Pulmonary edema clinic diagnostics intensive care. Pulmonary edema: symptoms, causes and emergency care

Pulmonary edema– a syndrome that occurs suddenly and is characterized by the accumulation of fluid in the lungs (in the interstitium, pulmonary alveoli), followed by disruption of gas exchange in the lungs and the development of hypoxia (lack of oxygen in the blood), manifested by cyanosis (cyanosis) of the skin, severe suffocation (lack of air).

The lungs are a paired organ that participates in the exchange of gases between the blood and the pulmonary alveoli. Participating in gas exchange are the walls of the pulmonary alveoli (thin-walled sac) and the walls of the capillaries (surrounding the alveoli). Pulmonary edema develops as a result of the transfer of fluid from the pulmonary capillaries (due to high pressure or low blood protein levels) into the alveoli of the lungs. Lungs filled with water lose their functional ability.
Pulmonary edema, depending on the causes, is of two types:

  • Hydrostatic edema– develops as a result of diseases that lead to an increase in intravascular hydrostatic pressure and the release of the liquid part of the blood from the vessel into the interstitial space, and subsequently into the alveoli;
  • Membranous edema– develops as a result of the action of toxins (endogenous or exogenous) that disrupt the integrity of the alveolar wall and/or capillary wall, with subsequent release of fluid into the extravascular space.
The first type of pulmonary edema is more common, this is associated with a high incidence of cardiovascular diseases, one of which is coronary heart disease (myocardial infarction).

Anatomy and physiology of the lung

The lung is a paired organ of the respiratory system, located in the chest cavity. The left and right lungs are located in separate pleural sacs (membranes), separated by the mediastinum. They differ slightly from each other in size and some anatomical structures. The lung resembles the shape of a truncated cone, with the apex facing upward (toward the collarbone) and the base downward. Lung tissue has high elasticity and extensibility, and is an important point in the performance of the respiratory function. A bronchus, vein, artery and lymphatic vessels pass through each lung from the inside.

In order to understand where exactly fluid accumulates during pulmonary edema, it is necessary to know their internal structure. The formation of the lung frame begins with the main bronchi, which flow into each lung, which in turn are divided into 3 lobar bronchi, for the right lung, and 2 for the left lung. Each of the lobar bronchi is divided into segmental bronchi, which end in bronchioles. All of the above formations (from the main bronchi to the bronchioles) form the bronchial tree, which performs the function of conducting air. The bronchioles flow into the secondary pulmonary lobules, and there they are divided into bronchioles of the 2nd-3rd order. Each secondary pulmonary lobule contains about 20 bronchioles of the 2nd-3rd order, and they, in turn, are divided into respiratory bronchioles, which, after division, flow into the respiratory passages, ending in alveoli (sacs). There are about 350 million alveoli in each lung. All alveoli are surrounded by capillaries, both of these structures actively participate in gas exchange; with any pathology of one of the structures, the process of gas exchange (oxygen and carbon dioxide) is disrupted.

  • The mechanism of external respiration and gas exchange in the lungs
When inhaling, which occurs with the help of the respiratory muscles (diaphragm, intercostal muscles and others), air from the atmosphere enters the respiratory tract. As atmospheric air moves through the respiratory tract (nasal or oral cavity, larynx, trachea, main bronchi, bronchioles), it is cleaned and warmed. Air (oxygen), having reached the level of the pulmonary alveoli, undergoes diffusion (penetration) through their wall, the basement membrane, and the wall of the capillaries (in contact with the alveoli). Oxygen that reaches the bloodstream attaches to red blood cells (erythrocytes) and is transported to tissues for nutrition and vital functions. In exchange for oxygen, carbon dioxide (from tissues) enters the alveoli from the blood. Thus, the cells and tissues of the human body breathe.
  • Lung circulation
To carry out the function of gas exchange, both arterial and venous blood flows to the lungs. Venous blood to the lungs flows through the branches of the pulmonary artery (it leaves the right ventricle), which pass into the lungs through their inner surface (the hilum of the lungs). As the bronchi divide, the arteries also divide, down to the smallest vessels called capillaries. Capillaries formed from the pulmonary arteries are involved in the release of carbon dioxide to the lungs. In return, oxygen from the alveoli enters through the venules, which form capillaries. Arterial blood (enriched with oxygen) flows through venules and veins. When leaving the lungs, many veins merge into 4 veins, which open into the left atrium. The entire path of blood covered above is called the pulmonary circulation. The systemic circulation is involved in the transfer of arterial blood (oxygen) to the tissues and their saturation.

Mechanisms of development of pulmonary edema

Pulmonary edema develops according to 3 main mechanisms:
  • Increased hydrostatic pressure (increased blood volume). As a result of an acute increase in pressure in the capillaries involved in the formation of the pulmonary circulation, the permeability of the capillary wall is disrupted, with the subsequent release of the liquid part of the blood into the interstitial tissue of the lung, which the lymphatic system is not able to cope with (drain), as a result of which the alveoli are saturated with liquid . Alveoli filled with water are unable to participate in gas exchange, which leads to an acute lack of oxygen in the blood (hypoxia), followed by blue discoloration of the tissues (accumulation of carbon dioxide) and symptoms of severe suffocation.
  • Reduced oncotic (low protein levels) blood pressure. A difference arises between the oncotic pressure of the blood and the oncotic pressure of the intercellular fluid, and in order to compare this difference, the fluid from the vessel exits into the extracellular space (interstitium). Thus, pulmonary edema develops with its clinical manifestations.
  • Direct damage to the alveolocapillary membrane. As a result of various causes, the protein structure of the alveolar capillary membrane is damaged, the release of fluid into the interstitial space is damaged, followed by the consequences listed above.

Causes of pulmonary edema

  • Decompensated heart diseases, accompanied by failure of the left side of the heart and stagnation in the pulmonary circulation (mitral valve defects, myocardial infarction). If the defects are pronounced and medical care is not provided during the procedure, the pressure in the pulmonary circulation (in the capillaries) increases, with the possible development of pulmonary edema, due to the mechanism of increased hydrostatic blood pressure. Also the causes of stagnation in the pulmonary circulation are: emphysema, bronchial asthma;
  • Thromboembolism of the pulmonary artery or its branches. In patients who are predisposed to the formation of blood clots (hypertension, varicose veins of the lower extremities or others), under certain unfavorable conditions a blood clot forms, or an existing blood clot breaks off. Through the blood flow, a thrombus can reach the pulmonary artery or its branches, and if the diameter of the thrombus and the diameter of the vessel coincide, a blockage occurs, which leads to an increase in pressure in the pulmonary artery ˃25 mm/Hg, and the pressure in the capillaries increases accordingly. All of the above mechanisms lead to an increase in hydrostatic pressure in the capillaries and the development of pulmonary edema;
  • Toxins (endogenous or exogenous) and diseases accompanied by the release of toxins that can disrupt the integrity of the alveolar capillary membrane. These include: overdose of certain medications (Apressin, Myelosan, Fentanyl and others), toxic effects of bacterial endotoxins during sepsis (infection entering the blood), acute lung diseases (pneumonia), inhalation and overdose of cocaine, heroin, radiation damage to the lungs and others . Damage to the alveolocapillary membrane leads to an increase in its permeability, release of fluid into the extravascular space and the development of pulmonary edema;
  • Diseases accompanied by a decrease in protein levels in the blood (low oncotic pressure): liver disease (cirrhosis), kidney disease with nephrotic syndrome and others. All of the above diseases are accompanied by a decrease in blood oncotic pressure and contribute to the possible development of pulmonary edema according to the mechanism described above;
  • Chest injuries, prolonged compression syndrome (Crash syndrome), pleurisy (inflammation of the pleura), pneumothorax (air in the pleural cavity);
  • Uncontrolled intravenous infusion of solutions, without forced diuresis (Furosemide), leads to an increase in hydrostatic blood pressure with the possible development of pulmonary edema.

Symptoms of pulmonary edema

Symptoms of pulmonary edema appear suddenly, most often at night (associated with the patient’s supine position) and begin with the following manifestations:
  • Attacks of severe, painful suffocation (lack of air), intensified in a lying position, so the patient must take a forced position (sitting or lying down), develop as a result of lack of oxygen;
  • Severe shortness of breath develops in a patient at rest (i.e. not associated with physical activity);
  • Pressing pain in the chest associated with lack of oxygen;
  • A sharp increase in breathing (shallow, bubbling, audible at a distance), associated with stimulation of the respiratory center by carbon dioxide that has not been released;
  • Rapid heartbeat due to lack of oxygen;
  • First, coughing, and then a cough with severe wheezing and the release of foamy, pink sputum;
  • The patient's facial skin is gray-bluish in color, with subsequent growth to other parts of the body, associated with the accumulation and disruption of the release of carbon dioxide from the blood;
  • Cold sticky sweat and pale skin develop as a result of centralization of blood (from the periphery to the center);
  • The veins in the neck swell, which occurs as a result of stagnation in the pulmonary circulation;
  • Increased blood pressure may develop;
  • The patient’s consciousness is confused, if medical care is not provided during the period, up to the absence of consciousness;
  • The pulse is weak, thread-like.

Diagnosis of the causes of pulmonary edema

Before carrying out all the necessary research methods, it is very important to carefully collect an anamnesis, in which you can find out the possible cause of the development of pulmonary edema (for example: heart failure, renal failure, or others).

If the patient is confused and unable to talk to him, then it is necessary to carefully evaluate all clinical manifestations in order to determine the possible cause of the development of pulmonary edema in order to eliminate its consequences. The plan of laboratory and instrumental examination methods for each patient is selected individually, depending on the clinical manifestations and the possible cause of pulmonary edema.

  • Percussion of the chest: dullness of the chest above the lungs. This method is not specific; it confirms that there is a pathological process in the lungs that contributes to the compaction of lung tissue;
  • Auscultation of the lungs: hard breathing is heard, the presence of moist, coarse rales in the basal parts of the lungs;
  • Pulse measurement: with pulmonary edema, the pulse is frequent, thread-like, weakly filled;
  • Blood pressure measurement: most often the pressure rises, above 140 mm/Hg;

Laboratory diagnostic methods

  • determining the concentration of gases in arterial blood: partial pressure of carbon dioxide 35 mm/Hg; and partial pressure of oxygen 60 mm/Hg;
  • Biochemical blood test: used to differentiate the causes of pulmonary edema (myocardial infarction or hypoproteinemia). If pulmonary edema is caused by myocardial infarction, then the level of troponins in the blood increases 1ng/ml and the MB fraction of creatine phosphokinase 10% of its total amount.
If the cause of pulmonary edema is hypoproteinemia (low protein levels in the blood), in this case, the level of total protein decreases
  • Coagulogram a (blood clotting ability) changes with pulmonary edema caused by pulmonary embolism. Increase in fibrinogen 4 g/l, increase in prothrombin 140%.

Instrumental diagnostic methods

  • Pulse oximetry (determines the concentration of oxygen binding to hemoglobin), detects low oxygen concentration, below 90%;
  • Measurement of central venous pressure (blood flow pressure in large vessels) using a Waldmann phlebotonometer connected to a punctured subclavian vein. With pulmonary edema, central venous pressure increases 12 mm/Hg;
  • Chest X-ray reveals signs confirming the presence of fluid in the lung parenchyma. A homogeneous darkening of the pulmonary fields is detected in their central sections, on both sides or on one side, depending on the cause. If the cause is related, for example, to heart failure, then edema will be noted on both sides; if the cause is, for example, unilateral pneumonia, then the edema will accordingly be unilateral;
  • Electrocardiography (ECG) allows you to determine changes in the heart if pulmonary edema is associated with cardiac pathology. The ECG may record: signs of myocardial infarction or ischemia, arrhythmias, signs of hypertrophy of the walls, left side of the heart;
  • Echocardiography (Echo CG, ultrasound of the heart) is used if the ECG reveals the above changes, to determine the exact cardiac pathology that caused pulmonary edema. The following changes may be noted on Echo CG: reduced cardiac ejection fraction, thickening of the walls of the heart chambers, the presence of valve pathology and others;
  • Pulmonary artery catheterization is a complex procedure and is not necessary for all patients. It is often used in cardiac anesthesiology, performed in the operating room, in patients with cardiac pathology, which is complicated by pulmonary edema, if there is no reliable evidence about the effect of cardiac output on pressure in the pulmonary artery.

Treatment of pulmonary edema

Pulmonary edema is an emergency condition, so at the first symptoms it is necessary to call an ambulance. Treatment is carried out in the intensive care unit, under the constant supervision of the doctor on duty.

A patient with pulmonary edema needs emergency medical care, which is provided during transportation to the hospital:

  • Place the patient in a semi-sitting position;
  • Oxygen therapy: applying a mask with oxygen or, if necessary, intubation of the lungs with artificial ventilation;
  • Apply venous tourniquets to the upper third of the thighs, but so that the pulse does not disappear (for no more than 20 minutes), the tourniquets are removed with gradual relaxation. This is done in order to reduce the flow to the right side of the heart to prevent further increases in pressure in the pulmonary circulation;
  • Nitroglycerin tablet under the tongue;
  • To relieve pain, intravenous administration of narcotic analgesics (Morphine 1% 1 ml);
  • Diuretics: Lasix 100 mg IV.

Treatment in the emergency department, treatment is carried out under strict constant monitoring of hemodynamics (pulse, pressure) and breathing. The attending physician prescribes treatment individually, depending on the clinic and the cause of pulmonary edema. The administration of almost all drugs is carried out through a catheterized subclavian vein.
Groups of drugs used for pulmonary edema:

  • Inhalation of oxygen in combination with ethyl alcohol is used to extinguish the foam that forms in the lungs;
  • Intravenous, drip administration of Nitroglycerin, 1 ampoule diluted with saline, the number of drops per minute depending on the level of blood pressure. Used in patients with pulmonary edema accompanied by high blood pressure;
  • Narcotic analgesics: Morphine - 10 mg IV, fractionally;
  • In case of pulmonary edema, accompanied by a decrease in blood pressure, Dobutamine or Dopamine drugs are administered to increase the force of heart contraction;
  • For pulmonary edema caused by pulmonary embolism, Heparin 5000 units is administered intravenously, then 2000-5000 units per hour, diluted in 10 ml of saline, for an anticoagulant effect;
  • Diuretics: Furosemide initially 40 mg, repeat the dose if necessary, depending on diuresis and blood pressure;
  • If pulmonary edema is accompanied by a low heartbeat, Atropine up to 1 mg, Eufillin 2.4% - 10 ml are administered intravenously;
  • Glucocorticoids: Prednisolone 60-90 mg IV infusion, for bronchospasm;
  • If there is insufficient protein in the blood, patients are prescribed an infusion of fresh frozen plasma;
  • For infectious processes (sepsis, pneumonia or others), broad-spectrum antibiotics (Ciprofloxacin, Imipenem) are prescribed.

Prevention of pulmonary edema

Prevention of pulmonary edema involves early detection of diseases leading to pulmonary edema and their effective treatment. Compensation for cardiac pathologies (coronary heart disease, hypertensive disease, acute cardiac arrhythmias, heart defects) helps prevent the development of pulmonary edema, of cardiac origin, which ranks first.

Also, patients suffering from chronic heart failure must adhere to a diet that includes: limiting the daily intake of table salt and fluid intake, eliminating fatty foods, eliminating physical activity, as it increases shortness of breath. Chronic pulmonary pathologies (pulmonary emphysema, bronchial asthma) are in second place as the causes of the development of pulmonary edema. To compensate for them, the patient must adhere to the following recommendations: be under constant supervision of the attending physician, supportive therapy on an outpatient basis, undergo treatment in a hospital twice a year, prevent possible factors that worsen the patient’s condition (acute respiratory diseases, contact with various allergens, avoidance of smoking and others). Prevention or premature and effective treatment of acute pulmonary diseases (pneumonia of various origins) and other conditions leading to pulmonary edema.



What can be the consequences of pulmonary edema?

The consequences of pulmonary edema can be extremely varied. As a rule, pulmonary edema creates favorable conditions for damage to internal organs. This is due to the fact that due to ischemia, there is a significant decrease in the flow of arterial blood to organs and tissues. Ischemia, in turn, occurs when the pumping function of the left ventricle is insufficient ( cardiogenic pulmonary edema). The most pronounced pathological changes are observed in tissues that require oxygen in large quantities - the brain, heart, lungs, adrenal glands, kidneys and liver. Abnormalities in these organs can aggravate acute heart failure ( decreased contractile function of the heart muscle), which can be fatal.

In addition, after pulmonary edema, some diseases of the respiratory system often occur.

Pulmonary edema can lead to the following diseases:

  • pulmonary atelectasis;
  • congestive pneumonia;
Pulmonary atelectasis is a pathological condition in which the alveoli of one or more lobes of the lung contain little or no air ( air is replaced by liquid). With atelectasis, the lung collapses and does not receive oxygen. It should be noted that large pulmonary atelectasis can displace mediastinal organs ( heart, large blood and lymphatic vessels of the chest cavity, trachea, esophagus, sympathetic and parasympathetic nerves) to the affected side, significantly impair blood circulation and negatively affect the functioning of these tissues and organs.

Pneumosclerosis is the replacement of functional lung tissue with connective tissue ( scar tissue). Pneumosclerosis occurs as a result of inflammatory-dystrophic processes caused by pulmonary edema. Pneumosclerosis is characterized by a decrease in the elasticity of the walls of the affected alveoli. The gas exchange process is also disrupted to a certain extent. In the future, due to the proliferation of connective tissue, bronchi of different calibers may become deformed. If pneumosclerosis is limited ( occurs in a small area of ​​lung tissue), then, as a rule, the gas exchange function does not change much. If pneumosclerosis is diffuse, affecting most of the lung tissue, then there is a significant decrease in the elasticity of the lungs, which affects the gas exchange process.

Congestive pneumonia is a secondary inflammation of the lung tissue that occurs against the background of hemodynamic disturbances ( circulatory disorder) in the pulmonary circulation ( ). Congestive pneumonia is a consequence of pulmonary veins overflowing with blood, which occurs due to impaired blood outflow due to insufficient function of the left ventricle of the heart. This pathology is manifested by cough, shortness of breath, separation of mucous and/or purulent sputum, increased body temperature to 37 - 37.5ºC, weakness, and in some cases, hemoptysis ( hemoptysis).

Emphysema is a pathological expansion of the terminal ( distal) bronchioles along with damage to the walls of the alveoli. With this pathology, the chest becomes barrel-shaped, and the supraclavicular areas bulge. When percussing the chest ( tapping) a clear boxed sound is revealed. Emphysema is also characterized by moderate or severe shortness of breath. This is where the disease usually begins. With this pathology, the gas composition of the blood is often disturbed ( ratio of carbon dioxide and oxygen in the blood).

It is worth noting that there is also a possibility of relapse ( reoccurrence) pulmonary edema. If the cause that led to pulmonary edema is not treated promptly ( heart failure, heart defects, etc.), then there is a high probability of recurrent pulmonary edema.

What is the treatment time for pulmonary edema?

The duration of treatment for pulmonary edema depends on the type of edema ( cardiogenic or non-cardiogenic), concomitant diseases, general health and age of the patient. As a rule, treatment periods can vary from 1 to 4 weeks.

If pulmonary edema occurs without complications ( in the absence of pneumonia, infection or pulmonary atelectasis), as well as with the provision of adequate and timely therapy, the treatment period in most cases does not exceed 5–10 days.

It is worth noting that the most severe form of pulmonary edema is toxic pulmonary edema, which occurs when poisoned by medications, poisons or poisonous gases. It is characterized by frequent development of complications such as pneumonia, emphysema ( ) or pneumosclerosis ( replacement of lung tissue with connective tissue). In rare cases, an exacerbation of tuberculosis may occur, which previously occurred in a latent state ( hidden) form or other chronic infectious diseases. In addition to the above-mentioned complications, toxic pulmonary edema may cause relapse ( re-occurrence) of this pathology against the background of acute heart failure ( most often occurs at the end of the second or beginning of the third week). That is why patients with toxic pulmonary edema should be under medical supervision for at least 3 weeks.

What are the forms and periods of toxic pulmonary edema?

There are two main forms of toxic pulmonary edema - developed and abortive. Developed ( completed) form of toxic pulmonary edema has 5 periods, and the abortive form has 4 ( there is no stage of completed pulmonary edema). Each period is characterized by certain manifestations and duration.

The following periods of pulmonary edema are distinguished:

  • stage of reflex disorders;
  • hidden period of attenuation of reflex disorders;
  • period of increasing pulmonary edema;
  • period of completed pulmonary edema;
  • period of reverse development of edema.
Stage of reflex disorders manifests itself as irritation of the mucous membranes of the upper and lower respiratory tract. The first stage is characterized by the occurrence of symptoms such as cough, shortness of breath, and lacrimation. It is worth noting that in this period, in some cases, respiratory and cardiac arrest is possible, which occurs when the respiratory and cardiovascular centers are depressed.

Hidden period of subsidence of reflex disorders characterized by subsidence of the above-mentioned manifestations and temporary well-being. This phase can last from 6 to 24 hours. With a thorough medical examination, bradycardia can be detected already in this period ( decrease in heart rate), as well as emphysema ( increased airiness of the lung tissue). These manifestations indicate impending pulmonary edema.

Period of increase in pulmonary edema lasts approximately 22 – 24 hours. The course of this phase is slow. Manifestations occur during the first 5–6 hours and then increase. This period is characterized by an increase in body temperature to 37ºC, a large number of neutrophils are found in the blood ( subtype of white blood cells). A painful and paroxysmal cough also appears.

Period of completed pulmonary edema characterized by the appearance of pronounced disturbances. The skin and mucous membranes become bluish due to the high content of carbon dioxide in the superficial blood vessels ( cyanosis). Subsequently, noisy, bubbling breathing appears with a frequency of up to 50–60 times per minute. Foamy sputum along with blood also often appears. If these manifestations are accompanied by collapse ( marked drop in blood pressure), then the upper and lower extremities become cold, the number of heart contractions increases significantly, the pulse becomes superficial and thread-like. Blood thickening is often detected ( hemoconcentration). It should be noted that improper transportation during this period can worsen the patient’s condition ( the patient should be transported in a semi-sitting position).

Period of reverse development of pulmonary edema occurs when providing quick and qualified medical care. Cough and shortness of breath gradually decrease, the skin returns to its normal color, and wheezing and foamy sputum disappear. Radiographically, large and then small lesions of the lung tissue disappear first. The composition of peripheral blood is also normalized. The duration of recovery can vary greatly depending on the presence of concomitant diseases, as well as complications that can often occur with toxic pulmonary edema.

It should also be noted that there is a so-called “silent” toxic pulmonary edema. This rare form can only be detected by X-ray examination of the respiratory organs, since clinical manifestations, as a rule, are extremely mild or completely absent.

What can lead to allergic pulmonary edema and how does it manifest?

Pulmonary edema can develop not only as a result of pathologies of the cardiovascular system, liver, poisoning or chest injuries, but also against the background of various allergic reactions.

Allergic pulmonary edema can occur when various allergens enter the body. Most often, pulmonary edema occurs with wasp and bee stings due to increased individual sensitivity to the poisons of these insects. Also, in some cases, this pathology may be caused by taking medications or may occur during blood transfusion.

Allergic pulmonary edema is characterized by the development of clinical manifestations within the first seconds or minutes after the allergen enters the human body. At the initial stage, a burning sensation occurs in the tongue. The scalp, face, upper and lower extremities begin to itch very much. In the future, these symptoms are accompanied by discomfort in the chest, pain in the heart, shortness of breath, and heavy breathing. Wheezing, which was initially heard in the lower lobes of the lungs, spreads to the entire surface of the lungs. Due to the accumulation of carbon dioxide, the skin and mucous membranes acquire a bluish tint ( cyanosis). In addition to these symptoms, other manifestations are also possible, such as nausea, vomiting and abdominal pain. In rare cases, urinary incontinence or fecal incontinence occurs. In case of prolonged hypoxia ( oxygen starvation) of the brain, caused by failure of the left ventricle of the heart, convulsions similar to epileptic ones may occur.

In case of allergic pulmonary edema, it is necessary to quickly remove the insect sting ( the sting should be removed with a sliding movement of a knife or nail, and a tourniquet should be applied above the bite site for 2 minutes at intervals of 10 minutes); stop blood transfusion ( blood transfusion) or taking medications that caused an allergic reaction. The patient should be placed in a semi-sitting position and an ambulance should be called immediately.

What can be the complications of pulmonary edema?

Pulmonary edema is a serious condition that requires urgent therapeutic measures. In some cases, pulmonary edema can be accompanied by extremely dangerous complications.

Pulmonary edema can lead to the following complications:

  • fulminant form of pulmonary edema;
  • respiratory depression;
  • asystole;
  • airway obstruction;
  • unstable hemodynamics;
  • cardiogenic shock.
Fulminant form of pulmonary edema may occur as a result of decompensated diseases ( depletion of compensatory functions of the body) cardiovascular system, liver or kidneys. With this form of pulmonary edema, clinical manifestations develop very quickly ( within the first few minutes) and, as a rule, it is almost impossible to save the patient’s life in this case.

Respiratory depression usually occurs with toxic pulmonary edema ( in case of poisoning with toxic poisons, gases or drugs). Most often this can occur after taking large doses of narcotic painkillers ( morphine), barbiturates ( phenobarbital) and some other medicines. This complication is associated with the direct inhibitory effect of the medication on the respiratory center located in the medulla oblongata.

Asystole represents a complete cessation of cardiac activity. In this case, asystole occurs due to severe disease of the cardiovascular system ( myocardial infarction, pulmonary embolism, etc.), which can lead to both pulmonary edema and asystole.

Airway obstruction occurs due to the formation of a large amount of foam. Foam is formed from fluid that accumulates in the alveoli. From approximately 100 milliliters of transudate ( liquid part of blood) 1 – 1.5 liters of foam is formed, which significantly disrupts the gas exchange process due to obstruction ( blockages) respiratory tract.

Unstable hemodynamics manifested by high or low blood pressure. In some cases, pressure drops can alternate, which has an extremely adverse effect on the walls of blood vessels. Also, these changes in blood pressure significantly complicate the implementation of therapeutic measures.

Cardiogenic shock represents severe failure of the left ventricle of the heart. With cardiogenic shock, there is a significant decrease in blood supply to tissues and organs, which can endanger the patient's life. With this complication, blood pressure drops below 90 mm Hg. Art., the skin becomes bluish in color ( due to the accumulation of carbon dioxide in them), and also decreases daily diuresis ( diuresis). Due to a decrease in the supply of arterial blood to brain cells, confusion may occur, including stupor ( deep depression of consciousness). It is worth noting that cardiogenic shock is fatal in most cases ( in 80 – 90% of cases), since in a short time it disrupts the functioning of the central nervous system, cardiovascular and other systems.

Does pulmonary edema occur again?

If the cause that led to pulmonary edema is not eliminated in time, a relapse is possible ( recurrence of the disease) of this pathology.

Most often, relapse of pulmonary edema can occur due to failure of the left ventricle of the heart. Severe congestion in the pulmonary veins leads to increased intravascular pressure in the capillaries ( ) lungs, which leads to the release of the liquid part of the blood into the intercellular space of the lung tissue. Subsequently, as pressure increases, the integrity of the alveoli is disrupted and penetration into them and into the respiratory tract occurs ( bronchioles) liquid ( actual pulmonary edema). If adequate therapy based on compensation of left ventricular failure is not carried out in a timely manner, then there is a real threat of relapse of cardiogenic ( caused by pathology of the cardiovascular system) pulmonary edema.

There is also a possibility of secondary pulmonary edema in people with chronic heart failure. In this case, recurrent pulmonary edema most often occurs within the first two or three weeks after the first one. In persons with chronic heart failure, in addition to carrying out basic therapeutic measures ( normalization of hydrostatic pressure in the vessels of the lungs, reduction of foaming in the lungs and increase in oxygen saturation in the blood) It is also equally important to continuously monitor the pumping function of the left ventricle of the heart for at least several weeks.

To prevent recurrent pulmonary edema, it is recommended to adhere to the following rules:

  • Complete and adequate therapy. It is necessary not only to provide timely and complete medical care at the pre-hospital and hospital stages, but also to carry out a set of measures aimed at compensating for the pathological condition that led to the occurrence of pulmonary edema. In case of cardiogenic pulmonary edema, coronary heart disease, arrhythmia, hypertension are treated ( increased blood pressure), cardiomyopathy ( structural and functional changes in the heart muscle) or various heart defects ( Mitral valve insufficiency, aortic valve stenosis). Treatment of non-cardiogenic edema is based on the detection and adequate treatment of a disease not related to the pathology of the cardiovascular system. Such a cause may be cirrhosis of the liver, acute poisoning with toxic substances or medications, an allergic reaction, chest injury, etc.
  • Limiting physical activity. Increased physical activity creates favorable conditions for the occurrence and intensification of shortness of breath. That is why people who have diseases predisposing to the occurrence of pulmonary edema ( diseases of the cardiovascular system, liver or kidneys), should avoid moderate to vigorous physical activity.
  • Dieting. Proper and balanced nutrition with the exception of large amounts of salt, fats and liquid intake is a necessary preventive measure. Following a diet reduces the load on the cardiovascular system, kidneys and liver.
  • Periodic observation by a doctor. It is equally important that if you already have pathologies of the cardiovascular system, respiratory system, liver or kidneys, see a doctor several times a year. It is the doctor who can identify in the early stages progressive conditions that can lead to pulmonary edema and promptly prescribe the necessary treatment.

What is the prognosis for pulmonary edema?

The prognosis depends on the type of pulmonary edema ( the reasons that caused it), severity, concomitant diseases, as well as how quickly and efficiently the medical care was provided.

The most unfavorable prognosis is observed with toxic pulmonary edema, which can be caused by an overdose of certain medications, inhalation of poisons or toxic fumes. It is with this form of pulmonary edema that the highest mortality rate is observed. This is due to the fact that quite often toxic pulmonary edema can lead to serious complications ( congestive pneumonia, pulmonary atelectasis, sepsis), and also manifest itself in a lightning-fast form, in which the patient dies within a few minutes. Also, toxic pulmonary edema is characterized by sudden cardiac or respiratory arrest.

The following pathological conditions worsen the prognosis for pulmonary edema:

  • myocardial infarction;
  • cardiogenic shock;
  • dissecting aortic aneurysm;
  • asystole;
  • sepsis;
  • cirrhosis of the liver;
  • unstable hemodynamics.
Myocardial infarction is one of the reasons that can lead to pulmonary edema ( cardiogenic pulmonary edema). During a heart attack, necrosis or necrosis of the muscle layer occurs ( myocardium) of the heart and, as a consequence, a decrease in its pumping function. Subsequently, in a short period of time, conditions are created for stagnation of blood in the pulmonary circulation ( vessels that are involved in transporting blood from the lungs to the heart and vice versa). This subsequently leads to pulmonary edema ( an increase in pressure in the vessels inevitably leads to the release of fluid from the capillaries into the alveoli). The presence of two severe pathologies at once, such as myocardial infarction and pulmonary edema, significantly worsens the prognosis.

Cardiogenic shock is an acute failure of the left ventricle of the heart, which is manifested by a pronounced decrease in the pumping function of the heart muscle. This pathological condition is characterized by a sharp decrease in blood pressure ( below 90 mm Hg. Art.). Excessively low blood pressure leads to decreased blood supply to tissues ( hypoperfusion) such vital organs as the heart, lungs, liver, kidneys, brain. Also, in addition to the collapse ( excessive drop in pressure) cyanosis of the skin and mucous membranes is observed ( the skin takes on a bluish tint) due to the accumulation of large amounts of carbon dioxide in surface vessels. It should be noted that cardiogenic shock, as a rule, occurs as a result of myocardial infarction and significantly worsens the prognosis, since in approximately 80–90% of cases it leads to death.

Dissecting aortic aneurysm It is also an extremely severe pathology, which very often leads to death. With this pathology, dissection occurs, and subsequently rupture of the largest artery in the human body - the aorta. Rupture of the aorta leads to massive blood loss, from which death occurs within minutes or hours ( loss of more than 0.5 liters of blood in a short time leads to death). As a rule, dissecting aortic aneurysm is fatal in more than 90% of cases, even with timely and adequate treatment.

Asystole characterized by complete cessation of cardiac activity ( heart failure). Asystole is most often a consequence of myocardial infarction, pulmonary embolism ( blockage of a pulmonary artery by a blood clot) or may occur with an overdose of certain medications. Only timely medical assistance within the first 5 to 6 minutes after asystole can save the patient’s life.

Sepsis(blood poisoning) is a serious condition in which pathogenic microorganisms circulate throughout the body along with the toxins they produce. With sepsis, the body's overall resistance drops sharply. Sepsis leads to an increase in body temperature above 39ºC or below 35ºC. There is also an increase in heart rate ( over 90 beats per minute) and breathing ( over 20 breaths per minute). An increased or decreased number of white blood cells is detected in the blood ( more than 12 or less than 4 million cells). Pulmonary edema, aggravated by severe sepsis, also has an extremely unfavorable prognosis.

Cirrhosis of the liver characterized by the replacement of functional liver tissue with connective tissue. Cirrhosis of the liver leads to a decrease in protein synthesis by the liver, due to which the oncotic pressure decreases ( blood protein pressure). Subsequently, the balance between the oncotic pressure of the intercellular fluid in the lungs and the oncotic pressure of the blood plasma is disrupted. In order to restore this balance again, some of the fluid from the bloodstream enters the intercellular space of the lungs, and then into the alveoli themselves, which causes pulmonary edema. Liver cirrhosis directly leads to liver failure, and in the future, against the background of this pathological condition, pulmonary edema can occur again.

Unstable hemodynamics manifested by sudden changes in blood pressure ( below 90 and above 140 mm Hg. Art.). These pressure differences significantly complicate the treatment of pulmonary edema, since completely different therapeutic measures are carried out at different blood pressure values.

Is pulmonary edema treated with folk remedies?

Pulmonary edema is an emergency condition that, if not treated promptly, can lead to serious consequences and sometimes death. That is why treatment of pulmonary edema should be carried out by experienced doctors in the hospital intensive care unit. However, traditional medicine can be resorted to when the patient’s condition has been successfully stabilized and the possibility of undesirable consequences remains extremely low. These folk remedies will help reduce the severity of some residual symptoms ( cough, sputum production), and can also be used as a prophylaxis for pulmonary edema.

During the period of convalescence(end of illness)You can use the following folk remedies:

  • A decoction of flax seeds. It is necessary to pour 4 teaspoons of flax seeds with one liter of water, and then boil for 5 - 7 minutes. Next, remove the pan with the contents from the heat and leave in a warm place for 4 – 5 hours. Take this decoction half a glass, 5 – 6 times a day ( after 2 – 2.5 hours).
  • Tincture of lovage roots. You need to take 40 - 50 grams of dried lovage roots, boil them in 1 liter of water for 10 minutes. Then the tincture should be left in a warm place for 30 minutes. You can take the tincture, regardless of meals, 4 times a day.
  • A decoction of parsley seeds. The seeds need to be finely crushed, and then take 4 teaspoons and pour 1 cup of boiling water over them and boil for 20 minutes. Next, you should cool the broth and strain. This decoction should be taken one tablespoon 4 times a day after meals.
  • A decoction of cyanosis roots. A tablespoon of well-chopped cyanosis roots is poured into 1 liter of water and then kept in a water bath for 30 minutes. The decoction should be taken 50 - 70 milliliters 3 - 4 times a day after meals.

It is worth noting that treatment with folk remedies is not an alternative to drug treatment for pulmonary edema. No medicinal decoctions and tinctures can replace modern medicines, as well as medical care provided by conscientious doctors. Also, some medicinal plants, interacting with prescribed medications, can lead to adverse reactions. That is why you should consult with your doctor when deciding to be treated with traditional medicine.

What are the types of pulmonary edema?

There are two types of pulmonary edema – cardiogenic and non-cardiogenic. The first type occurs against the background of some severe diseases of the cardiovascular system. In turn, non-cardiogenic pulmonary edema can occur as a result of pathologies absolutely unrelated to heart disease ( hence the name).

Types of pulmonary edema

Criteria Cardiogenic pulmonary edema Non-cardiogenic pulmonary edema
Pathological conditions that can lead to pulmonary edema
  • myocardial infarction;
  • mitral valve stenosis ( narrowing of the opening between the left atrium and ventricle);
  • cardiogenic shock ( severe left ventricular failure);
  • atrial fibrillation ( uncoordinated atrial contraction);
  • atrial flutter ( rapid contraction of the atria with maintenance of rhythm);
  • hypertensive crisis ( significant increase in blood pressure).
  • various allergic reactions ( Quincke's edema, anaphylactic shock);
  • cirrhosis of the liver;
  • renal failure;
  • chest injury;
  • inhalation of toxins and poisonous gases;
  • foreign bodies entering the lungs;
  • bronchial asthma;
  • ingress of blood clots or emboli ( foreign object) into the vessels of the lungs;
  • neurogenic pulmonary vasoconstriction ( pronounced vasoconstriction);
  • chronic lung diseases ( emphysema, bronchial asthma).

It is worth noting that, unlike cardiogenic pulmonary edema, non-cardiogenic pulmonary edema occurs somewhat less frequently. The most common cause of pulmonary edema is myocardial infarction.

The following subtypes of non-cardiogenic pulmonary edema are distinguished:

  • toxic pulmonary edema;
  • allergic pulmonary edema;
  • neurogenic pulmonary edema;
  • cancerous pulmonary edema;
  • traumatic pulmonary edema;
  • shock pulmonary edema;
  • aspiration pulmonary edema;
  • high-altitude pulmonary edema.
Toxic pulmonary edema occurs when certain particularly toxic gases and vapors enter the lower respiratory tract. Clinical manifestations begin with cough, shortness of breath and lacrimation due to irritation of the mucous membranes of the upper and lower respiratory tract. Subsequently, depending on the duration of inhalation of toxic substances, their properties and the state of the body itself, clinical manifestations of pulmonary edema develop. It is worth noting that toxic pulmonary edema is the most severe, since in some cases, already in the first minutes after inhaling toxic fumes, respiratory or cardiac arrest may occur ( due to inhibition of the activity of the medulla oblongata).

Allergic pulmonary edema occurs in individuals with high individual sensitivity to certain allergens. Most often, allergic pulmonary edema is caused by the bite of insects such as a wasp or a bee. In rare cases, this pathology can occur during massive blood transfusions ( allergic reaction to foreign proteins in the blood). If the impact of the allergen on the body is not eliminated in time, there is a high probability of developing anaphylactic shock ( immediate allergic reaction) and death.

Neurogenic pulmonary edema is a rather rare type of non-cardiogenic pulmonary edema. With this pathology, due to a violation of the innervation of the vessels of the respiratory system, significant spasm of the veins occurs. This subsequently leads to an increase in the hydrostatic pressure of the blood inside the capillaries ( the smallest vessels that participate together with the alveoli in the process of gas exchange). As a result, the liquid part of the blood leaves the bloodstream into the intercellular space of the lungs, and then enters the alveoli themselves ( pulmonary edema occurs).

Cancerous pulmonary edema occurs against the background of a malignant lung tumor. Normally, the lymphatic system should drain excess fluid in the lungs. In lung cancer, the lymph nodes are unable to function normally ( there is a blockage of the lymph nodes), which can subsequently lead to the accumulation of transudate ( edematous fluid) in the alveoli.

Traumatic pulmonary edema may occur when the integrity of the pleura is disrupted ( thin membrane that covers each lung). Most often, such pulmonary edema occurs with pneumothorax ( accumulation of air in the pleural cavity). With pneumothorax, capillary damage often occurs ( the smallest vessels), which are located near the alveoli. Subsequently, the liquid part of the blood and some formed elements of blood ( red blood cells) enter the alveoli and cause pulmonary edema.

Shock pulmonary edema is a consequence of a state of shock. During shock, the pumping function of the left ventricle drops sharply, which causes stagnation in the pulmonary circulation ( blood vessels connecting the heart and lungs). This inevitably leads to an increase in intravascular hydrostatic pressure and the release of some fluid from the vessels into the lung tissue.

Aspiration pulmonary edema occurs when stomach contents enter the airways ( bronchi). Airway obstruction inevitably leads to membranogenic pulmonary edema ( negative effect on the capillary membrane), in which there is an increase in the permeability of the capillaries and the release of the liquid part of the blood into the alveoli.

High altitude pulmonary edema one of the rarest types of pulmonary edema. This pathological condition occurs when climbing a mountain above 3.5 - 4 kilometers. With high-altitude pulmonary edema, the pressure in the blood vessels of the lungs increases sharply. Capillary permeability also increases due to increasing oxygen starvation, which leads to pulmonary edema ( alveoli are very sensitive to oxygen deprivation).

What are the features of pulmonary edema in children?

Pulmonary edema in children, unlike adults, rarely occurs against the background of any pathology of the cardiovascular system. Most often this occurs due to an allergic reaction ( allergic pulmonary edema) or by inhalation of toxic substances ( toxic pulmonary edema). At the same time, pulmonary edema can occur against the background of existing heart defects ( acquired heart defects), such as mitral valve insufficiency ( dysfunction of the mitral valve in which blood from the left ventricle is thrown into the left atrium) and aortic valve stenosis ( narrowing of the opening through which blood from the left ventricle enters the aorta).

Pulmonary edema in children can occur at any time of the day, but more often it occurs at night. The child becomes restless and frightened due to severe lack of air, which occurs with pulmonary edema. Sometimes a child may take a forced position in which he sits on the edge of the bed with his legs down ( in this position, the pressure in the vessels of the pulmonary circulation decreases slightly, which leads to a decrease in shortness of breath). In addition, there are a number of manifestations of pulmonary edema in children.

The following symptoms of pulmonary edema in children are distinguished:

  • dyspnea;
  • cough;
  • discharge of pink and frothy sputum;
  • wheezing;
  • cyanosis of the skin and mucous membranes.
Dyspnea represents an early symptom of pulmonary edema. Shortness of breath occurs when there is an increased amount of fluid in the alveoli ( pulmonary sacs in which gas exchange occurs), as well as with reduced elasticity of the lungs ( fluid in the lungs reduces the elasticity of lung tissue). Shortness of breath manifests itself as a lack of air. Depending on the cause, breathing may be difficult ( for diseases of the cardiovascular system) or exhale ( for diseases of the lungs and bronchi).

Cough with pulmonary edema it occurs reflexively due to an increase in the concentration of carbon dioxide in the blood ( With pulmonary edema, the process of gas exchange is disrupted). At first, the cough may be painful and without discharge ( unproductive), but then pink sputum is added to it.

Discharge of pink and frothy sputum occurs when there is a large amount of fluid in the lungs. The sputum is pink because it contains red blood cells from the capillaries ( the smallest vessels) penetrated the alveoli. Also, due to the foaming of liquid in the alveoli, sputum acquires a specific consistency ( becomes foamy). So, from 100 ml of blood plasma that enters the lungs, 1 - 1.5 liters of foam is obtained.

Wheezing are initially dry ( fluid in the lungs compresses the small caliber bronchi), but in a short period of time they become wet due to the accumulation of a large amount of fluid in the bronchi. During auscultation, moist small-, medium- and large-bubble rales can be heard ( wheezing occurs in small, medium and large bronchi).

Blueness of the skin and mucous membranes is a characteristic sign of pulmonary edema and occurs due to the accumulation of a large amount of reduced hemoglobin ( protein that carries carbon dioxide and oxygen) in the superficial vessels of the skin and mucous membranes, which gives such coloring.
It is worth noting that pulmonary edema can occur in children of all age groups, including newborns. Most often, pulmonary edema occurs against the background of some pathology that leads to hypoxia ( oxygen starvation). With a decrease in oxygen concentration in the blood, the permeability of the walls of the alveoli increases, which is one of the most important links in the mechanism of development of pulmonary edema. Also, the heart muscle and brain are extremely sensitive to hypoxia.

In newborns, pulmonary edema can occur against the background of the following pathologies:

  • Placental infarction represents the death of cells in a certain area of ​​the placenta. The most dangerous placental infarction is in the third trimester of pregnancy, since it is during this period that this pathology can significantly affect intrauterine development. During myocardial infarction, the blood supply to the fetus is disrupted, which can lead to hypoxia.
  • Aspiration of amniotic fluid– entry into the lower respiratory tract ( bronchi and alveoli) amniotic fluid. During the prenatal period, amniotic fluid penetrates up to the tracheal bifurcation ( division of the trachea into right and left bronchus). If a significant amount of this liquid enters the respiratory system, there may be a high likelihood of pulmonary edema.
  • Prenatal or birth brain injury often leads to disturbances in the blood supply to the brain. Prolonged oxygen starvation of the cells of the central nervous system causes reflex changes in blood supply throughout the body ( heart muscle, lungs, liver, kidneys). Subsequently, prolonged hypoxia causes pulmonary edema.
  • Heart defects also cause pulmonary edema. With aortic valve stenosis, as well as mitral valve insufficiency, pressure in the pulmonary circulation ( vessels that are involved in transporting blood from the lungs to the heart and vice versa) increases significantly. These heart defects lead to the release of blood plasma from the capillaries ( the smallest vessels) into the intercellular substance of the lungs, and subsequently into the alveoli themselves.

How to properly provide emergency care for pulmonary edema?

Pulmonary edema is a rather severe pathology and therefore requires immediate assistance. There are several general rules for providing emergency care for pulmonary edema.

Emergency care for pulmonary edema involves the following measures:

  • Place the patient in a semi-sitting position. If a person begins to experience symptoms of pulmonary edema, he should immediately be seated in a semi-sitting position with his legs down. In this position, congestion in the pulmonary circulation is reduced to a certain extent ( blood vessels that are involved in transporting blood from the lungs to the heart and vice versa), which manifests itself as a decrease in shortness of breath. Also in this position, the pressure in the chest decreases and the process of gas exchange improves.
  • Use of venous tourniquets. Venous tourniquets must be applied to the lower extremities. The duration of application of tourniquets should be from 20 to 30 minutes. The tourniquet is applied with medium force to each leg in the area of ​​the upper third of the thigh so that only the veins are compressed ( the pulse of the femoral artery should be palpable). This manipulation is carried out in order to reduce the flow of venous blood to the heart and, accordingly, reduce the severity of clinical manifestations of pulmonary edema.
  • Open access to fresh air. Staying in a stuffy room aggravates the course of pulmonary edema. The thing is that with low oxygen content in the air, the permeability of the alveoli increases ( special sacs in which gas exchange occurs). This leads to the fact that liquid from the capillaries ( the smallest vessels that, together with the alveoli, participate in the process of gas exchange) rushes first into the intercellular space of the lungs, and then into the alveoli themselves ( pulmonary edema develops).
  • Use of nitroglycerin. Nitroglycerin is indicated in cases where pulmonary edema was caused by myocardial infarction ( most common cause of pulmonary edema). It is recommended to take 1 or 2 tablets under the tongue at intervals of 3 to 5 minutes. Nitroglycerin reduces the stagnation of venous blood in the lungs and also dilates the coronary arteries that feed the heart.
  • Inhalation of alcohol vapor. Inhalation of alcohol vapor quite effectively neutralizes foaming during pulmonary edema. Foam is produced due to the rapid accumulation of fluid in the alveoli. A large amount of foam significantly complicates the process of gas exchange, as it leads to blockage of the respiratory system at the level of terminal ( end) bronchi and alveoli. Adults and children need to inhale vapors of 30% ethyl alcohol.
  • Constant monitoring of pulse and respiration. The respiratory rate and pulse of a patient with pulmonary edema should be constantly monitored. If necessary, perform cardiopulmonary resuscitation immediately ( indirect cardiac massage and/or artificial respiration).
Also, when the first symptoms of pulmonary edema appear, you should immediately call an ambulance.

Is it possible to cure pulmonary edema?

Pulmonary edema is a dangerous pathology that requires immediate and qualified medical care. The success of treatment depends on the form of pulmonary edema ( cardiogenic or non-cardiogenic pulmonary edema), degree of severity, the presence of concomitant diseases ( chronic heart failure, heart defects, hypertension, renal and liver failure, etc.), as well as how quickly and completely the medical care was provided.

Regardless of the cause that led to pulmonary edema, a number of therapeutic measures are performed in the intensive care unit aimed at relieving ( elimination) pain, reducing the degree of oxygen starvation, reducing the volume of circulating blood, reducing the load on the heart muscle, etc.

Urgent medical care for pulmonary edema

Therapeutic measures Mechanism of action
Taking narcotic pain medications ( morphine).

Morphine should be administered 10 milligrams intravenously in fractional doses.

These medications help eliminate shortness of breath and relieve psycho-emotional stress ( reduce the production of adrenaline and norepinephrine).

Morphine also leads to moderate dilation of the veins, which leads to a decrease in the severity of clinical symptoms of pulmonary edema.

Oxygen therapy ( oxygen inhalation) with ethyl alcohol vapor at a rate of 3 - 6 liters per minute. Significantly reduces hypoxia ( oxygen starvation). Hypoxia has an extremely adverse effect on the vessels of the lungs, increasing their permeability, as well as increasing stagnation in the pulmonary circulation ( vessels that are involved in transporting blood from the heart to the lungs and vice versa).

Oxygen therapy is one of the most important measures and is prescribed for any type of pulmonary edema ( with cardiogenic and non-cardiogenic).

Taking nitrates ( nitroglycerine) 1 – 2 tablets orally every 3 – 5 minutes.

Intravenous administration of up to 25 mcg bolus is also possible ( rapid injection of the entire contents of the syringe), and then drip administration with increasing doses.

Nitrates to a certain extent reduce the stagnation of venous blood in the lungs by expanding the walls of the veins. In large doses, nitrates can also dilate the coronary vessels that supply the heart.

Also, these drugs reduce the load on the myocardium ( muscle layer) left ventricle.

It should be noted that the use of nitrates is necessary only in cases where pulmonary edema was caused by myocardial infarction ( most common cause of pulmonary edema) and is strictly prohibited for hypertensive cardiomyopathy ( thickening of the muscle layer of the left ventricle).

Taking diuretics ( furosemide).

The medication is administered intravenously in a single dose of 40 milligrams.

In the future, furosemide can be reintroduced.

Diuretic medications ( diuretics) cause a decrease in circulating blood volume. Initially, furosemide slightly dilates the veins ( causes venodilation), and then, acting on the renal tubules, has a diuretic effect ( enhances the excretion of sodium, calcium, magnesium and chlorine ions).

When used intravenously, the therapeutic effect is observed within 10 minutes, and when taken orally ( tablet form) – within 30 – 60 minutes.

Taking ACE blocking drugs ( angiotensin converting enzyme).

Drugs of this group ( enalaprilat) are administered intravenously in a single dose of 1.25 to 5 milligrams.

ACE blockers to a certain extent reduce the volume of circulating blood by reducing the level of a special enzyme angiotensin. This enzyme not only constricts blood vessels, but also increases the production of the hormone aldosterone, which causes fluid retention in the body.

These drugs can dilate arterioles ( small caliber arteries) and thereby reduce the load on the left ventricle of the heart.


In addition to the above measures, treatment should also be aimed at the cause that caused pulmonary edema.

Treatment regimen for pulmonary edema depending on the cause and blood pressure

Pathological condition Treatment regimen
Myocardial infarction To eliminate pain, 10 milligrams of morphine are injected intravenously. To reduce the risk of blood clots, chew 250–500 milligrams of aspirin, and then administer 5000 units intravenously ( international units) heparin. Subsequently, the treatment algorithm depends on blood pressure readings.
Hypertensive crisis
(marked increase in blood pressure)
Under the tongue 1 or 2 tablets of nitroglycerin ( second tablet at intervals of 3 – 5 minutes). Nitroglycerin reduces blood pressure, and also to some extent reduces left ventricular failure.

Also, during a hypertensive crisis, furosemide is administered intravenously ( diuretic) 40 – 80 milligrams ( repeated administration of small doses is more effective).

In addition, enalaprilat is prescribed intravenously to lower blood pressure ( ACE blocker) 1.25 – 5 milligrams.

To reduce pain, 10 milligrams of morphine are injected intravenously.

Hypotension
(blood pressure drop below 90/60 mmHg)
To enhance cardiac activity and increase blood pressure, dobutamine is administered intravenously at a rate of 2.5 to 10 mcg/kg per minute.
The dose is gradually increased until systolic blood pressure stabilizes ( 90 or more mm Hg. Art.).

Subsequently, nitroglycerin and morphine are administered intravenously.

Anaphylactic shock
(immediate allergic reaction)
In the first minutes, it is necessary to administer 5 milliliters of a 0.1% adrenaline solution intramuscularly ( if there is no effect, the dose can be re-administered after 5 – 10 minutes). Adrenaline quickly eliminates excessive varicose veins. It is also able to expand the airways and influence the heart muscle, increasing its contractile function.

Glucocorticoids must be administered, which significantly reduce the concentration of immunoglobulins ( special proteins) and histamine ( biologically active substance), which support the allergic reaction.

Prednisolone is prescribed intravenously in large dosages - at least 150 mg ( or dexamethasone 20 mg), since in smaller doses the medication is ineffective.

To relieve pain, morphine is administered intravenously in an amount of 10 milligrams in fractions.

In addition to these medications, furosemide is also prescribed ( 40 mg intravenously) and aminophylline, which dilates the bronchi and also reduces pulmonary edema ( 2.4% solution 10 - 20 milliliters intravenously).


Treatment should be carried out until the following conditions are met:
  • normalization of blood pressure ( upper pressure should not be higher than 140 and lower than 90 mmHg. Art.);
  • normalization of the number of heartbeats ( norm is from 60 to 90 beats per minute);
  • decrease in respiratory rate to 22 or less in one minute;
  • absence of moist rales when listening ( auscultation) lungs;
  • absence of sputum and foam;
  • normalization of skin color and mucous membranes;
  • absence of symptoms of pulmonary edema when the patient moves to a horizontal position.
  • increased permeability of capillaries - alveoli (pneumonia, toxic poisoning (fluorine-containing compounds), in case of poisoning)
  • increased pressure in the pulmonary artery system (, severe renal failure with)
  • decreased contractility of the left ventricle (myocarditis, myocardial dystrophy, chronic heart failure)
In the clinic of pulmonary edema, two stages are distinguished interstitial and alveolar

Symptoms of pulmonary edema in the interstitial stage

Complaints: shortness of breath up to 25 - 30 per minute, feeling of suffocation, lack of air, dry cough
Upon objective examination:

  • the patient’s condition is forced (sitting in bed)
  • on auscultation: dry rales along the anterolateral surface, single wet rales in the inferolateral surfaces

Symptoms of pulmonary edema in the alveolar stage

  • increased shortness of breath up to 40 per minute
  • lack of air, suffocation
  • cough with frothy sputum that is white or sometimes pink due to red blood cells
  • bubbling breath “remote” wheezing- can be heard from a distance;
  • Auscultation: a mass of moist rales over the entire surface of the lungs

Treatment and emergency care for pulmonary edema

  • Sitting position with legs down
  • Morphine 1% - 1.0 per 20.0 physical. IV solution in a stream
  • Defoaming, oxygen through alcohol, antifomsilan
Further treatment tactics depend on blood pressure causes of pulmonary edema

If systolic blood pressure is less than 90 mm. rt. Art., then:
- Let's add debutamine 5.0 per 200.0 physical. solution intravenously or adrenaline 1.0 - 2.0 per 200.0 physical solution. IV drip
- In case of ineffectiveness and with blood pressure<60 мм. рт. ст. норадреналин 2,0 на 200,0 физ. р-ра в/в капельно или адреналин 1,0 - 2,0 на 200,0 физ. р-ра в/в капельно
- For pneumonia:
Prednisolone 60 - 120 mg. at 20.0 physical. iv solution in a jet
- For chronic heart failure - glycosides, digoxin 0.75 - 1.0 or strophanthin 0.05% 0.3 - 0.5 per 20.0 physical. iv solution in a jet

If systolic blood pressure is higher than 90 mm. rt. Art., then:
- Nitroglycerin under the tongue or intravenously under blood pressure control
- Lasix/furosemide 60 - 120 mg. i/v jet
- In the absence of myocardial infarction, cardiac arrhythmia and conduction disturbances:
Eufillin 24% - 10.0 to 20.0 physical. iv solution in a jet
Digoxin 0.75 - 1.0 or strophanthin 0.3 - 0.5 per 20.0 physical. iv solution in a jet
- If mechanical ventilation is ineffective

Pulmonary edema is the accumulation of fluid (transudate) in the lung tissues coming from the capillaries. This serious condition complicates the clinical picture of various diseases, and without timely assistance or incorrect treatment tactics, such a disorder can cause death, which with fulminant pulmonary edema can occur in a matter of minutes.

Pulmonary edema develops as a complication of cardiac, neurological, gynecological, urological diseases; diseases of the respiratory and digestive systems in children and adults can provoke this condition.

Regardless of the reason that caused the accumulation of fluid, pulmonary edema is distinguished according to the mechanism of development:

  • interstitial - transudate (non-inflammatory fluid) from the capillaries does not penetrate the pulmonary alveoli, which is manifested by symptoms;
    • , no sputum;
  • alveolar - the alveoli are flooded with transudate, signs of this process;
    • suffocation;
    • cough with foamy sputum;
    • audible wheezing in the lungs.

Penetration of fluid into the lung tissue (interstitium) and then into the pulmonary alveoli are two stages of pulmonary edema, this condition is characterized by increased clinical symptoms, which without emergency medical attention can lead to death.

The mechanism of development of interstitial pulmonary edema is that:

  • pressure in the capillaries of the lungs increases;
  • the extensibility of the lung tissue deteriorates - with fibrosis;
  • the total volume of fluid outside the blood vessels increases;
  • the resistance of small-caliber bronchi increases;
  • lymph flow increases.

Fluid accumulation in the interstitium occurs through a hydrostatic mechanism. Alveolar edema develops as a result of destruction of the membrane between the alveoli and capillaries, increasing its permeability.

Such edema is called membranous (membrane) and is characterized by the release into the lumen of the alveoli not only of transudate from the capillaries, but also of blood cells - red blood cells, proteins.

The consequences of membranous pulmonary edema are:

  • hypoxia – a state of insufficient oxygen content in the blood and tissues of the body;
  • hypercapnia - an increase in the concentration of carbon dioxide in the blood;
  • acidosis – increased acidity of body fluids, acidification.

The duration of the attack can range from several minutes with fulminant pulmonary edema to a day or more.

There are cases when signs of pulmonary edema in a person are discovered by chance during an X-ray examination when seeking treatment for another disease.

According to the duration of the attacks there are:

  • fulminant - death from pulmonary edema a few minutes after the onset of the attack;
  • acute – develops during acute conditions (heart attack, anaphylactic shock), lasts up to 4 hours;
  • subacute – wave-like progression of attacks is characteristic of edema of hepatic origin;
  • protracted – lasting longer than 12 hours, characteristic of chronic heart and lung diseases.

Causes

Among the causes of pulmonary edema are:

  1. Cardiogenic – caused by diseases of the heart and blood vessels
    1. heart diseases - heart attack, endocarditis, cardiosclerosis, congenital and acquired defects;
    2. vascular diseases - hypertension, aortitis, aortic insufficiency;
    1. lung diseases
      1. unilateral swelling with pneumothorax;
      2. thromboembolism;
      3. chronic diseases - asthma, COPD, emphysema, lung cancer;
      4. altitude sickness - a reaction to a sharp rise to an altitude of more than 3 km above sea level;
    2. kidney disease
    3. decrease in oncotic pressure, decrease in protein concentration in the blood during fasting, liver and kidney diseases
    4. diabetic coma
    5. infectious diseases – whooping cough, tetanus, polio
    6. neurogenic edema due to brain injury, epilepsy, stroke
    7. disturbance of lymph outflow in fibrosis, carcinomatosis
    8. allergy
    9. toxic effect of drugs during anesthesia, cardioversion, poisoning with barbiturates, ethyl alcohol

The main damaging factors in developing pulmonary edema of any origin are hypoxia and acidosis.

  1. Edema in the elderly

    In older people, a common cause of pulmonary edema and death is congestion in the pulmonary circulation, which develops as a consequence of a long-term recumbent state and is especially characteristic of adults with heart disease.

Signs of blood stagnation caused by pulmonary edema in adult bedridden patients after 65 years of age are similar in their external manifestations to the symptoms of respiratory failure in pneumonia and are characterized by:

  • severe weakness;
  • shortness of breath, rapid breathing, which is accompanied by rapid heartbeat;
  • cold sweat, pale skin;
  • swelling of the lower extremities;
  • cough with foamy discharge.

Among the causes of pulmonary edema in adults are long-term use of drugs containing salicylates, blood transfusions, a reaction to the administration of protein substances, or, as a reaction, in infectious diseases affecting the respiratory system.

Symptoms

Pulmonary edema can be assumed based on the appearance and characteristic position of the patient. He takes a forced position, tries to sit up or rise in bed. The patient's general health deteriorates sharply, he develops severe shortness of breath with the participation of the respiratory muscles.

When the patient inhales air, you can see how the subclavian fossa and the spaces between the ribs sink, and in both adults and children, during pulmonary edema, the respiratory muscles are activated as actively as possible.

And due to the lack of oxygen, muscle contractions become difficult, and the patient has to make considerable efforts just to inhale air.

At all stages of pulmonary edema in adults and children:

  • a decrease in the temperature of the skin, an increase in its humidity, and the appearance of a bluish tint;
  • severe shortness of breath, with difficulty in inhaling;
  • “bubbling” in the chest when breathing or talking;
  • dizziness;
  • fear of death, panic.

The intensity of symptoms depends on the stage of edema and the type of disease that caused the accumulation of fluid in the lungs. With interstitial edema, the patient develops wheezing, which at the stage of alveolar edema can be complicated by aperiodic Cheyne-Stokes breathing.

This type of breathing is characterized by shallow, frequent breaths, which gradually deepen towards the 5th-7th breath. The patient takes a breath, and then breathes shallowly again, gradually slowing down the frequency and depth of breaths.

The appearance of this symptom, especially in an elderly person, may indicate developing heart failure, which complicates the prognosis for pulmonary edema. Aperiodic breathing provokes attacks of arrhythmia, manifested by night awakenings and daytime drowsiness.

If the swelling is caused by a sharp increase in blood pressure (BP), then extremely high systolic pressure values ​​may be observed. But in general, the attack occurs against the background of no changes in blood pressure, not exceeding 95 - 105 mm Hg. Art.

With alveolar edema the following is noted:

  • swelling of the veins in the neck;
  • frequent heart contractions, reaching 160 beats per minute, with a thread-like pulse of weak filling.

If pulmonary edema becomes protracted, then blood pressure and heart rate decrease, while breathing is shallow and frequent, which does not saturate the blood with oxygen. During a prolonged attack, the patient’s condition is severe and threatens to stop breathing.

Treatment

Not only the timing of treatment and recovery after an attack, but also the patient’s life itself depends on the quality of treatment provided from the first minutes of the appearance of signs of pulmonary edema. And, even if it was possible to stop the attack, there is always the possibility of an undulating course of the disease and repeated exacerbation.

The patient should be under the supervision of a doctor for a year after the exacerbation, and to increase survival, treatment should begin when the first symptoms of pulmonary edema appear.

First aid

First aid for pulmonary edema should be provided to the victim by others. The patient must be seated comfortably, so that the legs hang down. This helps to reduce the return of venous blood to the heart and reduces the flow of blood into the pulmonary circulation.

If the swelling is caused by heart disease, loved ones should give the patient nitroglycerin under the tongue to support the heart and call emergency help.

To reduce venous return, diuretics (furosemide) are used. The drug is administered intravenously, and the correct dosage is selected by the doctor.

To reduce venous return, the doctor may cuff the legs and arm that are not receiving an IV. Air is pumped into the cuffs under a certain pressure, which partially compresses the veins through which blood flows to the heart.

To reduce the severity of the attack, the patient can be given a sedative (Relanium) before the doctors arrive. This will reduce the amount of catecholamines in the blood, eliminate spasm of peripheral blood vessels, and reduce venous blood flow to the heart.

If the patient begins to foam when breathing, he should be given a cotton swab moistened with medical alcohol to sniff. Ethyl alcohol vapor must be inhaled for 10–15 minutes for the defoaming effect to appear and bubbling breath to disappear.

Some people may have the opposite reaction to inhaling alcohol vapors, developing a cough or feeling short of breath. In such cases, it is impossible to treat a patient for pulmonary edema using an antifoam agent such as ethyl alcohol.

In medicine, in addition to ethanol, the defoamer antifomsilan is used, which is used in artificial respiration devices.

Health care

Medical assistance includes:

  1. Oxygenation – the patient’s oxygen supply is increased using an oxygen mask, and in severe cases, artificial ventilation.
  2. Administration of morphine as an analgesic and sedative.
  3. Administration of furosemide intravenously to reduce the return of blood to the pulmonary circulation.
  4. Administration of aminophylline, which acts as
    • bronchodilator;
    • increasing blood flow in the kidneys;
    • accelerating the removal of sodium from the body;
    • improves heart contractility;
  5. Blood pressure control
    • dobutamine and dopamine are administered for low blood pressure;
    • for high blood pressure, sodium nitroprusside is administered;
    • in case of hypertensive crisis, drugs that lower blood pressure are prescribed

The patient, depending on the cause of the swelling, is prescribed medications:

  • hormonal;
  • thrombolytics;
  • antibiotics;
  • antihistamines;
  • hepatoprotectors;
  • cardiac glycosides;
  • vasodilators.

Defoaming becomes a serious problem in the treatment of pulmonary edema. During an attack, the patient may produce so much foam that there is a danger of airway obstruction and death of the patient.

If the airways are blocked by foam, the doctor removes the foam mechanically, after which he uses antifoam agents, or injects an alcohol solution through the trachea, making a percutaneous puncture.

Prevention

Several factors that should be avoided can trigger pulmonary edema. Cardiogenic edema, which occurs in heart failure, can be triggered by physical activity, anxiety, or impaired drinking or diet.

Patients should limit salt intake, reduce daily fluid intake, and control weight. Physical activity should not cause shortness of breath in the patient.

Infectious respiratory diseases should not be allowed, as they can provoke pneumonia and pulmonary edema in weakened patients. In older adults, pulmonary edema associated with pneumonia significantly worsens survival prognosis.

Complications

Pulmonary edema, even with quick and successful relief of the attack, causes a lack of oxygen in the tissues. This leads to serious damage to the brain, heart tissue, and the lung itself.

The consequences of pulmonary edema can be:

  • ischemia of the heart and other organs;
  • pneumosclerosis;
  • emphysema;
  • congestion in the lungs.

In older people, hypoxia caused by edema negatively affects the viability of brain cells. Oxygen starvation of neurons leads to weakened memory and daytime sleepiness.

Forecast

On average, pulmonary edema in adults leads to death in 15-20% of cases. Life prognosis is determined by the cause of the attack. For edema caused by acute myocardial infarction, the mortality rate is extremely high, in adults it is 90%.

The timeliness and adequacy of treatment is of great importance. To a large extent, survival depends on the severity of seizure prevention measures.

Pulmonary edema is a disease that is characterized by pulmonary failure, presented in the form of mass waste transudate from the capillaries into the pulmonary region, resulting in infiltration of the alveoli. In simple words, pulmonary edema is a process in which fluid seeps through the blood vessels and stagnates in the lungs. The disease can be independent, or it can be a consequence of other serious ailments of the body.

The lungs are an organ that consists of alveoli filled with a large number of capillaries. The process of gas exchange occurs in this organ, as a result of which the body is filled with oxygen, which ensures good performance of the body. If in the alveolus liquid penetrates, not oxygen– this contributes to the formation of pulmonary edema.

Important . Pulmonary edema is a dangerous disease that can have such dangerous consequences as death. The disease affects both adults and children.

Prognosis and complications of the disease

Often the prognosis for pulmonary edema is unfavorable. This is due to the reasons that caused the disease. Non-cardiogenic edema is easy to treat, while cardiogenic edema is very difficult to treat. Even with effective treatment for cardiogenic edema, survival is only 50%. If the form is lightning, then the person cannot be saved. Toxic edema is a serious diagnosis and a favorable outcome is only possible with the use of large amounts of diuretics. It all depends on the individual characteristics of the body.

The consequences of pulmonary edema can be very diverse. Often, internal organs are damaged. The most pronounced changes occur in tissues that are more supplied with oxygen - lungs, heart, brain, liver, kidneys, adrenal glands. Disturbances in the functioning of these organs can cause heart failure. and even result in death. In addition, the following respiratory diseases occur:

  • Congestive pneumonia
  • Pulmonary atelectasis
  • Emphysema
  • Pneumosclerosis.

Causes of pulmonary edema

The causes of pulmonary edema are very different, but they need to be known, since the consequences of the disease are very serious, even fatal. Most often, pulmonary edema manifests itself as a complication of some disease. The main causes of pulmonary edema include:

  • Acute intoxication of the body. It manifests itself as a result of toxic elements entering the body, both non-infectious and infectious. Toxic elements have adverse effects on alveolar membranes. Intoxication of the body includes: excess medications, bacterial pneumonia, poisoning with drugs or poison.
  • General malaise of the left ventricle. As a result of this disease, pathological abnormalities of the cardiovascular system appear (heart disease, myocardial infarction, angina pectoris, arterial hypertension). Pulmonary edema may occur as a result of these diseases.
  • Chronic pulmonary disease. Among these are bronchial asthma, emphysema, pneumonia, and malignant tumors of the lung cavity.
  • Significant physical activity. For example, an athlete who climbs a mountain may experience pulmonary edema. It often occurs in female athletes rather than in males.
  • TELA. Pulmonary edema can occur due to blockage of the pulmonary arteries by blood clots. This can be fatal.
  • When oncotic pressure decreases. When pressure decreases, the amount of protein in the blood decreases, resulting in diseases such as liver cirrhosis and chronic hemorrhagic syndrome.
  • Long-term use of medications, especially intravenous drugs, if renal excretory function is impaired.
  • Severe head injuries
  • With long-term artificial ventilation
  • When vomit enters the respiratory organs. Often, this is observed in newborn children with incorrect posture during sleep.
  • In case of drowning
  • When various substances enter the respiratory tract.

Pulmonary edema may be cardiogenic and non-cardiogenic. Cardiogenic pulmonary edema occurs as a result of left heart failure. Insufficiency occurs for the following reasons:

  • Ventricular pathology – heart disease, myocardial infarction, myocarditis, cardiosclerosis.
  • Pathological deviations of the atrium.

Important . Non-cardiogenic edema occurs as a result of drug overuse.

Symptoms of pulmonary edema

Symptoms of the disease arise suddenly often at night (due to the patient’s supine position):

  • Attacks of painful, severe suffocation are intensified in a supine position, so the patient sits or stands. This is due to a lack of oxygen.
  • Shortness of breath occurs even at rest
  • Pain in the chest due to insufficient oxygen.
  • A sharp increase in breathing (due to stimulation of the respiratory center by carbon dioxide that has not been released).
  • Palpitations
  • Cough with pink sputum
  • The patient's face has a gray-bluish tint, and after a while it affects all parts of the body. This is due to changes in the release of carbon dioxide from the blood.
  • Pale skin and cold, clammy sweat
  • Veins in the neck area swell due to stagnation in the pulmonary circulation
  • Blood pressure increases
  • Patient's confusion
  • Thready, weak pulse

Diagnostics

In addition to a visual examination of the patient admitted with the first symptoms of pulmonary edema, the specialist must conduct instrumental and laboratory research, to confirm the accuracy of the diagnosis. Diagnostics involves the following procedures:

  1. Carrying out blood gas studies.
  2. Biochemical blood test.
  3. Electrocardiogram
  4. Ultrasound of the heart
  5. Breast X-ray.

The results of the procedures will allow us to determine not only the treatment regimen, but also the cause of the disease.

Pulmonary edema in children

Pulmonary edema in children most often manifests itself as a result of pathology of the cardiovascular system. This may be an allergic reaction or due to inhalation of toxic components. Swelling can occur at any time, but most often occurs at night. The baby is worried and even frightened by a significant lack of air. Among the main symptoms of pulmonary edema in children are:

  • Cough
  • Dyspnea
  • Foamy pink sputum
  • Wheezing
  • Blueness of the skin

In newborn babies, pulmonary edema can occur due to the following pathologies:

  • Placental infarction is the death of cells in a separate area of ​​the placenta. As a result, blood flows poorly to the fetus and hypoxia may occur.
  • Aspiration of amniotic fluid is penetration of amniotic fluid into the lower respiratory tract.
  • Prenatal or birth brain injury.
  • Heart defects.

First aid for pulmonary edema

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

  • Sit the patient so that the legs are down
  • Provide rapid access to a large peripheral vein
  • Organize then fresh air
  • Organize a hot foot bath
  • Allow the patient to inhale alcohol vapor
  • Track breathing and pulse
  • Apply venous tourniquets to the extremities
  • If the pressure is not reduced, you can take 1-2 tablets of nitroglycerin under the tongue.

Algorithm for the treatment of pulmonary edema

Therapy for pulmonary edema consists of 7 stages:

  1. Sedative therapy
  2. Defoaming
  3. Vasodilator therapy
  4. Diuretics
  5. Cardiac glycosides and glucocorticoids
  6. Blood exfusion
  7. Hospitalization of the patient.

Basic therapy includes:

  • For liver cirrhosis, a course of hepatoprotectors is prescribed
  • In case of pancreatic necrosis, drugs are initially prescribed that inhibit the functioning of the pancreas, and then drugs that stimulate the healing of necrosis.
  • Comprehensive treatment of myocardial infarction
  • For bronchopulmonary diseases, a course of antibiotics is required.
  • In case of toxic edema, detoxification therapy is necessary. Salt mixtures help replenish fluid that was lost due to the use of diuretics.
  • For asthma - expectorants, mucolytics, bronchodilators.
  • For toxic shock - antihistamines
  • Edema of any form requires the use of potent antibiotics and antiviral drugs.

The duration of therapy for pulmonary edema depends on the form of the disease, concomitant diseases, general condition and age of the patient. Often times can vary from 1 to 4 weeks.

Additional Information. If the swelling proceeds without any complications and with effective therapy, the treatment period is no more than 10 days.

Possible consequences after emergency care:

  1. Transition to lightning-fast degree of edema
  2. Due to the rapid production of foam, airway obstruction occurs
  3. Respiratory depression
  4. Tachyarrhythmia
  5. Asystole
  6. Angious pain. The pain is so severe that the patient may go into painful shock.
  7. Inability to normalize blood pressure. Often, pulmonary edema occurs with low or high blood pressure, which can alternate. The vessels cannot withstand these changes for a long period, as a result of which the patient’s condition worsens significantly.
  8. Pulmonary edema increases as a result of increased blood pressure.

Prevention

Prevention is based on early identification of the disease causing pulmonary edema. Patients suffering from chronic deficiency should follow a diet that is based on: limiting the amount of salt and fluid consumed, avoiding fatty foods and reducing physical activity. As a result of the presence of chronic pulmonary diseases, one should constantly consult with a specialist, carry out therapy on an outpatient basis, twice a year treat in a hospital, and prevent factors that could worsen the patient’s condition (interaction with allergens, acute respiratory diseases, smoking cessation).

First aid for pulmonary edema is a necessary measure to maintain human life.

First aid is a set of measures aimed at eliminating acute symptoms and providing life support.

If pulmonary edema occurs, then first aid is to call an ambulance, since in out-of-hospital conditions all the necessary medications and equipment are rarely available. While waiting for qualified doctors, people around the patient must take the necessary measures.

Pulmonary edema: clinic and emergency care

Pulmonary edema is a condition when too much fluid accumulates in the lungs. This is due to the large difference in colloid osmotic and hydrostatic pressure in the capillaries of the lungs.

There are two types of pulmonary edema:

Membranogenic– occurs if capillary permeability has increased sharply. This type of pulmonary edema often occurs as an accompaniment to other syndromes.

Hydrostatic– develops due to diseases in which hydrostatic capillary pressure increases sharply, and the liquid part of the blood finds its way out in such quantities that it cannot be removed through the lymphatic tract.

Patients with pulmonary edema complain of lack of air, have frequent shortness of breath and sometimes attacks of cardiac asthma that occur during sleep.

The skin is pale, and the nervous system may have inappropriate reactions in the form of confusion or depression.

With pulmonary edema, the patient develops cold sweat, and when listening to the lungs, wet rales are detected in the lungs.

At this time, it is very important to act quickly and accurately, since without support the situation can deteriorate sharply.

When the ambulance arrives, all specialists’ actions will be aimed at three goals:

  • reduce the excitability of the respiratory center;
  • relieve the load on the pulmonary circulation;
  • remove foaming.

In order to reduce the excitability of the respiratory center, the patient is administered morphine, which relieves not only pulmonary edema, but also an asthma attack. This substance is unsafe, but here it is a necessary measure - morphine selectively affects the brain centers responsible for breathing. Also, this medication makes the blood flow to the heart less intense and due to this, congestion in the lung tissue is reduced. The patient becomes much calmer.

This substance is administered either intravenously or subcutaneously, and its effect begins within 10 minutes. If the blood pressure is low, promedol is administered instead of morphine, which has a less pronounced but similar effect.

Strong diuretics (for example, furosemide) are also used to relieve pressure.

To relieve the pulmonary circulation, they resort to a dropper with nitroglycerin.

If there are symptoms of impaired consciousness, the patient is given a weak antipsychotic.

Along with these methods, oxygen therapy is indicated.

If the patient has persistent foam, this treatment will not give the desired effect, as it may block the airways. To avoid this, doctors give inhalation with 70% ethyl alcohol, which is passed through oxygen. Then specialists suck out excess fluid through the catheter.

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