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Pulmonary Embolism

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The most common cause of a pulmonary clot is a thrombus, which usually originates from the vein in the leg or pelvis. Once released into a venous circulation, clots expand onto both lungs in 65% of the cases; 25% to the right lung and 10% to the left lung. The lower areas are 4 times more likely to get affected than the upper ones.

The majority of the thromboembolism is accumulated in large or medium-sized pulmonary arteries, while 35% of them reach the smaller arteries. The fat embolus, which can occur after the fracture, as well as the amniotic fluid embolus, is the rare causes of the pulmonary embolism. They usually affect the pulmonary microcirculation (small venations – arterioles, capillaries), which can cause the respiratory distress syndrome (ARDS) in adults.

Clinical picture

The acute pulmonary embolism is a dynamic process – clots begin to dissolve immediately after reaching the lungs; yet, a massive embolism may cause death within minutes or hours, before the tissue arrest (pulmonary infarction) succeeds and develops. The embolic processes rarely reoccur over the following months and years, but when they do, they cause the advancing obstruction of the pulmonary artery with the chronically increased lung pressure, breathing difficulties, and consequential heart damage (pulmonary heart disease).

Clinical indicators of pulmonary embolism are non-specific and vary in intensity and frequency and may be asymptomatic when it comes to smaller clots. Clinical image develops suddenly and within minutes and, in the case of pulmonary infarction, within a few hours. It usually lasts for a few days, but it does get worse with time.
Embolism without infarction causes the shortage of breath. Hyperventilation is always present, which is characterized by a specific facial expression.


If intensive, pulmonary hypertension (increased pulmonary pressure) can cause severe chest pains. A significant number of patients develop headaches, dizziness, heart attack, neurological outbursts which are caused by a reduced blood flow to the brain. Cyanosis (face turning purple-blue) is usually present only in patients who are experiencing a massive pulmonary embolism.

Small clots on the lung peripherals may cause a pulmonary infarction without increasing the blood pressure. Lung findings, in this case, appear normal. The signs which can be a sign of an increased pulmonary pressure are a cough, coughing out blood, pleural pain (pleura), as well as the increased body temperature.


It is often difficult to diagnose the pulmonary embolism, with or without pulmonary hypertension, unless special methods are applied; radionuclide perfusion lung scan (monitors blood flow through lungs), pulmonary angiography (scanning lung arteries). If pulmonary infarction is not present, patient’s symptoms may be attributed to bad mood with increased breathing, due to the lack of the objective pulmonary symptoms.

Without pulmonary infarction, X-ray findings will usually be normal. Electrocardiogram will rule out the possible infarction of the myocardium. Low blood pressure indicates a massive embolism, and routine lab tests are poor contributors to the establishment of a valid diagnosis.


Mortality after the initial thromboembolism depends on the prevalence of the pulmonary embolism and the previous cardio-pulmonary status of a patient. The probability that the patient with the previously bad cardio-pulmonary status will pass away is very high (25%), unlike the patient with the previously normal cardio-pulmonary status if 50% of the lungs is not affected.

If the embolism is fatal, death usually occurs within 1 – 2 hours. The tendency towards the recurring embolisms in the untreated patients is 50%, and more than half of them can then be fatal. The anticoagulant therapy reduces the frequency of the reoccurrence to 5%, and only 20% of them will then be fatal.


The treatment of the pulmonary embolism is supportive; analgesics for pleural pain, tranquilizers, oxygen therapy in the case of a reduced tissue oxygenation. In the cases of pulmonary hypertension and acute pulmonary heart, medicines that affect the expansion of the pulmonary arteries are very effective, and so are the heart cardio-tonics (i.e. isoproterenol).

Norepinephrine is prescribed for the consequential blood pressure decrease as a pulmonary embolism complication. Also, thrombotic therapy is given intravenously (heparin), because it speeds up the “breakage“ of the clot and is recommended in patients with massive embolism and systemic hypotension (low blood pressure). In certain cases, the surgical clot removal is performed.

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