Clinically:

  • Massive PE – systemic hypotension with a systolic pressure <90mmHg, shock or cardiac arrest. Estimated mortality of 60% within first hour.
  • Sub-massive PE – normotension with imaging or enzyme evidence of RV dysfunction. Associated with 30 day mortality of 15-20%. Associated with development of cor pulmonale secondary to chronic thromboembolic PHT.
  • Non-massive PE – normotension without evidence of RV dysfunction.

Acute PE leads to acute rise in PVR.

May also be associated with pro-inflammatory state within RV.

Echo findings do not necessarily give true anatomic approximation of the RV but it does provide information of those at risk of deterioration.

CTPE required to assess clot burden.

Assessment:

2D – thrombus may be visualised in the right heart or proximal pulmonary arteries.

Acute cor pulmonale will result if large enough PE (usually >25% of pulmonary vascular tree obstruced):

  • RV dilatation present in over 25% of patients with PE.
  • RV-LV diameter ratio of >0.9.
  • TR Vmax & PG. In acute PE – PA pressures will usually not exceed 50mmHg.
  • 60-60 sign – pulmonary acceleration time (PAT) of <60ms with a PASP <60mmH Cg. Can be ~94% specific for PE.
  • May also see notching of PAT trace.
  • McConnell’s sign – regional RV dysfunction with apical sparing. Less reliable as has been reported in acute right ventricular infarction.
  • May see right to left shunting through PFO. Associated with increased mortality.