I Was Taught the Variables Before the System

Why haemodynamics is often understood poorly and taught worse

I used to think haemodynamics was difficult because there were too many variables.

I now think part of the problem is that we are often taught the variables before we are taught the system.

Blood pressure. Cardiac output. Stroke volume. Heart rate. Systemic vascular resistance. Preload. Afterload. Contractility. Central venous pressure. Mean systemic pressure. Fluid responsiveness. Venous return.

The words become familiar long before the machinery underneath them becomes clear.

This is not because cardiovascular physiology lacks great thinkers. It has been advanced by extraordinary physiologists, clinicians and experimentalists. Starling, Guyton and many others gave us ideas that remain powerful. The problem is what happens when parts of that work are taught too literally, too early, or in isolation from the rest of the system.

A model that explains one relationship becomes a complete story.

An equation becomes a mechanism.

A curve becomes a treatment instruction.

We learn Ohm’s law applied to the circulation. We learn that cardiac output is heart rate multiplied by stroke volume. We learn Starling curves. We learn cardiac function curves. We learn venous return curves. We learn that preload increases stroke volume, afterload opposes ejection, pressure gradients drive flow, and the heart pumps blood around the body.

None of this is useless.

The problem is subtler than that.

The problem is that these ideas are often taught in a way that makes relationships look like levers. A term in an equation starts to look like a controller. A pressure in a model starts to look like a real pressure pushing on the circulation. A curve on a graph starts to look like a direct treatment pathway. A dependent variable starts to look like a cause.

Take cardiac output. The equation is simple:

Cardiac output = heart rate × stroke volume.

It is a useful relationship. But it can also mislead. If cardiac output is heart rate multiplied by stroke volume, it is tempting to think that increasing heart rate must increase cardiac output. Sometimes it does. Often it does not.

Change heart rate and the rest of the system does not stay still. Filling time changes, so stroke volume tends to change in the opposite direction. Within a broad physiological range, cardiac output may therefore change surprisingly little. Ventricular interaction, myocardial oxygen demand and vascular loading may also change. The circulation does not simply obey the arithmetic. It settles into a new state. At very fast or very slow rates, the system fails for different reasons.

The equation remains true. The interpretation was the problem.

The same thing happens with cardiac function curves. We are shown that increasing inotropy shifts the curve upwards, and cardiac output rises. Again, there is truth in this. A stronger ventricle may eject better. But the circulation is not a ventricle in isolation. Output also depends on venous return, vascular tone, stressed volume, ventricular filling, arterial load, impedance, ventricular-arterial coupling and the ability of the heart to accept venous return without excessive rise in pressure.

The curve is useful. But the patient is not the curve.

Starling’s law is another example. It is often taught as if increasing right atrial pressure, or filling pressure, increases cardiac output. In one sense, that is the classic curve: more filling, more stretch, more stroke volume.

But at the bedside, right atrial pressure is usually not an independent handle we can turn. It is part of the state into which the system has settled.

A rising right atrial pressure is usually not evidence that venous return has improved. It is more often evidence that the heart is failing to accept what is being returned. That distinction is not a detail. It changes what fluid means.

This became hard to ignore in intensive care.

I trained in an era when much of haemodynamic resuscitation still aimed to increase cardiac output by giving large volumes of fluid. The logic was simple and fitted the diagrams. Fluid would increase filling pressure. Filling pressure would increase stroke volume. Stroke volume would increase cardiac output. Cardiac output would improve perfusion.

At the time, this felt like applying physiology. But the patients in front of me often seemed to get worse.

They were oedematous, ventilator dependent, vasoplegic, congested and still shocked. More fluid seemed to increase right atrial pressure without restoring useful flow. It raised venous pressure and capillary pressure while worsening organ function. The patient looked more “filled” while the circulation looked less coherent.

That was not just incomplete physiology. In many cases, it was wrong physiology. And wrong physiology can be dangerous.

Aiming for high right atrial pressures was not a sophisticated haemodynamic strategy. It was often a dangerous misunderstanding of what the pressure represented. The pressure was not proof that the circulation had been usefully loaded. It was often the sign that the system could no longer accept what we were giving it.

That realisation changed how I thought about haemodynamics.

The same problem appears in the way venous return is taught.

Guyton’s equation is elegant:

Venous return is related to the difference between mean systemic pressure and right atrial pressure, divided by resistance to venous return.

As an abstraction, this is powerful. It points to something real: the circulation has elastic properties; stressed volume matters; the vasculature is not just passive tubing; the heart and vessels interact.

But if taught too literally, the equation can become deeply misleading.

Mean systemic pressure is sometimes described as if it were a real upstream pressure source pushing blood back to the heart during flow. Right atrial pressure is described as a back pressure opposing venous return. The equation starts to sound like a hydraulic circuit with a hidden pressure reservoir at one end and the right atrium at the other.

But mean systemic pressure does not exist as a directly measurable pressure during ongoing flow. It is an abstract pressure defined under no-flow conditions. It tells us something about the elastic state of the circulation, but it is not a hidden motor sitting upstream of the right atrium.

Nor does the venous system supply energy for flow as though it were a second pump.

That point matters, because it prevents one simplification being replaced by another.

The heart does not simply “drive” the circulation alone. But neither does venous return “drive” cardiac output in isolation. The heart supplies energy. The vasculature stores, distributes and dissipates energy. The observed flow is the result of their interaction.

The circulation is a coupled system.

That sounds obvious, but it is often missing from the way haemodynamics is taught.

Change one part of the circulation and another usually changes with it. Increase vascular tone and you may alter arterial pressure, venous return, stressed volume, right atrial pressure, ventricular loading, cardiac output and regional flow. Give fluid and you may alter stressed volume, venous pressure, cardiac filling, cardiac output, capillary pressure and oedema formation. Improve cardiac function and you may lower right atrial pressure while increasing venous return and cardiac output. Raise downstream pressure and you may preserve global pressure while impairing regional perfusion.

The system re-solves.

That is the missing idea.

Equations and curves are often presented as if we can alter one term while the others politely stay still. Real circulations do not behave like that. The variables we measure are usually descriptions of a resolved system state, not independent causes waiting to be manipulated.

Pressure is a particularly good example.

We use pressure language constantly. Pressure pushes. Back pressure opposes. Afterload pushes back. Filling pressure fills. Venous pressure limits venous return. A pressure gradient drives flow.

Some of this language is useful shorthand. But it also smuggles in a mechanical picture that can become too simple.

Pressure gradients are required for flow in resistive pathways, but they are not free-standing causes detached from the system that generated them. Gradients arise with flow, energy input, elastic storage, dissipation, vascular tone, impedance and boundary conditions. A pressure difference is part of the solved state of the system. It is not an explanation by itself.

The same applies to afterload. We often speak as if the ventricle ejects and afterload pushes back. That is a useful image up to a point. But afterload is not a single pressure object sitting outside the ventricle. It reflects arterial pressure, elastance, impedance, vascular tone, wave reflection, timing and ventricular-arterial coupling. It is not one thing opposing another thing. It is a constraint imposed by the arterial system on ventricular ejection.

The language of drivers and opposition is tempting. It is also often too crude.

This is why haemodynamics becomes confusing. Not because clinicians are stupid. Not because the equations are useless. But because the language often turns system relationships into causal stories.

CVP becomes preload. Fluid responsiveness becomes hypovolaemia. Blood pressure becomes perfusion. Mean systemic pressure becomes a hidden upstream pressure. Right atrial pressure becomes a back pressure. Starling’s law becomes a treatment instruction. Cardiac output becomes what the heart does.

Each step is understandable. Each contains some truth. Each can mislead.

The more I have thought about cardiovascular physiology, the more I have moved away from looking for single drivers. I am more interested now in limits and constraints.

What is the system capable of doing? Where is energy being added? Where is energy being stored? Where is it being dissipated? What limits venous return? What limits cardiac acceptance? What limits ventricular ejection? What is the downstream boundary condition? What regional beds are being sacrificed to preserve global pressure?

And, most importantly:

Why has the system settled here?

Not merely: what is the blood pressure?

Not merely: what is the cardiac output?

Not merely: what is the CVP?

But: what combination of cardiac function, vascular tone, stressed volume, compliance, resistance, impedance, venous pressure, capillary pressure, ventricular interaction and regional perfusion has produced this state?

That is a different way of thinking.

It is not anti-equation. It is not anti-Guyton. It is not anti-Starling. It is not anti-echo, anti-monitoring, or anti-bedside shorthand.

It is anti-literalism.

The equations are useful when we understand what kind of thing they are. Curves are useful when we understand what has been held constant, what has been abstracted away, and what is actually being described. Pressures are useful when we understand whether they represent energy, constraint, consequence, boundary condition, or measurement artefact.

The problem is not that haemodynamics has too many variables.

The problem is that too often we are taught the variables before we are taught the system.

That is why this Substack is called The Dependent Variable. It captures the mistake I kept encountering: taking a measured output of a coupled system and treating it as the thing that controls the system.

I am not going to build this publication as a perfect textbook from chapter one onwards. That would be tempting, but probably fatal. What has helped me most is going back to first principles and asking whether the usual explanations remain coherent when tested against the underlying physics: pressure, flow, energy, resistance, impedance, compliance, capacitance and the behaviour of coupled physical systems. The aim is not to produce a finished doctrine, but to return to familiar haemodynamic ideas from that ground-up perspective.

Each topic has its own details. But the same question will keep returning:

Are we looking at a cause, a constraint, or the resolved state of a coupled system?

That question has changed how I think about haemodynamics.

I hope it changes how you think about it too.