Symptoms and methods of treatment of acute myocardial infarction. Myocardial infarction: causes and signs

That's all today more people complain of poor heart condition. If emergency assistance is not provided in time, the consequences can be very sad. The most dangerous condition of our motor is acute myocardial infarction. What kind of disease is this, how to fight it and provide quality treatment?

Description and causes of the disease

In Russia, tens of thousands of people die every year from myocardial infarction, 65,000 to be exact. Many others become disabled. This disease spares no one, neither the elderly nor the young. The whole point is the heart muscle, which is called the myocardium.

A blood clot blocks a coronary artery and heart cells begin to die

Blood flows through the coronary arteries to this muscle. A blood clot can block one of the arteries that supplies it. It turns out that this part of the heart remains without oxygen. In this state, myocardial cells can last about thirty minutes, after which they die. This is the immediate cause of a heart attack - arrest of coronary circulation. However, it can be caused not only by a blood clot. In general, the reasons for this situation in the vessels can be described as follows:

1. Atherosclerosis. In this case, a blood clot forms. If you do not interfere with its formation, it will grow very quickly and eventually block the artery. The above process occurs, which causes such a terrible disease;
2. Embolism. As you know, this is a process in which the blood or lymph contains particles that should not be in a normal state. This leads to disruption of local blood supply. If embolism is the cause of acute myocardial infarction, then most often it is in which droplets of fat enter the bloodstream. This happens with numerous bone fractures;
3. Spasm of heart vessels. This means that the clearance coronary arteries narrows sharply and suddenly. Although this process is temporary, the consequences can be the most unpleasant;
4. Surgical interventions, namely complete transverse dissection of the vessel or its ligation;

In addition, factors that influence the above reasons, and, accordingly, the occurrence acute course The disease we are discussing can be described as follows:

1. Diabetes is a dangerous disease, so its treatment should not be left to chance.
2. Smoking.
3. Stress.
4. Hypertension.
5. Age (the most common occurrence of myocardial infarction occurs in women after 50 years and men after 40 years).
6. Obesity.
7. Hereditary predisposition.
8. Low physical activity.
9. Already suffered a myocardial infarction.
10. Cardiovascular diseases.
11. Alcohol abuse.
12. Increased amount of triglycerides in the blood.

You can help your heart even before the disease worsens; you just need to change your life.

Signs of the disease

Symptoms that are quite pronounced will help determine the occurrence of a heart attack. The main thing is to recognize them in time and take action. necessary measures.

This disease has a clear sign that occurs very often - pain localized behind the sternum. However, for some, this feature may not be expressed strongly, and for those who have diabetes, it may not be present at all. In addition, pain can be felt in the abdomen, arm, neck, shoulder blade, and so on. But in many cases the pain will be burning and squeezing. A person may feel as if a hot brick has been placed on their chest. This state lasts for at least fifteen minutes. It can continue for several hours. If a heart attack affects the entire left ventricle, then the pain usually spreads, which is called irradiation.

Another significant symptom, which is also characteristic of myocardial infarction, is shortness of breath. It manifests itself due to the fact that the contractility of the heart decreases. If shortness of breath is accompanied by a cough, this indicates that the rate of pulmonary circulation is slowing down. In this case, necrosis of a significant area of ​​the left ventricle occurs. Even pulmonary edema and shock may occur due to the fact that the volume of the affected myocardium is quite large.

Other features that accompany a heart attack are weakness, profuse sweating, that is, too heavy sweating, and interruptions in heart function. In some cases, unexpected cardiac arrest may occur. It is worth paying attention to weakness and autonomic reactions, which will also help recognize this disease

This does not mean that the above symptoms occur all together and in every person. It is important to take into account individual characteristics and the fact that some signs may not manifest themselves. Recognizing symptoms is an important aid in managing them.

Classification of the disease

The development of acute myocardial infarction can be divided into four stages:

1. The sharpest phrase. This is otherwise called the damage phase. It lasts from 2 to 24 hours. During this period, the process of dying of the myocardium in the affected area is formed. Unfortunately, most people die during this period, so emergency care at this moment is especially important.
2. Acute phase. Its duration is up to 10 days, starting from the onset of the disease. This period is characterized by inflammation occurring in the area of ​​the heart attack. This means that your body temperature will increase. The area of ​​inflammation will become swollen and will put pressure on healthy areas of the myocardium, impairing its blood supply.
3. The subacute phase in which the scar is formed. It lasts from ten days to 4-8 weeks.
4. Scarring phase, which lasts 6 months. This stage is also called chronic.

In myocardial infarction, necrosis, that is, the disease itself, is localized in the following places:

• left ventricle;
• right ventricle;
• apex of the heart;
• interventricular septum;
• other combined localizations.

Based on size, infarction can be divided into large-focal and small-focal.

Diagnosis of the disease

Acute myocardial infarction myocardium can be diagnosed in several ways:

1. ECG. This is the main, objective method. Thanks to it, it is possible to determine where the myocardium was damaged.
2. Heart markers. These are enzymes released from myocardial cells in case of damage, which results in a heart attack. An increase in these markers is observed a day after the attack. However, treatment includes emergency care, which must be provided immediately. This is what you need to do, and within a day, cardiac markers will help establish an accurate diagnosis.
3. Angiography. This method is used when difficulties arise with diagnosis, as well as when it is possible to restore blood flow with endovascular surgery. The essence of angiography is that a catheter is inserted into a coronary vessel. A special substance is injected through it, which allows fluoroscopy to be performed in real time. Thus, the disease will become more understandable.

What to do?

Treatment of a disease such as acute myocardial infarction is a very responsible undertaking. It is not for nothing that we used the word “event”, since emergency care includes following several principles. Of course, it is important to know them, but despite this, only medical staff can provide truly qualified assistance. It turns out that the first thing you need to do is call ambulance. Over the phone, you must tell them what is happening to the patient and list the symptoms. The person's entire condition should be described in detail to the medical staff when they arrive. Next, it's up to them.

In total, the principles that treatment includes can be divided into several points:

1. Anesthesia. This process is necessary, since there is a strong production of catecholamines in response to a pain impulse. They compress the blood vessels of the heart. For pain relief, two types of analgesics are used - narcotic and non-narcotic. Morphine is often commonly used. But from the very beginning its use may be erroneous, as respiratory disorders may occur. Therefore, nitroglycerin is often given before using this drug, which can relieve pain. Nitroglycerin is contraindicated only if blood pressure is low, 90 to 60 or lower. There is an option for using analgin. If it does not help, morphine is used to relieve pain, which is administered intravenously in small doses. In case of acute heart attack, treatment with analgesics is required, which are used on the first day. High-quality assistance in this direction will weaken the disease.
2. Recovery. Emergency care also means restoring the patency of the coronary vessels. To do this, use drugs that affect blood clotting. After 3-6 hours have passed since it all started, thrombolytic agents such as alteplase, streptokinase, and so on are included in the treatment. To prevent re-development of thrombosis in the future, anticoagulants must be used: fragmin, heparin, fraxiparin. Antiplatelet agents contribute to the same goal: clopidogrel, aspirin, Plavix.

It is important to remember that until the ambulance arrives, the patient’s life is in the hands of whoever is nearby, so emergency care is more important than ever.

The patient needs to be put down, but if he does not want this, you should not force him, since such people often look for the most optimal body position for them. If there are no contraindications, nitroglycerin should be given under the tongue. If the pain persists, it can be applied every five minutes.

Sedatives will help enhance the effect of painkillers. In addition, you need to measure your blood pressure and pulse frequently, preferably every five minutes. As we have already said, in case of low blood pressure, nitroglycerin should be skipped. If the pulse is 60 beats per minute, then atenolol, 25 mg, can be given. This is done to prevent arrhythmia.

Treatment may also include surgical methods that help to overcome the disease to some extent. If surgery is performed as an emergency, in most cases it is done to restore blood flow. Stenting is used. This means that the area affected by thrombosis is metal structure. It expands, causing the vessel to expand. Today, this method often includes emergency care. In case of planned intervention, the goal is to reduce the area of ​​necrosis. Planned operations include coronary artery bypass grafting. Using this method, the risk of recurrence of an acute heart attack is further reduced.

If all necessary measures have been taken, this does not mean that the treatment stops there. Throughout his life, the patient must use hypolipidemic drugs and antiplatelet agents, for example, atorvostatin, simvostatin, and so on. This is important to ensure that the disease has as little chance as possible of returning. The first day of acute myocardial infarction is the most important, so you need to be on guard so that emergency care is provided if necessary. health care.

Therefore, at this time, medical staff must conduct multiple examinations, measure blood pressure, pulse, heart rate, and so on. In addition, nutrition is very important. During the first days, the patient’s diet should not include smoked foods, pickles, alcohol, or fatty meats. It is best to eat fruits, vegetables and purees from them.

During exercise, you need to carefully monitor your health so that help in case of an exacerbation is provided in a timely manner.

Everything described above is very important to know. This will help you be prepared if someone nearby has a seizure. The symptoms will help you understand what kind of disease is developing right before your eyes, and proper emergency care at such a moment will save a person’s life. Correctly selected treatment will prolong it and reduce the risk of complications. It is important to remember that everyone can reduce the risk of cardiovascular disease if they lead a healthy lifestyle.

Richard K. Pasternak, Eugene Braunwald, Joseph S. Alpert

Myocardial infarction is one of the most common diseases in Western countries. In the United States, approximately 1.5 million people suffer a myocardial infarction each year. With acute myocardial infarction, approximately 35% of patients die, and slightly more than half of them die before reaching the hospital. Another 15-20% of patients who underwent acute stage myocardial infarction, die within the first year. The risk of increased mortality among people who have had a myocardial infarction, even after 10 years, is 3.5 times higher than in people of the same age, but without a history of myocardial infarction.

Clinical picture

Most often, patients with acute myocardial infarction complain of pain. For some patients, it is so severe that they describe it as the worst pain they have ever experienced (Chapter 4). I am severe, squeezing, tearing pain usually occurs in the depths of the chest and is similar in nature to ordinary attacks of angina pectoris, but more intense and prolonged. In typical cases, pain is felt in the central part of the chest and/or in the epigastric region. In approximately 30% of patients it radiates to upper limbs, less often in the abdomen, back, capturing the lower jaw and neck. The pain can even radiate to the back of the head, but never radiates below the navel. Cases where the pain is localized below the xiphoid process, or when patients themselves deny the connection between the pain and a heart attack, are the reasons for the incorrect diagnosis.

The pain is often accompanied by weakness, sweating, nausea, vomiting, dizziness, and agitation. Unpleasant sensations usually appear at rest, often in the morning. If the pain begins during physical activity, then, unlike an attack of angina, it, as a rule, does not disappear after it stops.

However, pain is not always present. In approximately 15-20%, and apparently even in a larger percentage of patients, acute myocardial infarction is painless, and such patients may not seek medical help at all. More often, silent myocardial infarction is recorded in patients with diabetes mellitus, as well as in the elderly. In elderly patients, myocardial infarction is manifested by sudden shortness of breath, which can develop into pulmonary edema. In other cases, myocardial infarction, both painful and non-painful, is characterized by a sudden loss of consciousness, a feeling of severe weakness, the occurrence of arrhythmias, or simply an unexplained sharp drop in blood pressure.

Physical examination

In many cases, patients have a dominant reaction to chest pain. They are restless, agitated, trying to relieve pain by moving in bed, writhing and stretching, trying to induce shortness of breath or even vomiting. Patients behave differently during an attack of angina. They tend to take a stationary position for fear of renewed pain. Paleness, sweating and coldness of the extremities are often observed. Chest pain lasting more than 30 minutes and sweating observed at the same time indicate high probability acute myocardial infarction. Despite the fact that in many patients the pulse and blood pressure remain within normal limits, approximately 25% of patients with anterior myocardial infarction exhibit manifestations of sympathetic hyperreactivity nervous system(tachycardia and/or hypertension), and almost 50% of patients with inferior myocardial infarction exhibit signs increased tone sympathetic nervous system (bradycardia and/or hypotension).

The precordial area is usually unchanged. Palpation of the apical impulse may be difficult. In almost 25% of patients with anterior myocardial infarction, during the first days of the disease, altered systolic pulsation is detected in the periapical region, which may soon disappear. Other physical signs of left ventricular dysfunction that may occur during acute myocardial infarction, in descending order of frequency of occurrence, are as follows: IV (S4) or III (S3) heart sounds, muffled heart sounds and, rarely, paradoxical splitting of the second sound (ch. . 177).

Transient systolic murmur at the apex of the heart, which occurs primarily as a consequence of secondary insufficiency of the left atrioventricular valve (mitral regurgitation) due to dysfunction of the papillary muscles, is mid- or late-systolic in nature. During auscultation, many patients with transmural myocardial infarction occasionally hear a pericardial friction rub. In patients with right ventricular infarction, pulsation of the distended jugular veins often occurs, and there is a decrease in the volume of the pulse in the carotid arteries, despite normal cardiac output. In the 1st week of acute myocardial infarction, a rise in body temperature to 38 °C is possible, but if the body temperature exceeds 38 °C, other reasons for its increase should be looked for. Blood pressure varies widely. In most patients with transmural myocardial infarction, systolic blood pressure decreases by 10-15 mmHg. Art. from the initial level.

Laboratory research

To confirm the diagnosis of myocardial infarction, the following laboratory indicators are used: 1) non-specific indicators of tissue necrosis and inflammatory reaction; 2) electrocardiogram data; 3) results of changes in the level of serum enzymes.

A manifestation of the body's nonspecific reactivity in response to myocardial damage is polymorphic cell leukocytosis, which occurs within a few hours after the onset of anginal pain, persists for 3-7 days and often reaches values ​​of 12-15 109/l. ESR does not increase as quickly as the number of leukocytes in the blood, reaches a peak during the 1st week and sometimes remains elevated for 1-2 weeks.

Electrocardiographic manifestations of acute myocardial infarction are described in detail in Chap. 178. Although there is not always a clear connection between changes in the ECG and the degree of myocardial damage, the appearance of a pathological Q wave or the disappearance of the R wave usually makes it possible to diagnose transmural myocardial infarction with a high probability. The presence of non-transmural myocardial infarction is indicated in cases where the ECG reveals only transient changes in the ST segment and persistent changes in the T wave. However, these changes are very variable and nonspecific and therefore cannot serve as a basis for diagnosing acute myocardial infarction. In this regard, a rational nomenclature for the diagnosis of acute myocardial infarction should only distinguish the latter into transmural and non-transmural, depending on the presence of changes in the Q wave or ST-T waves.

Serum enzymes

Necrotic heart muscle secretes into the blood during acute myocardial infarction a large number of enzymes. The release rate of different specific enzymes varies. Changes in the level of enzymes in the blood over time have great diagnostic value. The dynamics of the concentration of enzymes most often used to diagnose acute myocardial infarction is shown in Fig. 190-1. Levels of two enzymes, serum glutamate oxaloacetate transaminase (SGOT) and creatine phosphokinase (CPK), rise and fall very quickly, while lactate dehydrogenase (LDH) rises more slowly and remains elevated longer. A disadvantage of the CGOT determination is that this enzyme is also found in skeletal muscle, liver cells, and red blood cells and can be released from these extracardiac sources. Therefore, at present, the determination of CGOT for the diagnosis of acute myocardial infarction is used less frequently than before, due to the nonspecificity of this enzyme and the fact that the dynamics of its concentration occupies an intermediate position between the dynamics of the concentration of CPK and the dynamics of the concentration of LDH, and therefore information about the level of CGOT becomes in most cases unnecessary. Determining the content of the MB isoenzyme CK has advantages over determining the concentration of CGOT, since this isoenzyme is practically undetectable in extracardiac tissue and is therefore more specific than CGOT. Because the rise in CPK or SGOT concentrations is detected within a short time, it may go undetected in cases where blood samples are taken more than 48 hours after the onset of myocardial infarction. The determination of MB-CPK has practical meaning in cases where there is suspicion of damage to skeletal muscle or brain tissue, since they contain significant amounts of this enzyme, but not its isoenzyme. The specificity of the MB isoenzyme for determining myocardial damage depends on the technique used. Radioimmunoassay is the most specific, but in practice, gel electrophoresis is more often used, which has less specificity and therefore more often gives false-positive results. In acute myocardial infarction, LDH levels rise on the first day, between the 3rd and 4th days they reach a peak and return to normal after an average of 14 days. When electrophoresis is carried out in starch gel, five isoenzymes of LDH can be isolated. Different tissues contain different amounts of these isoenzymes. The isoenzyme with the highest electrophoretic mobility is mainly found in the myocardium and is designated LDH). Isoenzymes with the lowest electrophoretic mobility are found predominantly in skeletal muscle and liver cells. In acute myocardial infarction, the level of LDH1 increases even before the level of total LDH increases, i.e., an increase in LDH content may be observed) with normal total LDH levels. Therefore, detection of elevated LDH levels | is a more sensitive diagnostic test for acute myocardial infarction than the level of total LDH, its sensitivity exceeds 95%.

Rice. 190-1. Dynamics of serum enzymes after a typical myocardial infarction.

CPK - creatine phosphokinase; LDH - lactate dehydrogenase; GOT - glutamate xaloacetate transaminase.

special clinical significance represents the fact that a 2-3-fold increase in the level of total CPK (but not MB-CPK) can be a consequence of intramuscular injection. There may be cases of paradoxical diagnosis of acute myocardial infarction in patients who have undergone intramuscular injection drugs due to chest pain not associated with heart pathology. In addition, potential sources of increased CPK levels may be: 1) muscle diseases, including muscular dystrophies, myopathies, polymyositis; 2) electrical pulse therapy (cardioversion); 3) cardiac catheterization; 4) hypothyroidism; 5) brain stroke; 6) surgical interventions; 7) damage to skeletal muscles due to injuries, convulsions, and prolonged immobilization. Cardiac surgery and electrical pulse therapy can often lead to increased levels of the CPK isoenzyme.

It is known that there is a correlation between the amount of enzyme released into the blood and the size of myocardial infarction. It has been demonstrated that the mass of the myocardium that has undergone necrosis can be determined from the concentration-time curve if the kinetics of enzyme release, its breakdown, distribution, etc. are known. Analysis of the concentration-time curve for MB - CPK allows us to determine the size of myocardial infarction in grams . While the area under the curve of changes in MB-CPK concentration over time reflects the size of myocardial infarction, the absolute values ​​of the concentration of this enzyme and the time to reach the maximum concentration are associated with the kinetics of leaching of MB-CPK from the myocardium. The appearance of a lumen in an occluded coronary artery, occurring either spontaneously or under the influence of mechanical action or pharmacological drugs V early dates acute myocardial infarction, causes a rapid increase in enzyme concentration. Peak concentrations are reached 1-3 hours after reperfusion. The total area under the concentration-time curve may be less than without reperfusion, which reflects the smaller size of the myocardial infarction.

A characteristic increase in enzyme concentrations is observed in more than 95% of patients with clinically proven myocardial infarction. At unstable angina the content of CPK, LDH, and SGOT usually does not increase. In many patients with suspected myocardial infarction, the initial level of enzymes in the blood remains within normal limits; during myocardial infarction, it can increase 3 times, but it does not exceed the upper limit of normal. This situation is observed in patients with minor myocardial infarction. Although such an increase in enzyme levels cannot be considered a strict diagnostic criterion for acute myocardial infarction, it is highly likely to raise suspicion. Determination of isoenzymes can provide practical assistance in such a situation.

Radionuclide techniques may be useful in diagnosing acute myocardial infarction or assessing its severity (Chapter 179). Scintigraphy in the acute phase of acute myocardial infarction (hot spot imaging) is performed with 99m"Tc-pyrophosphate containing divalent tin. Scinograms usually give positive result from the 2nd to the 5th day after the onset of myocardial infarction, more often in patients with transmural myocardial infarction. Despite the fact that the method makes it possible to determine the localization of myocardial infarction and its size (p. 887), in terms of diagnosis it is less accurate than determining the CPK content. Myocardial imaging with thallium-201, which is captured and concentrated by viable myocardium, reveals a perfusion defect (“cold spot”) in most patients in the first hours after the development of transmural myocardial infarction. This is a localized area. reduced radioactivity may fill over the following hours. However, differentiate acute infarction from old scar changes using this method impossible. Thus, thallium scanning is a very sensitive method for detecting myocardial infarction, but it is not specific for acute myocardial infarction. Using radionuclide ventriculography with erythrocytes labeled with 99mTe, contractility disorders and a decrease in left ventricular ejection fraction can be detected in patients with acute myocardial infarction. Radionuclide ventriculography is very valuable in assessing impaired hemodynamics in acute myocardial infarction and when it is necessary to establish a diagnosis of right ventricular myocardial infarction, when the ejection fraction of the right ventricle decreases. However, in general, the specificity of this method is low, since altered radionuclide ventriculograms are recorded not only in acute myocardial infarction, but also in other pathological conditions of the heart.

Two-dimensional echocardiography may also be useful in assessing the condition of patients with acute myocardial infarction. In this case, contractility disorders can be easily identified, especially in the area of ​​the septum and posteroinferior wall. And although echocardiography cannot differentiate acute myocardial infarction from contractility disorders due to the presence of scars or severe acute myocardial ischemia, the simplicity and safety of this method make it possible to consider it as an important stage in the examination of patients with acute myocardial infarction. In addition, echocardiography can be very informative for the diagnosis of right ventricular myocardial infarction, left ventricular aneurysm, and thrombus in the left ventricle.

Management of patients with acute myocardial infarction

In acute myocardial infarction, two main types of complications can be distinguished: complications caused by electrical instability (arrhythmias) and mechanical ones (pumping failure). The most common cause of “arrhythmic” death in acute myocardial infarction is ventricular fibrillation. Most patients with ventricular fibrillation die within the first 24 hours after the onset of symptoms, and more than half of them die within the first hour. Although ventricular extrasystole or ventricular tachycardia often precede ventricular fibrillation, the latter can develop without previous arrhythmias. This observation gave rise to the use of lidocaine for the prevention of spontaneous ventricular fibrillation in acute myocardial infarction. Therefore, the emphasis of treatment tactics has shifted from resuscitation measures to preventing situations in which the need for such measures arises. This has led to a decrease in the incidence of primary ventricular fibrillation over the past two decades. The reduction in in-hospital mortality for acute myocardial infarction from 30% to 10% was largely the result of such organizational measures as the rapid delivery of patients with acute myocardial infarction to medical institutions equipped with ECG monitoring devices and staffed (not necessarily with higher education). medical education), able to quickly recognize life-threatening ventricular arrhythmias and immediately prescribe appropriate treatment.

As the frequency decreased sudden death in the hospital, due to adequate preventive antiarrhythmic therapy, other complications of acute myocardial infarction, in particular insufficiency of the pumping function of the myocardium, began to come to the fore. And, despite advances in the treatment of patients with acute heart failure, the latter is currently the leading cause of death in acute myocardial infarction. The size of the area necrotic due to ischemia correlates with the degree of heart failure and mortality rate, both in the first 10 days and beyond. late dates. Killip was offered the original clinical classification, based on an assessment of the degree of cardiac dysfunction. According to this classification, patients are divided into four classes. Class 1 includes patients who do not have signs of pulmonary or venous stagnation; in the 2nd class - persons with moderate heart failure, in which wheezing is heard in the lungs, a gallop rhythm in the heart (Z3), there is shortness of breath, signs of failure of the right heart, including venous and hepatic congestion; in class 3 - patients with severe heart failure accompanied by pulmonary edema; in the 4th grade - patients in a state of shock with systemic pressure below 90 mm Hg. Art. and signs of peripheral vascular constriction, with sweating, peripheral cyanosis, confusion, oliguria. Some studies have calculated the risk of in-hospital mortality for each of the above-mentioned Killip clinical classes, it is for the 1st class - 0-5%, for the 2nd - 10-20%, for the 3rd - 35-45% and for 4th - 85-90%.

General Considerations

Thus, the main principles of treatment of patients with acute myocardial infarction are to prevent death due to rhythm disturbances and limit the size of myocardial infarction.

Rhythm disturbances can be corrected when they occur if qualified medical personnel and appropriate equipment are available. Since the greatest mortality from arrhythmia occurs in the first few hours of acute myocardial infarction, it is obvious that the effectiveness of medical care in intensive care units depends on how quickly the patient is delivered from them. The main delay is not due to shortcomings in transporting the patient to the clinic, but due to the fact that quite a lot of time passes between the onset of pain and the patient’s decision to seek medical help. Therefore, it is necessary to widely disseminate medical knowledge, explaining the importance of promptly seeking medical help when experiencing chest pain.

When treating patients with acute myocardial infarction, there are a number of general rules, which deserve special attention. The first and most important thing is to strive to maintain an optimal balance between the supply of oxygen to the myocardium and the need for it in order to maximize the preservation of myocardial viability in the area surrounding the focus of necrosis. To do this, it is necessary to provide the patient with rest, prescribe painkillers and moderate sedative therapy, create a calm atmosphere that helps reduce heart rate, the main value that determines the myocardial oxygen demand.

With severe sinus bradycardia (heart rate less than 45 per minute), the patient's lower limbs should be raised and atropine administered, or electrical stimulation performed. The latter is preferable in cases where bradycardia is accompanied by a drop in blood pressure or an increase in ventricular arrhythmias. Without severe bradycardia, atropine should not be prescribed to patients, as this can lead to a significant increase in heart rate. Patients with acute myocardial infarction with tachycardia and high blood pressure should be prescribed adrenergic blockers. First, 0.1 mg/kg propranolol (anaprilin) ​​or 15 mg metoprolol is administered intravenously, this dose is divided into three equal parts and administered sequentially. This prescription of these drugs is safe if it does not cause complications, such as heart failure, atrioventricular block, or bronchial asthma. All forms of tachyarrhythmias require immediate and specific treatment. Drugs with a positive notropic effect, such as cardiac glycosides, sympathomimetics affecting the heart muscle, should be prescribed only for severe heart failure and in no case for prophylactic purposes. If various sympathomimetic amines are available, it should be remembered that the administration of isoproterenol, which has a pronounced chronotropic and vasodilating effect, is least desirable. Dobutamine, which has a lesser effect on heart rate and peripheral vascular resistance, is preferable in cases where it is necessary to increase cardiac contractility. Dopamine has positive action in patients with left ventricular failure and systemic hypotension (systolic pressure less than 90 mm Hg). Diuretics are indicated for heart failure, in which case they are used before the prescription of pacemaker drugs, unless there are signs of hypovolemia and hypotension.

All patients need to inhale oxygen-enriched air (see below). Particular attention should be paid to maintaining adequate blood oxygenation in patients with hypoxemia, which can be observed in the case of chronic diseases lungs, pneumonia, left ventricular failure. In case of severe anemia, which may contribute to the expansion of the ischemic focus, red blood cells should be carefully administered, sometimes in combination with diuretics. Concomitant diseases, in particular infectious diseases, accompanied by tachycardia and increased myocardial oxygen demand, also require immediate attention. It is necessary to ensure that fluctuations in systolic blood pressure do not exceed 25 - 30 mmHg. Art. from the normal level for the patient.

Intensive coronary care units. Such units are designed to provide care to patients with acute myocardial infarction in order to reduce mortality among patients and increase knowledge about acute myocardial infarction. Intensive care units (ICUs) are nursing observation units staffed by highly qualified, experienced medical personnel capable of providing immediate assistance in emergency cases. Such a unit must be equipped with systems that allow constant monitoring of the ECG of each patient and monitoring of hemodynamic parameters in patients, have the required number of defibrillators, devices for artificial ventilation of the lungs, as well as devices for administering electrolytes for cardiac stimulation and floating catheters with inflatable balloons at the end . However, the most important thing is to have a highly trained nursing team capable of recognizing arrhythmias, administering appropriate antiarrhythmic drugs and performing cardiovascular resuscitation, including electropulse therapy when necessary. It is also important that you always have the opportunity to consult a doctor. However, it should be noted that nursing staff saved many lives as a result of timely correction of arrhythmias even before the doctor arrived.

The presence of intensive care units makes it possible to provide assistance to patients as early as possible during acute myocardial infarction, when medical care can be most effective. To achieve this goal, it is necessary to expand the indications for hospitalization and place patients in intensive care units even with suspected acute myocardial infarction. It is very easy to verify that this recommendation is being followed. To do this, it is sufficient to establish the number of patients with a proven diagnosis of acute myocardial infarction among all persons admitted to the intensive care unit. Over time, however, for a number of reasons this rule was broken. The availability of ECG monitoring and the presence of highly qualified personnel in the so-called intermediate observation blocks made it possible to hospitalize so-called low-risk patients (with no hemodynamic disorders and without rhythm disturbances). In order to save money and make optimal use of existing equipment, many institutes have developed guidelines for providing care to patients and selecting patients with suspected acute myocardial infarction. In the US, most such patients are hospitalized; in other countries, such as the UK, low-risk patients are treated at home. Among patients with acute myocardial infarction delivered to the hospital, the number of patients sent to intensive care units is determined both by their condition and by the number of beds in the units. In some clinics, beds in intensive observation units are primarily allocated for patients with a complicated course of the disease, especially for those who require hemodynamic monitoring. The mortality rate in intensive observation units is 5-20%. This variability is partly explained by differences in indications for hospitalization, the age of patients, the characteristics of the clinic, as well as other unaccounted factors.

Reperfusion

The cause of most transmural myocardial infarctions is a thrombus located either freely in the lumen of the vessel or attached to an atherosclerotic plaque. Therefore, a logical approach to reducing the size of myocardial infarction is to achieve reperfusion by rapidly dissolving the thrombus with a thrombolytic drug. It has been proven that in order for reperfusion to be effective, i.e., to contribute to the preservation of ischemic myocardium, it should be carried out within a short time after the onset of clinical symptoms, namely within 4 hours, and preferably 2 hours.

For the treatment of patients with acute myocardial infarction Department of Sanitary Supervision of Quality food products and medications considers it possible to administer streptokinase (SK) through a catheter installed in the coronary artery. Despite the fact that with the help of SA it is possible to lyse a blood clot, which causes a heart attack in 95% of cases, some issues related to the use of this drug remain unresolved. In particular, it is unknown whether the administration of SC reduces mortality. Intravenous administration of SA is less effective than intracoronary administration, but it has the great advantage of not requiring catheterization of the coronary arteries. Theoretically, tissue plasminogen activator has an advantage over SC; it lyses approximately 2/3 of fresh blood clots. When administered intravenously, it should exhibit a lysing effect at the site of fresh thrombosis and, as a result, have a less pronounced systemic thrombolytic effect. However, even if we have in mind an ideal thrombolytic drug, it is unknown whether, when routinely prescribed, it will actually help preserve ischemic myocardium, reduce the need for mechanical revascularization using coronary angioplasty and coronary artery bypass grafting, and significantly reduce mortality in patients with acute myocardial infarction. Research is currently being conducted that can answer these questions. At the time of writing, tissue plasminogen activator is not yet widely available. clinical application and his appointment has not yet been approved by the Biological Bureau. The optimal treatment tactics for severe obstruction (more than 80% of the lumen of the coronary artery) should be considered intravenous administration of streptokinase in the early stages of acute myocardial infarction (less than 4 hours after the onset of pain) or, if possible, intracoronary administration of streptokinase at the same time, and then percutaneous transluminal coronary angioplasty (PTCA). However, the need to have a qualified angiography team on constant readiness makes possible use Such treatment tactics are used only in a small number of patients with acute myocardial infarction. However, if current studies show that intravenous administration of tissue plasminogen activator followed by coronary angiography (1 to 2 days later) and, if necessary, PTCA can significantly reduce myocardial damage in the majority of patients, a practical approach to the treatment of patients with acute myocardial infarction. Then tissue plasminogen activator will be administered intravenously immediately after the diagnosis of acute myocardial infarction, and this administration can be carried out both in the intensive observation unit and in an ambulance, clinic, and even at the patient’s place of residence or work. After this, the patient will be admitted to the clinic, where within 2 days he will undergo coronary angiography and, if necessary, PTCA. This approach requires less highly qualified personnel, as well as less complex equipment.

It has been reported that urgent primary PTCA for acute myocardial infarction, i.e. PTCA performed without prior thrombolysis, may also be effective in restoring adequate reperfusion, but this procedure is very expensive because it requires constant availability of qualified personnel and complex equipment. .

The area of ​​the myocardium undergoing necrosis secondary to vascular occlusion is determined not so much by the localization of this occlusion as by the state of collateral blood flow in the ischemic tissues. The myocardium, well supplied with blood by collaterals, during ischemia is able to remain viable for several hours longer than the myocardium with a poorly defined collateral network. It is now known that the size of myocardial infarction can change over time under the influence of prescribed drugs. The balance between myocardial oxygen supply and the oxygen demand of ischemic areas ultimately determines the fate of these areas during acute myocardial infarction. Although there is currently no generally accepted therapeutic approach to reduce the size of myocardial infarction in all patients, the recognition of the fact that its size can increase under the influence of a number of drugs that adversely affect the relationship between myocardial oxygen demand and its delivery has led to a re-evaluation of a number of therapeutic options. approaches to the treatment of patients with acute myocardial infarction.

Treatment of a patient with uncomplicated infarction

Analgesia. Since acute myocardial infarction is most often accompanied by severe pain, pain relief is one of the the most important techniques therapy. The traditionally used morphine is extremely effective for this purpose. However, it may lower blood pressure by reducing arteriolar and venous constriction mediated through the sympathetic nervous system. The resulting deposition of blood in the veins leads to a decrease cardiac output. This should be kept in mind, but does not necessarily indicate a contraindication to morphine. .Hypotension resulting from the deposition of blood in the veins, as a rule, is quickly eliminated when raised lower limbs, although some patients may require saline administration. The patient may also experience sweating and nausea, but these phenomena usually resolve spontaneously. In addition, the beneficial effect of pain relief, as a rule, prevails over these unpleasant sensations. It is important to distinguish these side effects of morphine from similar manifestations of shock so as not to prescribe vasoconstrictor therapy unnecessarily. Morphine has a vagotonic effect and can cause bradycardia or high-grade heart block, especially in patients with inferoposterior myocardial infarction. These side effects of morphine can be eliminated by intravenous atropine at a dose of 0.4 mg. It is preferable to administer morphine in small (2 - 4 mg) divided doses every 5 minutes intravenously, rather than in large quantities subcutaneously, since in the latter case its absorption can lead to unpredictable consequences. Instead of morphine, meperedine hydrochloride or hydromorphone hydrochloride can be used successfully.

Most patients with acute myocardial infarction can be given sublingual nitroglycerin before initiating morphine therapy. Typically, 3 tablets of 0.3 mg, prescribed at 5-minute intervals, are enough to cause hypotension in the patient. Such nitroglycerin therapy, previously considered contraindicated in acute myocardial infarction, can help both reduce myocardial oxygen demand (by reducing preload) and increase oxygen delivery to the myocardium (by dilating the coronary vessels or collateral vessels in the area of ​​infarction). However, nitrates should not be prescribed to patients with low systolic blood pressure (less than 100 mmHg). We must remember about the possible idiosyncrasy of nitrates, consisting of a sudden decrease in blood pressure and bradycardia. This side effect of nitrates, which occurs most often in patients with lower myocardial infarction, can be eliminated by intravenous atropine.

To eliminate pain during acute myocardial infarction, adrenergic blockers can also be administered intravenously. These drugs reliably relieve pain in some patients, mainly as a result of a decrease in ischemia due to a decrease in myocardial oxygen demand. It has been proven that intravenous administration of adrenergic blockers reduces in-hospital mortality, especially among high-risk patients. β-blockers are prescribed in the same doses as in a hyperdynamic state (see above).

Oxygen. The routine use of oxygen in acute myocardial infarction is justified by the fact that the arteriolar horn is reduced in many patients, and oxygen inhalation, according to experimental data, reduces the size of ischemic damage. Oxygen inhalation increases the arteriolar horn and thereby increases the concentration gradient necessary for the diffusion of oxygen into the area of ​​ischemic myocardium from adjacent, better perfused zones. Although oxygen therapy may theoretically cause undesirable effects, such as increased peripheral vascular resistance and a slight decrease in cardiac output, practical observations justify its use. Oxygen is given through a loose mask or nasal tip during the first one to two days of acute myocardial infarction.

Physical activity. Factors that increase the work of the heart may contribute to an increase in the size of myocardial infarction. Circumstances that contribute to an increase in heart size, cardiac output, and myocardial contractility should be avoided. It has been shown that complete healing, i.e., replacement of the area of ​​myocardial infarction with scar tissue, requires 6 - 8 weeks. The most favorable conditions for such healing are provided by a decrease in physical activity.

Most patients with acute myocardial infarction should be placed in intensive care units and monitored. Observation of patients and constant ECG monitoring should continue for 2 to 4 days. A catheter is inserted into a peripheral vein and firmly secured so as to avoid its displacement. An isotonic glucose solution should be continuously injected slowly through the catheter or flushed with heparin. Such a catheter makes it possible, if necessary, to administer antiarrhythmic or other drugs. In the absence of heart failure and other complications, during the first 2-3 days the patient should remain in bed most of the day and sit down on a bedside chair for 15-30 minutes 1-2 times. A vessel is used for defecation. The patient should be washed. He can eat food on his own. The use of a bedside toilet seat is allowed in all hemodynamically stable patients with a stable rhythm, starting from the 1st day. The bed should be equipped with a footrest, and the patient should push firmly with both legs on this footrest 10 times per hour during the day to prevent venous stasis and thromboembolism, as well as to maintain muscle tone in the legs.

By the 3-4th day, patients with uncomplicated myocardial infarction should sit on a chair for 30-60 minutes 2 times a day. At this time, their blood pressure is measured to detect possible postural hypotension, which can become a problem once the patient begins to walk. In case of uncomplicated myocardial infarction, the patient is allowed to get up and gradually begin to walk between the 3rd and 5th day. First, they are allowed to go to the bathroom if it is in the patient’s room or nearby. The walking time is gradually increased and eventually walking along the corridor is allowed. Many clinics have special cardiovascular rehabilitation programs with a gradual increase in load, starting in the hospital and continuing after the patient is discharged. The duration of hospitalization for uncomplicated myocardial infarction is 7-12 days, but some doctors still consider it necessary to hospitalize patients with Q-myocardial infarction for 3 weeks. Patients with clinical class II or greater may require hospitalization for 3 weeks or more. The length of hospital treatment depends on how quickly the heart failure disappears and what home conditions await the patient after discharge. Many doctors consider it necessary to perform an exercise test (limited to reaching a certain heart rate) in some patients before discharge from the hospital. With the help of such a test, it is possible to identify patients from a high-risk group, i.e. those who have an attack of angina during exercise or immediately after it, changes in the ST segment, hypotension or ventricular extrasystole of high grades. These patients require special attention. They need to be prescribed antiarrhythmic drugs to combat rhythm disturbances and adrenergic blockers, long-acting nitrates or calcium antagonists to prevent myocardial ischemia. If patients experience ischemia at rest or with very little exercise, or if there is hypotension, coronary angiography (CAG) should be performed. If it is discovered that a large area of ​​viable myocardium is supplied by a critically narrowed artery, then revascularization with coronary artery bypass grafting (CABG) or coronary angioplasty may be required. An exercise test can also help develop an individualized exercise program, which should be more intense in patients who have better exercise tolerance and do not have the adverse symptoms noted above. Conducting an exercise test before discharge from the hospital helps the patient to see for himself his physical capabilities. Moreover, in cases where no arrhythmias or signs of myocardial ischemia occur during an exercise test, it is easier for the doctor to convince the patient that there are no objective signs of immediate danger to life or health.

The final phase of rehabilitation of a patient after an acute myocardial infarction is carried out at home. From the 3rd to the 8th week, the patient should increase the amount of physical activity by walking around the house and going outside in good weather. The patient should still sleep at least 8 to 10 hours at night. In addition, some patients benefit from additional periods of sleep in the morning and afternoon.

From the 8th week, the doctor should regulate the patient’s physical activity based on his tolerance to physical activity. It is during this period that an increase in the patient’s physical activity can cause general, severe fatigue. Postural hypotension may still be a problem. Most patients are able to return to work after 12 weeks, and some patients even earlier. Before the patient returns to work (after 6-8 weeks), a maximum exercise test is often performed. Recently, there has been a tendency towards earlier activation of patients, earlier discharge from the hospital and more rapid restoration of full physical activity in patients who have suffered acute myocardial infarction.

Diet. During the first 4-5 days, it is preferable for patients to be prescribed a low-calorie diet, taking food in small fractional doses, since an increase in cardiac output is observed after eating. If you have heart failure, you should limit your sodium intake. Since patients often suffer from constipation, it is quite reasonable to increase the proportion of plant foods containing large amounts of dietary fiber in the diet. In addition, patients receiving diuretics should be advised to eat foods high in potassium. During the 2nd week, the amount of food consumed can be increased. At this time, the patient must be explained the importance of limiting the calorie content of the diet, cholesterol content, and saturated lipids. This is necessary so that the patient consciously follows a rational diet. The desire to eat right and quit smoking is rarely more pronounced than in this early period of rehabilitation after acute myocardial infarction.

An unusual position in bed in the first 3-5 days of illness and the effect of narcotic analgesics used to relieve pain often lead to constipation. Most patients have difficulty using a bedpan, which causes them excessive straining, so it is recommended to use bedside chairs. A diet rich in fiber-rich plant foods and laxatives such as Dioctyl sodium sulfosuccinase 200 mg per day also help prevent constipation. If, despite the measures listed above, constipation persists, laxatives should be recommended. In case of acute myocardial infarction, it is possible to perform gentle digital massage. rectum.

Sedative therapy. Most patients with acute myocardial infarction require an appointment during hospitalization. sedatives to help better cope with the period of forced reduction in activity - diazepam 5 mg or oxazepam 15 - 30 mg 4 times a day. To provide normal sleep sleeping pills are indicated. The most effective is triazolam (from the group of short-acting benzodiazepines) at a dose of 0.25-0.5 mg. If necessary, to ensure a long-term hypnotic effect, you can prescribe Temazepam (15-30 mg) or Flurazepam (Flurazepam) at the same dose. This problem should be given special attention in the first few days of the patient’s stay in the intensive care unit, where a state of 24-hour wakefulness can lead to sleep disturbances in the future. It should be remembered, however, that sedative therapy in no way replaces the need to create a favorable psychological climate around the patient.

Anticoagulants. The most controversial opinions are expressed about the need for routine use of anticoagulants in acute myocardial infarction (AMI). However, the lack of reasoned, statistically based evidence of a reduction in mortality when using anticoagulants in the first few weeks of AMI indicates that the benefit of these drugs is small, and perhaps non-existent. Anticoagulant therapy to slow down the process of coronary occlusion in the initial phase of the disease currently has no clear justification, but it is currently attracting renewed interest, i.e., it is recognized that thrombosis plays an important role in the pathogenesis of AMI. It is recognized, however, that anticoagulant therapy certainly reduces the incidence of thromboembolism in both arteries and veins. Since it is known that the frequency of venous thromboembolism increases in patients with heart failure, shock, or a history of venous thromboembolism, routine, prophylactic use of anticoagulants is recommended for such patients while in intensive care units. Routine administration of anticoagulants for the prevention of venous thromboembolism is not recommended for patients in class I. In patients of classes III and IV, the risk of pulmonary embolism is increased, so they are recommended to undergo systemic anticoagulation during the first 10-14 days of hospitalization or until discharge from the hospital. This is best achieved with a continuous intravenous infusion of heparin using a pump. In this case, it is necessary to measure the coagulation time and partial thromboplastin time in order to regulate the rate of drug administration, increasing or decreasing it. After the patient is transferred from the intensive care unit, heparin is replaced with oral anticoagulants. It is acceptable to use small doses of heparin in the form subcutaneous injections(5000 units every 8-12 hours). Controversy exists regarding the treatment of class II patients with anticoagulants. It seems advisable for them to prescribe anticoagulants in cases where congestive heart failure exists for more than 3-4 days or when there is extensive anterior myocardial infarction.

The possibility of arterial embolism by a thrombus located in the ventricle in the area of ​​myocardial infarction, although small, is very definite. Two-dimensional echocardiography (ECHO-CG) allows early detection of blood clots in the left ventricle in approximately 30% of patients with infarction of the anterior wall of the left ventricle, but is rarely informative in patients with inferior or posterior myocardial infarction. The main complication of arterial embolism is hemiparesis when cerebral vessels are involved in the process and arterial hypertension when renal vessels are involved in the process. The low frequency of these complications contrasts with their severity, making it inappropriate to establish strict rules for the use of anticoagulants for the prevention of arterial embolism in acute myocardial infarction. The likelihood of thromboembolism increases with the prevalence of myocardial infarction, the degree of concomitant inflammatory reactions and endocardial stasis due to akinesia. Therefore, as in the case of venous thromboembolism, the indications for the use of anticoagulants for the prevention of arterial embolism expand with increasing size of acute myocardial infarction. In cases where the presence of a thrombus is clearly diagnosed using ECHO-CG or other methods, systemic anticoagulation is indicated (in the absence of contraindications), since the frequency of thromboembolic complications is significantly reduced. The exact duration of anticoagulant therapy is unknown, but it appears to be 3 to 6 months.

Adrenergic blockers. Intravenous administration of adrenergic blockers (BABs) is discussed above. Well-performed placebo-controlled studies have confirmed the need for routine administration of oral beta blockers according to at least within 2 years after acute myocardial infarction. Overall mortality, the frequency of sudden death and, in some cases, repeated myocardial infarction under the influence of beta blockers are reduced. Beta blockers are usually started 5 to 28 days after the onset of acute myocardial infarction. Typically, propranolol (anaprilin) ​​is prescribed at a dose of 60 - 80 mg 3 times a day or other slower-acting beta blockers in equivalent doses. Contraindications to the use of beta blockers are congestive heart failure, bradycardia, heart block, hypotension, asthma and labile insulin-dependent diabetes mellitus.

Arrhythmias (see also chapters 183 and 184). Advances in the correction of arrhythmias represent the most significant achievement in the treatment of patients with myocardial infarction.

Premature ventricular contractions (ventricular extrasystoles). Rare sporadic ventricular extrasystoles occur in most patients with acute myocardial infarction and do not require special treatment. It is generally believed that antiarrhythmic therapy for ventricular extrasystoles should be prescribed in the following cases: 1) the presence of more than 5 single ventricular extrasystoles per minute; 2) the occurrence of group or polytopic ventricular extrasystoles; 3) the occurrence of ventricular extrasystoles in the early diastole phase, i.e., superimposed on the T wave of the previous complex (i.e., the R on T phenomenon).

Intravenous administration of lidocaine has become the treatment of choice for ventricular extrasystole and ventricular arrhythmias, since the drug begins to act quickly and side effects disappear just as quickly (within 15-20 minutes after cessation of administration). To quickly achieve therapeutic concentrations in the blood, lidocaine is prescribed as a bolus of 1 mg/kg intravenously. This initial dose can eliminate ectopic activity, and then a continuous infusion at a rate of 2 - 4 mg/min is carried out to maintain the effect. If the arrhythmia persists, 10 minutes after the administration of the first bolus, a second one is administered at a dose of 0.5 mg/kg. In patients with congestive heart failure, liver disease, and shock, the dose of lidocaine is halved. As a rule, ventricular extrasystole disappears spontaneously after 72-96 hours. If significant ventricular arrhythmia persists even after this, long-term antiarrhythmic therapy is prescribed.

For the treatment of patients with persistent ventricular arrhythmias, procainamide, tocainide, and quinidine are usually used. BAB and disopyramide also eliminate ventricular arrhythmias in patients with acute myocardial infarction. In patients with left ventricular failure, disopyramide is prescribed with great caution, as it has a significant negative inotropic effect. If these drugs (Chapter 184), used as monotherapy or in combinations, are ineffective at usual doses, their blood concentrations should be determined. When prescribing large doses of these drugs, regular clinical and ECG monitoring is necessary to detect possible signs intoxication.

Ventricular tachycardia and ventricular fibrillation. During the first 24 hours of AMI, ventricular tachycardia (VT) and ventricular fibrillation (VF) often occur without preceding threatening arrhythmias. The risk of developing such primary arrhythmias can be significantly reduced by prophylactic intravenous lidocaine. Prophylactic administration of antiarrhythmic drugs is especially indicated for patients who cannot be placed in a clinic, or are in a clinic where the constant presence of a doctor is not provided in the hospital. For prolonged ventricular tachycardia, lidocaine is first prescribed. If, after one or two injections of the drug at a dose of 50-100 mg, the arrhythmia persists, electrical pulse therapy (electrocardioversion) is performed (Chapter 184). Electrical defibrillation is performed immediately in case of ventricular fibrillation, as well as in cases where ventricular tachycardia causes hemodynamic disturbances. If ventricular fibrillation continues for several seconds or more, the first shock of the defibrillator may be unsuccessful, in these cases it is advisable to perform indirect massage hearts, artificial ventilation lungs “mouth to mouth”, and also administer sodium bicarbonate intravenously (40-90 mEq). Improving tissue oxygenation and perfusion and correcting acidosis increases the likelihood of successful defibrillation (see also Chapter 30). For therapy-refractory ventricular fibrillation or ventricular tachycardia, administration of bretylium (ornid) may be effective. For ventricular fibrillation, bretylium is administered as a bolus of 5 mg/kg, then defibrillation is repeated. If the latter fails, another bolus of bretylium (10 mg/kg) is administered to facilitate defibrillation. Ventricular tachycardia can be eliminated by slow administration of bretylium at a dose of 10 mg/kg over 10 minutes. If arrhythmias recur after the first dose of bretylium, a continuous infusion of 2 mg/min can be performed. Severe orthostatic hypotension may occur following intravenous administration of bretylium. Therefore, during and after administration of the drug, patients should be in a supine position, in addition, they should be prepared to administer intravenous fluids.

With primary ventricular fibrillation, the long-term prognosis is favorable. This means that primary ventricular fibrillation is a consequence of acute ischemia and is not associated with the presence of predisposing factors such as congestive heart failure, bundle branch block, or left ventricular aneurysm. According to one study, 87% of patients with primary ventricular fibrillation remained alive and were discharged from the clinic. The prognosis for patients with secondary ventricular fibrillation, which developed as a result of insufficient pumping function of the heart, is much less favorable. Only 29% of them survive.

In the group of patients in whom ventricular tachycardia develops late in hospitalization, mortality within a year reaches 85%. Such patients require an electrophysiological study (Chapter 184).

Accelerated idioventricular rhythm. Accelerated idioventricular rhythm (“slow ventricular tachycardia”) is a ventricular rhythm with a frequency of 60 to 100 per minute. It occurs in 25% of patients with myocardial infarction. Most often it is recorded in patients with infero-posterior myocardial infarction and, as a rule, in combination with sinus bradycardia. The heart rate during accelerated idioventricular rhythm is similar to that during sinus rhythm preceding or following it. Accelerated idioventricular rhythm is difficult to diagnose clinically and is detected only with the help of ECG monitoring. This is due to the fact that the frequency of ventricular contractions differs little from that in sinus rhythm, and hemodynamic disturbances are minimal. Accelerated idioventricular rhythm arises and disappears spontaneously as sinus rhythm oscillations cause the atrial rate to decelerate below the accelerated escape level. In general, accelerated idioventricular rhythm is a benign rhythm disorder and does not mark the onset of classic ventricular tachycardia. However, a number of cases have been reported in which accelerated idioventricular rhythm was combined with more dangerous forms of ventricular arrhythmias or transformed into life-threatening ventricular arrhythmias. Most patients with accelerated idioventricular rhythm do not require treatment. Careful ECG monitoring is sufficient, since accelerated idioventricular rhythm rarely develops into more serious rhythm disturbances. If the latter does occur, accelerated idioventricular rhythm can be easily corrected with drugs that reduce the rate of ventricular escape rate, such as tocainide, and/or drugs that increase sinus rate (atropine).

Supraventricular arrhythmia. In this group of patients, supraventricular arrhythmias most often occur, such as junctional rhythm and junctional tachycardia, atrial tachycardia, atrial flutter and atrial fibrillation. These rhythm disturbances are most often secondary to left ventricular failure. Digoxin is usually used to treat patients. If the pathological rhythm persists for more than two hours and the ventricular rate exceeds 120 per minute or if the tachycardia is accompanied by the appearance of heart failure, shock or ischemia (as evidenced by repeated pain or changes in the ECG), then electrical pulse therapy is indicated.

Junctional rhythm disturbances have different etiologies; they do not indicate the presence of any specific pathology, therefore the doctor’s attitude towards such patients should be individualized. It is necessary to exclude an overdose of digitalis as a cause of nodal arrhythmias. In some patients with significantly impaired left ventricular function, loss of normal duration of atrial systole leads to a significant drop in cardiac output. In such cases, atrial stimulation or stimulation of the coronary sinus is indicated. The hemodynamic effect of these two types of stimulation is identical, but the advantage of stimulation of the coronary (coronary) sinus is that it achieves a more stable position of the catheter.

Sinus bradycardia. Opinions about the significance of bradycardia as a factor predisposing to the development of ventricular fibrillation are contradictory. On the one hand, it is known that the frequency of ventricular tachycardia in patients with prolonged sinus bradycardia is 2 times higher than in patients with normal frequency heartbeats. On the other hand, sinus bradycardia in hospitalized patients is considered an indicator of a favorable prognosis. Experience with mobile intensive care units suggests that sinus bradycardia occurring in the early hours of acute myocardial infarction is more clearly associated with subsequent ectopic ventricular rhythms than sinus bradycardia occurring later in acute myocardial infarction. Treatment for sinus bradycardia should be carried out in cases where (against its background) there is pronounced ectopic ventricular activity or when it causes hemodynamic disturbances. Sinus bradycardia can be eliminated by slightly elevating the patient's legs or the foot end of the bed. To accelerate sinus rhythm, it is best to use atropine, administering it intravenously at a dose of 0.4 - 0.6 mg. If after this the pulse remains less than 60 beats per minute, additional fractional administration of atropine of 0.2 mg is possible until the total dose of the drug is 2 mg. Persistent bradycardia (less than 40 per minute), which persists despite the administration of atropine, can be eliminated with electrical stimulation. Administration of isoproterenol should be avoided.

Conduction disorders. Conduction disturbances can occur in three various levels conduction system of the heart: in the area of ​​the atrioventricular node, atrioventricular bundle (His) or in more distal parts of the conduction system (Chapter 183). When a blockade appears in the area of ​​the atrioventricular node, as a rule, an escape rhythm of the atrioventricular junction occurs, with QRS complexes of normal duration. If the blockade occurs distal to the atrioventricular node, a replacement rhythm occurs in the ventricles, and the QRS complexes change their configuration and their duration increases. Conduction disturbances can occur in all three peripheral bundles of the conduction system, and recognition of such disturbances is important for identifying patients at risk of developing complete transverse block. In cases where there is a blockade of any two of the three bundles, they speak of the presence of a two-fascicle blockade. Such patients often develop complete atrioventricular block (complete transverse block). Thus, patients with a combination of blockade right leg His bundle and left anterior or left posterior hemiblock, or patients with new-onset left bundle branch block are at particularly high risk of developing a complete (transverse) block.

The mortality rate of patients with complete atrioventricular block accompanying anterior myocardial infarction is 80-90% and is almost 3 times higher than the mortality rate of patients with complete atrioventricular block accompanying inferior myocardial infarction (30%). The risk of subsequent death among patients who survived the acute stage of myocardial infarction is also significantly higher in the former. The difference in mortality is explained by the fact that heart block in inferior myocardial infarction is usually caused by ischemia of the atrioventricular node. The atrioventricular node is a small discrete structure and even mild ischemia or necrosis can cause its dysfunction. In myocardial infarction of the anterior wall, the appearance of heart block is associated with dysfunction of all three bundles of the conduction system and, therefore, is only a consequence of extensive myocardial necrosis.

Electrical stimulation is an effective means of increasing heart rate in patients with bradycardia that developed as a result of atrioventricular block, however, there is no certainty that such an increase in heart rate is always beneficial. For example, in patients with anterior wall myocardial infarction and complete transverse block, the prognosis is determined mainly by the size of the infarction and correction of the conduction defect does not necessarily have a beneficial effect on the outcome of the disease. Electrical stimulation, however, may be useful in patients with inferoposterior myocardial infarction, in whom complete transverse block is associated with the development of heart failure, hypotension, severe bradycardia or significant ectopic ventricular activity. Such patients with right ventricular myocardial infarction often respond poorly to ventricular pacing due to loss of atrial “beat” and may require biventricular sequential atrioventricular pacing.

Some cardiologists consider it necessary to place a prophylactic catheter for pacing in patients with conduction abnormalities, known as precursors to complete (transverse) block. There is no consensus on this matter. Continuous stimulation is recommended for patients who have permanent bifascicular blockade and temporary blockade III degree during the acute phase of myocardial infarction. Retrospective studies in small groups of such patients show that the likelihood of sudden death is reduced in cases where permanent pacing is performed.

Heart failure. Transient dysfunction of the left ventricle of varying degrees occurs in approximately 50% of patients with myocardial infarction. The most common clinical signs of heart failure are crackles in the lungs and S3 to S4 gallop rhythm. X-rays often show signs of pulmonary congestion. The appearance of radiological signs of pulmonary congestion, however, does not coincide in time with the appearance of such clinical signs as wheezing in the lungs and shortness of breath. Characteristic hemodynamic signs of heart failure are increased left ventricular filling pressure and pressure in the pulmonary trunk. It should be remembered that these signs may result from worsening left ventricular diastolic function (diastolic failure) and/or decreased stroke volume with secondary cardiac dilatation (systolic failure) (Chapter 181). With few exceptions, therapy for heart failure accompanying acute myocardial infarction is no different from that for other heart diseases (Chapter 182). The main difference lies in the use of cardiac glycosides. The beneficial effect of the latter in acute myocardial infarction is unconvincing. This is not surprising, since the function of non-infarcted myocardium may be normal, but it is difficult to expect that digitalis can improve the systolic and diastolic function of infarcted or ischemic myocardium. On the other hand, diuretics have a very good effect in the treatment of patients with heart failure due to myocardial infarction, since they reduce pulmonary congestion in the presence of systolic and/or diastolic heart failure. Intravenous administration of furosemide helps reduce left ventricular filling pressure and reduce orthopnea and dyspnea. Furosemide, however, should be administered with caution as it can cause massive diuresis and reduce plasma volume, cardiac output, systemic blood pressure and consequently reduce coronary perfusion. To reduce preload and symptoms of stagnation, various dosage forms of nitrates are successfully used. Oral isosorbide dinitrate or conventional nitroglycerin ointment are advantageous over diuretics because they reduce preload by venodilation without causing a decrease in total plasma volume. In addition, nitrates may improve left ventricular function through their effect on myocardial ischemia, as the latter causes an increase in left ventricular filling pressure. Treatment of patients with pulmonary edema is described in Chap. 182. Studies of vasodilators that reduce cardiac afterload have shown that its reduction leads to a decrease in cardiac work and, as a result, can significantly improve left ventricular function, reduce left ventricular filling pressure, reduce the severity of pulmonary congestion and, as a result, cause an increase in cardiac output.

Hemodynamic monitoring. Impaired left ventricular function becomes hemodynamically significant when contractility of 20–25% of the left ventricular myocardium is impaired. An infarction involving 40% or more of the left ventricular surface usually results in cardiogenic shock syndrome (see below). Pulmonary capillary wedge pressure and pulmonary diastolic pressure correlate well with diastolic pressure in the left ventricle, so they are often used as indicators of left ventricular filling pressure. Placement of a balloon floating catheter in the pulmonary trunk allows the physician to continuously monitor left ventricular filling pressure. This technique is advisable to use in patients who exhibit clinical signs of hemodynamic disturbances or instability. A catheter installed in the pulmonary trunk also makes it possible to determine the amount of cardiac output. If, in addition, intra-arterial pressure is monitored, it becomes possible to calculate peripheral vascular resistance, which helps control the administration of vasoconstrictor and vasodilator drugs. Some patients with acute myocardial infarction exhibit a significant increase in left ventricular filling pressure (> 22 mm Hg) and normal cardiac output (within 2.6-3.6 l/min per 1 m2), while in others have relatively low left ventricular filling pressure (
Cardiogenic shock is energy deficiency. With the introduction of effective methods for correcting arrhythmias in patients with acute myocardial infarction delivered to the clinic, cardiogenic shock has become the most common complication leading to death. It occurs in approximately 10% of such patients and causes death in approximately 60% of patients with acute myocardial infarction. We regret to note that improving the quality of treatment had no effect on the mortality of patients with acute myocardial infarction complicated by cardiogenic shock (Killip class IV); it continues to remain at the level of 85-95%.

It is advisable to consider cardiogenic shock as a form of severe left ventricular failure. This syndrome is characterized by severe hypotension with a decrease in systolic blood pressure to less than 80 mmHg. Art. and a significant decrease in cardiac index (
Pathophysiology of pump failure. The main cause of cardiogenic shock in acute myocardial infarction is a significant decrease in the mass of the contracting myocardium. All organs and systems are ultimately involved in the pathogenesis of cardiogenic shock. The function of the heart is impaired even with primary damage, this causes a decrease in blood pressure and, consequently, coronary blood flow due to the dependence of the latter on the perfusion pressure in the aorta (Fig. 190-2). A decrease in coronary perfusion pressure and myocardial blood flow leads to further impairment of myocardial function and may contribute to an increase in the size of myocardial infarction. Arrhythmias and acidosis, resulting from inadequate perfusion, also contribute to this process, perpetuating the existing pathological condition. It is this positive feedback that is responsible for the high mortality rate that accompanies cardiogenic shock.

Arterial blood pressure is a function of two factors - cardiac output and total peripheral resistance. A decrease in any of them without a compensatory increase in the other leads to a drop in blood pressure. In patients with myocardial infarction and shock, cardiac output is reduced. However, in many patients with myocardial infarction without cardiogenic shock, cardiac output is reduced to the same extent as in patients with cardiogenic shock. This indicates that the characterization of patients cannot be based only on a decrease in cardiac output. Peripheral vascular resistance, another important factor determining blood pressure levels, may be either normal or elevated in patients with myocardial infarction. Normally, a decrease in cardiac output is accompanied by a compensatory increase in peripheral vascular resistance. However, in patients with shock caused by acute myocardial infarction, there may not be an adequate increase in peripheral vascular resistance. It is necessary, however, to return to consideration of the heart itself as the organ that undergoes the greatest physiological damage during cardiogenic shock.

Rice. 190-2. Diagram of the sequence of events of the vicious circle when coronary artery obstruction leads to cardiogenic shock and progressive circulatory impairment.

A simple schematic diagram showing the relationship between left ventricular performance and filling pressure is shown in Fig. 190-3. The upper curve represents the well-known Frank-Starling relation in healthy heart; the lower curve shows the relationship that can be expected in a patient with shock secondary to myocardial infarction. It is obvious that in patients with acute myocardial infarction, at all values ​​of end-diastolic pressure, the functioning of the left ventricle is significantly impaired. At point B, the end-diastolic pressure is elevated, but at point B it may be normal, despite the fact that myocardial work is significantly reduced compared to the level that would be expected at a given value of diastolic pressure, as seen at point A.

Treatment for pump failure. A patient with pump failure requires, if possible, continuous monitoring of blood pressure and left ventricular filling pressure (as assessed by pulmonary capillary wedge pressure recorded using a balloon catheter installed in the pulmonary trunk), as well as regular determination of cardiac output. All patients with cardiogenic shock should be given 100% oxygen to correct hypoxia. In pulmonary edema, oxygenation is achieved through endotracheal intubation. It is very important to relieve pain, since in some cases reflex vasodepressor activity can be a consequence of severe pain. Drugs, however, are prescribed with great caution due to their ability to lower blood pressure.

Rice. 190-3. Schematic representation of the Frank-Starling relationship observed in patients with shock syndrome during myocardial infarction.

Treatment for cardiogenic shock is aimed at interrupting the vicious connection (see Fig. 190-2), as a result of which impaired myocardial function leads to a decrease in blood pressure, a decrease in coronary blood flow and a further deterioration in left ventricular function. This goal of maintaining coronary perfusion is achieved by increasing blood pressure with vasopressors (see below), using intra-arterial balloon counterpulsation, and adjusting blood volume to maintain an optimal level of left ventricular filling pressure (approximately 20 mmHg).

This can be achieved either by crystalloid infusion or by increasing urine output. In patients with a myocardial infarction duration of no more than 4 hours, reperfusion achieved with thrombolytic therapy and/or percutaneous transluminal coronary angioplasty can significantly improve left ventricular function.

Hypovolemia. This easily correctable condition contributes to the development of hypotension and vascular collapse in some patients with myocardial infarction. Fluid loss may be a consequence of previous treatment with diuretics, restriction of fluid intake for early stages illness and/or vomiting associated with pain or the use of diuretics. In addition, a state of relative hypovolemia may be observed, consisting of an acute decrease in contractility of the left ventricle and disruption of its function due to myocardial infarction; in these cases, vascular volume must be increased to maintain cardiac output. Due to the rapidity of this process, there is usually not enough time for compensatory fluid restoration, which leads to the development of relative hypovolemia in patients with normal fluid volume. In patients with acute myocardial infarction and hypotension, it is very important to recognize hypovolemia in a timely manner and correct it without resorting to more potent drugs, usually used to treat hypotension. If left ventricular filling pressure remains within normal limits, fluid should be administered until cardiac output is maximally increased. The latter is usually achieved at left ventricular filling pressures of approximately 20 mmHg. Art.

The optimal level of filling pressure of the left ventricle is the wedging pressure of the pulmonary trunk, but can vary significantly in different patients. The ideal blood pressure level for each patient is achieved by very careful fluid administration under close monitoring of oxygenation and cardiac output. Once a plateau of cardiac output is reached (see Fig. 190-3, B), a further increase in left ventricular filling pressure will only increase signs of congestion and reduce total oxygenation. Central venous pressure reflects the filling pressure of the right ventricle rather than the left ventricle. There is no need to record it in this situation, since left ventricular function in acute myocardial infarction is almost always impaired to a greater extent than right ventricular function.

Vasopressor drugs. There are many intravenous drugs that can be used to increase blood pressure and cardiac output in patients with cardiogenic shock. Unfortunately, many problems arise when using them; None of these drugs is able to affect the outcome of the disease in persons with established cardiogenic shock. Isoproterenol, a synthetic sympathomimetic amine, is now rarely used to treat patients with shock due to myocardial infarction. Although this drug increases myocardial contractility, it simultaneously causes peripheral vasodilation and an increase in heart rate. As a result of its action, the myocardial oxygen demand increases and coronary perfusion decreases, which can lead to an expansion of the area of ​​ischemic damage. Norepinephrine is a potential β-adrenergic drug with a powerful vasoconstrictor effect. It also has adrenergic activity and can therefore increase contractility. Norepinephrine effectively increases blood pressure. However, it causes an increase in afterload, in addition, the increase in contractility observed with its use contributes to a significant increase in myocardial oxygen demand. This drug is advisable to use in critical (hopeless) situations. It can also be used in patients with cardiogenic shock and decreased peripheral vascular resistance. Norepinephrine should be prescribed in the lowest possible doses (start infusion at a rate of 2-4 mcg/min) necessary to maintain blood pressure at 90 mmHg. Art. If blood pressure cannot be maintained at a given level when norepinephrine is administered. at a dose of 15 mcg/min, the likelihood that large doses of the drug will have an effect is very small.

Dopamine (dopamine) (Chapter 66) is very effective in many patients with insufficient contractile function of the heart. In small doses (2-10 mcg/kg per 1 min), the drug has a positive chronotropic and inotropic effect, which is a consequence of stimulation of receptors. In large doses, the vasoconstrictor effect of the drug is manifested, which is the result of stimulation of β-receptors. In very low doses (
Amrinone is a drug with a positive inotropic effect that is different in structure and action from catecholamines. In terms of pharmacological activity, it resembles dobutamine, although its vasodilating effect is more pronounced than that of the latter. First, a loading dose of 0.75 mg/kg is administered. If after this the desired effect is achieved, then the drug is infused at a rate of 10 mcg/kg per minute; if necessary, an additional bolus of 0.75 mg/kg is administered after 30 minutes.

If the cause of left ventricular failure and severe hypotension is global ischemia, as is the case, for example, in patients with critical stenosis of the main trunk of the left coronary artery, then a beneficial effect can be achieved using short-term administration of pure vasoconstrictors, rather than drugs with a positive inotropic effect . In such cases, improvement of coronary perfusion can be achieved by increasing blood pressure using vasoconstrictors. At the same time, drugs that have a positive inotropic effect can only increase the degree of ischemic damage to the myocardium, which is no longer capable of further increasing the work performed. In such cases, when Neosynephrine is prescribed as a vasoconstrictor at a dose of 10-100 mcg/min, treatment should be as short as possible and should be considered as preliminary therapy, during which preparation for intra-aortic balloon counterpulsation and/or to emergency surgical intervention on the coronary arteries.

Cardiac glycosides (ch. 182). Confirmation of the dominant role of myocardial dysfunction in the pathogenesis of cardiogenic shock suggests that the use of cardiac glycosides will be a fairly effective treatment method for this condition. Controlled studies, however, have failed to demonstrate a beneficial effect of cardiac glycosides in the early stages (0 - 48 hours) of acute myocardial infarction. Improvement in hemodynamics could only be observed in more late stages, however, even then this effect was insignificant. Since cardiac glycosides are not able to improve the function of necrotic myocardium, and the degree of pump failure is likely directly related to the total mass of myocardium undergoing infarction, the use of digitalis does not lead to a significant improvement in the condition of patients with acute myocardial infarction. However, the prescription of digitalis may be justified in patients with signs of left ventricular failure. It has been demonstrated that with sufficiently careful selection of the dose of cardiac glycosides, the risk of arrhythmias and myocardial rupture in patients with acute myocardial infarction receiving cardiac glycosides is no higher than in the control group. Therefore, the use of digitalis is relatively safe.

Aortic counterpulsation. The main manifestation of shock in acute myocardial infarction is myocardial dysfunction. Therefore, appropriate devices have been developed to maintain the pumping function of the heart during cardiogenic shock. The greatest clinical experience has been accumulated with the use of the intra-aortic balloon system to increase diastolic blood pressure. A sausage-shaped balloon with a catheter at the end is passed into the aorta through the femoral artery. The balloon is inflated in early diastole, thereby increasing coronary blood flow and peripheral perfusion. The balloon collapses during early systole, thereby reducing the afterload against which the left ventricle works. A significant proportion of patients experience hemodynamic improvement with this procedure, but the long-term prognosis still remains unfavorable. The balloon counterpulsation system is best reserved for those patients whose condition requires surgical intervention (with persistent ischemia, rupture of the interventricular septum, mitral regurgitation), as well as for patients in whom successful surgical treatment is more likely to resolve cardiogenic shock.

Unfortunately, there is reason to believe that the results of treatment for shock secondary to myocardial infarction, despite their gradual improvement due to special attention to the details of therapy described above, will still generally remain quite unfavorable because most patients with this syndrome resulting from diffuse coronary atherosclerosis is damage to a significant part of the myocardium. Despite individual cases of significant improvement in patients' condition achieved as a result of emergency surgical revascularization alone or emergency revascularization in combination with infarction, the results of this approach have been generally disappointing. It can be hoped that promptly initiated thrombolytic therapy will be able to reduce the volume of myocardium undergoing necrosis and thereby reduce the likelihood of developing cardiogenic shock.

Other complications. Mitral regurgitation. The systolic murmur of mitral regurgitation at the apex in the first five days after the onset of acute myocardial infarction is heard in more than 25% of patients, but hemodynamically significant mitral regurgitation is present only in a small proportion. In most patients, systolic murmur is recorded only in the acute stage of myocardial infarction and disappears subsequently. Most often, mitral regurgitation after myocardial infarction is caused by dysfunction of the papillary muscles of the left ventricle due to their infarction or ischemia.

Mitral regurgitation may also result from changes in the size or shape of the left ventricle due to impaired contractility or the formation of an aneurysm. Rupture of the papillary muscles may also occur, with the posterior papillary muscle being torn twice as often as the anterior one. When mitral regurgitation occurs against the background of acute myocardial infarction, left ventricular function can deteriorate very significantly. Mitral regurgitation should be differentiated from perforation of the interventricular septum (see below), and this is most conveniently done directly at the patient's bedside using a floating balloon catheter. In patients with hemodynamically significant mitral regurgitation, pulmonary capillary wedge may be detected when recording pressure. large V waves, and there is no so-called oxygen increase when the catheter moves from the right atrium to the right ventricle. Surgical replacement mitral valve can lead to a significant improvement in the condition of patients in whom acute heart failure is primarily a consequence of severe mitral regurgitation as a result of rupture of the papillary muscles or their dysfunction, and myocardial function is relatively preserved.

With a decrease in systolic pressure in the aorta in a patient with mitral regurgitation, a significant part of the stroke volume of the left ventricle is ejected antegrade, which leads to a decrease in the regurgitation fraction. Therefore, both intra-aortic balloon counterpulsation, which mechanically reduces systolic pressure in the aorta, and infusion of sodium nitroprusside at a dose of 0.5 - 8.0 mcg/kg per 1 min, which reduces peripheral vascular resistance, can be used as initial therapy for patients with severe mitral regurgitation accompanying acute myocardial infarction. Ideally, radical surgery should be delayed for 4 to 6 weeks after myocardial infarction. However, if the hemodynamic state and/or clinical condition the patient does not improve or stabilize, surgical intervention cannot be postponed even in the acute stage of myocardial infarction.

Heartbreak. Heart rupture is a serious complication of myocardial infarction, occurring, as a rule, during the 1st week from the onset of the disease. The incidence of this complication increases with the age of patients. Myocardial rupture often occurs during the first myocardial infarction in women, as well as in patients with concomitant arterial hypertension. Clinical manifestations of cardiac rupture include sudden disappearance of pulse and blood pressure, loss of consciousness, while sinus rhythm continues to be recorded on the ECG (actual electromechanical dissociation). The myocardium continues to contract, but blood does not expel from the heart due to the fact that the blood enters the pericardium. Cardiac tamponade develops (Chapter 194), while direct cardiac massage is ineffective. Heart rupture almost always ends in the death of the patient. There are only a few known cases in which this condition was promptly diagnosed and the patients were successfully treated with pericardiocentesis and emergency surgery.

Septal rupture. The pathogenesis of perforation of the interventricular septum is similar to that of myocardial rupture, but the treatment options for this condition are more extensive. Rupture of the interventricular septum usually manifests as severe heart failure, combined with a sudden onset of pansystolic murmur, often accompanied by parasternal flutter. This condition is often indistinguishable from that seen with rupture of the papillary muscles and resulting mitral regurgitation. Availability high wave V when recording pulmonary capillary wedge pressure, observed in both conditions, further complicates the differential diagnosis. The diagnosis of ventricular septal rupture can be made by demonstrating a left-to-right shunt (ie, oxygen elevation at the level of the right ventricle) with limited cardiac catheterization performed at the bedside using a floating balloon catheter. Patients with ventricular septal rupture require urgent surgical treatment. Although the latter carries a high risk of death, it is usually used to treat patients whose condition cannot be quickly stabilized. Prolonged periods of compromised hemodynamics can lead to organ damage and a number of complications that can be avoided with prompt intervention including sodium nitroprusside and intra-aortic balloon pumping. If the patient's condition has stabilized, surgery can be delayed for 4 to 8 weeks to allow scar tissue to form along the edges of the defect, which facilitates surgical correction. However, mortality from ventricular septal perforation is directly related to the total area of ​​myocardial damage and not to the timing of surgical intervention.

The physiological features of acute mitral regurgitation and acute ventricular septal perforation are similar in that the level of systolic pressure in the aorta partly determines the volume of regurgitation. The fundamental difference between these conditions is that the expulsion of the regurgitant blood volume occurs in different chambers. When the interventricular septum is perforated, part of the stroke volume of the left ventricle is thrown into the right ventricle. Therefore, as with mitral regurgitation, reducing the systolic pressure in the aorta using mechanical (intra-aortic balloon counterpulsation) and/or pharmacological (administration of nitroglycerin or sodium nitroprusside) means can reduce the degree of hemodynamic disturbance caused by perforation.

Ventricular aneurysm. The term "ventricular aneurysm" is usually used to refer to dyskinesia or paradoxical movement of a locally dilated myocardial wall. The degree of shortening of normally functioning myocardial fibers during the development of an aneurysm must increase to maintain stroke output and cardiac output. If this doesn't happen, general function the left ventricle is impaired. Aneurysms are made of scar tissue, so their existence does not predispose to heart rupture or indicate an increased risk of heart rupture.

Complications from a left ventricular aneurysm usually do not occur during the first weeks or months after a myocardial infarction. These complications include congestive heart failure, arterial embolism, and ventricular arrhythmias. Aneurysms of the left ventricular apex are the most common and easiest to recognize. The most reliable physical sign of an aneurysm is a double, diffuse or displaced apical impulse. A standard x-ray often shows a prominent curvature of the left border of the heart, but the x-ray may not be affected, especially if there is an aneurysm of the posterior wall of the left ventricle. On a resting ECG, 25% of patients with an aneurysm of the apex or anterior wall show ST segment elevation in the precordial leads. Left ventricular aneurysms are well detected using sectoral echocardiography. The latter also makes it possible to detect a parietal thrombus in the wall of the aneurysm, involving the anterior wall of the left ventricle or its apex. Left ventricular aneurysms can cause prolonged ventricular tachycardia. Such patients require treatment with antiarrhythmic drugs or endocardial resection (Chapter 184).

Right ventricular infarction. Approximately 1/3 of patients with inferoposterior myocardial infarction have right ventricular necrosis (at least minor). Sometimes in patients with inferoposterior left ventricular myocardial infarction, extensive right ventricular myocardial infarction is detected. V such patients usually have signs of severe right ventricular failure (swelling of the jugular veins, hepatomegaly) with or without hypotension. In most patients with right ventricular myocardial infarction, ST segment elevation is observed in the right precordial leads, especially in lead V4R. Radionuclide ventriculography and sectoral echocardiogram with a sufficient degree of sensitivity detect damage to the right ventricle associated with its infarction. Right heart catheterization often reveals hemodynamic signs resembling cardiac tamponade or constrictive pericarditis (Chapter 194). Measures aimed at increasing circulating blood volume are often successful in the treatment of patients with low cardiac output and hypotension associated with large right ventricular myocardial infarction.

Thromboembolism. Clinically significant thromboembolism complicates myocardial infarction in approximately 10% of patients, but embolic lesions are found on necropsy in 45% of patients, indicating that thromboembolism is often asymptomatic. It is believed that thromboembolism makes a significant contribution to the mechanism of death in 25% of patients with myocardial infarction who die during their hospital stay. The source of arterial emboli is usually mural thrombi in the left ventricle; most venous emboli originate from the veins of the lower extremities. Thromboembolism most often occurs in patients with extensive myocardial infarction complicated by heart failure. In patients with echocardiographic signs of thrombosis in the left ventricle, thromboembolism occurs very often; however, in patients without such signs, thromboembolism is a rare complication. The incidence of thromboembolism appears to be reduced by the use of anticoagulants, although this is not supported by well-controlled studies.

Pericarditis (see also Chapter 194). Pericardial friction rub and pericardial pain are common in patients with acute myocardial infarction. With this complication, patients can be treated with aspirin (650 mg 3 times a day). It is important to diagnose that chest pain is associated specifically with pericarditis, since errors in the interpretation of such pain can lead to an incorrect judgment about the presence of repeated myocardial ischemia and/or the spread of myocardial infarction and inadequate prescription of anticoagulants, nitrates, adrenergic blockers, and drugs. A clear connection and relationship between the use of anticoagulants and the development of cardiac tamponade or pericarditis has not been identified. However, the likelihood that the administration of anticoagulants during acute pericarditis can cause cardiac tamponade is quite high. Therefore, anticoagulants are considered contraindicated in patients with pericarditis, manifested by either persistent pain or a pericardial friction rub, unless there is a specific reason for their use.

Post-infarction Dressler syndrome (see also Chapter 194). The development of this syndrome, characterized by fever and pleuropericardial chest pain, is associated with the presence of autoimmune pericarditis, pleurisy and/or pneumonitis. Its signs appear within a few days to 6 weeks after the onset of acute myocardial infarction. The occurrence of Dressler's syndrome may be etiologically related to the early use of anticoagulants. The incidence of its development has decreased significantly in recent decades due to the significantly less frequent prescription of anticoagulants for acute myocardial infarction. Patients respond well to treatment with salicylates. IN in rare cases It may be necessary to prescribe corticosteroids to relieve severe pain that is refractory to treatment. If anticoagulants are prescribed, the effusion that appears in the pericardial cavity with Dressler's syndrome can become hemorrhagic.

Description:

This is one of clinical forms, occurring with the development of an ischemic area of ​​the myocardium, caused by an absolute or relative insufficiency of its blood supply.
Myocardial infarction is one of the most common diseases in Western countries. With acute myocardial infarction, approximately 35% of patients die, and slightly more than half of them die before reaching the hospital. Another 15-20% of patients who have suffered the acute stage of myocardial infarction die within the first year. The risk of increased mortality among people who have had a myocardial infarction, even after 10 years, is 3.5 times higher than in people of the same age, but without a history of myocardial infarction.

Symptoms:

Most often, patients with acute myocardial infarction complain of pain. For some patients, it is so severe that they describe it as the worst pain they have ever experienced. Severe, squeezing, tearing pain usually occurs deep in the chest and is similar in nature to regular attacks, but more intense and prolonged. In typical cases, pain is felt in the central part of the chest and/or in the epigastric region. In approximately 30% of patients, it radiates to the upper extremities, less often to the abdomen, back, involving the lower jaw and neck. The pain can even radiate to the back of the head, but never radiates below the navel. Cases where the pain is localized below the xiphoid process, or when patients themselves deny the connection between the pain and a heart attack, are the reasons for the incorrect diagnosis.
The pain is often accompanied by weakness, sweating, nausea, vomiting, dizziness, and agitation. Unpleasant sensations usually appear at rest, often in the morning. If pain begins during physical activity, then, unlike, it, as a rule, does not disappear after it stops.

However, pain is not always present. In approximately 15-20%, and apparently even in a larger percentage of patients, acute myocardial infarction is painless, and such patients may not seek medical help at all. More often, silent myocardial infarction is recorded in patients with diabetes mellitus, as well as in the elderly. In elderly patients, myocardial infarction is manifested by sudden shortness of breath, which can progress to. In other cases, myocardial infarction, both painful and non-painful, is characterized by a sudden loss of consciousness, a feeling of severe weakness, the occurrence of arrhythmias, or simply an unexplained sharp drop in blood pressure.

In many cases, patients have a dominant reaction to chest pain. They are restless, agitated, trying to relieve pain by moving in bed, writhing and stretching, trying to induce shortness of breath or even vomiting. Patients behave differently during an attack of angina. They tend to take a stationary position for fear of renewed pain. Paleness, sweating and coldness of the extremities are often observed. Chest pain lasting more than 30 minutes and sweating observed during this process indicate a high probability of acute myocardial infarction. Despite the fact that in many patients the pulse and blood pressure remain within normal limits, approximately 25% of patients with anterior myocardial infarction experience manifestations of hyperreactivity of the sympathetic nervous system (tachycardia and/or hypertension), and almost 50% of patients with inferior myocardial infarction experience signs of increased tone of the sympathetic nervous system (bradycardia and/or hypotension).

Causes:

Myocardial infarction develops as a result of obstruction of the lumen of the vessel supplying the myocardium (coronary artery). The reasons may be (by frequency of occurrence):

Acute myocardial infarction is a severe, dangerous pathological condition that occurs as a result of ischemia (long-term disturbance of the blood circulation of the heart muscle). Characterized by the appearance of necrosis (death) of tissue. Damage to the myocardium of the left ventricle of the heart is more often diagnosed.

This disease is included in the list of the main causes of disability and deaths among the country's adult population. The most dangerous is macrofocal (extensive) myocardial infarction. In this form, death occurs within an hour after the attack. With a small-focal form of the disease, the chances of a complete recovery are much higher.

The main reason for the development of a heart attack is considered to be blockage of a large blood clot. coronary vessel. In addition, common causes include a sharp spasm, contraction of the coronary arteries due to severe hypothermia or exposure to chemicals and toxic substances.

How does acute myocardial infarction manifest, what is emergency care, what consequences can this disease have? What folk remedies are recommended to be used after treatment? Let's talk about it:

Acute heart attack - symptoms

The pathological process develops gradually and has several main periods, each of which is characterized by certain symptoms. Let us briefly consider each of the periods:

Pre-infarction. It differs in varying degrees of duration - from several minutes to several months. During this period, frequent occurrence of angina attacks with pronounced intensity is noted.

Spicy. During this period, ischemia occurs and necrosis of the heart muscle develops. May be typical or atypical. In particular, the painful variant of the acute period is typical and is observed in the vast majority of cases (90%).

[u]The acute period is accompanied by certain symptoms: [u]

Pain appears in the area of ​​the heart, which is pressing, burning, or bursting or squeezing in nature. As the attack continues, the pain intensifies, radiating to the left shoulder, collarbone and scapula. May be felt in the left side of the lower jaw.

The attack can be short-lived or can last up to several days. Most often its duration is several hours. A characteristic feature of pain is the lack of connection between it and stress or physical activity (as, for example, with coronary artery disease).

However, it is not blocked by the usual heart medications Validol and Nitroglycerin. On the contrary, after taking the medicine, the pain continues to increase. This is what makes a heart attack different from another heart attack, for example, angina pectoris.

Besides the strong painful sensations, an acute heart attack is accompanied by a decrease in blood pressure, dizziness, and sometimes loss of consciousness. There are breathing problems, nausea and vomiting may occur. Skin pale and covered in cold sweat.

The severity of pain depends on the volume and area
defeats. For example, a large-focal (extensive) heart attack is characterized by more severe symptoms than a small-focal one.

If we talk about atypical variants of the course, then in these cases the signs of a heart attack can be disguised as attacks bronchial asthma. The abdominal version causes symptoms of an acute abdomen, and the arrhythmic one is similar to an attack of cardiac arrhythmia, etc.

In any case, if the above symptoms are observed, you should immediately call an ambulance.

What are the risks of acute myocardial infarction, and what are the consequences?

Consequences varying degrees severity can develop at any stage of this disease. They can be early or late. Early ones usually appear immediately after an attack. These include:

Cardiogenic shock, symptoms of the condition such as acute heart failure and blood clots;
- conduction disorders, as well as heart rhythm disturbances;
- very often ventricular fibrillation develops, pericarditis occurs;
- Cardiac tamponade is less common. This pathology develops due to a possible rupture of the wall of the heart muscle.

After suffered a heart attack Dangerous complications may also arise. They usually occur during a subacute course or in the post-infarction period - several weeks after the attack. Late complications include:

Post-infarction syndrome (Dressler's syndrome);
- chronic heart failure.
- cardiac aneurysm and possible thromboembolic complications;

Acute myocardial infarction - emergency care

If a heart attack is suspected, emergency medical care is required. So call immediately! Before the doctor arrives, open the windows and vents to allow fresh air into the room.

Place the patient in a semi-sitting position. Place a large pillow under your back. His head should be slightly raised.

Unbutton your collar and remove the tie that is restricting movement. Give the patient an Aspirin tablet (acetylsalicylic acid). For severe pain, give an anesthetic drug, for example, Analgin or Baralgin. You can put a mustard plaster on the chest area.

If cardiac arrest occurs, perform indirect cardiac massage as quickly as possible and give the patient artificial respiration.

To do this, place the patient on a flat, hard surface. Tilt his head back. Using the palms of your hands, apply four sharp pressures on the sternum and one inhalation. Again four presses and one breath, etc. You can find out more about the use of these resuscitation techniques on the website.

Home acute myocardial infarction - help for yourself:

If an attack occurs at home and no one is nearby, call an ambulance immediately. After which you need to open the windows, take painkillers and lie down on the bed in a semi-sitting position. The front door should be left unlocked. This will help doctors enter the apartment in case of loss of consciousness.

Further treatment is carried out in a hospital. The patient is placed in the cardiac intensive care unit.

Folk remedies after a heart attack

Mix an equal amount of crushed valerian roots, motherwort herb, marsh cudweed and also use medicinal plant astragalus. Add the same amount of finely broken wild rosemary shoots, calendula and clover flowers. Add the same amount of white willow bark, ground to a powder. Mix everything.

Pour boiling water (300 ml) into half a tablespoon of the mixture. It's better to cook in a thermos. The infusion will be ready in about 6 hours. It must be filtered, after which you can take a quarter glass, several times a day. Before taking the product, warm it up a little.

Combine an equal amount of dried horse chestnut flowers, motherwort herb, and corn silk. Add the same amount of arnica inflorescences, lavender herb, leaves of the coltsfoot plant and sedum. Add the fennel fruits, crushed to a powder. Pour 1 tsp of the mixture into 200 ml of boiling water. If you cook in a thermos, healing agent will be ready in 4 hours. Be sure to strain it and drink a quarter glass an hour before meals.

Heart pathologies are one of the most common problems and often lead to human death. Greatest danger for life represents acute myocardial infarction. What kind of disease is this?

What is an acute heart attack?

Myocardial infarction is a disease in which necrosis of heart muscle cells occurs. This pathology develops when the cells of an organ do not receive enough oxygen. This occurs due to the blocking of the blood vessel that feeds the tissue.

As a result, myocardial cells are not able to fully function, and the process of their death begins. This phenomenon is called a heart attack. The danger of the disease lies in the fact that the attack occurs unexpectedly, and it is necessary to quickly take measures to eliminate it. Otherwise the person may die.

Causes of acute heart attack

The culprit in the development of acute ST-segment elevation myocardial infarction is the occlusion of a blood vessel. This can happen due to the following reasons:

1. Blockage of a vessel by a blood clot that could appear in any part of the body.
2. Spasm of the coronary arteries. This disorder often occurs when stressful situations. Therefore, the phrase “bring to a heart attack” fully justifies itself. When a person experiences nervous shock, the blood vessels constrict and cut off oxygen supply to the heart.
3. Atherosclerosis. This vascular pathology is accompanied by a deterioration in the elasticity of the walls and their stenosis.

Such pathological phenomena develop under the systematic influence of provoking factors. The first of these are ischemic disease heart (CHD ) and angina. The presence of these diseases significantly increases the risk of myocardial infarction.

Also factors contributing to the development of cardiac pathology are:

• sedentary lifestyle;
• excess body weight;
• high blood pressure;
• frequent stressful situations;
• bad habits;
• hereditary predisposition;
• age of men over 45 years and women over 65 years.

People at risk should be more attentive to their heart health and be examined by a cardiologist every year.

Classification and stages of development

Myocardial infarction has its own classification. Doctors distinguish the following types of disease depending on the area of ​​the lesion: large-focal and small-focal. Based on the depth of myocardial damage, they are distinguished:

1. , affecting the entire thickness of the fabric.
2. Subendocardial, affecting only the inner layer.
3. Subepicardial, covering the anterior outer layer of the muscle.

Myocardial infarction occurs in several stages, each of which has its own characteristics. The following stages of pathology development are distinguished:

• The sharpest. Lasts from 30 minutes to 2 hours. At this stage, ischemia of the organ cells begins, which then smoothly transitions into the process of tissue death.
• Spicy. Lasts from 2 or more days. It is characterized by the formation of a necrotic focus in the myocardium. Often at this stage of development, the heart muscle ruptures, the lungs swell, and swelling occurs in the hands.
• Subacute. Develops over a period of one month. During this period, dead tissue is rejected, creating conditions for the formation of a scar on the muscle.
• Post-infarction. Rehabilitation of the patient can take about 5 months. At this stage, scarring occurs, the myocardium adapts to work in new conditions.

NOTE!!! The last stage of the development of a heart attack does not mean that the disease is over and no consequences will arise. The patient still requires doctor's supervision, as the risk of complications is high.

Symptoms

The main sign of a heart attack is pain in the chest area. It can have different intensity and character. Patients often describe it as burning, pressing, piercing. Pain occurs in the back of the sternum, radiates to left side body: arm, neck, lower jaw.

The symptom lasts over 20 minutes. For many people, the pain is very pronounced. As a result, a person experiences negative emotions, presented in the form of fear of death, anxiety, and apathy.

In addition to pain, the following manifestations of a heart attack are observed:

• increased sweating;
• pale skin;
• dyspnea;
• weak pulse.

If chest pain occurs, immediate emergency care and calling a doctor are required.

Diagnostics

The patient is examined using visual examination, blood tests and instrumental methods. Such a comprehensive diagnosis allows you to make an accurate diagnosis.

REFERENCE!!! For early detection of the disease, the patient himself can use it. It can be purchased at a pharmacy. This method allows you to accurately determine whether there is a heart attack or not.

Anamnesis

When a patient comes to the hospital, the doctor talks with him. The patient's complaints are clarified and his medical history is studied. It is important for the doctor to know whether there have been chest pains before, how intense they were, and whether the person is at risk for developing myocardial infarction.

Next, the specialist examines the patient for excess body weight, high blood pressure, and pale skin. If the patient indicates a pain duration of more than 20 minutes, then the doctor will first suspect a heart attack.

Laboratory methods

After being examined by a doctor, the patient must undergo laboratory testing. It includes the following types of blood tests:

• General clinical. In case of cardiac pathology, the interpretation of the result shows a high level of leukocytes and ESR.
• Biochemical. This study reveals an increase in the activity of the enzymes AlT, AsT, LDH, creatine kinase, and myoglobin. This indicator indicates that the myocardium is damaged.

Instrumental methods

To make an accurate diagnosis, the following activities are carried out:

• Electrocardiography. The infarction state is reflected on the ECG as negative tooth T, pathological QRS complex and other points. The procedure is performed in different leads, which helps to detect the localization of the necrosis focus.
• In acute myocardial infarction, the ECG looks at the ST segment. Acute myocardial infarction with ST segment elevation indicates the development.
• Ultrasound examination of the heart. Allows you to accurately determine where failure occurs in the contractions of the ventricular muscles.
• Coronary angiography. Designed to detect narrowing or blockage of the vessel that supplies the heart muscle. This diagnostic method is used not only to identify pathology, but also for its therapy.

Based on a comprehensive examination of the heart, the doctor makes a diagnosis and selects appropriate treatment tactics for each patient.

Complications

Adverse consequences from a heart attack do not occur immediately. Complications can develop gradually and affect not only the heart, but also other organs. The greatest danger to a person is the first year of life after a heart attack. It is during this period that most of the consequences that lead to death occur.

Complications often occur in the form of such diseases:

• Heart failure.
• Extrasystole.
• Aneurysm.
• Thromboembolism of the pulmonary artery.
• Thromboendocarditis.
• Pericarditis.

Fighting heart disease

Treatment for a heart attack begins with eliminating the attack before the ambulance arrives. The person next to the patient should take measures that will help gain time until doctors arrive.

To do this, it is necessary to ensure complete rest for the patient, open the windows and free his throat from constricting clothing so that as much oxygen as possible can flow. Then give the patient nitroglycerin.

If the patient has lost consciousness, his pulse is too weak, chest compressions and artificial respiration must be performed. Everyone should know how to do this correctly. Anyone can be close to someone who has an unexpected heart attack.

Specialized treatment

After first aid is provided, the patient is taken to the hospital, where intensive observation and treatment of acute myocardial infarction is carried out. First of all, drug therapy is prescribed. The patient is recommended to take the following medications:

• Narcotic analgesics and antipsychotics to relieve pain behind the sternum.
• Thrombolytic drugs that help dissolve blood clot, clogged the vessel. The administration of these drugs is effective within the first hour after the onset of a heart attack.
• Antiarrhythmic drugs to restore normal heartbeat.
• Medicines aimed at normalizing metabolism in the myocardium.
• Anticoagulants that help thin the blood, reduce its clotting and prevent the development of.

Surgery used in extreme cases. The following surgical treatment methods are used:

1. Balloon angioplasty of coronary vessels.
2. Installation of a stent in a vessel.
3. Arterial bypass.

The prognosis for acute myocardial infarction depends on how damaged the heart muscle is, where the focus of necrosis is located, how old the patient is, whether he has concomitant diseases, and from many other factors. The patient's risk of developing disability is very high.

Prevention

Preventive measures for myocardial infarction - actions that are aimed at preventing the development of this disease. Such measures will minimize the risk of developing heart disease.

1. To live an active lifestyle. Physical activity helps prevent the development of most diseases, including heart disease. Sport strengthens the muscle tissue of the organ, improves blood circulation, and normalizes metabolic processes.
2. To refuse from bad habits. Smoking and drinking alcohol significantly increase the risk of developing a heart attack, as they negatively affect the condition of blood vessels.
3. Eat properly. It is important that the diet is balanced and provides the body with everything it needs. useful substances. The menu should not include fast food or fatty foods.
4. Avoid stress. Negative feelings negatively affect the health of the heart. Therefore, it is worth getting as many positive emotions as possible.

Myocardial infarction is a serious pathology of the heart, often leading to death. To always keep the health of the main organ under control, you should regularly visit a cardiologist for a preventive examination.