Cardiac shock. Cardiogenic shock: clinic, emergency care
13. Cardiogenic shock during myocardial infarction: pathogenesis, clinical picture, diagnosis, emergency care.
Cardiogenic shock is an extreme degree of acute left ventricular failure, characterized by a sharp decrease in myocardial contractile function (a drop in stroke and cardiac 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.
The following forms of cardiogenic shock are distinguished:
Reflex,
True cardiogenic,
Areactive,
Arrhythmic,
Due to myocardial rupture.
Pathogenesis of true cardiogenic shock
It is this form of cardiogenic shock that fully corresponds to the definition of shock during myocardial infarction, which was given above.
True cardiogenic shock, as a rule, develops with extensive transmural myocardial infarction. In more than 1/3 of patients, the section reveals stenosis of 75% or more of the lumen of the three main coronary arteries, including the anterior descending coronary artery. Moreover, almost all patients with cardiogenic shock have thrombotic coronary occlusion (Antman, Braunwald, 2001). The possibility of developing cardiogenic shock increases significantly in patients with recurrent MI.
The main pathogenetic factors of true cardiogenic shock are the following.
1.Decreased pumping (contractile) function of the myocardium
This pathogenetic factor is the main one. The decrease in myocardial contractile function is primarily due to the exclusion of necrotic myocardium from the contraction process. Cardiogenic shock develops when the size of the necrosis zone is equal to or exceeds 40% of the mass of the left ventricular myocardium. An important role also belongs to the state of the peri-infarction zone, in which, during the most severe course of shock, necrosis forms (thus the infarction expands), as evidenced by a persistent increase in the blood level of CPK-MB and CPK-MBmass. A major 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 in patients with myocardial infarction, a pathophysiological vicious circle develops, 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 ultimately leads to a decrease in aortic pressure and a decrease in coronary perfusion pressure and, consequently, a decrease in coronary blood flow. In turn, a decrease in coronary blood flow aggravates myocardial ischemia and thereby further impairs the systolic and diastolic functions of the myocardium. The inability of the left ventricle to empty also leads to increased preload. Preload is understood as the degree of stretching of the heart during diastole; it depends on the amount of venous blood flow to the heart and the distensibility of the myocardium. An increase in preload is accompanied by expansion of the intact, well-perfused myocardium, which in turn, in accordance with the Frank-Starling mechanism, leads to an increase in the force of cardiac contractions. This compensatory mechanism restores stroke volume, but the ejection fraction, an indicator of global myocardial contractility, decreases due to an increase in end-diastolic volume. Along with this, 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 ventricular cavity and the radius of the ventricle, divided by the thickness of the ventricular wall. Thus, at the same aortic pressure, the afterload experienced by a dilated ventricle is higher than with a normal sized ventricle (Braunwald, 2001).
However, the magnitude of the 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. A decrease in cardiac output during cardiogenic shock leads to compensatory peripheral vasospasm, the development of which involves the sympathoadrenal system, endothelial vasoconstrictor factors, and the renin-angiotensin-II system. Increasing systemic peripheral resistance is aimed at increasing blood pressure and improving blood supply to vital organs, but it significantly increases afterload, which in turn leads to increased myocardial oxygen demand, worsening ischemia and a further decrease in myocardial contractility and an increase in left ventricular end-diastolic volume. The latter circumstance contributes to an increase in pulmonary congestion and, consequently, hypoxia, which aggravates myocardial ischemia and a decrease in its contractility. Then everything happens again as described above.
3. Disturbances in the microcirculation system and a decrease in circulating blood volume
As stated previously, in true cardiogenic shock there is widespread vasoconstriction and an increase in total peripheral vascular resistance. 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, ongoing 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, and venules more resistant to hypoxia remain spasmodic, as a result of which blood is deposited in the capillary network, which leads to a decrease in the mass of circulating blood. The release of the liquid part of the blood into the tissue interstitial spaces is also observed. A decrease in venous return of blood and the amount of circulating blood contributes to a further decrease in cardiac output and tissue hypoperfusion, further aggravating peripheral microcirculatory disorders up to the complete cessation of blood flow with the development of multiple organ failure. In addition, in the microvasculature, the stability of blood cells decreases, intravascular aggregation of platelets and erythrocytes develops, blood viscosity increases, and microthrombosis occurs. These phenomena aggravate 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 thrombosis of two or three coronary arteries is observed). The development of cardiogenic shock is also possible with extensive transmural infarctions of the posterior wall, especially with simultaneous spread of necrosis to the myocardium of the right ventricle. Cardiogenic shock often complicates the course of repeated myocardial infarctions, especially those accompanied by disturbances in heart rhythm and conduction, or in the presence of symptoms of circulatory failure even before the development of myocardial infarction.
The clinical picture of cardiogenic shock reflects severe disturbances in the blood supply to all organs, primarily vital ones (brain, kidneys, liver, myocardium), as well as signs of insufficient peripheral circulation, including in the microcirculatory system. Insufficient blood supply to the brain leads to the development of dyscirculatory encephalopathy, renal hypoperfusion leads to acute renal failure, insufficient blood supply to the liver can cause the formation of foci of necrosis in it, circulatory disorders in the gastrointestinal tract can cause acute erosions and ulcers. Hypoperfusion of peripheral tissues leads to severe trophic disorders.
The general condition of a patient with cardiogenic shock is severe. The patient is inhibited, consciousness may be darkened, complete loss of consciousness is possible, and short-term excitation is less common. The patient’s main complaints are complaints of severe general weakness, dizziness, “fog before the eyes,” palpitations, a feeling of interruptions in the heart area, and sometimes chest pain.
When examining the patient, attention is drawn to “gray cyanosis” or pale cyanotic coloration of the skin; there may be pronounced acrocyanosis. The skin is damp and cold. The distal parts of the upper and lower extremities are marble-cyanotic, the hands and feet are cold, and cyanosis of the subungual spaces is noted. The appearance of the “white spot” symptom is characteristic - an increase in the time it takes for the white spot to disappear after pressing on the nail (normally this time is less than 2 s). The above symptoms are a reflection of peripheral microcirculatory disorders, the extreme degree of which can be skin necrosis in the area of the tip of the nose, ears, distal parts of the fingers and toes.
The pulse on the radial arteries is thread-like, often arrhythmic, and often cannot be detected at all. Blood pressure is sharply reduced, always less than 90 mm. rt. Art. A decrease in pulse pressure is characteristic; according to A.V. Vinogradov (1965), it is usually below 25-20 mm. rt. Art. Percussion of the heart reveals an expansion of its left border; characteristic auscultatory signs are dullness of heart sounds, arrhythmias, soft systolic murmur at the apex of the heart, protodiastolic gallop rhythm (pathognomonic symptom of severe left ventricular failure).
Breathing is usually shallow and may be rapid, especially with the development of “shock” lung. The most severe course of cardiogenic shock is characterized by the development of cardiac asthma and pulmonary edema. In this case, suffocation occurs, breathing becomes bubbling, and there is a disturbing cough with pink, frothy sputum. When percussing the lungs, a dullness of the percussion sound in the lower parts is determined; crepitus and fine bubbling rales due to alveolar edema are also heard here. If there is no alveolar edema, crepitus and moist rales are not heard or are determined in small quantities as a manifestation of congestion in the lower parts of the lungs, a small amount of dry rales may appear. With severe alveolar edema, moist rales and crepitus are heard over more than 50% of the lung surface.
When palpating the abdomen, pathology is usually not detected; in some patients, liver enlargement may be detected, which is explained by the addition of right ventricular failure. The development of acute erosions and ulcers of the stomach and duodenum is possible, which is manifested by epigastric pain, sometimes bloody vomiting, and pain on palpation of the epigastric region. However, these changes in the gastrointestinal tract are rarely observed. The most important sign of cardiogenic shock is oliguria or oligoanuria; during bladder catheterization, the amount of urine released is less than 20 ml/h.
Diagnostic criteria for cardiogenic shock:
1. Symptoms of peripheral circulatory failure:
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 pressing on the nail > 2 s (decrease in the speed of peripheral blood flow)
2. Impaired consciousness (lethargy, confusion, possibly unconsciousness, less often - agitation)
3. Oliguria (decreased diuresis< 20 мл/ч), при крайне тяжелом течении - анурия
4. Decrease in systolic blood pressure to< 90 мм. рт. ст (по
some data less than 80 mm. rt. Art.), in persons with previous arterial
hypertension< 100 мм. рт. ст. Длительность гипотензии >30 min.
Reduction of pulse arterial pressure 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. for >= 30 min
7. Hemodynamic criteria:
pulmonary artery wedge pressure > 15 mm. rt. st (> 18 mm Hg, according to
Antman, Braunwald)
cardiac index< 1.8 л/мин/м2
increased total peripheral vascular resistance
increased left ventricular end-diastolic pressure
reduction in stroke and minute volumes
A clinical diagnosis of cardiogenic shock in patients with myocardial infarction can be made based on the detection of the first 6 available criteria. Determining hemodynamic criteria (point 7) for diagnosing cardiogenic shock is usually not mandatory, but is very advisable for organizing correct treatment.
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 allows the symptoms of shock to disappear),
Hemodynamic monitoring (catheterization of the central vein for insertion of a Swan-Ganz catheter).
2. Treatment of arrhythmias (arrhythmic form of cardiogenic shock)
3. Intravenous fluid administration.
4. Decrease in peripheral vascular resistance.
5. Increased myocardial contractility.
6. Intra-aortic balloon counterpulsation (IABC).
Intravenous fluid administration, which increases venous return to the heart, is one way to improve the pumping function of the left ventricle through the Frank-Starling mechanism. However, if the initial left ventricular end-diastolic pressure (LVEDP) is sharply increased, this mechanism ceases to work and a further increase in LVEDP 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 the PAWP is less than 15 mm. rt. Art. (if it is not possible to measure PAWP, they are monitored by CVP - fluid is administered if CVP is less than 5 mm Hg). During administration, signs of congestion in the lungs (shortness of breath, moist rales) are monitored most carefully. Usually 200 ml of 0.9% sodium chloride solution, low molecular weight dextrans (reopolyglucin, dextran -40) are administered; a polarizing mixture with 200 ml of 5-10% glucose solution can be used. You should drive up to the blood pressure system. more than 100 mm Hg. Art. or PAWP 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.
Reduced peripheral resistance (with blood pressure more than 90 mm Hg) - the use of peripheral vasodilators leads to a slight increase in cardiac output (as a result of reduced preload) and improved blood circulation in 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 systemic blood pressure, which is maintained at a level of at least 100 mm Hg. Art.
With blood pressure sys. less than 90 mm Hg. Art. and PAWP more than 15 mm Hg. Art. :
If blood pressure 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 system. up to 70-90 mm Hg. Art. - add dobutamine (5-20 mcg/kg/min), stop the administration of norepinephrine and reduce the dose of dopamine (to 2-4 mcg/kg/min - this is a “renal dose”, as it dilates the renal arteries)
If blood pressure sys. - 70-90 mm Hg. Art. – dopamine at a dose of 2-4 mcg/kg/min and dobutamine.
When diuresis is more than 30 ml/hour, it is preferable to use dobutamine. Dopamine and dobutamine can be used simultaneously: dobutamine as an inotropic agent + dopamine in a dose that increases renal blood flow.
If treatment measures are ineffective, IBD + emergency cardiac catheterization and coronary angiography. The purpose of IBD is to gain time for a thorough examination of the patient and targeted surgical intervention. In IBD, a balloon, inflated and deflated during each cardiac cycle, is inserted through the femoral artery into the thoracic aorta and positioned slightly distal to the ostium of the left subclavian artery. The main method of treatment is balloon coronary angioplasty (reduces mortality to 40-50%). Patients with ineffective BCA, mechanical complications of myocardial infarction, left main coronary artery disease, or severe three-vessel disease undergo emergency coronary artery bypass grafting.
Refractory shock – IBD and circulatory support before heart transplantation.
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– this is an extreme degree of manifestation of acute heart failure, characterized by a critical decrease in myocardial contractility and tissue perfusion. Symptoms of shock: drop in blood pressure, tachycardia, shortness of breath, signs of centralized blood circulation (pallor, decreased skin temperature, appearance of congestive spots), impaired consciousness. The diagnosis is made based on the clinical picture, ECG results, and tonometry. The goal of treatment is to stabilize hemodynamics and restore heart rhythm. As part of emergency treatment, beta blockers, cardiotonics, narcotic analgesics, and oxygen therapy are used.
ICD-10
R57.0
General information
Cardiogenic shock (CS) is an acute pathological condition in which the cardiovascular system is unable to provide adequate blood flow. The required level of perfusion is temporarily achieved due to the depleted reserves of the body, after which the decompensation phase begins. The condition belongs to class IV heart failure (the most severe form of cardiac dysfunction), mortality reaches 60-100%. Cardiogenic shock is more often recorded in countries with high rates of cardiovascular pathology, poorly developed preventive medicine, and lack of high-tech medical care.
Causes
The development of the syndrome is based on a sharp decrease in LV contractility and a critical decrease in cardiac output, which is accompanied by circulatory failure. A sufficient amount of blood does not enter the tissue, symptoms of oxygen starvation develop, blood pressure levels decrease, and a characteristic clinical picture appears. CABG can aggravate the course of the following coronary pathologies:
- Myocardial infarction. It is the main cause of cardiogenic complications (80% of all cases). Shock develops mainly with large-focal transmural infarctions with the release of 40-50% of the heart mass from the contractile process. It does not occur in myocardial infarctions with a small volume of affected tissue, since the remaining intact cardiomyocytes compensate for the function of dead myocardial cells.
- Myocarditis. Shock, leading to the death of the patient, occurs in 1% of cases of severe infectious myocarditis caused by Coxsackie viruses, herpes, staphylococcus, pneumococcus. The pathogenetic mechanism is damage to cardiomyocytes by infectious toxins, the formation of anticardiac antibodies.
- Poisoning with cardiotoxic poisons. Such substances include clonidine, reserpine, cardiac glycosides, insecticides, and organophosphorus compounds. An overdose of these drugs causes a weakening of cardiac activity, a decrease in heart rate, and a drop in cardiac output to levels at which the heart is unable to provide the required level of blood flow.
- Massive pulmonary embolism. Blockage of large branches of the pulmonary artery by a thrombus - pulmonary embolism - is accompanied by impaired pulmonary blood flow and acute right ventricular failure. Hemodynamic disorder caused by excessive filling of the right ventricle and stagnation in it leads to the formation of vascular insufficiency.
- Cardiac tamponade. Cardiac tamponade is diagnosed with pericarditis, hemopericardium, aortic dissection, and chest injuries. The accumulation of fluid in the pericardium complicates the work of the heart - this causes disruption of blood flow and shock phenomena.
Less commonly, pathology develops with papillary muscle dysfunction, ventricular septal defects, myocardial rupture, cardiac arrhythmias and blockades. Factors that increase the likelihood of cardiovascular accidents are atherosclerosis, old age, the presence of diabetes mellitus, chronic arrhythmia, hypertensive crises, and excessive physical activity in patients with cardiogenic diseases.
Pathogenesis
The pathogenesis is due to a critical drop in blood pressure and a subsequent weakening of blood flow in the tissues. The determining factor is not hypotension as such, but a decrease in the volume of blood passing through the vessels over a certain time. Deterioration of perfusion causes the development of compensatory and adaptive reactions. The body's reserves are used to supply blood to vital organs: the heart and brain. The remaining structures (skin, limbs, skeletal muscles) experience oxygen starvation. Spasm of peripheral arteries and capillaries develops.
Against the background of the described processes, activation of neuroendocrine systems occurs, the formation of acidosis, and the retention of sodium and water ions in the body. Diuresis decreases to 0.5 ml/kg/hour or less. The patient is diagnosed with oliguria or anuria, liver function is disrupted, and multiple organ failure occurs. In later stages, acidosis and cytokine release provoke excessive vasodilation.
Classification
The disease is classified according to pathogenetic mechanisms. At the prehospital stages, it is not always possible to determine the type of CABG. In a hospital setting, the etiology of the disease plays a decisive role in the choice of treatment methods. Misdiagnosis in 70-80% of cases ends in the death of the patient. The following types of shock are distinguished:
- Reflex– violations are caused by a severe pain attack. It is diagnosed when the volume of the lesion is small, since the severity of the pain syndrome does not always correspond to the size of the necrotic lesion.
- True Cardiogenic– a consequence of acute MI with the formation of a voluminous necrotic focus. The contractility of the heart decreases, which reduces cardiac output. A characteristic complex of symptoms develops. The mortality rate exceeds 50%.
- Areactive- the most dangerous variety. Similar to true CS, pathogenetic factors are more pronounced. Doesn't respond well to therapy. Mortality – 95%.
- Arrhythmogenic– prognostically favorable. It is the result of rhythm and conduction disturbances. Occurs with paroxysmal tachycardia, AV blockade of the third and second degree, complete transverse blockade. After the rhythm is restored, the symptoms disappear within 1-2 hours.
Pathological changes develop stepwise. Cardiogenic shock has 3 stages:
- Compensation. Decreased cardiac output, moderate hypotension, weakened perfusion in the periphery. Blood supply is maintained by centralizing the circulation. The patient is usually conscious, clinical manifestations are moderate. There are complaints of dizziness, headache, heart pain. At the first stage, the pathology is completely reversible.
- Decompensation. There is a comprehensive symptom complex, blood perfusion in the brain and heart is reduced. Blood pressure level is critically low. There are no irreversible changes, but there are minutes left before they develop. The patient is in stupor or unconscious. Due to the weakening of renal blood flow, urine formation is reduced.
- Irreversible changes. Cardiogenic shock enters the terminal stage. It is characterized by an intensification of existing symptoms, severe coronary and cerebral ischemia, and the formation of necrosis in the internal organs. Disseminated intravascular coagulation syndrome develops, and a petechial rash appears on the skin. Internal bleeding occurs.
Symptoms of cardiogenic shock
In the initial stages, cardiogenic pain syndrome is expressed. The localization and nature of the sensations are similar to a heart attack. The patient complains of squeezing pain behind the sternum (“as if the heart is being squeezed in the palm”), spreading to the left shoulder blade, arm, side, jaw. There is no irradiation on the right side of the body.
Complications
Cardiogenic shock is complicated by multiple organ failure (MOF). The functioning of the kidneys and liver is disrupted, and reactions from the digestive system are noted. Systemic organ failure is a consequence of untimely provision of medical care to the patient or a severe course of the disease, in which the rescue measures taken are ineffective. Symptoms of MODS are spider veins on the skin, vomiting “coffee grounds,” the smell of raw meat on the breath, swelling of the jugular veins, anemia.
Diagnostics
Diagnosis is carried out on the basis of physical, laboratory and instrumental examination data. When examining a patient, a cardiologist or resuscitator notes external signs of the disease (pallor, sweating, marbling of the skin) and assesses the state of consciousness. Objective diagnostic measures include:
- Physical examination. Tonometry determines a decrease in blood pressure below 90/50 mmHg. Art., pulse rate less than 20 mm Hg. Art. At the initial stage of the disease, hypotension may be absent, which is due to the inclusion of compensatory mechanisms. Heart sounds are muffled, moist fine rales are heard in the lungs.
- Electrocardiography. An ECG in 12 leads reveals characteristic signs of myocardial infarction: a decrease in the amplitude of the R wave, a displacement of the S-T segment, a negative T wave. Signs of extrasystole and atrioventricular block may be observed.
- Laboratory research. The concentration of troponin, electrolytes, creatinine and urea, glucose, and liver enzymes is assessed. The level of troponins I and T increases already in the first hours of AMI. A sign of developing renal failure is an increase in the concentration of sodium, urea and creatinine in plasma. The activity of liver enzymes increases with the reaction of the hepatobiliary system.
When carrying out diagnostics, it is necessary to distinguish cardiogenic shock from dissecting aortic aneurysm and vasovagal syncope. With aortic dissection, the pain radiates along the spine, persists for several days, and is wave-like. With syncope, there are no serious changes on the ECG, and there is no history of pain or psychological stress.
Treatment of cardiogenic shock
Patients with acute heart failure and signs of shock are urgently hospitalized in a cardiology hospital. The ambulance team responding to such calls must include a resuscitator. At the prehospital stage, oxygen therapy is provided, central or peripheral venous access is provided, and thrombolysis is performed according to indications. In the hospital, treatment started by the emergency medical team continues, which includes:
- Drug correction of disorders. To relieve pulmonary edema, loop diuretics are administered. Nitroglycerin is used to reduce cardiac preload. Infusion therapy is carried out in the absence of pulmonary edema and CVP below 5 mm Hg. Art. The infusion volume is considered sufficient when this figure reaches 15 units. Antiarrhythmic drugs (amiodarone), cardiotonics, narcotic analgesics, and steroid hormones are prescribed. Severe hypotension is an indication for the use of norepinephrine through a perfusion syringe. For persistent cardiac arrhythmias, cardioversion is used, and for severe respiratory failure, mechanical ventilation is used.
- High-tech assistance. When treating patients with cardiogenic shock, high-tech methods such as intra-aortic balloon counterpulsation, artificial ventricle, and balloon angioplasty are used. The patient receives an acceptable chance of survival with timely hospitalization in a specialized cardiology department, where the equipment necessary for high-tech treatment is available.
Prognosis and prevention
The prognosis is unfavorable. The mortality rate is more than 50%. This indicator can be reduced in cases where first aid was provided to the patient within half an hour from the onset of the disease. The mortality rate in this case does not exceed 30-40%. Survival is significantly higher among patients who underwent surgery aimed at restoring the patency of damaged coronary vessels.
Prevention consists of preventing the development of MI, thromboembolism, severe arrhythmias, myocarditis and heart injuries. For this purpose, it is important to undergo preventive courses of treatment, lead a healthy and active lifestyle, avoid stress, and follow the principles of a healthy diet. When the first signs of a cardiac catastrophe occur, an ambulance must be called.
Table of contents of the topic "Myocardial ruptures during myocardial infarction (MI, AMI). Complications of a hypertensive crisis. Treatment of complications of hypertensive crises.":1. Myocardial ruptures during myocardial infarction (MI, AMI). Rupture of the wall of the ventricles of the heart. Rupture of the interventricular septum. Rupture of the papillary muscle.
2. Cardiogenic shock. Classification of cardiogenic shock (Chazov). Clinic of cadiogenic shock.
4. Reflex cardiogenic shock. Emergency care for reflex cardiogenic shock.
5. Hypertensive crisis. Causes (etiology) of hypertensive crisis. Pathogenesis, classification of hypertensive crisis.
6. Clinic (clinical picture) of hypertensive crises. Hyperkinetic crises of type I (first). Hyperkinetic crises of type II (second).
7. Complication of hypertensive crisis. Variants of complications of hypertensive crises. Principles of emergency care for complications of hypertensive crisis.
8. Emergency care for hypertensive crisis of type I (first). Principles of treatment of type I crisis.
9. Emergency care for hypertensive crisis of type II (second). Principles of treatment of type II (second) crisis.
10. Treatment of complications of hypertensive crises. Treatment of complicated hypertensive crisis.
Principles of treatment of cardiogenic shock
1. True cardiogenic shock:
adequate pain relief;
sympathomimetics;
fibrinolytic drugs and heparin;
low molecular weight dextrans (reopolyglucin);
normalization of acid-base balance;
auxiliary circulation (counterpulsation).
2. Reflex shock:
adequate pain relief;
pressor drugs;
correction of bcc.
3. Arrhythmic shock:
adequate pain relief;
electropulse therapy;
electrical stimulation of the heart;
antiarrhythmic drugs.
4. Areactive shock:
adequate pain relief;
symptomatic therapy.
Since the therapy of various types of cardiogenic shock is not fundamentally different from treatment of complications of AMI, but only complements it, let us dwell on some individual issues.
True cardiogenic shock
Main difficulty treatment of true cardiogenic shock included in the pathogenesis - 40% or more of the left ventricular myocardium died. How can the remaining living 60% be made to work in double load mode, given that hypoxia, an inevitable companion to any state of shock, is itself a powerful stimulator of heart function? The issue is complex and not yet fully resolved. It is logical to start treatment with cardiac glycosides, but in experiments and in the clinic it has been proven that their effectiveness in this pathology is minimal. Hormones. Their minimal and rather short-term clinical effect can be detected only when using submaximal doses at the level of 2000 -3000 mg of prednisolone or its analogues. How can you really help a patient survive the acute phase of true cardiogenic shock?
The only group of drugs that have a specific positive effect in this pathology, are sympathomimetics. Drugs in this group have a specific effect on the cardiovascular system: they increase the tone of blood vessels in the microcirculation system (this creates additional resistance to the work of the heart!) and stimulate beta receptors of the heart, causing the development of positive inotropic and chronotropic effects. The main task of the doctor when using drugs of this group is to select such a dose and such a drug so that the positive effect on the heart outweighs the negative effect on the microcirculatory system.
Drug of choice in the treatment of true cardiogenic shock is dopmin (dopamine, dopamine). It is a sympathomimetic amine, which is apparently a precursor to norepinephrine in the body. Dopmin in small doses stimulates cardiac beta receptors, causing a noticeable inotropic effect with an increase in stroke volume, but without an increase in heart rate. The myocardial oxygen demand increases with the use of small doses of dopamine, but at the same time it is completely compensated by an increase in coronary blood flow. The effects of dopamine on blood vessels are completely different from those of other sympathomimetics. In small doses, it dilates the blood vessels of the kidneys (prevention of the prerenal form of acute renal failure) and intestines, while at the same time, the tone of other blood vessels, such as the veins of the skin and muscles, remains unchanged. The overall resistance of the peripheral circulation decreases somewhat, but tachycardia does not develop, since the increased volume of the heart compensates for the decrease in resistance.
Dopamine Available in 5 ml ampoules containing 40 mg of active substance per 1 ml. Enter dopmin IV, drip, usually at a dose of 2 to 10 mcg/kg/min, the contents of the ampoule (200 mg) are first diluted in 400 ml of rheopolyglucin or 400 ml of 5-10% glucose solution or 400 ml of isotonic sodium solution chloride (dopmin should not be mixed with alkaline solutions). This dilution creates a dopmin concentration of 500 mcg/1 ml or 25 mcg/1 drop. Knowing this, it is not difficult to calculate the required rate of drug administration in drops/min.
Note. 1 ml of solution contains 20 drops. At an infusion rate of 2-4 mcg/(kg min.) dopamine has a positive effect on beta1-adrenergic receptors, stimulating myocardial contractility and dopamine receptors in the kidneys, which increases renal blood flow (V.V. Ruksin, 1994).
At infusion rate 4-10 mcg\kg*min. The drug has a stimulating effect on beta2-adrenergic receptors, which leads to dilation of peripheral arteries (reduction of afterload) and a further increase in cardiac output. At this dosage, there is a noticeable increase in MOS, without any increase in blood pressure and heart rate and normalization of renal blood flow.
At injection rate over 20 mcg\kg*min. alpha-stimulating effects prevail, heart rate and afterload increase, and cardiac output decreases.
Selection of the required amount of the drug carried out individually. Infusions are carried out continuously over a period of several hours to 3-4 days. The average daily dose is usually 400 mg (in a patient weighing 70 kg).
The most common type is left ventricular heart failure. It usually follows myocardial infarction, severe arrhythmias and other dangerous conditions. Varieties of AHF include acute cardiogenic shock. It is caused by severe lesions for the body, in which the heart cannot pump blood normally.
The concept of cardiogenic shock
Emergency care for cardiogenic shock is necessary in the first minutes of its development. It should be remembered that this complication will not go away on its own. And in the absence of urgent treatment it will lead to death. Cardiogenic shock is a syndrome in which there is a decrease in cardiac output. Despite the compensatory increase in vascular resistance, the body cannot cope with this complication without the help of doctors.
Its main manifestations include a decrease in blood and pulse pressure, diuresis, and loss of consciousness. If help is not provided in time, death from cardiogenic shock occurs within a few hours after the onset of the disease. This condition does not occur on its own. It is always preceded by acute pathologies of the cardiovascular system.
What causes lead to cardiogenic shock?
The causes of cardiac shock include various cardiac and vascular diseases. The most common etiological factor is myocardial infarction. In this case, cardiogenic shock develops only in the case of massive shock and the absence of emergency assistance. Also common causes of its occurrence include life-threatening arrhythmias. They can bother a person for many years. But with their exacerbation and decompensation, these conditions are complicated by shock.
In some cases, a factor in the development of acute heart failure is considered to be a violation of vascular tone. This happens with massive bleeding, pain syndrome, acute renal failure. It must be remembered that cardiogenic shock is not an independent disease, but a complication of the underlying pathology. Therefore, doctors need to do everything to prevent its development.
Cardiogenic shock: classification of the disease
Depending on the cause and pathogenesis, several forms of cardiogenic shock are distinguished. Each of them has its own development mechanism. However, all variants result in the same symptoms. Regardless of the reason for its appearance, in case of cardiogenic shock it is necessary in any case. Since this condition is always equally dangerous. The following types of this complication are distinguished:
- True cardiogenic shock. It develops when heart tissue is damaged. In most cases, this form is caused by transmural necrosis of the myocardium.
- Arrhythmic shock. Its causes include flickering and extrasystole, severe bradycardia. In addition to arrhythmias, cardiac conduction disturbances can lead to shock.
- Reflex cardiogenic shock. With this option, cardiac dysfunction does not precede the complication. It usually develops with massive blood loss and renal failure.
- Areactive shock. Is the most dangerous option. It is placed in a separate group, since it almost always leads to death and cannot be treated.
True cardiogenic shock: mechanism of development
True cardiac shock is the most common. It occurs if a large part of the myocardium is affected (50% or more). In this case, necrosis spreads not only throughout the entire thickness of the muscle, but also occupies a large area. In addition to a heart attack, other illnesses can lead to true shock. Among them: septic endocarditis, severe heart defects, decompensated myodystrophies, etc. Acute hyperthyroidism and some genetic pathologies also lead to severe cardiac disorders.
As a result of necrosis of cardiac tissue, contractility is significantly reduced. Therefore, the organ cannot work at full capacity and supply blood vessels. The minute volume also decreases. This results in an increase in vascular resistance. Despite this, the heart still cannot cope with its job. The result is impaired blood supply to all organs and tissues.
Pathogenesis of arrhythmic cardiogenic shock
This form of the disease is based on disturbances in the conduction and rhythm of the heart. They can occur either spontaneously (as a result of myocardial infarction) or develop gradually. Most often, arrhythmias bother the patient for many years. The same applies to conduction disorders. However, life-threatening conditions develop over a short period. We are talking about hours and even minutes. Most often, cardiogenic shock is caused by ventricular rhythm disturbances. Among them: tachycardia, turning into fibrillation, and flutter. In addition, frequent group extrasystoles can lead to these processes.
Another condition that can lead to shock is sinus bradycardia. A decrease in heart rate is usually characterized by conduction disturbances. Less commonly, atrial fibrillation and flutter lead to cardiogenic shock. As a result of pathological contractions and ectopic foci in the myocardium (extrasystoles), the heart cannot perform its function. Therefore, there is a decrease in stroke and minute volume, a drop in pulse pressure, and blood pressure. With this option, the emergency doctor must first stop the arrhythmia by performing defibrillation or artificial cardiac massage.
What is reflex shock?
This form of shock develops due to reasons not initially related to damage to the heart muscle. The trigger for such a complication can be severe pain or bleeding. However, these symptoms are rarely related to the heart. Typically, such shock is diagnosed after an accident or acute renal failure.
This option has the most favorable prognosis. Emergency care for cardiogenic shock of a reflex nature should be aimed at eliminating its cause - pain, as well as stopping bleeding. As a result of these factors, the regulation of vascular tone is disrupted. Because of this, blood stagnates in the veins and arteries, and fluid leaks into the interstitial space, forming edema. All this leads to a decrease in venous flow to the heart. Further, the mechanism is the same as for other forms.
Causes and pathogenesis of areactive shock
Areactive cardiogenic shock occurs if the entire myocardium is affected. This occurs with repeated heart attacks. Cardiac tamponade may also be the cause. In this case, fluid appears in the pericardium, which compresses the organ, preventing it from contracting. In some cases, tamponade can lead to heart rupture. This condition leads to death. Unfortunately, it is not possible to help the patient in this case. The mechanism of shock development is associated with a complete cessation of cardiac function, unlike other forms in which cardiac output decreases. The mortality rate from this complication is close to 100%.
Symptoms of cardiogenic shock
The clinical picture is the same, regardless of what caused the cardiogenic shock. Symptoms of the complication are as follows: a drop in blood and pulse pressure, tachycardia, oliguria (decreased diuresis). Depending on the value of blood pressure and clinical data, there are 3 degrees of severity. When examining the patient, other signs of cardiogenic shock can be identified. These include:
- Cold and clammy sweat.
- Fear of death or lack of consciousness.
- Cyanosis is the blueness of the skin.
- The patient's facial features may be sharpened, facial expressions may be pained.
- In severe cases, the skin color takes on a gray tint.
How to diagnose shock?
Diagnosis of cardiogenic shock is usually based on clinical data and questioning of the patient's relatives. Since action must be taken immediately, doctors evaluate blood pressure, skin condition, pupil reaction, heart rate and respiratory rate. If the patient shows signs of shock, emergency care is provided immediately.
If medical personnel are available, the medical history is ascertained. The doctor asks: did the patient suffer from arrhythmia, angina pectoris, or perhaps have suffered a myocardial infarction before? If the complication develops at home or on the street, then the diagnosis of shock by emergency doctors ends there. When a patient is kept in an intensive care unit, in addition, pulse pressure, vascular resistance, and diuresis are measured. The gas composition of the blood is also examined.
Cardiogenic shock: emergency care, algorithm of actions
It is worth remembering that the patient’s life depends on how quickly and efficiently the assistance is provided. If there are signs of such a complication, doctors begin to take action immediately. If you do everything necessary in time, you can overcome cardiogenic shock. Emergency assistance - the algorithm of actions is as follows:
- Place the patient in a horizontal position with the leg end raised. In addition, it is necessary to provide access to air (unbutton clothes, open a window).
- Oxygen supply. It can be performed through a special mask or nasal catheter.
- Anesthesia. In case of myocardial infarction and reflex shock, narcotic drugs are used for this. The most commonly used medication is Morphine. It is diluted in saline and administered intravenously slowly.
- Restoration of blood volume and blood flow. To do this, administer the “Reopoliglucin” solution.
- If there is no effect, it is necessary to increase blood pressure using the drug "Atropine" 0.1%. Administer in an amount of 0.5-1 ml.
In addition, it is necessary to eliminate the cause of shock. In case of myocardial infarction, thrombolytic and antiplatelet therapy is carried out (drugs Alteplase, Clopidogrel, Aspirin). Heparin solution is also used to thin the blood. For ventricular arrhythmias, the drug Lidocaine is administered. In some cases, defibrillation is necessary.
Emergency care in a hospital setting
Emergency care for cardiogenic shock continues in the intensive care unit. There, constant monitoring of indicators is carried out, the causes of complications are determined. In case of myocardial infarction, surgical treatment is performed - arterial bypass surgery, stent placement. Surgical assistance is also necessary for some types of arrhythmia and conduction disorders. In this case, an artificial pacemaker is installed, which performs the contractile function of the heart.
Cardiogenic shock is a life-threatening condition that develops as a result of a sharp disruption of the contractile function of the left ventricle, a decrease in the minute and stroke volumes of the heart, resulting in a significant deterioration in the blood supply to all organs and tissues of the body.
Cardiogenic shock is not an independent disease, but develops as a complication of heart pathologies.
Causes
The cause of cardiogenic shock is a violation of myocardial contractility (acute myocardial infarction, hemodynamically significant arrhythmias, dilated cardiomyopathy) or morphological disorders (acute valvular insufficiency, rupture of the interventricular septum, critical aortic stenosis, hypertrophic cardiomyopathy).
The pathological mechanism for the development of cardiogenic shock is complex. Violation of myocardial contractile function is accompanied by a decrease in blood pressure and activation of the sympathetic nervous system. As a result, the contractile activity of the myocardium increases, and the rhythm becomes more frequent, which increases the heart’s need for oxygen.
A sharp decrease in cardiac output causes a decrease in blood flow in the renal arteries. This leads to fluid retention in the body. The increasing volume of circulating blood increases the preload on the heart and provokes the development of pulmonary edema.
Long-term inadequate blood supply to organs and tissues is accompanied by the accumulation of under-oxidized metabolic products in the body, resulting in the development of metabolic acidosis.
Mortality in cardiogenic shock is very high - 85-90%.
Kinds
According to the classification proposed by Academician E.I. Chazov, the following forms of cardiogenic shock are distinguished:
- Reflex. It is caused by a sharp drop in vascular tone, which leads to a significant drop in blood pressure.
- True. The main role belongs to a significant decrease in the pumping function of the heart with a slight increase in peripheral total resistance, which, however, is not enough to maintain an adequate level of blood supply.
- Areactive. Occurs against the background of extensive myocardial infarction. The tone of peripheral blood vessels sharply increases, and microcirculation disorders manifest themselves with maximum severity.
- Arrhythmic. Deterioration of hemodynamics develops as a result of significant disturbances in heart rhythm.
Signs
The main symptoms of cardiogenic shock:
- a sharp decrease in blood pressure;
- thread-like pulse (frequent, weak filling);
- oligoanuria (decrease in the amount of urine excreted to less than 20 ml/h);
- lethargy, even to the point of coma;
- pallor (sometimes marbling) of the skin, acrocyanosis;
- decreased skin temperature;
- pulmonary edema.
Diagnostics
The diagnostic scheme for cardiogenic shock includes:
- coronary angiography;
- chest x-ray (concomitant pulmonary pathology, dimensions of the mediastinum, heart);
- electro- and echocardiography;
- computed tomography;
- blood test for cardiac enzymes, including troponin and phosphokinase;
- arterial blood gas analysis.
Cardiogenic shock is not an independent disease, but develops as a complication of heart pathologies.
Treatment
- check airway patency;
- install a wide-diameter intravenous catheter;
- connect the patient to a cardiac monitor;
- deliver humidified oxygen through a face mask or nasal catheters.
After this, measures are taken to find the cause of cardiogenic shock, maintain blood pressure, and cardiac output. Drug therapy includes:
- analgesics (allow relief of pain);
- cardiac glycosides (increase the contractile activity of the myocardium, increase the stroke volume of the heart);
- vasopressors (increase coronary and cerebral blood flow);
- phosphodiesterase inhibitors (increase cardiac output).
If indicated, other medications are also prescribed (glucocorticoids, volemic solutions, β-blockers, anticholinergics, antiarrhythmic drugs, thrombolytics).
Prevention
Prevention of the development of cardiogenic shock is one of the most important measures in the treatment of patients with acute cardiopathology; it consists of rapid and complete relief of pain and restoration of heart rhythm.
Possible consequences and complications
Cardiogenic shock is often accompanied by the development of complications:
- acute mechanical damage to the heart (rupture of the interventricular septum, rupture of the left ventricular wall, mitral insufficiency, cardiac tamponade);
- severe left ventricular dysfunction;
- right ventricular infarction;
- disturbances of conductivity and heart rhythm.
Mortality in cardiogenic shock is very high - 85-90%.
