Pulmonary edema is an acute pulmonary insufficiency associated with a massive release of transudate from the capillaries into the lung tissue, which leads to infiltration of the alveoli and a sharp violation of gas exchange in the lungs. Disease is manifested by shortness of breath at rest, a feeling of tightness in the chest, suffocation, cyanosis, cough with foamy bloody sputum, bubbling breathing. Diagnosis involves auscultation, radiography, ECG, EchoCG. Treatment requires intensive therapy, including oxygen therapy, the introduction of narcotic analgesics, sedatives, diuretics, hypotensive agents, cardiac glycosides, nitrates, protein preparations.
ICD 10
J81 Pulmonary edema
Meaning
Pulmonary edema is a clinical syndrome caused by the effusion of the liquid part of the blood into the lung tissue and accompanied by a violation of gas exchange in the lungs, the development of tissue hypoxia and acidosis. Pathology can complicate the course of a variety of diseases in pulmonology, cardiology, neurology, gynecology, urology, gastroenterology, otolaryngology. In case of untimely provision of the necessary assistance, edema can be fatal.
Causes of pulmonary edema
The etiological prerequisites of pulmonary edema are diverse. In cardiological practice, disease can be complicated by various diseases of the cardiovascular system: atherosclerotic and postinfarction cardiosclerosis, acute myocardial infarction, infectious endocarditis, arrhythmias, hypertension, heart failure, aortitis, cardiomyopathy, myocarditis, atrial myxomas. Often, pulmonary edema develops against the background of congenital and acquired heart defects – aortic insufficiency, mitral stenosis, aneurysm, aortic coarctation, open ductus arteriosus, Eisenmenger syndrome.
In pulmonology, disease can be accompanied by a severe course of chronic bronchitis and croup pneumonia, pneumosclerosis and emphysema, bronchial asthma, tuberculosis, actinomycosis, tumors, PE, pulmonary heart. The development of disease is possible with chest injuries accompanied by prolonged crushing syndrome, pleurisy, pneumothorax.
In some cases, disease is a complication of infectious diseases that occur with severe intoxication: SARS, influenza, measles, scarlet fever, diphtheria, whooping cough, typhoid fever, tetanus, polio.
Pulmonary edema in newborns may be associated with severe hypoxia, prematurity, bronchopulmonary dysplasia. In pediatrics, the danger exists in all conditions associated with impaired airway patency – acute laryngitis, adenoids, foreign bodies of the respiratory tract, etc. A similar mechanism for the development of this disease is observed in mechanical asphyxia: hanging, drowning, aspiration of gastric contents into the lungs.
In nephrology, acute glomerulonephritis, nephrotic syndrome, renal failure can lead to pulmonary edema; in gastroenterology – intestinal obstruction, cirrhosis of the liver, acute pancreatitis; in neurology – ACA, subarachnoid hemorrhages, encephalitis, meningitis, tumors, TBI and brain surgery.
Often, pathology develops due to poisoning with chemicals (fluorinated polymers, organophosphates, acids, metal salts, gases), intoxication with alcohol, nicotine, drugs; endogenous intoxication with extensive burns, sepsis; acute poisoning with drugs (barbiturates, salicylates, etc.), acute allergic reactions (anaphylactic shock).
In obstetrics and gynecology, disease is most often associated with the development of eclampsia of pregnant women, ovarian hyperstimulation syndrome. It is possible to develop pulmonary edema against the background of prolonged ventilation with high oxygen concentrations, uncontrolled intravenous infusion of solutions, thoracocentesis with rapid simultaneous evacuation of fluid from the pleural cavity.
Pathogenesis
The main mechanisms of pulmonary edema development include a sharp increase in hydrostatic and a decrease in oncotic (colloidal osmotic) pressure in the pulmonary capillaries, as well as a violation of the permeability of the alveolocapillary membrane.
The initial stage of pulmonary edema is enhanced filtration of transudate into interstitial lung tissue, which is not balanced by the reabsorption of fluid into the vascular bed. These processes correspond to the interstitial phase of pulmonary edema, which is clinically manifested in the form of cardiac asthma.
Further movement of protein transudate and pulmonary surfactant into the lumen of the alveoli, where they mix with air, is accompanied by the formation of a persistent foam that prevents oxygen from entering the alveolar-capillary membrane, where gas exchange occurs. These disorders characterize the alveolar stage of edema. Shortness of breath resulting from hypoxemia helps to reduce intra-thoracic pressure, which in turn increases blood flow to the right parts of the heart. At the same time, the pressure in the small circle of blood circulation increases even more, and the perspiration of the transudate into the alveoli increases. Thus, a vicious circle mechanism is formed, causing the progression of edema.
Classification
Taking into account the triggers, cardiogenic (cardiac), non-cardiogenic (respiratory distress syndrome) and mixed form are distinguished. The term noncardiogenic pulmonary edema combines various cases not related to cardiovascular diseases: nephrogenic, toxic, allergic, neurogenic and other forms.
According to the variant of the course , the following types of pulmonary edema are distinguished:
- lightning-fast – develops rapidly, within a few minutes; always ending with a fatal outcome
- acute – increases rapidly, up to 4 hours; even with immediately initiated resuscitation measures, it is not always possible to avoid a fatal outcome. Acute pulmonary edema usually develops with myocardial infarction, TBI, anaphylaxis, etc.
- subacute – has a wave-like course; symptoms develop gradually, then increasing, then subsiding. Such a variant of the course of disease is observed with endogenous intoxication of various genesis (uremia, liver failure, etc.)
- prolonged – develops in the period from 12 hours to several days; it can occur erased, without characteristic clinical signs. Prolonged form occurs in chronic lung diseases, chronic heart failure.
Pulmonary edema symptoms
Pulmonary edema does not always develop suddenly and violently. In some cases, it is preceded by prodromal signs, including weakness, dizziness and headache, a feeling of tightness in the chest, tachypnea, dry cough. These symptoms may occur a few minutes or hours before the development of this pathology.
The clinic of cardiac asthma (interstitial pulmonary edema) can develop at any time of the day, but more often it occurs at night or in the early morning hours. An attack of cardiac asthma can be provoked by physical exertion, psychoemotional stress, hypothermia, anxious dreams, transition to a horizontal position, and other factors. In this case, there is a sudden suffocation or paroxysmal cough, forcing the patient to sit down. Interstitial pulmonary edema is accompanied by the appearance of cyanosis of the lips and nails, cold sweat, exophthalmos, excitement and motor anxiety. Objectively revealed BH 40-60 per minute, tachycardia, increased blood pressure, participation in the act of breathing auxiliary muscles. Breathing is intensified, stridorous; dry whistling wheezes may be heard during auscultation; there are no wet wheezes.
At the stage of alveolar pulmonary edema, severe respiratory failure, pronounced shortness of breath, diffuse cyanosis, puffiness of the face, swelling of the neck veins develops. Bubbling breathing can be heard in the distance; various wet wheezes are determined auscultatively. When breathing and coughing, foam is released from the patient’s mouth, often having a pinkish tinge due to the sweating of shaped blood elements.
With pulmonary edema, lethargy and confusion quickly increase, up to coma. In the terminal stage, blood pressure decreases, breathing becomes shallow and periodic, pulse is thready. The death of a patient with pulmonary edema occurs due to asphyxia.
Diagnostics
In addition to the assessment of physical data, indicators of laboratory and instrumental studies are extremely important in the diagnosis of pulmonary edema. All studies are carried out as soon as possible, sometimes in parallel with the provision of emergency care:
- Study of blood gases. With pulmonary edema, it is characterized by a certain dynamics: at the initial stage, moderate hypocapnia is noted; then, as pulmonary edema progresses, PaO2 and PaCO2 decrease; at a later stage, an increase in PaCO2 and a decrease in PaO2 are noted. Indicators of blood CBS indicate respiratory alkalosis.
- Biochemical screening. In order to differentiate the causes that led to pulmonary edema, a biochemical study of blood parameters (CPK-MV, cardiospecific troponins, urea, total protein and albumins, creatinine, liver samples, coagulograms, etc.) is carried out.
- ECG and EchoCG. An electrocardiogram with pulmonary edema often reveals signs of left ventricular hypertrophy, myocardial ischemia, and various arrhythmias. According to ultrasound of the heart, zones of myocardial hypokinesia are visualized, indicating a decrease in contractility of the left ventricle; the ejection fraction is reduced, the final diastolic volume is increased.
- Chest X-ray. Reveals the expansion of the boundaries of the heart and the roots of the lungs. With alveolar pulmonary edema, a homogeneous symmetrical butterfly-shaped darkening is detected in the central parts of the lungs; less often, focal changes. There may be a moderate or large pleural effusion.
- Catheterization of the pulmonary artery. Allows differential diagnosis between noncardiogenic and cardiogenic pulmonary edema.
Treatment for pulmonary edema
Treatment of pulmonary edema is carried out in the ICU under constant monitoring of oxygenation and hemodynamics. Emergency measures in the event of pulmonary edema include:
- giving the patient a sitting or half-sitting position (with a raised headboard), applying tourniquets or cuffs on the limbs, hot foot baths, bloodletting, which helps to reduce venous return to the heart.
- it is more expedient to supply moistened oxygen with this disease through defoamers – antifomsilane, ethyl alcohol.
- if necessary, transfer to a ventilator. If there are indications (for example, to remove a foreign body or aspiration of the contents from the respiratory tract), a tracheostomy is performed.
- the introduction of narcotic analgesics (morphine) to suppress the activity of the respiratory center.
- the introduction of diuretics (furosemide, etc.) to reduce BCC and dehydration of the lungs.
- the introduction of sodium nitroprusside or nitroglycerin to reduce afterload.
- the use of ganglioblockers (azamethonium bromide, trimetaphane) allows you to quickly reduce pressure in the small circle of blood circulation.
According to the indications, patients with pulmonary edema are prescribed cardiac glycosides, hypotensive, antiarrhythmic, thrombolytic, hormonal, antibacterial, antihistamines, infusions of protein and colloidal solutions. After the relief of an attack of pulmonary edema, the treatment of the underlying disease is carried out.
Prognosis and prevention
Regardless of the etiology, the prognosis for pulmonary edema is always extremely serious. In acute alveolar form, mortality reaches 20-50%; if edema occurs against the background of myocardial infarction or anaphylactic shock, mortality exceeds 90%. Even after successful relief of pulmonary edema, complications in the form of ischemic damage to internal organs, congestive pneumonia, lung atelectasis, pneumosclerosis are possible. In the event that the root cause of edema has not been eliminated, there is a high probability of its recurrence.
A favorable outcome is greatly facilitated by early pathogenetic therapy undertaken in the interstitial phase of disease, timely detection of the underlying disease and its targeted treatment under the guidance of a specialist of the appropriate profile (pulmonologist, cardiologist, infectious disease specialist, pediatrician, neurologist, otolaryngologist, nephrologist, gastroenterologist, etc.).
Literature
- Murray JF. Pulmonary edema: pathophysiology and diagnosis. Int J Tuberc Lung Dis. 2011 Feb;15(2):155-60, i. – link
- Ghofrani HA. [Pulmonary edema]. Internist (Berl) 2004 May;45(5):565-72. – link
- Ware LB, Matthay MA. Clinical practice. Acute pulmonary edema. N Engl J Med. 2005 Dec 29;353(26):2788-96. – link
- Rubenfeld GD, Caldwell E, Peabody E, Weaver J, Martin DP, Neff M, Stern EJ, Hudson LD. Incidence and outcomes of acute lung injury. N Engl J Med. 2005 Oct 20;353(16):1685-93. – link