Pulmonary edema

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Classification according to ICD-10
I50.14 cardiac pulmonary edema
J81 Pulmonary edema
ICD-10 online (WHO version 2019)
Pulmonary edema in ARDS

Lung edema ( pulmonary edema , colloquially water lung ) is a non-specific term for an accumulation of fluid in the lungs caused by the leakage of blood fluid ( plasma ) from the capillary vessels into the intermediate tissue and into the alveoli . Because of the edema, chronic congestive lungs are damp and heavy. As a result of this impregnation of the lungs , the affected person can no longer absorb sufficient oxygen into the bloodstream . As symptoms a contact respiratory distress as a result of increased work of breathing , a breathing rattling or a foamy ejection on. Depending on the cause, pulmonary edema is divided into permeability edema (ARDS, toxic pulmonary edema) and hydrostatic pulmonary edema (cardiac edema and altitude edema). Formally, the permeability (the flow of water through the vessel wall) is described by the Starling equation ( Starling concept).

to form

Pulmonary congestion

A lesser degree of pulmonary edema is the subacute or chronic form, which is known as pulmonary congestion . The consumption of heroin and consumption coagulopathy can also lead to pulmonary congestion and even pulmonary edema. A congested lung can also be associated with congestive bronchitis.

Cardiac pulmonary edema

The cardiac pulmonary edema (also called cardiogenic pulmonary edema ), the most common form of pulmonary edema is not a lung disease. It arises in acute left heart failure in the low pressure system . The cause of the failure of the left half of the heart is usually an acute decompensation of chronic heart failure , in which the left half of the heart can no longer fully cope with the return of blood from the lungs due to a weak pump. This leads to a backlog of blood in the pulmonary vessels and - because of the resulting increased intravascular blood pressure in the small circulation - to a leakage of fluid into the lung tissue. This severely restricts the gas exchange. Often the patients breathe panting ( asthma cardiale ), they are restless and have fear of suffocation (in the 19th century both asthma, cardiale or bronchial, as well as pulmonary edema were called stick flow ). There is usually marked cyanosis .

Acute pulmonary edema in left heart failure is a medical emergency which, if left untreated, can lead to respiratory failure and thus to death of the patient within a few minutes . An early alert of the ambulance service and the emergency doctor is required.


Treatment is emergency with elevation of the upper body, which can already be done by first aiders , with artificial ventilation in the form of oxygen, with opiates to combat pain and sedation as well as as an antitussive , with catecholamines , with nitroglycerin and, above all, with diuretics for forced diuresis . Sometimes kidney dialysis or (especially with simultaneous polycythemia ) bloodletting may be indicated. In the past, only "bubbling pulmonary edema" was treated with a ventilator ; In the event of improper ventilation, this sometimes even triggered or worsened pulmonary edema.

Noncardiac pulmonary edema

Acute respiratory failure

The acute lung injury (engl. Acute Respiratory Distress Syndrome ARDS) arises as a consequence of increased vascular permeability, either due to inflammatory processes , or due to toxins (toxic pulmonary edema). Clinically, the ARDS is defined by typical shadows in the X-ray image, hypoxemia , the exclusion of cardiac edema (see above) and its acute onset.

Common causes of ARDS are sepsis , multiple trauma , aspiration of the stomach contents or severe burns . The SARS virus, which has only been described for a few years, also leads to the clinical picture of ARDS. ARDS often occurs in connection with the failure of other organs ( multi-organ failure ). The mortality rate in the presence of ARDS is still around 50 percent even if therapy is started early.

High elevation pulmonary edema

A high altitude pulmonary edema (short: Höhenödem ., English high altitude pulmonary edema , HAPE) may, at the altitude sickness occur. It is caused by increased pulmonary arterial pressure as a result of hypoxia due to the Euler-Liljestrand mechanism . It usually develops one to three days after a quick ascent above 2700m. It is hypertensive edema with increased microvascular permeability and with excessive vasoconstriction . Symptoms are increasing shortness of breath, dry cough with frothy or bloody sputum, cyanosis , weakness of the body and, in later stages, a coma . The causal therapy is the immediate descent or a return to deeper layers. Similar are the symptoms of sub-acute mountain sickness in children especially the Han Chinese of births at high altitude and in the chronic altitude sickness great for long-term residents heights ( Monge's disease after the first person to describe Carlos Monge Medrano, 1925) with polycythemia and complaints as the Pickwick disease . As with high-altitude edema, pulmonary edema can also develop with barotrauma and drowning .

Post-obstruction pulmonary edema

A rare form of pulmonary edema is post-obstruction pulmonary edema (negative pressure pulmonary edema , NPPE). This is caused by negative air pressure in the lungs, which can occur when the upper airways are blocked and the upper airways are simultaneously inhaled deeply. Causes for this can be, for example, laryngospasm , biting of the endotracheal tube or the laryngeal mask during anesthesia drainage or other obstructions of the airways. In addition, improper suctioning procedures are another possible cause. The NPPE is characterized by a rapid onset after a corresponding incident.

Cerebral pulmonary edema

Cerebral or neurogenic pulmonary edema occurs in brain lesions , i.e. as a result of acute cerebral processes. One also speaks of central pulmonary edema, for example as a result of traumatic brain injuries or meningoencephalitis . Also one can sunstroke or epilepsy lead to cerebral edema. After a subarachnoid hemorrhage there may be a neurogenic centralization of the blood with increase in lung volume come.

This must be differentiated from the cerebral consequences of pulmonary edema and other effects on the central nervous system .


The symptoms are present in cardiac as well as toxic or allergic pulmonary edema.

Patients with pulmonary edema suffer from restlessness, fear of suffocation, severe shortness of breath (even at rest) and even cyanosis. You usually sit by yourself with an upright upper body to enable the use of the auxiliary breathing muscles ( orthopnea ). When inhaling and exhaling, boiling and wet rattling noises can be heard, possibly accompanied by spastic breathing noises ( boiling on the chest ). Further signs are damp and cool skin (cold sweat) with pallor, a tachycardiac pulse , sometimes also arrhythmic , and different blood pressure behavior (e.g. high with simultaneous hypertensive crisis or low with heart failure with cardiogenic shock). Foamy or even bloody sputum can appear when coughing.

X-ray diagnostics

In pulmonary edema, the lungs show typical changes visible in the chest x-ray, such as Kerley lines in interstitial pulmonary edema. Typical signs of an increased water content (located outside the blood vessels) in the lungs are also a blurred border of central structures or (in the case of pronounced alveolar pulmonary edema) blotchy confluent shadows.


  • Ulrike Bungeroth (Ed.): Basics Pneumology . 2nd Edition. Elsevier, Urban & Fischer, 2010, ISBN 978-3-437-42237-9 , pp. 72-73 .


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