Myocardial infarction

Myocardial infarction is a heart disease caused by acute insufficiency of its blood supply, with the emergence of a focus of necrosis in the heart muscle; The most important clinical form of ischemic heart disease.

The main factors of pathogenesis: coronary thrombosis (acute blockage of the lumen of the artery), leading to a large, more frequent, transmural necrosis of the myocardium; Coronary stenosis (acute narrowing of the artery lumen with a swollen atherosclerotic plaque, parietal thrombus) with large focal, as a rule, myocardial infarction; Stenosing widespread coronary sclerosis (a sharp narrowing of the lumen of 2-3 coronary arteries) usually against a background of marked myocardiosclerosis, leading to so-called small-focal, often-subendocardial myocardial infarctions. The last category of myocardial infarction is by no means "shallow" in its clinical significance, in the frequency of complications and in the consequences for the patient, especially in the case of subendocardial infarctions, when they are detected electrocardiographically in all the walls of the left ventricle of the heart (mortality in such myocardial infarctions Significantly exceeds mortality in transmural infarcts).

Symptoms, course. The beginning of a myocardial infarction is considered the appearance of an attack of intense and prolonged (more than 30 minutes, often many hours) chest pain (anginal disease), not being suppressed by repeated nitroglycerin; Rarer in the picture of the attack, choking or pain predominates in the epigastric region (asthmatic and gastralgic forms of acute infarction). Complications of an acute attack: cardiogenic shock; Acute left ventricular failure up to pulmonary edema; Severe tachyarrhythmias with arterial hypotension, sudden clinical death due to ventricular fibrillation (less often asystole). Ventricular ectopic arrhythmias in the first hours after an acute attack often reflect the restoration of the permeability of the coronary artery (lysis of the thrombus), which occurred either spontaneously or under the influence of thrombolytic therapy (streptodecase and other thrombolytic drugs).

In an acute period, hypertension is observed (often significant) that disappears after the pain subsides and does not require the use of antihypertensive drugs; Increased heart rate (not always); Increase in body temperature (from 2-3 days); Hyperleukocytosis, followed by a persistent increase in ESR; In the blood serum - a transient increase in glycemia, azotemia, fibrinogen level, activity of creatine kinase and its myocardial isoenzyme (within the first 48 h), ASAT (within 72 h), LDH and its isoenzyme LDG1 (within 5 days); Episthenocardial pericarditis (pain in the sternum, especially with breathing, often the noise of pericardial friction, heard at the left edge of the sternum).

On the ECG series, a significant, often dome-shaped rise of the ST segments is observed, followed by the appearance of broadened (not less than 0.04 s) Q teeth, a decrease in the amplitude of the R wave or the appearance of the QS form of the ventricular complex (sometimes only 24-48 hours and even 3- 5 days from the onset of myocardial infarction) in leads corresponding to the predominant localization of the lesion focus (zone) in the cardiac muscle. About 1/4 of all large-focal myocardial infarctions are either not accompanied by convincing changes on the ECG (especially with repeated infarctions, with intraventricular blockades), or such changes are detected only in additional leads. Diagnosis is evidenced by changes not in one ECG, but only by a certain sequence of changes in the QRS and ST segment recorded on the ECG series.

Complications of the hospital period of myocardial infarction: euphoria, uncritical behavior, right up to the psychotic state; Resumption of pain in the chest due to recurrence of the infarction, the appearance of fibrinous pericarditis, sudden fluctuations in frequency and regularity of the heart rhythm, attachment of a lung infarction (pleurisy!), The formation of an external rupture of the myocardium; Paroxysms of tachyarrhythmia, as well as early (near the T wave of the preceding cardiac complex) polytopic and group ventricular extrasystoles; Atrioventricular blockade of II-III degree; Syndrome of weakness of the sinus node: aneurysm of the left ventricle; Sudden death (terminal arrhythmia or a heart rupture with pericardial gemotemposada); Acute heart failure; Cardiogenic shock; Thromboembolism in the pulmonary artery system. Rare complications: embolic cerebral infarction; Thromboembolism of the branches of the mesenteric artery; Profuse bleeding from acute trophic ulcers of the mucous membrane of the stomach, intestines; Acute expansion of the stomach; Embolism of the arteries of the lower extremities; "Postinfarction syndrome" (Dressler); Rupture of the interventricular septum; Rupture "of the papillary muscle.

Heart failure is often manifested for the first time only when the patient begins to walk, and is the cause of "late" lung infarctions (thromboembolism of the pulmonary artery branches).

The diagnosis of myocardial infarction is conclusive if the patient has a clinical picture of an anginal attack (or asthmatic equivalent), hyperfermentemia at typical times, characteristic ECG changes described above. A typical clinical picture of a painful attack with the appearance (in a characteristic sequence) of hyperleukocytosis, hyperthermia, increased ESR, signs of pericarditis forces presuming myocardial infarction and appropriate treatment of the patient, even if the ECG lacks evidence of changes in the infarction. The diagnosis is confirmed by the analysis of the further course of the disease (detection of hyperfermentemia, complications, especially left ventricular failure). Similarly, a retrospective diagnostic assumption of myocardial infarction complicating the course of other diseases or the postoperative period is justified.

For the diagnosis of small-focal infarction, the patient needs the above-mentioned 3 components, but the intensity and duration of the pain attack, the reactive shifts on the part of the blood, body temperature, serum enzyme activity, and ECG changes are usually less pronounced. The reliability of the diagnosis based only on the appearance of negative T-wave on ECG in the absence of convincing clinical and laboratory data is questionable.As a rule, small-focal infarction is observed in persons who suffer from ischemic heart disease and cardiosclerosis for many years with various complications, the number and severity of which, As well as the tendency to recurrence increase with the addition of a heart attack, which is determined both by the duration and burden of the course of the latter, and by the severity of its immediate and distant prognosis.If it occurs in the early, initial phase of coronary heart disease, it is often a harbinger of a severe transmural cardiac infarction , Developing a few days or weeks later.These two features determine the clinical and prognostic evaluation of small focal infarction and the choice of treatment tactics.Differential diagnosis of myocardial infarction is performed with pericarditis (see), with pulmonary artery embolism (cm), with spontaneous pneumothorax (see) , With massive internal bleeding (see), with acute pancreatitis (see), with exfoliating aortic hematoma (see). Small-focal myocardial infarction is distinguished from coronarogenic focal dystrophy of the myocardium, from dyshormonal (climacteric) cardiopathy (see Cardialgia). Treatment. The main help in myocardial infarction: 1) continuous exposure to nitrates; 2) the administration of either a lysing thrombus preparation or a direct anticoagulant intravenously; 3) use of a drug that blocks beta-adrenergic effects on the heart; 4) the introduction of potassium chloride in the composition of the polarizing mixture. The totality of these measures, especially if they are taken in the first hours of the disease, is aimed at limiting the size of myocardial damage in the infarct and peri-infarction zones.

With an anginal condition, nitroglycerin is applied without delay, first sublinely (0.0005 g in a pill or 2 drops of 1% alcohol solution) repeatedly with an interval of 2-3 minutes until the intensity of angina pain significantly weakens, and in the meantime establish a system for In / in drip infusions and continue exposure to nitroglycerin by iv in continuous administration. To this end, an iodine (not alcoholic!) 0.01% solution of nitroglycerin containing 100 μg of the drug in 1 ml is diluted with a sterile isotonic sodium chloride solution so that the rate of iv administration of nitroglycerin to the patient may be 50 μg / min and increasing Every minute they achieve a stable antianginal action (usually - at a rate of no more than 200-250-300 μg / min); The effective speed is maintained for a long time. Only complete absence of alleviation of anginal pain, in spite of the adequate use of nitroglycerin, justifies the introduction of narcotic analgesics to the patient IV (not in / m and not /!): Either mixtures of 1-2 ml of a 2% solution of promedol, 1-2 ml 50% analgin and 1 ml 1% solution of diphenhydramine in 20 ml of 5-10% glucose solution; Or (in the absence of bradycardia, arterial hypotension) - 1 ml of 0.25% solution of droperidol with 1 ml of 0.005% solution of fentanide; Or (in the absence of arterial hypertension) 30 mg (i.e., 1 ml) of pentazocine (fortral). Potentiate analgesia by inhalation of a mixture of nitrous oxide and oxygen (1: 1) or by slowly (!) Injecting 20 ml of a 20% solution of sodium oxybutyrate (gamma-hydroxybutyric acid). It should not be rushed with hypotensive therapy for hypertension in the first hours of myocardial infarction. Nitroglycerin - if it is impossible to / in its introduction - continue to give in sublingual tablets, supporting the antianginal effect of the drug application on the skin of 2% ointment with nitroglycerin.

Heparin is administered intravenously, starting at 1000 units, then continuous intravenous infusion of heparin is preferred at a rate of 1000 units per hour, or a fractional introduction to the vein (can be done by catheter puncture) at least every 2 hours (!) At 2000 units. In the hospital, intravenous injection of heparin (1000 units per hour) is continued, controlled by repeated coagulograms or coagulation time (it should increase 2-3 times). Thrombolytic therapy is preferred, provided that the patient is taken to the hospital during the first hours of myocardial infarction (the ST segments of the ECG are still raised dome) and that the intensive hospital observation unit has the skills necessary to manage patients during thrombolysis; The latter is carried out by streptodease (usually at a dose of 3,000,000 units) or another thrombolytic drug.

Simultaneously with heparin (in particular after the introduction of streptodeacase or another thrombolytic drug) continue the administration of nitroglycerin (better iv) and adjust the introduction of a vein patient polarizing mixture (500 ml of 10% glucose solution + 1.5 g potassium chloride) +10 -12 ED of insulin), in combination with which it is possible to administer both heparin and other drugs. It is advisable to install a venous catheter into a large vein with the expectation of long-term use. Introduce the patient in / in the drip for about half an hour in a dose of 7-8 mg; 4 hours after the end of the infusion, the drug is started to be given inside, usually at a dose of 20-40 mg per dose every 4-6 hours. Ending heparin therapy, they switch from intravenous injection to injection into the subcutaneous fat layer of the anterior abdominal wall (only not intramuscularly!) 7500-5000 units 2-4 times a day. Admission of antiplatelet agents starts from the 3rd-4th day of the disease, as a rule, acetylsalicylic acid, taken at 100 mg (rarely 200 mg), once a day (after a meal) serves as such a preparation. It is necessary to control the response to blood in the stool.

Infusion heparin therapy is continued - with uncomplicated myocardial infarction - 5-7 days; Potassium salts - inward in the form of solutions of potassium chloride or acetate, or preparations "foamy potassium" or solnatrex (with food); Nitroglycerin infusions are gradually replaced with ointment applications with 2% nitroglycerin; The administration of an antiaggregant (acetylsalicylic acid) should not be discontinued until the completion of the rehabilitation period of the patient. Activity of the patient in bed - from the first day, sitting down - from 2-4 day, getting up and walking in the ward - on days 7-9-11. Recommended elastic bandaging of the feet, especially in obese persons (not massage!). The terms for transferring the patient to the regime of outpatient or sanatorium rehabilitation, as well as return to work and employment (according to the conclusion of the WTEC) are determined individually.

Treatment of complications. Frequent ventricular extrasystoles of high grades in Launus (early type R on T, polytopic, group, "tachycardia") during the first hours of myocardial infarction can be a consequence of recanalization (including spontaneous) of the coronary artery lumen, but at the same time - a harbinger of the early onset Ventricular tachycardia or ventricular fibrillation. Therefore, it is necessary to inject 10% to 20 ml of 1% xikain solution (xylocaine, lidocaine) v / v slowly, then titrate preventively injected drip for an hour (if necessary, repeatedly). Single extrasystoles do not require treatment. With supraventricular extrasystole, drip infusion of the polarizing mixture; Paroxysms of supraventricular tachycardia, flicker or atrial flutter if they cause symptoms of cardiac and vascular insufficiency, as well as infusion of the polarizing mixture in combination with the administration of 1 ml of 0.025% digoxin solution (not corglycon!) And 1-2 ml of 25% solution of cordiamine in / In, in the absence of such symptoms - observation, since these kinds of arrhythmias are usually transient. With paroxysm of ventricular tachycardia, immediate defibrillation is preferable to attempted drug therapy.

With an atrioventricular blockade of II-III degree, isadrin (novodrin) 0.005 g (dissolve the tablet in the mouth) or orciprenaline sulfate (alupent) 0.02 g (dissolve) or intravenously dripping in the form of 1-2 ml of 0.05% solution in 200 -300 ml isotonic sodium chloride solution at a rate of 12-16 drops per minute; The duration and repetition of the application are determined depending on the shifts in the degree of blockade. If the complete AV blockade with myocardial infarction of the posterior (lower) wall is often transient, then with anteroposterous myocardial infarction it sharply worsens the nearest prognosis and requires an electrocardiostimulation, which does not always, unfortunately, improve the prognosis. The blockade of branches of the bundle of the Hisnus usually does not require special medical treatment.

At the first even minimal signs of acute cardiac failure, more often left ventricular failure in any period of the disease shows the use of vasodilator drugs (nitrates, calcium antagonists) preferably in / in long periods, but can also be taken internally (nitrates and as an ointment). Stagnant phenomena lead to the appointment of diuretic drugs (furosemide, hypothiazide, triamterene, triampur, veroshpiron), which are used in small and moderate doses, but repeatedly, as needed.

With pulmonary edema, give nitroglycerin to the tongue and, if possible, start iv injection of nitroglycerin (see above), increasing the rate of its administration until the symptoms of edema are reduced. The panic mood of the patient may require the administration of intravenously or subcutaneously 1 ml of a 1% solution of morphine or other narcotic analgesics. In addition, 6-8 ml of a solution of furosemide as a diuretic (in the absence of signs of cardiogenic shock) is injected / in. Only with a sharp increase in diastolic blood pressure is it regulated (the danger of collapse!), Its decrease by dropwise intravenous administration of up to 250 mg of arfonade in 250-300 ml of a 5% solution of glucose, the speed of which (the number of drops per minute) is selected by measuring blood pressure every 1-2 Min.

With cardiogenic shock, i.e., with arterial hypotension combined with anuria or oliguria (less than 8 drops of urine per minute per catheter) and with acute heart failure (congestion in the lungs with shortness of breath, cyanosis, small cardiac output syndrome, pulmonary edema ), It is necessary first of all to stop anginal pain, as described in an anginal episode. Under mandatory control of central venous pressure, infusion or solutions replenishing a reduced volume of circulating blood - rheopolyglucin 100-200 and even 300 ml IV with caution (danger of pulmonary edema) are initiated; Or a solution of dopamine in 5% glucose or in isotonic sodium chloride solution (at the rate of 25 mg of dopamine per 125 ml of solution, while the rate of administration of 1 ml per 1 min, i.e. 16-18 drops per minute, will correspond to infusion 200 Μg of the drug per 1 minute). The rate of dopamine administration can and should vary depending on the response of cardiac activity and vascular tone, as well as the volume of urine released by the kidneys. The prognosis is extremely serious, especially if cardiogenic shock is combined with pulmonary edema. An indication of overcoming cardiogenic shock is the resumption of diuresis in a volume of 1 ml or more per minute; Do not focus only on increasing blood pressure. In specialized departments, the choice of tactics for treating shock and monitoring the course of treatment is facilitated by obtaining information on the pressure in the pulmonary artery, the volume of circulating blood, the parameters of central hemodynamics, oxygenation and blood pH, the value of minute diuresis, and also the radiographic picture of the blood filling of the lungs and some other Data.

With thromboembolism of the pulmonary artery branches, heparin therapy is all the more necessary as the diagnosis is more reliable; It should be combined with treatment of heart failure (often latent), which is the cause of peripheral, often asymptomatic phlebothrombosis (source of thromboembolism). Thrombolytic therapy is performed in specialized departments (see above).