Heart breaks

Heart ruptures or myocardial ruptures are observed in 2-6% of all myocardial infarction cases with ST segment elevation. This is the second most frequent cause of death in hospital patients. Usually heart ruptures occur during the first week of the disease, but in some cases are observed later (up to the 14th day). Particularly dangerous are the 1st and 3-5th day of the disease.

[1]

What causes heart ruptures?

• high blood pressure;
• non-compliance with the limitations of the motor regime;
• Preservation of a stressful state against the background of unchallenged pain syndrome;
• the effect of thrombolytic and anticoagulant therapy;
• early administration of large doses of cardiac glycosides.

As a rule, patients with a threat of heart rupture come in a more serious condition (circulatory insufficiency, cardiogenic shock or left ventricular failure). Duration, intensity of pain attacks and their number should alert the doctor with regard to the possibility of rupture of the myocardium. Characteristic typical intense, prolonged and recurrent pain, which have a cutting and tearing character. Therapy with analgesics for these pains is ineffective. At the height of non-stopping pains, there is a catastrophe with a fatal outcome. In other cases, against a background of improvement in well-being without any signs, sometimes in a dream, there is also a rapid death.

Heart ruptures are usually divided into external (they are accompanied by acute gemotamponade) and internal (perforation of the interventricular piecemeal and separation of the papillary muscle).

External cardiac ruptures

External heart ruptures occur in 3-8% of cases of myocardial infarction. Interventricular septal ruptures are less common than external ones. Highlights the rapid and slow occurrence of a heart rupture. It has been established that the rate of growth of cardiac hemotampoma depends on the size, shape and localization of the rupture, as well as on the rate of formation of blood clots, which, on the one hand, slow and stop bleeding, and on the other hand cause compression of the heart. In this regard, the life of the patient in this situation can last from several minutes to several days. Timely resuscitation measures started with a heart rupture "opt prolong the life of the patient for a while, which may be sufficient for urgent thoracotomy and suturing the place of rupture.

With a rapid heart rupture, which occurs in most patients, the cardiac hematoma is instantaneous. The general condition of the patient with myocardial infarction, which until then was relatively satisfactory, deteriorates sharply: there is an increase in the pain syndrome with loss of consciousness and a catastrophic drop in blood pressure, the disappearance of the pulse, a respiratory disorder that becomes rare and arrhythmic. Suddenly stop listening to heart tones, there is diffuse cyanosis, cervical veins swell, the boundaries of absolute cardiac dullness expand. Death can occur during sleep.

With the gradual formation of a heart rupture in the clinical picture, persistent anginal attacks appear in the foreground, in a number of cases they are not completely docked by narcotic drugs, as a result of which a cardiac shock refractory to therapy develops. There is a shortness of breath, a deafness of heart tones, sometimes a pericardial friction noise is heard above the apex of the heart and along the sternum. Pain with slowly current myocardial ruptures is extremely intense, tearing, tearing, dagger, burning. The pain persists until the rupture is complete. Identify the epicenter of pain with a slowly current heart break is difficult because of its extreme intensity.

Slowly flowing heart ruptures can last from several tens of minutes to several days (usually not more than 24 hours) and can have a two- or three-stage course. In surgical treatment, this option has a prognostically more favorable course.

[2], [3], [4], [5], [6]

Interventricular septal ruptures

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

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

To break the interventricular septum is characterized by a rapid increase in circulatory failure in the right ventricle type, widening the boundaries of the heart to the right, swelling of the cervical veins, enlargement of the liver and development of arterial hypotension. Echocardiography is quite informative in diagnosing an interventricular septal rupture.

The rupture of the papillary (papillary) muscle

The rupture of the papillary (papillary) muscle is an extremely dangerous, but a correctable complication. Most often, the posterior-medial muscle ruptures as a consequence of the lower myocardial infarction in the period from 2 days to the end of the first week of the disease. The rupture of the papillary muscle is manifested by severe heart failure, resistant to drug therapy. Mortality within the first 2 weeks is 90%. Noise from regurgitation, even if it is very pronounced, may not be heard. With echocardiography, the flotating valve of the mitral valve and the independently moving head of the papillary muscle are visible. The result of large regurgitation in the left atrium is hyperdynamics of the walls of the left ventricle.