Key result
Femoral pressure-derived effective arterial elastance correlates strongly with invasive reference measurements across shock states.
Why the study?
The accuracy of a simplified bedside formula for estimating effective arterial elastance in cardiogenic shock with rapidly evolving hemodynamics remained unknown.
Does a simplified bedside formula using femoral arterial pressure and stroke volume accurately estimate effective arterial elastance compared to invasive PV analysis in a porcine model of ischemic cardiogenic shock?
Does a simplified bedside formula using femoral arterial pressure and stroke volume accurately estimate effective arterial elastance compared to invasive PV analysis in a porcine model of ischemic cardiogenic shock?
Effect estimate: r = 0.72 (95% CI 0.58-0.82)
Absolute Event Rate: 2.04% vs 2.03%
p-value: p=<0.001
A simplified bedside formula using femoral arterial pressure and stroke volume reliably estimates effective arterial elastance in a porcine model of ischemic cardiogenic shock, potentially enabling continuous afterload monitoring without left ventricular catheterization.
Bedside Ea estimation may inform afterload management in ischemic CS; leaves open its impact on outcomes versus invasive measures.
Background During ischemic cardiogenic shock (CS), increased afterload overburdens the damaged myocardium and may worsen outcomes. The measure, effective arterial elastance (Ea), integrates systemic vascular resistance, arterial compliance, and heart rate, and reflects left ventricular (LV) afterload. While Ea is traditionally derived from invasive LV pressure–volume (PV) analysis, a simplified bedside formula (0.9 × systolic arterial pressure/stroke volume) has been validated in stable intensive care patients. Its accuracy in CS, characterized by rapidly evolving hemodynamics, remains unknown. Methods In total, 20 female Danish Landrace pigs were instrumented with a femoral arterial catheter, pulmonary artery catheter (PAC), and LV PV catheter. CS was induced by microsphere embolization of the left main coronary artery. Ea was estimated from femoral arterial pressure and stroke volume measured with the PAC and compared with PV-derived Ea as a reference. Ea was measured at healthy baseline, CS onset, 60 minutes of untreated CS and after a dobutamine infusion. Agreement was evaluated with Pearson correlation and Bland–Altman analysis. Results At baseline, onset of CS, and at established CS, correlations between the estimated and the PV-derived Ea remained strong ( r = 0.68–0.74, all P ≤ 0.002). During dobutamine infusion, correlation persisted ( r = 0.63, P = 0.020). Bland–Altman analysis showed negligible bias at healthy baseline and CS onset, slight underestimation during established CS, and modest overestimation during dobutamine-treated CS, with the widest limits of agreement observed during established untreated CS. Conclusions Estimated Ea reliably reproduced PV-derived Ea during disease states. This simple bedside measure may enable continuous monitoring of afterload in ischemic CS without LV catheterization.
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Hørsdal et al. (2026) studied Ischemic cardiogenic shock (n=20). Estimated effective arterial elastance (femoral pressure-derived) vs. Invasive LV pressure-volume derived effective arterial elastance was evaluated on Agreement between estimated and reference effective arterial elastance (Ea) (r = 0.72, 95% CI 0.58-0.82, p=<0.001). Estimated effective arterial elastance derived from femoral pressure reliably reproduced invasive pressure-volume derived measurements across healthy and cardiogenic shock states (r = 0.72).
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