Progressive Dyspnea

Medic 15 is called to a residential address for an 81-year-old female with shortness of breath. You and your partner arrive on scene at a single-story house. The patient is with her daughter, and both are able to provide you with a history-recurrent breast cancer, currently on chemotherapy and congestive heart failure.

The patient notes she’s developed worsening shortness of breath over the past 2-3 days. She denies having chest pain, upper back pain, cough, upper respiratory symptoms, fevers, chills or lower extremity swelling.

You place the patient on the monitor and find her to be in sinus tachycardia with a pulse of 124 and an oxygen saturation of 75% on room air.

Her initial blood pressure is 140/90, and her respiratory rate is 28. Your partner administers oxygen at 15 mL/min. via a non-rebreather mask (NRB), and the patient’s oxygen saturation quickly improves to 92%.

A physical exam reveals that the patient is awake, alert and oriented, with clear breath sounds bilaterally and no cardiac murmurs. She has no lower extremity edema.

The patient is placed on the stretcher and taken to the ambulance. While en route, an IV is established. The patient is taken to the closest ED, which is a community hospital affiliated with a large academic tertiary care center.

Hospital Course

On arrival, the patient’s vitals are unchanged. You move her to a hospital stretcher and the ED nurse places her on the monitor.

She remains hypoxic with oxygen saturation at 75% when she’s off of the non-rebreather, so she’s transitioned to bilevel positive airway pressure (BPAP) ventilation with settings of 10/5 mmHg.

Her oxygen saturation with a fraction of inspired oxygen (FiO2) of 100% is 95%, but she still has an increased respiratory rate of 24. Her systolic blood pressure remains in the 140s.

An ECG is performed and demonstrates evidence of right ventricular strain and tachycardia (see Figure 1), and her chest X-ray demonstrates clear lungs and a normal mediastinum without cardiomegaly.

A CT scan of the patient’s chest is obtained to assess for a pulmonary embolism.

The CT scan reveals a large saddle embolus with extension into the majority of the lobar and more distal pulmonary arterial branches resulting in significant right-sided heart strain. (See Figure 2, p. 20).

Figure 2: Patient’s CT scan confirming pulmonary embolism

Large saddle embolus with extension into the majority of the lobar
and more distal pulmonary arterial branches resulting in
significant right-sided heart strain.

She also has evidence of a small pericardial effusion and multiple areas of pulmonary infarct.

The ED providers discuss these findings with the interventional cardiologist on call, and after reviewing the patient’s images, he recommends transferring her to the associated academic tertiary care center. He’s determined that the patient is a good candidate for the interventional procedure of catheter-assisted thrombolysis with ultrasound and 12 hours of intra-arterial tissue plasminogen activator (tPA).

A heparin infusion is started. The university hospital’s flight service is dispatched. The patient remains on BPAP upon the flight crew arrival. She’s awake and alert, and she isn’t hypotensive but is still tachycardic.

The patient is placed on a transport ventilator with the same BPAP settings, is moved onto the stretcher and taken to the helicopter. Her transport is without incident.

On landing at the university hospital, the patient is immediately taken to the cardiac catheterization lab for catheter placement. Her hemodynamics and respiratory status are stable throughout the transfer and procedure.

The patient remains stable overnight and her catheter is removed the following morning. A bilateral lower extremity duplex demonstrates an occluding deep venous thrombosis (DVT) in the right mid-femoral and gastrocnemius veins. Her oxygenation status improves, and she’s able to be weaned to room air. She’s transitioned to enoxaparin and warfarin for anticoagulation. She remains stable and is discharged on hospital day three.

The patient follows up with her oncologist several times in the interim and remains stable and asymptomatic. She lives at home, is reportedly doing well, and is back to her pre-pulmonary embolism baseline.


Pulmonary embolism (PE) is a relatively common event that can lead to significant morbidity and mortality. The incidence of PE is estimated to be 60 to 70 per 100,000, and is the third most common type of cardiovascular disease after coronary artery disease and stroke.1

Autopsy evidence shows the highest incidence of fatal PE is in those 70-80 years of age. When PE is recognized and treated, the mortality is 8%, but climbs to 30% if unrecognized and untreated.1 Up to 10% of acute PE patients die suddenly.2,3

Given the morbidity and mortality associated with PE, novel interventions have been developed to improve patient outcomes. Many of these therapies such as those presented in our case involve the use of interventional techniques that require specialists at major centers.

Early recognition of the possibility of PE by prehospital crews can allow for appropriate treatment and transport as well as identification to the receiving ED so that these interventions can be explored early in the patient’s evaluation.

Patient risk factors include increased age, prior personal history of venous thromboembolism, active malignancy, disabling conditions such as cardiac or respiratory failure, congenital or acquired coagulation disorders, hormone replacement therapy and oral contraception.4 Virchow’s triad classically refers to the conditions of personal hypercoagulability risk factors described above, endothelial injury and stasis of blood flow. Stasis may be seen in any condition which limits mobility such as surgery or a long plane or car ride. Endothelial injury, which may be caused by central line placement, foreign bodies or shear stress also leads to increased risk of clot formation.

Patients typically present with sudden onset or worsening, progressive dyspnea.1 More than half endorse chest pain, which can sometimes be difficult to distinguish from anginal pain. The pain may be pleuritic or be described as “sharp.” Patients may also complain of cough, or less frequently, hemoptysis if the PE is also associated with pulmonary infarction. Around 15% will present with syncope.1

More than 90% of PE patients present with dyspnea, tachypnea or chest pain.2 Patients may present with tachycardia or tachypnea, although depending on the size of the PE and other co-morbidities or medications (such as beta-blockers), these findings may not be seen. The traditional triad of dyspnea, tachycardia and chest pain are only found infrequently together; their absence can’t be used to exclude PE clinically.

In the most severe cases, PE presents with hypotension, hypoxia or cardiac arrest. Patients suffering cardiac arrest from PE usually present in a pulseless electrical activity (PEA) rhythm.

An ECG may demonstrate evidence of right heart strain with findings such as ST depression and T wave inversion in the precordial leads (v1-v3) and the inferior leads (II, III, aVF), with III being the most prominent.

A new right bundle branch block may also be seen and patients may have the S1Q3T3 pattern with an S wave in lead I, Q wave in lead III and inverted T wave in lead III. (See Figure 3, p. 21.)

Figure 3: ECG demonstrating S1Q3T3 finding

Although not sensitive, this finding has been associated with massive PE. It’s characterized by an S wave in lead I, a Q wave found in lead III, and an inverted T wave in lead III.

High risk (massive) PE is defined by its hemodynamic instability, typically a systolic blood pressure < 90 mmHg, and carries a high mortality of 18-30%.5 Intermediate risk (submassive) PE patients have indications of right ventricular strain, either by laboratory markers (troponin, brain natriuretic peptide) or imaging studies (echocardiography, ECG) indicating that the right heart is pumping against the increased resistance caused by the clot in the pulmonary arteries.6 Patients with intermediate risk PEs aren’t hypotensive. Those with lower risk pulmonary emboli are typically hemodynamically stable and respond well to conservative treatment such as heparinization and transition to longer-term anticoagulation. Heparin and other anticoagulants don’t dissolve clots already present but do prevent further formation of clot.

Prehospital management of PE should be focused on the management of airway, breathing and circulation. Patients may require additional oxygen if hypoxic, and in severe cases, they may require intubation or bag valve mask ventilation (BVM) for respiratory failure. For hypotension, IV/intraosseous access should be obtained and IV fluids should be administered.

A complete set of vital signs will allow for risk stratification and a 12-lead ECG may demonstrate findings associated with PE, as well as rule out ST-segment elevated myocardial infarction (STEMI) as a cause of symptoms.

On arrival to the hospital, the diagnosis of PE is typically made via CT imaging of the chest. If a PE is discovered, this CT will also determine the extent of the PE, which will guide the next steps in treatment.

Patients with massive and submassive pulmonary emboli are candidates for intra-
arterial fibrinolytic therapy.7 Small PEs in patients without hemodynamic instability or right heart strain are placed on heparin or other anticoagulation.

Systemic fibrinolysis, such as IV alteplase or tenecteplase, carry a risk of bleeding. This risk is heightened in patients with known metastatic malignancy, thrombocytopenia, recent surgical interventions, pulmonary infarcts and prior intracerebral hemorrhage. In these patients with increased bleeding risk, systemic fibrinolysis can result in severe morbidity related to internal bleeding or death. Thus, in many instances, directed therapy may be beneficial for patients with significant clot burden. As was presented in our case, ultrasound-assisted fibrinolytic therapy was utilized to treat our patient. This technology functions by unwinding of fibrin strands, making the thrombus more permeable, and allowing the lytic to penetrate deeper while simultaneously accelerating dispersion of the lytic.8 This approach is performed by interventional cardiologists in a cardiac catheterization lab.

Ultrasound-assisted catheter-directed low-dose thrombolysis (USAT) delivers the efficacy of systemic fibrinolytics quickly, thus reducing right ventricular afterload and improving right ventricle size and function with a lower risk profile compared to systemic fibrinolytics.9 USAT should be considered in patients with acute massive and submassive PEs, especially those with contraindications to systemic fibrinolytics.9 Indeed, the risk profile with USAT is comparable to angicoagulation.10

In a randomized controlled trial comparing USAT to unfractionated heparin in patients with intermediate-risk PE, patients who received USAT demonstrated fewer cardiac effects such as dilation of the right ventricle than the group that received unfractionated heparin alone, without a significant increase in major bleeding.10

The SEATTLE II study further demonstrated safety and efficacy of USAT thrombolysis in patients with massive or submassive PEs.9 In our patient’s case, this approach was utilized with a good patient outcome.


We describe a case of a patient with a submassive PE who was rapidly diagnosed and treated using USAT. Early recognition of PE by identifying risk factors and clinical presentation may allow for rapid prehospital and ED diagnosis, evaluation, and management of patients which will further reduce morbidity and mortality. Appropriate recognition may improve patient outcomes by allowing for advanced, specialized treatment when indicated.


1. Bĕlohlávek J, Dytrych V, Linhart A. Pulmonary embolism, part I: Epidemiology, risk factors and risk stratification, pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism. Exp Clin Cardiol. 2013;18(2):129-138.

2. Torbicki A, Perrier A, Konstantinides S, et al. 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). Eur Heart J. 2008;29(18):2276-2315.

3. Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism: Clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER). Lancet. 1999;353(9162):1386-1389.

4. British Thoracic Society Standards of Care Committee Pulmonary Embolism Guideline Development Group. British Thoracic Society guidelines for the management of suspected acute pulmonary embolism. Thorax. 2003;58(6):470-483.

5. Mateo J, Oliver A, Borrell M, et al. Laboratory evaluation and clinical characteristics of 2,132 consecutive unselected patients with venous thromboembolism-Results of the Spanish Multicentric Study on Thrombophilia (EMET-Study). Thromb Haemost. 1997;77(3):444-451.

6. Hall RJ, Sutton GC, Kerr IH. Long-term prognosis of treated acute massive pulmonary embolism. Br Heart J. 1977;39(10):1128-1134.

7. Konstantinides S, Geibel A, Heusel G, et al. Heparin plus alteplase compared with heparin alone in patients with submassive pulmonary embolism. N Engl J Med. 2002;347(15):1143-1150.

8. Engelberger RP, Kucher N. Ultrasound-assisted thrombolysis for acute pulmonary embolism: A systematic review. Eur Heart J. 2014;35(12):758-764.

9. Piazza G, Hohlfelder B, Jaff MR, et al. A prospective, single-arm, multicenter trial of ultrasound-facilitated, catheter-directed, low-dose fibrinolysis for acute massive and submassive pulmonary embolism: The SEATTLE II study. JACC Cardiovasc Interv. 2015;8(10):1382-1392.

10. Kucher N, Boekstegers P, Muller OJ, et al. Randomized, controlled trial of ultrasound-assisted catheter-directed thrombolysis for acute intermediate-risk pulmonary embolism. Circulation. 2014;129(4):479-486.

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