Multi-Organ Congestion in Acute Heart Failure – Beyond the Loop

Acute heart failure (AHF) is frequently complicated by diuretic resistance, worsening renal function, and persistent congestion. Increasingly, AHF is recognized as a syndrome of systemic venous congestion affecting the kidneys, liver, and other end organs. Elevated central venous pressure contributes directly to cardiorenal dysfunction and complicates efforts to achieve effective decongestion without precipitating renal injury.

This session will review the mechanisms underlying diuretic resistance, including neurohormonal activation, distal nephron adaptation, and renal venous congestion. Faculty will discuss practical, evidence-based strategies for optimizing decongestion, including sequential nephron blockade and natriuresis-guided therapy, with particular attention to interpreting rising creatinine during treatment and distinguishing hemodynamic changes from intrinsic kidney injury.

Hepatic congestion will be examined within this broader framework of multiorgan dysfunction. Emerging evidence suggests that liver stiffness measurement (LSM), originally developed to assess fibrosis, may serve as a noninvasive surrogate of central venous pressure and a tool for risk stratification in AHF and advanced heart failure populations.

By integrating pathophysiology with practical management strategies, this session will provide clinicians with a physiology-driven approach to decongestion in acute heart failure.

Learning Objectives

• Explain the pathophysiologic relationship between elevated central venous pressure, hepatic congestion, and multiorgan dysfunction in acute heart failure (AHF).
• Interpret liver stiffness measurement (LSM) as a noninvasive surrogate of central venous pressure and assess its prognostic implications in AHF and advanced heart failure populations, including LVAD candidates.
• Integrate an understanding of venous congestion into clinical decision-making, including strategies to overcome diuretic resistance and manage cardiorenal interactions during aggressive decongestion.