CSC Oct-02
Echo in PE
Key Points:
• Acute PE cannot explain a PASP > 50 mm Hg
• Most patients with an acute PE will have some echocardiographic abnormality of the right
ventricle
• Positive troponin in acute PE seems to be correlated with RV dysfunction and increased mortality
1. What degree of pulmonary hypertension can be explained by an acute PE?
• Obstruction of > 50% of the pulmonary vascular bed is required to see significant elevation of
the PA pressures
• The normal RV is unable to generate PASP > 50 mm (mean 40) acutely
2. Aside from pulmonary HTN, what is the data about the utility of echocardiograms in acute
PE?
• More than 80% of patients with a documented PE have some type of right heart abnormality on
echo, most commonly one of the following:
-- Direct visualization of thrombus (rare)
-- RV dilatation
-- RV hypokinesis with apical sparing (a.k.a. McConnell’s sign)
-- Abnormal interventricular septal motion (a.k.a. “septal bowing”)
-- TR
-- PA dilatation
-- Lack of inspiratory collapse of IVC
• The presence of any 2 of the 3 following criteria has a 56% sensitivity and 90% specificity, in
one study, for acute PE (confirmed by P-Agram):
-- RV hypokinesis
-- RVEDD > 27 mm (without RV hypertrophy)
-- TR velocity of > 2.7 m/sec
• In the same study, using pre-test probabilities of PE of 10%, 50%, and 90%, the post-test
probabilities with a positive echo were 38%, 85%, and 98%. With a negative echo, post-test
probabilities were 5%, 33%, and 81%.
3. Please tell us about the latest data on troponin in PE!
• A prospective study of 106 patients with acute PE found that troponinI is elevated in 41% and
was correlated with echocardiographically detected RV dysfunction, “complicated in-hospital
course,” and overall mortality. The higher the troponin, the higher the mortality.
• Negative predictive value of troponins for a major clinical event was 93%
References
Goldhaber SZ in Braunwald. Heart Disease: A Textbook of Cardiovasc