Home > Biology, Computational Biology, Medicine > Cardiac Arrhythmias and Modeling (Part 2)

Cardiac Arrhythmias and Modeling (Part 2)

In Part 1, I gave an introduction to normal electrical conduction in the heart, and why it’s important.  Now, it’s time to look at how things can go wrong…


Arrhythmias: When the Conduction System Goes Awry

First of all, a word of reassurance: most of us will live full lives without experiencing any arrythmias, or at least being aware that one has occurred.  The cardiac conduction system is very reliable and works well under changing conditions, day in and day out, year after year.  While most arrhythmias are not harmful, there are some that are serious, or even lethal.

Arrhythmias can generally be placed into one of three groups: slow, fast, or irregular.  I won’t provide an exhaustive list of all arrhythmias here; I just want to provide a few examples.  Also, just as a reminder, here’s what a normal ECG looks like:


Image Credit: ambulance technician study


Slow Rhythms

Slow arrhythmias are called bradycardias, and are generally caused by problems with either the SAN or the AVN (SAN = sinoatrial node, AVN = atrioventricular node, see Part 1).  Below is an example of a severe bradycardia, third-degree heart block, which is often problematic because the result is a heart that is pumping too slowly to maintain adequate blood pressure.  You’ll notice two things about this ECG strip.  First, the P-waves are completely dissociated from the QRS complexes: the distance between a P-wave and the QRS complex that follows it changes with each beat and follows no pattern.  This is because signals that are being generated in the SAN and traveling through the atria down to the AVN are completely blocked upon arrival at the AVN.  Thus, there is the normal activity up in the atria, producing regularly spaced P-waves, and there is activation of the ventricles, producing regularly spaced QRS complexes, but there is no relationship between the two, owing to the complete block of signals at the AVN.


Image Credit: ambulance technician study

Second, the QRS complexes are much wider than those shown above in the “normal” example.  Most cardiac tissue has some ability to act as a pacemaker.  Here, the ventricles are being excited by a signal originating from somewhere below the AVN, at a rate slower than the P-waves which are being generated by the SAN.  Also, the fact that the ventricles are responding to a signal that originates from somewhere other than the SAN means that electrical activation within the ventricles follows a different pathway, which makes the QRS complexes look “wide and bizarre.”


Fast Rhythms

Fast arrhythmias are called tachycardias.  Below is an example of a particularly serious, and potentially lethal, tachycardia: ventricular tachycardia.  Ventricular tachycardia is dangerous for two reasons: 1) It results in the ventricles beating so fast that they don’t have time to fill in between beats, which severely limits the ability to pump blood, and 2) it can degrade into an even more disorganized rhythm: ventricular fibrillation.


Image Credit: ambulance technician study


Irregular Rhythmis (wait, is than an oxymoron?)

One type of arrhythmia in the “irregular” class is fibrillation.  Returning to the orchestra analogy from the last post, fibrillation is akin to what you hear before the start of an orchestra’s performance: random jumbles of sound as each musician practices and tunes on their own.  When a heart is fibrillating, each little region is being activated on its own and is not responding to directions from any sort of pacemaker.  This highly disorganized pattern of electrical activation results in a heart that quivers, rather than doing any sort of organized pumping.  It is a common occurrence for the atria to fibrillate, especially as people age, a condition called (unsurprisingly) atrial fibrillation.  Atrial fibrillation can cause a reduction in the heart’s pumping ability, since the ventricles are not being as fully loaded as they could be before they contract and force blood out to the rest of the body.  Atrial fibrillation is also problematic because it can lead to the development of blood clots.  If the atria are just sitting there quivering, blood may sit in one corner for too long, which promotes clotting.  Eventually the clotted blood finds its way down into the left ventricle, where it is then pumped out to the rest of the body.  If such a clot lodges in one of the brain’s blood vessels, a stroke can occur.  Below is an example of atrial fibrillation.  You’ll notice that there is “messy” electrical activity in between QRS complexes (which are themselves occurring irregularly), as opposed a clean baseline and distinct P-waves.


Image Credit: ambulance technician study

Ventricular fibrillation, as you can imagine, is much more dangerous, as no blood is being pumped anywhere.  The only way to correct V-fib is to apply a large electrical shock (just like when you see a patient being shocked with paddles on television).  In the ECG strip above, there was some disorganized electrical activity because the atria were fibrillating, but the ventricles were still producing distinct QRS complexes.  However, there are no QRS complexes in the ECG strip below since the entire heart is fibrillating.


Image Credit: ambulance technician study


Another type of arrhythmia in the “irregular” class is the premature complex.  A region of heart tissue can become excited on its own, and if this region is large enough, the resulting activation can propagate through the entire  heart resulting in a complex (or contraction) before one would be expected from the dominant pacemaker site.  These early activations, if originating from somewhere withing the ventricles, are called premature ventricular complexes (PVCs).  Now, PVCs on their own are fairly benign, but they can be worrisome for two reasons.  First, they often signify some underlying problem that’s manifesting itself as an abnormality with the heart’s electrical system.  Second, it’s possible for a PVC to occur during a “vulnerable window” and trigger something called a reentrant arrhythmia, one example being ventricular tachycardia.


Image Credit: ambulance technician study

There are two PVCs in the above ECG, occurring after the second and fifth normal beats.  These are multifocal PVCs – they originate from different locations within the ventricles – which means that the resulting activation follows a different path in space for each one, and is why the two PVCs look so different from one another.


Reentry: A “Short Circuit” Within the Heart

Reentry is a situation where some region of cardiac tissue is repeatedly (and rapidly) excited as an electrical activation wave travels round and round, following a circular path.  Once cardiac tissue has been excited, there is a period of time, called the refractory period, which must pass before the tissue is able to be excited again.  What this means is that normally electrical activation follows a path in one direction only; it cannot turn around and go back from where it came because the tissue at the trailing edge of the activation wave is still refractory.  A more detailed description of reentry can be found here.  I mention reentry because certain tachycardias (including ventricular tachycardia, mentioned above) and fibrillation (also mentioned above) are examples of reentrant arrhythmias.

Okay, so some particularly nasty arrhythmias result from reentrant pathways in the heart.  But what causes reentry in the first place?  There are two conditions, often working in concert, that greatly increase the chances of a reentrant pathway forming.  One of these conditions is slowed conduction.  If electrical activation travels more slowly in one region of heart tissue than another, this can help set the stage for reentry.  The second condition is referred to as unidirectional block.  Electrical activation in the heart  doesn’t occur in one-dimensional lines, but rather spreads in multiple directions.  If the spread of an electrical wave is blocked in one direction, but not the other, this can facilitate the development of reentry.

Now we’re moving into increasingly detailed explanations of some causes of cardiac arrhythmias.  Given that some arrhythmias are manifestations of reentry, and reentry can be established by slowed conduction and/or unidirectional block, what’s responsible for slowing conduction, or creating a unidirectional block?  Remember those PVCs I was talking about earlier?  They (or even smaller regions of depolarization that don’t manifest as PVCs) can create a unidirectional block.  I mentioned previously that cardiac tissue has a refractory period during which it is impossible (or much more difficult) to be excited again.  If a PVC occurs in one region of cardiac tissue, that region will now be refractory.  Now imagine a spreading activation wave, and what would happen if one part of that wave tried to spread into a region that had just been excited by a PVC.  Since the tissue is now refractory (thanks to the PVC), the spreading wave will be blocked in that direction, but will  still be able to spread in another direction into tissue that isn’t refractory.  Voilà!  You now have unidirectional block.

If you want to get a better idea of what I’m talking about, take a look at the animation at the top of Frank Starmer’s page, who is a researcher at Duke University.  The animation represents a two-dimensional sheet of excitable cells, with yellow representing non-excited cells and red representing excited cells.  At the start, a planar wave (red line spanning the entire yellow sheet) is initiated and propagates downward.  Shortly thereafter, a premature stimulus is delivered (shorter red line near the top of the sheet).  This premature stimulus cannot propagate downward, as the first wave has just passed through that region, leaving those cells in their refractory period.  But the tissue above the premature stimulus has had enough time to recover from its refractory period, and so the premature stimulus moves upward but not downward.  This unidirectional block sets up the spiral wave activity that you see in the last half of the animation.

Ultimately, many of the explanations for what causes slowed conduction or unidirectional block (including what causes a PVC to occur) are found at the level of individual cardiac cells, or even subcellular components.  Single-cell descriptions can take us only so far, but they are still very powerful.  In Part 3, I’ll talk about how we use computers to simulate individual cardiac cells, as well as larger regions of tissue.

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  1. Haitham
    January 10, 2011 at 09:44 | #1

    Very comprehensive and informative, thanks Byron, keep more coming.

  2. January 10, 2011 at 11:25 | #2

    Thanks, Haitham!

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