Chapter 21: Cardiac Electrophysiology and the Electrocardiogram

Welcome to Last Minute Lecture.

This free chapter overview is designed to help students review and understand key concepts.

These summaries supplement, not replace the original textbook and may not be redistributed or resold.

For complete coverage, always consult the official text.

Your heart, it's more than just a pump, isn't it?

It's this incredible electrical powerhouse silently running the show beat after beat.

Absolutely, a whole electrical orchestra inside us.

Exactly.

And today we're diving deep into that hidden world.

We're gonna unravel cardiac electrophysiology and the electrocardiogram, the ECG.

Yeah, and we're basing this discussion on chapter 21 of Boron and Bull Peep's Medical Physiology.

It's a cornerstone text, really dense stuff.

Right, but our mission here is to break it down, make it conversational, clear, so you can actually visualize these things without needing the book right in front of you.

And crucially, understand why it matters clinically.

We wanna turn that overwhelming info into those aha moments.

Think of it as your shortcut to understanding the heart's electrical symphony.

We'll build it up from the basics, connect it to the real world.

Sounds good.

So where should we start the origin?

Let's do it, the very beginning of that electrical spark.

Where does this whole symphony normally kick off?

Okay, so the heart's natural pacemaker, its conductor, you could say, is a tiny group of cells called the sinoatrial node, the SA node.

And that's up in the right atrium.

High up.

Exactly, high in the right atrium.

And what's amazing about these cells is they spontaneously generate their own electrical impulses.

They don't need telling.

So they set the pace themselves, the intrinsic heart rate.

Right.

Typically, at rest, that's somewhere between 60 and 100 beats per minute.

Because a SA node gets things going.

But the next part always fascinates me.

How does that signal spread so perfectly through the whole heart?

It's not like they're actual wires, is it?

No, not wires, but something almost as good.

Cardiac muscle cells are directly connected through these tiny little doorways called gap junctions.

Ah, gap junctions, like tunnels between cells.

Precisely.

Direct electrical tunnels.

They let the current, which is basically a flow of positive ions, zip straight from one cell into its neighbor.

Very efficient, because they're so tightly coupled.

And that flow of current is what makes the next cell fire off, right?

I feel like there's some basic physics involved here.

Ohm's law, does that apply?

You're spot on.

Ohm's law definitely applies, conceptually.

The current flow between two cells depends on the voltage difference between them, and critically, the resistance of those gap junctions.

So if the junctions are wide open, low resistance.

Current flows easily, signal spreads faster.

If they're more closed off, higher resistance, it slows down.

It's fundamental to how fast signals travel in the heart.

Okay, so the SA node fires, current flows through gap junctions.

How does that impulse path actually look?

Trace it for us.

Sure, so from the SA node, it spreads across the right atrium pretty quickly, and then over into the left atrium.

Okay, atria covered, then what?

Then it hits a really crucial spot.

The atrioventricular node, the AV node, this is like the only electrical bridge connecting the atria up top to the ventricles down below.

And something special happens there, right?

A delay.

A very important, deliberate delay, yeah.

About one tenth of a second, the signal slows right down as it goes through the AV node.

A delay seems weird for something that needs to pump blood efficiently.

Why pause?

What if it didn't pause?

No, it's absolutely critical.

That pause gives the atria enough time to finish contracting, to really squeeze blood down into the ventricles before the ventricles start their own contraction.

Ah, I see, so it synchronizes the chambers properly?

Without it, chaos.

Pretty much.

Atria and ventricles contracting together.

Very inefficient, you wouldn't move much blood.

So after that vital pause at the AV node, the signal basically explodes down through his Purkinje system.

That's the bundle of his and the Purkinje fibers?

Exactly, this is the superhighway.

It distributes the signal incredibly rapidly throughout both ventricles, making sure they contract forcefully

and almost simultaneously.

So we've got different speeds then.

Slow through the nodes, fast through the muscle and Purkinje fibers.

That's a key distinction.

We talk about slow action potentials in the SA and AV nodes and fast ones everywhere else.

Atrial muscle, ventricular muscle, Purkinje fibers.

And the Purkinje fibers are the absolute fastest.

By far.

About four meters per second.

Compare that to the SA and AV nodes, which are maybe 0 .05 meters per second.

Huge difference.

Perfectly designed for coordinated pumping.

And all this electrical movement, this flow of ions in and out of cells, that's what we actually pick up with an ECG.

That's exactly it.

As those action potentials propagate, positive and negative charges are moving inside and outside the cells.

This creates tiny electrical fields.

And the ECG sums it all up.

Right.

The ECG leads on the skin record, the sum of all those changing electrical vectors over time.

Every wave, every complex on that tracing is a snapshot of that electrical dance.

Okay, let's talk about that dance then.

The action potentials themselves.

You said they're different shapes in different parts of the heart.

Yeah, very different.

The shape, the duration, it all varies depending on the region.

And that's not random, it reflects their specific jobs.

Because they have different ion channels, different recipes, you called it.

Exactly.

Each cell type has a unique mix of ion channels, these little protein gates that control which ions can cross the membrane when.

So who are the main players, the key ion currents driving these action potentials?

Okay, there are four big ones to know.

First, probably the most dramatic is the sodium current, INA.

That's the fast one.

The really fast one.

It's responsible for that incredibly rapid upstroke, phase zero, in the atrial muscle, ventricular muscle, and Purkinje fibers.

Huge influx of positive sodium ions.

So it depolarizes the cell very quickly.

Very quickly.

It activates fast, then shuts off, or inactivates pretty quickly too.

Now, importantly, you don't find this fast sodium channel in the SA and AV nodes.

That's a key reason they depolarize more slowly.

And clinically, blocking this channel.

Right, that's how some antiarrhythmic drugs work.

Things like lidocaine, they block INA, slowing down conduction, which can terminate certain fast rhythms.

Okay, ion for the fast upstroke, what's next?

Calcium.

That sounds important for the actual muscle contraction?

Absolutely critical.

The calcium current, ICA, mostly flows through what we call L -type calcium channels.

Now, this current does two major things.

First, it's responsible for the slower upstroke, phase zero, in the SA and AV node cells.

Remember, they lack the fast I know.

Second, and this is huge, IK is the trigger for muscle contraction in all heart cells.

Calcium coming in tells the cell to squeeze.

And it also helps with that plateau phase, right?

Keeping the cell positive for longer.

Exactly.

It contributes significantly to phase two, the plateau, especially in ventricular cells.

Clinically, you know, calcium channel blockers for apamel diltiasm.

They target these L -type calcium channels so they can slow heart rate, reduce the force of contraction.

Makes sense.

So sodium for fast depolarization, calcium for slower depolarization and contraction trigger.

What about getting back to rest, repolarization?

That's primarily the job of potassium currents, IK.

There are actually several types, but generally these channels open more slowly and allow positive potassium ions to flow out of the cell.

So losing positive charge brings the voltage back down.

Precisely.

It's responsible for phase three, the repolarization phase, resetting the cell membrane potential back towards its negative resting state, the essential reset.

Okay, and the last one,

the funny current.

If, why funny?

Ah, if, the pacemaker current.

It got its nickname because it behaves,

well, funnily.

Most channels open when the cell gets more positive,

depolarizes.

If opens when the cell gets more negative, hyperpolarizes.

Right at the end of repolarization.

That is weird.

It is, it's a non -selectification channel letting some sodium and potassium through.

You only find it in pacemaker cells, SA node, AV node, Purkinje fibers.

And it provides this slow inward leak of positive charge during phase four.

Which slowly drifts the voltage up towards threshold.

Exactly, that's the spontaneous depolarization.

That's what makes pacemaker cells fire on their own.

It's the heart's internal metronome.

Okay, let's try to picture one of these action potentials, like a typical ventricular muscle cell.

Walk us through the phases.

Okay, imagine a ventricular cell just sitting there waiting.

That's phase four, the stable resting phase.

It's negative inside, maybe negative 90 millivolts.

Primed and ready.

Right, then a stimulus arrives from a neighbor cell.

Boom, phase zero, the rapid upstroke.

That's the fast sodium channels, IANA flying open.

Voltage shoots up to positive values.

Net a dip slightly.

Yeah, often a brief small dip called phase one early repolarization.

Some transient potassium channels open.

But then comes the really characteristic part, phase two, the plateau.

Where it stays positive for quite a while.

For a relatively long time, yeah.

Maybe 200 milliseconds or so.

Here, the inward calcium current, IK, is roughly balancing the outward potassium currents, IK.

So the voltage stays pretty flat and positive.

And you said this plateau is super important functionally.

Absolutely crucial.

Because the cell membrane is depolarized during this plateau, those fast sodium channels are inactivated.

They can't reopen yet.

Meaning the cell can't fire again immediately.

Exactly.

This creates the effect of refractory period, or ERP.

The cell is refractory, meaning it cannot be re -excited no matter how strong the stimulus.

The safety mechanism.

Prevents tetanus, like in skeletal muscle.

Precisely.

Tetanus in the heart would mean no pumping.

Just a sustained useless contraction.

The ERP ensures the heart has time to relax and refill between beats.

It's vital.

Okay, so after the plateau.

After the plateau, the calcium channels close.

And the main potassium channels, IK, really kick in, allowing lots of potassium to leave the cell.

This is phase three, rapid repolarization.

The voltage plummets back down towards the negative resting potential.

And then we're back at phase four, ready for the next beat.

Back at phase four.

Now remember, in pacemaker cells like the SA node, phase four isn't flat.

It has that slow upward drift thanks to the funny current.

Yeah.

That's the key difference.

Got it.

So we understand the individual cell now.

How does the body control the overall rhythm?

We know the SA node leads, but what if it falters?

Good question.

The heart has backups at the hierarchy.

The SA node is fastest, 6 ,100 BPM, so it normally drives everything.

But if it fails.

The AV node takes over.

The AV node can step in, yes.

It's a secondary pacemaker.

Its intrinsic rate is slower though, maybe around 40 beats per minute.

And if both fail.

Then you rely on the Purkinje fibers in the ventricles.

They are the tertiary pacemakers, but they're really slow.

Like 20 beats per minute, maybe even less.

It's an emergency backup.

Whichever pacemaker site is fastest at any given moment is the one in control.

Okay, and the body can obviously adjust this rate.

Like exercise versus rest.

How does that modulation happen?

Two main branches of the autonomic nervous system.

You have the parasympathetic system, mainly via the vagus nerve, releasing acetylcholine.

The rest and digest system.

That slows things down.

Right.

Acetyltcholine acts like the brake pedal.

It slows the heart rate.

That's called a negative chronotropic effect.

It does this mainly by decreasing the slope of that phase four depolarization in the SA node.

Making the if current less active and also making the cells start from a more negative potential.

Basically makes it harder and take longer for the SA node to fire.

Which explains why things like vagal maneuvers holding your breath, bearing down, can slow a fast heart rate.

Exactly.

Those maneuvers stimulate the vagus nerve, dumping acetylcholine onto the heart, slowing AV node conduction and SA node firing.

A direct clinical application.

Okay, so that's the brake.

What's the accelerator?

That's the sympathetic nervous system.

It releases catecholamines, norepinephrine directly from nerves onto the heart and epinephrine from the adrenal glands into the blood.

Fight or flight.

Speed things up.

Positive chronotropic effect.

Catecholamines bind to beta one receptors on the heart cells.

This increases the activity of the funny current if making that phase four depolarization steeper so the SA node fires more often.

It also enhances the calcium current, ICA.

And more calcium means?

A stronger contraction too.

So, sympathetic stimulation doesn't just increase rate chronotropy, it also increases the force of contraction inotropy.

Makes the heart beat faster and harder.

Wow, okay.

From the spark to the cell, the pathways, the modulation.

Now let's get to reading the story.

The ECG, what is it actually measuring?

Fundamentally,

the ECG measures the electrical potential differences on the body surface that are generated by the heart's electrical activity.

As that wave of depolarization and repolarization sweeps through the heart muscle.

It creates electrical fields we can detect outside?

Exactly.

Think of the ECG leads like little microphones listening to the electrical sound of the heart.

Or maybe cameras is a better analogy.

If the overall wave of positive charge is moving towards a camera, a positive electrode, you get an upward deflection on the ECG.

And if it moves away?

A downward deflection.

And if it moves perpendicularly across the camera's view?

Flat line.

Isoelectric.

Isoelectric, exactly.

It's that basic principle applied across multiple viewpoints.

Which brings us to the standard 12 lead ECG.

Why 12 leads?

Seems like a lot.

It gives us a comprehensive 3D -ish view.

You have electrodes on the arms and legs.

Those create the limb leads.

Looking at the heart in the frontal plane, like looking from the front.

Then you have electrodes across the chest.

The precordial leads giving you views in the transverse plane like slicing the body horizontally.

So 12 different angles to see the electrical wave moving.

Precisely.

Each lead provides a unique perspective.

Helping us pinpoint where electrical events are happening and in which direction they're moving.

Okay, let's look at a typical ECG strip.

Those bumps and wiggles.

P, QRS, T.

What do they represent?

Let's break it down.

The first little bump you usually see is a P wave.

That represents the depolarization, the electrical activation, spreading through both atria.

Okay, P wave equals atrial depolarization.

Then the big spiky thing.

That's the QRS complex.

It's usually much larger and sharper because the ventricles have so much more muscle mass.

The QRS represents the rapid depolarization of both ventricles.

Ventricular depolarization, got it.

And after that?

After the QRS, there's usually a flatter segment, the ST segment, and then comes the T wave.

The two wave represents ventricular repolarization, the ventricles resetting electrically.

And sometimes a U wave?

Yeah, occasionally a small U wave follows the T wave.

Its origin isn't totally certain, but it might be related to repolarization of the Purkinje fibers or pepillary muscles.

Not always seen.

Quick question about the T wave.

Depolarization is positive charge moving in, causing an upward QRS if it moves towards the lead.

Repolarization is positive charge moving out.

So why is the T wave usually upright like the QRS?

Shouldn't it be inverted?

That's a classic, excellent question.

It seems counterintuitive, right?

But the key is the sequence of repolarization.

In the ventricles, the cells that depolarize last, often in the outer layer, the epicardium, tend to repolarize first.

So the wave of repolarization effectively travels in the opposite direction to the wave of depolarization.

Sort of, because the last cells to get the GO signal, the first to get the reset signal, the overall direction of the repolarization vector ends up pointing similarly to the depolarization vector.

So if the QRS is upright in a lead, the T wave usually is too.

It's pretty neat.

That makes sense.

So when a clinician glances at an ECG, what are the first few things they're looking for?

The basics.

They're running through a systematic check.

First, rate.

How fast is the heart beating?

You can estimate it quickly from the RR interval, the distance between QRS complexes.

There's the 300, 150, 175, 60, 50 rule for counting boxes.

Right.

Then rhythm.

Is it regular?

Is it sinus?

Exactly.

Is there a P wave before every QRS?

Is QRS following the P wave consistently?

That tells you if the SA node is in charge and if conduction is proceeding normally, what we call normal sinus rhythm.

Then the intervals and durations.

Those tell you about conduction speed.

Precisely.

The PR interval from the start of the P wave to the start of the QRS tells you how long it takes the signal to get through the AV node.

Too long suggests an AV block.

And the QRS duration itself.

The QRS duration tells you how long it takes for the ventricles to depolarize.

If it's wide, it suggests the impulse isn't spreading through the fast Burkinje system properly, maybe due to a bundle branch block.

And the QT interval.

The QT interval from the start of the QRS to the end of the T wave reflects the total duration of ventricular electrical activity, both depolarization and repolarization.

A long QT interval is a red flag for increased risk of dangerous arrhythmias.

And finally, the axis.

What's that about?

The electrical axis is the overall average direction of the electrical current flow during ventricular depolarization.

Looking at the QRS in different leads tells you the axis.

If it's shifted way off normal, it can suggest things like one ventricle being abnormally enlarged or hypertrophy.

Okay, so that's the normal picture.

But what happens when things go wrong?

When the heart loses its rhythm, arrhythmias.

Right, and arrhythmias is basically any rhythm that isn't normal sinus rhythm.

Some are totally normal, like your heart speeding up with exercise, sinus tachycardia, others are definitely pathological.

And you said they basically boil down to two main problems.

Generally, yes.

Either problems with altered conduction, the signal gets blocked or takes a detour, or problems with altered automaticity cells start firing spontaneously when they shouldn't, or the normal pacemakers misbehave.

Let's tackle conduction problems first.

How can the signal get blocked?

Kishu damage is a big one.

Say from ischemia, lack of oxygen during a heart attack.

Damaged cells can become partially depolarized, which inactivates some crucial ion channels, like those fast sodium channels.

So the signal just can't get through as easily or at all.

Right, conduction slows down or it can block completely.

It's like a roadblock on the electrical highway.

And we see that on the ECG during a heart attack.

You mentioned ST elevation.

Yes, the ECG changes during a myocardial infarction, or MI, can be quite dramatic.

Early on, you might see tall peaked T waves, then often T wave inversion.

The classic sign of acute injury is ST segment elevation.

Why elevation?

The injured cells often have a less negative resting potential, closer to zero.

This creates a voltage difference between the injured and healthy areas during diastole when the ECG baseline is normally flat.

This difference makes the baseline appear shifted downward relative to the ST segment.

So the ST segment looks elevated.

Oh, okay.

And then later those deep Q waves appear.

If the tissue dies, becomes insarcted, it's electrically silent.

It can't conduct the impulse.

So electrodes looking at that area, see the electrical wave moving away from the dead zone, causing a deep negative deflection, a pathological Q wave.

That indicates irreversible damage.

So blocks can be complete, like in dead tissue, but also partial, right?

Just slowed down.

Absolutely.

We see different degrees of AV block, for example.

In first degree AV block, the signal gets through the AV node every time, just slower than normal.

So you see a consistently long PR interval on the ECG.

Okay, second degree.

In second degree AV block, some signals get through, but others don't.

It's intermittent block.

There are two main types, Mobitz type I or Finkebach, where the PR interval gets progressively longer, longer, longer, then suddenly a QRS is dropped.

Like the AV node is getting tired.

Kind of fatigues, yeah.

Then there's Mobitz type II, where the PR interval is constant, but suddenly, maybe every third or fourth beat, the QRS just doesn't appear.

That's often considered more serious, potentially progressing to complete block.

And you mentioned bundle branch blocks too, where the QRS widens?

Right.

If one of the main branches of the Hisprakinje system is blocked, the impulse has to spread through the ventricle on that side more slowly, cell to cell through the muscle instead of down the fast conduction highway.

That takes longer, widening the QRS complex.

And if the block is total,

like complete AV block?

That's third degree AV block or complete heart block.

No signals get from the atria to the ventricles through the AV node.

They're completely disconnected electrically.

So the atria beat at their own rate and the ventricles.

The ventricles have to rely on a backup pacemaker downstream, usually in the Purkinje fibers.

So the atria might be going at 70 BPM driven by the SA node, while the ventricles are plugging along independently at maybe 30 BPM.

This is called AV dissociation.

It's often an emergency requiring an artificial pacemaker.

Okay, another big cause of arrhythmias, especially fast ones, is reentry.

Sounds like the signal gets trapped.

That's a great way to put it.

Reentry or circus movement is probably the most common mechanism for sustained tech arrhythmias.

For it to happen, you generally need three things.

Okay, what are they?

One, you need a potential closed loop or circuit for the impulse to travel around.

Two, you need an area within that loop that has unidirectional block, meaning the impulse can travel one way through it, but not the other way back.

Three, the conduction around the loop needs to be slow enough so that by the time the impulse gets back to the start, the tissue is no longer refractory and can be excited again.

So the impulse just keeps going round and round the loop, re -exciting the tissue over and over.

Exactly, like an electrical dog chasing its tail.

Each lap around the circuit triggers another beat, leading to a very fast heart rate.

And conditions like Wolf -Parkinson -White syndrome, WPW, create these loops naturally.

WPW is a perfect example.

People with WPW are born with an extra electrical connection, an accessory pathway, like the Bundle of Kent, that bypasses the AV node.

Short -circuiting the delay.

Right.

This causes ventricular pre -excitation.

You see a short PR interval, and that characteristic slurred upstroke on the QRS called a delta wave.

More importantly, that accessory pathway can form one limb of a re -entrant circuit, allowing impulses to travel down the normal AV node and back up the accessory pathway or vice versa, creating a rapid supraventricular tachycardia, or SVT.

And when re -entry gets completely disorganized, fibrillation.

Yeah, fibrillation is like the ultimate chaotic form of re -entry.

Instead of one clean loop, you get multiple wandering, unstable re -entrant wavelets swirling around.

In the atria, that's AFib.

Right.

Atrial fibrillation, AFib, involves chaotic electrical activity all over the atria.

No coordinated atrial contraction, just quivering.

The AV node gets bombarded with hundreds of impulses per minute.

Thankfully, it blocks most of them, but the ones that get through are irregular, leading to that irregular ventricular rhythm on the ECG with no clear P waves.

Often tolerated, but carries risks like stroke.

Yes, because the stagnant blood in the fibrillating atria can form clots.

Treatment often involves controlling the ventricular rate or trying to restore normal rhythm, plus anticoagulation.

And the really bad one, ventricular fibrillation.

The tricular fibrillation, VFib, is catastrophic.

It's the same chaotic electrical activity, but now the ventricles, the heart muscle just quivers ineffectively.

There's no coordinated contraction, no cardiac output.

It's cardiac arrest.

Requires immediate defibrillation.

Absolutely.

The only effective treatment is a powerful electrical shock to try and reset everything simultaneously, hoping the SA node can regain control.

Okay, so that covers conduction problems.

What about the other category?

Altered automaticity.

Cells firing when they shouldn't.

Right, sometimes non -pacemaker cells can develop spontaneous activity, or normal pacemakers can fire abnormally.

One mechanism is called triggered activity, which depends on the preceding action potential.

Triggered, how does that work?

There are two main types.

Early after depolarizations, or EADs, happen during the repolarization phase, phase two or three.

If the action potential gets abnormally prolonged.

Like in long QT syndrome.

Exactly.

If it's prolonged, some calcium channels might recover from inactivation while the cell is still relatively positive, allowing a little inward current that causes the voltage to bump up again.

A little upward blip during repolarization?

Right, if that blip, that EAD, is large enough to reach threshold, it can trigger a full -blown extra action potential.

A premature beat, like a PVC.

And if that happens repeatedly?

It can lead to runs of ventricular tachycardia.

This is the mechanism behind the dangerous arrhythmia seen in long QT syndrome, LQTS,

called torsades de pointe, or twisting of the points.

The QRS complexes seem to spiral around the baseline.

LQTS can be genetic or acquired from drugs or electrolyte problems.

Okay, so EADs happen early.

Are there late ones too?

Yes, there are delayed after -depolarizations, or DDs.

These occur after the cell has fully repolarized, back near its resting potential.

They're often caused by calcium overload inside the cell.

Too much calcium, like with digitalis toxicity.

That's a classic cause.

Excess intracellular calcium can cause the sarcoplasmic reticulum, the cell's calcium store, to spontaneously release bursts of calcium.

This activates currents that cause a small depolarization, the DID.

If a day reaches threshold, again, it can trigger an extra beat or runs of tachycardia.

And other things can affect automaticity too, right?

Like metabolism.

Definitely.

For instance, during ischemia, lack of oxygen and ATP can cause special ATP -sensitive potassium channels, KATP, to open.

This lets potassium rush out, making the cell hyperpolarized and harder to excite, which actually slows conduction and can contribute to blocks, but might also be protective in some ways.

One last really critical situation,

electromechanical dissociation.

Ah, EMD, or now more commonly called pulseless electrical activity, PEA.

This is a dire situation where you see organized electrical activity on the ECG, maybe even looking like normal sinus rhythm, but the patient has no pulse.

The heart's electrics are working, but the mechanics aren't.

So the heart isn't pumping blood even though the ECG looks okay, why?

It's usually due to a major mechanical problem preventing the heart from pumping effectively, like severe hypovolemia, tension nomothorax, or cardiac tamponade, fluid squeezing the heart.

The electricity is there, but it can't translate into a useful contraction, a real emergency.

Wow, okay, we have covered a massive amount of ground from that first spark in the SA node, the ion channels dancing to create action potentials, the pathways, how we read it all on an ECG, and then the many ways it can go wrong with arrhythmias.

It really is a journey from basic cell physiology right through to complex clinical problems.

But understanding these core principles, the ions, the currents, the refractory periods, conduction, automaticity, it's absolutely the key to understand cardiology.

You've really got a solid foundation now.

Absolutely, and remember, you're part of the deep dive family.

You are definitely capable of mastering this stuff.

Keep digging into it, keep asking those questions.

The human body is complex, but you can unravel it.

Keep up the great work.

So here's a final thought to leave you with.

We've seen this incredible self -regulating electrical system.

Thinking ahead, beyond just pacemakers and drugs that block channels,

what might personalized cardiac medicine look like?

Could we one day tailor treatments right down to an individual's specific ion channel fingerprint?

What would that involve?