Pulmonary edema is a complication of various diseases, which is the excessive sweating of the transudate into the interstitial tissue, and then into the pulmonary alveoli. The term pulmonary edema is used as an association of a complex clinical symptoms arising from the accumulation of fluid in the pulmonary parenchyma.
According to the etiopathogenetic principle, two forms of pulmonary edema are distinguished: hydrostatic (occurs as a complication of diseases accompanied by an increase in hydrostatic pressure in the lumen of the vessels) and membranous (occurs when the toxins of various origin are damaged by the damage to the capillary-alveolar membrane).
The frequency of occurrence of hydrostatic pulmonary edema is much greater due to the fact that the pathology of the cardiovascular system prevails in the overall incidence of the population. The risk group for this pathology is people over 40 years old, but pulmonary edema can occur in children with congenital heart defects accompanied by left ventricular failure.
Lungs are the organ that provides all cells and tissues of the human body with oxygen. With edema of the lungs there is total hypoxia, which is accompanied by the accumulation of carbon dioxide in the tissues.
Pulmonary edema is not an independent nosological form, but is a complication of a number of diseases.
Among the main causes of pulmonary edema should be considered:
- Acute intoxication syndrome, due to ingestion of toxins of infectious and non-infectious origin (septic state, bacterial large-focal pneumonia, excessive accumulation of drugs, poisoning with poisons). Toxins exert a damaging effect on the alveolocapillary membranes and promote the release of transudate from pulmonary interstitium;
- acute left ventricular failure, which is a consequence of various pathologies of the cardiovascular system (acute myocardial infarction , mitral heart defects, persistent arterial hypertension, unstable angina , severe arrhythmia , cardiomyopathy , cardiosclerosis );
- chronic lung diseases (COPD, emphysema, bronchial asthma , large-focal pneumonia, malignant neoplasms in the lungs);
- pulmonary edema as a result of rapid ascent to a great distance (more than 3 km);
- unilateral swelling of the lung as a result of rapid evacuation of fluid or air from the pleural cavity (with pneumothorax and exudative pleurisy);
- diseases accompanied by a decrease in oncotic blood pressure as a result of a decrease in protein (nephrotic syndrome, liver cirrhosis, chronic hemorrhagic syndrome);
- uncontrolled excessive infusion of liquid medications by intravenous infusion in combination with impaired renal excretory function;
- Traumatic injury of the chest, accompanied by pneumothorax;
- severe craniocerebral trauma, accompanied by convulsive activity;
- the onset of pulmonary edema in diseases that occur with increased intracranial pressure (acute disturbance of cerebral circulation, neoplastic lesions of the brain)
- prolonged artificial ventilation of the lungs with a high concentration of oxygen;
- Aspiration syndrome with drowning, foreign body or vomiting in the respiratory tract.
Depending on the underlying cause of pulmonary edema, there is a classification that distinguishes cardiogenic and non-cardiogenic (neurogenic, nephrogenic, allergic, toxic) form of edema.
The pathogenetic mechanisms of any form of pulmonary edema consist of several stages. The debut of the pulmonary edema is the interstitial stage, during which the accumulation of transudate occurs in the pulmonary interstitium. At this stage, there are symptoms of cardiac asthma . Then, a fluid containing a high percentage of protein moves to the alveoli and whipped it with air, resulting in a viscous foam. Due to its thick consistency, the foam encircles the respiratory tract and there is an acute respiratory failure, which causes the accumulation of carbon dioxide in the tissues (hypercapnia), decompensated acidosis and hypoxia. All of the above metabolic disorders can cause irreversible processes in vital organs and result in a fatal outcome.
There are three pathomorphological mechanisms of pulmonary edema:
1. A sharp increase in hydrostatic pressure.
2. Decreased oncotic blood pressure.
3. Damage to the protein structure of the membrane located between the alveolus and the capillary and increasing the alveolar permeability.
With any form of pulmonary edema, a violation of the alveolocapillary wall occurs as a result of damage to the protein-polysaccharide complex of the membrane. When pulmonary edema occurs as a result of anaphylactic shock, severe intoxication of infectious nature, inhalation of toxic vapors and severe renal failure, this pathogenetic mechanism is leading in the development of manifestations of pulmonary edema.
As a result of a combination of increased hydrostatic pressure and reduced oncotic pressure, conditions are created to increase the filtration pressure in the lumen of the pulmonary capillaries. The cause of this condition is most often uncontrolled intravenous infusion of hypoosmotic solutions without taking into account daily diuresis. In addition, with severe renal and hepatic insufficiency, there is a deficiency of protein in the blood, which helps reduce oncotic pressure.
Among the pathogenetic causes of acute cardiogenic pulmonary edema, a sharp increase in hydrostatic pressure in the pulmonary circulation comes to the fore, exacerbated by the fact that outflow of blood to the left parts of the heart is difficult (myocardial infarction, mitral stenosis).
Swelling of the lungs symptoms
Clinical manifestations of pulmonary edema depend on the stage of the disease and on the speed of the transition from the interstitial to the alveolar. According to the terms of prescription, acute pulmonary edema (symptoms of alveolar edema develop within 4 hours maximum), prolonged (the symptoms of swelling increase gradually and reach a maximum after several days) and fulminant, which in almost 100% of cases ends in a lethal outcome, due to the extremely serious condition of the patient .
The cause of acute pulmonary edema is transmural myocardial infarction and mitral stenosis of the decompensation stage. A subacute variant of the development of pulmonary edema is observed with renal failure, an infectious lesion of the pulmonary parenchyma. Prolonged form of edema is characteristic for chronic inflammatory diseases with localization in the lung tissue.
The fulminant variant is observed in cardiogenic pulmonary edema, which is accompanied by a common cardiac pathology (extensive myocardial infarction, anaphylactic shock ). In subacute form, the first symptom of pulmonary edema is shortness of breath with physical activity, which gradually builds up and transforms into choking.
In practice, ambulance doctors use the clinical classification of pulmonary edema, in which 4 stages are distinguished: the stage of dyspnea (mass dry rales throughout the pulmonary fields and the absence of wet wheezes), the orthopnoietic stage (the prevalence of wet rales over the dry ones), the stage of pronounced orthopnea wet rales are heard at a distance without the use of a phonendoscope), the manifesting stage (bubbling breath, pronounced cyanosis of the skin, copious excretion of foamy sputum).
The peculiarity of the interstitial pulmonary edema is its appearance at night time against the background of complete well-being. The provoking factor may be excessive physical activity or psycho-emotional overstrain. A harbinger of edema development is coughing at night.
Symptoms of the interstitial phase of pulmonary edema: dyspnea with minimal physical activity and at rest, decreasing in the sitting position of the patient, severe shortage of air and inability to take a deep breath, dizziness and general malaise.
At the primary visual examination of the patient, attention is drawn to the sharp pallor and increased moisture of the skin, combined with cyanosis of the nasolabial triangle and the surface of the tongue, exophthalmos. Percussion of the lungs allows us to identify the symptoms of acute emphysema in the form of a boxed sound.
Auscultatory changes in the lungs are a bronchial type of breathing with a mass of dry buzzing rales all over the pulmonary fields on both sides. From cardiovascular changes there is a rapid heart rate, I tone is weakened in all auscultative points, in the projection of the pulmonary trunk there is an accent of II tone. Radiographic examination visualizes the structurelessness and expansion of the roots of the lungs, the indistinctness of the pulmonary pattern, the uniform symmetrical reduction in pneumotization, and the presence of Curly lines in the basal-lateral segments of the lungs.
Symptoms of the alveolar phase of pulmonary edema build up very intensively and suddenly, so they are difficult to tolerate by patients. The patient develops shortness of breath short of suffocation, the frequency of respiratory movements increases to 40 per minute, there is noisy stridor breathing and cough with copious discharge of foamy sputum with a trace of blood (in a short period of time the patient notes up to 2 liters of foamy sputum). In contrast to the interstitial edema, when patients choose a forced position and try not even to move, in the phase of alveolar edema the patient is extremely excited. With an external examination, diffuse cyanosis and hyperhidrosis of the skin of the face and trunk, lowering of arterial pressure and increased pulse of small filling, swelling of veins in the neck. Auscultatory changes - a mass of different-sized wet wheezing all over the pulmonary fields, tachycardia and tachypnea, heart sounds are not audible due to noisy breathing. X-ray pathology: homogeneous bilateral extensive obscuration in the basal area with fuzzy uneven contours and infiltrative changes in lungs of varying length and shape.
In the acute period there is an increase in the pulse to 160 beats per minute and an increase in blood pressure, and with prolonged flow and increase in hypoxia, there is a weakening of the pulse, a decrease in arterial pressure, and a rapid increase in respiratory movements, despite the fact that breathing becomes superficial.
Pulmonary edema can have a wavy course, when after relapsing the attack, a relapse of clinical manifestations occurs, so all patients need qualified medical care in a hospital.
Toxic pulmonary edema is accompanied by a lightning current and in most cases a fatal outcome. Signs of swelling build up within a few minutes, and acute respiratory failure ends with a complete stop of breathing when poisoning with nitrogen oxides. And at the same time, the toxic pulmonary edema caused by uremia may have a minor clinical symptomatology and a bright radiologic picture.
Clinical manifestations of pulmonary edema can occur in other diseases, therefore it is necessary to conduct careful differential diagnosis with such pathologies as: pulmonary embolism, asthmatic status in bronchial asthma, acute coronary syndrome. In some cases, there is a combination of pulmonary edema with the aforementioned diseases.
Pulmonary edema in bedridden patients
The pathogenetic mechanism of the development of pulmonary edema in a recumbent patient is due to the fact that in the horizontal position the volume of inhaled air is much less than when breathing in a vertical position. As a result of a decrease in the activity of respiratory movements, lung volume decreases, blood flow decreases, and stagnant changes in pulmonary interstitium occur. Conditions are created for the accumulation of phlegm containing the inflammatory component. Separation of sputum is difficult, in connection with which stagnant changes in the lungs are intensified.
Against the background of all the above-mentioned pathogenetic changes, stagnant pneumonia arises, a complication of which is pulmonary edema in the absence of adequate therapy.
A feature of pulmonary edema in bed patients is the gradual appearance and growth of clinical symptoms. The primary complaint of such patients is the unmotivated rapidity of breathing and the increasing shortness of breath, which patients describe as a feeling of lack of air. Because of the gradual increase in hypoxia, there is an oxygen starvation of the brain, which manifests itself in the form of drowsiness, dizziness, weakness. Despite the scarcity of clinical manifestations, an objective study has noted disturbances in the form of the presence of moist, large bubbling rales throughout the pulmonary fields with a maximum in the lower sections, as well as dullness of pulmonary sound during percussion.
In order to prevent the onset of pulmonary edema, all bed patients are advised to perform twice a day respiratory gymnastics - blowing air through a tube into a container of water, inflating balloons.
In order to avoid stagnation in a small circle of blood circulation, all lying patients are shown the position in bed with an elevated head end, therefore most of the stationary chambers are equipped with special functional couches.
In bed patients, it is possible to accumulate fluid not only in the lung tissue, as evidence of pulmonary edema, but also in the pleural cavities (hydrothorax, exudative pleurisy). In this situation, the use of a therapeutic puncture is shown, after which the majority of patients notice a significant improvement in the condition.
Pulmonary edema first aid
Kupirovanie a hypostasis of lungs should occur on a prehospital stage, and hospitalization in reanimation department it is necessary to make after stabilization of a status of the patient. In a situation where it is not possible to stabilize the patient's condition and the symptoms of respiratory and heart failure increase, it is necessary to take the patient to the profile hospital as carefully as possible in order to provide more qualified care. In the ambulance, all resuscitation measures are recommended to stabilize hemodynamic parameters.
To determine the necessary urgent measures, one should take into account not only the existing symptomatology, but also a kind of edema according to the pathogenetic criterion. However, there is a certain algorithm for urgent measures, which is observed in all cases of pulmonary edema.
It is necessary to provide the patient with fresh air and give the patient a semi-sitting position. With the patient should remove all the compressive clothing in the upper half of the trunk. The most effective and fastest way to reduce pressure in the system of the small circle of blood circulation is bloodletting. The recommended amount of blood is 300 ml and significantly reduces the stagnant changes in the lungs. Contraindication to the use of this method is - arterial hypotension and poorly expressed veins.
An alternative to bloodletting can serve as superposition of venous turnstiles for "unloading" of the small circle of blood circulation. When applying a tourniquet, it is necessary to check the pulsation of the arteries below the level of the tourniquet, so as not to stop arterial blood flow. Do not leave the venous tourniquet for more than an hour and change limbs once every 20 minutes. Absolute contraindication for the application of a tourniquet is thrombophlebitis . As a distraction, hot foot baths are used.
Emergency medical assistance for pulmonary edema is performed according to the following program:
- maintenance therapy by immediate adequate oxygenation, intubation of the trachea, ventilation in the 16-18 per minute mode and the volume of insufflated air 800-900 ml. Oxygenotherapy means permanent inhalation of 100% moistened oxygen through the nasal cannula. The criterion of adequate oxygenation of blood in the lungs in the absence of direct monitoring of transport and oxygen consumption should be a combination of oxygenation of arterial blood at a level of 70-80 mm Hg, and venous blood at a level of 35-45 mm Hg;
- reduction of intravascular hydrostatic pressure by the use of diuretics (Lasix 4-6 ml of intravenous solution or Furosemide 40-60 mg intravenously);
- sucking fluid from the upper respiratory tract with an aspirator;
- the use of antifoaming agents: inhalation of 30% ethanol solution, intravenous infusion of 5 ml of 96% ethyl alcohol together with 15 ml of 5% glucose solution, and with strong foam release, the endotracheal route of 2 ml 96% ethyl alcohol is applied by the method of tracheal puncture;
- heparin therapy is indicated for the normalization of pulmonary blood flow (bolus administration of Heparin in a dose of 6000-10000 ED intravenously-drip, then switch to subcutaneous injection of low-molecular heparins - Fraxiparin 0.3 ml twice daily);
- If there is a strong pain syndrome, then Fentanyl (2 ml of 0.005% solution) with Droperidol (4 ml of 0.25% solution) in 10 ml of isotonic sodium chloride solution should be administered to the patient;
- To eliminate the excitation of the respiratory center, Morphine is applied (1 ml of a 1% solution intravenously). With cardiogenic pulmonary edema, morphine is a pathogenetic agent and is used by all patients. Side effect of Morphine is vomiting, therefore, its administration is recommended to combine with intramuscular injection of 1 ml of Diphenhydramine or Pipolphen;
- with the inhibition of the respiratory center, which is accompanied by Cheyne-Stokes breathing, intravenous administration of Eufillin is indicated in a dosage of 10 ml of a 2.4% solution. Introduction Euphillin is accompanied by a decrease in blood pressure, which is important in cardiogenic edema with hypertension, but with the appointment of euphyllin should take into account side effects in the form of tachycardia and increased demand for cardiac muscle in oxygen;
- parenteral administration of corticosteroids (hydrocortisone 125 mg per 150 ml of 5% glucose solution) is used to improve the condition of the pulmonary membrane;
- antihistamines (Diphenhydram 1ml 1% solution intramuscularly, Suprastin 1 ml 2% solution intravenously);
- To control acidosis, intravenous drip injection of sodium bicarbonate with a 4% solution is recommended.
Immediate measures to stop acute cardiogenic pulmonary edema have their own peculiarities and are aimed at lowering preload on the heart, improving the contractile function of the myocardium and "unloading" the small circle of circulation.
To reduce preload on the heart, it is necessary to reduce the flow of blood from the peripheral vessels to the small circle of the circulation, for which peripheral vasodilators are used (Nitroglycerin in various dosage forms - Nitrospray, tablets with a periodicity of 1 tablet per 10 minutes, intravenous infusion of 0.01% solution at a rate of 1ml of solution in 4 minutes).
In cardiogenic edema, 1% Morphine solution is administered at a dose of 1 ml intravenously, as this preparation has a wide range of therapeutic properties: a vagotrophic effect, which inhibits the overexcited respiratory center, dilatation effect on pulmonary and peripheral veins, ganglion blocking properties that reduce inflow blood in the system of a small circle of blood circulation. If there are contraindications to the use of Morphine (bronchospastic syndrome, signs of cerebral edema), the drug of choice is Droperidol (2 ml of 0.25% solution intravenously).
To improve the contractile function of the myocardium, the administration of Dopamine at a dosage of 2 μg / kg / min with rheopolyglucose intravenously is indicated. To adverse reactions to the introduction of Dopamine are: paroxysmal tachycardia, vomiting and increasing dyspnea.
To "unload" the small circle of circulation, it is necessary to reduce the volume of circulating fluid and the pressure in the pulmonary artery. To this end, the diuretic preparations of the saluretic group are used (Furosemide 40-100 mg). The use of osmodiuretics is absolutely contraindicated, since these drugs contribute to the intensification of pulmonary edema.
The volume of infusion therapy should be reduced to 200-300 ml of 5% glucose.
With a pronounced concomitant bronchiolospastic component (expiratory dyspnea, auscultatory severe breathing is heard), there is a need to administer Prednisolone in a dose of 30-60 mg intravenously.
Cardiogenic pulmonary edema is often combined with acute cardiac rhythm disturbances, which may lead to electropulse therapy or electrostimulation.
It shows the use of drugs that have a stabilizing effect on the increased permeability of cell membranes (Counterline 40-60 thousand ED intravenously drip).
When combined cardiogenic pulmonary edema with increasing blood pressure, the algorithm of urgent measures consists of: intravenous infusion of nitroglycerin (30 mg per 300 ml of physiological sodium chloride solution) at a rate of 10 drops per minute under a constant control of arterial pressure, intravenous injection of 1 ml of 5% solution of Pentamine , and with severe arterial hypertension - 1 ml of 0.01% Clofelin solution.
Swelling of the lungs
After providing the first emergency care and stabilizing the condition, the patient is taken to the intensive care unit where treatment is continued. The main criteria for the patient's transportability are: the frequency of respiratory movements less than 22 per minute, the absence of excretion of foamy sputum, the absence of wet wheezes in auscultation of the lungs, the absence of cyanosis of the skin, stabilization of hemodynamic parameters.
In a hospital after careful medical research, conditions are created to identify the etiological factors that were the primary cause of pulmonary edema.
Among the diagnostic measures should be identified: a biochemical blood test with mandatory determination of the level of total protein and creatinine for evaluation of kidney function, a blood test for troponins for the diagnosis of acute coronary syndrome and myocardial infarction, determination of the gas composition of the blood, coagulogram for suspected pulmonary thromboembolism.
Chambers of intensive care are equipped with diagnostic equipment, which makes it possible to conduct instrumental research methods - pulse oximetry to determine the oxygen saturation of blood, phlebotometry for measuring venous pressure in the subclavian vein, chest X-ray to determine the stage of edema and possible complications, electrocardiography for the diagnosis of pathology cardiac activity.
After establishing the cause of pulmonary edema, etiological treatment is prescribed, for example, toxic pulmonary edema, in need of detoxification therapy, and in some cases, the administration of an antidote, and when swelling of the lungs against large focal pneumonia, antibacterial agents are indicated.
Medical activities in the intensive care unit are carried out under constant monitoring of hemodynamic parameters and parameters of external respiration. The introduction of most drugs is carried out through the central venous access, for which the resuscitator performs catheterization of the subclavian vein.
For successful treatment of any form of pulmonary edema, the psychoemotional state of the patient is of great importance, therefore, all patients are shown to carry out sedative and sedative therapy with 1% Morphine solution at a dose of 1 ml intravenously.
In the intensive care unit continues treatment of pulmonary edema with the use of medicines aimed at improving the work of the cardiovascular system and improving metabolic processes in the myocardium.
To improve the contractile function of the myocardium to a patient with pulmonary edema that appeared on the background of a hypertensive crisis and mitral valve insufficiency, it was justified the appointment of cardiac glycosides in a therapeutic dose (Korglikon 1 ml 0.06% solution intravenously). Contraindication to the use of cardiac glycosides is acute myocardial infarction.
In the intensive care unit, oxygenotherapy continues in combination with the use of antifoams, as well as the use of diuretics and peripheral vasodilators. Defoaming is carried out with the help of several methods: 95% ethyl alcohol is poured into the humidifier and oxygen is fed through it at a rate of 3 liters per minute, which is gradually brought to 7 liters per minute. On average, after 20 minutes of the procedure, gross respiratory disturbances and wet wheezing in the lungs disappear. An effective defoamer, which within 3 minutes stops the attack of pulmonary edema, is 10% alcohol solution of Antifemcilan, which is sprayed into the humidifier.
In severe pulmonary edema, intubation of the trachea and mechanical ventilation is recommended.
The appearance of recurrent pulmonary edema is an indication for surgical treatment of diseases accompanied by severe heart failure (surgical correction of heart defects, excision of aortic aneurysm).
Lung edema effects
Due to the fact that pulmonary edema provokes the development of respiratory failure, hypoxia develops in the human body. Prolonged hypoxia leads to irreversible destructive processes in the cells of the central nervous system and directly detrimental to the structure of the brain. The defeat of the central nervous system can manifest itself in the form of vegetative disorders that do not threaten the patient's life, but the defeat of vital brain structures leads to a fatal outcome.
Despite modern methods of diagnosis and treatment, mortality from alveolar pulmonary edema is at a high level and reaches 50%, and cardiogenic pulmonary edema in combination with acute myocardial infarction in 90% of cases leads to a lethal outcome. Therefore, timely diagnosis and a qualified and individual approach to the appointment of a particular treatment are very important for the successful management of clinical manifestations of edema. Coping an attack at the stage of interstitial edema improves the prognosis for the patient.
To prevent serious complications, it is recommended to carry out preventive measures to prevent pulmonary edema - timely diagnosis and treatment of cardiovascular pathologies, maintenance of chronic lung diseases at the compensation stage, prevention of contact with allergens and toxins of chemical origin, fighting smoking and adherence to a diet with limited salt intake .
The long-term consequences of pulmonary edema are congestive pneumonia, pneumofibrosis and segmental atelectasis. In addition, as a result of prolonged hypoxia and hypercapnia, conditions are created for ischemic damage of all organs and systems.
In order to avoid severe complications of pulmonary edema, there are prescriptions of traditional medicine that have positive effects in preventing re-edema. For this purpose, a decoction of flax seeds and cherry stems is used. The frequency of reception of this broth is 4 times a day for at least three months. It should be borne in mind that the reception of traditional medicine can cause an allergic reaction, which adversely affects the recovery process.