of the heart
For tachysystolic arrhythmias, cardiac glycosides are administered, as well as 10% novocainamide (5 - 10 ml) intravenously very slowly (1 ml/min) under the control of heart rate (using a phonendoscope) or electrocardiography. When the rhythm normalizes, administration should be stopped immediately to avoid cardiac arrest. If the initial blood pressure is low, it is advisable to take a very slow intravenous administration a mixture of drugs containing 10% novocainamide (5 ml), 0.05% strophanthin (0.5 ml) and 1% mezaton (0.25 - 0.5 ml) or 0.2% norepinephrine (0D5 - 0.25 ml). 10 - 20 ml of isotonic sodium chloride solution is used as a solvent. In order to normalize the rhythm, 1% lidocaine (10 - 20 ml) is prescribed intravenously slowly or drip, panangin (10 - 20 ml) intravenously (contraindicated in atrioventricular block). If treatment is carried out by a specialized team, then β-blockers are used: 0.1% inderal (obzidan, anaprilin, cordanum) 1 - 5 ml intravenously slowly under ECG control, as well as ajmaline, etmozin, isoptin, etc.
For bradysystolic arrhythmias, 0.1% atropine (0.5 - 1 ml), 5% ephedrine (0.6 - 1 ml) are administered. However, β-adrenergic receptor stimulants are more effective: 0.05% novodrin, alupent, isuprel 0.5 - 1 ml intravenously slowly or drip; combined administration with corticosteroids is indicated. If these measures are ineffective in a specialized team or cardiology department, electrical pulse therapy is performed: for tachysystolic forms (paroxysms of fibrillation, paroxysmal tachycardia) - defibrillation, for bradysystolic forms - electrocardiostimulation using special devices. Thus, the most effective treatment for complete atrioventricular block with Morgagni-Edams-Stokes attacks, accompanied by the development of cardiogenic arrhythmic shock, is electrical stimulation with a transvenous endocardial electrode inserted into the right ventricle (through the veins of the upper extremities).
The contractile function of the myocardium is increased. by using cardiac glycosides - 0.05% strophanthin (0.5 - 0.75 ml) or 0.06% korglykon (1 ml) slowly intravenously in 20 ml of isotonic sodium chloride solution or, better, intravenously drip in combination with plasma substitutes. It is also possible to use other cardiac glycosides: isolanide, digoxin, olitorizide, etc. In specialized cardiac care, glucagon is administered intravenously, which has a positive effect on the myocardium, but does not have an arrhythmogenic effect, and can be used in the development of cardiogenic shock due to an overdose of cardiac glycosides .
Normalization of blood pressure with the help of symptomimetics
Norepinephrine or mesaton are effective for this purpose. Norepinephrine is administered intravenously in a dose of 4 - 8 mg (2 - 4 ml of 0.2% solution) per 1 liter of isotonic solution of sodium chloride, polyglucin or 5% glucose. The rate of administration (20 - 60 drops per minute) is regulated by blood pressure, which should be monitored every 5 - 10 minutes, and sometimes more often. It is recommended to maintain systolic pressure around 100 mmHg. Art. Mezaton is used in a similar way, 2 - 4 ml of a 1% solution. If impossible drip administration sympathomimetics in as a last resort intravenous very slow (over 7 - 10 minutes) administration of 0.2 - 0.3 ml of 0.2% norepinephrine or 0.5 - 1 ml of 1% mesatone solution in 20 ml of isotonic sodium chloride solution or 5% glucose is also allowed. blood pressure control. In the conditions of a specialized cardiological ambulance team or hospital, dopamine is administered intravenously, which, in addition to the pressor effect, has a dilating effect on the renal and mesenteric vessels and helps to increase cardiac output and urine output. Dopamine is administered intravenously at a rate of 0.1 - 1.6 mg/min under ECG monitoring. Hypertensin, which has a pronounced pressor effect, is also used intravenously, 2.5 - 5.0 mg per 250 - 500 ml of 5% glucose at a rate of 4 - 8 to 20 - 30 drops per minute with regular blood pressure monitoring. To normalize blood pressure, hormones of the adrenal cortex - corticosteroids - are also indicated, especially if the effect of pressor amines is insufficient. Prednisolone is administered intravenously or intravenously in a drip at a dose of 60 - 120 mg or more (2 - 4 ml of solution), 0.4% dexazone (1 - 6 ml), hydrocortisone at a dose of 150 - 300 mg or more (up to 1500 mg per day) .
Normalization of rheological properties of blood(its normal fluidity) is carried out with the help of heparin, fibrinolysin, drugs such as hemodez, rheopolyglucin. They are used at the stage of specialized medical care. If there are no contraindications to the use of anticoagulants, they should be prescribed as early as possible. After intravenous simultaneous administration of 10,000 - 15,000 units of heparin (in an isotonic solution of glucose or sodium chloride) over the next 6 - 10 hours (if hospitalization is delayed), 7,500 - 10,000 units of heparin are administered in 200 ml of solvent (see above) with the addition 80,000 - 90,000 units of fibrinolysin or 700,000 - 1,000,000 units of streptolyase (streptase). Subsequently, in a hospital setting, anticoagulant therapy is continued under the control of blood clotting time, which in the first 2 days of treatment should not be less than 15-20 minutes according to the Masa-Magro method. With complex therapy with heparin and fibrinolysin (streptase), more favorable course myocardial infarction: mortality is almost 2 times less, and the frequency of thromboembolic complications is reduced from 15 - 20 to 3 - 6%.
Contraindications to the use of anticoagulants are hemorrhagic diathesis and other diseases accompanied by slow blood clotting, acute and subacute bacterial endocarditis, serious illnesses liver and kidneys, acute and chronic leukemia, cardiac aneurysm. Caution is necessary when prescribing them to patients with peptic ulcer, tumor processes, during pregnancy, in the immediate postpartum and postoperative periods(first 3 - 8 days). In these cases, the use of anticoagulants is permissible only for health reasons.
Correction of acid-base status necessary for the development of acidosis, aggravating the course of the disease. Usually a 4% solution of sodium bicarbonate, sodium lactate, trisamine is used. This therapy is usually carried out in a hospital under the monitoring of acid-base levels.
Additional treatments cardiogenic shock: for pulmonary edema - application of tourniquets to the lower extremities, oxygen inhalation With defoamers (alcohol or antifomsilane), administration of diuretics (4 - 8 ml of 1% Lasix intravenously), in an unconscious state - aspiration of mucus, insertion of an oropharyngeal airway, in case of breathing problems - artificial ventilation using various types of respirators.
In cases of severe areactive shock, specialized cardiac surgery departments use assisted circulation - counterpulsation, usually in the form of periodic inflation of an intra-aortic balloon using a catheter, which reduces the work of the left ventricle and increases coronary blood flow. A new treatment method is hyperbaric oxygen therapy using special pressure chambers.
The tactics of treating patients with cardiogenic shock at the prehospital stage has a number of features. Due to the extreme severity of the disease and poor prognosis, as well as the significant relationship between the timing of treatment and the completeness of therapy, emergency care at the prehospital stage must be started as early as possible.
Patients in a state of cardiogenic shock are not transportable and can only be transported to medical institutions from public place, enterprises, institutions, from the street while simultaneously providing necessary assistance. Upon the disappearance of the phenomena of cardiogenic shock or the presence of special indications (for example, intractable arrhythmic shock), a specialized cardiology team can transport such a patient for life-saving reasons, having previously notified the hospital of the appropriate profile.
Practical experience suggests the most rational scheme for organizing the provision of care to patients in a state of cardiogenic shock:
- examination of the patient; measurement of blood pressure, pulse, auscultation of the heart and lungs, examination and palpation of the abdomen, if possible - electrocardiography, assessment of the severity of the condition and establishment of a preliminary diagnosis;
- immediately call a medical team (preferably a specialized cardiology team);
- establishing intravenous drip administration of an infusion medium (isotonic sodium chloride solution, glucose, Ringer's solution, polyglucin, rheopolyglucin) initially at a low speed (40 drops per minute);
- further administration of medications by puncturing the rubber tube of the transfusion system or adding a particular drug to a bottle with an infusion medium. Puncture catheterization of the ulnar vein with a special plastic catheter is very rational;
- regular monitoring of the main indicators of the patient’s condition (blood pressure, pulse, heart rate, central venous pressure, hourly diuresis, the nature of subjective sensations, condition of the skin and mucous membranes);
- administration of drugs necessary for this type of shock (taking into account specific indications), only intravenously slowly with careful monitoring of the patient’s condition and with mandatory registration on a separate sheet of the time of administration and dose. At the same time, objective parameters of the patient’s condition are indicated. Upon arrival of the medical team, they are given a list of medications used to ensure continuity of therapy;
- use of medications taking into account existing contraindications, compliance with the established dosage and rate of administration.
Only with early diagnosis and early start intensive complex therapy, it is possible to obtain positive results in the treatment of this contingent of patients, to reduce the frequency of severe cardiogenic shock, especially its non-reactive form.
4.1.2. Cardiogenic shock.
Cardiogenic shock occurs, according to consolidated literature data, in 10-15% of cases (Malaya L.T. et al., 1981, Ganelina I.E., 1983, Chazov E.I., 1992, Rayn B., 1996). Currently, there are no simple, reliable laboratory and instrumental criteria that can be used to diagnose or confirm the presence of cardiogenic shock. Therefore, the following clinical criteria are considered the most informative.
Clinical criteria for cardiogenic shock.
1. Decrease in blood pressure below 90 mmHg. in patients without hypertension and below 100 mmHg. in hypertensive*;
2. Thread-like pulso*;
3. Pallor of the skin*;
4. Anuria or oliguria - diuresis less than 20 mm/hour (Haan D., 1973) o;
5. “Marbling of the skin” – on the back of the hands, against the background of pronounced pallor of the skin, blue veins with more than 4-5 branches are visible.
Note: * - criteria (first three), corresponding to collapse, o - cardiogenic shock (all five).
Classification of cardiogenic shock (Chazov E.I. et al., 1981):
1. Reflex,
2. Arrhythmic,
3. True,
4. Areactive.
Assessment of the severity of cardiogenic shock (Smetnev A.S., 1981, Chazov E.I., 1981). The severity of shock is characterized by the level of systolic blood pressure.
I degree of severity – BPsist. from 90 to 60 mm Hg.
II degree of severity – ADsyst. 60 to 40 mmHg
III degree of severity – ADsyst. below 40 mm Hg.
The mechanism of development of cardiogenic shock.
The triggering mechanism of cardiogenic shock is the following factors: the appearance of severe anginal pain and (or) a drop in stroke and minute blood volume, which leads to a decrease in blood pressure and regional blood flow. A decrease in minute blood volume can be caused by both systolic dysfunction due to the large size of the myocardial lesion (more than 40% of the area of the left ventricle), and diastolic or, less commonly, mixed dysfunction of the left ventricle. In addition, clinically significant hemodynamic disturbances can be observed as a result of the development of tachysystolic or bradysystolic forms of cardiac arrhythmia and conduction disturbances. In response to pain and a decrease in cardiac output, there is activation of the neurohumoral stress-limiting system (catecholamines, cortisol, serotonin, histamine, etc.), which overstimulate and then inactivate the corresponding receptors of arterioles, including baroreceptors that regulate the opening of the spicter between arterioles and capillaries (in Normally, the pressure in the capillaries is 2-3 mm Hg, and in the arterioles up to 4-7 mm Hg, and when the pressure in the arterioles increases to 6-7 mm Hg, the sphincter opens, blood is flowing along a pressure gradient from arterioles to capillaries, then, when the pressure between them equalizes, the sphincter closes). Due to the inactivation of baroreceptors, the axon reflex that regulates the opening of the sphincter between the arterioles and capillaries is disrupted, as a result of which the sphincter remains constantly open: the blood pressure in the arterioles and capillaries is equalized and the blood flow in them stops. As a result of the interruption of blood flow in the capillaries, shunts open between the arterioles and venules, through which blood is discharged from the arterioles into the venules, bypassing the capillaries. The latter, in turn, expand and are visible on the back of the hand in the form of a symptom of “skin marbling”, and anuria or oliguria also develops (see above).
. Reflex cardiogenic shock– characterized by the development of shock in the first hours of myocardial infarction in response to severe anginal pain as a result of extreme inhibition of the nervous system, including the vasomotor center. Another mechanism for the development of this type of shock is the involvement of the Berzold-Jarisch reflex during myocardial infarction with localization in the posterior wall of the left ventricle, manifested by severe bradycardia with a heart rate of less than 50-60 per minute and hypotension. This type of shock is most often encountered by ambulance and emergency physicians, and less often with in-hospital myocardial infarction.
r Treatment of reflex cardiogenic shock. The main method of treating reflex shock is to relieve pain - thalamonal (fentanyl 0.1 mg in combination with droperidol 5 mg, intravenously) or morphine up to 10-20 mg intravenously, in the case of bradycardia - atropine 1.0 mg intravenously. After eliminating the anginal syndrome, hypotension, as well as other signs of shock, stop. If the pain is not relieved, reflex shock gradually turns into true shock.
. Arrhythmic cardiogenic shock– characterized by the development of shock as a result of the development of tachy- or bradyarrhythmias, leading to a drop in stroke and minute blood volume.
r Treatment of arrhythmic cardiogenic shock. The main method of therapy is the elimination of heart rhythm disturbances. The main method of treatment of paroxysmal tachycardias (supraventric and ventricular), paroxysms of flicker and flutter of the atrial is electromypulsic therapy (defibrillation), and bradyarrhythmia (atrioventricular blockade of the II and III degree, atrioventricular rhythms, refusal of the sinus node, and more measures, and more measures. reigning bradyarrhythmia) - temporary transvenous electrocardiostimulation. After eliminating the arrhythmia, hypotension, as well as other signs of shock, are stopped. If cardiac arrhythmias are eliminated, but signs of shock persist, it is regarded as true cardiogenic shock with further appropriate therapy.
. True cardiogenic shock– characterized by the presence of all signs of shock (see above) in the absence of pain and arrhythmias. In the treatment of this type of shock, drugs are used to normalize blood flow from the arterioles to the capillaries by increasing the pressure in the arterioles and closing the shunts.
r Treatment of true cardiogenic shock. In the treatment of true shock, drugs with positive inotropic effects are used. Currently, these drugs are divided into three classes (see Table 4.1):
Inotropic substances with predominant vasoconstrictor properties;
Catecholamines with inotropic properties with little or no vasoconstriction;
Phosphodiesterase inhibitors are inotropic agents with predominant vasodilating properties.
+ Characteristics of vasoconstrictor inotropic drugs. These drugs are represented by dopamine and norepinephrine. When dopamine is administered, cardiac muscle contractility and heart rate increase through its direct stimulation of a- and b-adrenergic receptors, as well as through the release of norepinephrine from nerve endings. When prescribed at a low dose (1-3 mcg/kg/min), it mainly affects dopaminergic receptors, leading to dilation of renal vessels and a slight stimulation of cardiac muscle contractility through activation of b-adrenergic receptors. At a dose of 5-10 mcg/kg/min. The b-1-adrenergic effect predominates, leading to increased contractility of the heart muscle and an increase in heart rate. When this drug is administered in a larger dose, the effect on α-adrenergic receptors, manifested by vasoconstriction, dominates. Norepinephrine is an almost pure vasoconstrictor drug with a positive effect on myocardial contractility.
Catecholamine inotropic agents are represented by isoproterenol and dobutamine. Through their action on b-1 adrenergic receptors, they stimulate contractility, increase heart rate and cause vasodilation. Therefore they are not recommended except in urgent cases when low cardiac output due to severe bradycardia, and temporary cardiac pacing is not available.
Amrinone and milrinone (phosphodiesterase inhibitors) are characterized by positive inotropic and vasodilating effects. Increased mortality when milrinone is given orally for a long time, as well as high toxicity with long-term use of amrinone, have reduced the frequency of use of these drugs. Phosphodiesterase inhibitors are excreted by the kidneys and are therefore contraindicated in patients with renal failure.
When blood pressure is low (systolic blood pressure less than 90 mmHg), dopamine is the drug of choice. If blood pressure remains low with a dopamine infusion greater than 20 mcg/kg/min, additional norepinephrine may be added at a dose of 1-2 mg/kg/min. In other situations, dobutamine is the drug of choice. All catecholamines used intravenously have the advantage of a very short half-life, allowing the dose to be titrated minute by minute until a positive clinical effect is achieved. Phosphodiesterase inhibitors are reserve drugs for patients if there is no effect when using catecholamines, in the presence of tachyarrhythmias and tachycardia-induced myocardial ischemia during catecholamine therapy. Milrinone is administered intravenously at a dose of 0.25-0.75 mg/kg/min. Particular attention should be paid to patients with renal dysfunction, since this drug is excreted by the kidneys. It should be noted that when prescribing drugs with a positive inotropic effect, prednisolone can be used, which increases the sensitivity of dopamine, b- and a-adrenergic receptors to the maximum daily dose up to 1000 mg.
. Areactive cardiogenic shock– characterized by the presence of an irreversible stage of development of true cardiogenic shock or a slowly developing rupture of the cardiac muscle of the left ventricle (Ganelina I.E., 1977, 1983, Chazov E.I., 1981,1992).
r Treatment of areactive cardiogenic shock (see treatment of true cardiogenic shock).
The mortality rate for all types of caurdiogenic shock is, on average, 40%. With reflex and arrhythmic shock, patients should not die, and their death is often caused by late presentation of patients or inadequate treatment measures. The mortality rate for true shock is, on average, 70%, for areactive shock - 100%.
Table 4.1. Classification of inotropic drugs.
Drug Mechanism of action Inotropic influence Application
effect on blood vessels
Isoproterenol Stimulant ++ Dilatation Hypotension followed by
b-1 receptors cause bradycardia,
when it's impossible
carry out cardio-
__________________________________________________________________________________
Dobutamine Stimulant ++ Moderate Low Cardiac
b-1 receptor dilatation release during
HELL< 90 мм рт. ст.
__________________________________________________________________________________
Low doses Dopaminergic- ++ Renovascu- AD< 90 мм рт. ст.
which receptors are polar dila- or< 30 мм рт. ст.
tation from the usual
______________________________________________________________________________
Average doses: Stimulant ++ Constriction See above
b-1 receptors
______________________________________________________________________________
High doses: Stimulant ++ Severe See above
a-1 receptor constriction
__________________________________________________________________________________
Norepinephrine Stimulant ++ Severe Severe hypotonic
a-1-receptor constriction, despite
usage
dopamine
__________________________________________________________________________________
Amrinon Phosphorus inhibitor ++ Dilatation If absent
or dobutamine
__________________________________________________________________________________
Milrinone Phosphorus inhibitor ++ Dilatation If absent
dopamine effect fodiesterase
or dobutamine
__________________________________________________________________________________
Note: BP is blood pressure.
Retrospective studies have shown that mechanical reperfusion with coronary artery bypass grafting or angioplasty of occluded coronary arteries reduces mortality in patients with myocardial infarction, including those complicated by cardiogenic shock. In large clinical trials, when treated with thrombolytics, in-hospital mortality ranged from 50 to 70%, while when treated with mechanical reperfusion with angioplasty, the mortality rate dropped to 30%. A multicenter study using coronary artery bypass grafting in patients with acute coronary artery occlusion and cardiogenic shock noted a decrease in mortality from 9.0% to 3.4%. In these patients, in the case of cardiogenic shock complicating the course of myocardial infarction, immediate coronary artery bypass grafting was used in cases where other interventional treatments were ineffective. Data from the SHOCK study group confirmed that in a subset of patients with cardiogenic shock, immediate CABG was associated with a 19% reduction in mortality compared with thrombolysis. Urgent coronary artery bypass grafting, according to various authors, should be performed in patients with myocardial infarction only with multivessel lesions or cardiogenic shock, for whom thrombolytic therapy was not performed or was unsuccessful (Chazov E.I., 1992, Rayn B., 1996) . The recommended time for coronary artery bypass grafting is no more than 4-6 hours from the onset of symptoms of myocardial infarction.
