Hypoperfusion-Shock Continuum in Acute Decompensated Heart Failure.

Authors

Tijmen H Ris, Tim Balthazar, Paul Knaapen, Mariëlle C van de Veerdonk, Alexander Nap

Published in

Circulation. Heart failure. Volume 19. Issue 9. Pages e013797. Epub Sep 15, 2026.

Abstract

Acute decompensated heart failure is a clinical syndrome characterized by upregulation of neurohormonal compensatory mechanisms that, while intended to preserve organ perfusion as a response to reduced cardiac output, progressively exacerbate systemic congestion. Perfusion, defined by adequate oxygen delivery to the tissues, is more complex than simple cardiac output and arterial inflow, and is also significantly influenced by venous backpressure, as well as microcirculatory autoregulation. Therefore, as venous pressures continue to rise, these may ultimately contribute to hypoperfusion and, therefore, cardiogenic shock (CS). Other mechanisms, such as inflammation and increased organ capsular pressure, can contribute to further impairments in tissue oxygenation. This gradual and often clinically unrecognized deterioration from acute decompensated heart failure to heart failure-related CS (HF-CS) contrasts with acute myocardial infarction-related CS, where underlying compensatory mechanisms are more limited. Furthermore, prolonged and unrecognized hypoperfusion may further worsen HF-CS through progressive microcirculatory dysfunction with subsequent uncoupling of macrocirculation and microcirculation. At this point, normalization of macrocirculatory parameters may no longer restore tissue oxygenation. Early identification of hypoperfusion is, therefore, critical so that interventions targeting systemic hemodynamics may still improve tissue perfusion and reverse circulatory collapse. This review (1) outlines the pathophysiology of hypoperfusion in HF-CS; (2) summarizes invasive, biochemical, and imaging parameters to detect hypoperfusion; (3) phenotypes HF-CS profiles; and (4) proposes a monitoring framework for hypoperfusion in HF-CS.

PMID:
42743336
Bibliographic data and abstract were imported from PubMed on 16 Sep 2026.

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