Acute left ventricular failure

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

Such acute heart failure manifests itself primarily 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 heart failure with low cardiac output is characterized by low cardiac output and decreased (or normal) arterial pressure. Acute left ventricular failure is observed in acute coronary syndrome, mitral and aortic stenosis, myocarditis, acute myocarditis, acute dysfunction of the heart valves, pulmonary embolism, cardiac tamponade, etc. In some cases, the cause of low cardiac output is insufficient filling pressure of the ventricles of the heart.

Acute left ventricular failure with symptoms of pulmonary congestion most often develops with myocardial dysfunction in chronic diseases, acute myocardial ischemia and infarction, dysfunction of the aortic and mitral valves, heart rhythm disturbances, tumors of the left heart. The main non-cardiac causes are severe arterial hypertension, high cardiac output in anemia or thyrotoxicosis, tumor or brain injury.

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Acute left ventricular failure and myocardial infarction

Acute left ventricular failure is often encountered 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 contractile myocardium.

In the early stages, left ventricular failure is often caused by impaired diastolic function and may occur with a normal ejection fraction. The development of mitral regurgitation plays an important role in the development of heart failure. It may be caused by papillary muscle ischemia, damage to the mitral valve chords in lateral and anterior myocardial infarction, loss of significant myocardial mass, and/or ventricular dilation.

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 retention of sodium and water in the body, and the transience of the observed disorders.

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How does acute left ventricular failure develop?

One of the main pathogenetic moments of the development of left ventricular failure is an increase in hydrostatic pressure in the venous and capillary sections of the pulmonary circulation. Accumulation of excess fluid in the pulmonary interstitium leads to a decrease in the elasticity of the lungs. The lungs become more "rigid", restrictive disorders appear. Then the edematous fluid sweats into the alveoli. The alveoli filled with fluid cease to participate in gas exchange, which leads to the emergence of areas in the lungs with a reduced ventilation/perfusion index.

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

In the left atrium, blood from the unventilated alveoli (shunt) mixes with fully oxygenated blood. This results in a decrease in the total arterial partial oxygen tension. When the fraction of desaturated blood reaches a significant level, a state of hypoxemia develops.

In the initial stage of acute left ventricular failure, hypoxia is of a circulatory nature and is caused by “low” cardiac output.

As the failure worsens, hypoxia is added to circulatory hypoxia, caused by obstruction of the alveoli and tracheobronchial tree by foamy sputum.

Symptoms of acute left ventricular failure

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

Cardiac asthma is characterized by the development of interstitial pulmonary edema. It involves infiltration of peribronchial and perivascular spaces with serous fluid, which leads to an increase in pulmonary vascular and bronchial resistance and deterioration of metabolic conditions. 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 in nature and is caused by a "low" cardiac output. As the severity of failure increases, hypoxic hypoxia, caused by obstruction of the alveoli and tracheobronchial tree with foamy sputum, joins circulatory hypoxia.

Clinically, an attack of cardiac asthma manifests itself with symptoms of severe suffocation. The skin is moist and cold. There is pronounced acrocyanosis. Percussion of the lungs reveals dullness in the lower parts of the lungs. Auscultation reveals noisy breathing, dry wheezing is heard. Unlike bronchial asthma, exhalation is not difficult. There is tachycardia, an increase in the second tone over the pulmonary artery. Arterial pressure can fluctuate within wide limits, central venous pressure is increased.

As heart failure progresses, a picture of "classic" alveolar pulmonary edema develops. Large-bubble, sonorous wheezing appears and rapidly increases over the entire surface of the lungs, drowning out the heart tones. A gurgling, bubbling breath can be heard from a distance. The respiratory rate reaches 30-40 per minute. Sputum fills the entire tracheobronchial tree. A cough with liquid, foamy, pink sputum appears.

Cardiac output is not reduced in the early stages of heart failure due to a compensatory increase in heart rate and a positive left ventricular response to afterload. This period is generally characterized by high filling pressures, low stroke volume, tachycardia, and normal cardiac output.

X-ray examination reveals stage-specific changes in the lungs and heart. Edema fluid has a higher density for X-rays than air. Therefore, pulmonary edema is revealed on X-ray images by the presence of areas of increased density, which is revealed during chest X-ray earlier than the first clinical signs appear.

An early radiographic sign of pulmonary edema is an increase in the vascular pattern. Further, fuzzy vascular contours, an increase in the size of the cardiac shadow, the appearance of Kerley A lines (long, located in the center of the pulmonary field) and Kerley B lines (short, located on the periphery) may be observed. As the edema progresses, infiltration in the peribronchial areas increases, "bat silhouettes" or "butterfly" and acinar shadows (areas of consolidation with a spotty appearance) appear.

Treatment of acute left ventricular failure

Intensive care of such patients should be aimed at increasing cardiac output and improving tissue oxygenation (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 assess the magnitude 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 administration of up to 200 ml of a 0.9% sodium chloride solution over 10 minutes is recommended. If the infusion does not lead to a positive or negative effect, it is repeated. The infusion is stopped when the ACSSIST increases to 90-100 mm Hg or signs of venous congestion in the lungs appear.

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

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