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Review of Pulmonary Embolism

Contact Hours: 3

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Contact Hours: 3

This educational activity is credited for 3 contact hours at completion of the activity.

Course Purpose

The purpose of this course is to provide an overview of the various types of pulmonary embolism, their risk factors, and treatment options.


Pulmonary embolism is the third most common cardiovascular disease after coronary artery disease and stroke. It is a serious and deadly form of venous thromboembolic disease, for which an individual’s risk increases with age and multiple inherited and acquired factors. This independent learning activity provides an overview of pulmonary embolism, its risk factors, and treatment options.

Course Objectives

Upon completion of the independent study, the learner will be able to:

  • Define pulmonary embolism.
  • Differentiate the various types of pulmonary embolism.
  • Review risks factors for pulmonary embolism.
  • Review treatment options for pulmonary embolism.
  • Understand contraindications for thrombolysis.

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ArteriesA vessel that carries blood high in oxygen content away from the heart to the farthest reaches of the body.
Blood VesselsArteries, veins, and capillaries.
Blood A body fluid in the circulatory system that delivers nutrients and oxygen to the cells, and transports metabolic waste away from cells.
CapillariesBlood vessels that allow oxygen, carbon dioxide, nutrients, and waste products to pass into and out of cells.
Cardiogenic ShockHappens when the heart cannot pump enough blood and oxygen to the brain and other vital organs. 
Cardiopulmonary DiseaseConditions of the heart including structural and functional abnormalities.
Chronic Thromboembolic Pulmonary HypertensionA form of pulmonary hypertension, and a rare condition that causes high blood pressure in the small vessels of the lungs. 
Deep Vein Thrombosis Occurs when a blood clot (thrombus) forms in one or more of the deep veins in the body, usually in the legs.
EmbolectomyA procedure that removes a blood clot in the body.
EmbolusA blood clot, air bubble, piece of fatty deposit, or another object which has been carried in the bloodstream to lodge in a vessel and cause an embolism.
Extracorporeal Membrane Oxygenation (ECMO)Blood is pumped outside of your body to a heart-lung machine that removes carbon dioxide and sends oxygen-filled blood back to tissues in the body.
FondaparinuxA synthetic medication that is used to prevent blood clots.
HeartA muscular organ that pumps blood throughout the body.
Low-Molecular-Weight Heparin (LMWH)A long-lasting medication that prevents blood from clotting.
Patent Foramen OvaleA small opening between the two upper chambers of the heart, the right and the left atrium.
Post-Thrombotic Syndrome A condition that can happen to people who have had a deep vein thrombosis (DVT) of the leg
Pulmonary ArteryAn artery in the pulmonary circulation that carries deoxygenated blood from the right side of the heart to the lungs.
Pulmonary EmbolismA blood clot that travels to the lungs.
Thrombolysis An emergency treatment to dissolve blood clots that form in arteries feeding the heart and brain.
Unfractionated heparin (UFH)A strong,  fast-acting medication that  prevents clotting.
Veins These blood vessels return oxygen-depleted blood to the heart.
venous thromboembolism A blood clot that blocks the flow of blood through a vein.

The circulatory system, also called the cardiovascular system, consists of arteries, veins, capillaries, and the heart. The circulatory system’s function is to move blood throughout the body. The cycle begins when the right atrium receives deoxygenated blood from the inferior vena cava and superior vena cava. The tricuspid valve opens to allow blood to travel from the right atrium to the right ventricle. The right ventricle contracts, closing the tricuspid valve while opens the pulmonary valve. Blood then travels through the pulmonary valve to the lungs where it is reoxygenated. Oxygen-rich blood travels from the lungs to the left atrium through the pulmonary veins. The mitral valve then opens to send blood from the left atrium to the left ventricle. When the left ventricle contracts, it closes the mitral valve and opens the aortic valve. The heart then sends blood through the aortic valve to the aorta, where it flows to the rest of the body. Deoxygenated blood is then returned to the heart through the inferior vena cava and superior vena cava, repeating the cycle. When the cycle is slowed, or a change in blood flow or perfusion occurs, a blood clot may form.1 When a blood clot forms in one blood vessel and then breaks off, travels, and lodges into another body area, it is called an embolus.1 The blockage of a blood vessel by an embolus is called an embolism.1 A pulmonary embolism happens when a blood clot travels to the blood vessels in the lungs and restricts blood flow in that area.1,2

Pulmonary embolism is the third most common cardiovascular disease after coronary artery disease and stroke.3 It is a serious and deadly form of venous thromboembolic disease, for which an individual’s risk increases with age and multiple inherited and acquired factors.4 It is common after the age of 75 and has an overall annual incidence of  0.6 per 1000.3 It is a life-threatening disease with a high prevalence rate; despite this, only a few cases, around 30 to 45%, are diagnosed early, while others remain undiagnosed or silent.2,3  This course will discuss pulmonary embolism types, symptoms, causes, and treatment.

What is Pulmonary Embolism?

A blood clot that forms elsewhere in the body and then breaks off and travels to the blood vessels in the lungs and lodges there, restricting blood flow and interrupting gas exchange, resulting in a life-threatening disease, is called a pulmonary embolism.1,2,3 Blood clots can develop in both veins and arteries.1 Leg veins can be deep, located near the bone and surrounded by muscles, or superficial, located close to the surface of the skin.1 Many of the blood clots that end up in the lung are first formed in the legs as deep vein thrombosis (DVT), and thus, it is the most common cause of PE.1,2 The disease’s prognosis depends on the obstruction level and the number of blood vessels involved.2,4 A blood clot in the pulmonary artery blocks blood flow and prevents the lungs from picking up oxygen.2 If the unoxygenated blood moves to the heart’s left side, the body’s oxygen level will drop significantly and become dangerously low, causing stress and damage to all body organs, including the heart, brain, and kidneys.2 The blockage also increases pressure on the right side of the heart, causing it to work harder.2 The right side dilates, while the left side’s blood flow is reduced.2 This causes the heart’s left side to pump blood inefficiently and lower the patient’s blood pressure.2 All these effects can lead to death, either suddenly or in a short period if left untreated.2

Pulmonary embolism can also be caused by air bubbles, fat embolus, amniotic fluid embolus, or deep vein thrombosis in the upper body.1 However, lower extremity central DVTs are most likely to embolize and cause PE, up to 30% of the time, whereas upper extremity DVTs cause PE less than 10% of the time.4

Pulmonary Embolism Types

There are 3 different types of pulmonary embolism: acute, subacute, and chronic. These terms define the time from the initial event to the confirmed diagnosis.8

Acute Pulmonary Embolism

Acute pulmonary embolism is a common health concern with a variable clinical presentation that makes diagnosis challenging.5 Acute pulmonary embolism occurs when there is a disruption in blood flow in the lungs due to an embolus, initially formed elsewhere in the body, breaking off and lodging into the lungs’ blood vessels.5 The embolus is usually formed in the deep veins of the lower extremities and very rarely in the upper body.5 Since pulmonary embolism and deep vein thrombosis are on a similar spectrum, they are referred to as venous thromboembolism (VTE).5

Acute PE is further divided into two categories based on the presence or absence of hemodynamic stability.5 The hemodynamic effects relate to the location and size of the emboli and the presence or absence of underlying cardiopulmonary disease (CPD).4

Hemodynamically unstable PE, also known as massive PE, accounts for approximately 4.5%–10% of all PE cases and carries substantial morbidity and mortality that exceeds 50%.6 The word “massive” doesn’t describe the size of the embolus but its hemodynamic effect.6 It results in hypotension and can lead to right heart failure, cardiac arrest, cardiogenic shock, and death within a few minutes to hours after the event.5,6

The presence of any of the following factors defines massive pulmonary embolism:6

  • A thrombus that occludes greater than 50% of the pulmonary artery (PA) cross-sectional area or occludes two or more lobar arteries.
  • Hypotension or shock resulting from right heart failure or cardiovascular collapse.
  • If the patient is dependent on inotropic agents.

On the other hand, hemodynamically stable PE range from small and mildly symptomatic to asymptomatic PE.5 It doesn’t have any severe clinical findings, but patients show signs of dysfunction, right heart strain, or injury on echocardiogram or by laboratory biomarkers.6 It also causes mild hypotension but can be reversed by fluid therapy.5


Following are some of the common symptoms associated with acute pulmonary embolism:5,7

  • Abnormal pulmonary signs
  • Arrhythmias (atrial fibrillation)
  • Cough
  • Dyspnea (may be acute and severe in central PE or  mild and transient in small peripheral PE)
  • Fever
  • Hemodynamic collapse
  • Hemoptysis
  • Pleuritic chest pain (caused by pleural irritation due to distal emboli causing pulmonary infarction)
  • Presyncope or syncope
  • Tachycardia

Often, pulmonary embolism is asymptomatic and is incidentally discovered during workup for other diseases.5

Subacute Pulmonary Embolism

Subacute massive pulmonary embolism is characterized by symptom onset of 2 to 12 weeks, without a solid episode of cardiovascular collapse and pulmonary angiogram showing massive pulmonary embolus (>50% obstruction in major pulmonary arteries).9 It has a high mortality rate and occurs insidiously for weeks.9 It also leads to the development of pulmonary hypertension.9 However, the subacute presentation and similarity to acute PE make it difficult to diagnose and, thus, delay treatment.9  Moreover, the predisposing risk factors for subacute PE are unknown and, thus, could lead to recurrent emboli even after initial treatment is begun.9


Following are some of the common symptoms associated with subacute massive pulmonary embolism:9

  • Hemoptysis with the absence of cardiovascular collapse
  • Pleuritic chest pain
  • Progressive dyspnea

Chronic Pulmonary Embolism

Chronic thromboembolic pulmonary hypertension (CTEPH) is a long-term complication of acute PE.10,11 In most PE cases, patients are fully recovered once treated, with the emboli resolved and the blood flow restored, but in some cases, residual clots remain attached to pulmonary vessels walls, which leads to organization and fibrosis and results in blood flow impairment and increased pulmonary vascular resistance, this is known as CTEPH.11 It affects around 2-4% of PE survivors and is characterized by pulmonary hypertension and heart failure.10


Chronic pulmonary embolism symptoms are nonspecific and related to the development and progression of pulmonary hypertension.11 The following are some of the common symptoms associated with CTEPH:10,11

  • Atypical chest pain
  • Chronic nonproductive cough
  • Cor pulmonale
  • Edema
  • Fatigue
  • Progressive exertional dyspnea
  • Syncope
  • Tachycardia

In some patients, weeks or even years may pass after acute PE before any significant chronic symptoms become apparent, while during this time, chronic PE is present and progressing rapidly, which leads to poor quality of life and management.10 In the International CTEPH Registry, the median time from the last acute PE to CTEPH diagnosis was 13 months (interquartile range 5.7– 34 months).10

Thus, to facilitate earlier diagnosis, CTEPH should be considered in three categories of PE patients:10

  • Individuals presenting with symptoms that could indicate CTEPH.
  • Individuals with risk factors or predisposing conditions for CTEPH.
  • Individuals with signs indicative of CTEPH at the time of the acute PE diagnosis.
Causes and Risk Factors

The most common cause of PE is deep venous thrombosis (DVT). There are over 10 million cases per year of DVT, associated with high rates of morbidity and mortality.4 While the true incidence of PE is unknown, in the United States, it is estimated that nearly a third of hospitalized patients are at risk of developing DVT, and up to 600,000 cases of DVT are diagnosed per year, with 100,000 deaths related to these conditions.4 Deep vein thrombosis is a medical condition that defines a blood clot that forms in the deep veins, most commonly in the legs, pelvis, and thigh, but can also be developed in the arms and other upper body parts.12,13 One of the most severe complications of DVT is that the blood clot can break off and travel into the blood vessels in the lungs, resulting in PE and restricting blood flow to the entire body.12,13 Other complications include chronic venous insufficiency (a blood clot in the leg vein causes blood to pool and not flow to the heart, resulting in pain and swelling in the leg) and post-thrombotic syndrome (a long-term complication of a blocked vein in the leg, resulting in pain, swelling, redness, ulcers, and sores).13

Risk factors for DVT include:12,13

  • Age over 60 years
  • Blood clotting disorder
  • Chronic medical illnesses like heart disease, cancer, lung disease, inflammatory bowel disease, or lupus
  • Having a central venous catheter
  • Hormone replacement therapy
  • Injury to veins caused by a fracture or serious muscle injury
  • Long periods of no movement, paralysis, or confinement to bed
  • Overweight or obesity
  • Pregnancy
  • Surgery
  • Use of birth control pills

Surgery increases the risk of PE significantly due to long periods of limited mobility and inflammation.4 Common surgeries that lead to DVT and PE include orthopedic surgery, hip and knee replacement surgery, and traumatic hip fractures.4 Cancer diagnosis also plays a major role in PE.4 In a large population study including solid and hematologic malignancies, nearly 2% of patients were diagnosed with VTE (venous thromboembolism) within two years of their cancer diagnosis, with the highest rates of VTE seen with metastatic disease, particularly with pancreatic and colon cancer.4 The risk increases after diagnosis and initial treatment and decreases when cancer is in remission.4

Individuals above the age of 60 are also at an increased risk of PE due to limited mobility, obesity, and other comorbidities.4 Patients with severe obesity (BMI ≥ 35) have a sixfold higher risk of VTE compared with those of normal weight.4

There are also some acquired risk factors associated with DVT and PE, such as:4

  • Antithrombin deficiency
  • Factor V Leiden
  • Protein C deficiency
  • Protein S deficiency
  • Prothrombin gene mutation

Factor V Leiden is associated with a 5-fold increased risk of VTE with heterozygotes and a 10-fold risk with homozygotes.4 It is a common mutation that leads to hypercoagulability.4 Whereas antithrombin and protein C and S deficiencies are rare but potent and result in a 5 to 10-fold increase in venous thrombosis in affected patients.4 The prothrombin gene mutation can be detected in 7% of patients with VTE and increases the risk of thrombosis 3-fold.4

Other risk factors include:5

  • Chemotherapy
  • Heart or respiratory failure
  • History of VTE
  • Infection of the urinary tract or HIV
  • Postpartum period
  • Pregnancy (at highest risk for PE at six weeks after giving birth)
  • Thrombophilia
Diagnosis and Treatment

Diagnosis of pulmonary embolism is difficult as its symptoms are similar to those of multiple other diseases and conditions.1 Thus, the first step to providing optimal treatment involves risk stratification.14 Risk stratification of pulmonary embolism patients is based on hemodynamic consequences, including biomarker and imaging evidence of right ventricular strain.14 Based on this guideline, patients are divided into the following 4 categories:14

Table 1: PE patients’ risk stratification14

Risk levelCharacteristics
High-riskCardiac arrest Cardiogenic shock Vasopressor requirement Paradoxical bradycardia Hypotension Acute respiratory failure Ventricular tachyarrhythmia
Intermediate high-riskNormotensive with both:   Imaging evidence of RVS Elevated cardiac biomarkers
Intermediate low-riskNormotensive with either:   Imaging evidence of RVS, or Elevated cardiac biomarkers
Low-risksPESI=0 Normal cardiac biomarkers (if accessed) No imaging evidence of RVS (if accessed) PE may be incidental or asymptomatic

The classification of risk stratification is imperfect, and thus, the resulting interventions and treatments span multiple specialties, such as surgery, cardiology, and radiology.14 Because of this, many hospitals and centers have introduced Pulmonary Embolism Response Teams (PERT).14 This involves expertise from interventional cardiology, interventional radiology, cardiac surgery, cardiac imaging, and critical care, which helps in determining which treatment is suitable for which patient based on risk stratification.14

Common laboratory and diagnostic tests use to diagnose pulmonary embolism include:

D Dimer (blood test)A blood test that checks for the clot-dissolving substance D dimer. High levels may suggest an increased likelihood of blood clots, although many other factors can cause high D dimer levels.
Arterial Blood Gas (ABG)Measures the amount of oxygen and carbon dioxide in the blood. A clot in a blood vessel in the lungs may lower the level of oxygen in the blood.
Chest X-RayA noninvasive test that shows images of the heart and lungs on film. Although X-rays cannot diagnose a pulmonary embolism and may even appear fine when a pulmonary embolism exists, they can rule out other conditions with similar symptoms.
UltrasoundA noninvasive test known as duplex ultrasonography uses sound waves to scan veins to check for deep vein blood clots. This test can locate veins in the thigh, knee, calf, and sometimes the arms.
CT Pulmonary Angiography (CTPA)CT scanning generates X-rays to produce cross-sectional images. CT pulmonary angiography (CT pulmonary embolism study) creates 3D images that can find changes such as a pulmonary embolism within the arteries in lungs.
Ventilation-Perfusion (V/Q) ScanWhen there is a need to avoid radiation exposure or contrast from a CT scan due to a medical condition, a V/Q scan may be done. In this test, a small amount of a radioactive substance called a tracer is injected into a vein. The tracer maps blood flow and compares it with the airflow to the lungs to see if blood clots are causing symptoms of pulmonary hypertension.
Pulmonary AngiogramA test that provides a clear picture of the blood flow in the arteries of the lungs. It is the most accurate way to diagnose a pulmonary embolism.
Magnetic Resonance Imaging (MRI)A medical imaging technique that uses a magnetic field and computer-generated radio waves to create detailed images of the organs and tissues in the body. It is usually only done in those who are pregnant and in people whose kidneys may be harmed by dyes used in other tests.
Transthoracic Echocardiography (TTE)A test that uses ultrasound to create images of the heart. It should be performed in hemodynamically unstable patients, as well as in hemodynamically stable patients with specific elevated cardiac biomarkers and imaging features suspicious of pulmonary embolism. The decision to perform TTE should be based on clinical presentation.  
Initial Interventions

Respiratory Support

Supportive interventions are the initial treatment options for PE patients.5 For instance:5,15

  • Supplemental oxygen is administered to patients with an oxygen saturation <90%.
  • Mechanical ventilation and intubation should be considered in cases of severe hypoxemia, hemodynamic collapse, or respiratory failure.
  • In patients with massive PE, intravenous fluid resuscitation is considered only in patients with collapsible inferior vena cava/intravascular depletion.
  • In hemodynamically unstable patients with PE, mechanical cardiopulmonary support devices, such as extracorporeal membrane oxygenation (ECMO), may be used.


For acute PE, anticoagulation is a mainstay for treatment.5 For this purpose, both low-molecular-weight heparin (LMWH), fondaparinux, or unfractionated heparin (UFH) can be used for anticoagulation.5 They have their pros and cons; for instance, LMWH has a smaller risk of major bleeding or heparin-induced thrombocytopenia than UFH.5 unfractionated heparin is usually only considered in hemodynamically unstable patients for whom reperfusion treatment was ineffective, or in those who have renal impairment.5 Common anticoagulant medications include: 5

Unfractionated heparin (UFH) Strong and fast-acting medication that neutralizes antithrombin and thrombin to prevent clotting. UFH requires close monitoring with lab tests.
Low-molecular-weight heparin (LMWH)Low-molecular-weight heparin attaches to antithrombin, resulting in predictable, long-lasting effects. This
FondaparinuxA synthetic medication that works similarly to heparin. It  activates antithrombin but acts over a much longer period, but it is  not as strong as UFH or LMWH. This medication is often used to prevent clots rather than treat them.
WarfarinBlocks the use of vitamin K,  a key ingredient in the clotting process. Requires careful dosing and regular lab testing to prevent complications. 
Pixaban, Edoxaban and BetrixabanInhibitors of factor Xa (10-A), a key clotting component.
Dabigatran A thrombin inhibitor.

Anticoagulation for suspected PE patients is based on the type of PE, hemodynamically stable or unstable.5

Table 2: Anticoagulation for suspected PE patients5,15

Type of PEAnticoagulation
Hemodynamically stableHigh clinical suspicion – Anticoagulation is started before diagnostic imaging is received. Intermediate clinical suspicion – Diagnostic imaging is performed within 4 hours, and the results help determine a definitive diagnosis before starting anticoagulation. Low clinical suspicion – Diagnostic imaging is performed within 24 hours, and the results help determine a definitive diagnosis before starting anticoagulation.
Hemodynamically unstableHigh clinical suspicion requires portable perfusion scanning, emergent CTPA, or bedside transthoracic echocardiography whenever possible. Thrombolysis is the primary treatment option. Patients contradictive to thrombolysis undergo surgical pulmonary embolectomy or percutaneous catheter-directed therapy.

Hemodynamic Support

Patients that show clinical evidence of hypoperfusion, such as diminished urine output or changes in mental state, require hemodynamic support.15 It also depends on the patient’s baseline blood pressure; generally, intravenous fluids (IVF) of normal saline in small volumes are administered.15 Intravenous fluid is the first line of treatment for hypotension patients, but some studies suggest it could harm patients with right ventricular (RV) dysfunction.15 Thus, healthcare professionals should carefully assess volume status and treat as necessary.15

If intravenous fluid is unable to restore adequate perfusion, vasopressors should be administered.15 The most commonly used vasopressor is norepinephrine.15 It is less likely to cause tachycardia and is highly effective.15 Dobutamine is also sometimes used but results in systemic vasodilation which worsens hypotension, particularly at low doses.15 Thus, it is used in combination with norepinephrine to mitigate its effects.15

Definitive Therapies

When PE is diagnostically confirmed in patients, treatments are determined based on if they are hemodynamically stable or unstable.15

Hemodynamically Stable

Hemodynamically stable patients are heterogenous and include low-risk, intermediate-low-risk, and intermediate-high-risk PE patients.15 Treatment is also determined based on the risk of bleeding, for instance:15

  • Low risk of bleeding – Anticoagulant therapy is indicated.
  • High risk of bleeding – Inferior vena cava filter is placed.
  • Moderate risk of bleeding – The patient is viable for both treatment options, and a decision should be made based on the assessed risk-benefit ratio and values and preferences of the patient.


Anticoagulation therapy is further divided into initial, long-term, and indefinite based on the patient’s needs.15 For instance, initial anticoagulation therapy is administered as soon as possible to achieve therapeutic anticoagulation quickly.15 Whereas, after discharge, a patient continues a minimum of 3-month long-term anticoagulation treatment.15 Selected patients are chosen for indefinite anticoagulation based on their risk factors, nature of the event, risk of bleeding, recurrence rate, and preferences.15

Outpatient anticoagulation is also an option for PE patients. It involves getting the first dose of anticoagulant in the hospital and the remaining doses at home.15 patients that fulfill the following criteria may be considered for outpatient anticoagulation:15

  • Absence of concomitant DVT
  • Low risk of death
  • No history or risk factors for bleeding
  • No requirement for supplemental oxygen or narcotics for pain
  • No respiratory distress
  • No serious comorbid conditions like renal failure, cancer, or heart disease
  • Normal blood pressure and pulse
  • Normal mental status and good home support

Inferior Vena Cava Filter

An inferior vena cava filter is used to block the emboli’s path and prevent it from entering the pulmonary circulation.5 A vena cava filter is considered for the following patients:5,15

  • Patients with a high risk of bleeding
  • Patients with recurrent VTE despite anticoagulation
  • Patients with venous thromboembolism who have a contraindication to anticoagulants

In such cases, retrievable filters are considered so that the filters can be removed once the contraindication is resolved and the patient can be anticoagulated.5,15 Moreover, according to the Prevention of Recurrent Pulmonary Embolism by Vena Cava Interruption (PREPIC) study, the placement of a permanent vena cava filter resulted in a significant reduction in the risk of recurrent PE and a substantial increase in the risk of DVTs without any remarkable difference in the risk of recurrent VTE or death.5

Hemodynamically Unstable (Reperfusion Therapies)

Reperfusion therapies are considered for patients who become unstable from recurrence of embolism despite being on anticoagulation therrrapy.15 There are two types of reperfusion therapies, discussed below.


Thrombolysis, also known as thrombolytic therapy, is a widely accepted treatment for hemodynamically unstable PE patients.5,15 It reduces pulmonary artery pressure and resistance as compared to unfractionated heparin alone.5 It is recommended for patients with a symptom onset of 48 hours or whose symptoms began less than 14 days ago.5 The use of thrombolytics shows a significant reduction in mortality and recurrent PE.5

Thrombolysis is also considered for hemodynamically stable patients and has shown effective results in reducing the risk of hemodynamic decompensation or collapse.5 However, the risk of severe bleeding increases with this therapy.5

Thrombolysis is contraindicated in the following cases:5

  • Active bleeding or bleeding diathesis
  • Ischemic stroke within three months
  • Malignant intracranial neoplasm
  • Prior intracranial hemorrhage
  • Recent significant closed-head or facial trauma with radiographic evidence of bony fracture or brain injury
  • Recent surgery encroaching on the spinal canal or brain
  • Structural intracranial cerebrovascular disease (e.g., arteriovenous malformation)
  • Suspected aortic dissection


Embolectomy is considered for patients who are unsuitable for thrombolytic therapy or fail thrombolysis.15 In this procedure, the emboli are removed using a catheter or surgery.15 The choice between the two is made based on the diagnosis of pulmonary embolism, the expertise available, and the underlying comorbidities.15

Catheter-Directed Therapies

Multiple catheter-directed therapies are available that involve the insertion of a catheter into pulmonary arteries.5,15 The following table describes the modalities:

Table 3: Catheter-directed modalities5,15

Catheter-Directed TherapiesCharacteristics
Ultrasound-Assisted ThrombolysisThe high-frequency ultrasound enables the thrombolytic agent to penetrate the emboli better.
Suction EmbolectomyA hemostatic valve and aspiration syringe is used to manually aspirate the thrombus through a large lumen catheter.
Rotational EmbolectomyA rotating device at the catheter tip is used to fragment the thrombus while the fragmented clot is continuously aspirated.
Rheolytic EmbolectomyA catheter’s distal tip injects pressurized saline, and the macerated thrombus is aspirated through a catheter port.
Thrombus FragmentationThe thrombus is mechanically disrupted by manually rotating a standard pigtail or balloon angioplasty catheter into the thrombus.


Surgical embolectomy is indicated in hemodynamically unstable patients with a contraindication to thrombolysis or failed thrombolysis.5,15 Moreover, echocardiographic evidence of an embolus trapped within a patent foramen ovale or present in the right atrium or right ventricle is also indicative of surgical embolectomy.15 It has a high mortality rate, especially in the adult population.15


To conclude, PE patients are treated based on their risk profile and hemodynamic status.16 For instance, hemodynamically unstable PE patients at high risk are considered for thrombolysis.16 If thrombolysis is contraindicated or fails, catheter-directed modalities or surgical embolectomy are considered.16 However, anticoagulation remains the mainstay for PE treatment because even though reperfusion therapy shows life-saving results, it increases the risk of bleeding and thus is not indicated for all PE patients.16

Early discharge with a treatment regimen in place can be considered for patients that are not at high risk for sudden death, don’t have any severe comorbidities, have proper medical management at home, and when proper medical follow-up can be guaranteed.16 Long-term treatment involves anticoagulation therapy for 3 to 6 months; extension in administration depends on the risk of recurrence.16 Pulmonary embolism patients with a treatable or transient risk factor should be treated with anticoagulation therapy for three months.16

While direct-acting oral coagulants are the preferred treatment choice, patients that are pregnant or have severe renal impairment or antiphospholipid syndrome are recommended low-molecular-weight heparin and vitamin K antagonists, respectively.16 Pulmonary embolism patients with cancer are also treated with low-molecular-weight heparin.16

Inferior vena cava filters are also recommended for patients with contraindications to anticoagulation. However, they do not show any significant reduction in PR recurrence or mortality.16 All patients should get regular follow-up checkups because of increased cancer incidence, high risk of bleeding complications, or developing chronic thromboembolic pulmonary hypertension.16

Because DVTs may cause pulmonary embolism, preventive measures should target the limit of DVTs, such as compression stockings or pneumatic compression devices.1 Increased activity, like walking after surgery, is also recommended.1 it is also recommended to follow a healthy lifestyle by exercising regularly, maintaining a healthy diet and weight, taking medications as prescribed, and avoiding smoking.1

  1. Johns Hopkins Medicine. Pulmonary Embolism. Johns Hopkins Medicine. Published 2019. https://www.hopkinsmedicine.org/health/conditions-and-diseases/pulmonary-embolism
  2. American Thoracic Society. https://www.thoracic.org/patients/patient-resources/resources/pulmonary-embolism.pdf
  3. Clark AC, Xue J, Sharma A. Pulmonary Embolism: Epidemiology, Patient Presentation, Diagnosis, and Treatment. Journal of Radiology Nursing. 2019;38(2):112-118. doi:https://doi.org/10.1016/j.jradnu.2019.01.006
  4. Turetz M, Sideris A, Friedman O, Tripathi N, Horowitz J. Epidemiology, Pathophysiology, and Natural History of Pulmonary Embolism. Seminars in Interventional Radiology. 2018;35(02):92-98. doi:https://doi.org/10.1055/s-0038-1642036
  5. Vrinda Vyas, Amandeep Goyal. Acute Pulmonary Embolism. Nih.gov. Published August 10, 2020. https://www.ncbi.nlm.nih.gov/books/NBK560551/
  6. Martinez Licha CR, McCurdy CM, Maldonado SM, Lee LS. Current Management of Acute Pulmonary Embolism. Annals of Thoracic and Cardiovascular Surgery. 2020;26(2):65-71. doi:https://doi.org/10.5761/atcs.ra.19-00158
  7. Morrone D, Morrone V. Acute Pulmonary Embolism: Focus on the Clinical Picture. Korean Circulation Journal. 2018;48(5):365. doi:https://doi.org/10.4070/kcj.2017.0314
  8. Rali PM, Criner GJ. Submassive Pulmonary Embolism. American Journal of Respiratory and Critical Care Medicine. 2018;198(5):588-598. doi:https://doi.org/10.1164/rccm.201711-2302ci
  9. Solanki NN, Tanwar N, Solanki ND. Subacute Massive Pulmonary Embolism Treated With Streptokinase. Cureus. Published online October 25, 2020. doi:https://doi.org/10.7759/cureus.11157
  10. Klok FA, Couturaud F, Delcroix M, Humbert M. Diagnosis of chronic thromboembolic pulmonary hypertension after acute pulmonary embolism. European Respiratory Journal. 2020;55(6):2000189. doi:https://doi.org/10.1183/13993003.00189-2020
  11. Nishiyama KH, Saboo SS, Tanabe Y, Jasinowodolinski D, Landay MJ, Kay FU. Chronic pulmonary embolism: diagnosis. Cardiovascular Diagnosis and Therapy. 2018;8(3):253-271. doi:https://doi.org/10.21037/cdt.2018.01.09
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