Blood flow in the circulation may be governed by a threshold defined by critical closing pressure rather than a simple arterial–venous pressure gradient, according to a narrative review.
The review synthesizes physiological models, experimental data, and clinical observations to describe the “vascular waterfall” framework, in which flow depends on the difference between arterial pressure and critical closing pressure (Pcrit), with Pcrit acting as the effective downstream pressure, rather than downstream venous pressure. Drawing on prior studies in patients with shock and those receiving mechanical ventilation, the researchers outline how this model may apply to bedside hemodynamic assessment and therapy.
Across the evidence reviewed, when intravascular pressure falls below Pcrit, vessels partially collapse and flow becomes independent of downstream pressure. In this state, Pcrit functions as the effective backpressure, and perfusion depends on maintaining arterial pressure above this threshold. The authors describe how Pcrit and mean systemic filling pressure (Pmsf) can be estimated indirectly using pressure–flow relationships derived from bedside maneuvers and cardiac output curves.
In patients with vasoplegic shock, reduced vascular tone lowers Pcrit toward Pmsf, effectively abolishing the vascular waterfall and impairing autoregulation. Observational data cited in the review suggest norepinephrine improved perfusion only when it increased Pcrit more than Pmsf, restoring the pressure gradient required for flow. In these studies, Pcrit increased to about 40 mmHg in responders compared with about 20 mmHg in nonresponders, despite similar increases in mean arterial pressure.
The framework also explains hemodynamic effects during mechanical ventilation. Elevated alveolar and pleural pressures can act as external closing pressures, shifting pulmonary blood flow patterns and reducing venous return. High levels of positive end-expiratory pressure may convert regions of partial flow dependence into complete flow cessation, increasing right ventricular afterload and reducing cardiac output.
The authors note that interventions such as fluids, vasopressors, and ventilator settings may alter arterial pressure, Pcrit, and Pmsf in different directions. As a result, increases in mean arterial pressure alone may not improve perfusion if the underlying pressure gradient is not restored.
The review is limited by its narrative design and reliance on heterogeneous prior studies rather than a single data set. The vascular waterfall model assumes steady-state conditions and a relatively stable Pcrit, although both may vary dynamically in patients with sepsis, trauma, or other forms of shock. In addition, Pcrit cannot be measured directly and must be estimated using indirect methods that rely on simplifying assumptions.
“Blood flow may become independent of downstream pressure,” wrote Ricardo Castro, of Pontificia Universidad Católica de Chile, and colleagues, emphasizing that perfusion is governed by upstream pressure relative to Pcrit rather than venous pressure alone.
Disclosures: The authors reported no competing financial interests.
Source: Journal of Critical Care
