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Shock is complex. But our tools are often simplistic.
This paper proposes a new model:
🩸 Four circulatory interfaces that must stay coupled to maintain perfusion.
Uncouple any one — and shock worsens.
#Shock #MedX #FOAMcc
Here’s the framework.
🔗 doi.org/10.3390/jpm150… 2/
🔧 The model outlines 4 key interfaces:
1. LV to systemic arterial
2. Arteriolar to capillary
3. Capillary to venular
4. RV to pulmonary arterial

Each can be assessed. Each can fail. And each demands tailored therapy.

🧵 Starling’s Law: Misunderstood, Misapplied, and Still Misleading
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🚨 “Starling’s Law explains how the heart increases cardiac output.”

You’ve probably heard this a thousand times.
But it’s wrong.
Or at least - very incomplete.
Let’s fix it.
Because this matters - for heart failure, fluids, vasopressors, inotropes, afterload, and how we think about the whole system. 2
🫀 Textbook Starling curves show:

Preload (RAP or EDV) on the x-axis
Cardiac output on the y-axis
Upward shifts with “more inotropy” or “less afterload”
❌ But that’s not how the system really works.
Because in a real circulation, the system sets flow - not the heart.

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Most people think the heart drives circulation.
But what if that’s backwards?
Anderson’s model flips the whole idea of cardiac output on its head — and it changes how you think about fluid, flow, and failure.
🧵👇
#physiology #FOAMed #MedTwitter #criticalCare #cardiacOutput 2/
🚿The system sets the flow based on metabolic need.
It adjusts vascular tone and volume to change Pms (mean systemic pressure) and venous return.
The heart simply ejects what arrives — unless it fails.

Thanks for some great comments on this thread. Some nuance and further explanation is needed here.
Being ill activates the symp NS. I’m sure you have all noticed being tachy and having a bounding pulse when you have flu or are hungover! CO goes up to meet ⬆️ metabolic demand.

https://twitter.com/icmteaching/status/1788893274591088875

Sepsis of course is the same and can result in a ⬆️or ⬇️ cardiac output. The key factor is the balance between sepsis causing venoplegia (reducing Pms) and the sympathetic response trying to counter this (which increases Pms and HR).

#haemodynamics #hemodynamics myths.
Myth 1.
'Sepsis causes low SVR and high stroke volume/CO' This is a common misconception. Why? Because the moment a sick patient comes anywhere near a health care provider they get fluid boluses.

Post holiday season, @ICUltrasonica, @wilkinsonjonny & I are back to take you through the most most critical clinical questions on #haemodynamics that ultrasound can answer

We’re now on to question 3 of FUSIC HD

’Is the aorta abnormal?’

#FUSIC #echofirst #POCUS #FOAMus Aortic dissection is easily missed, carries a high mortality and should be on the differential of any patient with shock, abdo pain or chest pain. Contrary to popular belief the entire aorta can be imaged via transthoracic and abdominal ultrasound. Let’s start with some anatomy

We’ve seen how to measure VTI and stroke volume with #ultrasound
Our next #FUSIC haemodynamic question brought to you by @icultrasonica, @wilkinsonjonny and I is:

Q2. Does SV respond to fluid, vasopressors or inotropes?

#echofirst #POCUS #haemodynamics #foamed In Q1 we saw how to measure stroke volume (SV). Q2 helps us manage someone with an inappropriately low SV. Pressors, fluids and inotropes are all treatment options. If If used correctly, they will ↑SV. If not, they won’t, and they may even be harmful.

https://twitter.com/ICUltrasonica/status/1407111542814957575?s=20

@iceman_ex @avkwong Really interesting study. Before I read it I assumed that 'physiological assessment' would be lots of fluid responsiveness assessment and then filling to an unresponsive (pathological) state. In fact a lot of ultrasound was used. And there was no difference in fluid administered @iceman_ex @avkwong So why did US not help? Echo doesn't tell you whether there is hypovolaemia or not. A hyperdynamic heart is a feature of low venous return which is more often from venoplegia than hypovolaemia. Echo cannot distinguish between these.

Let's talk about fluids in COVID. @iceman_ex @Wilkinsonjonny @ThinkingCC @load_dependent
1/8 Early in the outbreak it was commonly advised to aim for a -ve fluid balance
More recently a higher than expected occurrence of AKI and RRT has been observed prompting calls for a more liberal fluid strategy.
All these miss the point about the type of fluid being administered
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