The position of the patient with pulmonary edema

- a condition in which as a result of stagnation ina small circle of blood circulation or toxic vascular lesions of the lungs, the serous-homorrhagic fluid swells into the pulmonary alveoli. The protein-rich transudate, when it comes into contact with air, gives a vigorous foaming, in the result of which its volume rises sharply, the respiratory surface of the lungs significantly decreases, and asphyxia threatens. The amount of foam can reach 2-3 liters; it is secreted through the upper respiratory tract in the form of bloody, foamy sputum. With pneumonia and phosgene poisoning, the increase in permeability of pulmonary capillaries plays a decisive role. Reduced plasma protein content may be an important cause of pulmonary edema in nephritis.

Pulmonary edema is most often observed with the samediseases like cardiac asthma (myocardial infarction, hypertension, atherosclerotic cardiosclerosis, heart defects) and is in these cases the most severe form of asthma.

Clinic. Lung edema develops suddenly, often at night, during sleep, and the patient wakes up in a state of suffocation, or in the daytime, with physical effort or excitement. In many cases, precursors of the attack are observed in the form of frequent coughing, the growth of wet wheezing in the lungs. With the onset of an attack, the patient assumes an upright position: the face expresses confusion, fear, pale gray shade or gray-cyanotic (with hypertensive crisis and acute disturbance of cerebral circulation it can be drastically hyperemic, and with a heart defect has a characteristic "mitral" appearance). The patient feels a painful suffocation, constriction or a pressing pain in the chest. Breathing is sharply increased, rattling rattles are audible from a distance, cough becomes more frequent, accompanied by a large amount of light or pink foamy sputum; in the most severe cases, the foam flows from the mouth and nose. Equally difficult to breathe in and out. Cyanosis grows, cervical veins swell, skin becomes covered with cold sticky sweat.

When listening to the lungs at the beginning of an attackOnly a small number of small bubbling rales and single large bubbling rales are detected. At the height of the attack, profuse, various, wet rales over various areas of the lungs are heard, the breathing above these sites is weakened or not at all, the percussion sound is shortened. Sites of a shortened percussion sound can alternate with areas of boxed sound (atelectasis of some segments of the lungs and acute emphysema - others). X-ray examination conducted during an attack reveals the enlarged roots of the lungs, large focal shadows with diffuse contours against the background of reduced transparency of the pulmonary fields.

Pulse is usually sharply increased, often up to 140-160 inminute, at the beginning of an attack of satisfactory filling, rhythmic. In more rare cases, there is a sharp bradycardia. Inspection, feeling, tapping and listening to the heart reveal symptoms that depend not so much on the attack itself as on the disease against which pulmonary edema has developed; as a rule, the boundaries of relative dullness of the heart are widened to the left, the heart sounds are deaf, often not heard at all due to noisy breathing and profuse wheezing. Arterial pressure depends on the initial levels, which can be both normal, and elevated and lowered.

With prolonged flow of pulmonary edema, the arterialpressure usually falls, the filling of the pulse weakens, it is difficult to probe. Breathing becomes superficial, less frequent, the patient assumes a horizontal position, he does not have the strength to cough up phlegm, death from asphyxia begins. Sometimes the attack ending with the death of the patient lasts only a few minutes (lightning-fast form), in other cases a short and light attack spontaneously passes without leaving a prolonged deterioration in the patient's condition. But most often, the attack lasts for several hours, which allows you to carry out the necessary medical measures. It is very important not to forget about the possibility of a wave-like course of pulmonary edema, when a patient, withdrawn from an attack and left without proper observation, develops a repeated severe attack, often ending with the death of the patient.

Significantly less common toxic edemalungs, which can be the result of poisoning with military poisonous substances, pesticides, barbiturates, alcohol, as well as professional poisonings with petrol vapors, nitrogen oxides, carbonyls of metals (carbon monoxide with iron, nickel, etc.), arsenic or uremia, liver or diabetic coma, burn. The clinical picture of the attack in these cases consists of the signs of the underlying disease or pathological process (upper respiratory tract infection, coma, burn disease, etc.) and the symptoms of the pulmonary edema itself.

It should be borne in mind that toxic pulmonary edema is more frequent than cardiac,

occurs without the typical clinical manifestations. So, with uremia toxic

Pulmonary edema is often characterized by a discrepancy between meager data and physical

(no bubbling breath, sharp cyanosis, excessive moisture

rales in the lungs) and expressed typical signs of edema at the X-

research. Poverty of clinical symptoms (only

dry cough, chest pain, tachycardia) against a background of severe general condition

patient is also typical for toxic pneumonia and pulmonary edema with otra

carbonyls of metals: X-ray examination and in these cases

teas gives a characteristic picture of large-focal drain with a blurred outline

shadows in diffuse opacification of pulmonary fields. At the same time, for example

measures for poisoning with nitrogen oxides, may be an expanded clinical

a picture of an attack with suffocation, cyanosis, noisy breathing, lemon yellow,

and sometimes pink foamy sputum, a change in the areas of blunting and a box

sound with percussion, abundant differently-sized wet rales

at listening of lungs, a tachycardia, depression of arterial pressure,

Treatment of pulmonary edema should be directed toreduction of stagnation in a small circle of circulation and overexcitation of the respiratory center, to fight with foaming, restoration of airway patency and elimination of oxygen starvation, dehydration (dehydration), lowering the permeability of pulmonary capillaries, normalization of arterial pressure. It is necessary to apply quickly and strongly acting means. Bleeding is a direct way of discharging a small circle of blood circulation. Extraction of 300 ml of blood leads to a rapid decrease in stagnation in the lungs. At low arterial pressure, anemia, poorly expressed veins, hampering the hemorrhage, it is more advisable to apply cuffs or tourniquets to the limbs (with compression of only the veins, the pulse should be palpated). When combined with pulmonary edema and collapse, which often complicates myocardial infarction, these methods are unsuitable. In hospital and specialized emergency care, ganglion blocking agents are widely used to reduce high pressure in pulmonary capillaries: with intravenous administration of 0.5-1.5 ml of a 5% solution of pentamine or 2% solution of benzohexonium, the vessels of a large circle expand, blood is deposited in them, the influx it is reduced to the heart. New ganglion blockers - arfonade and hygronium, which have a powerful effect and are suitable for continuous intravenous drip, are very effective in controlling pulmonary edema that occur against a background of high enough blood pressure. To increase the contractile ability of the myocardium in the absence of bradycardia, the patient is administered 0.5 ml of a 0.05% solution of strophanthin or 1 ml of a 0.06% solution of Korglikon (administered slowly, it is possible through the same needle with which bloodletting is performed). In one syringe with strophanthin and 10 ml of a 40% solution of glucose, it is advisable, if there is no reduction in blood pressure, to introduce 10 ml of a 2.4% solution of euphyllin that reduces pressure in the pulmonary artery stimulating the cardiac muscle and having a diuretic effect.

To reduce the excitability of the respiratory center1 ml of a 1% solution of morphine or 2% of an omnopon solution, additionally having a general soothing effect, is administered. To prevent vomiting caused by morphine, 1 ml of a solution of dimedrol, pipolphene, suprastin or atropine (the latter is preferable only with bradycardia and poisoning with organophosphorus poisons, but contraindicated in severe tachycardia) is administered concurrently with the morphine induced by the morphine. Morphine should not be administered with low blood pressure, with respiratory center depression, as evidenced by more shallow and less frequent breathing, disturbance of its rhythm, low position of the patient in bed.

To combat foaming,"Defoamers", the simplest of which are pairs of alcohol: 95% alcohol is poured instead of water into the humidifier, oxygen is passed through it from the bottle at an initial rate of 2-3 liters, and after a few minutes at a rate of 6-7 liters per minute; the patient breathes in pairs of alcohol with oxygen coming through the nasal catheter. Sometimes moistened with alcohol, cotton wool is put into the mask. Already in 10-15 minutes after the beginning of inhalation of alcohol vapors, a disappearance of bubbling breath can be observed; in other cases, the effect occurs only after a 2-3-hour inhalation. A much more active defoamer is antifosilan: 10% alcohol solution is poured into the humidifier of the respiratory apparatus or injected with a special nebulizer. The effect in this case occurs already on the 1-3th minute of inhalation: disappearing rattling rales, breathing becomes easier. It should be borne in mind the least effective, but the easiest way: spraying alcohol in front of the patient's mouth with any pocket inhaler or conventional spray.

Intravenous administration is used for dehydrationdiuretics: lasix (furosemide - 20-60 mg with 10 ml of physiological solution), uregit (ethacrynic acid 25-50-100 mg) and urea (1 g per 1 kg of the patient's weight in 200 ml of 10% glucose solution drip). Sometimes they inject a vein into a vein. To reduce the increased permeability of the pulmonary capillaries, 10 ml of a 10% solution of calcium chloride, 1-2 ml of a 2.5% solution of pipolphene, in a hospital - hydrocortisone, prednisolone are injected into the vein. Since the upper respiratory tract with lung edema is often filled with mucus, foamy secretions, it is necessary to suck them through a catheter connected to the suction. Specialized care includes, if necessary, measures such as intubation or tracheotomy, artificial respiration, which are used in the most severe cases. The combination of pulmonary edema and cardiogenic shock in myocardial infarction requires the use of complex therapy, including means that raise blood pressure, and analgesics.

All medical measures are carried out against the background ofmaximum rest patient. It is not transportable, since even shifting it onto a stretcher can cause an intensification or resumption of an attack. The doctor should be called "on himself." In the absence of a specialized ambulance, in which the entire volume of therapeutic measures can be performed, it is better to transport the patient to the hospital no earlier than 10-12 hours after the end of the attack. In this case, one should remember the undulating course of it and not leave the patient without observation, as it is usually in a state of drug sleep or stunning (drugs, pipolfen, etc.).

Treatment of toxic pulmonary edema includesspecific measures directed against the effect of the causative factor that caused the attack (for example, in the case of poisoning with gaseous substances, the patient is primarily endured with the danger zone), and the pulmonary edema itself, which is based on the same principles as cardiac pulmonary edema therapy.