Pulmonary embolism is a sudden occlusion of one or more pulmonary artery, primarily caused by a coagel of blood originating from the vein of another part of the body.
It is a solid mass of blood that comes from a vein:
- a leg (in 90% of cases),
- of the pelvis, especially in women,
- an arm (rare),
- may also originate from a thrombus of the pulmonary artery (for example, in sickle cell anemia) or from the right atrium (5% of cases).
The coagel prevents the tissues of the lungs from absorbing the necessary oxygen.
This structure, which is dragged from one place of the body to another, is called an embolus.
The embolus penetrates into the small and narrow pulmonary vessels and into the arterioles, which are so narrow that it can no longer penetrate further.
As a result, it is no longer possible for the blood to reach the entire lung tissue.
As a result, part of the lungs does not receive oxygen supply.
Lack of oxygen leads to the death of lung tissue (pulmonary infarction).
This disorder occurs most often:
- in the elderly,
- in people who have had surgery, even if they are adolescents or children.
Contents
Effects of pulmonary embolism (pathophysiology)
Deep vein thrombosis begins with a coagel that forms near a venous valve in the vein wall, where blood flow is more turbulent.
The vertebrae that form in this area can lead to detachment of all or part of the thrombus.
Acute pulmonary embolism can cause:
- sudden death,
- systemic hypotension (low arterial pressure) up to shock.
Sudden death does not depend on lung damage, but in the case of narrowing of a larger pulmonary vessel (for example, a pulmonary flap artery):
- a circulatory disorder of the right ventricle of the heart,
- decreased blood flow from the lungs to the left heart.
The sudden closure of the pulmonary circulation can also cause cardiac arrest.
Right atrium and ventricle dilate to pump more blood to the lungs because blood flow is reduced.
However, if the blockage has occurred suddenly, the heart does not adapt fast enough. Therefore, the pressure in the pulmonary arteries can increase by about 15-20mmHg, but does not exceed 55mmHg.
Consequences of dilation of the right ventricle are:
- regurgitation at the tricuspid valve (between the right atrium and ventricle),
- the left ventricle does not fill completely,
- low pressure because the left ventricle does not pump enough blood.
In these cases, the patient often suffers syncope and sudden death can occur.
Reducing pressure in the aorta and left ventricle can cause decreased blood flow to the coronary arteries.
In a subacute or gradual pulmonary embolism, many embolisms develop, which reach the lungs in a few weeks or months.
As this occlusion forms slowly, the right ventricle has time to adapt to it and hypertrophies (dilates).
The consequences are:
- pulmonary hypertension, higher than in acute embolism,
- the right heart muscle can significantly enlarge and press on the left ventricle,
- the ventricular septum may shift to the left.
If the left ventricle is shrinked, it pumps less blood into the body and can cause dyspnea.
With pulmonary embolism, pulmonary microinfarctions develop, which can lead to severe inflammation.
Inflammatory fluid accumulates in the area of the alveoli and squeezes them.
The result is a change in the ratio of ventilation (amount of air reaching the alveoli in one minute) / perfusion (blood flow per minute).
Nevertheless, pulmonary embolism does not cause hypoxia (reduction of oxygen in the blood).
Initially, a person with pulmonary embolism is hypocapnic (reduction of carbon dioxide in the blood), however, the baroreceptors of the lungs detect a decrease in carbon dioxide pressure and eventually the respiratory center is activated to increase the respiratory rate.
Types of pulmonary embolism
The composition of the embolus can be:
- Solid (fat, tumor mass), during a bone fracture or surgery on a long bone (for example, on the femur), fat can enter the blood circulation. The embolus can also be formed from cancer cells that tear themselves away from the tumor. Neoplasms produce thrombogenic substances.
- Liquid (amniotic fluid), can occur in a complicated birth.
- Gaseous, caused by an air bubble in the bloodstream and can occur:
- In the event of a medical error (for example, when inserting or moving venous catheters).
- An air embolism occurs in people who dive (divers) and resurface too quickly.
Classification of pulmonary embolism according to its severity
- Massive acute pulmonary embolism when involved:
- two lung branches,
- more than 50% of the blood vessels of the lungs.
- Submassive acute pulmonary embolism (or not massive) if involved:
- only one lung branch,
- about 30-40% of the vascular system of the lungs.
In this case, the heart is under stress, but the body still receives enough oxygenated blood.
There is a variant, the so-called paradoxical pulmonary embolism, which is characterized by the migration of an embolus from an artery into a vein.
It occurs in patients with an open foramen ovale: an abnormal hole between the right and left atrium that allows blood to pass from one chamber of the heart to the other.
Causes of pulmonary embolism
The most common cause is deep vein thrombosis (DVT). In this case, the embolism is caused by a coagel of blood that forms in the lower limbs.
The risk factors for forming a blood clot are:
Trauma or surgery
- Trauma or injury (especially to the legs)
- Recent surgery
- Injury to the spinal cord
- Hip fracture or femoral fracture
- Burns
Diseases and medications
- Heart attack or stroke
- Cardiac arrest
- Atrial fibrillation
- Cancer
- Estrogen therapy
- Oral contraceptives
- High blood pressure or hypertension
Coagulation disorders and genetic factors
Deficiency of some proteins or enzymes
A tendency to hypercoagulation can be acquired or congenital.
The factor V Leiden mutation (activated protein C resistance) is the most common risk factor. The factor V Leiden mutation is present in up to 5% of the normal population.
High risk factors include:
- Deficiency of antithrombin III
- Lack of protein C
- Lack of protein S
- Anomaly of plasminogen
- Plasminogen activator anomaly
- Anomaly of fibrinogen
- Resistance to activated protein C
The absence of these natural anticoagulants is responsible for 10% of venous thrombosis in younger patients.
Lifestyle
- Prolonged bed rest: vein narrowing leads to accumulation of platelets and thrombin in the veins
- Long flights in a sitting position (blood remains in the same position for a long time)
- Prolonged lack of exercise
Other factors
If the patient with an embolism has no risk factors, doctors refer to the condition as idiopathic (without an apparent cause) pulmonary embolism.
Symptoms of pulmonary embolism
Some people have no symptoms.
If the embolus is caused by deep vein thrombosis, the patient may develop signs of this disease.
Initial symptoms of deep vein thrombosis are muscle pain in the calf, but in about 25% of cases it is asymptomatic.
The leg can be:
- hot
- swollen,
- reddened
- painful to the touch.
Sometimes the patient also has discomfort when walking.
All this can pass within a few days.
When the embolus reaches the lungs, the symptoms are different.
Some of the signs observed are:
- anxiety and fear,
- Severe chest pain (gets worse when breathing and coughing), because the pulmonary artery (like the aorta) is strongly innervated and the nerves transmit the pain signals.
- Dry cough (with blood). The sudden increase in pulmonary pressure can lead to the rupture of a vessel.
- Low blood pressure,
- Tachycardia, an increase in heartbeat velocity, compensates for the decrease in cardiac output.
- sweating,
- shortness of breath at rest or under stress,
- tachypnea (rapid breathing),
- dizziness,
- feeling powerless,
- leg swelling,
- Mild fever.
If the clot is very large, the symptoms can be very severe:
- Low blood pressure and shock,
- Loss of consciousness
- cold welding,
- cyanosis on the face and fingers,
- pulmonary edema,
- Pulmonary infarction.
Pulmonary embolism can lead to the death of the patient in the course of a few hours due to cardiac arrest.
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