Pulmonary Embolism First Signs, Treatment & Life Expectancy (original) (raw)

• Introduction
  • What is a pulmonary embolism?
• Causes & Risk Factors
  • What are the causes and risk factors for pulmonary embolism?
• Symptoms
  • What are the signs and symptoms of pulmonary embolism?
• Diagnosis
  • What tests diagnose pulmonary embolism?
• Treatment
  • What is the treatment for pulmonary embolism?
• Prognosis
  • What is the prognosis of pulmonary embolism?
• Prevention
  • Can pulmonary embolism be prevented?

What is a pulmonary embolism?

A pulmonary embolus blocks blood flow and prevents the functioning of that part of the lung. Not only does it prevent the exchange of oxygen and carbon dioxide, but it also decreases blood supply to the lung tissue itself, potentially causing part of the lung tissue to die (infarct=tissue death).

The lungs are responsible for taking oxygen from the air and delivering it to the body. They also take carbon dioxide (a waste product of metabolism) from the bloodstream and exhale it, removing it from the body.

The exchange of air between the lungs and blood is through the arterial and venous systems. Both arteries and veins carry and move blood throughout the body, but the process for each is very different.

Arteries carry blood away from the heart, and veins return blood. Every time the heart pumps, it sends blood both to the lungs and the rest of the body.

The circulation pathway is as follows:

• The pulmonary arteries and their branches send blood from the heart to the lungs.
• Oxygen from the air is loaded onto hemoglobin in the red blood cells and then travels back to the heart through the pulmonary veins.
• The heart then pumps that oxygen-rich blood through the aorta and its branches to all the organs and tissues in the rest of the body, including the brain, the abdomen, and the arms and legs.
• After the hemoglobin delivers the oxygen into the tissues, it collects carbon dioxide, the waste product of metabolism.
• The carbon dioxide-laden blood then returns through veins back to the heart.
• The heart pumps this blood through the pulmonary arteries back to the lung.
• There, the carbon dioxide is returned to exhaled air and a new cargo of oxygen is uploaded to begin the circulation cycle again.

If a blood clot (thrombus) forms in one of the body's deep veins (deep vein thrombosis or DVT), it has the potential to break off and travel (embolize) back to the heart and into one of the pulmonary arteries where it can become stuck.

A pulmonary embolus blocks blood flow and prevents the functioning of that part of the lung. Not only does it prevent the exchange of oxygen and carbon dioxide, but it also decreases blood supply to the lung tissue itself, potentially causing part of the lung tissue to die (infarct=tissue death).

A pulmonary embolus is one of the life-threatening causes of chest pain that should always be considered when patients complain of chest pain and shortness of breath to their health care professionals.

There are special types of pulmonary embolus that are not due to blood clots but instead are due to other body materials. These are rare occurrences and include:

• Fat emboli from the interior of a large bone like a femur (thigh bone), which can occur because of a fracture or as a complication of surgery
• An amniotic fluid embolus in pregnancy
• Tumor tissue from cancer
• Air embolus is usually a complication of a medical procedure such as neurosurgery, dye injection, or central intravenous line placement

The signs and symptoms of a pulmonary embolus are caused by decreased lung function and the inability of the lung to provide adequate oxygen to the rest of the body.

What are the causes and risk factors for pulmonary embolism?

Picture how red blood cells and platelets form a blood clot

Pulmonary embolus is the result of a deep vein thrombosis or blood clot elsewhere in the body. Most commonly, DVT begins in the leg and lower abdomen (pelvis) or arm.

The risk factors for a pulmonary embolism are the same risks for developing deep vein thrombosis. These are referred to as Virchow's triad and include:

• Prolonged immobilization or alterations in normal blood flow (stasis)
• The increased clotting potential of the blood (hypercoagulability)
• Damage to the walls of the veins

Examples of these include:

Prolonged immobilization

• Extended travel (sitting in a car, airplane, or train)
• Hospitalization or prolonged bed rest
• Surgery

Increased blood clotting potential

• Medications
  • birth control pills
  • estrogen supplementation
  • phenothiazines
• Smoking
• Genetic predisposition. Examples include:
  • Factor V Leiden deficiency
  • MHFTHR mutation
  • Protein C or Protein S deficiencies
  • antithrombin III deficiency
  • Homocystinemia
  • Homocystinuria
  • Hyperlipidemia
• Blood disorders
  • Polycythemia
    * Increased number of red blood cells
    * (The opposite of anemia)
  • Thrombocytosis
    * Elevated platelet count
• Cancer
• Pregnancy, including the postpartum period up to 6 to 8 weeks after delivery

Damage to the vessel wall

• Prior deep venous thrombosis
• Trauma to the lower leg with or without surgery or casting
• Venography
• Pacemaker insertion
• IV drug abuse

SLIDESHOW A Visual Guide to Deep Vein Thrombosis (DVT) See Slideshow

What are the signs and symptoms of pulmonary embolism?

The most common symptoms of a pulmonary embolus are the acute onset of the following:

• Chest pain: The pain is often described as pleuritic, a sharp pain that worsens when taking a deep breath.
• Shortness of breath: The person may have difficulty catching his or her breath at rest, and the shortness of breath often worsens with activity.
• Hypoxia or hypoxemia: decreased oxygen concentration in the blood. (hypo=less + ox=oxygen + ia or emia= blood).

Vital signs (blood pressure, heart rate, respiratory rate, and oxygen saturation) may be normal or abnormal, depending upon the size of the embolus and how much lung tissue is affected. The larger the clot burden or load, the less stable the vital signs.

Abnormal vital signs may include:

• Tachycardia: elevated heart rate (tachy=fast + cardia=heart).
• Tachypnea: elevated respiratory (breathing) rate.(tachy=fast + pnea= breathing).
• Hypotension: decreased blood pressure (hypo=low + tension=blood pressure).
• Hypoxia: decreased SaO2. Oxygen saturation described how many hemoglobin molecules are carrying oxygen. Normal oxygen level is usually greater than 92%-93%.

The condition progresses as follows:

• The heart rate and respiratory rate may elevate as the body tries to compensate for the decreased oxygen transfer capabilities in the lung. This allows the oxygen that is available to be circulated more quickly, supplying the body's organ and tissue needs as best as possible.
• This may lead to anxiety, weakness, and lightheadedness as the body's organs are deprived of the necessary oxygen to function.
• If the clot burden is large enough, it may make it harder for the heart to pump blood through the blocked pulmonary arteries. This increases the work that the heart has to do, raising pressures inside the heart and straining the heart muscle itself.

Sudden death is the initial sign of the condition in up to 25% of cases. The person collapses, stops breathing, and his or her heart stops beating (cardiac arrest) without prior symptoms. Pulmonary embolus is the second leading cause of sudden death, behind coronary artery disease.

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What tests diagnose pulmonary embolism?

The healthcare professional should keep a high level of suspicion that a pulmonary embolus may be the cause of chest pain or shortness of breath. The first step in the diagnosis is taking a history of the chest pain, including its characteristics, its onset, and any associated symptoms that may direct the diagnosis to pulmonary embolism. The provider may also ask questions about risk factors for deep vein thrombosis.

A physical examination will concentrate initially on the heart and lungs, since chest pain and shortness of breath may also be the major complaints of heart attack, pneumonia, pneumothorax (collapsed lung), and dissection of an aortic aneurysm, among other conditions.

In 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 physical examination may also include examining the arms and legs and looking for signs of a DVT, including warmth, redness, tenderness, and swelling.
People with a pulmonary embolus may have no physical findings and have a normal physical exam.

PERC Rule for Pulmonary Embolus

It is important to be able to determine the risk for a pulmonary embolus to decide whether testing is needed to look for a PE.

One risk stratification tool is the PERC rule. If the patient has no risk factors for PE and normal vital signs, the potential for pulmonary embolism is low (less than 2%). No further testing may be necessary, depending on the situation.

A negative PERC test requires that NO is the answer to the following statements:

• Age older than 50
• Heart rate faster than 100
• SaO2 on room air is less than 95%
• Prior DVT or PE
• Trauma or surgery within the last 4 weeks
• Hemoptysis (coughing up blood)
• Hormone use
• Unilateral leg swelling (only one leg involved)

If the answer is YES to any of these questions, then the diagnosis of pulmonary embolus still needs to be considered.

Basic testing (CBC, electrolytes, BUN, creatinine blood test, chest X-ray, EKG)

Basic testing in the diagnosis of pulmonary embolism may include:

• CBC (complete blood count)
• Electrolytes
• BUN (blood urea nitrogen)
• Creatinine blood test (to assess kidney function; see below)
• INR, PTT (to measure blood clotting capabilities)
• Chest X-ray
• Electrocardiogram (Electrocardiography; EKG, ECG)

Chest X-ray is often normal in pulmonary embolism.

EKG may be normal, but may also show indirect signs of PE. These include tachycardia (heart rate >100), and changes associated with right ventricle strain.

D-dimer blood test

If the suspicion of pulmonary embolism is low, a D-dimer blood test can be used for reassurance that a blood clot may not be present. 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, cancer, or infection.

D-dimer is not helpful if the potential risk for a blood clot is high.

The purpose of the PERC rule and D-dimer test is to minimize the need for imaging studies and decrease radiation exposure risk.

CT scan

CT scan (computerized tomography) of the chest is usually the imaging test of first choice to look for pulmonary embolus. Dye is injected into a vein in the upper arm. This allows the pulmonary arteries to be outlined looking for blood clots. Care needs to be taken with people who have dye allergies, have kidney issues, or are in their first trimester of pregnancy.

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Pulmonary angiogram

Historically, the gold standard for the diagnosis of pulmonary embolus was a pulmonary angiogram, in which a catheter was threaded into the pulmonary arteries, usually from veins in the groin or wrist. Dye was injected into the pulmonary arteries and could identify whether blood clots were present. This is an invasive test and requires a skilled radiologist to insert the catheter.

CT scan is more commonly used today, and pulmonary angiography is most often performed in unusual circumstances.

Ventilation-perfusion scans

Ventilation-perfusion scans (V/Q scans) are another less commonly used test in people who cannot undergo a chest CT scan to make the diagnosis of pulmonary embolism.

The scan uses inhaled gas (V) and injected dye (Q) to compare areas of the lung where air can enter with those areas of the lung that are getting blood supply. If there is a mismatch, then there is a possibility that a blood clot exists.

V/Q scans take hours to perform and are read by a radiologist as low, medium, and high probability that a blood clot is present. A low probability result means that there is still a 5%-15% chance that a PE exists. For that reason, V/Q scans are not often performed.

Venous Doppler ultrasound

Instead of imaging the lung, an ultrasound of the legs (or arms, if clinically appropriate) may be used to look for blood clots in a patient suspected of having a pulmonary embolus. If a deep vein thrombosis (DVT) exists, it can be inferred that someone complaining of chest pain and/or shortness of breath may be suffering from a pulmonary embolism. The initial treatment for deep vein thrombosis and pulmonary embolus may be similar, depending upon the clinical situation.

Echocardiography

Echocardiography or ultrasound of the heart may be helpful in looking for right heart strain as a complication of a pulmonary embolus.

What is the treatment for pulmonary embolism?

The best treatment for a pulmonary embolus is prevention. Minimizing the risk of deep vein thrombosis is key in preventing a potentially fatal illness. Once the diagnosis of PE is made, it is important to know the severity of the illness and whether the patient needs to be hospitalized or whether treatment can occur at home.

• The Pulmonary Embolus Severity Index (PESI) can help risk-stratify who is stable and who may potentially be unstable. It takes the following factors into account:
  • Age
  • Sex
  • History of cancer, heart disease, lung disease
  • Vital signs
  • Mental status
• All patients with abnormal vital signs (heart rate, respiratory rate, blood pressure, and oxygen saturation) need to be admitted to the hospital.
• Those who have unstable social situations, have difficulty obtaining medication, or have difficulty understanding their medication may require observation before being discharged home.

When patients with PE are admitted to the hospital, it is because they are unstable with abnormal vital signs, or there is concern that they will become unstable. The initial treatment of choice is unfractionated heparin, an injectable blood thinner that is continuously given intravenously.

If vital signs are not stable, other alternative treatments may be considered based on the clinical situation. Complications can include shock with hypotension (low blood pressure), confusion, coma, or heart failure.

Tissue plasminogen activator (tPA) or alteplase is an injectable clot-busting drug.

Thrombolytic therapy

• Peripheral thrombolysis (thrombo= clot + lysis= dissolve) is the use of a clot-busting drug injected into a vein, with the expectation that it will “dissolve” the blood clot in the pulmonary artery.
• Catheter-directed thrombolytic therapy is the use of a catheter threaded into the pulmonary artery where the clot is lodged and the clot-busting drug is injected directly into it.

Thrombectomy, embolectomy

• A catheter is inserted into the pulmonary artery and the clot is sucked out.

Once vital signs are stable, anticoagulation with oral medication will follow intravenous heparin or tPA, and these will be maintained after discharge to home.

Anticoagulation

Anticoagulation, or blood-thinning, is the treatment of choice for both deep vein thrombosis and pulmonary embolism.

Anticoagulation prevents further blood clot formation and prevents the embolization of a clot to the lung from existing clots. Under normal conditions, the body will activate a system that will break down blood clots within 4 to 6 weeks.

The American College of Chest Physicians has published guidelines regarding the choice of medications to anticoagulant a patient with VTE. The recommendations were based on a review of multiple clinical trials and meta-analyses (statistical evaluation) in the medical literature.

• In patients with VTE and no cancer, the drug of choice is a direct oral anticoagulant (DOAC) such as:
  • apixaban (Eliquis)
  • rivaroxaban (Xarelto)
  • edoxiban (Sayvessa)
  • dabigatran (Pradaxa)
• In patients with VTE and active cancer, the drug of choice is enoxaparin (Lovenox).
  • The National Comprehensive Cancer Network suggests that DOACs may be an acceptable alternative to enoxaparin.

Apixaban and rivaroxaban are oral medications that have a relatively rapid onset of action and become effective within 3 to 4 days.

Edoxiban and dabigatran take a long to become effective and, therefore, there is a two-step process for their use. Either intravenous heparin or subcutaneous enoxaparin needs to be used until the oral medications become effective.

Coumadin (warfarin) has historically been the medication of choice for the treatment of VTE. It takes many days to reach its therapeutic range in the body and, therefore, it too requires the use of heparin or enoxaparin until the medicine is effective.

Certain clinical situations also affect the choice of anticoagulation. Pregnancy, those who are breastfeeding, the presence of liver or kidney failure, and the presence of antiphospholipid syndrome may require specific anticoagulation medications. The healthcare professional needs to match the clinical situation with the appropriate medication.

The dosing of Coumadin is monitored by a blood test. INR (international normalized ratio) is used to guide the amount of Coumadin that is taken each day to keep the blood appropriately thinned. Certain foods and medications can interact with Coumadin and affect the dosing.

DOACs do not need blood tests to monitor their effectiveness or dosing. There are drug interactions that need to be considered when they are prescribed.

Duration of Treatment

People usually take anticoagulation medications for a minimum of 3 to 6 months. At that time, the decision will be made based on their risk of developing recurrent clots as to whether they should continue with long-term therapy.

Risk stratification may include whether the blood clot was provoked or unprovoked. An example of a provoked blood clot would be a patient who broke his or her leg, was placed in a cast, and was sedentary. Those who have VTE often undergo hypercoagulable evaluations looking for genetic or familial causes of blood clots.

If the healthcare professional, in consultation with the patient (shared decision-making), decides that lifelong therapy is required, that decision should be reviewed every year to determine if the risk of clotting still exists and whether the risk of clotting is greater than the risk of bleeding.

What is the prognosis of pulmonary embolism?

Patient survival depends upon the following:

• The underlying health of the patient
• The clot burden of the pulmonary embolus
• The effect has on the heart and its ability to pump blood to the organs of the body
• Vital sign stability
• The cause of the pulmonary embolus
• The ability for the diagnosis to be made and early initiation of treatment

There are more than 900,000 cases of DVT and PE in the United States, and 60,000-100,000 people die each year from the condition. In addition, 25% of cases of PE cause sudden death, and 10%-30% of patients with PE will die within the first month of diagnosis.

Can pulmonary embolism be prevented?

Minimizing the risk of deep vein thrombosis minimizes the risk of pulmonary embolism. The embolism cannot occur without the initial DVT.

• In the hospital setting, the nursing 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.
  • Low-dose heparin or enoxaparin is prescribed for deep-vein thrombosis prevention.
• DVT in the legs may require the placement of vena cava filters to prevent clots in the legs from embolizing the lung. The filter sits in the large vein that leads from the legs to the heart.
• Those who have had hip or knee replacements may be prescribed DOACs to prevent DVTs.
• For long travel, getting up and walking or stretching every couple of hours may prevent clot formation.
• Compression stockings may help prevent recurrent DVT in people with a previous history of a clot.
• Those on hormone therapy, including birth control pills, should be counseled regarding the risk of DVT.
• Smoking cessation reduces the risk of clots.
• In those who are overweight, weight loss may decrease the risk of clot formation.

References

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Carman TL, Gegaj F. "Management of Pulmonary Embolism: 2010 State of the Art Update Curr Treat Options." Cardiovasc Med. 2010 Apr;12(2);168-184.

Centers for Disease Control and Prevention. "Data and Statistics on Venous Thromboembolism."
<https://www.cdc.gov/ncbddd/dvt/data.html> Updated 14Mar2019. Accessed 08Aug2019.

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Kearon C, Aki EA, et al. "Antithrombotic Therapy for VTE Disease." Chest. 2016. 149(2):315-352.

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Streiff MB, Holmstrom B, et al. "NCCN Guidelines Insights: Cancer-Associated Venous Thromboembolic Disease, Version 2." J Natl Compr Canc Netw. (2018) 16(11): 1289-1303.

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