Arteriolar Collapse and Haemodynamic Incoherence in Shock: Rethinking Critical Closing Pressure.

Area of Science:

• Physiology
• Critical Care Medicine
• Vascular Biology

Background:

• Critical closing pressure (CCP) and vascular waterfall concepts are used to explain shock-related perfusion failure.
• Current interpretations treat CCP as a downstream pressure, leading to flawed hemodynamic calculations.
• This has resulted in inconsistent understanding and application in clinical practice.

Purpose of the Study:

• To re-evaluate the physiological meaning of CCP and its role in perfusion failure.
• To demonstrate that CCP is a binary collapse threshold, not a continuous pressure.
• To propose a revised model for understanding circulatory coupling and shock states.

Main Methods:

• Analysis of classical vascular mechanics.
• Review of whole-bed flow studies and microvascular models.
• Integration of contemporary clinical physiology and research.

Main Results:

• CCP represents a threshold where smooth muscle tension surpasses intraluminal pressure, causing arteriolar collapse.
• Vessel collapse is tone-dependent and occurs heterogeneously across vascular beds at different pressures.
• This heterogeneity disconnects macro-hemodynamics from microcirculatory flow, leading to "hemodynamic incoherence."

Conclusions:

• Reframing CCP as a binary collapse threshold resolves contradictions in shock physiology.
• This mechanistic reinterpretation clarifies why MAP-centered targets often fail in critical illness.
• Therapeutic strategies should focus on reopening collapsed vessels rather than restoring a "waterfall."