Be like the AV Node
- Caroline Chen
- Oct 8, 2020
- 4 min read
Updated: Oct 9, 2020
This post is a bit science-heavy, but it's really cool info! At least I hope it is haha. Skip down to past the separation line if you want to get to the less science-y take-away. But I'd highly recommend to read the whole thing for sense to be made :)
In class, I recently learned about electrical conduction within the heart. At the end of lecture, I was particularly interested in what we call the "AV node delay". Without getting too much into the physiology, what's important to know is that our heart has these "autorhythmic" cells that serve as a pacemaker for our heart beat! This means that the heart can set its own contractile rhythm without input from the nervous system. Cool, right?!
Anyway... what interested me about the AV node delay is that it's really important for efficient heart function. Like really important. I guess we might need to go into a bit of signaling for this to make sense.
Basically, our heart has four chambers: the right atrium, right ventricle, left atrium, and left ventricle. Blood flows from the atria to their respective ventricles, and from the ventricles to either the lungs (to get oxygen) or to the rest of the body (to deliver oxygen to our tissues). And that's how we stay alive!
How do the different chambers of the heart "know" when to do their pumping? Well, near the "top" of the heart (called the "base"—kinda counterintuitive to what we might think), we have the sinoatrial (SA) node that serves as the main pacemaker for our heart. The electrical signals from this node cause the atria to contract and eject blood into the ventricles. These signals also reach the atrioventricular (AV) node. Some call the AV node the "gatekeeper" that relays the contractile signal of the SA node to the ventricles, causing ventricular contraction.
Important!! The atria need to finish ejecting all of their blood into the ventricles before the ventricles begin their part of the pumping. Kinda like passing on the baton in a race. Or else blood will remain in the atria and may lead to complications (e.g. blood clotting). Thus, there needs to be a delay in the electrical conduction, or else the ventricles will begin contracting before the atria have fully ejected all of their blood. (Here's a nice video on how the heart contracts for more background. Recommend watching at 2x speed.)
Alas, we have the AV node delay. And while we learned about its existence, I was curious as to how the delay happens. Like what actually causes the delay, or allows for it? So I consulted Dr. G (what my bio professor calls Google!) and found a paper that explained it pretty well!
In short, the delay happens because of slow conduction through the AV node, for several reasons.
Firstly, the myocytes (aka muscle cells) in this part of the heart have a smaller diameter, and since conduction velocity is related to diameter, a smaller diameter leads to slower conduction.
Secondly, the way the cells are arranged in the AV node make it such that the electrical signal follows a more "winding" path, slowing it down.
Thirdly, there's poor expression of Na+ channels, which are needed for signal propagation.
And lastly, there's simply poor electrical coupling between AV node cells due to their relatively few and small gap junctions. (Gap junctions are the bagel-shaped "holes" that connect cells and allow for the electrical signal to travel between them.)
The first thought I had when I discovered this explanation was... wow, there're so many faults with the AV node. "Poor" expression of channels, "few" gap junctions, "small" diameter. All things that I've been trained, or at least influenced, to think are *objectively* bad. Like, who wants "poor expression" of anything?! And why have "few" when you can have many?
And that really made me think. These characteristics that I deemed "imperfections" in the AV node are what make it work. They're necessary for healthy people to live their lives and not have to constantly worry about blood pooling in their atria and causing blood clots. Who's to say that poor expression is bad, or that fast conduction is good? To assign such a universal rule would be, in essence, incorrect. (I mean, in this case, it's the complete opposite.)
So, these "imperfections" are not imperfections. They're just facts. They're the truth. They're what they are. No judgement necessary.
It's interesting how the connotations of the descriptions associated with the AV node are so engrained as being things to avoid, rather than to appreciate. And it's intriguing how language can shape one's interpretation even of something that's objectively true.
When thinking about it, if we're using words like "few" and "poor", there must be something that we're comparing the AV node against, likely the SA node, since it's the main pacemaker of the heart. As humans, we're constantly comparing things to a certain gold standard to help us simplify and categorize the gazillion things running through our minds. What we define as the gold standard is usually what we're familiar with. Familiarity often dictates what we think of as "good".
But it's important to realize that there really is no binary. There's no absolute good or absolute bad. Just because something doesn't match up to the gold standard, doesn't mean it's lacking in any way. What even is the gold standard? There are so many external factors and individual circumstances that may confound comparisons, so is there even such a thing?
Anyway... I'd just like to recommend for us to be like the AV node: embrace your facts without judging too hard. Take your pre-existing gold standard with a grain of salt, and just be what works for you. Be like the AV node delay: take time to recuperate whenever you may need. A delay is not a fault, but rather—as you can tell from the evolution of our marvelous blood-pumping organ—is necessary to keep our bodies well and running. What works works, ya feel?
This shall be all for today. Stay grateful for the AV node and its delay. ❤
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