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Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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Pulmonary embolism echocardiography

Introduction

Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]

Overview

Overview

Routine echocardiography in patients with suspected pulmonary embolism (PE) is not required.[1] In fact, the majority of patients with PE have a normal echocardiography.[1] However if elevations in the cardiac troponins or brain natriuretic peptide are present, then acute right ventricular (RV) dysfunction may be present and echocardiography is warranted.[2] Echocardiography is also valuable for the evaluation of hemodynamically unstable patients with acute dyspnea, right heart failure, or syncope who are suspected to have PE.[1] The presence of right ventricular dysfunction is a predictor of early death among patients with PE.[3] When evidence of RV dysfunction is present, PE is risk stratified into submassive PE or massive PE depending on the absence or presence of hypotension respectively.[4][5]

Echocardiography

Echocardiography

  • Echocardiography may also show akinesia of the mid-free wall but normal apical motion of the right ventricle. This is referred to as the McConnell sign. The sensitivity and specificity of the McConnell sign for the diagnosis of acute PE are 77% and 94% respectively.[6]

Shown below is an echocardiogram that demonstrates McConnell sign: {{#ev:youtube|Tklaxe-kPrk}}

References

References

  1. ↑ 1.0 1.1 1.2 1.3 Goldhaber SZ (2002). “Echocardiography in the management of pulmonary embolism”. Ann Intern Med. 136 (9): 691–700. PMID 11992305.
  2. ↑ Kucher N, Goldhaber SZ (2003). “Cardiac biomarkers for risk stratification of patients with acute pulmonary embolism”. Circulation. 108 (18): 2191–4. doi:10.1161/01.CIR.0000100687.99687.CE. PMID 14597581.
  3. ↑ 3.0 3.1 3.2 Goldhaber SZ, Visani L, De Rosa M (1999). “Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER)”. Lancet. 353 (9162): 1386–9. PMID 10227218.
  4. ↑ 4.0 4.1 Jaff MR, McMurtry MS, Archer SL, Cushman M, Goldenberg N, Goldhaber SZ; et al. (2011). “Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association”. Circulation. 123 (16): 1788–830. doi:10.1161/CIR.0b013e318214914f. PMID 21422387.
  5. ↑ 5.0 5.1 Cannon CP, Goldhaber SZ (1996). “Cardiovascular risk stratification of pulmonary embolism”. Am. J. Cardiol. 78 (10): 1149–51. PMID 8914880. Retrieved 2011-12-21. Unknown parameter |month= ignored (help)
  6. ↑ McConnell MV, Solomon SD, Rayan ME, Come PC, Goldhaber SZ, Lee RT (1996). “Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism”. Am. J. Cardiol. 78 (4): 469–73. PMID 8752195.
  7. ↑ Torbicki A, Galié N, Covezzoli A, Rossi E, De Rosa M, Goldhaber SZ; et al. (2003). “Right heart thrombi in pulmonary embolism: results from the International Cooperative Pulmonary Embolism Registry”. J Am Coll Cardiol. 41 (12): 2245–51. PMID 12821255.
  8. ↑ Konstantinides S, Geibel A, Kasper W, Olschewski M, Blümel L, Just H (1998). “Patent foramen ovale is an important predictor of adverse outcome in patients with major pulmonary embolism”. Circulation. 97 (19): 1946–51. PMID 9609088. Retrieved 2011-12-21. Unknown parameter |month= ignored (help)