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Acute left ventricular failure

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.

While using GLs of ultra-short effect one should always have a syringe

with phenylephrine hydrochloride in readiness. GLs are advantageous because they decrease a release of adrenalin and thereby eliminate one of the most important moments in the pathogenesis of pulmonary edema.

— Spasmolytics — euphilline 2.4% — 240-480 mg, papaverine 2% — 2.0. They exert a spasmolytic effect on the vessels of systemic circuit, decrease spasm of pulmonary vessels.

— Morphine — 10-20 mg, decreases the tone of pulmonary vessels and in combination with atropine it diminishes a vagotonic effect. At the same time, it causes hypoventilation at the expense of inhibition of respiratory center and a decrease of blood flow with development of compensatory tachycardia, thereby contributng to the shift of blood from the system of high pressure to the system with low pressure.

— Application of talamonal by 2 ml is possible.

2. Improvement of myocardial contractility:

— Glucose-polarizing mixture with insulin that has pronounced anabolic properties, increases metabolism and contributes to synthesis and transport of ATP. To 400 ml 10% glucose we add 12 units of insulin, 10 ml 5% ascorbinic acid, riboxinum — 200-400 mg, 50 ml 3% KC1 and 5 ml MgS0₄.

— Cardiac glycosides are not applied since they decrease coronary blood f ow that leads to a decrease of myocardial efficiency. The effect of cardiac glycosides advances slowly. Besides, they cause a spasm of arterioles elevating TPVR and so increasng the load on the myocardium. Therefore, cardiac glycosides may be prescribed as a preventive agent after a pulmonary edema is arrested. In mitral stenosis, cardiac glycosides cann't be applied because of the load upon the right heart that leads to intensification of congestion in the pulmonary circuit.

Administration of calcium gluconate— 10% solution 5-10 ml intravenously slowly per 5-10 ml 0.9% NaCl solution is also possible.

3. Improvement of patency of respiratory tracts:

— glucocorticoids and antihistaminic agents with the purpose to decrease
permeability of pulmonary capillaries.

4. Improvement of alveolar ventilation:

— inhalations of oxygen passed through vapours of 33% alcohol;

— antifoam agents: 96° alcohol — 2 ml into the trachea through microtracheostoma or endotracheal tube, 10-20% alcohol i/v up to 80 ml, 10% silicon, 10% antiphosmilan;

— sanitation of tracheobronchial tree;

— APV with positive pressure on the expiration (+ 5-10 cm water column that improves the work of the heart by 20-25%);

— dehydration with lasix. Under no circumstances do not use osmotic diuretics (mannite, mannitol) that, at the first phase of their action, cause hypervolemia that provokes progression of pulmonary edema. Soda is added to an infusion therapy with great caution because of the danger of development

of respiratory alkalosis. After arresting an acute pulmonary edema such patients need in rest and strict, intensive observation, since the recurrence of pulmonary edema is possible if its cause is not eliminated.

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