Ashley Miller Profile picture
Nov 9 14 tweets 3 min read Read on X
1️⃣
We can remove fluid at rates up to 12 mL/kg/h and blood pressure often holds.
That limit isn’t arbitrary – it comes from dialysis data showing steep rises in hypotension and mortality above it.
It marks the upper boundary of how fast plasma can be refilled from the interstitium and lymph 👇
2️⃣ The background

In most tissues, fluid filters out of capillaries and returns via the lymphatics.
At steady state, filtration ≈ lymph flow (~10 L/day ≈ 400 mL/h), so plasma and interstitial volumes stay constant.
This is the equilibrium that ultrafiltration later exploits.
3️⃣ What ultrafiltration actually does

Removing plasma water slightly lowers blood volume and triggers reflex arteriolar constriction (↑ Ra).
That drops capillary pressure (Pc), pushing the microcirculation left on the J-curve.
Filtration falls toward zero — you’ve effectively turned off the tap that was sending ~400 mL/h into the interstitium.
4️⃣ Two sources of safe refill

Fluid can be removed without hypotension because refill is funded by:
• Stopped filtration (~400 mL/h you no longer lose)
• Ongoing lymphatic return (often 0.5–1 L/h in oedema)

Together they support removal rates approaching 12 mL/kg/h in oedematous patients.
5️⃣ The paradox resolved

If re-absorption “never happens,” how do we refill?
Because UF stops filtration while lymph keeps flowing.
Refill is therefore lymph-mediated, not venular suction – the circulation stays stable because lymph replaces what’s removed.
6️⃣ Why oedematous patients tolerate higher rates

In oedema, interstitial pressure (Pi) is raised and lymphatics are already pumping hard.
Lymph flow can reach 0.5–1 L/h.
When Pc falls and filtration ceases, that lymph stream becomes a ready source of refill – the physiological reason we can remove up to ~12 mL/kg/h safely.
7️⃣ The compliance piece

While oedema is present, Pi is high and lymph flow is brisk – so fluid can be removed rapidly without hypovolaemia.
As UF continues and tissues de-oedematize, Pi falls, lymph drainage slows, and the refilling circuit collapses.
Beyond that point, further fluid removal draws directly from plasma volume – causing hypovolaemia.
8️⃣ Putting numbers on it

A 70 kg patient at 12 mL/kg/h ≈ 840 mL/h:
• You “save” ~400 mL/h by stopping filtration
• Add ~400–600 mL/h lymph return in oedema
That’s why MAP and filling pressures can stay stable even during aggressive fluid removal.
9️⃣ When refill limits are reached

Two microvascular regimes set the ceiling for safe UF 👇
1/ Leaky circuit – glycocalyx injury
The oncotic brake is lost, so filtration persists even at low Pc.
Refill becomes lymph-limited: the faster the lymph drains, the faster you can safely remove fluid.

2/ Sealed circuit – intact glycocalyx, low Pc
Here Jv ≈ 0 once Pc falls left of the J-point.
The ~400 mL/h that normally filters out is “saved,” adding to lymph flow and allowing faster UF – until lymph drainage slows as oedema resolves.

Clinical signs of reaching the limit: rising HR, falling MAP, delayed cap-refill, haemoconcentration.
🔟 Tailoring the rate

Safe removal depends on clinical state, not a single number.
Severe oedema with organ failure: lymph flow high → remove fluid quickly.
Mild oedema, limited organ failure: lymph reserve low → go slower to avoid hypovolaemia.

Lowering Pc (via α-tone or relieving venous congestion) reduces further filtration, preserving plasma volume as lymph continues to drain.
1️⃣1️⃣RRT hypotension – often misattributed

When RRT first starts, the extracorporeal circuit briefly sequesters 300–500 mL of blood, causing a transient dip in circulating volume and pressure before lymphatic refill and vascular tone re-equilibrate.
Hypotension on RRT has many causes (for another thread), but true hypovolaemia is usually low on the list – it’s often blamed because we misunderstand refill physiology.
1️⃣2️⃣The takeaway

You’re not “sucking blood volume out” with RRT – you’re harvesting lymph while turning off filtration.
That’s why the circulation stays full even as total body water falls.
The 12 mL/kg/h limit reflects the maximum rate that refilling circuit can sustain.
1️⃣3️⃣ One-liner to teach with

“Safe ultrafiltration works because you stop making interstitial fluid and keep draining it.”
Not re-absorption – lymph-mediated refill.
1️⃣4️⃣ Next time

We’ll tackle the myth of being “oedematous but intravascularly dry” and why that's impossible at steady state.

If you've found this thread useful please like, comment and repost

#FOAMed #ICU #Physiology #CRRT @NephroP

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More from @icmteaching

Nov 6
1️⃣We talk endlessly about “capillary leak” – but most of what we say about it is wrong.

Here’s what actually drives fluid movement across the microcirculation – and why Starling’s model needed an upgrade. A 🧵👇
2️⃣ The old picture
Starling (1896) imagined that filtration dominates early in the capillary and re-absorption later, where pressure is lower.
In most tissues, direct re-absorption almost never happens.
Capillary pressure (Pc) slightly exceeds oncotic pressure along the whole capillary, so filtration (Jv) predominates at both ends.
All that filtrate returns to the circulation through the lymphatics.

Fluid leaves the circulation continuously – and the lymphatics bring it back.
3️⃣ The extended Starling principle

Jv = Lp · S · ( (Pc − Pi) − σ · (πc − πg) )

• Pc – capillary hydrostatic pressure
• Pi – interstitial pressure
• πc – plasma oncotic pressure
• πg – oncotic pressure just beneath the glycocalyx (the effective gradient)

That thin, protein-free layer (πg ≈ 0) is what really opposes filtration.
Read 15 tweets
Oct 16
🧩 Part 3 – Why you usually can’t move one curve without the other
1️⃣
So far, we’ve treated the cardiac and venous return curves as two lines that meet.
In theory, you can move one without the other – and sometimes that’s true.
But in physiology, they almost always move together – because they share the same inlet.
2️⃣
Both curves hinge on the same gateway: the inlet to the heart.
That’s where Ivr – inlet impedance – lives.
Any change in relaxation, stiffness, or pericardial pressure alters Ivr, so both curves tend to shift together.
3️⃣RVR vs Ivr – Anderson’s key insight:

RVR assumes static pipe resistance (captures geometry, compression but ignores compliance & timing).
Ivr represents dynamic inlet impedance (stiffness, relaxation, pericardial coupling).

RVR treats veins as plumbing; Ivr treats them as a living inlet.
When the heart stiffens or relaxes, Ivr changes – and both curves move.
Read 11 tweets
Oct 13
🧵 Part 2 — The Venous Return Curve

1️⃣
Last time, we fixed the cardiac function curve.
Now let’s look at the other half of the story — venous return — and how the circulation really feeds the heart.

#FOAMed #MedX #physiology Image
2️⃣
The venous return (VR) curve describes how blood flows into the heart for any steady state of the venous system.
It’s not about forcing RAP up or down — it shows the equilibrium between flow and pressure for a given system tone and volume.
3️⃣
Mathematically:

VR = (Pms - RAP) / Ivr

• Pms = mean systemic filling pressure → “push” from stressed volume & venous tone
• Ivr = inlet impedance – how easily blood enters the heart (similar to Guyton’s RVR but dynamic, not fixed)
• RAP = dependent feedback pressure where inflow = outflow
Read 10 tweets
Oct 10
🧵 The Cardiac Function Curve — why it misleads (Part 1)
1/
The cardiac function curve is one of the most recognisable images in physiology.
Unfortunately, it’s also one of the most misdrawn, mislabelled, and misunderstood.
Let’s redraw it — and see what it really tells us about the circulation.

#MedX #FOAMed #physiologyImage
2/
Textbooks teach: ↑ filling pressure → ↑ output.
But that’s backwards.
The heart doesn’t decide flow — it matches whatever venous return delivers.
It’s a servo, not a suction pump.
3/
This cardiac function curve shows what the heart alone can do at different right-atrial pressures.
But cardiac output isn’t set by the heart in isolation — it’s where this curve meets the circulation’s ability to return blood.
We’ll come to that next time in part 2
Read 16 tweets
Oct 6
1️⃣
Some patients with severe venous congestion have almost no oedema — and that’s confusing at first.
It only starts to make sense once you unpack the physiology. 👇
Venous congestion ↑RAP → ↑venous pressure (Pv) → potentially ↑capillary pressure (Pc).
But the rise in Pc — and thus filtration — depends on arteriolar tone (Ra)
Pc = (Rv / (Ra + Rv)) * Pa + (Ra / (Ra + Rv)) * Pv Image
3️⃣
If arterioles constrict (↑Ra), most of the pressure drop occurs before the capillary → Pc stays low and changes little even if Pv rises.
If they dilate (↓Ra), Pc shifts toward Pa → filtration ↑ → oedema.

Tight = protected.
Dilated = leaky.Image
Read 7 tweets
Sep 16
1/
SVR looks precise: (MAP – RAP)/CO.

But this neat number hides traps. It’s not “afterload,” it’s not pure “tone,” and sometimes it’s not even valid.

A thread on why systemic vascular resistance misleads — and when it still helps. 🧵 #MedX Image
2/
SVR isn’t measured.
It’s calculated from MAP, right atrial pressure, and CO.
That makes it a derived ratio — not a direct property of the circulation.
3/
Because it has “resistance” in the name, we imagine SVR = arteriolar tone.
It doesn’t.
It’s just arithmetic.
Read 15 tweets

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