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MYOCARDIAL INFARCTION

A B C D E F G H I J K L M N O P Q R S T U V W X Y Z

MYOCARDIAL INFARCTION - a disease caused by necrosis of a part of the heart muscle due to acute ischemia, most often associated with clogging of any branch of the coronary (coronary) heart arteries with a blood clot; form of coronary heart disease. In some cases, myocardial infarction develops as a result of spasm of the coronary artery, blockage by its embolus, atherosclerotic plaque with hemorrhage at its base. Most often, myocardial infarction is observed in patients with coronary artery atherosclerosis.

Clinical symptoms and course. An acute myocardial infarction is usually preceded by angina pectoris of various durations of the course, which shortly before the development of a heart attack often acquires a progressive character: its attacks become more frequent, their duration increases, they are poorly stopped by nitroglycerin. In some cases, myocardial infarction develops suddenly in patients without a clinically manifest heart disease. However, careful questioning often allows one to establish in such cases that a few days before the patient’s state of health worsened: there was rapid fatigue, weakness, decreased mood, and there were vague unpleasant sensations in the chest.

Typical manifestations of myocardial infarction are a feeling of severe compression or pain behind the sternum, or somewhat to the left or right of it. The pain is most often constricting, pressing, tearing (a feeling of a stake in the chest), sometimes burning. Stitching or cutting aching pain is not typical. Irradiation of pain in the left shoulder girdle, shoulder, arm, less often in the neck and lower jaw, sometimes in the right half of the shoulder girdle, into the interscapular space is characteristic. Relatively rarely (mainly with infarction of the posterior wall of the left ventricle), the pain is localized in the epigastric region - a gastralgic variant of myocardial infarction. Unlike angina pectoris, pain in myocardial infarction lasts more than half an hour, usually several hours, and in case of pericarditis, several days. Accepted nitroglycerin brings only minor and short-term relief. Many patients note that pain behind the sternum limits a deep breath, however, intensification of pain during deep breathing is not characteristic of myocardial infarction (if it is not complicated by pericarditis) and suggests another reason for the pain. Sometimes the leading symptom may be shortness of breath with mild pain or its absence. No matter how severe the pain, severe weakness and cold sweat are often noted. Often in the acute stage of myocardial infarction, patients experience nausea , vomiting , hiccups , and bloating, which have a reflex character. In some cases, a heart attack the myocardium is almost asymptomatic.

The patient's face during the period of pain has a painful appearance, the skin is usually pale, sometimes with a cyanotic hue. Hands, feet, and often the entire skin are cold and wet. Breathing is rapid and often superficial. Blood pressure at the time of pain may increase, but soon drops to an unusually low level for the patient. A soft and frequent (sometimes, on the contrary, very rare) pulse of weak filling is detected. Cardiac sounds are weakened, sometimes an additional third tone (diastolic gallop rhythm) is heard during diastole above the apex of the heart and in the fourth intercostal space to the left of the sternum. In most patients, various cardiac arrhythmias can be detected. With uncomplicated myocardial infarction, the occurrence of heart murmurs is irregular; in some patients a weak systolic murmur is detected above the apex of the heart. The sudden appearance of pronounced noise is characteristic of complicated myocardial infarction (aneurysm, septal rupture, papillary muscle infarction, etc.). On the 2nd – 5th day of illness, about a quarter of patients have a pericardial friction noise above the front surface of the heart due to the development of fibrinous pericarditis. A few hours after the onset of the disease, body temperature rises (rarely exceeding 38.5 ° C), usually normalizing over the next 5 days.

Myocardial infarction can begin or be combined with a picture of acute cerebrovascular accident, confusion, speech disorders (cerebral form). Cerebral symptoms are based on cerebrovascular accidents due to decreased cardiac output and cerebrovascular spasm.

The clinical course of myocardial infarction is extremely diverse. Some patients carry it on their feet, while others have it, although with typical clinical symptoms, but without serious complications, in some cases - as a serious long-term illness with dangerous complications, which can lead to death. In some patients, sudden death occurs as a result of myocardial infarction.

Complications The most formidable complications in the acute period of myocardial infarction are cardiogenic shock , acute heart failure , manifested as cardiac asthma , pulmonary edema, rupture of the necrotic wall of the ventricle of the heart.

Cardiogenic shock is caused by a decrease in myocardial contractility and is manifested by a sharp drop in blood pressure (systolic - below 90 mm Hg) and symptoms of severe peripheral circulation disorders. The patient's appearance is characteristic: the skin is pale with a grayish-cyanotic shade, the facial features are sharpened, the face is covered with cold sticky sweat, the saphenous veins collapse and they cannot be distinguished upon examination. Hands and feet of the patient are cold to the touch. Pulse is threadlike. Heart sounds are deaf, at the top of the heart II tone is louder than the first. Urine does not separate or almost does not separate. At first the patient is inhibited, later falls into an unconscious state.

Cardiac asthma and pulmonary edema are manifestations of acute left ventricular heart failure, which is most often also due to a decrease in contractile function of the myocardium of the affected left ventricle, and in some cases is associated with acute mitral insufficiency due to myocardial papillary muscle infarction. In some cases, especially in elderly patients, pain is absent or slightly expressed, and the main manifestation of myocardial infarction becomes an asthma attack - an asthmatic variant of the disease. Increasing dyspnea is characteristic, passing into suffocation, the patient is forced to stand in an elevated position, a cough appears (first dry, then with more and more plentiful foamy, often pink sputum), moist rales are heard first at first over separate sections of the lungs (mainly finely bubbly), then, as they develop pulmonary edema, they become abundant medium and coarse bubbles, audible at a distance. The patient seeks to take a sitting position (orthopnea); not only intercostal and abdominal muscles begin to take part in the respiratory act, but also the facial muscles of the face (the wings of the nose are swollen, the patient swallows air with his mouth open). The borders of the heart are expanded to the left, blood pressure is often increased (if suffocation is accompanied by collapse, the prognosis is poor), tachycardia is determined. Heart sounds are deaf, the gallop rhythm can be heard. Rupture of the ventricular wall and associated cardiac tamponade in the vast majority of cases lead to death within a few minutes.

Violations of the rhythm and conduction of the heart with myocardial infarction are extremely diverse. Often there is ventricular extrasystole of varying severity, which can go into ventricular tachycardia and ventricular fibrillation. Atrial rhythm disturbances are less frequently recorded: extrasystole, paroxysmal tachycardia , atrial fibrillation. Atrial arrhythmias , unlike ventricular, are generally not life threatening. Among the conduction disorders associated with necrosis in the area of ​​the conduction pathways of the heart, the most dangerous is atrioventricular block. With an arrhythmic variant of myocardial infarction, rhythm disturbances are its only clinical manifestation.

A frequent complication of an extensive heart attack, especially localized in the anterior wall of the left ventricle, is an aneurysm of the heart, the development of which contributes to the occurrence of arrhythmias and heart failure.

Parietal thrombosis of the heart cavities can cause embolism of the arteries supplying blood to the internal organs (brain, kidneys, spleen, etc.) and limbs.

Myocardial infarction is diagnosed based on the presence of at least two of the three main criteria: 1) a prolonged attack of pain in the chest; 2) ECG changes characteristic of ischemia or myocardial necrosis; 3) increased activity of blood enzymes.

Thus, in the vast majority of cases, the correct diagnosis can be made at the prehospital stage on the basis of the clinic and ECG.

A special role in the diagnosis of myocardial infarction belongs to electrocardiography. By changes in the ECG, one can determine the location of the heart attack, its extent and depth - large-focal, small-focal, transmural (through) or intramural (lying in the thickness of the myocardium), sometimes also prescription (in the first weeks) and a number of other features. For acute transmural myocardial infarction, the disappearance of the R wave, the appearance of a deep and wide QS wave, the rise of the ST segment above the isoelectric line are characteristic, and in the first 1 - 2 days it merges with the positive T wave. With a large focal infarction, a pathologically wide and deep O wave is formed , R wave decreases, but does not disappear; ST segment elevation is less pronounced than with transmural infarction; from the 5th day of acute myocardial infarction, a constant decrease in the ST segment and the formation of a negative isosceles T wave are noticeable. Echocardiography and radionuclide research methods are also used to clarify the size and localization of myocardial infarction. Biochemical changes in the blood occur on the 2nd – 3rd day of the disease and cannot serve as a basis for early diagnosis. Thus, the activity of the heart fraction of creatine phosphokinase increases after 8-10 hours from the onset of myocardial infarction and returns to normal after 48 hours, the activity of lactate dehydrogenase increases by 3-5 days, aspartic aminotransferase within 3 days.

A differential diagnosis in an atypical clinical picture of myocardial infarction is carried out with pulmonary embolism, stratified aortic aneurysm, pleurisy, spontaneous pneumothorax. A differential diagnosis can be difficult with a gastralgic variant of a heart attack, when patients often have a perforated gastric ulcer, acute cholecystitis , and pancreatitis . Diagnostic difficulties are exacerbated by the fact that in the elderly a number of acute diseases of the abdominal organs can be combined with reflex angina pectoris. In such cases, diagnosis is facilitated by a carefully collected medical history and proper examination of the patient. With cholecystitis, there are indications of attacks of hepatic colic in the past, sometimes followed by obstructive jaundice, the pain is localized mainly in the right upper quadrant of the abdomen, radiating to the right scapula and right shoulder. Acute pancreatitis is characterized by localization of pain in the epigastric region and to the left of the navel, their girdle nature, and profuse repeated vomiting . As with pancreatitis, and with acute cholecystitis, the disease often occurs after ingestion of fatty foods. When a stomach or duodenal ulcer is perforated, the starting points for a differential diagnosis are a history of peptic ulcer , the relatively young age of patients, sudden dagger pains in the abdomen, as well as the patient's appearance and pronounced muscle tension of the anterior abdominal wall. The significance of the differential diagnosis is due to differences in management tactics and the nature of emergency care. If in acute surgical diseases of the abdominal cavity, the use of narcotic analgesics before examination by the surgeon is unacceptable, then with myocardial infarction, which occurs with pain in the epigastric region, the same therapy is used as for pain with sternal localization.

With pericarditis, intense prolonged pain in the upper half of the chest is often associated with respiratory movements and body position, combined with fever. An objective examination may listen to the pericardial friction noise. On the ECG, in the initial period of the disease, an ST segment elevation is recorded in all standard and chest leads, only after lowering it to the isoline do negative T waves begin to form (with myocardial infarction, negative T waves arise long before the ST segment decreases to the isoline). In addition, pericarditis is not characterized by a decrease in the amplitude of the R wave and the appearance of a pathological O wave in the dynamics.

Treatment . If repeated administration of nitroglycerin does not reduce pain, narcotic analgesics are administered - promedol (1-2 ml of a 2% solution), morphine (1-2 ml of a 1% solution), omnopon (1-2 ml of a 1% solution) with 0.5 ml 0 , 1% solution of atropine subcutaneously, intramuscularly or intravenously, fentanyl (1-2 ml of 0.005% solution) with antipsychotic droperidol (1-2 ml of 0.25% solution) in 20 ml of 5% glucose solution or the same amount of isotonic sodium chloride solution (administered intravenously slowly).

With severe suffocation, the patient should be given a semi-sitting position with legs down (with low blood pressure, only slightly raise the head end of the bed), allow oxygen to be inhaled through gauze moistened with 70% ethyl alcohol. In addition, at the prehospital stage, 10,000 units of heparin are injected intravenously and 300 mg of aspirin are given inside (tablets should be chewed).

Regardless of whether it was possible to relieve the pain in whole or in part, emergency hospitalization is indicated for all patients with myocardial infarction. The patient is transferred to a vehicle on a stretcher. In houses with narrow stairs, you can transfer the patient in a sturdy chair, slightly thrown back. The patient is transported to the hospital in a prone position: if there are signs of left ventricular failure (suffocation, bubbling breathing), the head end of the stretcher should be raised, and the patient should be breathed in alcohol and oxygen.

If possible, patients with acute myocardial infarction are hospitalized in special wards (units) of intensive care, equipped with equipment that allows monitor monitoring - constantly monitor the ECG and other blood circulation parameters.

In a hospital, if no more than 6 hours have passed since the development of a heart attack, in the absence of contraindications, treatment is started aimed at dissolving the thrombus in the coronary artery (streptokinase is most often used) or preventing thrombosis progression (heparin is administered).

In order to stop the spread of myocardial necrosis, drip intravenous administration of nitroglycerin is prescribed (reduces the load on the heart), taking anaprilin and other drugs that reduce myocardial oxygen demand.

Surgical treatment is indicated if stenosis of a large branch of the coronary artery is revealed on angiograms after dissolution of the thrombus. The operation is used to expand the narrowed section of the artery using a special catheter, at the end of which a balloon is attached that can expand (but not stretch) when liquid is injected into it under pressure. In the acute period, an aortocoronary or mammaro-coronary artery bypass grafting is sometimes performed (bypassing the prosthesis between the aorta or internal mammary artery and the coronary artery below the narrowing site).

Of particular importance in preserving the patient’s life is the timely and sufficiently energetic treatment of complications of myocardial infarction. With cardiogenic shock, the patient is given a horizontal position. In the absence of a doctor, the average health worker can slowly inject 0.5 ml of a 1% solution of mesatone in an isotonic solution of sodium chloride into a vein slowly, while observing that the systolic pressure does not exceed 110 mm Hg. Art. According to the doctor’s prescription, mesatone , norepinephrine or dopamine (dopamine) are injected intravenously, focusing on the same indicator of systolic pressure.

With the development of severe cardiac arrhythmias (ventricular extrasystole of high degrees or ventricular tachycardia), 5–6 ml of a 2% lidocaine solution is injected intravenously, after which it is infused at a rate of 2–4 mg / min (if 10 ml of the solvent contains 10 ml 2% lidocaine solution, the average injection rate of about 60 drops in 1 min). In the case of ventricular tachycardia, electropulse therapy can be indicated, with progressive atrial-ventricular blockade - temporary endocardial electrical stimulation of the heart.

With cardiac asthma or pulmonary edema, the head end of the bed is raised. Lasix (40 - 160 mg), narcotic analgesics (morphine, promedol , omnopon) or fentanyl with droperidol are administered intravenously, and nitrates are dripped intravenously. Nitroglycerin (nitro Mac, perlinganite) is administered in an isotonic sodium chloride solution, intravenously, at a rate of 10 μg / min, followed by an increase in speed by 20 μg / min every 5 min under constant monitoring of blood pressure and heart rate. Typically, the effect is achieved at a rate of administration of 50-100 μg / min, the maximum rate of administration - 400 μg / min In the absence of a dispenser, 4 ml of a 1% solution of nitroglycerin is diluted in 400 ml of an isotonic sodium chloride solution and injected intravenously at a rate of 6-8 drops in 1 min. The rate of administration is increased if the pain syndrome persists, provided stable hemodynamics. Using special suction, foamy sputum is evacuated from large bronchi. To destroy the foam in small bronchi, inhalation of oxygen with vapors of ethyl alcohol is used (50% when breathing through a mask and 70% when using a nasal catheter). Sometimes they resort to artificial ventilation of the lungs under high pressure, as well as to ultrafiltration of the blood - removing part of the water contained in the blood with electrolytes dissolved in it using special devices.

The regimen of a patient with myocardial infarction depends on the size of the focus or foci (if there are several) of damage to the heart muscle and the time elapsed since the onset of the disease. With a small focal infarction, non-strict bed rest is prescribed for 1 to 2 days. If the doctor makes sure that there is no tendency to expand or relapse of a heart attack, the patient is transferred to the ward, and after a week he is allowed to move within the department with a gradual further activation. With uncomplicated transmural infarction, the patient is usually put in bed with the help of a nurse or exercise therapy practitioner on the 7th day of illness, they are allowed to walk around the ward on the 14th day; discharged from the hospital after about 28 to 30 days from the onset of the disease.

The patient’s nutrition in the first days of the disease includes digestible food (juices, jelly, soufflé, soft-boiled eggs, kefir). Excluded products that cause increased gas formation in the intestine. From the 4th day of the disease, the diet is gradually expanded and by the end of the week they are switching to diet No. 10.

An important role in the rehabilitation system of patients belongs to physiotherapy exercises. It contributes to the stimulation of auxiliary circulatory mechanisms that facilitate the work of the heart, the training of contractile function of weakened heart muscles and the apparatus for regulating systemic hemodynamics. Under the influence of physiotherapy exercises, breathing is moderately activated, the tone of the nervous system increases, the function of the gastrointestinal tract improves, which is especially important during the patient’s stay in bed.

Care for patients with acute myocardial infarction, especially in the early days of the disease, when the patient is in strict bed rest, should ensure the exclusion of unacceptable physical and emotional stress for the patient. During this period, as a rule, a nurse should feed the patient, although with the patient’s insistent desire, he can eat on his own with the permission of the doctor, especially if the bed is equipped with a bedside table. In the early days of the disease, the nurse washes the patient daily, later, when the patient is allowed to sit, helps him wash himself. If the patient’s stay in bed is delayed due to complications, it is necessary to turn the patient in bed daily, wipe his skin with camphor alcohol, eau de toilette or cologne. In the first 2-3 days of illness, the patient is not allowed to shave on their own.

The regulation of physiological functions is important. As a rule, patients in the first days develop constipation, for the elimination of which non-salt laxatives are used (buckthorn, Alexandrian leaf, liquid paraffin or vegetable oil). Often you have to cleanse the intestines with an enema. With prolonged absence of stool, there may be a need for finger destruction in the rectum of the fecal plug. Sometimes the doctor allows patients who cannot empty the intestines while lying in bed to transplant for this purpose on the bedside chair from the 2nd to 3rd day of illness (in cases where the patient’s efforts spent on emptying the intestines in bed significantly exceed the efforts required for transfer to a toilet seat with the help of a nurse). It is necessary that the patient's stool be at least once every 2 days. Straining during bowel movements can lead to recurrence of pain attacks and even to the sudden death of the patient.

With a delay in the patient's urine, the doctor determines its cause. If necessary, the bladder is emptied through the urinary catheter, in some cases the catheter is left in the urinary tract for 1-2 days, after which the patient is allowed to empty the bladder on his own. If the patient empties the bladder while standing, then the nurse should help him get out of bed with minimal load: first he needs to be turned on his right side, asked to bend his legs; then they lower the legs of the lying patient, after which they help him to sit in bed, and after 2 to 3 minutes of rest, get up. During urination, the patient must be maintained.

Rehabilitation (rehabilitation therapy) of patients begins already in the hospital. It is aimed at restoring, if possible, a full-fledged general physical and mental state of the patient. Allowing the patient to eat and shave on their own is one of the rehabilitation measures: most patients, having received such permission, believe that they have already begun to recover. Rehabilitation measures include the timely expansion of the regime, the appointment of physiotherapy exercises. By the end of his stay in the hospital, the patient masters walking for 1.5 - 2 km and 2 flights of stairs. A confidential conversation with the patient about other patients who were in a hospital with the same disease, and now leading full-time work and normal family life, is psychologically useful.

The prognosis depends on the extent of the heart attack, as well as on the presence and nature of complications in the acute and subsequent periods. With uncomplicated and not very extensive or small-focal myocardial infarction, the prognosis for life and restoration of disability is usually favorable. It is significantly worse with extensive heart attack (especially with acute left ventricular aneurysm), as well as with complications - severe cardiac arrhythmias and conduction, heart failure. Almost complete recovery is sometimes observed only with small focal, less intramural and very rarely with a small area of ​​lesion transmural myocardial infarction, proceeding without complications. In other cases, recovery for one reason or another is regarded as partial, since the presence of a post-infarction scar predisposes to heart rhythm disturbances and the gradual development of heart failure, especially if myocardial infarction is complicated by aneurysm of the heart.

Prevention is reduced to the fight against risk factors for the development of atherosclerosis, to medical or surgical treatment of coronary heart disease and diseases accompanied by an increase in blood pressure, to timely hospitalization of patients with frequent, elongated and resistant to nitroglycerin attacks of angina pectoris.