Открытая медицинская библиотека

Статьи и лекции по медицине ✚ Библиотека студента-медика ✚ Болезни и способы их лечения.

Фармакология Acute left ventricular failure
просмотров - 227

It is manifested in the form of cardiac asthma or pulmonary edema.

The causes are: hypertensive disease, acute myocardial infarction, atherosclerosis, angina pectoris, valvular defects — mitral incompetence and aortic incompetence.

Blood overfills the left atrium that leads to the pressure increase in it. The right ventricle, preserved its working capacity, continues to pump into the pulmonary vessels all the blood received from caval veins. The left ventricle does not accommodate the whole volume of blood from the lungs. This remainder stays too long in the pulmonary circuit, as a result a hydrostatic pressure elevates in the pulmonary circuit.

This leads to the increase of percolation pressure, it becomes directed from the capillaries to alveoli. The interstitial pulmonary edema arises with slowing down of gas diffusion from alveoli into capillaries and development of hypoxia, hypercapnia, ARF.

Clinically appears a feeling of shortage of air, as well as dyspnea, headache, disorder of consciousness, decrease of diuresis, progression of myocardial insufficiency.

Disorders of blood supply of the brain, liver, kidneys and heart define their functional incompetence.

Upon auscultation there are no rales still in the lungs at this stage of acute left ventricular failure. On X-ray examination of the organs of the chest we may mark symptoms of interstitial pulmonary edema.

In continuing growth of congestion and hydrodynamic pressure in the pulmonary circuit a fluid transudes from the interstitial space into alveoli. The interstitial edema turns into alveolar edema that is characterized by the appearance of exudate in the alveoli and bronchi, foamy sputum. As a result of erythrocytes transudation (per diapedesem) exudate may obtain a rose colour. Crepitant and later moist, small bubbling rales are auscultated. The transition from interstitial edema to the alveolar one may be very fast — in the course of a few minutes. Here, the expressivity of hypoxia and hypoxemia progressively aggravates.

Treatment of pulmonary edema is directed to:

— decrease of venous return;

— improvement of myocardial contractility;

— improvement of patency of respiratory tracts;

— improvement of alveolar ventilation.

I- Decrease of venous return to the heart with the purpose to lower pulmonary hypertension:

— sitting position;

— deposition of some portion of blood by means of application of venous tourniquets on the extremities;

— ganglionics (GL) of ultra-short effect: arphonad 50 mg drop-by-drop per 100 ml of liquid under AP control, benzohexonium— 10-25 mg, pentamine — 10-20 mg, peripheral dilatators — nitroglycerin from 5 to 13 mg, isoket — 100 mg, perlinganit — 100 mg. A rational application of gangliolytics excludes a need in bloodletting.