Right Ventricular-Pulmonary Artery Pressure Relationship in Experimental Acute Lung Injury

Monday, March 23, 2026

2:30 PM - 3:30 PM Central Time

Location: Connections Central - RST 12

Rima Othman, MD (she/her/hers)

Johns Hopkins University, Maryland

Disclosure(s): No relevant financial relationship(s) to disclose.
MC

Mingfeng Cao, N/A

Doctoral Candidate
Johns Hopkins University

Disclosure information not submitted.
IW

Ian Woodward, phD

Staff Engineer
Johns Hopkins University

Disclosure information not submitted.
YA

Yousra Ahmed, MBBS

Postdoctoral Research Fellow
Johns Hopkins University

Disclosure information not submitted.
Mm

Madison malfitano, MD

Postdoctoral Research Fellow
Johns Hopkins University

Disclosure information not submitted.
KL

Kelley Leadingham, N/A

Staff Engineer
Johns Hopkins Hospital

Disclosure information not submitted.
QW

Qihong Wang, MBBS

Senior Researcher
Johns Hopkins University

Disclosure information not submitted.
SK

Steven Keller, MD, phD

Primary Investigator
Johns Hopkins Hospital

Disclosure information not submitted.

Introduction: The right ventricular–pulmonary artery (RV–PA) relationship is a key determinant of cardiopulmonary function, particularly during increased pulmonary vascular load. In acute lung injury (ALI), the right ventricle experiences abrupt increases in afterload due to elevated pulmonary vascular resistance (PVR), risking right ventricular (RV) failure. Understanding hemodynamic changes in ALI is critical to develop RV-protective strategies.

Methods: A large-animal swine model was used to study RV–PA hemodynamics during ALI. Sepsis-induced ALI was simulated via intravenous lipopolysaccharide (50 µg/kg over 30 minutes). Hemodynamic parameters—including RV pressures, cardiac output, central venous pressure, and pulmonary artery (PA) pressure—were recorded using high-fidelity catheterization and synchronized data acquisition systems. Key metrics included pulmonary artery pulsatility index (PAPi) and transpulmonary vascular pressure gardient (TPVG).

Results: In this representative swine study of LPS-induced ALI, pulmonary artery pulsatility index (PAPi) decreased progressively from baseline (0.72) to 0.41 at 120 minutes post-injury, suggesting impaired right ventricular function. TPVG increased substantially from baseline (32 mmHg) to a peak of 48 mmHg at 120 minutes, indicating elevated pulmonary vascular resistance. These combined metrics reflect worsening RV afterload and compromised pulmonary hemodynamics over time, consistent with progressive lung injury severity.

Conclusions: ALI significantly disrupts RV–PA coupling and increases pulmonary vascular load. In this septic model, RV efficiency deteriorated markedly, underscoring the vulnerability of the right heart in early ALI. These findings highlight the need for integrated cardiopulmonary monitoring and support the use of RV-protective strategies in critical care settings.