Areactive cardiogenic shock. Extreme insufficiency of the contractile function of the heart or cardiogenic shock: are there any chances? Cardiogenic shock in children
Article publication date: 06/08/2017
Article last updated: 12/21/2018
From this article you will learn: what is cardiogenic shock, what first aid is provided for it. How is it treated, and is there a large percentage of survivors. How to avoid cardiogenic shock if you are at risk.
Prevention
To avoid cardiogenic shock, it is necessary to prevent myocardial infarction.
To get rid of factors that increase its risk:
- bad habits;
- excessive consumption of fatty, salty foods;
- stress;
- lack of sleep;
- excess weight.
For diseases and pathological conditions that lead to a heart attack (for example, coronary disease heart disease, atherosclerosis, hypertension, thrombophilia), receive appropriate preventive therapy.
It, depending on the disease, may include taking statins and polyunsaturated acids(with atherosclerosis, coronary artery disease), ACE inhibitors or beta-blockers (for hypertension), antiplatelet agents (for atherosclerosis, thrombophilia).
For prevention acute myocarditis start treatment on time infectious diseases. Always with an increase in body temperature and feeling unwell consult a doctor and do not self-medicate. In case of systemic rheumatism during exacerbations, immediately begin the treatment prescribed by the rheumatologist.
For prevention, if you have an increased risk of its occurrence, take antiarrhythmic drugs prescribed by a cardiologist or arrhythmologist. Or, have a pacemaker fitted with defibrillation-cardioversion if indicated.
Once every 1-2 years preventive examination see a cardiologist if you are healthy. Once every 6 months - if you suffer from cardiovascular diseases, endocrine disorders(first of all, the risk of heart attack is increased with diabetes).
If you have already experienced one myocardial infarction, take it seriously preventive measures, since the risk of cardiogenic shock and death is significantly increased with a second heart attack.
13. Cardiogenic shock in myocardial infarction: pathogenesis, clinic, diagnosis, emergency care.
Cardiogenic shock is an extreme degree of acute left ventricular failure, characterized by a sharp decrease in contractile function myocardium (fall in shock and minute output), which is not compensated by an increase in vascular resistance and leads to inadequate blood supply to all organs and tissues. It is the cause of death in 60% of patients with myocardial infarction.
There are the following forms of cardiogenic shock:
Reflex,
true cardiogenic,
areactive,
arrhythmic,
due to myocardial rupture.
The pathogenesis of true cardiogenic shock
It is this form of cardiogenic shock that fully corresponds to the definition of shock in myocardial infarction, which was given above.
True cardiogenic shock, as a rule, develops with extensive transmural myocardial infarction. More than 1/3 of patients on the section show stenosis of 75% or more of the lumen of the three main coronary arteries, including the anterior descending coronary artery. However, almost all patients with cardiogenic shock have thrombotic coronary occlusion (Antman, Braunwald, 2001). The possibility of developing cardiogenic shock is significantly increased in patients with recurrent MI.
The main pathogenetic factors of true cardiogenic shock are as follows.
1. Decreased pumping (contractile) function of the myocardium
This pathogenetic factor is the main one. The decrease in the contractile function of the myocardium is primarily due to the exclusion of the necrotic myocardium from the contraction process. Cardiogenic shock develops when the size of the necrosis zone is equal to or greater than 40% of the mass of the myocardium of the left ventricle. A large role also belongs to the state of the peri-infarction zone, in which, with the most severe course shock, necrosis is formed (thus, the infarction expands), as evidenced by a persistent rise in the blood level of CK-MB and CK-MBmass. An important role in reducing the contractile function of the myocardium is also played by the process of its remodeling, which begins already in the first days (even hours) after the development of acute coronary occlusion.
2. Development of a pathophysiological vicious circle
With cardiogenic shock, patients with myocardial infarction develop a pathophysiological vicious circle, which aggravates the course of this terrible complication of myocardial infarction. This mechanism begins with the fact that as a result of the development of necrosis, especially extensive and transmural, there is a sharp decrease in the systolic and diastolic function of the left ventricular myocardium. A pronounced drop in stroke volume leads, ultimately, to a decrease in aortic pressure and a decrease in coronary perfusion pressure and, consequently, to a decrease in coronary blood flow. In turn, a decrease in coronary blood flow exacerbates myocardial ischemia and thus further disrupts the systolic and diastolic functions of the myocardium. The inability of the left ventricle to empty also leads to increased preload. Under preload understand the degree of stretching of the heart during diastole, it depends on the amount of venous blood flow to the heart and the extensibility of the myocardium. An increase in preload is accompanied by an expansion of the intact, well-perfused myocardium, which in turn, in accordance with the Frank-Starling mechanism, leads to an increase in the strength of heart contractions. This compensatory mechanism restores stroke volume, but ejection fraction - an indicator of global myocardial contractility - decreases due to an increase in end-diastolic volume. Along with this, the dilatation of the left ventricle leads to an increase in afterload - i.e. the degree of myocardial tension during systole in accordance with Laplace's law. This law states that the tension of the myocardial fibers is equal to the product of the pressure in the cavity of the ventricle and the radius of the ventricle, divided by the thickness of the wall of the ventricle. Thus, at the same aortic pressure, the afterload experienced by a dilated ventricle is higher than that of a normal ventricle (Braunwald, 2001).
However, the amount of afterload is determined not only by the size of the left ventricle (in this case, the degree of its dilatation), but also by systemic vascular resistance. decline cardiac output in cardiogenic shock, it leads to compensatory peripheral vasospasm, in the development of which the sympathoadrenal system, endothelial vasoconstrictor factors, and the renin-angiotensin-II system take part. An increase in systemic peripheral resistance is aimed at increasing blood pressure and improved blood supply to vital important organs, but it significantly increases afterload, which in turn leads to an increase in myocardial oxygen demand, aggravation of ischemia and a further decrease in myocardial contractility and an increase in the end-diastolic volume of the left ventricle. The latter circumstance contributes to an increase in pulmonary stagnation and, consequently, hypoxia, which exacerbates myocardial ischemia and its decrease. contractility. Then everything happens again as described above.
3. Violations in the microcirculation system and a decrease in the volume of circulating blood
As previously stated, widespread vasoconstriction and an increase in total peripheral vascular resistance occur in true cardiogenic shock. This reaction is compensatory in nature and is aimed at maintaining blood pressure and ensuring blood flow in vital organs (brain, kidneys, liver, myocardium). However, continued vasoconstriction acquires pathological significance, as it leads to tissue hypoperfusion and disturbances in the microcirculation system. The microcirculatory system is the largest vascular capacity in the human body, accounting for over 90% of the vascular bed. Microcirculatory disorders contribute to the development of tissue hypoxia. Metabolic products of tissue hypoxia cause dilatation of arterioles and precapillary sphincters, while venules more resistant to hypoxia remain spasmodic, resulting in blood being deposited in the capillary network, which leads to a decrease in the mass of circulating blood. There is also an exit of the liquid part of the blood into the tissue interstitial spaces. A decrease in venous blood return and the amount of circulating blood contributes to a further decrease in cardiac output and tissue hypoperfusion, further exacerbates peripheral microcirculatory disorders up to a complete cessation of blood flow with the development of multiple organ failure. In addition, the stability of blood cells decreases in the microcirculatory bed, intravascular aggregation of platelets and erythrocytes develops, blood viscosity increases, and microthrombosis occurs. These phenomena exacerbate tissue hypoxia. Thus, we can assume that a kind of pathophysiological vicious circle develops at the level of the microcirculation system.
True cardiogenic shock usually develops in patients with extensive transmural myocardial infarction of the anterior wall of the left ventricle (often with thrombosis of two or three coronary arteries). The development of cardiogenic shock is also possible with extensive transmural infarcts of the posterior wall, especially with the 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 disorders heart rate 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 pronounced 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 microcirculation system. Lack of blood supply to the brain leads to the development of dyscirculatory encephalopathy, kidney hypoperfusion - to acute kidney 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 the patient with cardiogenic shock is severe. The patient is inhibited, consciousness may be darkened, complete loss of consciousness is possible, short-term excitation is less often observed. The main complaints of the patient are complaints of severe general weakness, dizziness, "fog before the eyes", palpitations, a feeling of interruptions in the region of the heart, sometimes retrosternal pain.
When examining a patient, “gray cyanosis” or pale cyanotic coloration of the skin attracts attention, there may be pronounced acrocyanosis. The skin is wet and cold. The distal parts of the upper and lower extremities are marble-cyanotic, the hands and feet are cold, cyanosis of the subungual spaces is noted. Characterized by the appearance of the symptom of "white spot" - lengthening the time of disappearance white spot 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, auricles, distal parts of the fingers and toes.
Pulse on radial arteries filiform, often arrhythmic, often not defined at all. Arterial pressure is sharply reduced, always less than 90 mm. rt. Art. Characterized by a decrease pulse pressure, according to A. V. Vinogradov (1965), it is usually lower than 25-20 mm. rt. Art. Percussion of the heart reveals an expansion of its left border, characteristic auscultatory signs are deafness of heart tones, arrhythmias, a soft systolic murmur at the apex of the heart, a protodiastolic gallop rhythm (pathognomonic symptom of severe left ventricular failure).
Breathing is usually shallow, may be rapid, especially with the development of a "shock" lung. The most severe course of cardiogenic shock is characterized by the development of cardiac asthma and pulmonary edema. In this case, suffocation appears, breathing becomes bubbling, coughing with a pink, foamy sputum is disturbing. With percussion of the lungs, dullness of percussion sound in the lower sections is determined, crepitus, small 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 a small amount as a manifestation of stagnation 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.
On palpation of the abdomen, pathology is usually not detected, in some patients an enlarged liver may be determined, which is explained by the addition of right ventricular failure. Perhaps the development of acute erosions and ulcers of the stomach and duodenum, which is manifested by pain in the epigastrium, sometimes bloody vomiting, pain on palpation of the epigastric region. However, these changes gastrointestinal tract are rarely observed. The most important sign of cardiogenic shock is oliguria or oligoanuria; during catheterization of the bladder, the amount of urine separated is less than 20 ml / h.
Diagnostic criteria for cardiogenic shock:
1. Symptoms of peripheral circulatory insufficiency:
pale cyanotic, "marbled", moist skin
acrocyanosis
collapsed veins
cold hands and feet
decrease in body temperature
prolongation of the time of disappearance of the white spot after pressure on the nail > 2 s (decreased peripheral blood flow)
2. Violation of consciousness (lethargy, confusion, possibly unconsciousness, less often - arousal)
3. Oliguria (decreased diuresis< 20 мл/ч), при крайне тяжелом течении - анурия
4. Decrease in systolic blood pressure to the value< 90 мм. рт. ст (по
some data less than 80 mm. rt. st), in persons with previous arterial
hypertension< 100 мм. рт. ст. Длительность гипотензии >30 min.
Decrease in pulse arterial pressure up to 20 mm. rt. Art. and below
Decreased mean arterial pressure< 60 мм. рт. ст. или примониторировании снижение (по сравнению с исходным) среднего артериального давления >30 mm. rt. Art. within >= 30 min
7. Hemodynamic criteria:
pressure "jamming" in the pulmonary artery> 15 mm. rt. st (> 18 mm Hg, according to
Antman, Braunwald)
cardiac index< 1.8 л/мин/м2
increase in total peripheral vascular resistance
increased left ventricular end-diastolic pressure
decrease 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. The definition of hemodynamic criteria (point 7) for the diagnosis of cardiogenic shock is usually not mandatory, but it is highly advisable to organize the correct treatment.
General activities:
Anesthesia (of particular importance in the reflex form of shock - it allows you to stabilize hemodynamics),
oxygen therapy,
Thrombolytic therapy (in some cases, effective thrombolysis can achieve the disappearance of symptoms of shock),
Hemodynamic monitoring (cathetarization of the central vein for the introduction of the Swan-Ganz catheter).
2. Treatment of arrhythmias (arrhythmic form of cardiogenic shock)
3. Intravenous fluid.
4. Decreased peripheral vascular resistance.
5. Increased myocardial contractility.
6. Intra-aortic balloon counterpulsation (IBC).
Intravenous fluid administration, which increases venous return to the heart, is one way to improve left ventricular pumping by the Frank-Starling mechanism. However, if the original final diastolic pressure of the left ventricle (LVDD) is sharply increased, this mechanism ceases to work and a further increase in LVDD will lead to a decrease in cardiac output, deterioration of the hemodynamic situation and perfusion of vital organs. Therefore, intravenous administration of fluids is carried out when PAWP is less than 15 mm. rt. Art. (in the absence of the ability to measure PZLA, they are controlled by CVP - fluid is injected if CVP is less than 5 mm Hg). During the introduction, the signs of stagnation in the lungs (shortness of breath, wet rales) are most carefully controlled. Usually, 200 ml of 0.9% sodium chloride solution, low molecular weight dextrans (rheopolyglucin, dextran-40) are injected, a polarizing mixture can be used with 200 ml of 5-10% glucose solution. Drive should be up to BP sys. more than 100 mm Hg. Art. or PZLA more than 18 mm Hg. Art. The rate of infusion and the volume of injected fluid depends on the dynamics of PAWP, blood pressure, and clinical signs of shock.
Decreased peripheral resistance (with blood pressure over 90 mm Hg) - the use of peripheral vasodilators leads to a slight increase in cardiac output (as a result of a decrease in preload) and an improvement in the circulation of vital organs. The drug of choice is sodium nitroprusside (0.1-5 mcg / min / kg) or nitroglycerin (10-200 mg / min) - the infusion rate depends on the blood pressure system, which is maintained at a level of at least 100 mm Hg. Art.
With AD sys. less than 90 mm Hg. Art. and DZLA more than 15 mm Hg. Art. :
If BP sys. less than or equal to 60 mm Hg. Art. - norepinephrine (0.5-30 mcg / min) and / or dopamine (10-20 mcg / kg / min)
After increasing blood pressure sys. up to 70-90 mm Hg. Art. - add dobutamine (5-20 mcg/kg/min), stop norepinephrine administration and reduce the dose of dopamine (to 2-4 mcg/kg/min - this is the "renal dose", as it dilates the renal arteries)
If BP sys. - 70-90 mm Hg Art. - dopamine at a dose of 2-4 mcg / kg / min and dobutamine.
With a urine output of more than 30 ml / hour, it is preferable to use dobutamine. Dopamine and dobutamine can be used simultaneously: dobutamine as an inotropic agent + dopamine at a dose that increases renal blood flow.
With inefficiency medical measures– IBD + emergency cardiac catheterization and coronary angiography. The goal of IBD is to buy time for a thorough examination of the patient and targeted surgical intervention. In IBD, a balloon that is inflated and deflated during each cardiac cycle, injected through the femoral artery into the thoracic aorta and located slightly distal to the mouth of the left subclavian artery. The main method of treatment is balloon coronary angioplasty (reduces mortality to 40-50%). Patients with ineffective BCA, with mechanical complications of myocardial infarction, lesions of the left coronary artery trunk, or severe three-vessel disease undergo emergency coronary bypass grafting.
Refractory shock - IBD and circulatory support prior to heart transplantation.
Cardiogenic shock is a severe condition caused by severe heart failure, accompanied by a significant decrease in blood pressure and a decrease in myocardial contractility. In this condition, a sharp decrease in the amount of minute and stroke volume of blood is so pronounced that it cannot be compensated by an increase in vascular resistance. Subsequently, this condition causes severe hypoxia, lowering blood pressure, loss of consciousness and serious violations in the circulation of vital organs and systems.
Thromboembolism large branches pulmonary artery can cause cardiogenic shock in the patient.
Cardiogenic shock in almost 90% of cases can lead to the death of the patient. The reasons for its development can be:
- acute valvular insufficiency;
- acute stenosis of the heart valves;
- myxoma of the heart;
- severe forms;
- septic shock, provoking dysfunction of the heart muscle;
- gap interventricular septum;
- heart rhythm disturbances;
- rupture of the wall of the ventricle;
- squeezing;
- cardiac tamponade;
- tension pneumothorax;
- hemorrhagic shock;
- rupture or dissection of an aortic aneurysm;
- coarctation of the aorta;
- massive.
Classification
Cardiogenic shock is always caused by a significant violation of the contractile function of the myocardium. There are such mechanisms for the development of this serious condition:
- Decreased pumping function of the myocardium. With extensive necrosis of the heart muscle (during a myocardial infarction), the heart cannot pump the necessary volume of blood, and this causes severe hypotension. The brain and kidneys experience hypoxia, as a result of which the patient loses consciousness, and he has urinary retention. Cardiogenic shock can occur when 40-50% of the myocardial area is affected. Tissues, organs and systems abruptly cease their functioning, develops DIC syndrome and death comes.
- Arrhythmic shock (tachysystolic and bradysystolic). Such a form state of shock develops with paroxysmal tachycardia or complete atrioventricular block with acute bradycardia. Violation of hemodynamics occurs against the background of a violation of the frequency of contraction of the ventricles and a decrease in blood pressure to 80-90 / 20-25 mm. rt. Art.
- Cardiogenic shock in cardiac tamponade. This form shock occurs when the septum ruptures between the ventricles. The blood in the ventricles mixes and the heart loses its ability to contract. As a result, blood pressure is significantly reduced, hypoxia in tissues and organs increases and leads to a violation of their function and death of the patient.
- Cardiogenic shock caused by massive pulmonary embolism. This form of shock occurs when the pulmonary artery is completely blocked by a thrombus, in which blood cannot flow into the left ventricle. As a result, blood pressure drops sharply, the heart stops pumping blood, increases oxygen starvation all tissues and organs and death of the patient occurs.
Cardiologists distinguish four forms of cardiogenic shock:
- True: accompanied by a violation of the contractile function of the heart muscle, microcirculatory disorders, a metabolic shift and a decrease in diuresis. May be complicated by severe (cardiac asthma and pulmonary edema).
- Reflex: due reflex influence pain syndrome on myocardial function. Accompanied by a significant decrease in blood pressure, vasodilation and sinus bradycardia. Microcirculation disorders and metabolic disorders are absent.
- Arrhythmic: develops with severe brady- or tachyarrhythmia and is eliminated after the elimination of arrhythmic disorders.
- Areactive: proceeds quickly and severely, even intensive therapy for this condition often does not work.
Symptoms
In the early stages, the main signs of cardiogenic shock largely depend on the cause of the development of this condition:
- with myocardial infarction, the main symptoms are pain and a sense of fear;
- in case of heart rhythm disturbances - interruptions in the work of the heart, pain in the region of the heart;
- with pulmonary embolism - pronounced shortness of breath.
As a result of lowering blood pressure, the patient develops vascular and autonomic reactions:
- cold sweat;
- pallor, turning into cyanosis of the lips and fingertips;
- severe weakness;
- restlessness or lethargy;
- fear of death;
- swelling of the veins in the neck;
- cyanosis and marbling of the skin of the head, chest and neck (with pulmonary embolism).
After the complete cessation of cardiac activity and respiratory arrest, the patient loses consciousness, and, in the absence of adequate assistance, death may occur.
It is possible to determine the severity of cardiogenic shock by indicators of blood pressure, duration of shock, severity metabolic disorders the body's response to drug therapy and the severity of oliguria.
- I degree - the duration of the state of shock is about 1-3 hours, blood pressure drops to 90/50 mm. rt. Art., slight severity or absence of symptoms of heart failure, the patient quickly responds to drug therapy and relief of the shock reaction is achieved within an hour;
- II degree - the duration of the state of shock is about 5-10 hours, blood pressure drops to 80/50 mm. rt. Art., peripheral shock reactions and symptoms of heart failure are determined, the patient slowly responds to drug therapy;
- III degree - long-term shock reaction, blood pressure drops to 20 mm. rt. Art. or not determined, signs of heart failure and peripheral shock reactions are pronounced, 70% of patients have pulmonary edema.
Diagnostics
The generally accepted criteria for diagnosing cardiogenic shock are the following indicators:
- decline systolic pressure up to 80-90 mm. rt. Art.
- Decrease in pulse (diastolic pressure) up to 20-25 mm. rt. Art. and below.
- A sharp decrease in the amount of urine (oliguria or anuria).
- Confusion, agitation, or fainting.
- Peripheral signs: pallor, cyanosis, marbling, cold extremities, thready pulse on the radial arteries, collapsed veins on the lower extremities.
If it is necessary to perform a surgical operation to eliminate the causes of cardiogenic shock, the following is performed:
- Echo-KG;
- angiography.
Urgent Care
If the first signs of cardiogenic shock appeared in a patient outside the hospital, then it is necessary to call a cardiological ambulance. Before her arrival, the patient must be laid on a horizontal surface, raise his legs and ensure peace and fresh air.
Emergency care for cardiogenic care begins to be performed by ambulance workers:
During drug therapy for continuous monitoring of the functions of vital organs, the patient is given urinary catheter and connect heart monitors that record heart rate and blood pressure.
With the possibility of using specialized equipment and the ineffectiveness of drug therapy to provide emergency care A patient with cardiogenic shock may be prescribed the following surgical techniques:
- intra-aortic balloon counterpulsation: to increase coronary blood flow during diastole, blood is injected into the aorta using a special balloon;
- percutaneous transluminal coronary angioplasty: through the puncture of the artery, the patency of the coronary vessels is restored, this procedure is recommended only in the first 7-8 hours after the acute period of myocardial infarction.
Cardiogenic shock is characterized by a steady drop in blood pressure. Top pressure while falling below 90 mm Hg. In most cases, this situation occurs as a complication of myocardial infarction, and you should be prepared for its occurrence in order to help the core.
The occurrence of cardiogenic shock contributes (especially in the left ventricular type), in which many myocardial cells suffer. The pumping function of the heart muscle (especially the left ventricle) is impaired. As a result, problems begin in target organs.
First of all, they fall into dangerous conditions kidneys (the skin clearly turns pale and its moisture increases), the central nervous system, pulmonary edema occurs. long-term storage state of shock invariably leads to death of the core.
Due to its importance, cardiogenic shock microbial 10 is separated into a separate section - R57.0.
Attention. True cardiogenic shock is the most dangerous manifestation AHF (acute heart failure) of the left ventricular type, due to severe myocardial damage. The probability of a lethal outcome in this condition is from 90 to 95%.
Cardiogenic shock - causes
More than eighty percent of all cases of cardiogenic shock are a significant decrease in blood pressure in myocardial infarction (MI) with severe damage to the left ventricle (LV). To confirm the occurrence of cardiogenic shock, more than forty percent of the volume of the LV myocardium must be damaged.
Much less often (about 20%), cardiogenic shock develops due to acute mechanical complications of MI:
- acute insufficiency mitral valve due to rupture of the papillary muscles;
- complete separation of the papillary muscles;
- myocardial ruptures with the formation of an IVS defect (interventricular septum);
- complete rupture of the IVS;
- cardiac tamponade;
- isolated right ventricular MI;
- acute cardiac aneurysm or pseudoaneurysm;
- hypovolemia and a sharp decrease in cardiac preload.
The incidence of cardiogenic shock in patients with acute MI ranges from 5 to 8%.
Risk factors for the development of this complication are:
- anterior infarction,
- the patient has a history of myocardial infarction,
- old age of the patient,
- the presence of underlying diseases:
- diabetes,
- chronic renal failure,
- severe arrhythmias,
- chronic heart failure,
- LV systolic dysfunction (left ventricle),
- cardiomyopathy, etc.
Types of cardiogenic shock
- true;
- reflex (development of pain collapse);
- arrhythmogenic;
- areactive.
True cardiogenic shock. developmental pathogenesis
For the development of true cardiogenic shock, the death of more than 40% of LV myocardial cells is necessary. At the same time, the remaining 60% should start working at a double load. The critical decrease that occurs immediately after a coronary attack systemic circulation stimulates the development of response, compensatory reactions.
Due to the activation of the sympathetic-adrenal system, as well as the action of glucocorticosteroid hormones and the renin-angiotensin-aldosterone system, the body tries to increase blood pressure. Due to this, in the first stages of cardiogenic shock, blood supply to the coronary system is maintained.
However, activation of the sympathetic-adrenal system leads to the appearance of tachycardia, increased contractile activity cardiac muscle, an increase in myocardial oxygen demand, vasospasm of the microvasculature, and an increase in cardiac afterload.
The occurrence of generalized microvascular spasm enhances blood clotting and creates a favorable background for the occurrence of DIC.
Important. Severe pain associated with severe damage to the heart muscle also exacerbates existing hemodynamic disorders.
As a result of impaired blood supply, renal blood flow decreases and renal failure develops. Fluid retention leads to an increase in circulating blood volume and an increase in cardiac preload.
Violation of LV relaxation in diastole contributes to rapid rise pressure inside the left atrium, venous congestion of the lungs and their edema.
A "vicious circle" of cardiogenic shock is formed. That is, in addition to compensatory maintenance of coronary blood flow, there is an aggravation of the already existing ischemia and a worsening of the patient's condition.
Attention. Prolonged tissue and organ hypoxia leads to a violation of the acid-base balance of the blood and the development of metabolic acidosis.
Pathogenesis of the development of reflex cardiogenic shocks
The basis for the development of this type of shock is an intense pain syndrome. The severity of pain in this case may not correspond to the true severity of damage to the heart muscle.
Unlike true cardiogenic shock, with timely medical care, the pain syndrome is quite easily stopped by the introduction of analgesics and vascular preparations, as well as carrying out infusion therapy.
A complication of reflex cardiogenic shocks is a violation of vascular tone, an increase in capillary permeability and the appearance of a shortage of circulating blood volume due to plasma leakage from the vessel into the interstitium. This complication leads to a decrease in blood flow to the heart.
Attention. Infarcts with posterior localization are characterized by bradyarrhythmia ( low frequency heart rate), which increases the severity of shock and worsens the prognosis.
How does arrhythmia shock develop?
The most common causes of this type of shock are:
- paroxysmal tachyarrhythmia;
- ventricular tachycardia;
- atrioventricular blockade of the second or third degree;
- sinoatrial blockade;
- sick sinus syndrome.
Development of areactive cardiogenic shock
Important. Unlike true cardiogenic shock, given state can occur even with a small area of damaged LV myocardium.
At the basis of pathogenesis areactive shock there is a reduced ability of the heart muscle to contract. As a result, microcirculation, gas exchange are disturbed and disseminated intravascular coagulation develops.
Areactive shock is characterized by:
- high risk of death;
- complete lack of response to the introduction of pressor amines to the patient;
- the presence of paradoxical pulsation of the heart muscle (bulging, rather than contraction of the damaged part of the myocardium during systole);
- a significant increase in the need of the heart for oxygen;
- a rapid increase in the ischemic zone in the myocardium;
- the onset or worsening of symptoms pulmonary edema, in response to the introduction of vasoactive agents and an increase in blood pressure.
Cardiogenic shock - symptoms
The leading symptoms of cardiogenic shock are: 
- pain (high-intensity, widely radiating, burning, squeezing, pressing or "dagger character"). Dagger pain is most specific for slow ruptures of the heart muscle);
- decrease in blood pressure (indicative of a sharp decrease of less than 90 mmHg, and mean blood pressure less than 65 and the need for vasopressor medicines in order to maintain blood pressure. Average blood pressure is calculated based on the formula = (2 diastolic blood pressure + systolic) / 3). In patients with severe arterial hypertension and original high pressure, the level of systolic blood pressure in shock can be more than 90;
- severe shortness of breath;
- the appearance of a thready, weak pulse, tachycardia of more than one hundred beats per minute or bradyarrhythmia of less than forty beats per minute;
- microcirculation disorders and the development of symptoms of tissue and organ hypoperfusion: cold extremities, the appearance of sticky cold sweat, pallor and marbling skin, renal failure with oliguria or anuria (decrease in volume or complete absence urine), disorders acid-base balance blood and the occurrence of acidosis;
- deafness of heart tones;
- increasing clinical symptoms of pulmonary edema (appearance of moist rales in the lungs).
There may also be disturbances of consciousness (the appearance of psychomotor agitation, severe lethargy, stupor, loss of consciousness, coma), collapsed, unfilled peripheral veins and a positive symptom of a white spot (the appearance of a white, long-lasting spot on the skin back side hands or feet, after light pressure with a finger).
Diagnostics
In the vast majority of cases, cardiogenic shock develops after acute MI. When a specific clinical symptoms cardiogenic shock should be additional research in order to differentiate shock from:
- hypovolemia;
- cardiac tamponade;
- tension pneumothorax;
- thromboembolism of the pulmonary artery;
- internal bleeding from ulcers and erosions of the esophagus, stomach or intestines.
For reference. If the data obtained are in favor of a shock, it is necessary to determine its type (the further algorithm of actions depends on this).
It should be remembered that patients old age with NMK (violation cerebral circulation) and long-term diabetes, cardiogenic shock may occur against the background of painless ischemia.
For fast differential diagnosis carry out:
- ECG recording (against the background of clinical symptoms of shock significant changes absent); pulse oximetry (quick, non-invasive assessment of the degree of blood oxygen saturation);
- monitoring of arterial pressure and pulse;
- assessment of the level of plasma serum lactate (the most significant factor for the prognosis). A lactate level of more than 2 mmol/l testifies in favor of true cardiogenic shock. The higher the lactate level, the higher the risk of death).
Extremely important! Remember the half hour rule. The patient's chances of survival increase if assistance is provided within the first half hour after the onset of shock. In this regard, all diagnostic measures should be carried out as quickly as possible.
Cardiogenic shock, emergency care. Algorithm
Attention! If cardiogenic shock does not develop in a hospital, you should immediately call ambulance. All attempts to provide first aid on their own will only lead to a loss of time and make the patient's chances of survival zero.
Emergency care for cardiogenic shock:
Cardiogenic shock - treatment
Treatment of cardiogenic shock consists of several stages:
- Holding general events with adequate pain relief, oxygen therapy, thrombolysis, stabilization of hemodynamic parameters;
- Infusion therapy (according to indications);
- Normalization of microcirculation and reduction of peripheral vascular resistance;
- Increased contractility of the heart muscle;
- Intra-aortic balloon counterpulsation;
- Operational intervention.
Treatment depending on the type of shock:
Medical therapy
Ataralgesia is also indicated - the introduction of NSAIDs (ketoprofen) or narcotic analgesic(fentanyl) in combination with diazepam.
In order to increase the contractile activity of the heart muscle, strophanthin, corglicon and glucagon are used.
To normalize blood pressure, norepinephrine, mezaton, cordiamine, dopamine are used. If the effect of increasing blood pressure is unstable, the introduction of hydrocortisone or prednisolone is indicated.
When conducting thrombolytic therapy, a combination of thrombolytics with low molecular weight heparins is administered.
In order to normalize the rheological properties of blood and eliminate hypovolemia, rheopolyglucin is administered.
Also, elimination of violations of the acid-base balance of the blood, repeated anesthesia, correction of arrhythmia and cardiac conduction disorders are performed.
According to indications, balloon angioplasty and coronary artery bypass grafting are performed.
Prevention, complications and prognosis
Cardiogenic shock is the most severe complication of MI. Mortality in the development of true shock reaches 95%. The severity of the patient's condition is determined by severe damage to the heart muscle, tissue and organ hypoxia, the development of multiple organ failure, metabolic disorders and DIC.
For pain and arrhythmogenic shock the prognosis is more favorable, as patients usually respond adequately to ongoing therapy.
For reference. There is no prevention of shock.
After the shock is eliminated, the treatment of the patient corresponds to the therapy for CHF (chronic heart failure). There are also specific rehabilitation measures which depend on the cause of the shock.
According to the indications, extracorporeal membrane oxygenation (invasive O2 blood saturation) is performed and the patient is transferred to an expert center to resolve the issue of the need for a heart transplant.
Pathologies of the heart vascular system ranks first in terms of mortality among the population. In severe heart failure or complicated myocardial infarction, patients are at risk of developing such a critical condition as cardiogenic shock, which in 70-85% leads to lethal outcome. What is cardiogenic shock, what are its symptoms and how to treat it first first aid with cardiogenic shock?
What is cardiogenic shock?
Cardiogenic shock is a critical state of the body, in which there is a sharp decrease in blood pressure, followed by a deterioration in blood circulation in all internal organs and systems. The danger of cardiogenic shock lies in the fact that during its development, the rheological property blood, its viscosity increases, microthrombi are formed in the body. With cardiogenic shock, a decrease in heart rhythms occurs, which entails the development of disorders in the whole organism. All vital organs cease to receive oxygen, as a result, hypoxia develops: necrosis of the liver, kidneys, metabolic processes are disturbed, work deteriorates nervous system and the whole organism. Despite advances in modern cardiology and medicine, only 10% of patients who develop symptoms of cardiogenic shock can be saved.
Types of cardiogenic shock
In medicine, there are three main types of cardiogenic shock, each of which has its own severity and causes of development:
- reflex - mild form cardiogenic shock, in which extensive damage to the myocardium occurs. A decrease in blood pressure occurs against the background of a strong pain syndrome in the chest area. Timely rendered health care help to stop the symptoms, improve the prognosis for further treatment.
- Arrhythmic shock is the result of acute bradyarrhythmia. With the timely introduction of antiarrhythmic drugs, the use of a defibrillator acute period can be bypassed.
- Areactive shock - may occur with repeated myocardial infarction, when there is no positive response to drug therapy. In development this disease are happening irreversible changes in tissues with a 100% lethal outcome.
Regardless of the type of cardiogenic shock and its severity, the pathogenesis is practically the same: a sharp decrease in blood pressure, severe oxygen hypoxia internal organs and systems.
Signs and symptoms of cardiogenic shock
The clinic of cardiogenic shock is pronounced, develops within a few hours and is characterized.
- A sharp drop in blood pressure.
- changing appearance large: sharp and panicked facial features, pallor of the skin.
- Cold sweat breaks out.
- Breathing, rapid.
- Weak pulse.
- Loss of consciousness.
With the development of cardiogenic shock, the blood supply to the brain is disrupted, as a result of untimely assistance to the patient - 100% mortality. The only way save a person or increase the chances of life before the arrival of the ambulance team - to provide first aid to the patient. Of course, if cardiogenic shock has developed in a hospital, the patient has a better chance of life, since doctors will be able to quickly provide emergency care for cardiogenic shock.
First aid for cardiogenic shock
Any person who is nearby should help the patient with cardiogenic shock. It is very important to "remove" the panic, gather your thoughts and realize that a person's life depends on your actions. The emergency care algorithm for cardiogenic shock, before the arrival of the resuscitation team, consists of the following actions:
- Lay the patient on his back.
- Call a team of doctors, while clearly describing to the dispatcher the symptoms of the person and his condition.
- To increase blood flow to the heart, you can slightly raise your legs.
- Provide free air to the patient, unbutton his shirt, open the windows.
- Measure blood pressure.
- If necessary, when the patient has lost consciousness, perform cardiopulmonary resuscitation.
- After the arrival of the doctors, tell them what actions you have taken and all other information about the person's health, of course, if it is familiar to you.
If a person does not have medical education or does not know what medicines are allowed for a particular patient, it makes no sense to give heart drops or nitroglycerin, and painkillers or medicines for hypertension can harm the patient even more. Even if a person knows the cardiogenic shock algorithm, and can provide all needed help patient, there is no 100% guarantee that the patient will live, especially in severe forms of critical condition.
If the patient's condition is critical, it cannot be transported. Medical workers must carry out all emergency procedures on the spot. Only after the pressure stabilizes, the patient can be hospitalized in the department intensive care where he will be provided further assistance. It is very difficult to give a prognosis for cardiogenic shock, it all depends on the degree of damage to the heart and internal organs, as well as the age of the patient and other features of his body.
