Acute cardiovascular failure in the presence of AMI can be manifested as left ventricular, right ventricular, and mixed (total) forms.
Acute left ventricular heart failure (cardiac asthma)
This pathological syndrome in the clinic of internal diseases is traditionally called cardiac asthma .
Etiology . Its occurrence is possible with some forms of coronary heart disease: against AMI, in the presence of post-infarction cardiosclerosis: some heart defects and a number of other conditions.
Pathogenesis . The basis of an attack of cardiac asthma is sudden acute left ventricular failure – a pathological syndrome characterized by a decrease in contractility of the left ventricle, with a corresponding decrease in stroke volume of the sickle, with preserved, or even increased venous return, which causes an increase in intravascular pressure in the pulmonary circulation. The fluid from the vascular bed begins to “sweat” into the interstitial space.
There is an increase in the distance between the endothelial cells of the capillaries, which allows the macromolecules to enter the interstitial space. An interstitial pulmonary edema is formed . A further increase in intravascular pressure leads to the rupture of tight junctions between the cells lining the alveoli and the ingress of fluid containing erythrocytes and macromolecules into the alveoli. Clinically, this is manifested by the appearance of finely bubbly wet rales. With a deepening of the rupture of the alveolar-capillary membrane, the liquid floods the alveoli and respiratory tract. From this moment, a vivid clinical picture of alveolar pulmonary edema develops with the development of signs of ODN. One of the pathogenetic factors in the occurrence of ODN is the foaming with each breath of fluid that has entered the alveoli, which causes airway obstruction. So, from 100 ml of sweating plasma 1 – 1.5 l of foam is formed. Foam not only violates the airway, but also destroys the surfactant of the alveoli, this causes a decrease in the extensibility of the lungs, the load on the respiratory muscles increases, hypoxia and edema increase.
Gas diffusion through the alveolar-capillary membrane is also impaired due to disorders of lymph circulation, impaired collateral ventilation , drainage function and capillary blood flow. There is a shunting of blood and hypoxia increases. From the point of view of pathophysiology, an attack of cardiac asthma is a beginning alveolar pulmonary edema.