#FUSIC Haemodynamics National Lead. ICS trustee. BSE level 2. BJJ ⬛️⬛️🟥⬛️ @Turningthe_Tide #foamed #pocus #haemodynamics

United Kingdom
I’ve started a Substack: The Dependent Variable. X is great for short-form discussion, but it’s not ideal for building a coherent archive. This will be the home for longer-form writing on cardiovascular physiology, haemodynamics, fluids, shock, ultrasound and critical care reasoning. All in one place, easier to follow and return to. First post: open.substack.com/pub/icmtea…
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Twenty years ago, someone handed me a photocopied article about Stewart’s approach to acid–base. I needed an explanation that started several steps earlier. So I’ve written one. Whose hydrogen is it anyway? From first principles to the disorders a normal pH can hide. thedependentvariable.com/p/a…
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Here @Turningthe_Tide, we discuss Bozeat et al's paper on whether crystalloid still belongs in the first hours of trauma haemorrhage - When fluid has a job - When it does not - How permissive hypotension and vasopressors fit - Why “the bag is already up” is not an indication. #FOAMed #FOAMcc fluids.info/members/articles…
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The Surviving Sepsis Campaign has shaped sepsis care for decades. But do some of its core recommendations now lag behind the physiology and the evidence? Rory Spiegel @TheEMNerd led this new dissenting opinion, which I was very pleased to contribute to. We challenge: • fixed 30 mL/kg fluid loading • chasing lactate with fluid • fluid responsiveness as a sufficient reason to give fluid • pressure-centric resuscitation • the omission of POCUS from modern haemodynamic assessment • rigid bundle-driven care The argument is not for less treatment. It is for more individualised, physiology-driven treatment of shock. authors.elsevier.com/c/1npdk… The 2026 Surviving Sepsis Campaign Guidelines: The dissenting opinion Spiegel et al. AJEM, just published.
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Next up on The Dependent Variable: a two-part dive into acid–base physiology. Not Stewart versus Henderson–Hasselbalch. Both can be correct. The more interesting question is: Which variables are independent, which are dependent, and which equations are simply different descriptions of the same chemical state? We’ll get into: • why hyperchloraemia acidifies • what SID actually represents • why bicarbonate can raise pH even when the Na–Cl gap barely changes • what is actually happening to H⁺ • and why this is not simply a story of water dissociating into H⁺ and OH⁻ The aim is to make difficult physiology simple without making it less true. If that sounds like your kind of thing, subscribe here: thedependentvariable.com Part 1 coming soon.
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Every 5-years the SSC publishes their updated guidelines, and every 5-years we pen our dissenting opinion. Just published in AJEM our respectful dissent. sciencedirect.com/science/ar…
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High praise (exaggerated I think) from one of the greatest POCUS educators of our time 🙌🏻
. @icmteaching, one of the greatest hemodynamic educators of our time, gives a fantastic talk on circulation - making pressures, volumes, and all the other confusing stuff feel simple and intuitive. #HR26
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An IV-fluid shortage accidentally created a fascinating experiment. Nearly 39,000 operations. Intraoperative crystalloid use ↓ 75%. What happened? AKI: 2.5% → 2.5% No meaningful increase in hypotension, vasopressor use, respiratory complications or major cardiovascular events. Urine output fell but kidney injury didn't increase. And the proportion of operations receiving no crystalloid at all rose from 6.7% to 28%. This isn't an RCT and doesn't prove that giving less fluid is better. But when scarcity forced clinicians to ask whether each bag was really necessary, they managed to give dramatically less without an obvious signal of harm. Perhaps the most interesting question isn't “How restrictive should perioperative fluids be?” It's: How much of what we normally give was necessary in the first place? New TTT commentary: fluids.info
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💗Want to keep your finger on the pulse of critical care? 📑Tired of 40 tabs, dying inboxes and trawling journals at 23:00 after a night shift? 👏Here’s the solution🤷‍♂️ And it’s free🆓 Constant. Live. Updating 📈📉 👇 icuwaveform.grok.me/ #FOAMed #FOAMcc #POCUS #CriticalCare
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Afterload is not SVR. It is not simply arterial pressure. And the same arterial load does not impose the same myocardial load on every heart. In this week’s The Dependent Variable: – why the ventricle really does eject against pressure – why resistance matters because it dissipates energy – why geometry changes wall stress – why Ea is only a lumped descriptor – why coupling matters more than any single number Afterload is not the hill. It is the mechanical burden of climbing it. thedependentvariable.com/p/t…
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Blood pressure is not afterload. SVR is not afterload. And the same arterial load does not impose the same burden on every heart. Coming Monday at 12.00 GMT. Everything you need to know about afterload in a way you can understand. Free to read on thedependentvariable.com
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Two new studies this week look at predicting fluid responsiveness. A meta-analysis found changes in EtCO₂ during preload challenge had reasonable diagnostic accuracy: Sensitivity 75% Specificity 85% SROC AUC 0.87 A second small study found IVC collapsibility predicted an increase in stroke volume reasonably well, while renal resistive index did not. Useful? Potentially. But neither answers the question clinicians often quietly substitute for “fluid responsiveness”: Should I give this patient fluid? Fluid responsiveness means cardiac output rises when preload rises. It does not mean: • the patient is hypovolaemic • cardiac output is inadequate • organ perfusion will improve • IV fluid is the best intervention • more volume is safe • the patient “needs fluid” A patient with pulmonary oedema and developing systemic venous congestion may still be fluid responsive. • The better sequence is: • Is there a clinical problem that increasing flow might improve? • Can flow increase if preload rises? • Is IV fluid the safest way to achieve that? • Did the patient actually improve? • Should we stop? The monitor may tell us whether cardiac output can rise. It cannot tell us that another bag of fluid should be prescribed. New TTT Evidence Watch: fluids.info
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Only a handful of spots left. Closing registration tonight, if anyone forgot or was on the fence, this is your chance! Bedside applied physiology in shock and respiratory failure at it’s very best. Magder/Marino/Crager/Denault/Weingart/Augustin/Miller/Spiegel/Haycock hrpresents2026.squarespace.c…
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For logistics and organizational purposes, we will close the virtual registration tonight and the in-person on sunday september 12th midnight. So if anyone was dragging their feet to attend #HR2026, now is the time! We are super excited for next week! Planning the workshops, etc, and we may even get CME for the VExUS and Hemodynamic Course in time as a bonus for those registered! (we do have CME for the main conference, naturally!) hrpresents2026.squarespace.c…
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I’ve been so excited about this one!
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Preload is what drives cardiac output, right? Give fluid → increase preload → move up the Frank–Starling curve → increase stroke volume → increase cardiac output. But yet… Why can an almost empty heart contract violently? Why can a small hyperdynamic ventricle sit inside a circulation with a cardiac output of 10 L/min? And what is Frank–Starling actually doing if it isn’t simply “more preload → more cardiac output”? What determines how much additional volume the heart can tolerate before filling pressure rises sharply? Coming soon on thedependentvariable.com: The Preload Problem.
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