Acute left ventricular failure

Acute left ventricular failure often develops in patients with myocardial infarction, hypertensive disease, heart defects and coronary atherosclerosis.

There is such acute heart failure, especially in the form of pulmonary edema. Pathogenetically, and depending on the mechanism of development, two forms of pulmonary edema are distinguished.

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Causes of acute left ventricular failure

Acute congestive heart failure with low cardiac output is characterized by low cardiac output and reduced (or normal) arterial pressure. Acute left ventricular failure is observed in acute coronary syndrome, mitral and aortic stenoses, myocarditis, acute myocarditis, acute dysfunction of the heart valves, pulmonary thromboembolism, cardiac tamponade, etc. In some cases, the reason for low cardiac output is the insufficient filling pressure of the ventricles of the heart.

Acute left ventricular failure with symptoms of stagnation in the lungs most often develops with myocardial dysfunction in chronic diseases, acute ischemia and myocardial infarction, aortic and mitral valve dysfunction, heart rhythm disorders, left heart tumor. The main non-cardiac causes are severe arterial hypertension, high cardiac output in case of anemia or thyrotoxicosis, swelling or trauma of the brain.

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Acute left ventricular failure and myocardial infarction

Acute left ventricular failure is common in myocardial infarction. It can develop simultaneously with myocardial infarction, but often appears several days after its development. In the latter case, its occurrence is due to the loss of a significant mass of the contractile myocardium.

In early terms, left ventricular failure is often due to a diastolic dysfunction and may occur with a normal ejection fraction. An important role in the development of heart failure in this case is the development of mitral regurgitation. It can be caused by ischemia of the papillary muscle, damage to the chords of the mitral valve with lateral and anterior myocardial infarction, loss of a significant mass of the myocardium and / or dilatation of the ventricle.

The development of acute left ventricular failure in the first hours and days in patients with myocardial infarction is characterized by a normal or reduced volume of circulating blood, a moderate decrease in cardiac output, minimal sodium and water retention, and transientness of the observed disorders.

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How does acute left ventricular failure develop?

One of the main pathogenetic moments of development of left ventricular failure is an increase in hydrostatic pressure in the venous and capillary parts of the small circle of the circulation. The accumulation of excess fluid in the pulmonary interstitium leads to a decrease in the elasticity of the lungs. The lungs become more "rigid", there are restrictive disorders. Next, swollen fluid swims into the alveoli. Liquid-filled alveoli cease to participate in gas exchange, which leads to the appearance in the lungs of sites with a reduced rate of ventilation / perfusion.

Initially, edematous fluid accumulates in the surrounding tissues of the alveoli and then spreads along the pulmonary venous trunks and along the pulmonary arterial and bronchial trunks. There is infiltration of serous fluid peribronchial and perivascular spaces, which leads to an increase in pulmonary vascular and bronchial resistance, worsening the conditions of metabolism. The fluid can accumulate in the bronchioles, which leads to a narrowing of the airways and is recognized by the occurrence of wheezing.

In the left atrium, blood from unventilated alveoli (shunt) is mixed with completely oxygenated blood. This leads to a decrease in the total arterial partial pressure of oxygen. When the fraction of desaturated blood reaches a significant level, the state of hypoxemia develops.

In the initial stage of acute left ventricular failure, hypoxia is circulatory and is caused by a "small" cardiac output.

With aggravation of insufficiency to circulatory hypoxia, hypoxic, due to obturation of alveoli and tracheobronchial tree by foamy sputum, is added.

Symptoms of acute left ventricular failure

Acute left ventricular failure includes cardiac asthma, pulmonary edema and a shock symptom complex. One of the main pathogenetic moments of its development is an increase in hydrostatic pressure in the venous and capillary parts of the small circulatory system.

Cardiac asthma is characterized by the development of interstitial pulmonary edema. With it, the serous fluid infiltrates the peribronchial and perivascular spaces, which leads to an increase in pulmonary vascular and bronchial resistance, and a worsening of the conditions of metabolism. Further penetration of fluid from the vascular bed into the lumen of the alveoli leads to the development of alveolar pulmonary edema and severe hypoxemia. In the initial stage of acute left ventricular failure, hypoxia is circulatory and is caused by a "small" cardiac output. When the severity of insufficiency increases, circulatory hypoxia is associated with a hypoxic, conditioned by obturation of alveoli and tracheobronchial tree by foamy sputum.

Clinically, an attack of cardiac asthma is manifested by symptoms of severe choking. Skin wet and cold. There is pronounced acrocyanosis. Percussion of the lungs reveals blunting in the lower parts of the lungs. Auscultatory breathing is noisy, dry rales are heard. Unlike bronchial asthma, exhalation is not difficult. There is a tachycardia, amplification of II tone above a pulmonary artery. Arterial pressure can fluctuate within wide limits, central venous pressure is increased.

With the progression of heart failure, a picture of the "classic" alveolar edema of the lungs develops. Above the entire surface of the lungs there appear and rapidly grows sonorous large bubbling rales that drown out the heart sounds. At a distance you can hear buzzing, gurgling breath. The frequency of respiratory movements reaches 30-40 per minute. Sputum fills all the tracheobronchial tree. There is a cough with a liquid frothy, pink-colored phlegm.

Cardiac output does not decrease in the early stages of heart failure due to a compensatory increase in the number of heartbeats and a positive response of the left ventricle to afterload. For this period, as a whole, high filling pressure, low shock volume, tachycardia and normal minute volume of blood circulation are characteristic.

Radiographic examination determines the stage-specific changes in the lungs and heart. The edematous fluid, in comparison with air, has a high density for x-rays. Therefore, pulmonary edema on radiographs reveals itself by the presence of areas of increased density, which when chest X-ray is detected earlier than the first clinical signs appear.

An early radiographic evidence of pulmonary edema is the strengthening of the vascular pattern. Fuzzy contours of vessels, an increase in the size of the cardiac shadow, the appearance of the Curly A lines (long, located in the center of the pulmonary field), and the Curly B lines (short, located on the periphery) can be observed. As the edema progresses, infiltration increases in the peribronchial regions, "bat silhouettes" or "butterflies" and acinar shadows appear (consolidation areas having a spotted appearance).

Treatment of acute left ventricular failure

Intensive therapy of such patients should be aimed at increasing cardiac output and improving oxygenation of tissues (vasodilators, infusion therapy to maintain sufficient ventricular filling pressure, short-term inotropic support).

Most often at the stage of emergency care it is difficult to estimate the value of the filling pressure of the ventricles of the heart. Therefore, in patients with acute heart failure without congestive wheezing in the lungs, a trial intravenous injection of up to 200 ml of a 0.9% solution of sodium chloride in 10 minutes is recommended. If the infusion does not lead to a positive or negative effect, then it is repeated. Infusion is stopped when ACSIST is raised to 90-100 mm Hg. Art. Or the appearance of signs of venous stasis in the lungs.

It is extremely important for low cardiac output caused by hypovolemia, to find and eliminate its cause (bleeding, excessive dose of diuretics, vasodilators, etc.).

In intensive care of a condition such as acute left ventricular failure, vasodilators, diuretics, narcotic analgesics, bronchodilators and respiratory support are used.