CEP

I would like for people who don’t specialize in electrophysiology to understand things that I write about. I also want to have a stock explanation of cardiac electrophysiology basics for presentations to non-technical audiences and for curious people. As such, I’m building and maintaining this page. Please send suggestions or questions to me via any of my contact info.

Additional Cardiac Electrophysiology information, at varying levels of complexity, may be found under the Cardiac Electrophysiology category of my blog.

An alternate version of this slide reads, “The basics with as little jargon as possible.” If we didn’t use jargon in the field, our conversations would take forever, and people would be tripping over their words all of the time. However, when communicating with educated “laypeople”, the use of jargon is both natural to us and confusing to them. I’ll try to keep things as conceptual and jargon-free as I can.

Motivation

Now, on to the motivation for why people do such research. Assuming that the heart beats 60 times per minute, that’s a pretty large number per year:

Given all of the things that can go wrong, it’s amazing that we’re alive at all. However, the heart has a lot of failsafe mechanisms and redundancies. Once you learn about those, it’s a little more understandable. Things do go wrong, though:

29.1 percent of deaths in the US are from heart disease.

CDC, 1999-2003

In sudden cardiac arrest, the normal, coordinated pumping of the heart is disrupted and becomes chaotic. As a result, the heart stops pumping blood to the body. Once the heart enters sudden cardiac arrest, there’s only one (practical) way to stop it — electrical defibrillation. You’ve probably seen the paddles used on TV or whatever:

These paddles are used to apply a massive shock to the body. This forces the heart into a resting state, eventually, and allows it to start beating normally again. It’s a little more complicated than that, but I’ll save the explanation for later. If doctors suspect someone will have a sudden cardiac arrest in the future, they can implant a device that will automatically perform the procedure:

The little device you see on the right is called an “Implantable Cardioverter-Defibrillator” or ICD. The name means that it’s implanted (duh), can gain control of the heart beat, and can stop sudden cardiac arrest (or fibrillation) via defibrillating shocks. If you look closely at the X-ray, you can see the wires leading from the device to the heart. Even with the device in the body, the shocks required for defibrillation are quite high. Patients are shocked without warning with enough energy to cause their muscles to contract, to inflict pain, and to even cause them to black out. Numerous studies have shown that this is detrimental to people’s mental well-being:

As such, people are continually trying to find ways to reduce (a) the number of times a person must be shocked and (b) the strength of those shocks.

Background

The heart contains two pumps that function together. The smaller of the two, the right heart, takes “used” blood from the body and pumps it to the lungs. The lungs release carbon dioxide and allow oxygen into the blood. The blood is then returned to the larger of the two pumps, the left heart, which pushes the “refreshed” blood out to the rest of the body. This is illustrated schematically below. Try to follow the path of the blood, starting with the right atrium. It follows a sort of figure-of-eight:

This pumping is done periodically, rather than continuously. This is why you have a pulse. Every second or so, the whole heart contracts, moving blood into the lungs and the body. It then relaxes, pulling in blood from the lungs and the body. This pumping is coordinated by electrical pulses in the heart. There is an extensive network of fibers that carries out this coordination, the key part of which is highlighted in red below. The red fibers are insulated — the atria (upper chambers) are activated first, and then the fibers carry the impulse to the furthest part of the heart ventricles (lower chambers). Blood is thus squeezed out of the ventricles from the “bottom” up, like the way you’re supposed to squeeze your toothpaste out of the tube:

To send and carry signals, heart cells expend energy by moving charged particles (ions) around. They prepare to do this by building up a store of electrochemical energy and waiting, at “rest”, until a signal is received. This is similar to a camera flash:

Often you can hear the capacitor charging up after taking a picture. This is so that the flash will be ready when you take another picture. You won’t have to wait for it to charge once you press the shutter button. Thus, heart cells at rest are always ready to fire immediately without having to “charge up”. How do cells charge up?

The line of squiggles down the middle is what’s called a “phospholipid bi-layer”. All you need to know is that it’s the membrane that makes up the border of a cell. It helps to keep stuff inside / outside of the cell. Charged particles, such as potassium (K), sodium (Na), calcium (Ca), and chloride (Cl) ions can’t cross the layer. As illustrated in the picture, the inside of the cell contains a lot of potassium, and not much sodium, chloride, or calcium. The outside of the cell contains large numbers of these, but not much potassium. Because of the properties of diffusion, these imbalances of ions exert something like a pressure on the membrane. The ions “want” to be in equal concentrations on both sides of the membrane. Potassium (green circles/arrow) wants to leave the cell, and calcium, chlroide, and sodium (white/orange/pink) want to enter the cell. The separation of these ions into different compartments requires energy. Because these ions have charge, and the membrane separates them, the mechanism is actually nicely analogous to charging the capacitor in a camera flash. This is where energy is stored in preparation for “firing”. The energy balance is such that the cell has a negative polarization with respect to the outside. When the cell fires, ions are let through the membrane in specific orders and amounts:

In the diagram above, sodium ions are being allowed to pass through the membrane via an ion channel. Because they are positive, they cause the cell’s polarization to move in a positive direction. Since the cell is normally negatively polarized at rest, and this moves the potential toward a zero potential (no polarization), this is called de-polarization. De-poliarization is the equivalent of the camera flash. Unlike such a flash, in the heart it follows an elongated time course:

This time course of depolarization and repolarization is usually referred to as an “action potential”, although this is technically an inaccurate abbreviation of “action potential trace”. The potential to fire is actually what should be called an action potential. I’ll call it an action potential (or AP) anyway. In the beginning of the AP, sodium (Na) is allowed to rush into the cell, as in the previous illustration. This pushes the cell’s potential up. Potassium (K) then begins to rush out, which should bring the potential down. However, at the same time, calcium (Ca) enters the cell. These opposite currents result in a balance for a period of time, so the AP “plateaus”. Finally, calcium (Ca) current is reduced, and potassium (K) takes over, returning the cell to rest. The number of ions involved is quite small. It only uses a small amount of the stored energy in the cell. Even without regeneration of stored energy, the cell can fire in this way many times. This process is controlled by gates in the ion channels. Some channels are gated, some are not. There are many, many types of channels, gated and ungated, as well as pumps that help to keep the cell charged (or polarized). A thorough explanation of that is beyond the scope of this write-up.