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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Why did we ever think ScvO₂ told us what to do in shock? Part 1 of 'Complicated Ways to Learn Very Little' is out on Friday at thedependentvariable.com Sound on....

We have spent decades drawing a pressure gradient from mean systemic pressure (Pms) to right atrial pressure (RAP) and calling it the driver of venous return. Write the equivalent equation on the arterial side and the same logic says Pms is a back pressure that reduces cardiac output. It can’t be both. The Pressure–Volume State Part 2 is now live. thedependentvariable.com/p/f…

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Can VExUS estimate CVP in ventilated children? A new prospective PICU study looked at 56 mechanically ventilated children with simultaneous invasive CVP and ultrasound of the IVC, hepatic, portal and intrarenal veins. The conventional categorical 0–3 VExUS-style score was only moderately good at identifying CVP >12 mmHg: • AUROC 0.74 • Sensitivity 45% • Specificity 98% They also tested a more granular 0–7 score: • Abnormal IVC = 1 point • Hepatic vein = 0–2 • Portal vein = 0–2 • Intrarenal vein = 0–2 This performed much better: • AUROC 0.94 • Sensitivity 82% • Specificity 91% Intrarenal venous Doppler alone had an AUROC of 0.92. The 0–7 score is not yet an established standard. It was proposed and tested in this paediatric study, although a very similar “extended VExUS” approach has also appeared in recent adult work. The useful physiological message is that a more graded description of venous waveform abnormalities may track RAP/CVP better than the usual coarse categorical system. And the bigger point remains: VExUS is principally a readout of the venous pressure/pulsatility environment, not a volume meter. Same CVP does not always mean the same waveform: intrathoracic pressure, abdominal pressure, tricuspid regurgitation, venous compliance and local tissue pressure all modify transmission. Carioca F de L, Franzon NH, Krzesinski LDS, et al. Pediatric Venous Excess Ultrasound Score (P-VExUS): a novel approach to assess central venous pressure in the PICU. Eur J Pediatr. 2026;185(11):855. doi.org/10.1007/s00431-026-0… Interested to hear the thoughts of @ThinkingCC @khaycock2 @NephroP @ross_prager

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The heart supplies the energy for circulation. The flow that results depends on two constraints. The systemic pressure–volume state is one of them. If you’ve ever been confused by 'venous return' terminology, you are not alone. So I went back to first principles. Start with a single elastic container. Build V₀. Add volume. Add compliance. Then show how those pieces determine pressure, where blood resides, and why Pms is the pressure signature of the whole vascular pressure–volume state, not simply a measure of stressed volume. This is the foundation. Part 2 will turn the pump on and asks how that pressure–volume state constrains venous return. thedependentvariable.com/p/t…

Here’s a little follow up. After my first intervention, this is where we are at, with a VTI of 9 to 10. What might I have done? And what might I do next.

A new meta-analysis reports lower mortality with “personalised” fluid resuscitation in sepsis: OR 0.62 (95% CI 0.42–0.93). Impressive – but fragile. Fewer than 1,000 patients contributed to the mortality analysis, mostly from small single-centre trials using very different strategies. Remove any one of 3 influential trials and statistical significance disappears. And there was no clear improvement in RRT, ventilation, vasopressor duration or ICU stay. The useful message isn't “fluid responsiveness saves lives”. It is that fixed-volume fluid prescribing is increasingly hard to justify. Fluid responsiveness tells us whether flow can increase with preload. It does not tell us whether flow needs to increase or whether fluid should be given. New TTT commentary: fluids.info Original paper: Nagy et al., Intensive Care Medicine Experimental

When I started The Dependent Variable, one of my worries was that I might eventually run out of things I wanted to write about. I now have the opposite problem. Already outlined is an article exploring terms such as stressed volume, unstressed volume, compliance, capacitance, venous tone and mean systemic filling pressure. They are closely related. They are often used almost interchangeably. But they are not the same thing. Also mapped out is a six-part series on the way we often over-complicate haemodynamics by measuring or calculating ever more numbers: ScvO₂. The CO₂ gap. P(v−a)CO₂ / C(a−v)O₂. Pulse pressure, diastolic shock index, PPV and SVV. Dynamic arterial elastance: Eadyn = PPV/SVV. Ees/Ea and ventriculo-arterial coupling. For each of them, I want to start from zero (no prior knowledge assumed) work through what the number actually represents, where it comes from, what physiology sits underneath it, and whether it genuinely helps us make better clinical decisions. The aim is to take you from novice to expert without making the subject unnecessarily complicated. Lots more to come from thedependentvariable.com Stay tuned.

How to read a blood gas: Parts 1 and 2 explain the chemistry. But even if you haven’t read them, Part 3 will let you quickly work out what is driving the metabolic component of an acid–base disturbance. Anion gap, albumin, lactate, Story’s method and how opposing effects can hide inside a single base excess. Part 3 is out now and it's free to read. thedependentvariable.com/p/a…

Introducing our growing section editors 👏 This is no solo project! ICU — @iceman_ex POCUS — @icmteaching, @ICUltrasonica & @PARADicmSHIFT EM / PHEM — @emccdoc The experts, shaping the feeds..

The Normosol vs LR result was completely predictable from the chemistry. Lactate and acetate disappear rapidly. Gluconate persists. Once you count the anions that actually remain in plasma, the effective SID of the two fluids converges. Similar bicarbonate and BE was the obvious result. Looking for differences in mortality, dialysis or ventilator days was worse. There is no plausible route from this tiny compositional difference to major clinical outcomes. This is what happens when trials are designed without letting basic physiology veto bad questions. The chemistry is in my latest substack series.

Part 3 of the acid–base series is nearly ready. This is the bedside episode: anion gap, albumin, lactate, Story’s method, and how several metabolic effects can cancel each other out and leave a deceptively simple blood gas. The aim is a practical way to work out what is contributing to the result. If you missed the previous episodes then start with part 1 here: thedependentvariable.com/p/a…

This isn’t another article listing Stewart’s three “independent variables”. It tackles the awkward questions most explanations skip: If lower SID means more H⁺, where does that H⁺ actually come from? If water dissociates, what happens to the OH⁻? Why does low albumin alkalinise if albumin is a buffer? And how can Henderson–Hasselbalch and Stewart both be right? Often we learn the equations without ever quite joining the chemistry together. Part 2 of the series is out now. thedependentvariable.com/p/a…