Pulmonary edema- a pathological condition caused by excessive sweating of the liquid part of the blood into the lung tissue. This terrible syndrome can occur in many diseases: infections, intoxications, drowning, allergic conditions, damage to the central nervous system, etc.

Reasons

But more often pulmonary edema develops as a result of acute left ventricular failure with arterial hypertension, atherosclerotic cardiosclerosis, acute myocarditis, heart defects; It often develops with pulmonary embolism and chronic cor pulmonale (chronic bronchitis, diffuse pneumosclerosis), as a result of the use of certain medications and the transfusion of excessive volumes of fluid. Medical manipulations can also provoke pulmonary edema: rapid removal of pleural transudate or ascitic fluid.

Development

In the development of pulmonary edema, regardless of the cause, an acute increase in hydrostatic pressure in the capillaries of the pulmonary circulation and an increase in the permeability of the capillary wall are important. Hypertension of the pulmonary circulation in acute left ventricular failure and increased permeability of the vascular wall create conditions for the liquid part of the blood to sweat into the interstitial tissue and alveoli. Protein-rich transudate forms a stable foam in the alveoli, which reduces the respiratory surface of the lungs and leads to the development of severe respiratory failure.

Acute left ventricular failure complicates the course of a number of pathological conditions: myocardial infarction (paroxysmal tachycardia), detachment of the papillary muscle, hypertensive crisis; it occurs in atherosclerotic and post-infarction cardiosclerosis, aortic heart defects (usually aortic valve stenosis), myocarditis, and cardiomyopathy.

The picture of pulmonary edema can develop in a practically healthy person with significant physical activity due to rupture of the chordae tendineae of the mitral valve, leading to acute mitral regurgitation.

Pulmonary edema can be caused by a sharp increase in blood flow to the heart due to excessive blood transfusions and transfusions of non-protein solutions. Rapid administration of large volumes of plasma expanders or any drugs can also increase the hydrostatic pressure in the pulmonary capillaries due to reflex irritation of the baroreceptors of the vascular wall. This is especially true when administering chilled medications.

Any overload of the bloodstream due to chronic heart failure - be it excessive fluid intake, or salty foods, or taking drugs that retain sodium in the body (salicylates, butadione) can lead to pulmonary edema.

Another mechanism causing pulmonary hypertension is associated with obstruction of the pulmonary outflow tract, such as left atrioventricular orifice stenosis. Increased permeability of the vascular wall is a leading factor in the pathogenesis of pulmonary edema caused by infectious diseases (influenza, lobar pneumonia, measles, etc.), endogenous (uremia, liver failure) or exogenous intoxication (poisoning with household and industrial poisons), allergies.

Excessive pressure in the pulmonary circulation can be caused by a sharp increase in pulmonary vascular resistance due to mechanical obstacles to blood flow - thromboembolism, thrombosis of the pulmonary arteries, reflex vascular spasm as a result of hypoxia, a decrease in the volume of the vascular bed in chronic nonspecific lung diseases (obstructive emphysema, diffuse or focal pneumosclerosis) . Alveolar hypoxia is of independent importance in the development of pulmonary edema in climbers during rapid ascent to high altitudes (“high-altitude pulmonary edema”).

When the level of blood catecholamines (adrenaline, norepinephrine, etc.) increases, peripheral vasoconstriction (spasm) occurs, which complicates the functioning of the left ventricle due to an increase in systemic blood pressure and tachycardia. This is the mechanism of pulmonary edema in diseases accompanied by increased intracranial pressure and cerebral edema (traumatic brain injury, acute cerebrovascular accident, brain tumors, epileptic seizure). A decrease in negative intraocular pressure is important in the development of pulmonary edema. This kind of effect occurs in acute total obstruction of the respiratory tract (status asthmaticus, laryngeal edema during anaphylactic shock, drowning).

Pulmonary edema can occur with the administration of large volumes of liquid drugs (see above), sympathomimetics (“adrenaline pulmonary edema”), drugs that inhibit myocardial contractility (beta-adrenergic receptor blockers).

Stages of pulmonary edema

Distinguish interstitial and alveolar stages of pulmonary edema.

• The interstitial stage (clinically manifested by cardiac asthma) is characterized by the infiltration of serous fluid throughout the lung tissue, which causes an increase in pulmonary vascular and bronchial resistance. Increasing hypoxia promotes increased permeability of the alveolocapillary membrane.
• The appearance of the liquid part of the blood in the alveoli marks the alveolar stage (pulmonary edema itself). Penetrating fluid damages pulmonary surfactant - a phospholipid that regulates the surface tension of the mucous membrane of the pulmonary alveoli, preventing them from completely collapsing during exhalation.

In the alveoli, the transudate is whipped with inhaled air, forming a protein foam (from 200 ml of liquid, 2-3 liters of foam are obtained), the stability of which is due to its honeycomb-like structure, which prevents the leakage of liquid. Obstruction of the airways by foam causes rapidly increasing respiratory failure. Hypoxemia stimulates the respiratory center, increasing shortness of breath, which does not correspond to the degree of oxygen debt. Deep and frequent breathing helps reduce negative intrathoracic pressure, which entails increased blood flow to the right heart. Blood pressure in the pulmonary circle increases, fluid leakage into the alveoli, whose permeability is reduced due to hypoxia, increases. A picture of pulmonary edema develops, and all the mechanisms of its pathogenesis interact according to the principle of a vicious circle.

Clinic

Cardiac (interstitial pulmonary edema) occurs at any time of the day, but more often at night or in the early morning hours. The attack is provoked by physical exertion, hypothermia, psycho-emotional stress, nightmares, the patient’s transition from a vertical to a horizontal position, while the pulmonary blood volume increases by an average of 300 ml.

Choking occurs or gets worse suddenly. The equivalent of shortness of breath may be a paroxysmal cough. The patient is forced to take a sitting position with his legs dangling from the bed (orthopneic position). The auxiliary respiratory muscles are involved in the act of breathing. Cyanosis of the lips and nails, perspiration, and exophthalmos appear. Patients are excited and restless. Extremities are cold. There may be phenomena of bronchospasm due to swelling of the bronchial mucosa. Cough is dry, superficial or hacking, shortness of breath up to 40-60 per minute. Typical tachycardia. Blood pressure is usually elevated. When percussing the lungs, a boxy sound is noted due to acute pulmonary emphysema. Breathing is loud and intense. When bronchospasm occurs, dry, whistling, scattered wheezes are heard. Moist rales are not detected at this stage of the disease. Heart sounds are difficult to hear due to noisy breathing and wheezing; An enlarged, painful liver and swelling of the lower extremities may be detected.

Cardiac asthma requires differential diagnosis with an attack of bronchial asthma (see table), which is not always easy, especially if bronchospasm occurs in the clinical setting of cardiac asthma. It should be borne in mind that a severe attack of bronchial asthma is often complicated by alveolar pulmonary edema, due to total spasm of the pulmonary vessels.

A chest x-ray may help in diagnosis. In case of cardiac asthma, the image reveals a blurred pulmonary pattern and decreased transparency of the hilar regions of the lungs.

Symptoms

Alveolar pulmonary edema is characterized by severe respiratory failure: severe shortness of breath, increasing diffuse cyanosis. The consciousness of the patients is confused. As the swelling increases, the lethargy deepens, even to the point of coma. The face is puffy, the veins of the neck are swollen. The skin is moist, and during a stroke it is hot due to hyperthermia of central origin. Wheezing in the lungs can be heard from a distance as bubbling. Foam bubbles on the lips of the patients. Its pink color is due to the formed elements of blood penetrating into the alveoli, which is characteristic of influenza and lobar pneumonia. The chest is expanded; during percussion, the percussion sound is mosaic: areas of tympanitis alternate with foci of dullness. When auscultating the lungs, along with dry rales, a mass of sonorous moist rales of various sizes (from small to large bubbles) is heard. The auscultatory picture is dynamic; Wheezing is best heard in the upper and middle parts of the lungs. Blood pressure is often elevated if edema does not occur against the background of shock, but in the terminal stage blood pressure progressively decreases, the pulse becomes thready, breathing is shallow, then of the Cheyne-Stokes type. The patient is unconscious. Death occurs as a result of asphyxia.

X-rays with pulmonary edema reveal intense symmetrical darkening in the central parts of the lungs in the form of a butterfly.

There is a “fulminant”, “hurricane” pulmonary edema, which very quickly leads to death (within a few minutes). This form of acute pulmonary edema can be observed in anaphylactic and poisoning with various poisons, damage to the central nervous system. Subacute pulmonary edema lasting up to 12 hours is characterized by an undulating course: its symptoms increase gradually, sometimes intensifying, sometimes weakening. More often this is characteristic of endogenous intoxication (uremia, liver failure). Protracted forms of pulmonary edema, lasting up to several days, complicate chronic heart failure and chronic nonspecific lung diseases. In the latter case, diagnosis can be difficult. The appearance of moist rales in the lungs against the background of whistling dry rales is difficult to determine.

Treatment

Clarification of the genesis of pulmonary edema is important for the success of therapy (although this is not always possible). In cardiac patients, the main tactical direction should be to reduce hydrostatic pressure in the pulmonary vessels. This is achieved by facilitating the work of the left ventricle by reducing systemic blood pressure. For these purposes, ganglion blockers are used: 0.5-1 ml of a 5% solution of pentamine in 20 ml of isotonic sodium chloride solution is administered slowly intravenously under blood pressure control. To avoid severe hypotension, it is not necessary to administer the entire volume of the drug - after the blood pressure level has decreased by more than the initial systolic blood pressure, the infusion can be stopped.

Controlled hypotension is achieved by intravenous drip administration of arfonade -250 mg in 100-150 ml of saline or 5% glucose solution. The rate of administration is adjusted depending on blood pressure; if it decreases, the flow of solution into the vein is stopped and blood pressure rises slightly.

In recent years, “peripheral vasodilators” have been used - drugs similar to ganglion blockers: nitroglycerin, sodium nitroprusside. Their action is based on reducing venous tone and venous return to the heart, relieving pulmonary vasospasm and reducing overall pulmonary resistance. Due to this, pulmonary hypertension is eliminated. In addition, sodium nitroprusside has a bronchodilator effect: its use is the method of choice for mitral regurgitation: it reduces the resistance to the outflow of blood from the left ventricle into the aorta, which eliminates the reverse flow of blood into the left atrium and thereby reduces the pressure in the pulmonary circle. Therapy can be started by taking the tablet form of nitroglycerin: 1-2 tablets under the tongue, then switch to intravenous drip administration of 1 ml of 0.01% nitroglycerin solution or 50 mg of sodium nitroprusside in 500 ml of 5% glucose solution at a rate of 6-7 drops per minute under blood pressure control. It should be borne in mind the possibility of using ganglion blockers and peripheral vasodilators not only at high, but also at moderately elevated and normal blood pressure.

To reduce the volume of circulating blood and dehydrate the lungs, fast-acting diuretics are used: furosemide (Lasix) 80-120 mg, ethacrynic acid (Uregit) 100-200 mg, administered intravenously as a bolus without dilution. The effect occurs almost immediately (even before diuresis appears) due to the redistribution of blood from the small circle to the large circle.

Diuresis should not be very abundant (no more than 2-3 liters on the first day) due to possible electrolyte disorders. In case of prolonged pulmonary edema, when there is no effect from the administered drugs, osmodiuretics are added - urea at the rate of 1 g of dry matter per 1 kg of patient weight in the form of a 30% solution in a 10% glucose solution is administered intravenously at a rate of 40-60 drops per minute. Urea is contraindicated in severe liver and kidney failure, cerebral edema, stroke, intracranial bleeding. For cerebral edema, mannitol can be used.

Reducing venous flow to the heart is achieved by applying tourniquets to the lower extremities. The latter are compressed in such a way that the pulsation in the arteries is preserved. After the swelling is relieved, the tourniquets are released gradually due to the danger of a sharp increase in the mass of circulating blood. In case of thrombophlebitis, the application of tourniquets is contraindicated. Hot foot baths can also be used. Rapid bloodletting (400-600 ml) is possible for mitral stenosis, if blood pressure allows. To unload the small circle, artificial pulmonary ventilation (ALV) with increased expiratory pressure (10-15 mm water column) is also used.

For pulmonary edema, morphine is effective - 1 ml of a 1% solution intravenously as a bolus: it has a calming effect on the central nervous system, relieves pathological impulses of the overexcited respiratory center, and relieves the pulmonary circulation. The side effects of morphine - activation of the vomiting center and increased bronchospasm - are eliminated to some extent by a combination with 2 ml of droperidol. Administration of morphine is contraindicated in case of bronchospasm and in patients with low breathing volume (hypoventilation).

The use of aminophylline for pulmonary edema is limited by its side effects: it increases the myocardial oxygen demand, causes tachycardia, and activates the respiratory center. We observed cases of rapid transition of cardiac asthma during myocardial infarction to alveolar pulmonary edema after intravenous injection of aminophylline. Its administration is advisable for severe bronchospastic syndrome, mitral stenosis, hypertensive crisis, and stroke. Inject slowly 10 ml of 2.4% aminophylline solution intravenously. Cardiac glycosides, as agents that improve myocardial contractility and reduce heart rate, are used in pulmonary edema very limitedly due to possible toxic effects, increased contractile function of the right ventricle, and lack of rapid effect after administration. For mitral stenosis, glycosides are indicated only for atrial fibrillation. Use corglicon - 1 ml of 0.06% solution, strophanthin - 0.5 ml of 0.05% solution slowly intravenously under heart rate control.

Clearing fluid from the respiratory tract

An indispensable condition for the treatment of pulmonary edema is oxygen therapy. When foaming occurs, when the airways are blocked by foamed liquid, it is necessary to clean the nose and oral cavity using suction. To destroy foam in the bronchi, defoamers are used, which are administered by inhalation: ethyl alcohol (30-40% if the patient is in a coma), through which oxygen is passed in the Gorsky apparatus, 10% alcohol solution of antifomsilane. Inhalation of antifoam agents is alternated with inhalation of oxygen. In the absence of effect, increasing symptoms of respiratory and heart failure, tracheal intubation is performed and the patient is transferred to mechanical ventilation. If the patient is conscious, sodium hydroxybutyrate is used for anesthesia - 10 ml of a 20% solution, talamonal - 2-4 ml intravenously. In addition to the above measures, acidosis is combated: a 4% sodium bicarbonate solution is administered intravenously by drip under the control of the acid-base state. To reduce the increased permeability of alveolocapillary membranes, antihistamines are used (diphenhydramine 1 ml of 1% solution, suprastin 1 ml of 2% solution).

Prescribing calcium gluconate or calcium chloride is ineffective, and in combination with cardiac glycosides it is dangerous (!)

Pulmonary edema that occurs against the background of anaphylactic and cardiogenic shock, drowning, severe bronchospasm, poisoning with medicinal or industrial poisons requires corticosteroid therapy. The latter have antiallergic, bronchodilator and antishock effects. Prednisolone is administered in an average dose of 90-150 mg, hydrocortisone - 150-300 mg (up to 1 g) intravenously. It must be taken into account that large doses of glucocorticoids have a depressant effect on the central nervous system.

Due to the large volume of treatment measures for pulmonary edema in conditions of acute time shortage (pulmonary edema requires immediate intensive care) It is mandatory to carry out the following activities and comply with the following rules: 1) the patient should be in a semi-sitting or sitting position (even with myocardial infarction), if there is no arterial hypotension; 2) morphine, droperidol, thalamonal, sodium hydroxybutyrate are administered intravenously; 3) carry out aspiration of foam from the upper respiratory tract and inhalation of oxygen with an antifoam agent; 4) apply tourniquets to the lower extremities; 5) diuretics, ganglion blockers, peripheral vasodilators are administered intravenously, and for low blood pressure - corticosteroids; 6) sodium bicarbonate, cardiac glycosides, etc. are used. Considering the severity of the patient’s condition and the need for long-term intensive infusion therapy, it is advisable to puncture the subclavian vein using the Seldinger method.

Patients are hospitalized immediately after pulmonary edema is relieved. This is due to the fact that the severity of their condition requires monitoring of the main hemodynamic parameters, taking measures to prevent recurrence of pulmonary edema and its complications (pneumonia).

What are the tactics for intractable pulmonary edema, when, despite all the measures taken, respiratory and heart failure increases? In these cases, hospitalization of the patient is possible even if edema develops on the street, at work, etc. In this case, it is desirable to achieve stabilization of hemodynamics - to reduce elevated blood pressure or ensure its rise in shock. Determining the disease, the complication of which was pulmonary edema, is also important for specialized hospitalization. Thus, patients with intractable pulmonary edema due to mitral orifice stenosis must be taken to a cardiac surgery hospital for emergency mitral commissurotomy.

Hospitalization should be as gentle as possible, in conditions of absolute rest. A relative contraindication for it is off-road use. The patient is not changed, but wrapped in a blanket or blanket. They are delivered to the car on a stretcher with the head end raised. In case of arterial hypotension, the patient’s body position is strictly horizontal. In the ambulance, mask inhalation of oxygen is carried out. If necessary, intravenous drip administration of medicinal solutions is continued under the control of blood pressure and heart rate.

Therapy of pulmonary edema, a syndrome that puts the patient on a narrow line between life and death, requires the physician to exert maximum mental and physical strength.

Pulmonary edema, a life-threatening pathology, requires emergency care and urgent hospitalization of the patient. This condition is characterized by overflow of the pulmonary capillaries, transudation (leakage) of fluid from the vessels into the alveoli and bronchi.

It happens that pulmonary edema appears at night, when a person is sleeping (as a complication of the underlying disease) and during severe physical exertion.

Classification

Pulmonary edema as a complication occurs when there is a disruption in the regulation of the amount of fluid entering and leaving the lungs. Simply put, with this complication, the lymphatic vessels do not have time to remove excess blood filtered from the capillaries. And due to high blood pressure and low protein levels, fluid moves from the pulmonary capillaries to the alveoli of the lungs. That is, the lungs fill with fluid and cease to perform their functions. The causes of pulmonary edema are divided into two groups, with the main one in first place – heart disease:

• Hydrostatic edema– occurs due to diseases in which intravascular hydrostatic pressure increases and fluid leaks from the vessel into the interstitial space, and then into the alveolus. The main cause of this swelling is cardiovascular disease.
• Membranous edema– occurs under the influence of toxins, when the walls of the capillary or alveoli are damaged and the fluid escapes into the extravascular space.

There are two types of this complication: interstitial and alveolar. These, in fact, are stages of the whole process, since the fluid overcomes two barriers (histohematic and histoalveolar). Comparative characteristics of both processes:

	Interstitial	Alveolar
Symptoms of pulmonary edema	Shortness of breath, cough, no sputum	Cough, foamy sputum, wheezing (dry and then wet) heard
Liquid barrier	Histohematic (on the blood-tissue path)	Histoalveolar (on the tissue-alveolus path)
Characteristic	The fluid passes into the interstitial space from the vessel, only the lung parenchyma swells	Blood plasma, overcoming the wall of the alveoli, sweats into its cavity
without providing medical help with progression	Transitions into alveolar	Suffocation, death

Another classification is based on the severity of manifestations.

Causes and development

Cardiogenic – develops in acute left heart failure

Scheme of development of cardiogenic pulmonary edema

The cause of AHF (acute heart failure) may be:

• pathology of the atrium - mitral stenosis
• and the ventricle - myocardial infarction, hypertension, heart defects, as a result of which the contractile functions of the heart muscles are reduced.

With decompensated heart disease, with stagnation in the pulmonary circulation (which also happens with bronchial asthma, emphysema), in case of increased pressure in the capillaries and untimely provision of medical care, pulmonary edema may develop.

In children, cases of cardiogenic pulmonary edema are extremely rare. Their main causes are others: poisoning with harmful substances (for example, turpentine or kerosene fumes), shock, inflammatory reactions, drowning.

Not cardiogenic

• Arose as a result of other reasons:
  • aspiration - foreign matter entering the lungs
  • traumatic - chest injuries
  • shock - in all three cases the pathology is associated with membrane damage
  • cancerous - the lymphatic system of the lungs is disrupted, that is, the outflow of fluid is hampered
  • neurogenic - here the causes of pulmonary edema lie in central mechanisms; with intracranial hemorrhage, with severe convulsions or due to brain surgery, fluid accumulation in the lungs is possible.
• With a sharp ascent to high altitudes (3 km), high-altitude pulmonary edema may occur.
• ARDS - acute respiratory distress syndrome occurs due to injury, severe infectious disease, inhalation of toxins, or pulmonary infections, which disrupts the integrity of the alveoli and increases the risk of fluid leaking into them from the vessels.
• With a sharp process of expansion of the lungs, for example with pneumothorax, with exudative pleurisy - in this case, swelling usually occurs on one side of the lung - unilateral.
• Rare causes include pulmonary embolism, when a blood clot enters the vessels of the lung and clogs them.

Scientists have found that athletes who expose themselves to enormous physical activity have a certain risk of developing pulmonary edema. These are marathon athletes, freedivers, scuba divers, long-distance swimmers, and climbers who climb to great heights. Moreover, some of them experienced mild swelling after receiving the load, and this fact was detected more often in women than in men.

Symptoms

A person subjectively feels the following symptoms of pulmonary edema.

In the initial stage (interstitial edema)	As alveolar edema progresses, the existing sensations are added to
severe inspiratory dyspnea (difficulty in inhaling) with increased breathing at rest, that is, does not depend on physical activity increased sweating dry severe paroxysmal cough growing weakness increased heart rate the cough intensifies while lying down, so the person takes a forced position - the patient sits with his legs dangling anxiety	cough with a lot of foamy, pinkish sputum breathing is wheezing at first, then bubbling, wheezing suffocation veins in the neck swell acrocyanosis (outflow of blood from the extremities, they turn blue and become cold) possible fear of death

Attention! When initial symptoms of pulmonary edema appear, it is important to seek qualified medical attention as soon as possible. help, so you should urgently call an ambulance.

Basic diagnostic methods

History taking	During the interview, the doctor finds out the factors that contributed to pulmonary edema to choose the right treatment tactics. Heart diseases provoke cardiogenic edema, others mentioned above are not cardiogenic.
External examination, during which the doctor reveals:	inspiratory shortness of breath with retraction of the intercostal spaces during inspiration and supraclavicular fossa forced position of the patient cyanosis (blue discoloration) of the face and acrocyanosis (blue discoloration of the extremities) bulging veins in the neck cough is dry or with phlegm wheezing audible in the distance profuse sweating
Auscultation (listening):	interstitial edema - hard breathing, tachycardia (increased heart rate), dry scattered, subsequently wheezing alveolar edema - ringing crepitus, moist rales (starting from the base of the lungs, and then large bubbles over their entire surface), dull heart sounds, a gallop rhythm is heard (a heart rhythm that appears when the heart muscle is damaged), an accent of the second tone over the pulmonary artery (this means increased vibrations of the pulmonary artery leaflets due to increased pressure in the pulmonary circulation)
Percussion	a boxy tone of the sound, dullness over the posterior lower parts of the lungs, and an increase in the borders of the liver are determined.
Palpation	a weak, frequent pulse is detected, the filling of the neck veins is detected, and the degree of moisture of the skin is determined.

An experienced doctor can easily determine the severity of a patient’s condition by the moisture of the skin:

• not severe – dry skin
• moderate severity – forehead with perspiration
• heavy - wet chest
• extremely severe – wet chest and stomach

Additional diagnostic methods

• X-ray examination:
  • interstitial edema – blurred pulmonary pattern, decreased transparency of the perihilar regions
  • alveolar edema – changes in the hilar and basal regions in the form of a focal, diffuse (widespread) form or “butterfly wings”.

• Electrocardiography - reveals signs of heart disease, as well as overload of its left side.
• Echo CG - performed for non-acute pulmonary edema to determine the concomitant disease that provoked this complication.
• Measurement of pulmonary capillary wedge pressure (hydrostatic pressure) using a catheter inserted into the pulmonary artery. This indicator is needed to make a correct diagnosis, since PCWP increases with cardiogenic edema, and remains the same with non-cardiogenic edema.
• A biochemical blood test (transaminases) also allows you to distinguish cardiogenic edema (transaminases are elevated) from non-cardiogenic edema (normal values).

Differential diagnosis

It is important to distinguish pulmonary edema from bronchial asthma in time.

	Pulmonary edema	Bronchial asthma
Anamnesis	Most often cardiac	Allergic
Dyspnea	Inspiratory (difficulty breathing)	Expiratory (difficulty exhaling)
Breath	Bubbling, wheezing, orthopnea	Wheezing involving auxiliary muscles
Sputum	Foamy with a pinkish tint	Viscous, difficult to separate
Percussion	Boxy sound, dullness over some areas	Boxed sound
Auscultation	Hard breathing, moist, coarse rales	Exhalation is prolonged, vesicular breathing with an abundance of whistling, buzzing dry rales
ECG	Overload of the left departments	Changes in the right side of the heart

First aid for swelling

Before the doctor arrives, you can do the following on your own:

• Place the patient in a sitting or half-sitting position with legs down
• Provide reliable access to a large peripheral vein (for subsequent catheterization)
• Organize access to fresh air
• Allow the patient to inhale alcohol vapors (96% for adults, 30% for children)
• Take a hot foot bath
• Use venous tourniquets on the limb (from 30 minutes to 1 hour)
• Constantly monitor your breathing and pulse
• In the presence of nitroglycerin and not low blood pressure - 1-2 tablets under the tongue.

Emergency care for pulmonary edema, provided by the ambulance team before arriving at the hospital, is as follows:

• Oxygen therapy (active oxygen saturation)
• Foam suction and anti-foam therapy (oxygen inhalation through ethyl alcohol solution)
• Diuretic therapy (Lasix, Novurit) – removes excess fluid from the body; for low blood pressure, reduced doses of drugs are used
• If there is pain, take painkillers (analgin, promedol)
• Other drugs depending on blood pressure level:
  • high – ganglion blockers (promote blood outflow from the heart and lungs and flow to the extremities: benzohexonium, pentamine), vasodilators (dilate blood vessels: nitroglycerin)
  • normal – reduced doses of vasodilators
  • low – inotropic agents (increase myocardial contractility: dobutamine, dopmin).

Treatment of pulmonary edema

In a hospital setting, therapy is continued.

• Oxygen therapy - inhalation of oxygen with ethyl alcohol to extinguish foam in the lungs
• Narcotic analgesics (painkillers) and antipsychotics (drugs to reduce psychomotor agitation): reduce hydrostatic pressure in the pulmonary vessels and reduce venous blood flow. Drugs: morphine, fentanyl
• Diuretics - reduce the volume of circulating blood, cause dehydration of the lungs: furosemide
• Cardiac glycosides (provide a cardiotonic effect): strophanthin, corglycone
• Other drugs for the treatment of pulmonary edema depending on the blood pressure level (see above)
• Relief and prevention of bronchospasm: aminophylline, aminophylline
• Glucocorticosteroids, surfactant therapy: used for non-cardiogenic pulmonary edema.
• For infectious diseases (pneumonia, sepsis) - broad-spectrum antibiotics.

Important to know: cardiac glycosides are mainly prescribed to patients with moderate congestive heart failure; Glucocorticosteroids are contraindicated for cardiogenic pulmonary edema.

Prevention

For chronic heart failure, ACE inhibitors (medicines for the treatment of hypertension) are prescribed. For recurrent pulmonary edema, isolated blood ultrafiltration is used.

Prevention also involves avoiding factors that provoke pulmonary edema: timely treatment of heart disease, lack of contact with toxic substances, adequate (not increased) physical and respiratory stress.

Pulmonary edema is an acute pathology accompanied by massive movement of fluid from the pulmonary capillaries into the interstitium of the lungs or the cavity of the alveoli.

Etiology

Depending on the etiological factor, swelling of the lung tissue is classified into two groups:

1) Cardiogenic origin.

Developing against the background of myocardial infarction, myocarditis, hypertensive crisis, cardiac arrhythmias, decompensation of valve defects, left ventricular failure provokes an increase in pressure in the pulmonary circulation.

2) Extracardiac origin.

Decrease in oncotic pressure against the background of hypoproteinemia.

Increase in hydrostatic pressure in the vessels of the lungs:

• overhydration due to oliguria or anuria (with kidney failure);
• Iatrogenic fluid overload due to inadequate infusion therapy without taking into account water balance, pressure in the central vessels and diuresis during the day.

Decreased pressure in the alveoli:

• swelling during puncture of the pleural cavities as a result of too rapid release of pleural fluid (drainage of more than 1.5 liters per day is unacceptable);
• swelling at high altitudes, for example in the mountains, associated with a lack of oxygen in combination with spasm of the capillaries of the lungs (Korotkoff reflex).

Increased pulmonary capillary permeability:

• Allergic origin (anaphylactic shock).
• Toxic origin (poisonous gases, aspiration of stomach contents, heroin poisoning, in the elderly taking acetylsalicylic acid). The causes of toxic pulmonary edema are often the same as in the case of respiratory failure due to exposure to toxins.

Other reasons:

Neurogenic edema due to traumatic brain injury, seizures, circulatory disorders in the vessels of the brain. Pulmonary embolism, trauma or surgery on the chest organs, other surgical intervention, etc.

In childhood, compared to adults, pulmonary edema develops mainly against the background of an allergic reaction and is accompanied by symptoms of anaphylaxis. In newborns, its development can be associated with heart defects, meconium aspiration, and trauma during childbirth. The main cause among elderly patients is heart failure.

Mechanism of edema development

The pathogenesis of pulmonary edema is associated with the predominance of fluid filtration in the lung tissue over its reabsorption. An imbalance between fluid secretion and absorption may be based on the following:

1) Increase in hydrostatic pressure.

With an increase in blood volume in the pulmonary circulation, the load on the capillary wall increases. An increase in pressure provokes sweating of the liquid component of the blood into the interstitium of the lung, and then into the alveoli. Filled with liquid, they cease to perform their functions, as a result of which gas exchange is disrupted.

2) Decrease in oncotic pressure.

A pathological decrease in plasma protein leads to a decrease in oncotic pressure in the bloodstream and its relative increase in the interstitium. The release of fluid from the vessels into the intercellular space is an attempt to compensate for this difference.

3) Damage to the alveolocapillary membrane.

Damage to the protein structure of the membrane leads to a violation of its integrity and triggers the process of fluid leakage into the interstitium. The consequence is respiratory dysfunction.

Insufficiency of respiratory function in all cases develops due to a decrease in vital capacity and compliance of the lungs, as well as an increase in resistance in the respiratory tract.

Developing according to one of the pathomechanisms, edema always at the initial stage affects the interstitial space, later accompanied by the penetration of fluid into the cavity of the alveoli. There are four stages during the process:

1. Interstitial pulmonary edema (fluid penetration into the interstitium).
2. Alveolar edema (exudation and transudation of serous fluid into the cavity of the alveoli and bronchioles).
3. Pronounced development of edema, formation of foam in the sputum with an increase in the initial volume of fluid in the lungs.
4. Gas exchange disorders, and as a result, asphyxia.

Clinic

The most common symptoms of interstitial edema are:

• increased breathing (tachypnea), disturbance of the rhythm of respiratory movements, shortness of breath, increasing in a horizontal position, mainly at night and in the morning;
• Auscultation - hard breathing, dry wheezing;
• cough with watery sputum, sometimes mixed with blood;
• orthopnea (forced sitting position);
• anxiety, increased sweating.

Alveolar pulmonary edema, in addition to the listed symptoms, is characterized by:

• severe shortness of breath, accompanied by a feeling of fear, turning into suffocation;
• pale skin or cyanosis of the face and upper half of the body;
• puffiness of the face, swelling of the veins of the neck;
• auscultation - moist rales (in the most severe cases they can be heard remotely);
• frothy sputum, possibly mixed with blood;
• tachycardia, blood pressure may fluctuate (its increase is noted during a hypertensive crisis, and decrease during shock).

In each situation, the clinical picture is individual and depends primarily on the cause of the swelling. In one case, signs of pulmonary edema are combined with symptoms of left ventricular failure (edema of the extremities, enlarged liver). In another, there are, for example, symptoms of inhalation poisoning, overhydration or injury.

Diagnostics

The disease is diagnosed based on clinical, instrumental and laboratory data.

Pulse oximetry is required - registration using a sensor of the degree of oxygen saturation of the blood (with edema, the parameters are reduced).

X-ray examination reveals opacities in the lungs diffusely on both sides. In the case of left ventricular failure - expansion of the borders of the heart, Kerley lines (horizontal bilateral stripes in the phrenic-costal sinuses).

Electrocardiography and ultrasound examination of the heart provide information in the case of cardiogenic genesis of the pathology. In case of poisoning, material is taken for analysis (for example, urine and blood for drugs).

Laboratory tests that are necessary include a general and biochemical analysis of blood, urine, coagulogram, and a study of the acid-base composition of arterial blood. In the latter, there is a decrease in the partial pressure of oxygen, signs of respiratory alkalosis, subsequently with acidosis and a decrease in blood pH (at a late stage).

It is necessary to differentiate between non-cardiogenic pulmonary edema and edema of cardiac origin. Signs that allow you to reliably diagnose the latter are:

1. An increase in pulmonary artery wedge pressure (PAWP) above 18–20 mm Hg. Art.
2. Increased central venous pressure (CVP) more than 120 mmHg. Art.
3. Decreased cardiac output.
4. ECHO and electrocardiographic signs of heart failure of various etiologies.

In addition, edema is differentiated from pneumonia. Distinctive signs of inflammation are rather unilateral changes in lung tissue, auscultatory signs of infiltration, and hyperthermia.

With bronchial asthma, pulmonary edema is distinguished on the basis of anamnesis (asthmatic attacks in the past), the nature of shortness of breath (expiratory in the first case, mixed with edema). The clinic also makes it possible to distinguish these two diseases (asthma is characterized by dry wheezing and dry skin during an attack).

Treatment

Emergency care for swelling includes a number of points:

1. Oxygen therapy through nasal catheters or a face mask.
2. The use of defoamers by inhalation or into a vein (ethyl alcohol reduces the surface tension of foam in sputum and promotes its deposition).
3. Sanitation of the oropharynx and tracheobronchial tree.
4. Giving the patient an optimal sitting position with his legs lowered, applying venous tourniquets to the limbs for a short time is allowed. This helps to reduce venous return, and thereby the hydrostatic pressure in the pulmonary capillaries.
5. Sedation: Morphine or Diazepam under the control of respiratory parameters (contraindicated in respiratory depression, hypotension, lack of consciousness).
6. Reducing afterload in a patient with cardiogenic pulmonary edema: Furosemide or Nitroglycerin (in tablets under the tongue, in an aerosol or intravenous infusion). Prescribing the drug requires caution in case of hypotension (it is rational to administer it together with Dopamine).
7. Inotropic support in case of reduced myocardial contractility and severe hypotension (Dopamine, Dobutamine, Norepinephrine).
8. Glucocorticosteroids for edema of an allergic or toxic nature. Steroid therapy is also used to prevent swelling due to inhalation of gases that irritate the mucous membranes. Toxic pulmonary edema can occur even after a latent stage lasting more than 12 hours.
9. The use of non-invasive methods of breathing support (CPAP therapy - oxygen supply through a mask under constant positive pressure) is effective. In case of increasing respiratory failure, tracheal intubation and transfer to artificial ventilation in the mode with positive end-expiratory pressure (PEEP) are performed.
10. Toxic pulmonary edema that does not respond to conservative treatment may require the use of extracorporeal membrane oxygenation (ECMO).

In the future, etiological therapy includes influencing the factor that provoked the swelling:

• reduction of pre- and afterload during hypertensive crisis;
• treatment of acute left ventricular failure (for example, thrombolytic therapy or percutaneous angioplasty for myocardial infarction);
• treatment of heart rhythm disturbances;
• dialysis therapy for renal failure with overhydration;
• for edema caused by altitude, oxygen therapy and delivery of the patient to a lower location is indicated.

Prognosis and prevention

The prognosis of the disease depends on the triggering factor, the age and health of the patient, and the timeliness of treatment. A toxic form of edema, often occurring at lightning speed, is associated with an unfavorable prognosis. Cardiogenic edema is also prognostically unfavorable, especially against the background of myocardial infarction, shock, and ventricular arrhythmias. The disease is more difficult for older patients with a history of concomitant pathology.

Mortality is significantly increased by complications:

• From the lungs - pneumonia, atelectasis, asphyxia.
• From the heart - cardiogenic shock, asystole, hemodynamic instability.
• Sepsis, etc.

Primary prevention is based on the prevention of edema in patients at risk. It includes timely diagnosis and treatment of arrhythmias, heart failure, hypertension, restriction of activity of patients with severe pathology of the kidneys and liver. Compliance with the doctor’s prescriptions and recommendations also allows you to avoid relapses of the disease, which are usually more difficult to tolerate.

Pulmonary edema is a pathological process, the occurrence of which is associated with the release of transudate of non-inflammatory origin from the capillaries into the interstitium of the lung, and then into the alveoli. The result of this process is reduced performance of the alveoli and impaired gas exchange, and hypoxia is formed. Significant changes also occur in the gas composition of the blood, as the carbon dioxide content increases. In combination with hypoxia, the patient has a strong suppression of the central nervous system. All this requires immediate medical attention, otherwise the consequences can be dire.

Symptoms

If you identify the symptoms of the pathology in time, then emergency care for pulmonary edema will significantly reduce the risk of complications. If the disease is in an advanced phase, the patient has difficulty breathing due to shortness of breath. It does not matter what condition the patient is in: performing physical activity or just lying down.

Pulmonary edema is a pathology that leads to oxygen starvation, which negatively affects the functioning of other organs. During examination with a stethoscope, wheezing may be heard, indicating fluid accumulation in the alveoli.

In addition, pulmonary edema can be recognized by the following symptoms:

1. Dizziness is a common symptom of the pathology.
2. Often, against this background, the patient develops drowsiness and apathy.
3. If the disease takes a lightning-fast form, then this is fraught with suffocation, which affects a person at night.
4. Cough, the formation of sputum, which over time becomes very liquid and resembles ordinary water.
5. Difficulty breathing, wheezing and whistling.
6. Pale skin and increased sweating.

Very often, a person experiences illness associated with thoughts of death. The duration of the attack is 30 minutes, so first aid is very important at this time. Only if it is carried out correctly can the death of the victim be avoided.

Classification of pathology

In addition to the indicated symptoms, for proper first aid, it is important to know the types of pulmonary edema:

1. Membranogenic - formed against the background of a sharp increase in capillary permeability. This pathology develops against the background of other syndromes.
2. Hydrostatic – affects due to diseases characterized by a sharp increase in hydrostatic pressure in the vessels. The liquid part of the plasma can come out in such a volume that it cannot be removed through the lymphatic pathways.

Correct condition assessment

Taking into account the rate of transformation of the interstitial stage of edema into the alveolar stage, it is necessary to assess the condition of the victim. If there are chronic diseases, then the development of edema occurs slowly and smoothly, more often at night. This pathological process can be easily eliminated with medications. If the edema is caused by mitral valve defects or damage to the pulmonary parenchyma, then an increase in its symptoms is observed. The patient's condition noticeably worsens. Acute pathology requires a quick response and first aid, since its development occurs very rapidly.

First aid

Having discovered signs of a pathological process in a person, it is necessary to immediately begin providing emergency care. In this case, first aid for pulmonary edema involves the following algorithm of actions:

1. Place the victim in a semi-sitting position.
2. Remove foam from the upper respiratory tract. For these purposes, it is necessary to use oxygen inhalation through 33% ethanol.
3. Relief of acute pain syndrome. Neuroleptics will help in resolving this issue.
4. Restore heart rhythm.
5. Correct electrolyte balance.
6. Normalize acid-base balance.
7. Bring hydrostatic pressure in the pulmonary circulation back to normal. For this purpose, narcotic analgesics such as Omnopon and Promedol are used. Their action is aimed at suppressing the respiratory center, eliminating tachycardia, reducing blood flow in the veins, lowering blood pressure, reducing anxiety and fear of death.
8. Give the victim vasodilator medications. Nitromint aerosol has an excellent effect. When used, it is possible to reduce vascular tone and intrathoracic plasma volume. When using nitroglycerin preparations, it is possible to facilitate the outflow of blood from the lungs by affecting peripheral vascular resistance.
9. Application of venous tourniquets to the lower extremities. Such measures must be carried out in order to reduce CTC. This method has been actively used for several decades. To dehydrate the lung parenchyma, Lasix is ​​used in an amount of 40 ml. He is being administered intravenously. Its effect is achieved within a couple of minutes and lasts 3 hours. The drug is capable of removing 2 liters of urine in a short time. With a reduced blood volume and increased colloid osmotic pressure, the edema fluid passes into the bloodstream. Filtration pressure decreases. Giving the victim diuretics is allowed only after blood pressure has normalized.
10. Administration of cardiac glycosides to increase myocardial contractility.
11. Urgent hospitalization.

Consequences of an ambulance

Often, when providing first aid to a patient, the condition may, on the contrary, worsen and cause a number of the following complications:

1. Formation of a transient form of pathology.
2. Frequent foam production causes airway obstruction.
3. Respiratory depression.
4. Anginal pain. Such pain syndrome becomes simply unbearable, so the patient may develop pain shock, which negatively affects the overall prognosis.
5. Blood pressure cannot stabilize. Often the pathology occurs against a background of low and high blood pressure. Indicators can alternate within a significant amplitude. The vessels cannot withstand such a load, so the patient’s condition worsens.

Treatment of the disease

After providing first aid, the patient must be urgently hospitalized. Already in a hospital setting, the victim will be prescribed the following treatment:

1. Inhalation of oxygen in combination with ethyl alcohol. Such activities will help remove foam from the lungs.
2. Painkillers and medications to reduce psychomotor agitation. To reduce hydrostatic pressure in the vessels of affected organs and reduce the flow of venous blood, Morphine or Fentanyl is prescribed.
3. Diuretics, the action of which is aimed at reducing the volume of moving blood. Furosemide, which dehydrates the lungs, is considered effective.
4. Cardiac glycosides help achieve a cardiotonic effect. Strophanthin and Korglikon are prescribed.
5. To remove bronchospasm and for prevention purposes, the patient takes Euphyllin and Aminophylline.
6. If there is an infectious disease, then broad-spectrum antibiotics are indispensable.

Pulmonary edema is a very serious and dangerous disease, since if emergency assistance is not provided, there is a risk of death. If all treatment measures were carried out on time and correctly, then there is no need to worry, since after effective therapy prescribed by the doctor, the victim’s condition will noticeably improve.

Pulmonary edema is not a separate disease, but rather a complication of a number of pathologies. Its essence lies in the excessive accumulation of fluid in the tissues of the lung, its sweating into the lumen of the alveoli, which leads to a deterioration in respiratory function and the death of the patient.

Anatomy and physiology of the pulmonary gas exchange system

The lungs are a complex of hollow tubes of small diameter, at the end of each of which there are alveoli - saccular thin-walled formations filled with air. All these structures are shrouded in threads consisting of connective tissue. These threads form a kind of framework that forms the lung itself and is called the interstitium. Part of the interstitium is the interalveolar septa, penetrated by capillaries.
The wall of the alveoli and capillary, together with the interstitial tissue, form an alveolo-capillary membrane (ACM) 0.2-2 microns thick, through which oxygen and carbon dioxide diffuse into/from the blood.

Mechanism and causes of development of pulmonary edema

The appearance of pulmonary edema (PE) can be caused by many reasons, but regardless of the factor that caused the complication, the mechanism of its development is the same - the accumulation of excess fluid in the interstitial tissues, the resulting thickening of the alveolar-capillary membrane and a decrease in the diffusion of gases (primarily oxygen). As a result, tissue hypoxia occurs (oxygen starvation of all tissues) and acidosis - a shift in the acid-base balance, leading to the inevitable death of the patient if he is not given emergency assistance.
There is no unified classification of pulmonary edema, but according to the pathogenetic mechanism it can be divided into:

1. OB due to increased capillary pressure as a result of:
   • acute;
   • cardiac;
   • cardiomyopathies;
   • myocarditis;
   • exudative pericarditis;
   • pulmonary artery stenosis;
   • massive infusion of blood replacement solutions;
   • renal failure in the anuric phase.
2. OB due to increased permeability of the capillary wall with:
   • acute respiratory distress syndrome;
   • intoxications (for example, narcotic drugs);
   • anticancer chemotherapy;
   • use of X-ray contrast agents;
   • inhalation of toxic substances;
   • allergies.
3. OB due to impaired lymphatic drainage due to cancerous lesions of the lymphatic vessels.
4. OB due to changes in intrathoracic interstitial pressure during decompression sickness and evacuation (removal) of fluid from the pleural cavity.
5. OL due to a decrease in protein content in the blood plasma.
6. Mixed OL:
   • neurogenic;
   • postoperative;
   • with eclampsia;
   • with ovarian hyperstimulation syndrome;
   • with altitude sickness.

Previously, a classification was used that included types of pulmonary edema such as interstitial and alveolar. Currently, it has been abandoned, since these two types of OA are actually only stages of the development of the syndrome. In addition, in terms of diagnosis and treatment, such a division does not provide any useful function.
Normally, only a small amount of fluid from the interstitium penetrates into the alveoli. Almost all of it is absorbed into the blood and lymphatic capillaries and removed from the alveolo-capillary membrane. However, if the permeability of the ACM is impaired, there is too much fluid and it does not have time to move all of it into the vessels. In this case, it permeates the interstitium, increasing its thickness, and in the most advanced situation it begins to enter the lumen of the alveoli, further worsening gas exchange.

The symptoms of pulmonary edema depend little on the factors that led to its development. The difference between OB caused by disorders in the cardiovascular system and edema not associated with cardiac causes lies only in the speed of development of the pathology.

OL associated with disorders in the circulatory system

With cardiogenic pulmonary edema (caused by circulatory disorders), the first symptom is cardiac asthma, manifested by shortness of breath at rest, increased respiratory movements, a feeling of severe lack of air, and suffocation. Most often, the attack begins at night, the patient immediately wakes up and takes a sitting position in which it is easier for him to breathe. At the same time, he lowers his legs from the bed and rests his hands on its edge. This is the orthopnea position, which is accepted by almost every patient.
The onset of pulmonary edema is characterized by a desire to go to the window and breathe fresh air. In this state, the patient practically does not speak, but emotional stress is clearly visible on his face. As doctors put it, “the patient completely surrenders to the struggle for air.” The skin becomes pale, the nasolabial triangle becomes bluish (acrocyanosis). This indicates an increase in hypoxia. Cold, sticky sweat may appear - a sign of impending cardiogenic shock, which is an extremely severe complication of any cardiac pathology. With further development, the patient's breathing becomes noisy, bubbling in his chest can be heard even at a distance, and pink, foamy sputum may be released in large volumes. At this stage, the amount of liquid already far exceeds the capacity of the capillaries to remove it, and the liquid part of the blood begins to penetrate into the alveoli.

Non-cardiogenic edemalungs

In this case, the phenomenon of pulmonary edema occurs due to damage to the alveolo-capillary membrane by various factors (microbial toxins, chemicals, allergy mediators, etc.). Unlike cardiogenic, this type of OA appears only after a relatively long time after exposure to the damaging agent (up to 48 hours). The symptoms of non-cardiogenic pulmonary edema are exactly the same as those of its cardiac form. The only difference is that cardiogenic OA is much easier to treat and resolves faster, completely disappearing after 2-4 days. Non-cardiogenic edema has to be treated for 1-3 weeks, very often (up to 80% of cases) it ends in death. But even in case of successful treatment, this form of OA is accompanied by persistent residual effects.

Diagnosis of pulmonary edema

Anamnesis data are very important for diagnosing pulmonary edema. And although sometimes it is not possible to obtain them, it is information about existing diseases that can lead the doctor to think about the causes of the complication. After clarifying the medical history, the patient is examined and auscultated. At this moment, changes in the color of the skin and mucous membranes, profuse sweat are detected, attention is drawn to the patient’s posture when breathing, and his behavior. When listening to the lungs, wheezing and hard breathing are noted; when listening to the heart, there is a muffled sound, a “gallop” rhythm, and murmurs. The main indicator of pulmonary edema is a decrease in blood oxygen saturation. To identify it, pulse oximetry is used - a method available to any ambulance team.
Hemodynamic disorders are detected by measuring blood pressure and counting heart rate. It is necessary to conduct emergency electrocardiography taking into account the patient's condition - this method allows you to identify the causes of the cardiogenic form of edema and develop optimal treatment tactics. In a hospital setting, an additional chest x-ray is performed, which reveals signs of pulmonary edema and some pathologies that led to it. Using this study, it is possible to relatively accurately differentiate the causes of the disease. Other methods for diagnosing pathology are also used:

• echocardiography, which allows to identify abnormalities or pathology of the heart valves leading to hemodynamic disorders;
• catheterization of the pulmonary artery to detect changes in pressure indicators in this vessel;
• transpulmonary thermodilution, which allows you to determine the degree of edema;
• biochemical blood test, which identifies some pathological conditions that can lead to OL;
• blood gas composition is the most important analysis that provides information about the saturation of the blood with oxygen and carbon dioxide.

Treatment and emergency care for pulmonary edema

The first step in treatment of OA is oxygen therapy. Inhaling pure oxygen to patients can reduce the degree of hypoxia, straighten the alveoli and improve the transport of gases into the blood. This gives doctors the necessary time to administer medications that can eliminate the pathology. In the presence of hemorrhagic foam, oxygen is passed through an aqueous-alcohol solution, since ethanol is capable of destroying bubbles. If there is no effect from standard oxygen therapy, they switch to inhaling oxygen through a breathing mask under pressure. In particularly severe cases, tracheal intubation and artificial ventilation may be required. Drug therapy depends on the pathology that led to the development of pulmonary edema:

Decrease in systolic blood pressure below 90 mm Hg. Art. is an unfavorable sign. In this case, nitrates are contraindicated even in the presence of a heart attack; dopamine drugs are prescribed instead. A frequent “companion” of cardiogenic pulmonary edema is bronchospasm. When this syndrome is detected, bronchodilators are prescribed.

Prevention of pulmonary edema

Since this syndrome most often occurs in people suffering from chronic diseases, timely treatment can reduce the likelihood of pulmonary edema. It is impossible to completely exclude its occurrence, especially with long-term arrhythmias, coronary heart disease, heart defects and heart failure. However, careful monitoring of the condition by a doctor and strict adherence to all medical recommendations helps to avoid decompensation of these diseases, and therefore the development of their complications, including pulmonary edema. Bozbey Gennady, medical columnist, emergency doctor