Pulmonary wave intensity analysis to assess ventriculo-arterial interactions in cardiogenic shock

Pulmonary wave intensity analysis (WIA) uses pressure and velocity measurements to characterize the type, direction, and timing of energy waves within the pulmonary circulation. Its application to assess ventriculo-arterial (VA) interactions in patients with cardiogenic shock (CS) receiving mechanical circulatory support (MCS) has not been previously described. We hypothesized that forward wave intensity would be reduced in CS, with preserved or augmented reflected wave intensity and/or speed.

In this prospective cohort study, 19 patients with CS requiring MCS were compared with 10 patients with normal pulmonary artery (PA) hemodynamics. PA pressure was measured via right heart catheterization (RHC), and PA flow via Doppler transthoracic echocardiography (TTE). WIA was derived from the product of pressure and velocity change. Statistical significance was defined as p < 0.05.

We studied 19 CS patients (54 ± 9 years, 17 male) and 10 controls (52 ± 16 years, 7 male). Compared with controls, CS patients had lower LVEF (16 ± 7 vs 50% ± 15%), lower RV FAC (21 ± 11 vs 39% ± 13%), and higher PCWP (25 ± 10 vs 9 ± 4 mmHg; all p < 0.01). CS was associated with more negative net wave intensity (-0.05 ± 0.07 vs -0.02 ± 0.02) and higher wave speed (7.1 ± 7.4 vs 1.8 ± 1.0 cm/s; both p < 0.05). Following MCS initiation, peak backward compression wave timing was delayed (0.13 ± 0.07 vs 0.17 ± 0.05 s, p = 0.048). IABP support was associate with increased forward decompression wave magnitude (p = 0.04) and reduced reflection index (p = 0.046), whereas Impella 5.5 delayed backward compression wave return (p = 0.03), without consistent changes in mPAP or PVR. WIA parameters demonstrated associations with LVEDV (BDW: R² = 0.13, p = 0.02), LA volume (BCW: R² = 0.23, p < 0.01), RV EDA (BCW: R² = 0.31, P < 0.01), TAPSE (R² = 0.08, p = 0.08), and inotrope dose (dobutamine: NWI R² = 0.30, p = 0.02; milrinone: TTP R² = 0.37, p < 0.01).

In CS, net wave intensity was more negative, and wave speed increased. MCS was associated with changes in forward and reflected wave characteristics, consistent with altered RV-pulmonary arterial coupling. WIA parameters were associated with structural and functional cardiac measures and reflected physiologic changes not consistently captured by conventional hemodynamic or echocardiographic indices. These exploratory findings warrant validation in larger prospective cohorts.