Low perfusion in heart failure is often concealed at discharge and reflects discordance across hemodynamic layers, requiring structured assessment to guide therapy and prevent early relapse.
Heart failure clinicians are trained to treat congestion. We look for jugular venous distention, rales, orthopnea, and the “wet” clinical narrative that unfolds before us 1. Congestion is visible, actionable, and immediately rewarding; with diuresis, symptoms improve, and discharge becomes feasible. Contrastingly, low perfusion is often framed as a late-stage finding, synonymous with hypotension, shock, or the need for inotropes. In practice, hypoperfusion exists along a continuum that begins earlier, frequently without overt hypotension, and may persist even when congestion appears “resolved” 2. This mismatch – between the importance of perfusion and how inconsistently we evaluate it – remains a persistent gap in everyday heart failure care.The core reason low perfusion is often missed is conceptual. “Perfusion” represents layered physiology rather than a single measurable variable. At the macrocirculatory level, flow is inferred from blood pressure (BP) patterns, pulse pressure, or measured cardiac output. At the organ level, clinicians read the body’s ledger – renal function trajectory, mentation, liver enzymes, lactate, and urine output – signals that reflect supply-demand balance rather than flow alone. At the peripheral and microcirculatory levels, assessment relies on skin temperature, capillary refill, temperature gradients, and plethysmography-derived indices that integrate flow, vascular tone, and sympathetic activation. Crucially, these layers often disagree. Systolic pressure may be preserved through vasoconstriction while sacrificing peripheral – and occasionally renal – perfusion. Conversely, a patient may appear warm with acceptable vitals yet remain “functionally cold” because microvascular flow is impaired or vascular tone is pathologically elevated. When hypoperfusion is defined solely by hypotension, it is systematically underestimated 3.The operational reality further reinforces this problem. Congestion establishes bedside grammar, whereas perfusion does not. Many signs of impaired perfusion are subjective (e.g., cool extremities), environment-dependent, or poorly standardized (e.g., capillary refill assessment). Objective surrogates can also be difficult to incorporate into routine care: lactate is not drawn from every stabilized patient, invasive hemodynamics are limited, and echocardiography – although informative – is not easily repeated as a serial monitoring tool. This result is paradoxical: clinicians recognize the importance of low perfusion, yet lack a simple, repeatable signal that integrates into routine discharge workflows.Contemporary patient populations also include cases of concealed hypoperfusion. Older patients and those with heart failure with preserved ejection fraction (HFpEF), or high systemic vascular resistance may have preserved BP despite marginal forward flow. Atrial fibrillation, anemia, peripheral arterial disease, and autonomic dysfunction further blur bedside perception. In such settings, hypoperfusion may not be declared until after discharge owing to early deterioration or recurrent admission. Therefore, the peri-discharge window is an optimal time to refine perfusion assessment because apparent clinical improvement may obscure limited physiologic reserve. A pragmatic approach is to conceptualize perfusion assessment as a triad and focus on reconciling discordances rather than seeking a single definitive measure 4.1.Macro-circulation (“Can the pump deliver?”): BP, pulse pressure, and, if available, cardiac output/cardiac index – necessary but insufficient because compensation can preserve pressure despite impaired flow.2.Organ perfusion (“Are organs supplied?”): renal function trajectory, mentation, transaminases, lactate/acid-base status, urine output – clinically relevant outcomes but often appear late and can be confounded by other factors.3.Peripheral/microcirculation (“What does the periphery show?”): skin temperature patterns, capillary refill, plethysmographic, or thermal indices – early and repeatable, but sensitive to vascular tone and environmental conditions.Hypoperfusion becomes apparent easily when all three layers align. When they diverge, the discordance signals limited physiologic reserves and should prompt a more cautious discharge strategy. This layered framework and pragmatic peri-discharge workflow are summarized in Figure 1.Kasai and Kawasaki 5 are notable for advancing perfusion assessment toward a simple bedside metric by evaluating a finger plethysmography-derived perfusion index (PI) measured shortly before discharge in patients hospitalized with acute heart failure. Under standardized conditions, a low PI identified a higher risk group for post-discharge events, with prognostic performance comparable to a clinically defined “cold” profile. The key contribution is not that PI diagnoses hypoperfusion, but that a periphery-facing, quantitative signal can serve as an implementable risk stratifier at discharge – precisely when concealed hypoperfusion is most clinically relevant.What should change when hypoperfusion is suspected near discharge? First, residual congestion must be assessed. Cool extremities may partially reflect unresolved venous congestion and elevated filling pressures. When hypoperfusion is suspected, clinicians should evaluate orthopnea, lung findings (or ultrasonography), jugular venous distention, net diuresis, weight trajectory, and natriuretic peptide trends. By explicitly assessing congestion and perfusion, the immediate therapeutic target can be clarified as “wet” (residual congestion) or “cold” (true hypoperfusion) 6, 7. Second, therapy should be reconciled with physiology. Hypoperfusion signals should trigger structured medication and volume reviews, rather than reflex escalation to inotropes 8. Has diuresis been excessive? Is the vasodilator burden too high for the patient’s forward-flow reserve? Is bradycardia or uncontrolled tachyarrhythmias limiting the output? Can anemia, infection, or thyroid disease increase metabolic demand? Is peripheral arterial disease distorting the interpretation of peripheral metrics? This is where perfusion assessment becomes actionable: it identifies patients whose discharge regimen requires adjustment rather than simple continuation. Third, the post-discharge safety net should be strengthened even when symptoms improve. Residual hypoperfusion should be interpreted as a marker of vulnerability, not stability. This does not mandate aggressive inpatient intervention but often warrants a safer outpatient trajectory 9, including earlier follow-up, clear diuretic titration plans, prompt laboratory reassessment, remote monitoring when feasible, and education that enables rapid self-recognition of relapse. Finally, when hypoperfusion persists despite apparent decongestion and acceptable BP, the underlying phenotype should be revisited 10. Potential contributors include HFpEF with elevated afterload, hypertrophic or restrictive physiology (including amyloidosis), right ventricular failure, significant valvular disease, pulmonary hypertension, and recurrent atrial arrhythmias. In such patients, peripheral signals may reveal what routine vital signs conceal, indicating limited forward-flow reserve.If peripheral quantitative signals enter routine practice, the next step is not to perfect a single number but to standardize the habit of measurement: specify conditions, understand within-patient variability, and define what constitutes a meaningful change, particularly in phenotypes where BP may mislead (HFpEF, atrial fibrillation, anemia, and peripheral vascular disease) 11. Crucially, future work should test whether a perfusion-informed discharge strategy – including tight-loop follow-up, explicit diuretic adjustment rules, and early laboratory reassessment – can prevent early relapse rather than merely predicting it 9.Risk markers are most valuable when they inform decisions. The central message is simple: low perfusion is not synonymous with hypotension; it reflects discordance across hemodynamic layers and is often concealed at discharge. Congestion remains the visible half of heart failure physiology, but outcomes may depend on whether we also recognize, and act upon, the invisible half.T.O. and S.Y. are affiliated to a department sponsored by Medtronic (Japan). T.O. received research grants from Pfizer Japan, Alnylam Japan Pharmaceuticals, and Alexion Pharmaceuticals, and lecture fees from AstraZeneca, Pfizer Japan, Alnylam Japan Pharmaceuticals, and Toa Eiyo, which were not connected to this work. H.H. received research grants from Konica Minolta, Inc., the Konica Minolta Science and Technology Foundation, and the Kowa Life Science Foundation. T.M. has received honoraria from Bayer, Daiichi Sankyo, Dainippon Sumitomo Pharma, Kowa, MSD, Mitsubishi Tanabe, Nippon Boehringer Ingelheim, Novartis Pharma, Pfizer Japan, Sanofi, and Takeda Pharma, which are also unrelated to this work. Dr. T.O. was a member of the journal’s Editorial Board at the time of submission.This article was not supported by any sponsor or funder.T.O. drafted the manuscript. H.H., S.Y., and T.M. critically revised the manuscript for important intellectual content.
Okumura et al. (Wed,) conducted a editorial in Heart failure. Perfusion assessment was evaluated. Low perfusion in heart failure is often concealed at discharge and reflects discordance across hemodynamic layers, requiring structured assessment to guide therapy and prevent early relapse.