Acute left ventricular failure (VLF) of cardiac origin occurs due to a rapid decrease in LV pumping function (2 times or more) with subsequent stagnation of blood in the lung and lungs (fluid accumulation in the interstitial tissue and alveolar space) while maintaining contractile function of the pancreas.
Acute left ventricular failure contributes to the acute development of LH or its increase against the background of an increase in blood pressure in the left ventricle and / or in the lung. In most cases, VLVF is a manifestation of myocardial weakness due to its acute pathology (massive myocardial infarction), severe rhythm disturbances (PVT with a heart rate of more than 180 beats / min) that occur on the “affected” heart, or a sharp increase in the load on the myocardium, with which it does not coping (for example, hypertensive crisis).
Acute left ventricular failure has two conditional stages: CA (interstitial OL) and true, alveolar OL (with further disturbance of the water-electrolyte balance). With a decrease in the pumping function of the heart, hypoxemia develops and arteriovenous oxygen extraction increases. The appearance of shunt hypoxia (due to arteriovenous shunting) is also possible. Against this background, respiratory failure (DN) is also formed due to the involvement of the lungs in the pathological process.
Insufficiency of the propulsive ability of the heart favors the growth of blood pressure in the left ventricle and the subsequent retrograde increase in pressure in the pulmonary circulation. This forms a passive, postcapillary PH. The pathophysiological characteristic of cardiogenic OL is the transudation of excess fluid into the lung tissue due to the secondary nature of the increase in pressure in the lung. Changes in the hemodynamics of the pulmonary circulation during VLF occur under conditions when there is no primary increase in the permeability of endothelial cells of capillaries and epithelial cells of the distal airways.
Acute left ventricular failure
Cardiac asthma (CA) is a dramatic manifestation of acute left ventricular failure. The basis of its development is systolic or diastolic LV dysfunction. Usually there is a sharp decrease in the contractile function of the myocardium (for example, when more than 20% of its mass falls out of the contraction process during MI), an increase in the pressure of filling the left ventricle, followed by the retrograde development of passive PH (hydrostatic pressure exceeds 28 mm Hg, first in the pulmonary veins, and then in the arteries) and jamming pressure in LA (DZLA) of more than 18 mm Hg. Art.
This helps to increase the permeability of pulmonary capillaries , reduce oncotic pressure (the balance between oncotic and hydrostatic pressure and arteriolar and venous pressure is disturbed) and subsequent sweating of blood elements into interstitial tissue and easy soaking of the walls of the alveoli. So there is swelling of the mucous membrane of the bronchial tree (compression of the bronchi from the outside) and subsequent bronchial obstructive syndrome (BOS).
Bronchioles (located in the same interstitial bed with pulmonary capillaries) are compressed, their mucous membrane swells, becomes edematous, which determines the clinical picture of cardiac asthma.