A 70-year-old female with a past history of prior tobacco dependence, an inferoposterior MI years ago, LV systolic dysfunction (EF 45-50% two years prior), known AAA (3cm), and peripheral artery disease presented to the ED with a chief complaint of decreased appetite. She reported that over the last week she had felt fatigued and did not feel like eating. She specifically denied chest pain, shortness of breath, abdominal pain, nausea, vomiting, and diarrhea.


Initial VS: BP 82/52, HR 70, RR 27, SpO2 85% on RA


Physical exam revealed a woman sitting up in bed, shivering. She was tachypnic. Her lungs were clear to auscultation bilaterally. Cardiac exam revealed regular rate and rhythm without murmur, gallop, or rub appreciated.


Within minutes of arrival to the ED, a large work-up was initiated with an EKG, bedside cardiac ultrasound, CXR, lactate, BNP, troponin, chemistry panel, CBC, UA, and venous blood gas. A liter of intravenous fluid was also ordered and started infusing. She was placed on oxygen with slight improvement of her oxygen saturation.


The initial differential was broad and included hypovolemia, silent MI, ruptured AAA, sepsis, and pulmonary embolism.


Here is the initial EKG:

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This was interpreted as a non-specific EKG.


Bedside ultrasound of the heart was done rapidly as has become standard of care in our ED in patients presenting with hypotension of unknown etiology. Here is the first image obtained in the parasternal long view:

Notice anything abnormal? We hope you do!


The right ventricle, which is sitting at the top of the screen, is huge. In the parasternal long view you can often only see a small sliver of the RV. So what was the suspected diagnosis?


You guessed it! A pulmonary embolism was suspected, and not just any old pulmonary embolism, a MASSIVE pulmonary embolism.


Here is the parasternal short view:

You can see that again, the RV is huge. It is also causing septal bowing into the left ventricle. Remember that normally the LV has much higher pressures than the RV and, bowing into the LV should not occur unless there is some type of pathology present. This septal bowing is referred to as the D-sign because when it bows, it looks like a D.


Here are two more views. One is an apical view and the other we will call a pseudo-apical view. It almost looks like it is a cross between an apical view and a substernal view.


Again, in these views, you can appreciate how massively enlarged the right side of the heart is compared to the left. You can also see the septal bowing again.


Now, we should note that there are other conditions that can cause RV strain, such as, pulmonary hypertension. This woman, however, had an echo from 2 years prior without any evidence of this, so we can presume that this is a new condition likely representative of PE.


In the ED, her BP continued to be hypotensive and the decision to give thrombolytics was made based off of the beside ultrasound and vital signs. Before the tPA was given, norepinephrine had been started. After the administration of the first bolus of 10 mg tPA, her blood pressure improved, and the norepinephrine was weaned off. She was then given a subsequent 90 mg of tPA over 2 hours.


Labs later returned significant for a creatinine of 2.47, troponin of 0.048 (normal <0.03), a BNP of 11682, and a normal lactate.


In this case, PE was diagnosed off of a bedside ultrasound that was done within minutes of arrival. If the clinicians taking care of this patient had not reached for the ultrasound, this patient’s diagnosis and treatment could have been significantly delayed, which could have been detrimental to this very ill patient. This patient had a creatinine of 2.47 and, therefore, contrasted CT to look for PE would have not been able to be obtained. This patient also had bibasilar opacities on CXR, which would have made a VQ scan difficult or impossible to interpret.


We should mention that ultrasound is not the preferred means of diagnosing a PE because it is insensitive and, patients often lack evidence of PE on echo. Only 30-40% of those presenting with a PE will have evidence on echo. Signs of a PE that can been seen on echo are increased RV size and decreased function, tricuspid regurgitation, RV thrombus (see example by clicking here), pulmonary artery thrombus, and a McConnell’s sign. A McConnell’s sign is RV akinesia of the mid-free wall that spares the right ventricular apex. This sign has a 94% specificity, but is only 77% sensitive. It can be used to distinguish acute PE from pulmonary hypertension if present because the regional wall motion abnormality in pulmonary hypertension will not spare the apex.


She required a short course of intubation secondary to hypercapnic respiratory failure, however, was then extubated without incident. The patient did well, and was discharged from the hospital on anticoagulation with ongoing work-up for etiology of the massive PE.


Bottom Line: We believe that if you know the limitations of cardiac ultrasound in PE, it can be used as one of the initial diagnostic tests in someone with suspected PE, particularly if the patient is hemodynamically unstable. To us, the benefit of finding one of the signs of PE on echocardiography very rapidly outweighs any reason not to do the study.




  1. Gibson NS, Sohne M, Buller HR. Prognostic value of echocardiography and spiral computed tomography in patients with pulmonary embolism. Curr Opin Pulm Med. 2005;11(5):380-384.
  2. Kucher N, Rossi E, De Rosa M, Goldhaber SZ. Prognostic role of echocardiography among patients with acute pulmonary embolism and a systolic arterial pressure of 90 mm Hg or higher. Arch Intern Med. 2005;165(15):1777-1781.
  3. McConnell MV, Solomon SD, Rayan ME, Come PC, Goldhaber SZ, Lee RT. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol. 1996;78(4):469-473.
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