Cardiac ruptures

Heart ruptures, or myocardial ruptures, occur in 2-6% of all cases of myocardial infarction with ST segment elevation. This is the second most common immediate cause of death in hospitals. Heart ruptures usually occur during the first week of the disease, but in some cases they are observed later (up to the 14th day). The 1st and 3-5th days of the disease are considered especially dangerous.

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What causes heart ruptures?

• high blood pressure;
• failure to comply with restrictions on physical activity;
• persistence of a stressful state against the background of uncontrolled pain syndrome;
• the influence of thrombolytic and anticoagulant therapy;
• early administration of large doses of cardiac glycosides.

As a rule, patients with a risk of cardiac rupture are admitted in a more serious condition (circulatory failure, cardiogenic shock or left ventricular failure). The duration, intensity of pain attacks and their number should alert the doctor to the possibility of myocardial rupture. Typical intense, prolonged and recurrent pains of a cutting and tearing nature are characteristic. Analgesic therapy for these pains is ineffective. At the height of the pain that does not stop, a catastrophe with a fatal outcome occurs. In other cases, against the background of an improvement in well-being without any signs, sometimes in a dream, a rapid fatal outcome also occurs.

Ruptures of the heart are usually divided into external (they are accompanied by acute hemotamponade) and internal (perforation of the interventricular septum and rupture of the papillary muscle).

External cardiac ruptures

External cardiac ruptures occur in 3-8% of myocardial infarction cases. Interventricular septal ruptures are less common than external ones. Rapid and slow cardiac ruptures are distinguished. It has been established that the rate of cardiac hemotamponade growth depends on the size, shape and location of the rupture, as well as on the rate of formation of blood clots, which, on the one hand, slow down and stop bleeding, and on the other hand, cause compression of the heart. In this regard, the patient's life in this situation can last from several minutes to several days. Timely resuscitation measures for cardiac rupture can "optimal prolong the patient's life for some time, which may be sufficient for urgent thoracotomy and suturing of the rupture site.

In the case of rapid rupture of the heart, which occurs in most patients, cardiac hemotamponade occurs instantly. The general condition of the patient with myocardial infarction, which up to this point was relatively satisfactory, deteriorates sharply: there is an increase in pain syndrome with loss of consciousness and a catastrophic drop in blood pressure, disappearance of the pulse, respiratory distress, which becomes rare and arrhythmic. Heart sounds suddenly cease to be heard, diffuse cyanosis appears, the jugular veins swell, the boundaries of absolute cardiac dullness expand. Death can occur during sleep.

With gradual development of cardiac rupture, persistent angina attacks come to the fore in the clinical picture, in some cases not relieved by narcotic drugs at all, resulting in the development of cardiogenic shock refractory to therapy. Dyspnea increases, heart sounds become dull, sometimes a pericardial friction rub is heard above the apex of the heart and along the sternum. The pain with slowly flowing myocardial ruptures is extremely intense, tearing, ripping, stabbing, burning. The pain persists until the rupture is complete. It is difficult to determine the epicenter of pain with a slowly flowing cardiac rupture due to its extreme intensity.

Slowly flowing cardiac ruptures can last from several tens of minutes to several days (usually no more than 24 hours) and can have a two- or three-stage course. With surgical treatment, this variant has a more favorable prognosis.

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Interventricular septal ruptures

Acute rupture of the interventricular septum is observed in lower (basal) and anterior (apical) myocardial infarction in 2-4% of patients. It most often develops in the first week. These cardiac ruptures are often accompanied by the development of pulmonary edema.

The clinical picture of perforation of the interventricular septum resembles a relapse of myocardial infarction, accompanied by severe pain behind the sternum, tachycardia, the appearance of a rough "scraping" systolic murmur over the entire area of the heart with the epicenter in the region of the 4-5 sternocostal joint on the left. The amplitude, duration and shape of the murmur depend on the force of contraction of the left ventricle, the size of the interventricular septal defect, its shape, pressure in the right ventricle and pulmonary artery. The pain syndrome can have painless intervals from 10-20 minutes to 8-24 hours. Perforation of the interventricular septum can be preceded by an increase in the frequency of angina attacks, deterioration of the general condition.

Rupture of the interventricular septum is characterized by rapid increase in right ventricular circulatory failure, expansion of the heart borders to the right, swelling of the jugular veins, enlargement of the liver, and development of arterial hypotension. Echocardiography is quite informative in diagnosing rupture of the interventricular septum.

Rupture of the papillary muscle

Rupture of the papillary muscle is an extremely dangerous but correctable complication. Most often, rupture of the posteromedial muscle occurs as a consequence of inferior myocardial infarction in the period from 2 days to the end of the first week of the disease. Rupture of the papillary muscle is manifested by severe heart failure resistant to drug therapy. Mortality during the first 2 weeks is 90%. The noise from regurgitation, even if it is very pronounced, may not be heard. Echocardiography shows a floating mitral valve leaflet and an independently moving head of the papillary muscle. The result of large regurgitation into the left atrium is hyperdynamics of the walls of the left ventricle.