Determinants of Right Ventricular Performance in Severe Acute Pulmonary Embolism

Severe acute pulmonary embolism (PE) induces hemodynamic compromise due to a failing right ventricle (RV) and a "dry" hyperdynamic left ventricle (LV). RV systolic dysfunction is the key parameter to determine acute PE risk stratification, clinical management, and prognosis. The present study delineates the determinants of RV performance in acute PE resulting in RV dysfunction.

This was a single-center, retrospective analysis of a high-volume PE response team database of patients with intermediate-high-risk or high-risk PE with an echocardiogram prior to escalation of care.

The RV free wall motion (total RVFW motion score = 8.1 ± 2.8) was correlated with the magnitude of RV systolic depression (RV fractional area change [FAC] = 29 ± 13%, tricuspid annular planar systolic excursion = 1.57 ± 0.49 cm, and S' velocity = 10.57 ± 3.14 cm/s). LV preload and stroke volume were markedly reduced (LV end diastolic size = 4.04 ± 0.68 cm and volume = 73.6 ± 25.8 mL; LV stroke volume = 46.2 ± 16.6 mL). LV preload deprivation was correlated with the severity of RV systolic dysfunction (total RVFW motion score, r = -0.11, P = .39; FAC, r = 0.25, P = .04; S' velocity, r = 0.27, P = .03). RV overload induced reversed interventricular septal curvature reflected by LV end diastolic eccentricity index = 1.21 ± 0.21, which correlated with RV systolic dysfunction (total RVFW motion score, r = 0.47, P < .001; FAC, r = -0.35, P < .005; S' velocity, r = -0.43, P < .001) and RV dilation.

Afterload strain imposed by PE may induce severe RV systolic dysfunction attributable to marked RVFW dysfunction. RV systolic pressure generation and transpulmonary flow are generated through systolic ventricular interactions mediated by primary septal contraction and paradoxical septal motion.