Cardiac asthma and pulmonary edema – a syndrome that is clinically accompanied by an asthma attack, complicating the course of many diseases and requiring urgent measures. This syndrome occurs as a result of the rapid accumulation of tissue fluid (transudate) in the interstitial tissue of the lungs and alveoli.
The exit of the liquid part of the blood through the wall of the capillaries into the lung tissue is associated: 1) with an increase in hydrostatic pressure in the capillaries of the lungs; 2) a decrease in the oncotic pressure of the blood plasma; however, some excess of interstitial fluid can be removed through the lymphatic system of the lungs, and therefore its pathology (with carcinomatosis, various fibrosis) can also lead to pulmonary edema;
3) an increase in the permeability of the capillary wall. The first pathophysiological process that causes the development of pulmonary edema is an increase (sudden) in hydrostatic pressure in the vessels of the pulmonary circulation. The increase in pressure in the capillaries of more than 30 mm Hg leads to the fact that it is compared with oncotic blood pressure, and plasma begins to actively pass into the lung tissue. An important link is the failure of the left ventricle: a sharp decrease in blood outflow from the small circle or an increase in inflow into the small circle. Overexcitation of the respiratory center due to a violation of its blood supply is also of certain importance.
The second pathophysiological in pulmonary edema is a violation of the permeability of endothelial cells of the alveolar capillaries and changes in the colloid osmotic pressure of the plasma.
An increase in alveolar-capillary permeability is associated with a chain of reactions starting with exposure to a chemotactic factor leading to neutrophil adhesion to endothelium. At the same time, various proteases and other mediators are released; metabolites of arachidonic acid, which not only increase permeability, but also lead to hemodynamic changes that contribute to the development of pulmonary edema. The fluid that accumulates in the interstitial tissue of the lungs contains protein, accounting for 69% of the blood plasma protein, while in the first mechanism the amount of protein does not exceed 40%. This once again emphasizes the role of high permeability of capillaries of the lungs in the formation of adult respiratory syndrome. Initially, the peribronchial and perivascular spaces of the lungs are impregnated with serous fluid. The area of contact with air decreases – interstitial pulmonary edema develops, which is clinically manifested by cardiac asthma. The latter represents only a certain stage during pulmonary edema, the peak of which is the alveolar form of the latter. Subsequently, the liquid penetrates into the lumen of the bronchi and alveoli, and it contains not only blood proteins, but also shaped elements.
As a result of mixing in the alveoli, air passing through them, the edematous fluid foams, increases in volume, fills the pulmonary alveoli, forms a stable protein foam – alveolar edema occurs, which disrupts the ventilation of the lungs and prevents normal gas exchange, as a result of which hypoxia rapidly builds up. In patients with heart failure in 12%, the cause of nosocomial mortality is pulmonary edema, while the annual mortality in these patients is 40%.
The European recommendations highlight the main causes that can lead to the development of acute heart failure : – diseases associated with direct heart damage, – background diseases or conditions not related to heart damage.
Diseases associated with direct damage to the heart :
• Decompensation of heart failure.
• Acute coronary syndrome – myocardial infarction, unstable angina pectoris, right ventricular infarction.
• Hypertensive crisis.
• Acute arrhythmia – ventricular tachycardia, atrial fibrillation or flutter, other supraventricular tachycardia.
• Valvular regurgitation – endocarditis, rupture of tendon chords, strengthening of existing regurgitation.
• Severe aortic stenosis.
• Acute myocarditis.
• Cardiac tamponade.
• Rupture of aneurysm of the heart.
• Postpartum cardiomyopathy.
Diseases and conditions not associated with heart damage :
• Decreased adherence to the pharmacotherapy regimen.
• Volume overload.
• Infectious diseases (especially pneumonia and septicemia).
• Acute cerebrovascular accident.
• Postoperative condition.
• Kidney dysfunction.
• Bronchial asthma.
• Dependence on psychoactive substances.
• High ejection syndrome.
You should remember the factors that provoke the development of this syndrome , most often these are: • previous inadequate physical activity; • neuropsychic stresses; • overfilling of the gastrointestinal tract (plentiful food, drink), especially late in the evening: • late pregnancy; • joining intercurrent diseases to the main process or • its aggravation; • some iatrogenic factors – uncontrolled therapy (glycosides, b-blockers, circulatory overload: the introduction of large amounts of fluid, including plasma-substituting solutions, enhancing the volley and flow to the right heart; emptying the bladder too quickly, discharge of ascitic fluid, pleural effusion).