Sameed M
5.6K posts
@_MSAMEED
Pulmonary & Critical Care @ClevelandClinic. #FOAMed. 🏴🇵🇰🇺🇸Tweets reflect my personal opinion. Director ILD clinic @JeffHealthEH @WeAreJefferson
Today at 3pm at The Learning Studio in the Networking Super Center, join us for a session targeted towards transitions in training for IMGs @atscommunity @atsearlycareer #ats2026
Why critical closing pressure (CCP) always felt wrong For years, I found CCP papers confusing — not because the idea of vessel collapse is wrong, but because CCP was often treated as something that exists all the time, as if it continuously governs perfusion in normal, open-flow states. That framing immediately caused problems and led to some very strange ideas. CCP was frequently presented as a downstream opposing pressure — something to subtract from MAP. Hence formulas like tissue perfusion pressure (TPP) = MAP − CCP. But a collapse threshold cannot be a back-pressure. CCP is only relevant once arterioles have collapsed. CCP was also used to explain autoregulation, even though autoregulation occurs in proximal arterioles at much higher pressures than those at which CCP becomes relevant in distal arterioles. CCP − Pms was then used to describe capillary perfusion, even though a collapse threshold cannot be an input pressure. This is simply a category error. CCP marks the point at which arterioles close. Above that point, flow is governed by ordinary arterial–venous pressure gradients and arteriolar tone — not by CCP. A waterfall analogy — developed for passive collapsible tubes (veins, zone-1 lung) — was exported into arteriolar physiology. But arterioles are not floppy veins. They possess active smooth-muscle tone, making them functionally open or closed, in a way veins are not. A true waterfall would make venous pressure irrelevant for organ blood flow — which it plainly is not. And here lies the central contradiction: If capillary perfusion were governed by CCP − Pms, how could there simultaneously be a “waterfall” in which venous pressure does not matter? The framework collapses under its own assumptions. From this came papers proposing that we might manipulate — even widen — waterfalls, which would in fact imply closing off more vascular beds rather than improving perfusion. In healthy physiology, there should be no collapse and no waterfall. None of this fits with clinical observation: • Raising MAP does not reliably restore perfusion • SVR does not reliably reflect tone • Oedema and venous congestion clearly impair organ blood flow • Monitors can reassure while tissues suffer The problem was never CCP. The problem was how it was framed. Active arteriolar closure was conflated with passive Starling-resistor behaviour. In reality, CCP is a conditional collapse threshold: vessels are either open or closed. It is not continuously “acting” when flow is normal. Once those ideas are separated, the contradictions disappear. CCP stops adding confusion and instead explains haemodynamic incoherence. CCP always felt wrong because it was being asked to do jobs it was never meant to do. Used correctly, it simplifies physiology — and supports genuinely personalised care. And that leads to the most important practical point: What matters clinically is restoring flow continuity across the macro-to-micro interface — reducing excessive tone, relieving external or venous constraint, and avoiding pressure strategies that worsen collapse rather than reopen closed beds. That is what CCP is actually useful for and why it finally makes sense. Read our full paper here 👇 @ThinkingCC @khaycock2 @EMNerd_ mdpi.com/2075-4426/16/2…
