A pulmonary embolism (short: LE ) or pulmonary artery embolism (short: LAE ) is a blockage ( embolism ) of a blood vessel in the lungs or the pulmonary circulation . It is usually by a blood clot (blood clot), called thrombus (she will also Lungenthrombembolie , pulmonary thromboembolism or Pulmonalarterienthrombembolie called), rarely by gas bubbles, such as in a diving accident or during surgery aspirated air, or (in bold fat embolism , about caused by fat from the fat marrow in bone fractures). Because pulmonary embolism is potentially life threatening , first aid measures are always required. The falling blood pressure ( hypotension ) can lead to obstructive shock with cardiac arrest .
Typical symptoms are acute shortness of breath ( dyspnoea ) and / or chest pain when inhaling. The lack of oxygen ( hypoxia ) causes a resting pulse of over 100 / min ( tachycardia ), which is accompanied by a high respiratory rate ( tachypnea ). The other symptoms are very variable and can include cough (lat .: tussis), blood in the sputum ( hemoptysis ) and cardiac arrhythmias . If there is an additional ( comorbidity ) existing deep vein thrombosis ( deep vein thrombosis - DVT), the affected leg is usually swollen and painful. Because of the increased pumping resistance in the pulmonary circulation ( pulmonary hypertension ), the right ventricle is more stressed ( cor pulmonale ), which can lead to heart failure .
In addition to supplying oxygen as required , lysis therapy is carried out to dissolve the thrombus. For the inhibition of blood coagulation ( anticoagulants used) intravenously appliqué heparin . After the acute symptoms have subsided, long-term therapy with orally administered anticoagulants (see Medical measures ) is usually necessary to avoid renewed thrombosis .
A blood clot that triggers a pulmonary embolism occurs in up to 80% of all cases in the deep leg or pelvic veins and reaches both pulmonary arteries via the inferior vena cava , the right atrium and ventricle of the heart . In the process, the thrombus gets stuck and closes the vessel. The larger the thrombus, the larger the area of the lung that is no longer supplied with blood. Often there are several thrombi, which at the same time or at a time interval completely or partially block the lung vessels. Both lungs of a patient can also be affected. Under the birth it can also cause amniotic fluid embolism , in fractures of the long bones (eg. As the femur ) to fat embolism occur. Even bone marrow embolisms are possible in the lungs. Furthermore, in the event of injuries or medical measures, air or other gases (for example CO 2 during laparoscopy ) can get into the venous vascular system.
Pulmonary embolism is one of the most frequently overlooked causes of death.
The lethality of an untreated severe pulmonary embolism is very high at 30%. Prompt treatment can reduce mortality to 2–8%.
The embolus blocks one or more branches of the pulmonary arteries. This is all the more serious, the larger the inner diameter of the affected vessel. The congestion of blood in front of the thrombus leads to a more or less strong increase in pressure in the pulmonary circulation ( pulmonary hypertension ) and thus to stress on the right part of the heart, which can partially or even completely fail. If the right half of the heart does not fail, at least the amount of blood that can pass through the lungs and reach the left half of the heart is reduced. However, the left half of the heart can only continue to pump as much blood as it receives. The consequence of the reduced delivery rate is a reduced oxygen supply to the important organs. It can be used to (cardiogenic) shock coming. Depending on the extent, the oxygen content of the blood - hypoxemia - may decrease .
Smaller pulmonary embolisms can also lead to right heart problems. The increase in pressure in the small circulation is not so severe here, and the acute survival rate of the patient is therefore significantly higher. In most cases, the thrombi are broken down and the vascular system is free again. Nevertheless, in the further course of the disease, chronic pulmonary hypertension can develop in some patients (especially with recurrent minor pulmonary embolisms) . It can then be a CTEPH .
Subsequent to the acute event, an infection of the no longer adequately supplied lung tissue can lead to so-called infarct pneumonia . The lung area located behind the embolus can the particular for greater embolism with destruction of a portion of connective tissue lung backbone infarzieren . In spite of the high regenerative power of the lung tissue, whole areas then die permanently. If the organism survives this, functionless scars develop. If larger areas are affected with a corresponding loss of functionality, there is shortness of breath , reduced resilience and often persistent coughing . The easier invasion of germs into the initially necrotic , then fibrotically altered - and largely inaccessible to antibiotics - scarred tissue later leads to pneumonia more frequently . The fibrotic remodeling processes also slightly increase the risk of later lung cancer . There is a high rate of late complications, especially with re-embolism.
Causes and Triggers
There are certain risk patients who are prone to thrombosis and thus pulmonary embolism.
Disposing factors in the patient's history are: fracture (hip or leg), total hip or knee endoprosthesis , major surgery, lung disease, hormone replacement therapy, malignant tumor, oral contraception, stroke, pregnancy, phase shortly after birth, previous venous embolism , Blood clotting disorder , old age, high homocysteine levels .
With a corresponding predisposition , any immobilization , especially of the lower limbs, can become a trigger that promotes the growth of a thrombus (similar to "condensation") through stasis of the blood: Blood congestion with long knees bent, for example on long bus trips or long-distance flights, travel thrombosis , after fractures and sprains as well as being bedridden of any kind.
The point in time of the acute onset, however, is only determined by the later detachment of a thrombus and its floating into the lungs. This typically happens through mobilization after resting, i.e. sometimes clearly after getting up, during pressing (bowel movements) and other first physical exertions afterwards. What they all have in common is the sudden change in blood pressure in the venous system with dilation of the vessels after inactivity. (Sources below)
Typical signs of a pulmonary embolism are acute shortness of breath and / or chest pain when inhaling. The other symptoms are very variable and often characterized by an increase in the resting heart rate ( over 100 / min, tachycardia with cardiac arrhythmia ) and breathing rate ( tachypnea ). Occasional coughing is occasionally associated with blood in the sputum . The low blood pressure ( hypotension ) can lead to shock .
Pleural effusion occurs in 20 to 55% of cases of pulmonary embolism .
If a sudden onset ( fulminant ) pulmonary embolism leads to cardiac arrest , then, within the framework of resuscitation measures, jammed jugular veins (as a sign of upper congestion in the presence of "forward failure " of the heart) can often be recognized. Due to the insufficient supply of blood with oxygen is classically called "ring cyanosis " (or "Swedish collar") recognizable: neck and décolleté seem dark marbled.
According to Grosser
|Severity I||Severity II||Severity III||Severity IV|
|clinic||discreet, in 80% clinically silent||Acute dyspnea , tachypnea , thoracic pain, anxiety, hemoptysis , fever, pleural effusion (due to transudate or exudate )||Additionally shock symptoms|
|Blood pressure||normal||possibly slightly lowered||humiliated||greatly degraded|
|Vascular occlusion||peripheral branches||Segmental arteries||PA branch or multiple lobed arteries||One PA branch and several lobed arteries|
According to ESC (European Society for Cardiology) 2008
|low (<1%)||medium (3–15%)||high (> 15%)|
|Shock or hypotension||No||No||yes (triggers therapy)|
|RV dysfunction||No||no Yes*||possible|
|Troponin increased||No||no Yes*||possible|
|* at least one of the two criteria|
|therapy||early discharge||Hospital treatment||Thrombolysis or embolectomy|
The PESI (Pulmonary Embolism Severity Index) is a scoring system for the risk stratification of non-massive pulmonary embolisms (systolic blood pressure> 90 mmHg). The patients are divided into five risk classes based on 11 criteria. With a PESI risk class of I or II, the mortality rate is low and outpatient therapy can be considered.
|Age||Number of years|
|Pulse ≥ 110 / min||20th|
|Systolic blood pressure <100 mmHg||30th|
|Respiratory rate ≥ 30 / min||20th|
|Temperature <36 ° C||20th|
|Decreased state of consciousness||60|
|Oxygen saturation <90%||20th|
|PESI risk class||Points|
If a pulmonary embolism is clinically suspected, which results from a careful history taking and assistance from the Wells Score or Geneva Score , the fastest way to confirm the diagnosis is to use contrast-enhanced computed tomography . In the conventional X-ray there are indeed described X-ray signs of a pulmonary embolism ( Hampton hump , Westermark and Fleishner signs ), but these are rarely present and often ambiguous.
A pulmonary embolism can be ruled out with a high degree of certainty in the laboratory if the dimers are normal . Elevated D-dimers do not allow a statement, as they easily become false positive. D-dimers are often increased after operations, sports or accidents.
Signs of right heart strain as indirect signs of pulmonary embolism can be detected in the ECG (so-called SIQIII type) and in the echocardiography . The blood gas analysis shows a reduced pO 2 with a simultaneously reduced pCO 2 as a result of hyperventilation in hypoxemia .
Smaller embolisms that could escape the CT can be detected by lung scintigraphy . However, this method is used less often because of its limited availability and the length of the examination compared to modern CT. In many cases, however, nuclear medicine with lung perfusion and inhalation scintigraphy can make a valuable contribution to the diagnosis of pulmonary embolism: Computed tomography with contrast agent cannot be performed in patients with contrast agent allergy , with overactive thyroid or with poor kidney values (increased creatinine) ; in these cases the exact diagnosis can only be made through nuclear medicine. The lung perfusion scintigraphy shows whether the radioactive tracer applied into a vein is regularly displayed in both lungs or whether there are wedge-shaped weakenings or defects in the lungs, which can be an indication of a pulmonary embolism. In the case of inhalation scintigraphy, the tracer is inhaled and then a comparison is made as to whether the representations of both examinations are the same (same: no indication of pulmonary embolism) or whether there is a difference (difference between perfusion and inhalation scintigraphy: evidence of pulmonary embolism).
The magnetic resonance imaging (MRI) allows for the diagnosis of pulmonary embolism. However, given the current spread of suitable devices, this is rarely used with this question.
Conventional angiography of the pulmonary circulation, which was often performed in the past, provides good results. However, it is carried out less often because of the technical complexity involved, the considerable burden on the patient and the risk associated with the introduction of a catheter into the patient's pulmonary circulation.
Symptom assessment and diagnosis is often made more difficult because several, even small, thrombi can be involved at time intervals. The Wells-Score , a point system for the probability of an embolism, which can be combined well with the result of the D-dimer test, is an aid to diagnosis .
The main symptoms of severe pulmonary embolism (shortness of breath, chest pain , circulatory instability) comes as a differential diagnosis of primary heart attack in question, possibly a pneumonia , a pneumothorax or an aortic dissection .
Predicting pulmonary embolism for a first responder is usually quite difficult and requires prior knowledge. However, if you suspect such a thing, you have to act quickly as a first aider. Measures that can be carried out as a first aider are:
- Immediately alert the ambulance service via 112 (in Europe) or another local emergency number
- Position the patient with the upper body raised
- Calm the patient down and encourage them to breathe calmly
- Do not allow the sick person to exercise
- Provide fresh air and open tight clothing
- Further general measures in the context of first aid
Pulmonary embolism can be life threatening. Small pulmonary embolisms in stable patients can also be treated on an outpatient basis.
In addition to the oxygen feed one in each case is thrombolysis with intravenously applique heparin to inhibit blood coagulation ( anticoagulants performed). After acute symptoms have subsided, long-term thrombosis prophylaxis with direct oral anticoagulants (DOAC) is carried out to avoid recurrence of thrombosis. Corresponding preparations are apixaban (trade name Eliquis ; manufacturer: Bristol-Myers Squibb / Pfizer ), rivaroxaban (trade name Xarelto ; manufacturer: Bayer ) or dabigatran (trade name Pradaxa ; manufacturer: Boehringer Ingelheim ). The coumarin preparations Phenprocoumon (trade name Marcumar or Falithrom ) and warfarin (trade name Coumadin ) have been on the market for much longer .
In the case of severe pulmonary embolism with shock symptoms and the severe stress on the right heart as described , circulatory stabilization and rapid "recanalizing" measures are necessary. In addition to lysis therapy, catheter-based mechanical “breaking up” of localized thrombi as well as surgical removal ( embolectomy ) should be considered as acute life-saving measures . In the surgical evacuation of the embolic material, there are procedures without the use of the heart-lung machine and those with its use. If necessary, the operation is carried out with continuous resuscitation of the patient as a so-called ultima ratio (a high-risk, but perhaps life-saving measure).
If artificial ventilation of the patient becomes necessary due to a lack of oxygen in the blood, the ventilator should be set to the lowest possible pressure in the exhalation phase ( PEEP ) and in the inhalation phase. Too high ventilation pressure would put additional strain on the right part of the heart, which is already stressed by the pulmonary embolism.
The anticoagulant substances must be taken for a few months after a pulmonary embolism, in some cases (with certain congenital disorders of the coagulation system as well as with recurrent pulmonary embolism) for life in order to avoid recurrence of thrombosis and pulmonary embolism.
The best protective measure is thrombosis prophylaxis, which is mainly used in bedridden patients and postoperatively. The patient is given an anticoagulant drug (usually a so-called low molecular weight heparin) injected into the subcutaneous fatty tissue or given in tablet form. Wearing compression stockings has also proven its worth. Rapid patient mobilization is also important for prophylaxis .
The number of deaths from pulmonary embolism within the European Union is estimated at around 370,000 annually. The estimated cost of treatment for pulmonary embolism caused by deep vein thrombosis is estimated at around three billion euros across Europe.
Literature and Sources
- German Society for Angiology - Society for Vascular Medicine: Diagnosis and therapy of venous thrombosis and pulmonary embolism. (PDF) January 2005, accessed on July 13, 2015 .
- European Society for Cardiology: Guidelines on the diagnosis and management of acute pulmonary embolism. (PDF; 1.1 MB) 2008, accessed on July 5, 2009 (English).
- Alexander Schellhaaß, Andreas Walther, Stavros Konstantinides, Bernd W. Böttiger: Diagnostics and therapy for acute pulmonary embolism . In: Dtsch Arztebl Int . No. 107 (34-35) , 2010, pp. 589-595 ( abstract ).
- Drahomir Aujesky: The outpatient treatment of pulmonary embolism . In: PrimaryCare . No. 2 , 2013, p. 30–31 ( online [PDF]).
- German Society for Angiology - Society for Vascular Medicine e. V .: Thrombosis risk campaign. Berlin 2015, 
- after: W. Huckenbeck (Institute for Forensic Medicine, University of Düsseldorf): Forensic medicine aspects of the causal chain thrombosis - pulmonary embolism - death. In: Phlebology. Issue 6, 1998, summary on: Schattauer.de ( Memento from December 17, 2013 in the Internet Archive )). , pp. 181-209 (
- Diedrich Bühler, Vera Wittenberg: What is a pulmonary embolism? In: TK medical texts. Techniker Krankenkasse , March 7, 2019, accessed April 7, 2019 .
- Herbert Lippert: Textbook anatomy. 4th edition. Urban & Schwarzenberg Publishing House, p. 190.
- A. Rahimtoola, JD Bergin: Acute pulmonary embolism: an update on diagnosis and management. In: Current problems in cardiology. 2005 Feb; 30 (2), pp. 61-114.
- Berthold Jany, Tobias Welte: Pleural effusion in adults - causes, diagnosis and therapy. In: Deutsches Ärzteblatt. Volume 116, No. 21, (May) 2019, pp. 377-385, here: pp. 377-381 and 383.
- Austrian Red Cross General Secretariat: Medical aid training. 7th edition, March 2016 version, ISBN 978-3-902332-18-9 .
- Guidelines on the diagnosis and management of acute pulmonary embolism. The Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). In: European Heart Journal . (2008), 29, pp. 2276-2315, doi: 10.1093 / eurheartj / ehn310 .
- Samuel Z. Goldhaber: Deep Venous Thrombosis and Pulmonary Embolism. In: Dan L. Longo, Anthony S. Fauci, Dennis L. Kasper, Stephen L. Hauser, J. Larry Jameson: Harrisons's Principles of Internal Medicine. Volume 2, New York 2012, p. 2170.