Ashley Miller

Left atrial “reservoir strain” (LARS) is usually taught as an atrial property.
That framing fails physiologically.
LARS is best understood as a signal of ventriculo–atrial coupling.

2/
Start with a hard constraint: volume conservation.
During LV systole, ventricular volume falls.
Total cardiac volume changes little.
That displaced volume must go somewhere → atrial expansion.

3/
The physical coupler is the AV plane.
LV longitudinal shortening pulls it downward (MAPSE).
The LA lengthens passively above it.
Same motion. Same driver.

4/
This is why MAPSE and LARS track so closely (R² ≈ 0.95).
LARS ≈ MAPSE indexed to LA length.
Measuring it from the atrial side does not make it an intrinsic atrial material property.

5/
The &lt;100% correlation is the key insight.
If the atrium were a passive balloon, LARS would mirror MAPSE perfectly.
The residual variance reflects modulation of coupling, not noise.

6/
LA compliance, geometry (size & shape), fibrosis, and timing determine whether AV-plane motion is stored as reservoir volume or manifests as pressure rise.
This defines coupling efficiency.

7/
This resolves the paradoxes.
LARS falls in HFpEF and predicts outcomes not because it measures LA distensibility, but because impaired coupling means LV longitudinal work is no longer stored as atrial reservoir volume.

8/
Bottom line:
LARS is not LA strain, stiffness, or distensibility.
It is a ventriculo–atrial coupling signal dominated by LV systolic longitudinal function and modulated by atrial properties.
MAPSE tells you how much the ventricle pulls; LARS tells you how that pull is

🧵What makes the blood go round?

And why does such a simple sounding question cause such heated arguments between physiologists?

Everyone agrees on the observations.
The disagreement is about causality. 👇

#FOAMed #Physiology #MedX

2/ What everyone agrees on

At steady state:
• Venous return = cardiac output
• Flow is always associated with pressure differences
• Sustained flow requires a pump

So why the disagreement?
Because the same observations can be given very different causal interpretations.

3/ One framing: circulation-first

In the classic Guyton framework, venous return depends on:

• Pms (stressed volume)
• RAP
• Resistance to venous return (RVR)

This suggests the circulation sets flow, and the heart permits it.
This view is associated with Guyton, Magder, and

4/ Why this framing was compelling
It:
• explains fluid responsiveness
• fits many experimental observations
• produces intuitive venous-return curves
• works well for teaching and bedside reasoning

But critics argue it embeds a hidden causal assumption.

5/ The opposing objection: heart-first

The counter-argument is that:
• RAP is not a control knob
• It cannot be independently set
• It changes because flow changes

So treating RAP as a “backpressure” that causes flow is misleading.
This critique is associated with

6/ Independent vs dependent variables

This is where the camps diverge.

One view treats Pms, RVR, and RAP as independent inputs to venous return,
with RAP acting as a downstream backpressure.

The other argues RAP is always dependent, emerging from the balance of venous return

7/ Why this was often misunderstood

Guyton did not claim that RAP is a freely adjustable control variable in normal physiology.

RAP was treated as independent in experimental models to map venous return. But plotting RAP on the x-axis and writing...

VR = (Pms − RAP)/RVR

8/ The energy-source dispute

Another core disagreement is where the energy driving circulation comes from.

One intuition emphasises the vessels:
• elastic arteries store energy in systole
• recoil releases that energy in diastole
• this appears to help “drive” flow

The

9/ The deeper issue underneath

So the real argument is not about curves or equations.

It’s about:
• whether pressure differences are causes or consequences of flow
• whether volume sets causation or conditions
• and what role the heart really plays

Until these are

10/ Setting up the resolution

To resolve this, we need to be precise about:

• what “drive” actually means
• which variables are independent
• and what volume and elasticity really do

That’s what the next thread will tackle.

🧵 What drives blood flow – the heart or the vessels?

Eminent physiologists have argued this for decades.

The disagreement survives because of imprecise causality.

Here’s the resolution 👇

2/ To resolve the heart vs circulation debate, we first need to be precise about one word:

“Drive.”

Do we mean:
– supplying energy?
– setting conditions?
– constraining what’s possible?

Most confusion comes from mixing these up.

3/ Start with first principles.

A circulation is a hydraulic circuit.

In any hydraulic system:
– Energy must come from a pump
– Flow requires a pressure gradient
– Gradients cannot persist without energy input

These are physical constraints, not opinions.

4/ So what does the heart do?

The heart is the only sustained energy source in the system.

It:
– adds energy to blood
– raises pressure at its outlet
– lowers pressure at its inlet
– redistributes pressure around the circuit

Without ongoing cardiac work, pressures drift toward

5/ So why doesn’t “pumping harder/faster” always increase output?

Because the heart usually has reserve.

As long as it has:
– volume reserve
– energy reserve

it simply passes forward whatever venous return arrives.

In this range, the heart behaves like a Type 3 pump –

6/ So what usually sets venous return?

Two independent controlling variables:

– Mean systemic pressure (Pms) – how much stressed volume is available
– Inlet impedance (Zin) – how hard it is for blood to enter the heart

Together, they determine how much flow can reach the pump.

7/ What is Pms, really?

Pms is not a source of energy.

It is an operating condition, set by total blood volume, venous compliance, and venous tone.

Elasticity and volume determine what pressures are possible in the system – not what drives flow.

8/ This resolves the first paradox:

How can Pms “drive” flow if it exists only at zero flow?

Answer:
• It doesn’t drive flow
• It defines the pressure field the pump can work within

Changing Pms changes what pressure gradients are possible – but sustained flow still requires

9/ What is Zin?

Zin is the impedance to venous return at the heart.

It limits flow by restricting how easily blood can enter the heart – whether through reduced compliance or inlet narrowing.

Zin can severely limit venous return even when Pms is high.

10/ This resolves a major source of confusion.

As Zin rises:
– venous return falls
– blood pools upstream
– RAP usually rises

Because RAP often mirrors Zin, it is easy to mistake RAP for a controller.

But RAP is a signal, not the control.

11/ So what is RAP?

RAP is a dependent variable.

It reflects the equilibrium between:
– Pms (how much volume is available)
– Zin (how hard it is to enter the heart)
– cardiac pumping capacity
– external pressures

RAP changes because the system rebalances.
It is not a control

12/ Pressure and flow – what’s necessary, what’s causal

Flow requires a pressure difference – but a pressure difference alone never guarantees flow.

Pressure gradients are necessary conditions, not causal agents.

They exist only while energy is being supplied to the system.

13/ What pressure actually represents

Pressure is a state variable: stored potential energy in an elastic, constrained system.

Flow occurs when that energy is allowed to dissipate along a conductive pathway.

The heart supplies energy.
Pressure reflects it.
Impedance governs

14/ What about elastic recoil?

Vascular elastic recoil stores energy during systole and releases it during diastole.

This explains:
– pulsatile smoothing (the Windkessel effect)
– continued diastolic flow

But recoil does not supply net energy.
It only redistributes energy

15/ Why do fluids and vasopressors increase flow?

Because both primarily act by increasing stressed volume:

– fluids increase total volume
– vasopressors increase venous elastance

Both shift blood into the stressed compartment – raising the Pms analogue.

If Zin is low and the

16/ Why does Pms responsiveness disappear?

Because:
– as Pms continues to rise..
– Zin rises in parallel
– the heart reaches its volume limit

Once Zin dominates:
– pressure rises faster than flow
– RAP increases
– venous return plateaus

Loss of Pms responsiveness reflects

17/ Final synthesis

The heart does not “pull” blood.
The vessels do not “push” blood.

The heart supplies energy.
Pms and Zin set the limits.
RAP reports the balance.

Flow is the equilibrium that satisfies all three.

That is how the blood goes round.

#physiology #FOAMed #MedX

@iceman_ex @ThinkingCC @ross_prager @khaycock2 @nickmmark @IM_Crit_ @msiuba

🧵 Inlet impedance: the missing determinant of cardiac output
1/
What really limits cardiac output: the heart or the circulation delivering blood to it?
This question has sparked heated arguments between physiologists for decades.
To answer it, you first need to understand inlet

2/
Guyton taught venous return using resistance (as if the system were an electrical circuit).
Anderson reframed it using inlet impedance (Zin) because veins and hearts are compliant, deformable, and state-dependent.

3/
Zin replaces venous resistance in the denominator:

VR ∝ (Pms − RAP) / Zin

Higher Zin means poorer conversion of pressure into flow.

4/
Think of venous return as blood entering the heart through a doorway.
Pms is the push from behind.
Zin describes how hard it is to get through the door.

5/
There are two fundamental ways inlet impedance (Zin) can increase – two ways the doorway can be affected.

They often coexist, but the pressure signatures differ.

6/
🚪 The door is small
Flow is limited by a choke before the heart.

Examples:
• IVC compression
• Abdominal hypertension
• True Starling-resistor behaviour

Pressure builds upstream of the door.

7/
🔩 The hinges are stiff
The heart is hard to open.

Examples:
• RV dilatation with septal shift
• LV diastolic dysfunction
• Pericardial constraint
• High intrathoracic pressure (PEEP – constraint-dominant)

Pressure rises inside the heart.

8/
⚠️ Sometimes both are true
The door is small and the hinges are stiff.

Examples:
• Very high PEEP
• Tamponade physiology
• Severe RV failure in a tight pericardium

Here, inlet impedance skyrockets.

9/
🔩 Stiff hinges
Small increases in flow require large rises in filling pressure.

At the new equilibrium:
• RAP rises
• congestion is central
• fluids give pressure ≫ flow

10/
🚪 Small door 
Flow is limited upstream.
Pressure accumulates before the heart.

At equilibrium:
• RAP may be normal or low
• congestion is extra-cardiac
• fluids worsen pooling without meaningful CO gain

11/
This is why RAP is a dependent variable, not a cause.
High RAP often reflects high inlet impedance – not “backpressure” opposing venous return.

12/
Increasing stressed volume (↑Pms) increases the driving pressure for venous return.
But when Zin is high, the pressure-to-flow gain is poor.
Most of the added volume appears as congestion, not flow.

13/
So the real clinical question isn’t:
“Is the CVP high?”

It’s:
“Is venous return limited by a small door, stiff hinges or both?”

14/
Cardiac output depends on pressure (Pms), the pump (the heart), and how easily blood can enter it (Zin).
High RAP in heart failure reflects impaired filling, not blocked flow.

This sets up the real debate: what actually drives the circulation – the heart or the venous

Thanks Stephen. I’m not 100% sure what question(s) you are asking. Can you clarify? Also apologies but those photos are too much effort to read 😆