What is a pulmonary embolism?
The lungs are a pair of organs in the chest that are primarily responsible for the exchange of oxygen and carbon dioxide between the air we breathe and blood. The lung is composed of clusters of small air sacs (alveoli) divided by thin, elastic walls (membranes). Capillaries, the tiniest of blood vessels, run within these membranes between the alveoli and allow blood and air to come near each other. The distance between the air in the lungs and the blood in the capillaries is very small, and allows molecules of oxygen and carbon dioxide to transfer across the membranes.
Arteries and veins both carry and move blood throughout the body, but the process for each is very different.
- Arteries carry blood from the heart to the body.
- Veins return blood from the body to the heart.
- The heart is a two-sided pump.
- Oxygen-carrying blood travels from the left side of the heart to all the tissues of the body. The oxygen is extracted by the tissue, and carbon dioxide (a waste product) is delivered back into the blood.
- The blood now deoxygenated and with higher levels of carbon dioxide, is returned via the veins to the right side of the heart.
- The blood is then pumped out of the right side of the heart to the lungs, where the carbon dioxide is removed and oxygen is returned to the blood from the air we breathe in, which fills the lungs.
- Now the blood, high in oxygen and low in carbon dioxide, is returned to the left side of the heart where the process starts all over again.
- The blood travels in a circle and is therefore referred to as circulatory system.
If a blood clot (thrombus) forms in the one of the body's veins (deep vein thrombosis or DVT), it has the potential to break off and enter the circulatory system and travel (or embolize) through the heart and become lodged in the one of the branches of the pulmonary artery of the lung. A clot that travels through the circulatory system to another location is known as an embolus (plural emboli). A pulmonary embolus clogs the artery that provides blood supply to part of the lung. The embolus not only prevents the exchange of oxygen and carbon dioxide, but it also decreases blood supply to the lung tissue itself, potentially causing lung tissue to die (infarct). A pulmonary embolus is one of the life-threatening causes of chest pain and should always be considered when a patient presents to a healthcare provider with complaints of chest pain and shortness of breath.
Non-thrombus causes of pulmonary embolus are rare but include:
- an amniotic fluid embolus in pregnancy,
- fat emboli from a broken femur, and
- In some cases, tumor tissue from cancer.
The presentation is the same as that of a blood clot, caused by blockage of part of the arterial tree of the lung.
What are the causes and risk factors for pulmonary embolism?
Pulmonary embolus is the end result of a deep vein thrombosis or blood clot elsewhere in the body. Most commonly deep vein thrombosis' are seen in the leg, but can also occur in veins within the abdominal cavity or in the arms. The risk factors for a pulmonary embolism are the same as the risk factors for deep vein thrombosis. These are referred to as Virchow's triad and include:
- Any damage to the walls of the veins.
- increased clotting potential of the blood (hypercoagulability)
- prolonged immobilization, alterations in normal blood flow (stasis)
Examples of these include the following:
Damage to vessel wall
- Trauma to the lower leg with or without surgery or casting
- Prior deep venous thrombosis
Increased blood clotting potential
- Medications: birth control pills, estrogen
- Genetic predisposition
- Polycythemia(increased number of red blood cells, the opposite of anemia)
- Pregnancy, including 6-8 weeks post partum
- Hospitalization or prolonged bed rest
- Extended travel (sitting in a car, airplane, train, etc.)
What are the signs and symptoms of pulmonary embolism?
A pulmonary embolus may present with the sudden onset of chest pain and shortness of breath. The pain is classically sharp and worsens when taking a deep breath, often called pleuritic pain or pleurisy. There may be cough that produces bloody sputum.
The patient may have stable vital signs (blood pressure, heart rate, respiratory rate, and oxygen saturation) but frequently presents with an elevated heart rate. A severe pulmonary embolus can present with shock (low blood pressure) or cardiac arrest, particularly when a large clot blocks the outflow of blood from the right side of the heart to the lungs (saddle embolus). Depending on the amount of blood clot (clot burden or clot load), oxygen saturation can be variably compromised as can the blood pressure and heart rate. In a classic presentation, the heart rate and respiratory rate are elevated as the body tries to compensate.
The patient may be cyanotic (a blue tinged discoloration of the skin caused by red blood cells without oxygen), lightheaded, and weak.
Oxygen saturation may be decreased (red blood cells that do not have oxygen molecules attached to them). Oxygen saturation in a healthy individual approaches 100% at sea level.
In some cases, pulmonary embolus will present with sudden death, where the patient collapses, stops breathing, and their heart stops beating (cardiac arrest).
How is pulmonary embolism diagnosed?
Physical examination and History
There always needs to be a high a level of doubt that a pulmonary embolus may be the cause of chest pain or shortness of breath. The healthcare provider will take a history of the type of chest pain, including its onset and associated symptoms that may direct the diagnosis to pulmonary embolism. It may include asking about risk factors for deep vein thrombosis. Physical examination will concentrate initially on the heart and lungs, since chest pain and shortness of breath may also be the presenting complaints for heart attack, pneumonia, pneumothorax (collapsed lung), and dissection of an aortic aneurysm, among others. With pulmonary embolism, the chest examination is often normal, but if there is some associated inflammation on the surface of the lung (the pleura), a rub may be heard (pleura inflammation may cause friction which can be heard with a stethoscope). The surfaces of the lung and the inside of the chest wall are covered by a membrane (the pleura) that is full of nerve endings. When the pleura becomes inflamed, as can occur in pulmonary embolus, a sharp pain can result that is worsened by breathing, so-called pleurisy or pleuritic chest pain.
The physical examination may include looking for signs of a deep vein thrombosis in an extremity:
- swelling, and
It is important to note, however, that the signs associated with deep vein thrombosis may be completely absent even in the presence of a clot. Again, risk factors for clotting must be taken into consideration when making an assessment.
Basic testing may include:
- Creatinine blood test (to assess kidney function),
- CBC (complete blood count)
- Chest x-ray,
- BUN (blood urea nitrogen), and
- Electrocardiogram (EKG or ECG).
The chest x-ray is often normal in pulmonary embolism. The EKG may be normal, but usually demonstrates a rapid heart rate, so-called sinus tachycardia (heart rate > 100 bpm). If there is significant blockage in a pulmonary artery, it acts like a dam and it is harder for the heart to push blood past the obstructing clot or clots. This can result in a change in the electrical signal passing through the heart by stretching the heart muscle, revealed on an EKG a so-called right heart strain.
Since the cost of missing the diagnosis of pulmonary embolus can be death, the approach to diagnosis is to prove that no pulmonary embolus exists.
The gold standard for the diagnosis of pulmonary embolus is a pulmonary angiogram in which a catheter is threaded into the pulmonary arteries, usually from veins in the leg. Dye is injected and a clot or clots can be identified on imaging studies. This is considered an invasive test and should be performed only by someone with expertise in this procedure. Fortunately, there are other, less invasive ways to make the diagnosis. The decision as to which test might best make the diagnosis needs to be individualized to the patient and their presentation and situation.
d-Dimer blood test
If the healthcare provider's suspicion for pulmonary embolism is low, a d-Dimer blood test can be used. The d-Dimer blood test measures one of the breakdown products of a blood clot. If this test is normal, then the likelihood of a pulmonary embolism is very low. Unfortunately, this test is not specific for blood clots in the lung. It can be positive for a variety of reasons including pregnancy, injury, recent surgery, or infection. Looking at the list of deep vein thrombosis risk factors, one can imagine that a d-Dimer blood test may not be helpful in those with significant risk factors for deep vein thrombosis.
Venous Doppler study
Ultrasound of the legs, also known as venous Doppler studies, may be used to look for blood clots in the legs of a patient suspected of having a pulmonary embolus. If a deep vein thrombosis exists, it can be inferred that chest pain and shortness of breath may be due to a pulmonary embolism.
If there is greater suspicion, then computerized tomography (CT scan) of the chest with angiography can be done. Contrast dye is injected into an intravenous line in the arm while the CT is being taken, and the pulmonary arteries can be visualized. There are some restrictions of the test, especially if a pulmonary embolism involves the smaller arteries in the lung. There are risks with this test since some patients are allergic to the dye, and the contrast dye can be harsh on kidney function especially if the patient's kidney function (as measured by blood tests) is marginal. It may be wise to limit the patient's exposure to radiation, especially in pregnant patients. However, since pulmonary embolus can be fatal, even in pregnancy this test can be performed, preferably after the first trimester.
The first step in stable patients with pulmonary embolism is anticoagulation. This is a two step process. Warfarin (Coumadin) is the drug of choice for anti-coagulation. It is taken by mouth beginning immediately upon the diagnosis of pulmonary embolism, but may take up to week for the blood to be appropriately thinned or anti-coagulated. As an immediate solution and as a bridge until the Coumadin becomes effective, low molecular weight heparin [enoxaparin (Lovenox)] is administered at the same time. It thins the blood via a different mechanism. Enoxaparin injections can be administered as an outpatient.
It is also essential to realize that warfarin (Coumadin) is in the same family of chemicals as rat poison. Rats eat this chemical and bleed to death internally. A clever clinician recognized that if this process was carefully monitored, this medication could be used therapeutically to treat clotting disorders. It is of the essence that anyone taking Coumadin be carefully monitored with blood tests and that this medication (as with all medication) be kept in a safe place.
For those patients who have contraindications to the use of enoxaparin (Lovenox) (for example, kidney failure does not allow the drug to be metabolized), intravenous heparin can be used as the first step. This requires admission to the hospital and careful patient monitoring with blood tests.
Anticoagulation is usually suggested for a minimum of six months, but each patient will have their treatment regimen individualized. The blood test utilized to monitor warfarin therapy is referred to as the prothrombin time or PT. This test can be performed by finger stick or venous stick depending on the laboratory procedures. Since different reagents are used to measure the prothrombin time, a ratio has been developed for comparison of this test between different labs. It is referred to as the International Normalized Ratio or INR. Usually, for these clotting conditions, your physician will want you to take enough warfarin to keep your INR between two and three. To participate in their health management it is very helpful for the patient by keeping a diary of their warfarin dose, the date of testing, and their INR values.
Ventilation-perfusion scans (VQ scans) use labeled chemicals to identify inhaled air into the lungs and match it with blood flow in the arteries. If a mismatch occurs, meaning that there is lung tissue that has good air entry but no blood flow, it may be indicative of a pulmonary embolus. These tests are read by a radiologist as having a low, moderate, or high probability of having a pulmonary embolism. There are limitations to the test, since there may be a 5%-10% risk that a pulmonary embolism exists even with a low probability V/Q result.
Echocardiography (EKG, ECG)
Echocardiography or ultrasound of the heart may be helpful if it shows that there is strain on the right side of the heart.
If non-invasive tests are negative and the healthcare provider still has significant concerns, then the healthcare provider and the patient need to discuss the benefits and risks of treatment versus invasive testing like angiography.
What is the treatment for pulmonary embolism?
Prevention is the best treatment for a pulmonary embolus. Minimizing the risk of deep vein thrombosis is a key in preventing a potentially fatal illness.
The initial decision is whether the patient requires hospitalization. Those patients with a small pulmonary embolus, who are hemodynamically, stable (normal vital signs) and who can be compliant with treatment, may be treated at home with close outpatient care.
Those who are unstable need to be admitted to the hospital.
Pulmonary embolism can be fatal, especially if involves a large amount of clot. When the patient is unconscious, has low or no blood pressure or are not breathing, clot busting or thrombolytic therapy using medications like TPA (tissue plasminogen activator) may be considered. It is also often considered when signs of right heart strain are present. Some physicians argue that thrombolytic therapy should be used more often, since the source clot is also dissolved as well as the pulmonary embolus. This therapy is associated with a slightly greater risk of bleeding and is contraindicated if recent surgery or significant trauma has occurred.
What is the prospect for pulmonary embolism?
Patient survival depends upon:
- size of the pulmonary embolus,
- the cause of the pulmonary embolus
- the ability for a diagnosis to be made and treatment initiated, and
- The underlying health of the patient.
Usually, the mortality risk is much less in most patients. In older patients, the higher incidence of death occurs, have other underlying illnesses, or have a delay in diagnosis. Racial differences may also exist, but probably are due more to access to quality care than a specific genetic difference.
How can pulmonary embolism be prevented?
Minimizing the risk of deep vein thrombosis is a key in preventing a potentially lethal illness.
- For those who travel, it is recommended that they get up and walk every couple of hours during a long trip.
- Compression stockings may be helpful in preventing future deep vein thrombus formation in patients with a previous history of a clot.
- In the hospital setting, the staff works hard to minimize the potential for clot formation in immobilized patients. Compression stockings are routinely used. Surgery patients are out of bed walking (ambulatory) earlier and low dose heparin or enoxaparin is being used for deep vein thrombosis prophylaxis (measures taken to prevent deep vein thrombosis).
Pulmonary Embolism at a Glance
- Pulmonary embolism is a diagnosis that should be considered in patients with chest pain and is one of the causes of sudden death.
- The diagnosis of pulmonary embolism may be difficult to make, and is often missed. Diagnostic strategies need to be individualized to each patient and situation.
- Anticoagulation is the treatment of choice for pulmonary embolism and the patient may be required to continue treatment for months.
Prevention is the best treatment for pulmonary embolism, which can be accomplished by minimizing the risk factors for deep venous th