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Myocardial infarction


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

K l and n and chie cal symptoms and current. Acute myocardial infarction is usually preceded by angina of different duration of the course, which, shortly before the development of a heart attack, often becomes progressive in nature: its attacks become more frequent, their duration increases, they are poorly controlled by nitroglycerin. In some cases, myocardial infarction develops suddenly in patients without clinically manifested heart disease. However, careful questioning often makes it possible in such cases to establish that a few days before this the patient’s condition worsened: rapid fatigability, weakness, decreased mood, and vague chest discomfort appeared.

Typical manifestations of myocardial infarction - a feeling of strong compression or pain behind the sternum or slightly to the left or to the right of it. The pain is most often squeezing, pressing, tearing (cola feeling in the chest), sometimes burning. Stitching or cutting pains are not typical. Irradiation of pain is characteristic in the left shoulder girdle, shoulder, arm, less often in the neck and lower jaw, sometimes in the right half of the shoulder girdle, in the interscapular space. Relatively rarely (mainly in infarction of the posterior wall of the left ventricle), pain is localized in the epigastric region — a gastralgic variant of myocardial infarction. Unlike angina pectoris, myocardial infarction pain lasts more than half an hour, usually several hours, and in the case of pericarditis, several days. Accepted nitroglycerin provides only minor and short-term relief. Many patients note that the pain behind the sternum limits deep inhalation, but increased pain during deep breathing is not typical of myocardial infarction (unless it is complicated by pericarditis) and suggests another cause of the pain. Sometimes the leading symptom may be shortness of breath with mild pain or its absence. Regardless of the degree of pain, severe weakness and cold sweat are often noted. Often in the acute stage of myocardial infarction in patients with nausea , vomiting , hiccups , bloating, having a reflex nature. In some cases, heart attack myocardium is almost asymptomatic.

The face of the patient during the period of pain has a pained appearance, the skin is usually pale, sometimes with a cyanotic shade. Brushes, feet, and often the entire skin is cold and wet. Breathing quickened and often superficial. Blood pressure at the time of pain may increase, but soon drops to an unusually low level for the patient. Soft and frequent (sometimes, on the contrary, very rare) pulse of weak filling is detected. The gongs of the heart are weakened, sometimes over the apex of the heart and in the fourth intercostal space to the left of the sternum, an additional third tone is heard during diastole (diastolic canter rhythm). In most patients, it is possible to identify various cardiac arrhythmias . In uncomplicated myocardial infarction, the occurrence of heart murmurs is irregular; in some patients, a weak systolic murmur is detected over the apex of the heart. The sudden appearance of pronounced noise is characteristic of a complicated myocardial infarction (aneurysm, septal rupture, papillary muscle infarction, etc.). On the 2nd — 5th day of the disease, about a quarter of patients have a pericardial rubbing noise over the anterior surface of the heart due to the development of fibrinous pericarditis. After a few hours from the onset of the disease, the body temperature rises (rarely exceeding 38.5 ° C), normalizing usually within the next 5 days.

Myocardial infarction can begin or be combined with a picture of acute cerebral vascular catastrophe, confusion, speech disorders (cerebral form). Cerebral symptoms are based on disorders of cerebral circulation due to a decrease in cardiac output and a spasm of brain vessels.

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

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

Cardiogenic shock is caused by a decrease in myocardial contractility and is manifested by a sharp drop in blood pressure (systolic - below 90 mmHg) and symptoms of severe disorders of the peripheral circulation. The patient's appearance is characteristic: the skin is pale with a grayish-bluish tinge, the features are pointed, the face is covered with cold, sticky sweat, the saphenous veins fall down and cannot be distinguished upon examination. Patient's hands and feet are cold to the touch. Pulse is thready. Heart sounds are deaf, at the top of the heart is II tone louder than the first. Urine does not separate or hardly separates. The patient is initially 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 the contractile function of the left ventricular myocardium, and in some cases associated with acute mitral insufficiency due to papillary muscle infarction. In some cases, especially in elderly patients, the pain syndrome is absent or slightly expressed, and the main manifestation of myocardial infarction is an attack of suffocation - an asthmatic variant of the disease. Growing dyspnea is characteristic, turning into asphyxiation, the patient is forced to occupy an elevated position, a cough appears (first dry, then co more and more abundant foamy, often pink phlegm), moist rales are heard first at first over certain areas of the lungs (mostly finely bubbly), then as they develop pulmonary edema, they become copious medium- and large-bubble, audible at a distance. The patient tends to take a sitting position (orthopnea); Not only the intercostal muscles and the abdominal muscles, but also the facial muscles of the face begin to take part in the respiratory act (the wings of the nose swell up, the patient swallows the air with his mouth open). Borders of the heart are extended to the left, blood pressure is often increased (if choking is accompanied by collapse, the prognosis is poor), tachycardia is determined. Heart sounds are deaf, a canter rhythm can be heard. The rupture of the ventricular wall and the cardiac tamponade associated with it in most cases lead to death within a few minutes.

Cardiac rhythm and conduction disturbances in myocardial infarction are extremely diverse. Often there is ventricular premature beats of varying severity, which can turn into ventricular tachycardia and ventricular fibrillation. Less common are atrial rhythm disturbances: extrasystole, paroxysmal tachycardia , atrial fibrillation. Unlike ventricular arrhythmias, atrial arrhythmias are generally not life-threatening. Among conduction disorders associated with necrosis in the area of ​​the cardiac pathways, atrial-ventricular blockade is the most dangerous. With an arrhythmic variant of myocardial infarction, rhythm disturbances are the only clinical manifestations of it.

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

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

The diagnosis of myocardial infarction is made on the basis of the presence of at least two of the three main criteria: 1) a long attack of chest pain; 2) ECG changes characteristic of ischemia or myocardial necrosis; 3) increased activity of blood enzymes.

Thus, in the overwhelming 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. The ECG changes can determine the localization of the infarction, its vastness and depth - large-focal, small-focal, transmural (cross-cutting) or intramural (lying in the thickness of the myocardium), sometimes also old (in the first weeks) and a number of other features. Transmural myocardial infarction in the acute period is characterized by the disappearance of the R wave, the appearance of a deep and wide QS tooth, the rise of the ST segment above the isoelectric line, and in the first 1–2 days it merges with the positive T wave. When the large-focal infarction is formed, a pathologically wide and deep O wave forms. R wave decreases, but does not disappear; ST elevation is less pronounced than in 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 noticeably. Echocardiography and radionuclide studies are also used to clarify the magnitude and localization of myocardial infarction. Biochemical changes in blood occur on the 2-3rd day of illness and cannot serve as a basis for early diagnosis. Thus, the activity of the cardiac fraction of creatine phosphine kinase 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, and asparaginine transferase is within 3 days.

A differential diagnosis in an atypical clinical picture of myocardial infarction is performed with pulmonary thromboembolism, dissecting aortic aneurysm, pleurisy, and spontaneous pneumothorax. Differential diagnosis may be difficult in case of gastralgia infarction, when patients often mistakenly recognize perforated gastric ulcer, acute cholecystitis , pancreatitis . Diagnostic difficulties are aggravated by the fact that in elderly people a number of acute diseases of the abdominal organs can be combined with reflex angina. In such cases, the diagnosis is facilitated by a carefully collected history and proper examination of the patient. With cholecystitis, there are indications of bouts of hepatic colic in the past, sometimes with subsequent mechanical jaundice, 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 shingles, and abundant repeated vomiting . Both with pancreatitis and acute cholecystitis, the disease often occurs after ingestion of fatty foods. In case of perforation of gastric or duodenal ulcers, the starting points for the differential diagnosis are a history of peptic ulcer , a relatively young age of patients, sudden dagger pains in the abdomen, as well as the appearance of the patient and pronounced tension of the muscles of the anterior abdominal wall. The value of the differential diagnosis is due to differences in the tactics of patient management and the nature of emergency care. If in acute surgical diseases of the abdominal cavity, the use of narcotic analgesics before the examination by the surgeon is unacceptable, then for myocardial infarction occurring with pain in the epigastric region, the same therapy is used as for pain with chest 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 can be heard pericardial friction noise. On the ECG, in the initial period of the disease, a rise in the ST segment is recorded in all standard and chest leads, only after it is lowered to the isoline, negative T teeth begin to form (during myocardial infarction, negative T teeth appear long before the ST segment decreases to the isoline). In addition, a decrease in the amplitude of the R-wave and the appearance of the pathological O-wave in the dynamics are not characteristic of pericarditis.

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 of 0 , 1% solution of atropine subcutaneously, intramuscularly or intravenously, fentanyl (1-2 ml of a 0.005% solution) with a neuroleptic droperidol (1-2 ml of a 0.25% solution) in 20 ml of a 5% glucose solution or the same amount of isotonic sodium chloride solution (administered intravenously slowly).

In case of severe asphyxiation, the patient should be given a half-sitting position with the legs lowered (with low blood pressure, only a few raise the head end of the bed), let oxygen be inhaled through gauze moistened with 70% ethanol. In addition, 10 000 IU of heparin is intravenously administered intravenously at the prehospital stage and 300 mg of aspirin are given orally (tablets should be chewed).

Regardless of whether it was possible to relieve the pain completely or partially, emergency hospitalization is indicated for all patients with myocardial infarction. The patient is transferred to the vehicle on a stretcher. In homes with narrow staircases, you can move the patient on a solid chair, somewhat thrown back. In the hospital, the patient is transported in the supine position: if there are signs of left ventricular insufficiency (asphyxiation, bubbling breathing), the head end of the stretcher needs to be lifted, to allow the patient to inhale alcohol vapors with oxygen.

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

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

In order to stop the spread of myocardial necrosis, intravenous drip of nitroglycerin is administered (reduces the load on the heart), anaprilin and other drugs that reduce the need for myocardium in oxygen are taken.

Surgical treatment is indicated if, after dissolution of a blood clot on angiograms, stenosis of a large branch of the coronary artery is revealed. An operation is performed to expand the narrowed area of ​​the artery using a special catheter, at the end of which a balloon is strengthened, capable of straightening (but not stretching) when fluid is injected under pressure. In the acute period, an aortocoronary or mamma-coronary bypass surgery is sometimes performed (creating bypass prostheses bypassing the aorta or the internal artery of the breast and the coronary artery below the narrowing area).

Of particular importance in preserving the life of the patient is the timely and sufficiently vigorous treatment of the complications of myocardial infarction. In cardiogenic shock, the patient is given a horizontal position. In the absence of a physician, the average health worker can, by vital indications, slowly inject 0.5 ml of a 1% solution of mezaton in an isotonic solution of sodium chloride into a vein, and it should be observed that the systolic pressure does not exceed 110 mm Hg. Art. At the doctor's prescription, mezaton , norepinephrine or dopamine (dopamine) is injected intravenously, guided by the same systolic pressure.

With the development of severe cardiac arrhythmias (high degree ventricular arrhythmia or ventricular tachycardia), 5-6 ml of a 2% lidocaine solution are administered by intravenous injection, and then drip infusion is adjusted at a rate of 2-4 mg / min (if there is 10 ml in 200 mg of solvent 2% solution of lidocaine, the average injection rate of about 60 drops in 1 min). In the case of ventricular tachycardia, electropulse therapy can be indicated, with progressive atrioventricular blockade, temporary endocardial electrical stimulation of the heart.

With cardiac asthma or pulmonary edema, raise the head end of the bed. Lasix (40-160 mg), narcotic analgesics (morphine, promedol , omnopon) or fentanyl with droperidol, intravenously drip nitrates are injected intravenously. Nitroglycerin (nitro mak, perlinganite) is injected in isotonic sodium chloride solution, intravenously at a rate of 10 mg / min, followed by an increase in speed of 20 μg / min every 5 minutes under constant control of blood pressure and heart rate. The effect is usually achieved at an injection rate of 50-100 μg / min, the maximum injection rate is 400 μg / min. In the absence of a dispenser, 4 ml of a 1% solution of nitroglycerin are diluted in 400 ml of an isotonic solution of sodium chloride and injected intravenously at a rate of 6 to 8 drops per minute. The rate of administration is increased if pain syndrome persists provided stable hemodynamics. With the help of special suction evacuate frothy sputum from the large bronchi. For the destruction of foam in the 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 elevated pressure, as well as to ultrafiltration of blood - the removal of 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 lesion or lesions (if there are several) of the lesion of the heart muscle and the time elapsed since the onset of the disease. In case of small focal infarction, non-severe bed rest is prescribed for 1 - 2 days. If the doctor is convinced that there is no tendency to enlargement or recurrence 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 an uncomplicated transmural infarction, the patient is usually started to be implanted in bed with the help of a nurse or a physiotherapist on the 7th day of illness, they allow him to walk around the ward on the 14th day; discharged from the hospital after about 28 - 30 days from the onset of the disease.

Nutrition of the patient in the first days of the disease includes easily digestible food (juices, kissels, souffles, 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 switch to diet No. 10.

In the system of rehabilitation of patients, an important role is played by physical therapy. It contributes to the stimulation of auxiliary circulatory mechanisms that facilitate the work of the heart, training the contractile function of the weakened heart muscle and the systemic system of hemodynamic regulation. Under the influence of physiotherapy exercises, respiration is moderately activated, the nervous system tone increases, the function of the gastrointestinal tract improves, which is especially important during the patient's stay on bed rest.

Caring for a patient with acute myocardial infarction, especially in the early days of the disease, when the patient is on strict bed rest, should ensure the exclusion of physical and emotional overvoltages that are unacceptable for the patient. During this period, the nurse should usually be fed to the patient, although with the patient's insistent desire, with the permission of the doctor, he can eat on his own, especially if the bed is equipped with a bedside table. In the first days of the illness, the nurse washes the patient daily; later, when the patient is allowed to sit, she helps him to wash. If the patient’s stay on bed rest is delayed due to complications, it is necessary to turn the patient in bed every day, wipe his skin with camphor alcohol, toilet water or cologne. In the first 2-3 days of illness, the patient is not allowed to shave on his 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, Alexandria leaf, vaseline or vegetable oil). Often it is necessary to clean the intestines with an enema. With prolonged absence of stool, it may be necessary to finger destruction in the rectum fecal stopper. Sometimes the doctor allows patients who cannot empty the intestines lying in bed to change to the bedside stool for this purpose already from the second to third day of illness (in cases where the patient’s efforts, the intestinal efforts in the bed significantly exceed the efforts required for transfer to the toilet seat with the help of a nurse). It is necessary that the patient's chair was at least once every 2 days. Straining during bowel movements can lead to recurrence of painful attacks and even to the sudden death of the patient.

When a patient is urine retained, the doctor determines its cause. If necessary, the bladder is emptied through a 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 independently. If the patient empties the bladder while standing, the nurse should help him get out of bed with a minimum load: first, he should turn on his right side, ask him to bend his legs; then they lower the legs of the lying patient, after which they help him sit up in bed, and after 2 - 3 minutes of rest - stand up. During urination the patient must be supported.

Rehabilitation (rehabilitation therapy) of patients begins 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 shaving independently is one of the rehabilitation measures: the majority of patients, having received such permission, believe that they have already begun to recover. Rehabilitation measures include the timely expansion of the regimen, the appointment of physiotherapy exercises. By the end of the inpatient stay, the patient learns to walk 1.5 - 2 km and 2 flights of stairs. A trusting conversation with a patient about other patients who were in the hospital with the same disease, and now leading full-fledged work activities 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. When uncomplicated and not very extensive or small focal myocardial infarction, the prognosis for life and rehabilitation is usually favorable. It is much worse with extensive heart attack (especially with acute left ventricular aneurysm), as well as with complications - severe disturbances of heart rhythm and conduction, heart failure. Almost complete recovery is sometimes observed only with small focal, less intramural, and very rarely with a small area of ​​transmural myocardial infarction, which was uneventful. In other cases, recovery for one reason or another is regarded as partial, since the presence of a post-infarction scar predisposes to cardiac rhythm disturbances and the gradual development of heart failure, especially if myocardial infarction is complicated by heart aneurysm.

Prevention comes down to combating risk factors for atherosclerosis, to medical or surgical treatment of coronary heart disease and diseases associated with an increase in blood pressure, to timely hospitalization of patients with frequent, prolonged and resistant to nitroglycerin strokes.