Myocardial infarction: complications

Electrical dysfunction occurs in more than 90% of patients with myocardial infarction. Electrical dysfunction, which usually leads to death in the first 72 hours, includes tachycardia (from any source) with a sufficiently high heart rate, capable of reducing cardiac output and lowering blood pressure, an atrioventricular block of the Mobitz II type (2 degrees) or complete (grade 3), ventricular tachycardia (VT) and ventricular fibrillation (VF).

Asystole is rare, except in cases of extreme manifestations of progressive left ventricular failure and shock. Patients with heart rhythm disturbances should be examined for hypoxia and electrolyte disturbances, which can be both a cause and a concomitant factor.

[1], [2], [3], [4]

Violations of the functions of the sinus node

In the case of an artery, which supplies a sinus node, it is possible to develop sinus node dysfunction. This complication is more likely in the event that there was a previous lesion of the sinus node (often found among the elderly). Sinus bradycardia, the most frequent dysfunction of the sinus node, usually does not require treatment, except for cases of arterial hypotension or heart rate <50 per minute. Lower heart rate, but not critical, leads to a decrease in the workload on the heart and helps to reduce the heart attack zone. With bradycardia with arterial hypotension (which can reduce the blood supply of the myocardium) use atropine from 0.5 to 1 mg intravenously; In case of insufficient effect, the administration can be repeated in a few minutes. The administration of several small doses is better, since high doses can cause tachycardia. Sometimes a temporary pacemaker is required.

Persistent sinus tachycardia is usually a menacing symptom, often indicative of a lack of left ventricular low cardiac output. In the absence of left ventricular failure or other obvious cause, this variant of arrhythmia can respond to the administration of b-blockers intravenously or inward, depending on the degree of urgency.

Atrial arrhythmias

Atrial rhythm disturbances (atrial extrasystole, atrial fibrillation and rarely atrial flutter) develop in approximately 10% of patients with myocardial infarction and may reflect the presence of left ventricular failure or myocardial infarction of the right atrium. Paroxysmal atrial tachycardia is rare and usually in patients who have had similar episodes before. Atrial extrasystole usually proceeds benignly, but it is believed that an increase in frequency can lead to the development of heart failure. Frequent atrial extrasystole may be sensitive to the appointment of b-blockers.

Atrial fibrillation is usually transient if it occurs within the first 24 hours. Risk factors include age over 70 years, heart failure, previous myocardial infarction, extensive previous myocardial infarction, atrial infarction, pericarditis, hypokalemia, hypomagnesemia, chronic lung diseases and hypoxia. The use of fibrinolytic agents reduces the likelihood of this complication. Repeated paroxysms of atrial fibrillation are a poor prognostic factor, increasing the risk of systemic embolism.

With atrial fibrillation, heparin is usually prescribed, since there is a risk of systemic embolism. Intravenous administration of b-adrenoblockers (for example, atenolol 2.5 to 5.0 mg for 2 minutes before reaching the full dose of 10 mg for 10-15 minutes, metoprolol 2 to 5 mg every 2-5 minutes to a full dose of 15 mg for 10-15 minutes) slows down the frequency of ventricular contractions. Careful monitoring of heart rate and blood pressure is necessary. Treatment is stopped with a marked decrease in heart rate or systolic blood pressure <100 mm Hg. Art. Intravenous administration of digoxin (less effective than b-adrenoblockers) is used cautiously and only in patients with atrial fibrillation and left ventricular systolic dysfunction. It usually takes about 2 hours to reduce heart rate when using digoxin. In patients with no apparent left ventricular systolic dysfunction or conduction disorders, which are manifested by the appearance of a wide QRS complex, intravenous administration of verapamil or diltiazem can be considered. The last drug can be administered in the form of intravenous injections to maintain a normal heart rate for a long time.

If atrial fibrillation disturbs the systemic circulation (for example, leading to the development of left ventricular failure, arterial hypotension, or chest pain), an emergency cardioversion is indicated. In the case of recurrence of atrial fibrillation after cardioversion, the possibility of intravenous administration of amiodarone should be considered.

With atrial flutter, heart rate is controlled in the same way as in atrial fibrillation, but heparin is not administered.

Of the supraventricular tachyarrhythmias (if sinus tachycardia is not considered), atrial fibrillation is most often observed in the acute period of myocardial infarction - in 10-20% of patients. All other variants of supraventricular tachycardia with myocardial infarction are very rare. If necessary, standard medical measures are taken.

Early atrial fibrillation (the first day of myocardial infarction), as a rule, is transient, its occurrence is associated with ischemia of the atria and epistenocardic pericarditis. The occurrence of atrial fibrillation in later periods is in most cases a consequence of the dilatation of the left atrium in patients with left ventricular dysfunction (arrhythmia of heart failure). In the absence of noticeable violations of hemodynamics, atrial fibrillation does not require medical treatment. In the presence of pronounced violations of hemodynamics, the method of choice is an emergency electrical cardioversion. With a more stable condition, there are 2 options for managing patients: (1) a decrease in heart rate with tachysystolic form, on average, up to 70 per min with iv injections of beta-blockers, digoxin, verapamil, or diltiazem; (2) an attempt to restore the sinus rhythm by intravenous administration of amiodarone or sotalol. The advantage of the second option is the possibility of achieving recovery of sinus rhythm and at the same time a rapid decrease in heart rate in the case of atrial fibrillation. In patients with obvious heart failure, a choice is made between two drugs: digoxin (iv administration of about 1 mg fractional doses) or amiodarone (iv 150-450 mg). All patients with atrial fibrillation are shown IV injection of heparin.

Bradyarrhythmias

Violation of the sinus node function and atrioventricular blockade is more often observed with myocardial infarction of the lower localization, especially in the first hours. Sinus bradycardia rarely presents any problems. When combined sinus bradycardia with severe hypotension ("bradycardia syndrome-hypotension") use intravenous atropine.

Atrioventricular (AV) blockades are also more common in patients with lower myocardial infarction.

On the ECG signs of acute coronary syndrome with the rise of the segment STII, III, aVF (in the leads I, aVL, V1-V5 there is reciprocal depression of the ST segment). The patient has a complete AV-blockade, the rhythm of AV-connection with a frequency of 40 per min.

The incidence of AV blockade of MI degree with lower myocardial infarction reaches 20%, and if there is concomitant myocardial infarction of the right ventricle - AV blockade is observed in 45-75% of patients. AV-blockade with myocardial infarction of the lower localization, as a rule, develops gradually: at first the prolongation of the PR interval, then the AV blockade of the II degree of the type I (Mobits-1, Samoilov-Wenckebach periodicals) and only after this - the complete AV blockade. Even complete AV blockade with lower myocardial infarction is almost always transient and lasts from several hours to 3-7 days (in 60% of patients - less than 1 day). However, the occurrence of AV blockade is a sign of a more pronounced lesion: hospital mortality in uncomplicated lower myocardial infarction is 2-10%, and in the event of AV blockade reaches 20% or more. The cause of death in this case is not the AV blockade itself, but cardiac insufficiency, due to a more extensive myocardial lesion.

On the ECG, the rise of the ST segment in leads II, III, aVF and in V1-V3 is recorded. Elevation of the ST segment in leads V1-V3 is a sign of right ventricular involvement. In the leads I, aVL, V4-V6, there is a reciprocal depression of the ST segment. The patient has a complete AV-blockade, the rhythm of the AV connection at a frequency of 30 per min (in the atria, a sinus tachycardia with a frequency of 100 / min).

In patients with lower myocardial infarction in the event of complete AV blockade, the slipping rhythm from the AV-connection, as a rule, provides full compensation, no significant violations of hemodynamics are usually noted. Therefore, in most cases, treatment is not required. With a sharp decrease in heart rate - less than 40 per min and the appearance of signs of circulatory insufficiency, intravenous atropine is used (0.75-1.0 mg, if necessary repeatedly, the maximum dose is 2-3 mg). Interest reports on the efficacy of IV in the administration of aminophylline (euphyllin) in AV blockade, resistant to atropine ("atropine-resistant" AV blockade). In rare cases, infusion of beta-2 stimulants may be required: adrenaline, isoproterenol, alupent, asthmopent or inhalation of beta-2 stimulants. The need for an electrocardiostimulation is extremely rare. Exceptions are cases of lower myocardial infarction involving the right ventricle, when right ventricular failure in combination with pronounced hypotension to stabilize hemodynamics may require conducting a two-chamber electrostimulation, tk. With myocardial infarction of the right ventricle it is very important to preserve the systole of the right atrium.

With myocardial infarction of the anterior location AV blockade II-III degree develops only in patients with very massive myocardial damage. At the same time, the AV blockade occurs at the level of the Gisa-Purkinje system. The prognosis in such patients is very poor - mortality reaches 80-90% (as in cardiogenic shock). The cause of death is heart failure, up to the development of cardiogenic shock or secondary ventricular fibrillation.

Precursors of the occurrence of AV blockade in anterior myocardial infarction are: the sudden appearance of the blockade of the right bundle of the bundle, the deviation of the electrical axis and the prolongation of the PR interval. In the presence of all three signs, the probability of occurrence of a complete AV blockade is about 40%. In cases of occurrence of these signs or registration of AV blockade II degree II (Mobits II), a prophylactic introduction of a stimulation probe-electrode into the right ventricle is indicated. A means of choice for the treatment of complete AV blockade at the level of branches of the bundle with a slow idioventricular rhythm and hypotension is temporary cardiostimulation. In the absence of a pacemaker, infusion of epinephrine (2-10 μg / min) is used, it is possible to use infusion of isadrin, astmopent or salbutamol at a rate that provides a sufficient increase in heart rate. Unfortunately, even in cases of AV-conduction recovery, the prognosis in such patients remains unfavorable, the lethality is significantly increased both during hospital stay and after discharge (according to some data, the mortality in the first year reaches 65%). True, in recent years there have been reports that after discharge from the hospital the fact of a transient complete AV blockade no longer affects the long-term prognosis of patients with anterior myocardial infarction.

[5], [6], [7], [8], [9], [10], [11], [12], [13], [14]

Conductivity disorders

Blockade of Mobitz type I (Wenkebach blockade, progressive lengthening of PR interval ) often develops with lower diaphragmatic myocardial infarction; she rarely progresses. A blockade of the Mobitz II type (rare contractions) usually indicates the presence of massive anterior myocardial infarction, as well as complete atrioventricular blockade with wide QRS complexes (atrial impulses do not reach the ventricles), but both types of blockages are infrequent. The incidence of complete (grade III) AV blockade depends on the localization of the infarction. Complete AV blockade occurs in 5-10% of patients with lower myocardial infarction and is usually transient. It occurs in less than 5% of patients with uncomplicated anterior myocardial infarction, but up to 26% with the same form of myocardial infarction, accompanied by blockage of the right or posterior branch of the left branch of the bundle.

A blockade of the Mobitz type I usually does not require treatment. In the case of a true blockade of the Mobitz type II low heart rate or with AB blockade with rare wide QRS complexes, a temporary pacemaker is used. You can use an external pacemaker before implanting a temporary pacemaker. Despite the fact that the administration of isoproterenol can temporarily restore the rhythm and heart rate, this approach is not used, since there is an increase in myocardial oxygen demand and the risk of arrhythmias. Atropine at a dose of 0.5 mg every 3-5 minutes until a total dose of 2.5 mg can be prescribed with AV blockade with a narrow ventricular complex and a small heart rate, but it is not recommended for AB blockade with the first wide ventricular complex.

[15], [16], [17], [18], [19], [20], [21], [22]

Ventricular arrhythmias

Most often, myocardial infarction is marked by ventricular extrasystole.

Until recently, ventricular extrasystole with myocardial infarction was given very great importance. The concept of so-called "preventive arrhythmias" was popular, according to which ventricular extrasystoles of high gradation (frequent, polymorphic, group and early - type "R to T") are precursors of ventricular fibrillation, and treatment of ventricular extrasystoles should help reduce the incidence of fibrillation. The concept of "preventive arrhythmias" was not confirmed. It has now been established that extrasystoles arising from myocardial infarction are themselves safe (they are even called "cosmetic arrhythmia") and are not precursors of ventricular fibrillation. And most importantly - treatment of extrasystole does not affect the incidence of ventricular fibrillation.

The recommendations of the American Heart Association for the Treatment of Acute Myocardial Infarction (1996) specifically emphasized that recording ventricular extrasystoles and even unstable ventricular tachycardia (including polymorphic ventricular tachycardia, up to 5 complexes) is not an indication for prescribing antiarrhythmic drugs (!). Negative prognostic value is the detection of frequent ventricular extrasystoles in 1-1.5 days from the beginning of myocardial infarction, tk. In these cases, ventricular extrasystoles are "secondary" and, as a rule, result from extensive lesion and severe left ventricular dysfunction ("markers of left ventricular dysfunction").

Unstable ventricular tachycardia

Unsustainable ventricular tachycardia is called episodes of ventricular tachycardia, lasting less than 30 seconds ("jogging" of tachycardia), not accompanied by hemodynamic disorders. Many authors, unstable ventricular tachycardia, as well as ventricular extrasystoles, are referred to as "cosmetic arrhythmias" (they are called "enthusiastic" slipping rhythms ").

Antiarrhythmic drugs are prescribed only for very frequent, usually group extrasystoles and unstable ventricular tachycardia, if they cause hemodynamic disorders with the onset of clinical symptoms or are subjectively very poorly tolerated by patients. The clinical situation with myocardial infarction is very dynamic, arrhythmias are often transient, and it is very difficult to assess the effectiveness of treatment. However, currently it is recommended to avoid the use of antiarrhythmic drugs of class I (with the exception of lidocaine), and in the presence of indications for antiarrhythmic therapy, preference is given to beta-blockers, amiodarone and, possibly, sotalol.

Lidocaine is administered intravenously - 200 mg for 20 minutes (usually with repeated boluses of 50 mg). If necessary, infusion is carried out at a rate of 1-4 mg / min. In the absence of the effect of lidocaine, beta-blockers or amiodarone are more often used. In Russia, currently the most available beta-blocker for intravenous administration is propranolol (obzidan). Obsidan with myocardial infarction is administered at a rate of 1 mg for 5 minutes. The dose was observed with an iv administration of 1 to 5 mg. If there is an effect, they switch to taking beta-blockers inside. Amiodarone (cordarone) is administered intravenously slowly in a dose of 150-450 mg. The rate of administration of amiodarone with prolonged infusion is 0.5-1.0 mg / min.

Stable ventricular tachycardia

The incidence of stable ventricular tachycardia (tachycardia, which does not pass spontaneously) reaches 15% in the acute period of myocardial infarction. In the case of severe hemodynamic disorders (cardiac asthma, hypotension, loss of consciousness), the method of choice is conducting electrical cardioversion with a discharge of 75-100 J. In a more stable state of hemodynamics, lidocaine or amiodarone is primarily used. Several studies have shown the advantage of amiodarone over lidocaine in the management of ventricular tachyarrhythmias. If the ventricular tachycardia continues, then with the preservation of stable hemodynamics one can continue the empirical selection of therapy, for example, to assess the effect of iv administration of oszydan, sotalol, magnesium sulfate or conduct a planned electrical cardioversion.

The interval between the administration of various drugs depends on the patient's condition and with good tolerability of the tachycardia, the absence of signs of ischemia and relatively stable hemodynamics ranges from 20-30 minutes to several hours.

For treatment of polymorphic ventricular tachycardia of the "pirouette" type, the drug of choice is magnesium sulfate - iv administration of 1-2 g for 2 min (if necessary again) and subsequent infusion at a rate of 10-50 mg / min. In the absence of the effect of magnesium sulfate in patients without prolonging the QT interval (in sinus complexes), the action of beta-blockers and amiodarone is evaluated. If there is an extension of the QT interval, electrocardiostimulation with a frequency of about 100 / min is used. It should be noted that in patients with acute myocardial infarction, even with prolongation of the QT interval, the use of beta-blockers and amiodarone may be effective in the treatment of pirouette-type tachycardia.

Ventricular fibrillation

It is known that approximately 50% of all cases of ventricular fibrillation occur in the first hour of myocardial infarction, 60% in the first 4 hours, 80% in the first 12 hours of myocardial infarction.

If you speed up calling an emergency doctor for 30 minutes, you can prevent about 9% of deaths from ventricular fibrillation due to timely defibrillation. This far exceeds the effect of thrombolytic therapy.

The incidence of ventricular fibrillation after admission of the patient to the intensive care unit is 4.5-7%. Unfortunately, less than 20% of patients enter the first hour, about 40% within 2 hours. Calculations show that if you accelerate the flow of patients for 30 minutes, approximately 9 patients out of 100 can be saved from fibrillation. Basically this is the so-called primary ventricular fibrillation (not associated with recurrence of myocardial infarction, ischemia and circulatory insufficiency).

The only effective method of treatment of ventricular fibrillation is the immediate conduct of electrical defibrillation. In the absence of a defibrillator, resuscitation during ventricular fibrillation is almost always unsuccessful, moreover, with every minute the probability of successful electric defibrillation decreases. The effectiveness of immediate electrical defibrillation with myocardial infarction is about 90%.

The prognosis in patients who underwent primary ventricular fibrillation, as a rule, is quite favorable and, according to some data, practically does not differ from the prognosis in patients with uncomplicated myocardial infarction. Ventricular fibrillation, occurring at a later date (after the first day), in most cases is secondary and usually occurs in patients with severe myocardial infarction, recurrent myocardial infarction, myocardial ischemia, or signs of heart failure. It should be noted that secondary ventricular fibrillation can be observed during the first day of myocardial infarction. An unfavorable prognosis is determined by the severity of myocardial damage. The incidence of secondary ventricular fibrillation is 2.2-7%, including 60% in the first 12 hours. In 25% of patients, secondary ventricular fibrillation is noted against a background of atrial fibrillation. The effectiveness of defibrillation in secondary fibrillation ranges from 20 to 50%, repeated episodes occur in 50% of patients, the mortality rate of patients in the hospital is 40-50%. There are reports that after discharge from the hospital, the presence in the history of even secondary ventricular fibrillation does not exert any additional influence on the prognosis.

Thrombolytic therapy allows a sharp (in dozens of times) to reduce the incidence of stable ventricular tachycardia and secondary ventricular fibrillation. Reperfusion arrhythmias do not present a problem, mostly frequent ventricular extrasystoles and accelerated idioventricular rhythm ("cosmetic arrhythmias") - an indicator of successful thrombolysis. Rarely occurring more serious arrhythmias tend to respond well to standard therapy. 

Heart failure

Patients with extensive myocardial infarction (according to ECG or serum markers) and violation of myocardial contractility, AH or diastolic dysfunction are more likely to develop heart failure. Clinical manifestations depend on the size of the infarction, increasing the filling pressure of the left ventricle, and the degree of reduction in cardiac output. Often there are shortness of breath, inspiratory wheezing in the lower parts of the lungs and hypoxemia.

Heart failure in myocardial infarction

The main cause of death of patients with myocardial infarction in hospital is acute heart failure: pulmonary edema and cardiogenic shock.

Clinical manifestations of acute left ventricular failure are shortness of breath, orthopnea, a feeling of lack of air, up to suffocation, increased sweating. With an objective examination, paleness, cyanosis, an increase in the frequency of breathing, and often the swelling of the cervical veins are noted. When auscultation - a variety of wheezing in the lungs (from creping to wet large bubbles), III tone (proto diastolic rhythm of the gallop), systolic noise. In most cases, sinus tachycardia and a decrease in blood pressure, a pulse of weak filling or a filiform pulse are noted.

In case of myocardial infarction, the classification of acute heart failure according to Killip is used: I class - there are no stagnant phenomena, II class - signs of moderate stagnant phenomena: wheezing in the lower parts of the lungs, listening to III tone or moderate right ventricular failure (swelling of the veins of the neck and enlargement of the liver), III class - pulmonary edema, class IV - cardiogenic shock.

Typical clinical manifestations of heart failure are observed with a sufficiently pronounced degree of circulatory failure, when it is "easier to diagnose than treat". Early detection of heart failure by clinical signs is a very difficult task (clinical manifestations at early stages are non-specific and do not accurately reflect the state of hemodynamics). Sinus tachycardia may be the only sign of compensated circulatory failure (compensation due to sinus tachycardia). The group of patients with an increased risk of circulatory failure includes patients with a common myocardial infarction of anterior localization, with repeated myocardial infarction, with AV blockades of II-III degree in the presence of lower myocardial infarction (or with signs of right ventricular involvement, with severe depression of the ST segment in anterior leads), patients with atrial fibrillation or severe ventricular arrhythmias, intraventricular conduction disorders.

Ideally, all patients with an increased risk or initial signs of heart failure should be treated with invasive monitoring of hemodynamics. For this purpose, it is most convenient to use the "floating" catheters of Swan-Ganz. After insertion of the catheter into the pulmonary artery, the so-called "wedging" pressure in the branches of the pulmonary artery or diastolic pressure in the pulmonary artery is measured. Using the thermodilution method, it is possible to calculate cardiac output. The use of invasive control of hemodynamics greatly facilitates the selection and conduct of therapeutic measures in acute heart failure. To ensure adequate hemodynamics in patients with acute myocardial infarction, the diastolic pressure in the pulmonary artery (reflecting the filling pressure of the left ventricle) should be in the range of 15 to 22 mm Hg. Art. (an average of about 20 mm). If the diastolic pressure in the pulmonary artery (DDLA) is less than 15 mm Hg. Art. (or even in the range of 15 to 18 mm) - the cause of circulatory failure or a factor contributing to its appearance, may be hypovolemia. In these cases, amid the introduction of fluid (plasma-substituting solutions), there is an improvement in hemodynamics and the state of patients. In case of cardiogenic shock, cardiac output decreases (cardiac index less than 1.8-2.0 l / min / m ² ) and increased left ventricular filling pressure (DDLA greater than 15-18 mm Hg if there is no concomitant hypovolemia). However, the situation in which there is the possibility of invasive hemodynamic control for most institutions of practical health care (especially in an ambulance environment) is indeed ideal, i.e. One that does not really exist.

With moderate cardiac insufficiency, clinically manifested by a slight shortness of breath, creping rales in the lower parts of the lungs, with normal or slightly elevated blood pressure, nitrates are used (nitroglycerin under the tongue, nitrates inwards). At this stage it is very important not to "heal", i.e. Do not cause an excessive decrease in the filling pressure of the left ventricle. Use the appointment of small doses of ACE inhibitors, less commonly used furosemide (lasix). Nitrates and ACE inhibitors have an advantage over diuretics - they reduce preload without decreasing the BCC.

The sequence of medical measures in the appearance of clinical signs of cardiac asthma or pulmonary edema:

• inhalation of oxygen,
• nitroglycerin (under the tongue repeatedly or intravenously),
• morphine (iv in 2-5 mg),
• Lasix (w / v of 20-40 mg and more),
• breathing with positive exhalation pressure,
• artificial ventilation.

Even with the unfolded clinical picture of pulmonary edema after sublingual administration of 2-3 nitroglycerin tablets there may be a noticeable positive effect after only 10 minutes. Instead of morphine, you can use other narcotic analgesics and / or relanium. Lasix (furosemide) for pulmonary edema in patients with myocardial infarction is used last, cautiously, starting at 20 mg if persistent shortness of breath persists, if necessary increasing the dose by 2 times with each repeated administration. When swelling of the lungs in patients with myocardial infarction, as a rule, there is no fluid retention, so when overdosage of lasix can develop pronounced hypovolemia and hypotension.

In some cases, it is enough to use only one of the drugs (most often nitroglycerin), sometimes you have to inject all 3 drugs almost simultaneously, without waiting for the appearance of the effect of each drug separately. Inhalation of oxygen is carried out with moisturizing, passing through sterile water or alcohol. At the expressed foam formation it is possible to pierce a trachea with a thin needle and to enter 2-3 ml of 96 ° alcohol.

When there is a pulmonary edema against a background of increased blood pressure, the treatment measures are almost the same as with normal blood pressure. However, with a sharp increase in blood pressure or the preservation of high blood pressure, in spite of the introduction of nitroglycerin, morphine and lasix, additionally use droperidol, pentamine, sodium nitroprusside infusion.

Swelling of the lungs against the background of a decrease in blood pressure - an especially difficult condition. This is a cardiogenic shock with a predominance of symptoms of stagnation in the lungs. In these cases, nitroglycerin, morphine and lasix are used in reduced doses on the background of infusion of inotropic and vasopressor drugs: dobutamine, dopamine or norepinephrine. With a slight decrease in blood pressure (about 100 mm Hg), one can start with the infusion of dobutamine (from 200 μg / min, if necessary, increasing the injection rate to 700-1000 μg / min). With a sharper decrease in blood pressure, dopamine is used (150-300 μg / min). An even more pronounced decrease in blood pressure (less than 70 mm Hg) shows the administration of noradrenaline (from 2-4 μg / min to 15 μg / min) or intra-aortic balloon counterpulsation. Glucocorticoid hormones with cardiogenic pulmonary edema are not shown.

Treatment depends on the severity. With moderately severe heart failure, loop diuretics are prescribed (for example, furosemide 20 to 40 mg intravenously once a day) to reduce the filling pressure of the ventricles, and this is often enough. In severe cases, vasodilators (eg, intravenous nitroglycerin) are used to reduce pre- and post-loading; During treatment, pulmonary artery wedge pressure is often measured by catheterization of the right heart chambers (using the Swan-Ganz catheter). ACE inhibitors are used as long as systolic blood pressure remains above 100 mm Hg. Art. For the initiation of therapy, it is preferable to use ACE inhibitors of short duration in small doses (for example, captopril at 3,125-6,25 mg every 4-6 hours, increasing the dose for tolerability). As soon as the maximum dose is reached (maximum for captopril is 50 mg 2 times a day), an ACE inhibitor of a longer duration (eg, fosinopril, lisinopril, ramipril) is prescribed for a long time. If heart failure persists at the level of NYHA functional class II or higher, an aldosterone antagonist (eg, eplerenone or spironolactone) should be added. In severe heart failure, intra-arterial balloon counter-pulsation is used to provide temporary hemodynamic support. In those cases where it is impossible to perform revascularization or surgical correction, consider the question of heart transplantation. Long-term left ventricular or biventricular implantable devices can be used prior to transplantation; if heart transplant is not possible, these auxiliary devices sometimes apply as a permanent method of treatment. Sometimes the use of such devices leads to the restoration of the functions of the ventricles, and the device can be removed after 3-6 months.

If heart failure leads to the development of hypoxemia, oxygen inhalation is prescribed through the nasal catheters (to maintain pO at a level of approximately 100 mmHg). This can promote oxygenation of the myocardium and limiting the area of ischemia.

Lesions of papillary muscles

Functional deficiency of papillary muscles occurs in approximately 35% of patients during the first few hours of a heart attack. Ischemia of the papillary muscles leads to incomplete closure of the valves of the mitral valve, which then passes in the majority of patients. However, in some patients the appearance of scarring in the papillary muscles or the free wall of the heart leads to a constant mitral regurgitation. Functional deficiency of the papillary muscles is manifested by late systolic noise and usually disappears without treatment.

The rupture of the papillary muscle most often occurs with lower-back myocardial infarction associated with occlusion of the right coronary artery. This leads to the appearance of acute expressed mitral regurgitation. The rupture of the papillary muscle is characterized by the sudden appearance of loud, holosystolic murmur and jitter at the apex, usually with pulmonary edema. In some cases, when regurgitation does not cause intense auscultative symptoms, but clinically suspect a complication, echocardiography is performed. An effective method of treatment is plastic or replacement of the mitral valve.

Myocardial rupture

A rupture of the interventricular septum or free ventricular wall occurs in 1% of patients with acute myocardial infarction and causes 15% of hospital mortality.

The rupture of the interventricular septum, also a rare complication, occurs 8-10 times more often than the rupture of the papillary muscle. The rupture of the interventricular septum is characterized by the sudden appearance of loud systolic murmur and jitter, determined at the level from the middle to the apex of the heart, along the left edge of the sternum at the level of the third and fourth intercostal spaces, accompanied by arterial hypotension with signs of left ventricular failure or without them. The diagnosis can be confirmed by using balloon catheter catheterization and comparing the saturation of O2 or pO2 in the right atrium, the right ventricle and the pulmonary artery. The significant increase in pO2 in the right ventricle is diagnostic as significant as the data of Doppler echocardiography. The treatment is surgical, it should be delayed for 6 weeks after myocardial infarction, since the maximum healing of the damaged myocardium is necessary. If persistent hemodynamic instability persists, earlier surgical intervention is performed, despite the high risk of mortality.

The frequency of ruptures of the free wall of the ventricle increases with age, more often such a break occurs in women. This complication is characterized by a sudden drop in blood pressure with the preservation of sinus rhythm and (often) signs of cardiac tamponade. Surgical treatment is rarely successful. The rupture of a free wall is almost always fatal.

Aneurysm of the ventricle

Limited vyhuhanie walls of the ventricle, often the left, can occur in the zone of extensive myocardial infarction. Aneurysm of the ventricle often occurs with large transmural myocardial infarctions (usually the anterior ones). Aneurysm can develop several days, weeks or months after myocardial infarction. Rupture of aneurysms occurs rarely, but they can lead to recurrent ventricular arrhythmias, low cardiac output, and parietal thrombosis with systemic embolism. Ventricular aneurysms are suspected when paradoxical movements are detected in the precordial region. The ECG demonstrates a constant rise in the ST segment , and a chest X-ray reveals a characteristic bulge of the cardiac shadow. Echocardiography is performed to confirm the diagnosis and to identify thrombi. In the presence of left ventricular failure or arrhythmia, surgical excision can be prescribed. The use of ACE inhibitors during acute myocardial infarction reduces myocardial remodeling and can reduce the incidence of aneurysms.

Pseudoaneurysm is an incomplete rupture of the free wall of the left ventricle, limited to the pericardium. Pseudoaneurysms almost always contain thrombi and are often completely ruptured. Treatment is performed surgically.

[23], [24], [25], [26]

Arterial hypotension and cardiogenic shock

Arterial hypotension may be due to a decreased filling of the ventricles or a decrease in the force of contraction due to extensive myocardial infarction. Significant arterial hypotension (systolic BP <90 mm Hg) with tachycardia and signs of insufficient blood supply to peripheral organs (decreased urine output, impaired consciousness, excessive sweating, cold extremities) is called cardiogenic shock. With cardiogenic shock, pulmonary edema develops rapidly.

The decrease in the left ventricle filling is most often caused by the reduced venous return caused by hypovolemia, especially in patients receiving intensive therapy with loop diuretics, however it can be a sign of myocardial infarction of the right ventricle. Pronounced pulmonary edema indicates a loss of strength of the contractions of the left ventricle (left ventricular failure), which caused shock. Treatment depends on the cause of this condition. Some patients need a catheterization of the pulmonary artery to measure intracardiac pressure to determine the cause. If the pulmonary artery wedge pressure is below 18 mmHg, more likely a reduction in filling associated with hypovolemia; if the pressure is above 18 mm Hg. St., Left ventricular failure is likely. With arterial hypotension associated with hypovolemia, careful substitution therapy with 0.9% sodium chloride solution is possible without the development of an overload of the left chambers of the heart (excessive pressure increase in the left atrium). However, sometimes the functioning of the left ventricle is so changed that fluid recovery sharply increases the pulmonary artery wedge pressure to a level characteristic for pulmonary edema (> 25 mm Hg). If the pressure in the left atrium is high, arterial hypotension is probably associated with a deficiency of the left ventricle, and with ineffectiveness of diuretics, inotropic therapy or support of adequate blood circulation may be required.

In cardiogenic shock, a- or b-agonists may be temporarily effective. Dopamine, catecholamine, which acts on receptors and is prescribed in a dose of 0.5-1 μg / kg per minute with an increase to a satisfactory response or until a dose of approximately 10 μg / kg per minute is achieved. Higher doses stimulate vasoconstriction and cause atrial and ventricular arrhythmias. Dobutamine, a-agonist, can be administered intravenously at a dose of 2.5-10 μg / kg per minute or more. This often leads to the development of arterial hypotension or strengthens it. The appointment is most effective when hypotension is caused by a low cardiac output with a high peripheral vascular resistance. Dopamine can be more effective than dobutamine, when a vasopressor effect is needed. In refractory cases, a combination of dopamine and dobutamine may be used. Intra-aortic balloon counterpulsation can be used as a temporary measure. Directed lysis of the thrombus, angioplasty or emergency CABG can significantly improve the function of the ventricle. NOVA or CABG is treated with persistent ischemia, refractory ventricular arrhythmia, hemodynamic instability or shock, if the anatomical features of the arteries allow it.

[27], [28], [29]

Ischemia or myocardial infarction of the right ventricle

Approximately half of patients with lower myocardial infarction have right ventricular involvement, including 15-20% hemodynamically significant. Clinically, such patients experience hypotension or shock in combination with signs of venous congestion in a large circle: swelling of the veins of the neck, enlargement of the liver, peripheral edema (signs of venous stasis may be absent with concomitant hypovolemia and appear after infusion of fluid). "Classical triad of myocardial infarction of the right ventricle": swelling of the cervical veins, absence of stagnation in the lungs and hypotension. In addition, pronounced dyspnea without orthopnea is noted. The clinical picture resembles a cardiac tamponade, constrictive pericarditis, pulmonary artery thromboembolism. With myocardial infarction of the right ventricle, AV blockade of II-III degree and atrial fibrillation occur more often. One of the signs of involvement of the right ventricle is a sharp decrease in blood pressure, down to syncope, when taking nitroglycerin.

On ECG-signs of myocardial infarction, usually lower localization, and in the lead V1 and in the right thoracic leads (VR4-R6), the rise of the ST segment is recorded. In the case of involvement of the posterior-basal parts of the left ventricle in leads V1-V2, depression of the ST segment and an increase in the height of the R wave are observed. When the right heart is probing, there is an increase in pressure in the right atrium and ventricle (diastolic more than 10 mm Hg). With echocardiography, there is a violation of contractility and an increase in the size of the right ventricle, a lack of significant effusion in the pericardial cavity and tamponade.

The main way to treat hypotension with myocardial infarction of the right ventricle is IV injection of fluid ("volume-dependent myocardial infarction"). Infusion of plasma-substituting solutions (saline solution, rheopolyglucin) is carried out at a rate providing an increase in diastolic pressure in the pulmonary artery up to 20 mm Hg. Art. Or blood pressure to 90-100 mm Hg. Art. (with signs of venous congestion in the large circle and CVP increasing) - the only "driving force" in myocardial infarction of the right ventricle - increased pressure in the right atrium. The first 500 ml is injected with a bolus. In some cases it is necessary to introduce several liters of plasma-substituting solutions - up to 1-2 liters in 1-2 hours (according to one of the cardiologists: "it is necessary to pour the liquid, down to the anasarca").

When signs of stagnation in the lungs appear, the rate of infusion is reduced or the introduction of plasma-substituting solutions is stopped. If the effect of infusion of the liquid is insufficient, dobutamine (dopamine or norepinephrine) is added to the treatment. In the most severe cases, intraaortic counterpulsation is used.

Contraindicated appointment vasodilators (including nitroglycerin and narcotic analgesics) and diuretics. Under the influence of these drugs, there is a sharp decrease in blood pressure. Increased sensitivity to the action of nitrates, morphine and diuretics is a diagnostic sign of myocardial infarction of the right ventricle. The most effective way to treat myocardial infarction with right ventricular involvement is to restore coronary blood flow (thrombolytic therapy or surgical revascularization). The prognosis for correct treatment of patients with myocardial infarction of the right ventricle is generally quite favorable in most cases, improvement in the function of the right ventricle is noted in the first 2-3 days, and signs of stagnation in the large circle usually disappear within 2-3 weeks. With proper treatment, the prognosis depends on the condition of the left ventricle.

A severe and, unfortunately, often observed complication of myocardial infarction of the right ventricle is a complete AV blockade. In these cases, it may be necessary to carry out a two-chamber electrocardiostimulation, since with right ventricular myocardial infarction, it is very important to maintain an effective systole of the right atrium. In the absence of the possibility of two-chamber pacing, intravenous euphyllin and ventricular electrostimulation are used.

Thus, the detection and timely correction of three curable states: reflex hypotension, hypovolemia and myocardial infarction of the right ventricle allows to achieve significant improvement in this group of patients even in the clinical picture of shock. Equally important is the fact that improper treatment, such as the use of vasopressors with hypovolemia, vasodilators or diuretics in myocardial infarction of the right ventricle, is often the cause of the acceleration of death.

Continuing ischemia

Any chest pain that persists or recurs within 12-24 hours after myocardial infarction may be a manifestation of ongoing ischemia. Postinfarction ischemic pain indicates that there is a risk of developing a heart attack of large areas of the myocardium. Usually, ongoing ischemia can be identified by reversible changes in the ST-T interval on an electrocardiogram; it is possible to increase blood pressure. However, since ongoing ischemia can be painless (ECG data changes in the absence of pain syndrome), approximately one third of patients usually receive an ECG series every 8 hours on the first day and then daily. With ongoing ischemia, treatment is similar to unstable angina. The intake of nitroglycerin under the tongue or intravenously is usually effective. To preserve ischemic myocardium, it is advisable to consider the question of coronary angioplasty and NOVA or CABG.

[30], [31], [32], [33]

Pristenochny thrombosis

Near-wall thrombosis develops in approximately 20% of patients with acute myocardial infarction. Systemic embolism is detected in approximately 10% of patients with thrombi in the left ventricle. The risk is highest in the first 10 days, but it persists for at least 3 months. The highest risk (more than 60%) in patients with extensive anterior myocardial infarction (especially involving distal parts of the interventricular septum and apex), an enlarged left ventricle, common areas of hypokinesia, or a constant ciliary arrhythmia. To reduce the risk of embolism, anticoagulants are prescribed. In the absence of contraindications, intravenous intravenous heparin is administered, intravenously administered warfarin for 3-6 months with maintenance of MHO between 2 and 3. Anticoagulant therapy is carried out for a long time if the patient has advanced with advanced areas of left ventricular hypokinesia, left ventricular aneurysm or constant atrial fibrillation. Also, long-term use of acetylsalicylic acid.

Pericarditis

Pericarditis develops due to the spread of myocardial necrosis through the ventricular wall to the epicardium. This complication develops in approximately one third of patients with acute transmural myocardial infarction. Friction noise pericardium usually appears from 24 to 96 hours after the onset of myocardial infarction. Earlier appearance of friction noise is unusual, although hemorrhagic pericarditis sometimes complicates the early stage of myocardial infarction. Acute tamponade is rare. Pericarditis is diagnosed with an ECG that demonstrates the diffuse rise of the STn segment (sometimes) the depression of the PR interval . Echocardiography is performed often, but usually the data is normal. Sometimes a small amount of fluid is detected in the pericardium or even an asymptomatic tamponade. The intake of acetylsalicylic acid or other NSAIDs usually reduces manifestations. High doses or a durable use of NSAIDs or glucocorticoids can inhibit the healing of the infarction, which must be taken into account.

Postinfarction syndrome (Dressler's syndrome)

Postinfarction syndrome develops in some patients in a few days, weeks or even months after an acute myocardial infarction. In recent years, the frequency of its development has been decreasing. The syndrome is characterized by fever, pericarditis with pericardial friction noise, the appearance of fluid in the pericardium, pleurisy, fluid in the pleural cavity, pulmonary infiltrates and common pain. This syndrome is caused by an autoimmune reaction to the necrotic tissue of the myocytes. It can be repeated. Differential diagnosis of postinfarction syndrome with the progression or repetition of myocardial infarction can be difficult. However, with postinfarction syndrome there is no noticeable increase in the number of cardiospecific markers, and ECG data changes are undefined. NSAIDs are usually effective, but the syndrome can be repeated several times. In severe cases, a short intensive course of another NSAID or glucocorticoid may be required. High doses of NSAIDs or glucocorticoids are not used for longer than a few days, as they may interfere with early healing of the ventricle after acute myocardial infarction.