Myocardial infarction: complications

Electrical dysfunction occurs in more than 90% of patients with myocardial infarction. Electrical dysfunction that usually causes death within 72 hours includes tachycardia (from any source) with a heart rate high enough to decrease cardiac output and lower blood pressure, Mobitz type II (2nd degree) or complete (3rd degree) atrioventricular block, ventricular tachycardia (VT), and ventricular fibrillation (VF).

Asystole is rare except in extreme cases of progressive left ventricular failure and shock. Patients with cardiac arrhythmia should be evaluated for hypoxia and electrolyte disturbances, which may be either the cause or a contributing factor.

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Sinus node dysfunction

Sinus node dysfunction may develop if the artery supplying the sinus node is affected. This complication is more likely if there is previous sinus node damage (common in the elderly). Sinus bradycardia, the most common sinus node dysfunction, usually does not require treatment unless there is arterial hypotension or a heart rate < 50 bpm. A lower heart rate, although not critical, reduces the workload of the heart and helps to reduce the infarction area. In bradycardia with arterial hypotension (which can reduce myocardial blood supply), atropine 0.5 to 1 mg intravenously is used; if the effect is insufficient, the administration can be repeated after 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 an ominous sign, often indicating left ventricular failure and low cardiac output. In the absence of left ventricular failure or other obvious cause, this type of arrhythmia may respond to intravenous or oral beta-blockers, depending on the degree of urgency.

Atrial arrhythmias

Atrial rhythm disturbances (atrial extrasystole, atrial fibrillation, and less commonly 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 occurs in patients who have had similar episodes before. Atrial extrasystole is usually benign, but it is believed that an increase in frequency may lead to the development of heart failure. Frequent atrial extrasystole may be sensitive to the administration of beta-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, previous large myocardial infarction, atrial infarction, pericarditis, hypokalemia, hypomagnesemia, chronic lung disease, and hypoxia. Fibrinolytic agents reduce the incidence of this complication. Recurrent paroxysms of atrial fibrillation are a poor prognostic factor, increasing the risk of systemic embolism.

In atrial fibrillation, sodium heparin is usually prescribed because of the risk of systemic embolism. Intravenous beta-blockers (eg, atenolol 2.5 to 5.0 mg over 2 min to a full dose of 10 mg over 10 to 15 min, metoprolol 2 to 5 mg every 2 to 5 min to a full dose of 15 mg over 10 to 15 min) slow the ventricular rate. Careful monitoring of heart rate and blood pressure is necessary. Treatment is stopped if heart rate drops significantly or systolic blood pressure is < 100 mm Hg. Intravenous digoxin (less effective than beta-blockers) is used cautiously and only in patients with atrial fibrillation and left ventricular systolic dysfunction. It usually takes about 2 h for heart rate to decrease with digoxin. In patients without obvious left ventricular systolic dysfunction or conduction disturbances manifested by a wide QRS complex, intravenous verapamil or diltiazem may be considered. The latter drug can be given intravenously to maintain a normal heart rate over a long period of time.

If atrial fibrillation compromises the systemic circulation (eg, causing left ventricular failure, hypotension, or chest pain), emergency cardioversion is indicated. If atrial fibrillation recurs after cardioversion, intravenous amiodarone should be considered.

In atrial flutter, heart rate is monitored in the same way as in atrial fibrillation, but sodium heparin is not administered.

Of the supraventricular tachyarrhythmias (excluding sinus tachycardia), atrial fibrillation is most often observed in the acute period of myocardial infarction - in 10-20% of patients. All other variants of supraventricular tachycardia during myocardial infarction are very rare. If necessary, standard treatment measures are carried out.

Early atrial fibrillation (in the first 24 hours after myocardial infarction) is usually transient and is associated with atrial ischemia and epistenocardic pericarditis. Later onset of atrial fibrillation is in most cases due to left atrium distension in patients with left ventricular dysfunction (arrhythmia of heart failure). In the absence of significant hemodynamic disturbances, atrial fibrillation does not require treatment. In the presence of significant hemodynamic disturbances, the method of choice is emergency electrical cardioversion. In a more stable condition, there are 2 options for patient management: (1) slowing the heart rate in the tachystolic form to an average of 70 bpm using intravenous beta-blockers, digoxin, verapamil, or diltiazem; (2) attempting to restore sinus rhythm using intravenous amiodarone or sotalol. The advantage of the second option is the possibility of achieving restoration of sinus rhythm and simultaneously rapid slowing of heart rate in case of persistence of atrial fibrillation. In patients with obvious heart failure, the choice is made between two drugs: digoxin (IV administration of about 1 mg in fractional doses) or amiodarone (IV 150-450 mg). All patients with atrial fibrillation are indicated for IV administration of heparin.

Bradyarrhythmia

Sinus node dysfunction and atrioventricular blocks are more often observed in myocardial infarction of the lower localization, especially in the first hours. Sinus bradycardia rarely presents any problems. In combination with sinus bradycardia and severe hypotension ("bradycardia-hypotension syndrome"), intravenous atropine is used.

Atrioventricular (AV) blocks are also more often recorded in patients with inferior myocardial infarction.

The ECG shows signs of acute coronary syndrome with ST segment elevation II, III, aVF (reciprocal ST segment depression is noted in leads I, aVL, V1-V5). The patient has complete AV block, AV junctional rhythm with a frequency of 40 bpm.

The incidence of grade II-III AV block in inferior myocardial infarction reaches 20%, and if there is a concomitant right ventricular myocardial infarction, AV block is observed in 45-75% of patients. AV block in inferior myocardial infarction, as a rule, develops gradually: first, prolongation of the PR interval, then grade II AV block type I (Mobitz-1, Samoilov-Wenckebach periodicity), and only after that - complete AV block. Even complete AV block in inferior 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 block is a sign of a more severe lesion: hospital mortality in uncomplicated inferior myocardial infarction is 2-10%, and in the case of AV block it reaches 20% or more. The cause of death in this case is not the AV block itself, but heart failure, due to more extensive myocardial damage.

The ECG shows ST segment elevation in leads II, III, aVF and V1-V3. ST segment elevation in leads V1-V3 is a sign of right ventricular involvement. Reciprocal ST segment depression is noted in leads I, aVL, V4-V6. The patient has complete AV block, AV junctional rhythm with a frequency of 30 bpm (sinus tachycardia in the atria with a frequency of 100 bpm).

In patients with inferior myocardial infarction, in the event of complete AV block, the escape rhythm from the AV junction, as a rule, ensures complete compensation, and significant hemodynamic disturbances are usually not observed. Therefore, treatment is not required in most cases. In case of a sharp decrease in heart rate - less than 40 bpm and the occurrence of signs of circulatory failure, intravenous atropine is used (0.75-1.0 mg, repeated if necessary, the maximum dose is 2-3 mg). Of interest are reports on the effectiveness of intravenous administration of aminophylline (euphylline) in AV blocks resistant to atropine ("atropine-resistant" AV blocks). In rare cases, infusion of beta-2-stimulants may be required: adrenaline, isoproterenol, alupent, astmopent or inhalation of beta-2-stimulants. The need for electrical cardiac pacing occurs extremely rarely. An exception is cases of inferior myocardial infarction involving the right ventricle, when, in the case of right ventricular failure combined with severe hypotension, dual-chamber electrical stimulation may be required to stabilize hemodynamics, since in the case of right ventricular myocardial infarction, it is very important to maintain right atrial systole.

In anterior myocardial infarction, grade II-III AV block develops only in patients with very massive myocardial damage. In this case, AV block occurs at the level of the His-Purkinje system. The prognosis for 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.

The precursors of AV block in anterior myocardial infarction are: sudden onset of right bundle branch block, axis deviation, and prolongation of the PR interval. In the presence of all three signs, the probability of complete AV block is about 40%. In cases of these signs or registration of type II (Mobitz II) AV block, prophylactic insertion of a stimulating probe electrode into the right ventricle is indicated. The drug of choice for the treatment of complete AV block at the level of the bundle branches of His with a slow idioventricular rhythm and hypotension is temporary electrical pacing. In the absence of a pacemaker, adrenaline infusion (2-10 mcg/min) is used; isadrine, astmopent, or salbutamol infusion may be used at a rate that ensures a sufficient increase in heart rate. Unfortunately, even in cases of restoration of AV conduction, the prognosis for such patients remains unfavorable, mortality is significantly increased both during hospital stay and after discharge (according to some data, mortality during the first year reaches 65%). However, in recent years there have been reports that after discharge from hospital, the fact of transient complete AV block no longer affects the long-term prognosis of patients with anterior myocardial infarction.

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

Conduction disturbances

Mobitz type I block (Wenckebach block, progressive prolongation of the PR interval) often develops in inferior diaphragmatic myocardial infarction; it rarely progresses. Mobitz type II block (sparse beats) usually indicates the presence of massive anterior myocardial infarction, as does complete atrioventricular block with wide QRS complexes (atrial impulses do not reach the ventricles), but both types of blocks are uncommon. The frequency of complete (grade III) AV blocks depends on the location of the infarction. Complete AV block occurs in 5-10% of patients with inferior myocardial infarction and is usually transient. It occurs in less than 5% of patients with uncomplicated anterior myocardial infarction, but up to 26% in the same type of myocardial infarction accompanied by right or left posterior fascicle block.

Mobitz type I block usually does not require treatment. In the case of true Mobitz type II block with low heart rate or in AV block with rare wide QRS complexes, a temporary pacemaker is used. An external pacemaker can be used until a temporary pacemaker is implanted. Although the administration of isoproterenol can temporarily restore the rhythm and heart rate, this approach is not used because it increases the myocardial oxygen demand and the risk of developing arrhythmias. Atropine at a dose of 0.5 mg every 3-5 minutes to a full dose of 2.5 mg can be prescribed for AV block with a narrow ventricular complex and a slow heart rate, but it is not recommended for AV block with a new-onset wide ventricular complex.

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

Ventricular arrhythmias

Most often, ventricular extrasystole is observed during myocardial infarction.

Until recently, ventricular extrasystoles in myocardial infarction were considered very important. The concept of so-called "warning arrhythmias" was popular, according to which high-grade ventricular extrasystoles (frequent, polymorphic, grouped, and early - "R on T" type) are precursors of ventricular fibrillation, and treatment of ventricular extrasystoles should help reduce the incidence of fibrillation. The concept of "warning arrhythmias" has not been confirmed. It has now been established that extrasystoles that occur in myocardial infarction are safe in themselves (they are even called "cosmetic arrhythmia") and are not precursors of ventricular fibrillation. And most importantly, treatment of extrasystoles does not affect the incidence of ventricular fibrillation.

The American Heart Association's guidelines for the treatment of acute myocardial infarction (1996) specifically emphasized that the recording of ventricular extrasystoles and even unstable ventricular tachycardia (including polymorphic ventricular tachycardia lasting up to 5 complexes) is not an indication for prescribing antiarrhythmic drugs (!). The detection of frequent ventricular extrasystoles 1-1.5 days after the onset of myocardial infarction has a negative prognostic value, since in these cases ventricular extrasystoles are "secondary" and, as a rule, occur as a result of extensive damage and pronounced dysfunction of the left ventricle ("markers of left ventricular dysfunction").

Non-sustained ventricular tachycardia

Unstable ventricular tachycardia is defined as episodes of ventricular tachycardia lasting less than 30 s (tachycardia "runs"), not accompanied by hemodynamic disturbances. Many authors classify unstable ventricular tachycardia, as well as ventricular extrasystole, as "cosmetic arrhythmias" (they are called "enthusiastic" escape rhythms).

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

Lidocaine is administered intravenously - 200 mg over 20 minutes (usually in repeated boluses of 50 mg). If necessary, an infusion is performed at a rate of 1-4 mg / min. If lidocaine is ineffective, beta-blockers or amiodarone are more often used. In Russia, the most accessible beta-blocker for intravenous administration is currently propranolol (obzidan). Obzidan for myocardial infarction is administered at a rate of 1 mg over 5 minutes. The dose of obzidan for intravenous administration is from 1 to 5 mg. If there is an effect, beta-blockers are switched to orally. Amiodarone (cordarone) is administered intravenously slowly at a dose of 150-450 mg. The rate of administration of amiodarone during prolonged infusion is 0.5-1.0 mg / min.

Sustained ventricular tachycardia

The incidence of sustained ventricular tachycardia (tachycardia that does not resolve spontaneously) in the acute period of myocardial infarction reaches 15%. In case of severe hemodynamic disturbances (cardiac asthma, hypotension, loss of consciousness), the method of choice is electrical cardioversion with a discharge of 75-100 J. In a more stable hemodynamic state, lidocaine or amiodarone are used first. Several studies have shown the advantage of amiodarone over lidocaine in stopping ventricular tachyarrhythmias. If ventricular tachycardia continues, then with stable hemodynamics, empirical selection of therapy can be continued, for example, assess the effect of intravenous administration of obsidan, sotalol, magnesium sulfate, or perform planned electrical cardioversion.

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

For the treatment of polymorphic ventricular tachycardia of the "pirouette" type, the drug of choice is magnesium sulfate - intravenous administration of 1-2 g over 2 minutes (repeated if necessary) and subsequent infusion at a rate of 10-50 mg / min. If there is no effect from magnesium sulfate in patients without prolongation of the QT interval (in sinus complexes), the effect of beta-blockers and amiodarone is assessed. In the presence of prolongation of the QT interval, electrical cardiac pacing is used at a frequency of about 100 / min. It should be noted that in patients with acute myocardial infarction, even with prolongation of the QT interval, beta-blockers and amiodarone can be effective in the treatment of tachycardia of the "pirouette" type.

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 can speed up the call to an ambulance doctor by 30 minutes, you can prevent about 9% of deaths from ventricular fibrillation due to timely defibrillation. This is much greater than the effect of thrombolytic therapy.

The incidence of ventricular fibrillation after admission to the intensive care unit is 4.5-7%. Unfortunately, less than 20% of patients are admitted within the first hour, and about 40% within 2 hours. Calculations show that if we accelerate the admission of patients by 30 minutes, we can save about 9 patients out of 100 from fibrillation. This is mainly the so-called primary ventricular fibrillation (not associated with recurrent myocardial infarction, ischemia, and circulatory failure).

The only effective method of treating ventricular fibrillation is immediate electrical defibrillation. In the absence of a defibrillator, resuscitation measures for ventricular fibrillation are almost always unsuccessful, moreover, the probability of successful electrical defibrillation decreases with each passing minute. The effectiveness of immediate electrical defibrillation for myocardial infarction is about 90%.

The prognosis for patients who have had primary ventricular fibrillation is usually quite favorable and, according to some data, is virtually no different from the prognosis for patients with uncomplicated myocardial infarction. Ventricular fibrillation that occurs later (after the first day) is secondary in most cases and usually occurs in patients with severe myocardial damage, recurrent myocardial infarctions, myocardial ischemia, or signs of heart failure. It should be noted that secondary ventricular fibrillation can also be observed during the first day of myocardial infarction. The 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 observed against the background of atrial fibrillation. The effectiveness of defibrillation in secondary fibrillation ranges from 20 to 50%, repeated episodes occur in 50% of patients, and the mortality rate of patients in hospital is 40-50%. There are reports that after discharge from hospital, even a history of secondary ventricular fibrillation no longer has an additional effect on the prognosis.

Conducting thrombolytic therapy allows to reduce sharply (by tens of times) the incidence of stable ventricular tachycardia and secondary ventricular fibrillation. Reperfusion arrhythmias are not a problem, mainly frequent ventricular extrasystoles and accelerated idioventricular rhythm ("cosmetic arrhythmias") - an indicator of successful thrombolysis. Rarely occurring more serious arrhythmias, as a rule, respond well to standard therapy.

Heart failure

Patients with extensive myocardial infarction (as determined by ECG or serum markers) and impaired myocardial contractility, hypertension, or diastolic dysfunction are more likely to develop heart failure. Clinical manifestations depend on the size of the infarction, the increase in left ventricular filling pressure, and the degree of decrease in cardiac output. Dyspnea, inspiratory wheezing in the lower lungs, and hypoxemia are common.

Heart failure in myocardial infarction

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

Clinical manifestations of acute left ventricular failure are dyspnea, orthopnea, a feeling of lack of air, up to suffocation, increased sweating. During an objective examination, pallor, cyanosis, increased respiratory rate, and often swelling of the jugular veins are noted. During auscultation, various wheezing in the lungs (from crepitant to moist large-bubble), the third tone (protodiastolic gallop rhythm), systolic murmur are noted. In most cases, sinus tachycardia and decreased blood pressure, a weak or threadlike pulse are noted.

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

Characteristic clinical manifestations of heart failure are observed at a sufficiently pronounced degree of circulatory failure, when it is "easier to diagnose than to treat". Early detection of heart failure by clinical signs is a very difficult task (clinical manifestations in the early stages are nonspecific and do not very 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 widespread myocardial infarction of the anterior localization, with repeated myocardial infarction, with AV blocks of II-III degree in the presence of inferior myocardial infarction (or with signs of right ventricular involvement, with pronounced depression of the ST segment in the anterior leads), patients with atrial fibrillation or pronounced ventricular arrhythmias, intraventricular conduction disorders.

Ideally, all patients with increased risk or initial signs of heart failure should undergo invasive hemodynamic monitoring. The most convenient method for this purpose is to use a floating Swan-Ganz catheter. After inserting the catheter into the pulmonary artery, the so-called "wedge" pressure in the branches of the pulmonary artery or diastolic pressure in the pulmonary artery is measured. Using the thermodilution method, cardiac output can be calculated. The use of invasive hemodynamic monitoring significantly facilitates the selection and implementation of therapeutic measures in acute heart failure. To ensure adequate hemodynamics in patients with acute myocardial infarction, the diastolic pressure in the pulmonary artery (reflects the filling pressure of the left ventricle) should be in the range of 15 to 22 mm Hg (on average, about 20 mm). If the diastolic pressure in the pulmonary artery (DPPA) is less than 15 mm Hg, then the diastolic pressure in the pulmonary artery (DPPA) is less than 15 mm Hg. (or even within the range of 15 to 18 mm) - the cause of circulatory failure or a factor contributing to its occurrence may be hypovolemia. In these cases, against the background of the introduction of fluid (plasma-substituting solutions), an improvement in hemodynamics and the condition of patients is noted. In cardiogenic shock, a decrease in cardiac output (cardiac index less than 1.8-2.0 l/min/ ^m2 ) and an increase in left ventricular filling pressure (DPLA more than 15-18 mm Hg, if there is no concomitant hypovolemia) are noted. However, the situation in which there is a possibility of invasive hemodynamic monitoring for most practical healthcare institutions (especially in emergency care conditions) is really ideal, i.e. one that does not exist in reality.

In moderate heart failure, clinically manifested by slight dyspnea, crepitant wheezing in the lower parts of the lungs, with normal or slightly elevated blood pressure, nitrates are used (nitroglycerin sublingually, nitrates orally). At this stage, it is very important not to "overtreat", i.e. not to cause an excessive decrease in the filling pressure of the left ventricle. Small doses of ACE inhibitors are prescribed, less often furosemide (lasix) is used. Nitrates and ACE inhibitors have an advantage over diuretics - they reduce preload without reducing the BCC.

Sequence of treatment measures when clinical signs of cardiac asthma or pulmonary edema appear:

• oxygen inhalation,
• nitroglycerin (sublingually, repeatedly or intravenously),
• morphine (IV 2-5 mg),
• lasix (IV 20-40 mg or more),
• positive pressure breathing on exhalation,
• artificial ventilation of the lungs.

Even with a full-blown clinical picture of pulmonary edema, after sublingual administration of 2-3 nitroglycerin tablets, a noticeable positive effect can be seen after 10 minutes. Other narcotic analgesics and/or relanium can be used instead of morphine. Lasix (furosemide) is used last in patients with pulmonary edema after myocardial infarction, cautiously, starting with 20 mg if severe dyspnea persists, increasing the dose by 2 times with each repeated administration if necessary. As a rule, there is no fluid retention in patients with pulmonary edema after myocardial infarction, so an overdose of Lasix can lead to severe hypovolemia and hypotension.

In some cases, it is enough to use only one of the drugs (most often nitroglycerin), sometimes it is necessary to administer all 3 drugs almost simultaneously, without waiting for the effect of each drug separately. Oxygen inhalation is carried out with humidification, passing through sterile water or alcohol. In case of pronounced foaming, you can puncture the trachea with a thin needle and administer 2-3 ml of 96° alcohol.

When pulmonary edema occurs against the background of elevated blood pressure, the treatment measures are almost the same as for normal blood pressure. However, if blood pressure increases sharply or remains high despite the administration of nitroglycerin, morphine and lasix, droperidol, pentamine and sodium nitroprusside infusion are additionally used.

Pulmonary edema with decreased blood pressure is a particularly severe condition. This is a cardiogenic shock with predominant symptoms of pulmonary congestion. In these cases, nitroglycerin, morphine, and lasix are used in reduced doses with infusion of inotropic and vasopressor drugs: dobutamine, dopamine, or norepinephrine. With a slight decrease in blood pressure (about 100 mm Hg), you can start with an infusion of dobutamine (from 200 mcg/min, increasing the rate of administration to 700-1000 mcg/min if necessary). With a more pronounced decrease in blood pressure, dopamine is used (150-300 mcg/min). With an even more pronounced decrease in blood pressure (less than 70 mm Hg), norepinephrine administration is indicated (from 2-4 mcg/min to 15 mcg/min) or intra-aortic balloon counterpulsation. Glucocorticoid hormones are not indicated for cardiogenic pulmonary edema.

Treatment depends on the severity. In moderate heart failure, loop diuretics (eg, furosemide 20 to 40 mg intravenously once daily) to reduce ventricular filling pressures are often sufficient. In severe cases, vasodilators (eg, intravenous nitroglycerin) are used to reduce pre- and afterload; pulmonary artery occlusion pressure is often measured during treatment by right cardiac catheterization (using a Swan-Ganz catheter). ACE inhibitors are used as long as systolic blood pressure remains above 100 mmHg. Short-acting ACE inhibitors in low doses (eg, captopril 3.125 to 6.25 mg every 4 to 6 hours, titrated as tolerated) are preferred for initiation of therapy. Once the maximum dose is reached (maximum for captopril is 50 mg twice daily), a longer-acting ACE inhibitor (eg, fosinopril, lisinopril, ramipril) is started long-term. If heart failure persists at NYHA class II or higher, an aldosterone antagonist (eg, eplerenone or spironolactone) should be added. In severe heart failure, intra-arterial balloon pumping may be used to provide temporary hemodynamic support. When revascularization or surgical correction is not possible, cardiac transplantation should be considered. Durable left ventricular assist devices or biventricular assist devices may be used pending transplantation; if cardiac transplantation is not possible, these devices are sometimes used as a permanent treatment. Occasionally, use of these devices results in restoration of ventricular function, and the device can be removed after 3 to 6 months.

If heart failure leads to the development of hypoxemia, oxygen inhalations through nasal catheters are prescribed (to maintain PaO at a level of approximately 100 mm Hg). This can promote myocardial oxygenation and limit the ischemic zone.

Papillary muscle lesions

Papillary muscle insufficiency occurs in approximately 35% of patients within the first few hours of infarction. Papillary muscle ischemia results in incomplete closure of the mitral valve leaflets, which then resolves in most patients. However, in some patients, scarring of the papillary muscles or free wall of the heart leads to persistent mitral regurgitation. Papillary muscle insufficiency is characterized by a late systolic murmur and usually resolves without treatment.

Rupture of the papillary muscle most often occurs in inferoposterior myocardial infarction associated with occlusion of the right coronary artery. This leads to the appearance of acute severe mitral regurgitation. Rupture of the papillary muscle is characterized by the sudden appearance of a loud holosystolic murmur and thrill at the apex, usually with pulmonary edema. In some cases, when regurgitation does not cause intense auscultatory symptoms, but there is a clinical suspicion of this complication, echocardiography is performed. An effective method of treatment is mitral valve repair or replacement.

Myocardial rupture

Rupture of the interventricular septum or ventricular free wall occurs in 1% of patients with acute myocardial infarction and is the cause of 15% of hospital mortality.

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

The incidence of ventricular free wall rupture increases with age and is more common in women. This complication is characterized by a sudden drop in blood pressure with maintenance of sinus rhythm and (often) signs of cardiac tamponade. Surgical treatment is rarely successful. Free wall rupture is almost always fatal.

Ventricular aneurysm

A localized bulging of the ventricular wall, most often the left one, may occur in the area of a large myocardial infarction. Ventricular aneurysm is common in large transmural myocardial infarctions (usually anterior). An aneurysm may develop days, weeks, or months after the myocardial infarction. Rupture of aneurysms is rare, but they may cause recurrent ventricular arrhythmias, low cardiac output, and mural thrombosis with systemic embolism. Ventricular aneurysm is suspected when paradoxical movements are detected in the precordial area. An ECG shows persistent ST segment elevation, and a chest X-ray reveals a characteristic bulging cardiac shadow. Echocardiography is performed to confirm the diagnosis and detect thrombi. Surgical excision may be indicated if left ventricular failure or arrhythmia is present. The use of ACE inhibitors during acute myocardial infarction reduces myocardial remodeling and may reduce the incidence of aneurysms.

A pseudoaneurysm is an incomplete rupture of the free wall of the left ventricle, limited to the pericardium. Pseudoaneurysms almost always contain thrombi and often rupture completely. Treatment is surgical.

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

Arterial hypotension and cardiogenic shock

Arterial hypotension may be due to decreased ventricular filling or decreased contractile force 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, profuse sweating, cold extremities) is called cardiogenic shock. In cardiogenic shock, pulmonary edema develops rapidly.

Decreased left ventricular filling is most often caused by decreased venous return due to hypovolemia, particularly in patients receiving intensive loop diuretic therapy, but it may be a sign of right ventricular myocardial infarction. Severe pulmonary edema indicates loss of left ventricular force of contraction (left ventricular failure), causing shock. Treatment depends on the cause. In some patients, pulmonary artery catheterization to measure intracardiac pressure is necessary to determine the cause. If the pulmonary artery occlusion pressure is below 18 mm Hg, decreased filling due to hypovolemia is more likely; if the pressure is above 18 mm Hg, left ventricular failure is likely. In hypotension associated with hypovolemia, cautious replacement therapy with 0.9% saline is possible without causing left atrial overload (excessive increase in left atrial pressure). However, sometimes left ventricular function is so altered that fluid replacement dramatically increases pulmonary artery wedge pressure to levels characteristic of pulmonary edema (> 25 mm Hg). If left atrial pressure is high, hypotension is likely due to left ventricular failure, and inotropic therapy or circulatory support may be required if diuretics are ineffective.

In cardiogenic shock, α- or β-agonists may be temporarily effective. Dopamine, a catecholamine that acts on α receptors, is given at a dose of 0.5 to 1 mcg/kg per minute and titrated to a satisfactory response or to a dose of approximately 10 mcg/kg per minute. Higher doses stimulate vasoconstriction and cause atrial and ventricular arrhythmias. Dobutamine, an α-agonist, may be given intravenously at a dose of 2.5 to 10 mcg/kg per minute or more. It often causes or worsens hypotension. It is most effective when hypotension is due to low cardiac output with high peripheral vascular resistance. Dopamine may be more effective than dobutamine when a pressor effect is needed. A combination of dopamine and dobutamine may be used in refractory cases. Intra-aortic balloon counterpulsation may be used as a temporary measure. Directed thrombolysis, angioplasty, or emergency CABG may significantly improve ventricular function. NOVA or CABG is considered in cases of persistent ischemia, refractory ventricular arrhythmia, hemodynamic instability, or shock if the anatomical features of the arteries allow it.

[ 27 ], [ 28 ], [ 29 ]

Right ventricular myocardial ischemia or infarction

Approximately half of patients with inferior myocardial infarction have right ventricular involvement, including hemodynamically significant involvement in 15-20%. Clinically, such patients present with hypotension or shock in combination with signs of venous congestion in the systemic circulation: venous distension in the neck, liver enlargement, peripheral edema (signs of venous congestion may be absent with concomitant hypovolemia and appear after fluid infusion). "The classic triad of right ventricular myocardial infarction": venous distension in the neck, no pulmonary congestion, and hypotension. In addition, severe dyspnea without orthopnea is noted. The clinical picture resembles cardiac tamponade, constrictive pericarditis, and pulmonary embolism. In right ventricular myocardial infarction, grade II-III AV block and atrial fibrillation occur more often. One of the signs of right ventricular involvement is a sharp decrease in blood pressure, even to the point of fainting, when taking nitroglycerin.

ECG signs of myocardial infarction, usually of the lower localization, and in lead V1 and in the right chest leads (VR4-R6) an elevation of the ST segment is recorded. In case of involvement of the posterobasal sections of the left ventricle in leads V1-V2 there is depression of the ST segment and an increase in the height of the R wave. When probing the right sections of the heart, an increase in pressure in the right atrium and ventricle is noted (diastolic more than 10 mm Hg). Echocardiography shows impaired contractility and an increase in the size of the right ventricle, the absence of significant effusion in the pericardial cavity and tamponade.

The main method of treating hypotension in right ventricular myocardial infarction is intravenous fluid administration ("volume-dependent myocardial infarction"). Infusion of plasma-substituting solutions (saline, rheopolyglucin) is carried out at a rate that ensures an increase in pulmonary artery diastolic pressure to 20 mm Hg or blood pressure to 90-100 mm Hg (in this case, signs of venous congestion in the systemic circulation and central venous pressure increase) - the only "driving force" in right ventricular myocardial infarction is increased pressure in the right atrium. The first 500 ml are administered as a jet (bolus). In some cases, several liters of plasma-substituting solutions have to be administered - up to 1-2 liters in 1-2 hours (according to one cardiologist: "it is necessary to pour in fluid, right up to anasarca").

If signs of pulmonary congestion appear, the infusion rate is reduced or the administration of plasma-substituting solutions is stopped. If the effect of fluid infusion is insufficient, dobutamine (dopamine or norepinephrine) is added to the treatment. In the most severe cases, intra-aortic counterpulsation is used.

Contraindicated are vasodilators (including nitroglycerin and narcotic analgesics) and diuretics. These drugs cause a sharp decrease in blood pressure. Increased sensitivity to nitrates, morphine and diuretics is a diagnostic sign of right ventricular myocardial infarction. The most effective treatment for myocardial infarction involving the right ventricle is restoration of coronary blood flow (thrombolytic therapy or surgical revascularization). With proper treatment of patients with right ventricular myocardial infarction, the prognosis is quite favorable in most cases; improvement in right ventricular function is noted in the first 2-3 days, and signs of congestion in the systemic circulation usually disappear within 2-3 weeks. With proper treatment, the prognosis depends on the condition of the left ventricle.

A severe and, unfortunately, frequently observed complication of right ventricular myocardial infarction is complete AV block. In these cases, dual-chamber pacing may be required, since in right ventricular myocardial infarction, maintaining effective systole of the right atrium is of great importance. If dual-chamber pacing is not possible, intravenous euphyllin and ventricular pacing are used.

Thus, detection and timely correction of three curable conditions: reflex hypotension, hypovolemia and right ventricular myocardial infarction allows achieving significant improvement in this group of patients even with a clinical picture of shock. No less important is the fact that incorrect treatment, for example, the use of vasopressors in hypovolemia, vasodilators or diuretics in right ventricular myocardial infarction, is often the cause of accelerated death.

Ongoing ischemia

Any chest pain that persists or recurs within 12 to 24 hours after myocardial infarction may represent ongoing ischemia. Postinfarction ischemic pain indicates that large areas of the myocardium remain at risk for infarction. Ongoing ischemia can usually be identified by reversible changes in the ST-T interval on the electrocardiogram; blood pressure may be elevated. However, because ongoing ischemia may be silent (ECG changes in the absence of pain), serial ECGs are usually performed every 8 hours on the first day and then daily in about one third of patients. If ongoing ischemia occurs, treatment is similar to that for unstable angina. Sublingual or intravenous nitroglycerin is usually effective. Coronary angioplasty and NOVA or CABG may be considered to preserve ischemic myocardium.

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

Mural thrombosis

Mural 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 persists for at least 3 months. The highest risk (more than 60%) is in patients with extensive anterior myocardial infarction (especially with involvement of the distal interventricular septum and apex), a dilated left ventricle, widespread areas of hypokinesis, or persistent atrial fibrillation. Anticoagulants are prescribed to reduce the risk of embolism. In the absence of contraindications, sodium heparin is administered intravenously, warfarin is prescribed orally for 3-6 months with the INR maintained between 2 and 3. Anticoagulant therapy is carried out for a long time if the patient has an enlarged left ventricle with widespread hypokinesis zones, left ventricular aneurysm, or permanent atrial fibrillation. Long-term use of acetylsalicylic acid is also possible.

Pericarditis

Pericarditis results from extension of myocardial necrosis through the ventricular wall to the epicardium. This complication develops in approximately one third of patients with acute transmural myocardial infarction. A pericardial friction rub usually appears 24 to 96 hours after the onset of myocardial infarction. Earlier onset of a friction rub is unusual, although hemorrhagic pericarditis sometimes complicates early myocardial infarction. Acute tamponade is rare. Pericarditis is diagnosed by ECG, which shows diffuse STn segment elevation and (sometimes) PR interval depression. Echocardiography is often performed but is usually normal. Occasionally, a small amount of pericardial fluid or even asymptomatic tamponade is found. Aspirin or other NSAIDs usually reduce manifestations. High doses or prolonged use of NSAIDs or glucocorticoids may inhibit infarction healing and should be taken into account.

Post-infarction syndrome (Dressler syndrome)

Post-infarction syndrome develops in some patients days, weeks, or even months after an acute myocardial infarction. In recent years, its incidence has decreased. The syndrome is characterized by fever, pericarditis with pericardial friction rub, pericardial fluid, pleurisy, pleural fluid, pulmonary infiltrates, and widespread pain. The syndrome is caused by an autoimmune reaction to necrotic myocyte tissue. It may recur. Differentiating post-infarction syndrome from progression or recurrence of myocardial infarction may be difficult. However, post-infarction syndrome does not markedly increase cardiac markers, and ECG changes are uncertain. NSAIDs are usually effective, but the syndrome may recur several times. In severe cases, a short, intensive course of another NSAID or a glucocorticoid may be required. High doses of NSAIDs or glucocorticoids are not used for more than a few days because they may interfere with early ventricular healing after acute myocardial infarction.