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

## TL;DR

This paper redefines critical closing pressure in shock, showing it as a binary threshold for vessel collapse rather than a continuous pressure, explaining why traditional metrics like MAP can be misleading.

## Contribution

The paper reframes critical closing pressure as a binary collapse threshold, resolving contradictions in shock physiology and offering a new model for personalized perfusion management.

## Key findings

- Critical closing pressure is a threshold for vessel collapse, not a continuous downstream pressure.
- Perfusion becomes heterogeneous as different vascular beds collapse at different pressures.
- Systemic variables like MAP may appear normal even when tissues are under-perfused, causing haemodynamic incoherence.

## Abstract

Critical closing pressure (CCP) and the vascular waterfall have long been used to explain perfusion failure in shock, yet their physiological meaning has been inconsistently interpreted. CCP is frequently treated as a continuous downstream pressure and inserted into formulas such as mean arterial pressure (MAP) − CCP, implying that a collapse threshold behaves like an opposing pressure even when vessels remain open. Drawing on classical vascular mechanics, whole-bed flow studies, microvascular models, and contemporary clinical physiology, we show that this interpretation is incorrect. Tone-dependent arteriolar collapse does not behave as a Starling resistor: CCP is a threshold at which smooth-muscle tension exceeds intraluminal pressure and vessels close, not a pressure governing flow in patent vessels. Perfusion becomes heterogeneous because different vascular beds reach their collapse thresholds at different pressures (via excessive tone, extrinsic compression, or profound hypotension), disconnecting macro-haemodynamics from microcirculatory flow. This explains why systemic variables such as MAP and systemic vascular resistance (SVR) may appear adequate even while tissues are under-perfused, a phenomenon now termed haemodynamic incoherence. Reframing CCP as a binary collapse threshold resolves longstanding contradictions in the literature, clarifies why MAP-centred targets often fail, and unifies the behaviour of shock states within a four-interface model of circulatory coupling. Therapeutically, the aim is not to “restore a waterfall” but to reopen closed vascular territories by lowering excessive tone, relieving external pressure, or raising truly low arterial inflow. This mechanistic reinterpretation provides a more coherent, physiologically grounded approach to personalised perfusion management in critical illness.