Written by: Sean Hickey, MD (@seanhickey92 – Resident Physician, Icahn School of Medicine at Mount Sinai) and Stephen Alerhand, MD (@SAlerhand – Assistant Professor, Rutgers New Jersey Medical School) // Edited by: Manpreet Singh MD (@MPrizzleER – Assistant Professor of Emergency Medicine – Harbor-UCLA Medical Center) and Brit Long, MD (@long_brit)

This write up has been adapted from the above authors’ review in JEM: (PMID 31745658)

Pulmonary Embolism Classification

Half of pulmonary embolisms (PE’s) are diagnosed in the emergency setting [1, 2]. They can be categorized into three groups (Table 1) [3, 4]:

Table 1: Classification of Pulmonary Embolism [5] 

* Hemodynamic instability:

  • Sustained hypotension with systolic blood pressure (SBP) < 90 mm Hg for at least 15 min or requiring inotropic support that is not due to another cause other than PE
  • Pulselessness
  • Persistent profound bradycardia (heart rate < 40 bpm) with signs or symptoms of shock

** Right ventricular (RV) strain:

  • Bedside echocardiography
  • Elevated laboratory markers (BNP > 500 pg/mL, Troponin I > 0.4 ng/mL or troponin T > 0.1 ng/mL)
  • New ECG changes (incomplete or complete right bundle branch block, anteroseptal ST elevation or depression, anterolateral T wave inversion)


Background on Pulmonary Embolism Management

  • In brief, evidence supports the use of thrombolytics for massive PE, as long as there are no contraindications [3, 6-9].
  • Non-massive PE’s do not warrant thrombolytics, and some may even be safely treated at home [10, 11].
  • It is for the sub-massive PE category that the evidence is less clear [4, 12-16]. This decision may depend on the patient’s clinical course and warrants discussion with the patient and consultants. A detailed synopsis can be found HERE.


Right Ventricular Structure and Dynamics in Pulmonary Embolism

  • The RV has an unusual geometric shape which precludes the straight-forward assessment of volume and ejection fraction.
    • It appears triangular-shaped when viewed from the side and crescent-shaped when viewed in cross-section [17, 18]. Its three parts are the inlet, highly trabeculated body, and smooth outlet portion (known as the conus or infundibulum) [19].
  • The contraction of the RV is a complex process.
    • It begins at the proximal portion and ends at the infundibulum and outflow tract. The inlet and outlet portions contract perpendicularly to each other.
    • The RV carries superficial muscle fibers for circumferential contraction and deep subendocardial fibers for longitudinal contraction [20, 21], the latter of which contributes 80% of the cardiac output [10, 22].
  • The RV and pulmonary arterial vasculature constitute a low-resistance, high-capacitance system.
    • The RV is thus better able to handle increased preload than increased afterload [23].
  • In the setting of a PE, there is an abrupt increase in pulmonary vascular resistance and RV afterload.
    • The RV cannot overcome the increased pressure needed to overcome the large clot burden and associated mechanical obstruction.
      • Even an obstruction of >25-30% of the pulmonary arteries is associated with an increase in pulmonary pressures [24] and 30% reduction in RV stroke volume [25]. Outright RV failure may be seen when 50-75% of the pulmonary vasculature is obstructed by thrombi [24]. This strain on the RV will first lead to chamber dilation and regional wall stress, followed by systolic dysfunction and septal deviation [26]. In this display of ventricular interdependence, the decrease in preload will lead to compromise of the cardiac output [27]. Hypotension, decreased coronary perfusion, and ischemia will follow.
  • European and American guidelines have stated that RV dysfunction and cardiac biomarker elevations are more relevant for risk stratification than the anatomic burden and distribution of pulmonary artery clots [5, 28].
  • RV dysfunction can help prognosticate outcomes in normotensive patients with PE.
    • In the short-term, this finding on bedside echocardiography can portend development of hypotension, cardiorespiratory deterioration, or death despite the initiation of anticoagulation.
    • In the long-term, patients treated with standard anticoagulation and not thrombolytics may end up with persistent RV strain and functional limitation [29, 30]. It is these patients who ought to be considered for systemic or catheter-based thrombolytics, or at least more intensive clinical monitoring and disposition. In contrast, those without any signs of RV dysfunction may be considered for extended observation or even treated as an outpatient [11, 31].


Role of Echocardiography After the Diagnosis of Pulmonary Embolism

  • The goal of echocardiography in cases of established PE is to identify high-risk patients (and thus direct care) before they may decompensate.
  • Making matters difficult, the RV is difficult to evaluate using bedside echocardiography due to the complex geometric shape and contractile pattern described above.
    • No single echocardiographic parameter (i.e. RV:LV ratio, D-shaped intraventricular septum, McConnell’s sign, tricuspid regurgitation) provides a clear-cut assessment of RV function.


TAPSE for Evaluation of Right Ventricular Dysfunction

Tricuspid annular plane systolic excursion (TAPSE) has gained traction as a risk-stratification and prognostic tool through its assessment of global RV function and ejection fraction. In the apical 4-chamber view, this one-dimensional measure of RV systolic function is obtained by measuring the vertical movement of the tricuspid annulus between the end of diastole and end of systole in M-mode. This reflects the longitudinal contraction of the RV.

  • Approximates RV ejection fraction with 80% sensitivity and 75% specificity [32].
  • Used by cardiologists to reliably assess RV dysfunction and ejection fraction correlated with cardiac MRI and right heart angiography [32-34].
  • The mid-esophageal 4-chamber view of transesophageal echocardiography (TEE) was validated as a good correlate to RV systolic function as reflected by RV fractional area change [35].
  • Validated against the RV ejection fraction calculated from the biplanar Simpson’s rule [36].
  • Can assess for RV dysfunction in patients with heart failure with preserved ejection fraction [37-39].


TAPSE as a Prognostic Tool in Patients with Pulmonary Embolism

  • The numerical value of TAPSE is decreased in patients with acute PE [40, 41].
    • Abnormal TAPSE is independently predictive of increased short-term mortality [42] and increased length-of-stay in the intensive care unit (ICU) [43, 44].
    • In those who are normotensive, it reflects RV function and independently predicts survival [42], while demonstrating superiority for risk stratification compared to RV/LV ratio [45].
    • TAPSE measurements can even be used to predict acute decompensation in patients undergoing acute pulmonary artery embolectomy [46].
    • TAPSE may recover incompletely after 3 months [40], and is independently associated with a decreased long-term survival [47].


Why makes TAPSE so attractive as a measurement tool?

  • Unlike the other qualitative RV parameters of RV dysfunction, TAPSE provides a quantitative value that corresponds to RV systolic function. This allows an easy determination of normal compared to abnormal.
  • TAPSE can be reproduced by physicians with high interobserver reliability [48-50].
  • It is less dependent on optimal image quality.


What are the cut-off measurements of TAPSE?

There is no consensus measurement or cut-off for TAPSE values in prognostication [42, 43, 45, 46, 51].


Limitations to TAPSE

  • TAPSE measures the longitudinal excursion of the tricuspid annulus in one dimension. It does not incorporate the transverse contribution to ejection fraction of the RV free wall and septum. Therefore, TAPSE may be less accurate in patients with regional differences in RV function.
  • The numerical value may be affected by the angle of the M-mode cursor over the tricuspid annulus.
  • The precise cut-off value of numerical estimation has not been established.
  • A decreased TAPSE is not specific to PE. It may also result from pulmonary hypertension and congestive heart failure [48].


How to Obtain TAPSE

Obtain an apical 4-chamber view of the heart.

Place the M-mode cursor over the lateral aspect of the tricuspid annulus. Measure the distance of the maximal longitudinal displacement. Calculate the average of three consecutive cardiac cycles.


Case 1

In a patient with diagnosed PE who has normal vitals, ECG, and biomarkers, you put the US probe on this patient and find that the TAPSE is 13 mm. He has a sub-massibve PE, so you decide to admit this patient to Stepdown instead of just Telemetry.

Case 2

In a patient with diagnosed PE who has normal vitals, ECG, and biomarkers, you put the US probe on this patient and find that the TAPSE is 14 mm. Given the association between abnormal TAPSE and worse prognosis, you discuss this finding with the patient and convince him that his condition requires admission and closer monitoring, rather than discharge on apixaban and close outpatient follow-up with his Cardiologist.

Bottom Line

TAPSE provides a quantitative value that serves as a surrogate for RV function. It is easy to obtain and reproducible. In patients diagnosed with PE, it can serve as a risk-stratification tool by guiding the decision of whether to administer thrombolytics, and also determining which type of hospital disposition the patient’s condition warrants.


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