echo in venous thrombo

Evaluation of the critically ill patient with suspected or confirmed pulmonary embolism remains a challenging clinical quandary. Critical care echo (CCE) can be a valuable bedside adjunct in patients who are too sick to be transported or continue to deteriorate, despite escalating intensive therapy. Whether it is used as a diagnostic adjunct, in hemodynamic evaluation, or prognostically to evaluate risk of deterioration, CCE can provide critical insights in a patient with severe cardiorespiratory and/or hemodynamic deterioration. CCE may also unveil potential confounders such as acute valvular regurgitation and biventricular failure.

Characteristic findings such as inter-ventricular septal flattening, RV dilatation and poor RV systolic movement can all signify an acute RV process, which may occur in the setting of acute pulmonary embolism. In fact, detection of RV dysfunction in the patient with confirmed pulmonary embolism is associated with a significantly increased in-hospital morbidity and mortality (1,2). CCE plays a critical role in risk assessment and guiding treatment decisions in patients who are severely hemodynamically compromised (3). Despite the appeal, CCE is not advised as a routine procedure in hemodynamically stable patients with confirmed pulmonary embolism (3).

conflicting findings

Acute pulmonary embolism may also result in a distinct pattern of regional RV dysfunction. The, “McConnell sign”, describes severe hypokinesia of the RV free wall with preserved contraction of the apical segment (4). This finding was originally reported to have a specificity as high as 94% 4; however, subsequent studies have found significantly lower specificities (5).  A free-floating thrombus may also be visualized in the right heart, a finding which is uncommon. Overall, it is likely that the diagnostic utility of CCE for PE is limited as the calculated sensitivity and specificity of comprehensive trans-thoracic echocardiography has been reported between 29% and 52% and between 96% and 87%, respectively (6). The specificity can also be greatly reduced in the presence of comorbidities which may chronically elevate RV afterload including obstructive sleep apnea, pulmonary hypertension, interstitial lung disease and chronic obstructive pulmonary disease.

more on McConnel

In this clip we see an enlarged right ventricle (>2/3 LV, non-foreshortened) with a grossly hypokinetic RV free wall. Further, the RV apex is hyperkinetic, a combination of findings known as, “McConnell sign”. The hyperdynamic, low-volume LV cavity is typical for this obstructive form of shock. This individual had a massive saddle pulmonary embolus.

Common error in acquisition

One of the more common errors in estimating RV size (as a proportion of LV) is foreshortening. This clip demonstrates how, by a simple change in axis, the RV, which is normal (Image A) can appear to seem roughly the same proportion (Image B).

Confirmation of distal VTE

Compression ultrasound in the lower extremities can also be used to provide critical information on the presence of a venous thromboembolism. While this should not be used as rule-out test, the presence of an obvious clot can be assist in the presumptive diagnosis of PE (+ cardiac fundings).

Hemodynamic progression of a pulmonary embolism

The bottom line (or two)

Although CCE is only one element of assessment of the patient with suspected or confirmed PE, it remains an important one in critical illness. Likely where the application of CCE remains most compelling is in the application to hemodynamically unstable patients in refractory circulatory shock (systolic BP <90 mm Hg for >15 minutes or evidence of circulatory shock) and/or refractory hypoxemia. If the suspicion for PE remains high and conventional testing is considered unsafe (i.e. computed tomography, transport), findings of acute RV dysfunction in setting of refractory hypoxia or hypotension may justify the use of life-saving therapy, balanced against the risk of adverse effects (including intra-cranial hemorrhage) (3). Furthermore, CCE may enhance the ability to monitor the effect of thrombolysis as regional RV dysfunction may actually reverse with thrombolysis (7).


1. ten Wolde M, Söhne M, Quak E, Mac Gillavry MR, Büller HR. Prognostic value of echocardiographically assessed right ventricular dysfunction in patients with pulmonary embolism. Arch Intern Med. 2015;164:1685-1689.

2. Ribeiro a., Lindmarker P, Juhlin-Dannfelt a., Johnsson H, Jorfeldt L. Echocardiography Doppler in pulmonary embolism: Right ventricular dysfunction as a predictor of mortality rate. Am Heart J. 1997;134:479-487.

3. Goldhaber SZ. Echocardiography in the management of pulmonary embolism. Ann Intern Med. 2002;136:691-700.

4. McConnell M V., 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;78:469-473.

5. Casazza F, Bongarzoni A, Capozi A, Agostoni O. Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular infarction. Eur J Echocardiogr. 2005;6:11-14.

6. Bova C, Greco F, Misuraca G, et al. Diagnostic utility of echocardiography in patients with suspected pulmonary embolism. Am J Emerg Med. 2003;21(2):180-183.

7. Nass N, McConnell M V., Goldhaber SZ, Chyu S, Solomon SD. Recovery of regional right ventricular function after thrombolysis for pulmonary embolism. Am J Cardiol. 1999;83(98):804-806.

8. Vonk Noordegraaf A, Westerhof BE, Westerhof N. The Relationship Between the Right Ventricle and its Load in Pulmonary Hypertension. J Am Coll Cardiol. 2017;69(2):236-243.