I wrote this post to answer some of the questions, I had as a medical student, when I first learned about cardiac arrhythmias. Mainly, what are the conditions required to initiate and maintain a reentrant arrhythmia? That is, a state where the heart muscles are continuously activated by a self-sustaining loop, independent of the normal pace-making system. These arrhythmias can be benign, as with AV-nodal reentry tachycardia (AVNRT); a common, and usually harmless, cause of palpitations in young people. Or they can be deadly, as with ventricular fibrillation.
Heart muscle cells (cardiomyocytes) have some interesting properties. When they are activated, they depolarize. Depolarization causes the cell to contract, but also activates neighboring cells, setting of a chain reaction.
For the following demonstrations, we use i highly simplified model of heart. Below is a grid of simulated cardiomyocytes, each ready to activate their neighboring cells. They all start in a resting state, ready to be activated.
Activated cells are black. After a short moment, they become inactive and refractory. Refractory cells cannot be activated. In the simulation, refractory cells go from dark gray to light gray, until they have regained their resting state, and are ready for a new activation.
👆️ Click/tap anywhere in the box below to activate a cell.
Notice, that the activation is not entirely symmetric and predictable. To give the simulation a more organic feel, I added a bit of randomness to the activation of cells. Each cell is activated with a higher probability the more of its four neighbors are active (33% chance if one neighbor is active, 100% chance when 3 or 4 neighbors are active).
Pacemaker cells
Another interesting property of cardiomyocytes is their automaticity; cardiomyocytes spontaneously activate if they are not stimulated by a neighboring cells for a period. Cells in the sinoatrial node (sinus node) in the right atrium have the fastest rate of spontaneous activation, and thus activate the remaining heart, making the sinus node the heart’s pacemaker.
In the following simulation, a cluster of cells in the top left corner act as pacemaker cells.
👆️ Move the slider below the simulation to change the rate of spontaneous depolarization (heart rate).
When the spontaneous depolarization of the sinus node determines the heart rate, the heart is said to be in sinus rhythm, which is the normal (physiological) activation path of the heart. If the sinus node paces the heart at a rate faster than 100 beats per minute, the rhythm is called sinus tachycardia. Sinus tachycardia (together with increased stroke volume) increases the flow of blood from the heart, and is the physiological response to exercise.
Reentry tachycardia
In reentry tachycardia, the heart is not paced by the sinus node, but instead from a group of cells that have formed a circuit, where a wave of depolarization can loop around and stimulate itself over and over. This requires a non-responsive area among the cells (an area that cannot be activated), so a circuit can form around it.
In the simulation below, the red cells are non-responsive (dead). They could represent scar tissue after a myocardial infarction—a common cause of ventricular tachycardia. Or the simulation could illustrate atrial flutter, where a reentrant loop can form around the tricuspid valve.
👆️ To stop the reentrant tachycardia, shock the cardiac cells by pressing the “⚡️ Defibrillate!” button.
After defibrillation, the system is in sinus rhythm. The pacemaker cells were always there, but were suppressed by the reentrant loop.
The simulation above illustrates how a reentrant loop can sustain itself around a dead area, but how does it start in the first place?
👆️ You can try to click/tap on the simulation above to set of an ectopic beat (a depolarization starting outside the sinus node), but you will not be able to initiate a reentrant loop again.
How does a reentrant loop start?
To initiate a reentrant loop, the wave of depolarization must be traveling only one way around the dead area. Otherwise the two waves traveling in opposite will just eliminate each other when they meet at the other side. However, if one pathway has cells with a longer refractory period, a wave of depolarization can arrive exactly when one pathway is ready to depolarize, while the other is still refractory.
In the simulation below, cells in the lower left corner have a longer refractory period.
👆️ Try initiating an ectopic beat (click/tap) next to the area with a longer refractory period, while the area is still refractory.
👆️ You can get the system back in sinus rhythm either by ⚡️ defibrillation, or by cleverly timing a new ectopic beat to block the reentrant loop.
Fibrillation
Another common cardiac arrythmia is fibrillation—atrial fibrillation or ventricular fibrillation. Fibrillation is a reentrant arrhythmia, but the wave of depolarization does not propagate around a fixed anatomical area, but rather meanders irregularly through the myocardium.
In the simulation below, cells have different refractory times. An ectopic depolarization will activate some cells, while others are still refractory. This can create a quite complex pattern of depolarization, and may create a reentrant loop, without any dead area to loop around.
👆️ Try setting of a few ectopic beats in the simulation below, and see if you can initiate one or more reentrant loops.
Make the system more unstable by changing the scale (with high scale, nearby cells have similar refractory times) and range (overall range of refractory times in the system). High range and low scale makes the system unstable.
Stimulating the system while some cells are refractory, while others are not, corresponds to an ectopic beat occurring during the T-wave of an ECG—a high-risk situation for ventricular fibrillation. Also, a high range of refractory times, corresponds to a wide T-wave in the ECG.
Acknowledgment
This article is inspired by Bartosz Ciechanowski’s amazing interactive articles.