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Prehospital Stabilization of Pulmonary Embolism


This CE activity is approved by EMS World Magazine, an organization accredited by the Continuing Education Coordinating Board for Emergency Medical Services (CECBEMS) for 1 CEU. To take the CE test that accompanies this article, go to to take the test and immediately receive your CE credit. Questions? E-mail


  • Describe the U.S. incidence of pulmonary embolism
  • Explain the risk factors for developing a pulmonary embolism
  • Identify the common and classic symptoms of pulmonary embolism
  • Describe the prehospital care for a patient experiencing pulmonary embolism

A 48-year-old male patient has phoned 9-1-1 for severe respiratory distress. You arrive to find an anxious neighbor waiting to take you to the second floor of a two-story flat. Hustling up the stairs, the neighbor advises you that he’s been helping care for Henry, his neighbor, after Henry had surgery to repair his right lower leg following a motorcycle accident. Henry has been home for five days.

You find Henry seated upright on the side of his bed in a tripod position, with pale and diaphoretic skin, breathing 40 times a minute. In one-word answers he denies any medical history other than his recent leg surgery, reports no allergies and says he’s taking morphine for pain from the surgery. He specifically denies any prior breathing problems.

Working quickly, your partner administers oxygen 15 lpm via nonrebreather mask while you determine that Henry’s pulse is 124/min. with a narrow-complex tachycardic rhythm on the cardiac monitor. His SpO2 is 78% on room air, and his blood pressure is 74/50 mmHg. Henry is unable to walk, so your partner leaves to retrieve the stair-chair while you establish a 16-gauge IV in the right antecubital region and begin a 500-cc normal saline fluid bolus. By the time your partner returns, Henry’s SpO2 has increased to 84% on oxygen, and you’ve determined that he has slight crackles in the bases of both lungs, jugular vein distention, cyanosis to the lips and is negative for chest pain, abdominal distress and peripheral edema. His level of respiratory distress appears to be increasing.


Acute pulmonary embolism (PE) is a life-threatening emergency during which an obstruction occurs in a pulmonary artery or arteriole. Pulmonary embolism occurs in more than 650,000 people annually.1 While more than 75% of patients with PE remain stable, around 10% die within the first few hours of symptom onset, and overall mortality remains around 30%.2 With 10% of patients with PE rapidly deteriorating in just a few hours, PE remains the second-leading cause of sudden death (following sudden cardiac death).3 Thus it is important for all prehospital professionals to understand when to suspect and how to manage acute pulmonary embolisms.

One out of every 1,000 Americans is diagnosed with an acute PE annually.2 This rate rose each year from 2001–2010 due to improved ED diagnostic capabilities, including the availability of CT scanners.2,3 Most experts believe the rising incidence can be attributed improved recognition of previously missed PEs, not a true rise in the overall occurrence.

Women 55 and older are at greater risk for PE than men of the same age, but death rates are 20%–30% higher in men. There is also an interesting correlation between PE and race: The incidence and mortality from PE is nearly 50% higher in blacks than whites, and the mortality is 50% higher for whites than it is for other races (Asians, South Americans, Native Americans, etc.).3

Between 60%–80% of patients diagnosed with PE first have a deep vein thrombosis (DVT). A DVT is complete occlusion of a deep vein and occurs in 10%–13% of all patients who have been on bed rest for seven or more days, and in over 25% of patients with pulmonary disease who are on bed rest for three or more days.3 Thus most patients ordered extended bed rest are placed on DVT prophylaxis to help mitigate the risk of DVTs developing.

Examples of DVT prophylaxis include anticoagulation medications and the application of compression stockings with around 20 mmHg of pressure. When a DVT is diagnosed early and treated with anticoagulants, the patient has no greater risk of dying from PE than they do from anticoagulant-associated fatal hemorrhage (less than 1%).4 While an in-depth discussion on DVTs is beyond the scope of this article, it is important to understand that DVT prophylaxis reduces the risk of PE development, making the untreated DVT a potential ticking time bomb. Virchow’s triad (Figure 1) identifies the three primary factors that predispose a patient to venous thrombus formation, placing them at risk for PE: endothelial injury, stasis or turbulent blood flow, and blood hypercoagulability.1

The etiology of PE in adult patients is not always clear, so in addition to Virchow’s triad, there are many risk factors for which all patients with shortness of breath should be screened. These are outlined in Table 1. One of the most notable is recent surgery. DVTs following major surgery primarily occur in a lower (58%) or upper (18%) extremity.3 While not common when prophylactic measures are used, DVTs are most common following orthopedic surgery, particularly following surgeries of the hip, pelvis and spine. Traumatic injury also predisposes patients to embolisms, with the greatest risk occurring with fracture of the tibia or femur.3

Unlike adults, most (98%) children with pulmonary embolism have a clearly identifiable risk factor, and between 20%–36% of these patients have a central venous catheter.3 One hypothesis for this increased prevalence is that the thrombus forms around the catheter, then becomes dislodged when it is removed.


Fundamentally, pulmonary embolism is not a disease in and of itself; it is a complication of other venous thrombosis or disease, most commonly a deep vein thrombosis. In addition to arising from a lower-extremity DVT, an embolus can develop from thrombi that originate in the pelvic, renal or upper-extremity deep veins, as well as in the right heart chambers. Deep veins are almost always beside an artery and are found beneath the fascia. Superficial veins, on the other hand, are near the body’s surface.

Atrial thrombus formation most frequently occurs when the heart is in atrial fibrillation. A thrombus is a blood clot that forms inside a vessel and remains at its place of origin, while an embolism occurs when a piece of that clot breaks loose, travels through the bloodstream and becomes lodged in another part of the body. In the case of a pulmonary embolism originating outside a right heart thrombus, the blood clot travels up the inferior vena cava, through the right side of the heart and into the pulmonary artery system (Figure 2). Blood clots are the most common emboli, but emboli can also occur from fatty tissue or bone marrow being released when a bone fractures, as well as from air, a piece of tumor, sheared IV catheter or any other foreign body that enters the bloodstream.

Thrombosis, the formation of a blood clot, normally occurs to help tamponade hemorrhage following injury. When it occurs within the vessels, thrombosis usually takes place on the valves in the lower extremities. The thrombus then grows as platelets and fibrin aggregate, leading to thrombus formation. When the thrombus occurs in a deep vein, it is considered a DVT; it is an occlusive thrombus if it interrupts blood flow.

When a piece breaks loose, an embolism develops. Emboli that break free in the venous system travel through veins that continuously gain diameter size until they reach the heart; thus it is unlikely for emboli to occlude a vessel prior to passing through the heart. Once the embolism passes through the heart, it enters the pulmonary arteries, where vessels progressively decrease in size until they become the pulmonary capillary bed. The embolus then becomes lodged once its size is larger than the artery through which it is traveling. Small emboli tend to travel distally within the pulmonary artery tree and lead to micro-occlusion, which can produce minimal symptoms that include pleuritic chest pain that develops from the lung tissue’s inflammatory response to the emboli. Large emboli may lodge at the bifurcation of the main pulmonary artery or proximally in the lobar artery branches, resulting in rapid hemodynamic instability.

Largely impacted by the emboli’s original size, the acute pulmonary embolism is characterized as either central or peripheral. A central PE is found in the central vasculature of the pulmonary tree, which includes the main pulmonary artery, anterior trunk, right and left interlobar arteries, left upper lobe trunk, right middle lobe artery, and right and left lower lobe arteries.3 When both pulmonary arteries are involved, or when the PE causes hemodynamic compromise, it is considered massive. The saddle pulmonary embolism (Figure 3) bridges across bifurcation of the main pulmonary artery and can interrupt blood flow to both lungs, causing rapid deterioration and death. Peripheral PEs lodge in the segmental and subsegmental arterioles, are small in size by comparison, and because they disrupt little blood flow, they typically do not cause hemodynamic compromise. Most peripheral PEs occur in the lower lung lobes and are multiple in nature, meaning more than one embolism occurs at a time.3

The physiologic effects of a PE are largely determined by the embolism’s size and where it becomes lodged. Once lodged in the pulmonary artery, the PE disrupts distal blood flow, inhibiting the exchange of oxygen and carbon dioxide and causing a pressure backup within the cardiovascular system. As a result, clinicians are likely to see a manifestation of primarily respiratory and cardiovascular symptoms.

Within the respiratory system, PE leads to:

  • Increased dead air space (VQ mismatch);
  • Hypoxemia;
  • Hyperventilation;
  • Pulmonary infarction.

Within the cardiovascular system, PE can lead to:

  • Increased pulmonary vascular resistance;
  • Increased right ventricular afterload;
  • Decreased stroke volume and cardiac output;
  • Right ventricular failure (massive PE only);
  • Pulmonary artery constriction (reflex mechanism);
  • Tachycardia;
  • Jugular vein distention;
  • Cardiovascular collapse.


Since patients with pulmonary embolisms frequently complain of mild dyspnea and chest pain, begin assessing them as you would any other patient with a chest-related complaint. Developing a differential diagnosis requires ruling out other possible etiologies of chest pain and dyspnea through detailed history-taking and a thorough assessment. While obtaining a medical history, pay attention to any risk factors for DVT and PE, as well as prior medical conditions (e.g., asthma) that need to be ruled in or out as potential causes. Since it can be difficult to rule in or out a pulmonary embolism, several scoring systems have been developed to help determine whether a patient’s symptoms are in fact caused by a PE. One such tool is the Modified Wells Prediction Rule (Table 2), which relies on a patient’s medical history, assessment and vital signs.5

Patients experiencing large PE classically develop sudden-onset pleuritic chest pain with shortness of breath and hypoxia that is difficult to improve with oxygen. In reality, though, this “classic” triad of symptoms is rarely seen. Often there are few obvious symptoms when a PE forms, and particularly when patients are suffering from a small embolism, their symptoms may develop over time, with mild shortness of breath and intermittent mild chest pain. The most common are:

  • Acute shortness of breath;
  • Cough;
  • Chest pain;
  • Tachycardia;
  • Tachypnea;
  • Signs of DVT.

Complete a thorough set of vital signs and accurately count respirations; nearly all patients present with tachycardia and tachypnea.3 Determine a baseline SpO2 and monitor for change with oxygen administration. Do not be surprised if a patient with a suspected PE does not experience a significant rise in SpO2 with supplemental oxygen. Patients may also experience tachycardia, so establish cardiac monitoring as a part of your assessment and perform a 12-lead ECG—it is not uncommon to identify new-onset atrial fibrillation.

Pulmonary embolism won’t cause ST-segment elevation or depression, but it is likely to cause changes consistent with right heart strain, which include non-sinus rhythms, incomplete or complete right bundle branch block, the S1Q3T3 pattern, and T-wave inversions in leads V1–V2, V1–V3 or V1–V4. A multicenter trial that reviewed more than 6,000 12-lead ECGs found that the presence of these ECG changes, consistent for right heart strain, increased the odds a patient without prior cardiopulmonary disease was experiencing a pulmonary embolism.6 The S1Q3T3 pattern is a large S-wave in lead I, a Q-wave in lead III and an inverted T-wave in lead III. While the absence of these changes doesn’t rule out PE, their presence is concerning. Massive pulmonary embolisms are defined as presenting with a systolic blood pressure less than 90 mmHg; these patients are at risk for dying within hours and should be considered critically unstable. Patients with massive PE are in shock and will have poor peripheral perfusion and present pale, diaphoretic and often with mental status changes.

Perform a thorough head-to-toe examination. Neurological symptoms are typically only found when patients experience a large PE. They may include seizures, syncope (most common) and mental status changes. On the neck, inspect for jugular vein distention. Listen to lung sounds; many patients with PE develop mild pulmonary edema as a result of increased pulmonary artery pressures. In addition, they may experience a nonproductive cough, and lung sounds may reveal wheezes or fine rales in the bases. Hemoptysis can occur, although it is rare.

One clue to suspecting PE in shock patients is the presence of a systolic murmur louder on inspiration along the left sternal border. This suggests tricuspid valve regurgitation. Abdominal pain is more likely when the PE results from a DVT in the renal or pelvic veins. When examining the extremities, pay close attention for evidence of a deep vein thrombosis. An extremity with a DVT is unlikely to lose pulses, but patients may have nonspecific leg pain and tenderness (particularly in the calf muscles) and increased warmth and swelling isolated to the affected extremity. Pay close attention to the patient's skin; diaphoresis and clammy skin are common, and peripheral cyanosis in the hands and feet may rapidly progress to central cyanosis on the face, neck and trunk.

It’s important to consider PE whenever a patient experiences shortness of breath or hypoxia. But because pulmonary embolism is not a disease but rather a complication of other coagulopathy, illness or injury elsewhere in the body, work to rule in or out other diagnoses that can more easily explain the symptoms before treating for PE. Many illnesses and diseases present with symptoms similar to PE:

  • Sickle cell disease;
  • Pleurisy;
  • Pericarditis;
  • Angina;
  • Anxiety;
  • Atrial fibrillation;
  • Cor pulmonale;
  • Pneumonia;
  • Acute coronary syndrome;
  • Pneumothorax.

Lab Values That May Suggest PE

For prehospital professionals working with point-of-care lab testing capabilities as well as those working in nontraditional settings, some laboratory values may be useful in helping strengthen suspicion for PE. These include D-dimer, lactic acid, ABG, troponin levels, and brain natriuretic peptide (BNP).3 An elevated BNP over 500 ng/L is associated with increased mortality.

D-dimer testing is most helpful for patients with low to moderate Wells prediction scores. In these patients a normal D-dimer can essentially rule out pulmonary embolism. D-dimer should never be used on patients with high Wells scores or to rule in PE because it lacks sufficient sensitivity or specificity to do so.

In one study of 270 patients with an ED diagnosis of pulmonary embolism, an elevated serum lactate (over 2 mmol/L) correlated with high risk of death and adverse outcomes independently from shock, hypotension or elevated troponin.7

An arterial blood gas can be used to determine how well any patient with a respiratory complaint is oxygenating and to titrate oxygen delivery. However, an ABG should rarely be used to rule in or out pulmonary embolism, as it is a nonspecific test for hypoxemia. One exception to this would be patients with no known pulmonary disease who develop sudden respiratory distress (especially following surgery); in these patients a low PO2 has a high predictive value for pulmonary embolism.

While not a laboratory value, end-tidal CO2 (EtCO2) is a popular prehospital assessment tool for patients with respiratory complaints. And while it may seem reasonable to consider EtCO2 in the assessment of patients suspected to have PE, a meta-analysis of 14 trials determined it has a probability of less than 10% of accurately indicating pulmonary embolism as a diagnosis.8 If you use it, expect a patient with a suspected PE to have a normal (35–45 mmHg) to slightly low EtCO2, resulting from tachypnea, and a normal waveform.


Prehospital treatment of acute pulmonary embolism is driven by patient stability and focuses on early recognition and supportive measures. Patients with small pulmonary embolisms generally only require comfort care. Manage pain with local analgesia protocols; avoid drugs such as morphine, which may exacerbate hypotension. Unstable patients with large PEs demand aggressive intervention to protect the ABCs.

Administer all suspected PE patients oxygen to maintain SpO2 above 94%. This may be accomplished with a nasal cannula for some patients, while others will remain hypoxic on a nonrebreather mask. Patients with persistent hypoxia may benefit from noninvasive positive-pressure ventilation (CPAP or BiPAP). While this will not correct the underlying problem, it will help maximize oxygen delivery to the blood that’s reaching the lungs without harming the patient. The benefit of improved oxygenation may outweigh the risk of slight blood pressure decline in patients with borderline blood pressures. Patients in shock with declining level of consciousness need early advanced airway management, including rapid sequence intubation (RSI). If intubation is performed, consider adding a PEEP valve onto the bag-valve mask and ventilate the patient with supplemental PEEP to help maximize oxygen delivery to blood reaching the lungs.

Early IV access is important, as patients with PE who are going to deteriorate are most likely to do so during the first hour of care. Establishing large-bore IV access allows for the rapid administration of IV fluids; treat hypotension with up to a liter of isotonic fluids to help increase stroke volume and cardiac output. If the patient’s blood pressure does not respond to initial IV fluids, initiate a vasopressor. Norepinephrine is the preferred first-line vasopressor for PE patients, as dopamine will only worsen the already-present tachycardia, reducing the ventricular filling time and leading to a further decrease in stroke volume.

Transport teams with anticoagulants such as Lovenox and heparin should consider early administration for patients with high risk of pulmonary embolism when not contraindicated. The American College of Chest Physicians recommends immediate anticoagulation for any suspected PE patient, as doing so reduces mortality. In these patients intravenous heparin administration is preferred, as it will not interfere with fibrinolytic therapy, should it be required.9 Lovenox administration requires the patient to have a properly functioning renal system, so in the prehospital setting it is best avoided in any patient who may have renal disease.

In patients with intermediate and low risk for PE, it is recommended to wait until ED arrival so a definitive diagnosis can be made prior to administration.9 Once a diagnosis is made, patients are placed on either heparin or warfarin for anticoagulation before being bridged to Coumadin, leading to resolution within a few weeks. Surgical removal of the clot, known as a pulmonary embolectomy, may be considered by an interventional radiologist when the patient is not a candidate for fibrinolytics or when they improve following fibronlytic administration. For unstable hypotensive patients with massive PEs, definitive care includes the administration of fibrinolytics. Typically fibrinolytics are not indicated in the absence of hypotension because of their associated risk of hemorrhage.


After quickly moving Henry to the ambulance, you direct your partner to begin the 18-minute lights-and-siren transport to the hospital. During the transport you determine Henry’s Wells prediction score is 6 and switch him from a nonrebreather mask to CPAP with a PEEP of 7.5 cm H2O to attempt to improve his oxygenation, as his SpO2 remains at 85%. CPAP brings his SpO2 up to 90%, but he continues to breathe 40 times a minute, and his heart rate and blood pressure remain unchanged after a 500-mL fluid bolus.

When you arrive in the emergency department, the ED physician performs rapid sequence intubation and has a stat CT scan performed. Henry is diagnosed with a saddle PE and administered tPA.

Acute pulmonary embolisms can range from asymptomatic to rapid-onset life-threatening emergencies during which patients rapidly deteriorate. Because PE is not a disease in its own right, diagnosis is made by completing a thorough history and assessment and ruling out other, more likely illnesses. Diagnosing a PE requires a high index of suspicion and is aided by determining a PE risk assessment score. When treating a patient suspected to have a PE, protect the critical systems, provide adequate oxygen and anticipate the potential for rapid patient deterioration. Be prepared to intervene!


1. York NL, Kane CJ, Smith C, Minton LA. Care of the patient with an acute pulmonary embolism. Dimens Crit Care Nurs, 2015 Jan–Feb; 34(1): 3–9.

2. Schissler AJ, Rozenshtein A, Schluger NW, Einstein AJ. National trends in emergency room diagnosis of pulmonary embolism, 2001–2010: a cross-sectional study. Respir Res, 2015 Mar 24; 16: 44.

3. Oullette DR. Pulmonary Embolism. Medscape,

4. Munoz-Torrero JF, Bounameaux H, Pedrajas JM, et al. Effects of age on the risk of dying from pulmonary embolism or bleeding during treatment of deep vein thrombosis. J Vasc Surg, 2011 Dec; 54(6 Suppl): 26S–32S.

5. Chagnon I, Bounameaux H, Aujesky D, et al. Comparison of two clinical prediction rules and implicit assessment among patients with suspected pulmonary embolism. Am J Med, 2002 Sep; 113(4): 269–75.

6. Marchick MR, Courtney DM, Kabrhel C, et al. 12-lead ECG findings of pulmonary hypertension occur more frequently in emergency department patients with pulmonary embolism than in patients without pulmonary embolism. Ann Emerg Med, 2010 Apr; 55(4): 331–5.

7. Vanni S, Viviani G, Baioni M, et al. Prognostic value of plasma lactate levels among patients with acute pulmonary embolism: the thrombo-embolism lactate outcome study. Ann Emerg Med, 2013 Mar; 61(3): 330–8.

8. Manara A, D’hoore W, Thys F. Capnography as a diagnostic tool for pulmonary embolism: a meta-analysis. Ann Emerg Med, 2013 Dec; 62(6): 584–91.

9. Kearon C, Akl EA, Comerota AJ, et al. Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed.: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest, 2012 Feb; 141(2 Suppl): e419S–94S.

Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT, is an educator, e-learning content developer and author of numerous articles and textbook chapters. He is also the clinical education coordinator for AirLink/VitaLink in Wilmington, NC, and a lead instructor for Wilderness Medical Associates. Contact him at

Sean M. Kivlehan, MD, MPH, NREMT-P, is an international emergency medicine fellow at Brigham & Women’s Hospital, Harvard Medical School. E-mail

Scott R. Snyder, BS, NREMT-P, is a faculty member at the Public Safety Training Center in the Emergency Care Program at Santa Rosa Junior College, CA. He is also a paramedic with AMR: Sonoma Life Support in Santa Rosa, CA. E-mail




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