This course will be updated or discontinued on or before Sunday, November 9, 2025
Nationally Accredited
CEUFast, Inc. is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation. ANCC Provider number #P0274.
CEUFast, Inc. is an AOTA Provider of professional development, Course approval ID #9719. This distant learning-independent format is offered at 0.2 CEUs Intermediate, Categories: OT Foundational Knowledge
AOTA does not endorse specific course content, products, or clinical procedures. AOTA provider number 9757.
CEUFast, Inc. (BOC AP#: P10067) is approved by the Board of Certification, Inc. to provide education to Athletic Trainers (ATs).
FPTA Approval: CE24-1122634, CE25-1122634. Accreditation of this course does not necessarily imply the FPTA supports the views of the presenter or the sponsors.
Outcomes
≥ 92% of participants will know how to recognize the signs and symptoms of pulmonary embolisms (PE).
Objectives
Upon completion of this course, the participant will be able to meet the following objectives:
Differentiate between the types of pulmonary embolisms (PE).
Analyze risk factors of PE.
Identify signs and symptoms of PE.
Review the diagnostic criteria for PE.
Compare various treatment options for PE.
CEUFast Inc. and the course planners for this educational activity do not have any relevant financial relationship(s) to disclose with ineligible companies whose primary business is producing, marketing, selling, re-selling, or distributing healthcare products used by or on patients.
Last Updated:
$39 Unlimited Access for 1 Year (Includes all state required Nursing CEs)
No Tests Required (Accepted by most states & professions)
Nursing Assistants from California, only. You must read the material on this page before you can take the test. The California Department of Public Health, Training Program Review Unit has determined that is the only way to prove that you actually spent the time to read the course. Less
A pulmonary embolism (PE) is a frightening and potentially fatal diagnosis. For reference, it is important to differentiate between venous thromboembolism (VTE), deep vein thrombosis (DVT), and PE.
DVT: A DVT is a blood clot that forms within the body's deep veins, often occurring in the lower extremities. The cerebral and mesenteric veins and the upper extremities can also be affected (Waheed et al., 2023).
PE: PE is a piece of the blood clot or DVT that has broken off and traveled to the lungs (Reyes & Abe, 2023).
VTE: VTE refers to a thromboembolic event encompassing a DVT, PE, or both (Waheed et al., 2023).
Blood Clot
Healthcare providers often refer to a blood clot that has traveled as an 'embolus.' When the traveling clot or embolus blocks a blood vessel, it is termed an "embolism'. When an embolism is impeding blood flow in the lungs, it is called a 'pulmonary embolism' (Penn Medicine, 2023).
The worldwide disease burden caused by PE is significant. Nearly one million individuals in the United States are affected by PE each year, with 30% dying within one month of the diagnosis (American Lung Association, 2023). Over 30% of individuals have a PE reoccurrence within ten years (Centers for Disease Control and Prevention [CDC], 2023a). Medical costs for PE are patient-dependent, but it is not uncommon for a PE diagnosis to cost up to $20,000 per patient; this averages to $10 billion yearly for our nation (CDC, 2023b).
PE is a dangerous and frightening diagnosis that deserves prompt attention and awareness to prevent morbidity and mortality.
In order to prevent the potentially devastating effects of PE, it is pertinent to differentiate between the various types.
Acute: An acute PE develops suddenly, and symptoms develop rapidly. It is often the most serious form of PE and must be addressed and treated quickly to prevent fatalities (Morrone & Morrone, 2018).
Subacute: A subacute PE develops gradually, with symptoms often developing over two to 12 weeks. Because of the progressively developing symptoms, subacute PE can be difficult to diagnose as many patients delay treatment. The difficulty in diagnosis leads to higher mortality rates in subacute PE versus acute PE (Solanki et al., 2020).
Chronic: A PE is considered chronic when it remains attached to the wall of the blood vessel after treatment. Because of this continued blockage, increased vascular resistance results, and blood flow is impeded (Nishiyama et al., 2018).
Beyond these categories, PE can be classified into stable versus unstable.
Hemodynamically stable PE: Patients diagnosed with a hemodynamically stable PE will have symptoms ranging from asymptomatic to moderately symptomatic. Patients with this type of diagnosis are usually classified as low to intermediate risk. Most patients with presenting PE symptoms are classified as hemodynamically stable (Vyas & Goyal, 2022; Weinberg & Rali, 2023).
Hemodynamically unstable PE: Hemodynamically unstable PE usually presents with severe symptoms that result in instability. Cardiac resuscitation may be necessary for patients with this diagnosis. Patients are often considered high-risk, requiring prompt intervention to prevent fatalities (Vyas & Goyal, 2022; Weinberg & Rali, 2023).
Though these are the major PE categories, further types exist. For example, some patients may be diagnosed with saddle PE. In this instance, the PE is considered intermediate or high-risk and often lodges in the bifurcation of the main pulmonary artery (Bull & Hountras, 2023b). Though rare, they can cause life-threatening complications.
The true incidence of PE is unknown, as some cases go undiagnosed or misdiagnosed, or they are only diagnosed if an autopsy is performed. Besides the above statistics, almost a third of hospitalized patients are at risk of developing PE.
PE is more likely to occur in older adults. For instance, adults over 70 are three times more likely to be diagnosed with PE than adults aged 45-69. Those aged 45-69 are actually three times more likely to experience PE than adults aged 20-44 (Turetz et al., 2018).
There is no sound evidence when comparing the incidence of PE in males versus females. However, an analysis of PE cases between 1979 and 1998 revealed that PE was 30% likely to occur and cause fatalities in males. The analysis also indicated that African Americans have mortality rates 50% higher than Caucasians. Mortality rates in Caucasians were 50% higher than in Asian and American Indian races (Horlander et al., 2003).
Risk factors for PE can be separated into inherited and acquired. Inherited risk factors are passed through families via genes.
Inherited risk factors include the following (Turetz et al., 2018):
Protein C and/or protein S deficiency
Prothrombin gene mutation
Factor V Leiden
Antithrombin deficiency
Examples of acquired risk factors include the following (Turetz et al., 2018):
Surgical procedures
Trauma
Aging
Obesity
Risk factors can further be divided into minor and major risk factors.
Minor risk factors include hypertension, oral contraception use, obesity, sitting for long periods (traveling), chronic dialysis, and inflammatory bowel disease.
Major risk factors include major surgeries, such as of the abdomen or knee, late pregnancies, metastatic cancer, geriatric care, and a prior history of VTE (Bĕlohlávek et al., 2013).
The pathogenesis of PE depends on the type of PE the patient is diagnosed with.
In a thromboembolic event, a DVT dislodges or detaches, travels through the veins, and occludes one or more pulmonary arteries. The place where the PE lodges, the size of the PE, and the quantity, if there is more than one, determines the signs and symptoms.
Thrombosis
Nonthrombotic sources of PE include foreign bodies, fat, air, infected materials or cells, and tumors (Bull & Hountras, 2023a). There are other less common sources of PE.
Foreign body embolism results when foreign matter enters the pulmonary system, usually via injection, such as with heroin use.
A fat embolism occurs when bone marrow (fat) is introduced systemically, often from orthopedic procedures or long bone fractures. Patients may experience symptoms comparable to acute respiratory distress syndrome when there is a fat embolus.
An air embolism occurs when air is introduced and moves through the venous system into the pulmonary arterial system. Air can be introduced when there is blunt trauma, through surgical procedures, or with defective venous catheters.
When infected material enters the lungs, a septic embolism may result. Intravenous (IV) drug use and some forms of carditis may cause a septic embolism with signs and symptoms similar to pneumonia.
A tumor embolism, though rare, is a direct complication of cancer. This form of embolism occurs when neoplastic cells enter the pulmonary arterial system and impede blood flow (Bull & Hountras, 2023a).
Signs and symptoms of PE are dependent on the type and size of the clot. Because of the increased risk of mortality, promptly recognizing the symptoms associated with PE is pertinent.
Common signs of PE include tachypnea, dyspnea, tachycardia, pleuritic pain, calf pain and swelling, and cough (Tarbox & Swaroop, 2013). Acute PE may also present with abnormal pulmonary signs, fever, syncope, cyanosis, and vascular collapse (Morrone & Morrone, 2018).
Up to 30% of patients with acute PE will present with sudden death. The risk of sudden death with PE increases with comorbid conditions and major risk factors. Studies have shown that PE should be expected in sudden death when there is a non-shockable rhythm.
Acute PE may also present as respiratory failure with symptoms such as hypocapnia and hypoxia. However, it may be increasingly difficult to recognize PE in patients with a history of respiratory conditions, such as chronic obstructive pulmonary disease. Even scans and imaging may not show evidence of PE in patients with respiratory conditions, as these conditions have caused pulmonary changes.
PE is also known to induce asthmatic symptoms, making this condition difficult to diagnose in patients with a history of asthma. Breathlessness can occur acutely and gradually progress to sluggishness within a few days. Other signs, similar to asthma, include a widespread wheeze, difficulty finishing sentences, and tachypnea (Morrone & Morrone, 2018).
Patients with PE may present with atypical signs and symptoms, which may include the following:
Delirium, often in older adults
Atrial fibrillation
Seizures
Syncope or faintness
Flank pain
Patients with a massive PE present with symptoms of shock that may include tachycardia, tachypnea, hypotension, and a pale and weak appearance. They may also experience pulmonary hypertension, as evidenced by a loud systolic murmur, a right ventricular s3 gallop, and a palpable impulse at the second left intercostal space (Ouellette, 2020).
A complete and thorough history should be taken to determine the potential probability or likelihood of a PE.
Healthcare providers should assess risk factors, such as pregnancy, cancer, stroke, obesity, varicose veins, a history of VTE, and any other inherited or acquired risk factors discussed above.
Potential triggers of PE should also be assessed. Triggers can include the following:
Significant blunt trauma
Prolonged sitting (often due to travel)
Major surgery (such as a hip or knee replacement)
Prepartum status
Fractures
If patients have a past medical history of VTE, it is important to determine the age when the event occurred and the location of the VTE.
It is pertinent to assess for a past history of diseases that increase the probability of PE, such as polycythemia vera, collagen vascular disease, heart failure, atherosclerosis, and autoimmune diseases.
Of note, certain medications can increase the likelihood of PE. Glucocorticoids, tamoxifen, phenothiazine-derived medications, and hydralazine can increase the risk of PE development (Anderson & Spencer, 2003; Torbicki et al., 2008).
Though symptoms may lead to a PE diagnosis, it is crucial to obtain diagnostics and imaging to ensure the appropriate diagnosis is made. Many diagnostic tools can be used to support a PE diagnosis.
Depending on the severity of PE, including the size and location, vital signs may be abnormal. If vital signs are abnormal, the most affected are heart and respiratory rate and oxygen saturation. The heart rate is often > 100 beats per minute (bpm), and the oxygen saturation may be below 95% (Cakal, n.d.). The respiratory rate may also be increased, at times, significantly.
Beyond reviewing vital signs, blood samples should be taken to perform laboratory (lab) tests to assist with diagnosing and determining the PE's severity.
D-dimer: A D-dimer is one of the most common lab tests reviewed with a PE. This dimer is produced by plasmin, and the level is usually low in our bodies. D-dimer can increase in many conditions, such as heart disease and inflammation. However, an elevated d-dimer can also indicate PE (Gao et al., 2018). Because of false positives and negatives associated with this test, other diagnostic tests should be employed to ensure an accurate diagnosis is made.
A normal d-dimer is anything < 0.50 milligrams per liter (mg/L), depending on the scale being used (Bounds & Kok, 2023). When reviewing the d-dimer, anything > 1.96 mg/L suggests a high risk for PE (Fu et al., 2020). If any elevation is seen, further imaging and scans should be performed.
Arterial blood gas (ABG): Because ventilation and alveolar perfusion are affected in PE, hypoxemia and hypocapnia occur. Therefore, an ABG may be measured to help support the diagnosis of PE. It should not be used alone as a diagnostic measure (Gharib et al., 2016; Maloba & Hogg, 2005).
Table 1: Normal ABG Levels
pH
7.35-7.45
PaO2
35-45 mmHg
PaCO2
35-45 mmHg
HCO3
22-26 meq/L
SaO2
95-100%
Base excess/deficit
-4 to +2
(Castro et al., 2022)
With hypoxemia and hypocapnia, the patient usually experiences respiratory alkalosis. If hemodynamically unstable, mixed acidosis may be present. In respiratory alkalosis, the pH will usually be above the threshold (> 7.45), and the PaCO2 will be below the normal range (< 35 millimeters of mercury [mmHg]). It is not uncommon to see patients with a PaO2 > 85 mmHg (Castro et al., 2022).
Brain natriuretic peptide (BNP): Because of the physiological process and symptoms of PE, the right ventricle becomes stressed. Therefore, reviewing cardiac lab tests may be useful in diagnosing PE (Bi et al., 2021). BNP levels are considered normal when < 100 picograms per milliliter (pg/mL). N-terminal pro-b-type natriuretic peptide (NT-proBNP) can also support a PE diagnosis. NT-proBNP is considered normal in patients under 75 years of age when it is < 125 pg/mL and when it is < 450 pg/mL in patients over 75 years of age. When BNP and/or NT-proBNP levels are increased, there is a heightened risk of death occurring in the short-term future; high levels can be indicative of an impending adverse effect. However, these tests should not be used alone for diagnosing PE but in conjunction with other supportive diagnostic measures (Corteville et al., 2007).
Troponin: Another cardiac biomarker often used to help diagnose PE is troponin; troponin T (TnT) and troponin I (TnI) are often drawn in patients with PE symptoms. Because elevated troponins are indicative of myocardial injury, and PE can cause right ventricular dysfunction, it is not uncommon to see elevations with this test. Like other tests, the normal level of troponin in the body is generally low. Normal levels of TnI range from 0 to 0.04 nanograms per milliliter (ng/mL), and the normal range for TnT is 0 to 0.01 ng/mL (Cleveland Clinic, 2022b). Though it is not considered a diagnostic test, elevated troponin is associated with higher morbidity and mortality in PE diagnoses.
Different scans can be performed to detect PE, some more sensitive and specific than others.
Chest x-ray (CXR): A CXR is not diagnostic in the case of PE as it is nonspecific and because blood clots are not visible on CXRs. However, a CXR is often performed to rule out other diagnoses, such as pneumonia (National Blood Clot Alliance, 2018).
Nonetheless, there are some signs seen on a CXR that can be indicative of a PE; they include the following (Shahul et al., 2019):
Westermark sign- focal area of oligemia (reduction of blood volume)
Palla sign- dilated or prominent pulmonary artery
Hampton's hump- wedge-shaped opacity
Ventilation-perfusion (VQ) scan: This scan is performed to assist with diagnosing PE by reviewing and measuring blood and air flow distribution in the lungs. Though some studies have questioned its efficacy, it is often used to assess the probability of PE in patients who are unable to tolerate contrast, such as with severe renal insufficiency. Generally, the scan takes at least 30-45 minutes, addressing ventilation and perfusion using radioactive components.
The VQ ratio is considered normal when it is 0.8, which is derived from a ratio of normal ventilation (4 liters [L] of air per minute) and normal perfusion (5 L of blood per minute). A high VQ score indicates that ventilation exceeds perfusion. One common cause of a high VQ score is when blood flow is impeded in the lungs, such as with PE. A low VQ score indicates that perfusion exceeds ventilation. A low VQ score could also indicate PE if over-perfusion occurs as blood flow is being diverted from the affected region (Mirza & Hashmi, 2023).
Computed tomography pulmonary angiogram (CPTA): Often, a CPTA is the preferred imaging source when aiming to diagnose PE. It appears to be cost-effective, minimally invasive, and often readily accessible. However, they are usually contraindicated in pregnancy (Moore et al., 2018).
Pulmonary Angiography
Usually, the vessels will appear white from the injected contrast. However, the vessels will be darker if there is a filling defect. With this imaging, often the size of the heart's ventricles can be assessed. If the right ventricle is larger than the left, it may indicate PE (Lewis et al., 2015).
CPTA has high sensitivity, and now that the imaging technique has had modifications, the amount of false negatives is low. If a CPTA is positive, often, no further tests are performed, and treatment for PE is initiated (Doğan et al., 2015).
Magnetic resonance angiography (MRA): MRA, sometimes termed pulmonary contrast-enhanced MRA (CE-MRA), is a newer option for patients suspected of having PE. Many providers use CE-MRA over CPTA because it does not expose patients to radiation. However, it may work best in patients with a lower suspicion of PE and females < 35 years old.
Various studies have found that CE-MRA may not be as sensitive when the PE is smaller than one centimeter (cm); however, sensitivity increases when the PE is larger.
When a filling defect is noted on a CE-MRA, it indicates PE. Other findings pointing toward this diagnosis include high signal T1 intensity clots, a double bronchus sign, and an arterial cutoff sign (Tsuchiya et al., 2018). A double bronchus sign is when the artery, which is air-filled, appears similarly to a bronchus that runs alongside another bronchus (Moser et al., 2017). The arterial cutoff sign often called the knuckle sign, is when the pulmonary artery abruptly appears to taper off or disappear due to PE (Leitman & McDermott, 2019).
Ultrasound and echocardiogram: This form of diagnostic testing may often be called a point-of-care cardiac ultrasound or POCCUS (Myers et al., 2017). Though it is not the gold standard, ultrasound may be used in the diagnosis of PE as it may identify right ventricle strain, often seen in PE. However, other criteria should be used to ensure an accurate diagnosis because right ventricle strain can be seen in various conditions, such as pleural effusion.
Typically, pulmonary consolidation is present with a round-shaped or wedge-shaped area (Zhu & Ma, 2017). There may be evidence of what is known as the "D" sign, which is where the left ventricle takes on a "D" shape due to right ventricular overload or pressure causing a shift (Dinh, n.d.).
An echocardiogram, a type of ultrasound scan, can also be performed for early risk stratification for PE. Findings such as right ventricle overload and right systolic dysfunction can help healthcare providers diagnose PE (Oh & Park, 2023).
Electrocardiogram (EKG): An EKG or ECG is a standard procedure for many conditions, and PE is no exception. The most common EKG finding in PE is sinus tachycardia.
Sinus Tachycardia
There are more findings on an EKG that may indicate PE. For example, the McGinn-White Sign may be seen in a small subset of patients. The McGinn-White sign, also known as the S1Q3T3 pattern, is characterized by a large S wave in lead 1, a Q wave in lead III, and a late inverted T wave in lead III (Healio, n.d.). Even though this sign is considered classic in PE, an EKG is not near specific or sensitive enough to be the only diagnostic test used. In fact, around 18% of patients with PE have a normal EKG result (Burns & Buttner, 2021).
A couple of popular risk stratification scores are used to determine the probability of PE.
Wells score: This test, developed in 1998, aims to clinically predict and classify patients suspected of having PE into risk categories.
It was originally developed to guide the type of diagnostic imaging, such as VQ scanning or angiography, to ensure an accurate diagnosis. An algorithm was used with the first version of the scale, and patients were classified with a low, moderate, or high probability. When healthcare providers started using d-dimers more frequently, the score was revised. Now, patients are classified into either two groups, including low versus high risk, or three groups, including low, moderate, or high risk (Wells et al., 1998; Wells et al., 2000).
The criteria for the Wells score include the following (van Belle et al., 2006):
Symptoms of DVT, such as leg swelling = 3 points
If other diagnoses are less likely and PE is suspected as the primary diagnosis = 3 points
Heart rate higher than 100 bpm = 1.5 points
If the patient has been immobilized for > three days or has had surgery in the past four weeks = 1.5 points
A previous diagnosis of DVT or PE = 1.5 points
Hemoptysis, or coughing up blood = 1 point
Malignancy = 1 point
Traditional Wells criteria scoring includes the following (van Belle et al., 2006):
Low probability = < 2 points
Moderate probability = 2-6 points
High probability = > 6 points
If using the simplified or modified version, the patient is classified into two groups, including the following (van Belle et al., 2006):
PE unlikely = < 4 points
PE likely = > 4 points
Geneva score: The Geneva score is another prediction tool utilized in assessing the probability of PE in patients. There is the original Geneva score, the revised Geneva score, and the simplified Geneva score (Wicki et al., 2001).
The original Geneva score ranges from zero to 16, classifies patients into high, intermediate, or low risk, and is based on several factors (Hacking, 2021).
Age:
60-79 years = 1 point
80+ years = 2 points
VTE history = 2 points
Surgery within a month = 3 points
Heart rate higher than 100 bpm = 1 point
The partial pressure of CO2 in arterial blood:
< 35 mmHg = 2 points
35-39 mmHg = 1 point
The partial pressure of O2 in arterial blood:
< 49 mmHg = 4 points
49-59 mmHg = 3 points
60-71 mmHg = 2 points
72-82 mmHg = 1 point
CXR findings:
Hemidiaphragm elevation = 1 point
Band atelectasis = 1 point
Table 2: Original Geneva score probability
Probability
Points
Low
< 5
Intermediate
5-8
High
> 8
(Hacking, 2021)
The revised Geneva score eliminates the CXR and ABG categories.
Table 3: Revised Geneva Score
Factor
Points
> 65 years
1
VTE history
3
Surgery/fracture history within a month
2
Active malignancy
2
Unilateral lower extremity pain
3
Pain on deep vein palpation and edema
4
Hemoptysis
2
Heart rate: 75-94 bpm
3
Heart rate: > 94 bmp
5
(Hacking, 2021)
The score is then tallied, and the probability is determined. Probability categories include the following (Hacking, 2021):
Low probability = 0-3 points
Intermediate probability = 4-10 points
High probability = > 10 points
The simplified Geneva score weights everything with one point, except if the heart rate is > 94 bpm, then two points are assigned. Clinical probability is low if the score is < 1 point, intermediate if the score is 2-4 points, and high if the score is > 5 points (Robert-Ebadi et al., 2017).
There is an adapted Geneva score specifically for pregnant women. Some factors were removed, and some thresholds changed for this version.
Table 4: Pregnancy Adapted Geneva Score
Factor
Points
≥ 40 years old
1
VTE history
3
Surgery/lower limb fracture within a month
2
Unilateral lower limb pain
3
Hemoptysis
2
Heart rate ≥ 110 bpm
5
Pain on deep vein palpation and edema
4
(Robert-Ebadi et al., 2021)
Each scale is easy to use and compute and can detect PE.
Treatment of PE depends on the severity of the situation. The primary goal is to stabilize the patient and maintain oxygen levels. Hemodynamic stability should be assessed, and treatment should occur based on the patient's needs.
When oxygen saturation (SaO2) is less than 90%, supplemental oxygen is necessary. Depending on the patient's status, nasal cannulas, face masks, or a nonrebreather can be used. If these mechanisms are unsuccessful, a high-flow nasal cannula can be used, or mechanical ventilation can be initiated (Pérez-Nieto et al., 2023).
If hemodynamically unstable and experiencing hypotension, the patient may be given IV fluids. However, this could worsen symptoms for patients with right ventricular dysfunction (Konstantinides et al., 2014).
It is often necessary for patients to receive inotropes and vasopressors. The three most common medications used include epinephrine, norepinephrine, and dopamine. These medications should increase right ventricular function and mean arterial pressure while maintaining pulmonary vascular resistance. When administering these medications to patients, it is pertinent to observe for worsening hypotension (Sekhri et al., 2012).
At times and often with massive PE, patients become unstable due to the size and movement of the clot, and rapid action is necessary to prevent death from occurring. Thrombolytic therapy is often used when time is of the essence. However, there are contraindications to using thrombolytics. Absolute contraindications include the following (Ucar, 2019):
Active bleeding
Prior intracranial hemorrhage
Malignant neoplasm of the brain
Significant closed-head trauma within 90 days
Relative contraindications include the following (Ucar, 2019):
Pregnancy
Severe and uncontrolled hypertension
Older than 75 years of age
Major surgery within the past three weeks
Internal bleeding within the past month
The most common thrombolytics used include recombinant tissue plasminogen activator or rt-PA or alteplase, urokinase, and streptokinase.
Alteplase, or rt-PA, a fibrinolytic agent, converts plasminogen to plasmin, lysing fibrin and fibrinogen. This medication is available in 50 and 100-mg vials but must be reconstituted before administration. The initial half-life is fewer than five minutes.
For PE, the recommended administration is 100 mg infused over two hours. Anticoagulation via a parenteral route should be started immediately following the infusion when the partial thromboplastin or thrombin time is lower than twice normal (Reed et al., 2023).
Urokinase is another thrombolytic agent used for lysis of PE, often when patients are hemodynamically unstable. The initial dose is 4400 international units (IU) per kilogram (kg) over 10 minutes, given at a rate of 90 mL per hour. The recommended maintenance dose is 2200-4400 IU/kg over 12 hours at 15 mL per hour (Ucar, 2019).
Streptokinase is no longer commercially available in the United States, but generic versions and derivatives of it may still be used. This medication causes an ongoing thrombolytic state, sometimes lasting up to 48 hours. The loading dose is 250,000 IU over 30 minutes. The maintenance dose is 100,000 IU per hour for 24 hours (Edwards & Nagalli, 2023).
Anticoagulants are another type of medication used to treat and prevent PE. Initially, they are often used for the first week to a week and a half after the event. In the long term, they can be used for three to six months to prevent PE reoccurrence. However, it is not uncommon to see anticoagulants being used for over six months (Agnelli & Becattini, 2015).
Different types of anticoagulants can be used for patients with PE, such as IV or injectable and oral forms.
Heparin: This medication activates antithrombin and works to inhibit clotting. Contraindications include active and uncontrollable bleeding when the platelet count is lower than 100,000 per microliter or the patient has a history of heparin-induced thrombocytopenia (Warnock & Huang, 2023). There are two commonly used types of heparin.
Unfractionated heparin (UFH) – This form of heparin usually comes in 10,000 units/mL in 5 mL vials. Prophylactically, UFH can be given as 5,000 IU subcutaneously (SQ) every eight to 12 hours or 7,500 IU SQ every 12 hours. Therapeutically, UFH can be given as 8,000-10,000 IU SQ every eight hours or 15,000-20,000 IU SQ every 12 hours. To treat PE, UFH can be given as 80 units/kg in an IV bolus followed by a continuous infusion of 18 units/kg/hour or as a 5000 unit IV bolus followed by a continuous infusion of 1300 units/hour.
Many different dosages and rates exist depending on diagnosis, weight, risk factors, and comorbidities. UFH must be monitored very closely to ensure dosages are correct based on lab results (UC San Diego Health, n.d.).
Low-molecular-weight heparin (LMWH) – this form of heparin is longer-lasting and, therefore, does not need to be monitored as often. Examples of LMWH include enoxaparin and dalteparin. The same contraindications exist for this form of heparin.
Enoxaparin, better known as Lovenox, comes in prefilled and graduated prefilled syringes from 30 mg to 150 mg. Therapeutically, it can be given as 1 mg/kg bid. It can be given at 40mg/day as a prophylactic medication. Dosages depend on weight and patient condition.
Dalteparin, or Fragmin, comes in 2,500 - 25,000 IU prefilled syringes. Therapeutically, it can be given as 100-200 units/kg bid. As a prophylactic measure, up to 5,000 IU per day can be given (Miesner & Trewet, 2012; Solari & Varacallo, 2023).
A synthetic derivative of heparin is fondaparinux. It works over a long period and is not as strong as the other forms of heparin. It is often used for prevention rather than treatment of PE (Panahi et al., 2021).
Warfarin: Warfarin is a vitamin K antagonist used to treat PE. It is often used with other medications, such as UFH or LMWH. It is usually contraindicated in hemorrhage or excessive bleeding, pregnancy, threatened abortion, and malignant hypertension (Patel et al., 2023).
The maintenance dose is generally between two and 10 mg daily, depending on lab results (Mayo Clinic, 2023). The onset of action of warfarin is between one and three days, and the peak therapeutic effect is seen at days five to seven. Frequent monitoring is necessary with warfarin and is usually accomplished by reviewing the International Normalized Ratio or INR (Patel et al., 2023).
Patients should be educated that foods high in vitamin K, such as nuts and green vegetables, may inhibit the efficacy of warfarin (Panahi et al., 2021).
Direct oral anticoagulants: Direct oral anticoagulants (DOACs) are a popular alternative for preventing and treating PE. Common DOACs include rivaroxaban (Xarelto®), apixaban (Eliquis®), dabigatran (Pradaxa®), edoxaban (Savaysa®), and betrixaban (Bevyxxa®). Contraindications include mitral stenosis, liver disease, and renal insufficiency (Chen et al., 2020). Dosages, maintenance, and monitoring guidelines depend on the patient's history and indications for use.
This list is not all-inclusive; many other medications, such as aspirin, are used to prevent PE, and many others are used for treatment, maintenance, and long-term prevention.
Various surgical procedures can be used to treat PE.
Embolectomy: This procedure can restore pulmonary blood flow and circulation by clearing the obstruction. Catheter-based and surgical-based procedures can be effective at treating PE.
A catheter embolectomy is more minimally invasive than a surgical embolectomy. However, a surgical embolectomy may be necessary to free the clot. With a catheter embolectomy, a catheter is inserted into a small incision that has been made and placed into the vessel where the clot is. Imaging is used to ensure the placement is correct. A catheter is used to aspirate out the clot and restore blood flow. After clot removal, the catheter is removed, and dressings are placed (Cleveland Clinic, 2022a).
A surgical embolectomy is a more invasive procedure. It is often used when there are contraindications to anticoagulation, the patient is or is likely to experience shock that may cause death, or the catheter embolectomy failed (Fukuda & Daitoku, 2017). A sternotomy, where a vertical incision is created, allows access. Then, an incision is made into the pulmonary artery and potentially the branches. Once the clot is identified, it is extracted using suction catheters and forceps (Kim, 2022).
Balloon pulmonary angioplasty: This procedure is often used for patients with multiple clots or those who may not be suitable for procedures such as a surgical embolectomy. This procedure uses a local anesthetic, and a thin tube is threaded into and along the femoral vein, through the heart's chambers, and into the lung's arteries. After placement, a balloon is inflated, which widens the vessel and increases the blood flow. Often, this procedure may have to be performed more than once (Northwestern Medicine, n.d.).
Balloon Angioplasty
Vena Cava Filter: These prevent PE from reoccurring and stop clots from moving into the lungs or heart. Vena cava filters can be separated into the following (Cleveland Clinic, 2022c):
Inferior vena cava (IVC) filter- this prevents clots from the lower body.
Superior vena cava (SVC) filter- this prevents clots from the upper body.
For both of these filters, a small incision is made, and a thin tube is threaded into the vein and the area of the vena cava that is needed. A collapsed filter sent in with the catheter is left in place. The catheter is removed, and the filter, once expanded, attaches itself to the vena cava's walls (Johns Hopkins Medicine, n.d.).
There are complications associated with PE; major complications include chronic thromboembolic pulmonary hypertension (CTEPH), cardiogenic shock, right-sided heart failure, and reoccurring PE.
CTEPH, though rare, is a serious consequence of PE. Pulmonary hypertension occurs due to traveling emboli that do not resolve and obstruct the arteries. It is more common in patients who have hypothyroidism, have a history of PE, or have an inflammatory condition. If CTEPH is not identified and treated early, death can occur because of right-sided heart failure (Medrek & Safdar, 2016). Symptoms include shortness of breath, fatigue, chest tightness, and palpitations (Sahay et al., 2020).
Cardiogenic shock from PE also has a high mortality rate. Blood flow is impeded when the clot is obstructed in the pulmonary arteries. The right ventricle experiences volume overload, potentially leading to failure, and the left ventricle experiences a reduction in filling volume (Bangalore et al., 2023). Cardiogenic shock and right-sided heart failure can progress to cardiac arrest if not treated promptly.
Recurrent PE is more likely to occur within the first two weeks after diagnosis. The risk increases when patients are not on an anticoagulant regimen that is strong enough or correct for the situation or there is poor medication adherence (Vyas & Goyal, 2022).
When untreated, PE can cause fatalities in up to 30% of patients. Anticoagulation treatment decreases the mortality rate significantly (Weinberg & Rali, 2023).
Besides maintenance medication for prevention, there are other measures patients can use to prevent PE. Prevention measures include the following (Mayo Clinic, 2022):
Maintain a healthy weight
Tobacco cessation
Regular hydration
Elevation of the legs- this can be accomplished by raising the bottom of the bed by six inches
Physical activity
Compression socks/stockings
Prevention measures may also be used when patients are traveling, such as for long hours in a car or plane. Additional steps to take when traveling include moving ankles and toes every 30 minutes and moving around the cabin of the plane every hour if possible (Mayo Clinic, 2022).
After a PE diagnosis, patients should be monitored closely. How often monitoring should occur depends on the patient's overall health status, severity of the diagnosis, and medication regimen. Typically, follow-up visits should be scheduled for two weeks to three months out, and a new plan should be devised from there (Rivera-Lebron et al., 2019).
Andrew is a 45-year-old male who presents to the emergency department with complaints of chest pain, cough, and acute dyspnea. His past medical history includes hypertension, obesity, and melanoma, for which he is currently being treated.
Clinically, the patient presents with unstable vital signs that include the following:
Blood pressure- 88/52 mmHg
Pulse- 129 bpm
Respiratory rate- 33 breaths per minute
Oxygen saturation- 87%
A physical exam was completed, and no murmurs, adventitious breath sounds, or lower extremity edema were noted. An EKG was performed, and sinus tachycardia was evident. Pulmonary angiography was performed and denoted a saddle PE across both pulmonary arteries with evidence of right-sided heart strain.
Intervention/strategies
Oxygen therapy was initiated.
Mechanical thrombectomy, specifically a catheter-directed thrombectomy, was performed successfully. Anticoagulant therapy was also initiated. The patient was hospitalized for several days.
Follow-up was scheduled for four weeks after discharge from the hospital.
Discussion of outcomes
Based on the symptoms and clinical presentation, the healthcare provider could recognize the severity of the situation. After confirmation of the diagnosis by pulmonary angiography, the healthcare provider also knew the patient would be considered hemodynamically unstable, and immediate action was necessary.
Strengths and weaknesses of the approach used in the case
The healthcare provider performed the steps necessary to make an accurate diagnosis. The saddle PE may have been missed if the healthcare provider did not perform diagnostics. If the healthcare provider did not prescribe the right anticoagulants or did not perform the right procedure, the risk of mortality significantly increases.
A PE can be a deadly diagnosis if not identified and treated promptly. Patients should be aware of the risk factors of PE. Healthcare providers should recognize the signs and symptoms of PE to diagnose and treat the condition accurately. Chosen interventions and the prognosis depend on the type of PE, such as saddle PE, and whether the patient is hemodynamically unstable. Understanding the pathophysiology of PE can help providers with risk-stratifying measures to prevent the occurrence and reoccurrence of PE.
Select one of the following methods to complete this course.
Take TestPass an exam testing your knowledge of the course material.
OR
No TestAttest that you have read and learned all the course materials.
Implicit Bias Statement
CEUFast, Inc. is committed to furthering diversity, equity, and inclusion (DEI). While reflecting on this course content, CEUFast, Inc. would like you to consider your individual perspective and question your own biases. Remember, implicit bias is a form of bias that impacts our practice as healthcare professionals. Implicit bias occurs when we have automatic prejudices, judgments, and/or a general attitude towards a person or a group of people based on associated stereotypes we have formed over time. These automatic thoughts occur without our conscious knowledge and without our intentional desire to discriminate. The concern with implicit bias is that this can impact our actions and decisions with our workplace leadership, colleagues, and even our patients. While it is our universal goal to treat everyone equally, our implicit biases can influence our interactions, assessments, communication, prioritization, and decision-making concerning patients, which can ultimately adversely impact health outcomes. It is important to keep this in mind in order to intentionally work to self-identify our own risk areas where our implicit biases might influence our behaviors. Together, we can cease perpetuating stereotypes and remind each other to remain mindful to help avoid reacting according to biases that are contrary to our conscious beliefs and values.
Agnelli, G., & Becattini, C. (2015). Anticoagulant treatment for acute pulmonary embolism: a pathophysiology-based clinical approach. European Respiratory Journal, 45(4), 1142–1149. Visit Source.
American Lung Association. (2023). Learn About Pulmonary Embolism. American Lung Association. Visit Source.
Anderson, F. A., Jr, & Spencer, F. A. (2003). Risk factors for venous thromboembolism. Circulation, 107(23 Suppl 1), I9–I16. Visit Source.
Bangalore, S., Horowitz, J. M., Beam, D., Jaber, W. A., Khandhar, S., Toma, C., Weinberg, M. D., & Mina, B. (2023). Prevalence and Predictors of Cardiogenic Shock in Intermediate-Risk Pulmonary Embolism: Insights From the FLASH Registry. JACC. Cardiovascular interventions, 16(8), 958–972. Visit Source.
van Belle, A., Büller, H. R., Huisman, M. V., Huisman, P. M., Kaasjager, K., Kamphuisen, P. W., Kramer, M. H., Kruip, M. J., Kwakkel-van Erp, J. M., Leebeek, F. W., Nijkeuter, M., Prins, M. H., Sohne, M., Tick, L. W., & Christopher Study Investigators (2006). Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing, and computed tomography. JAMA, 295(2), 172–179. Visit Source.
Bĕlohlávek, J., Dytrych, V., & Linhart, A. (2013). Pulmonary embolism, part I: Epidemiology, risk factors and risk stratification, pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism. Experimental and clinical cardiology, 18(2), 129–138.
Bi, W., Liang, S., He, Z., Jin, Y., Lang, Z., Liu, H., Wang, Y., & Li, S. (2021). The Prognostic Value of the Serum Levels of Brain Natriuretic Peptide, Troponin I, and D-Dimer, in Addition to the Neutrophil-to-Lymphocyte Ratio, for the Disease Evaluation of Patients with Acute Pulmonary Embolism. International journal of general medicine, 14, 303–308. Visit Source.
Bounds, E. J., & Kok, S. J. (2023). D Dimer. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Visit Source.
Bull, T. M. & Hountras, P. (2023a). Nonthrombotic Pulmonary Embolism. Merck Manual Professional Version. Visit Source.
Bull, T. M. & Hountras, P. (2023b). Pulmonary Embolism (PE). Merck Manual Professional Version. Visit Source.
Burns, E. & Buttner, R. (2021). ECG changes in Pulmonary Embolism. Life in the Fastlane. Visit Source.
Cakal, E. D. (n.d.). Pulmonary Embolism. International Emergency Medicine Education Project. Visit Source.
Castro, D., Patil, S. M., & Keenaghan, M. (2022). Arterial Blood Gas. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Visit Source.
Centers for Disease Control and Prevention (CDC). (2023a). Data and Statistics on Venous Thromboembolism. Centers for Disease Control and Prevention. Visit Source.
Centers for Disease Control and Prevention (CDC). (2023b). Impact of Blood Clots on the United States. Centers for Disease Control and Prevention. Visit Source.
Chen, A., Stecker, E., & A. Warden, B. (2020). Direct Oral Anticoagulant Use: A Practical Guide to Common Clinical Challenges. Journal of the American Heart Association, 9(13). Visit Source.
Corteville, D. C., Bibbins-Domingo, K., Wu, A. H., Ali, S., Schiller, N. B., & Whooley, M. A. (2007). N-terminal pro-B-type natriuretic peptide as a diagnostic test for ventricular dysfunction in patients with coronary disease: data from the heart and soul study. Archives of internal medicine, 167(5), 483–489. Visit Source.
Dinh, V. (n.d.). The D Sign – Right Heart Strain from Pressure vs Volume Overload. Pocus 101. Visit Source.
Doğan, H., de Roos, A., Geleijins, J., Huisman, M. V., & Kroft, L. J. (2015). The role of computed tomography in the diagnosis of acute and chronic pulmonary embolism. Diagnostic and interventional radiology (Ankara, Turkey), 21(4), 307–316. Visit Source.
Edwards, Z., & Nagalli, S. (2023). Streptokinase. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Visit Source.
Fu, Z., Zhuang, X., He, Y., Huang, H., & Guo, W. (2020). The diagnostic value of D-dimer with simplified Geneva score (SGS) pre-test in the diagnosis of pulmonary embolism (PE). Journal of cardiothoracic surgery, 15(1), 176. Visit Source.
Fukuda, I., & Daitoku, K. (2017). Surgical Embolectomy for Acute Pulmonary Thromboembolism. Annals of vascular diseases, 10(2), 107–114. Visit Source.
Gao, H., Liu, H., & Li, Y. (2018). Value of D-dimer levels for the diagnosis of pulmonary embolism: An analysis of 32 cases with computed tomography pulmonary angiography. Experimental and therapeutic medicine, 16(2), 1554–1560. Visit Source.
Gharib, A., Khattab, A., Housset, B., Saeed, A., Gomaa, N., & Bermejo, J. G. (2016). Role of arterial blood gases, continuous positive airway pressure and ddimers to rule out pulmonary embolism suspected in obese patients. European Respiratory Journal, 48(suppl 60). Visit Source.
Hacking, C. (2021). Geneva score. Radiopaedia. Visit Source.
Horlander, K. T., Mannino, D. M., & Leeper, K. V. (2003). Pulmonary embolism mortality in the United States, 1979-1998: an analysis using multiple-cause mortality data. Archives of internal medicine, 163(14), 1711–1717. Visit Source.
Kim, T. S. (2022). Surgical Embolectomy of Acute Pulmonary Embolism. Annals of Phlebology, 20(1), 15–18. Visit Source.
Konstantinides, S. V., Torbicki, A., Agnelli, G., Danchin, N., Fitzmaurice, D., Galiè, N., Gibbs, J. S., Huisman, M. V., Humbert, M., Kucher, N., Lang, I., Lankeit, M., Lekakis, J., Maack, C., Mayer, E., Meneveau, N., Perrier, A., Pruszczyk, P., Rasmussen, L. H., Schindler, T. H., … Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). (2014). 2014 ESC guidelines on the diagnosis and management of acute pulmonary embolism. European heart journal, 35(43), 3033–3069k. Visit Source.
Leitman, E. M., & McDermott, S. (2019). Pulmonary arteries: imaging of pulmonary embolism and beyond. Cardiovascular diagnosis and therapy, 9(Suppl 1), S37–S58.
Lewis, G., Hoey, E. T., Reynolds, J. H., Ganeshan, A., & Ment, J. (2015). Multi-detector CT assessment in pulmonary hypertension: techniques, systematic approach to interpretation and key findings. Quantitative imaging in medicine and surgery, 5(3), 423–432. Visit Source.
Maloba, M., & Hogg, K. (2005). Best evidence topic report. Diagnostic utility of arterial blood gases for investigation of pulmonary embolus. Emergency medicine journal : EMJ, 22(6), 435–436. Visit Source.
Mayo Clinic. (2022). Pulmonary Embolism. Mayo Clinic. Visit Source.
Mayo Clinic. (2023). Warfarin (Oral Route). Mayo Clinic. Visit Source.
Medrek, S., & Safdar, Z. (2016). Epidemiology and Pathophysiology of Chronic Thromboembolic Pulmonary Hypertension: Risk Factors and Mechanisms. Methodist DeBakey cardiovascular journal, 12(4), 195–198. Visit Source.
Miesner, A. R., & Trewet, C. B. (2012). Clarification of Once-Daily Low-Molecular-Weight Heparin Dosing in Pulmonary Embolism. Chest, 142(4), 1074–1075. Visit Source.
Mirza, H., & Hashmi, M. F. (2023). Lung Ventilation Perfusion Scan (VQ Scan). In: StatPearls [Internet]. Treasure Island (FL). Visit Source.
Moore, A. J. E., Wachsmann, J., Chamarthy, M. R., Panjikaran, L., Tanabe, Y., & Rajiah, P. (2018). Imaging of acute pulmonary embolism: an update. Cardiovascular diagnosis and therapy, 8(3), 225–243. Visit Source.
Morrone, D., & Morrone, V. (2018). Acute Pulmonary Embolism: Focus on the Clinical Picture. Korean circulation journal, 48(5), 365–381. Visit Source.
Moser, J., Sheard, S., Patel, J., Sayer, C., Madden, B., & Vlahos, I. (2017). Iatrogenic peripheral pulmonary air embolism following intravenous contrast administration for CT pulmonary angiography: proposal of the "double bronchus sign". BJR case reports, 3(2), 20160097. Visit Source.
Myers, S. J., Kelly, T. E., & Stowell, J. R. (2017). Successful Point-Of-Care Ultrasound-Guided Treatment of Submassive Pulmonary Embolism. Clinical practice and cases in emergency medicine, 1(4), 340–344. Visit Source.
National Blood Clot Alliance. (2018). How is PE Diagnosed? National Blood Clot Alliance. Visit Source.
Nishiyama, K. H., Saboo, S. S., Tanabe, Y., Jasinowodolinski, D., Landay, M. J., & Kay, F. U. (2018). Chronic pulmonary embolism: diagnosis. Cardiovascular diagnosis and therapy, 8(3), 253–271. Visit Source.
Oh, J. K., & Park, J. H. (2023). Role of echocardiography in acute pulmonary embolism. The Korean journal of internal medicine, 38(4), 456–470. Visit Source.
Ouellette, D. R. (2020). Pulmonary Embolism (PE) Clinical Presentation. Medscape. Visit Source.
Panahi, L., Udeani, G., Horseman, M., Weston, J., Samuel, N., Joseph, M., Mora, A., & Bazan, D. (2021). Review of Medical Therapies for the Management of Pulmonary Embolism. Medicina (Kaunas, Lithuania), 57(2), 110. Visit Source.
Patel, S., Singh, R., Preuss, C. V., & Patel, N. (2023). Warfarin. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Visit Source.
Penn Medicine. (2023). Pulmonary Embolism (Pulmonary Embolus). Penn Medicine. Visit Source.
Pérez-Nieto, O. R., Gómez-Oropeza, I., Quintero-Leyra, A., Kammar-García, A., Zamarrón-López, É. I., Soto-Estrada, M., Morgado-Villaseñor, L. A., & Meza-Comparán, H. D. (2023). Hemodynamic and respiratory support in pulmonary embolism: a narrative review. Frontiers in medicine, 10, 1123793. Visit Source.
Reed, M., Kerndt, C. C., & Nicolas, D. (2023). Alteplase. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Visit Source.
Reyes, N., & Abe, K. (2023). Deep Vein Thrombosis & Pulmonary Embolism. Centers for Disease Control and Prevention. Visit Source.
Rivera-Lebron, B., McDaniel, M., Ahrar, K., Alrifai, A., Dudzinski, D. M., Fanola, C., Blais, D., Janicke, D., Melamed, R., Mohrien, K., Rozycki, E., Ross, C. B., Klein, A. J., Rali, P., Teman, N. R., Yarboro, L., Ichinose, E., Sharma, A. M., Bartos, J. A., Elder, M., … PERT Consortium (2019). Diagnosis, Treatment and Follow Up of Acute Pulmonary Embolism: Consensus Practice from the PERT Consortium. Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis, 25, 1076029619853037. Visit Source.
Robert-Ebadi, H., Mostaguir, K., Hovens, M. M., Kare, M., Verschuren, F., Girard, P., Huisman, M. V., Moustafa, F., Kamphuisen, P. W., Buller, H. R., Righini, M., & Le Gal, G. (2017). Assessing clinical probability of pulmonary embolism: prospective validation of the simplified Geneva score. Journal of Thrombosis and Haemostasis, 15(9), 1764–1769. Visit Source.
Robert-Ebadi, H., Elias, A., Sanchez, O., Le Moigne, E., Schmidt, J., Le Gall, C., Aujesky, D., Roy, P. M., Moumneh, T., Chauleur, C., Rouyer, F., Le Gal, G., & Righini, M. (2021). Assessing the clinical probability of pulmonary embolism during pregnancy: The Pregnancy-Adapted Geneva (PAG) score. Journal of thrombosis and haemostasis : JTH, 19(12), 3044–3050. Visit Source.
Sahay, S., Levine, D. J., & Peters, J. (2020). Chronic Thromboembolic Pulmonary Hypertension (CTEPH). American College of Chest Physicians. Visit Source.
Sekhri, V., Mehta, N., Rawat, N., Lehrman, S. G., & Aronow, W. S. (2012). Management of massive and nonmassive pulmonary embolism. Archives of medical science : AMS, 8(6), 957–969. Visit Source.
Shahul, H. A., Manu, M. K., & Mohapatra, A. K. (2019). Hampton's hump, Westermark's sign and Palla's sign in acute pulmonary thromboembolism: a rare concurrence. BMJ case reports, 12(9), e231693. Visit Source.
Solanki, N. N., Tanwar, N., & Solanki, N. D. (2020). Subacute Massive Pulmonary Embolism Treated With Streptokinase. Cureus, 12(10), e11157. Visit Source.
Solari, F. & Varacallo, M. (2023). Low-Molecular-Weight Heparin (LMWH). In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Visit Source.
Tarbox, A. K., & Swaroop, M. (2013). Pulmonary embolism. International journal of critical illness and injury science, 3(1), 69–72.
Torbicki, A., Perrier, A., Konstantinides, S., Agnelli, G., Galiè, N., Pruszczyk, P., Bengel, F., Brady, A. J., Ferreira, D., Janssens, U., Klepetko, W., Mayer, E., Remy-Jardin, M., Bassand, J. P., & ESC Committee for Practice Guidelines (CPG). (2008). Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). European heart journal, 29(18), 2276–2315. Visit Source.
Tsuchiya, N., van Beek, E. J., Ohno, Y., Hatabu, H., Kauczor, H. U., Swift, A., Vogel-Claussen, J., Biederer, J., Wild, J., Wielpütz, M. O., & Schiebler, M. L. (2018). Magnetic resonance angiography for the primary diagnosis of pulmonary embolism: A review from the international workshop for pulmonary functional imaging. World journal of radiology, 10(6), 52–64. Visit Source.
Turetz, M., Sideris, A. T., Friedman, O. A., Triphathi, N., & Horowitz, J. M. (2018). Epidemiology, Pathophysiology, and Natural History of Pulmonary Embolism. Seminars in interventional radiology, 35(2), 92–98. Visit Source.
Ucar, E. Y. (2019). Update on Thrombolytic Therapy in Acute Pulmonary Thromboembolism. The Eurasian journal of medicine, 51(2), 186–190. Visit Source.
UC San Diego Health. (n.d.). UFH and LMWH Dose. UC San Diego Health. Visit Source.
Vyas, V., & Goyal, A. (2022). Acute Pulmonary Embolism. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Visit Source.
Warnock, L. B., & Huang, D. (2023). Heparin. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Visit Source.
Weinberg, A. S., & Rali, P. (2023). Treatment, prognosis, and follow-up of acute pulmonary embolism in adults. UpToDate. Visit Source.
Wells, P. S., Ginsberg, J. S., Anderson, D. R., Kearon, C., Gent, M., Turpie, A. G., Bormanis, J., Weitz, J., Chamberlain, M., Bowie, D., Barnes, D., & Hirsh, J. (1998). Use of a clinical model for safe management of patients with suspected pulmonary embolism. Annals of internal medicine, 129(12), 997–1005. Visit Source.
Wells, P. S., Anderson, D. R., Rodger, M., Ginsberg, J. S., Kearon, C., Gent, M., Turpie, A. G., Bormanis, J., Weitz, J., Chamberlain, M., Bowie, D., Barnes, D., & Hirsh, J. (2000). Derivation of a simple clinical model to categorize patients probability of pulmonary embolism: increasing the models utility with the SimpliRED D-dimer. Thrombosis and haemostasis, 83(3), 416–420.
Wicki, J., Perneger, T. V., Junod, A. F., Bounameaux, H., & Perrier, A. (2001). Assessing clinical probability of pulmonary embolism in the emergency ward: a simple score. Archives of internal medicine, 161(1), 92–97. Visit Source.
Zhu, R., & Ma, X. C. (2017). Clinical Value of Ultrasonography in Diagnosis of Pulmonary Embolism in Critically Ill Patients. Journal of translational internal medicine, 5(4), 200–204. Visit Source.
We're sorry! All our support agents are unavailable to chat at the moment.
Need Immediate Assistance? Please visit our FAQ section which provides answers to many common inquiries.
Get in Touch Directly via Email If your query is urgent or you'd prefer to reach us directly, we invite you to submit a support ticket through our Contact Us page. Our dedicated support team will review your inquiry and get back to you as soon as possible.
Support Hours Our chat support is typically available Monday to Friday, 9:00 AM - 6:00 PM EST. For support outside of these hours, please use our email contact
Are you sure?
You should NOT select "Remember me for 30 days" if you are on a public or shared computer.
