1.3 Sinoatrial Node Physiology and Autonomic Nervous System

• One thing that you'll come to realize is that the high frequency of the spectral power of heart rate variability is associated with the parasympathetic system, whereas the low frequency is associated with both the parasympathetic and the sympathetic nervous system. And I'm going to explain to you why that is. 
• So in the SA node, which is we know the pacemaker, there are four important ion channels on the SA node cell membranes, you have the sodium channel, potassium channel, actually to potassium channels in a calcium channel, and within the cell is electrically negative relative to the outside of the cell. And so there's a 65 millivolt difference so that the inside is 65 millivolts, slower than the outside of the cell. 
• So when you have positive ions move across the cell membranes, through the ion channels, it neutralizes for decreases this electrical potential difference. And so what we say is that depolarize is the the cell membrane or the cell. 
• On the other hand, if you have potassium channels, which goes in the opposite direction, it enhances this polarization or V colorizes, or hyperpolarizing Salmone, right. And this is sort of a diagram to illustrate this. 
• So you have a measurement of the voltage potential difference across the cell membrane. And as it goes up, you know, from negative 65, millivolts, to zero and even positive potential difference, it's depolarization. And as it goes down, it's repolarization. 
• The sodium channel has what's called a leaky current. And this leaky currents will causes a depolarization, a very slow depolarization of the cell membrane. And what happens is that slowly as it reaches a threshold, as denoted by this dashed line here, it causes the calcium channel to open up. And this causes a rush of calcium channels into the cell, and then actively leads the depolarization of the SA node cells. 
• Subsequently, the potassium channels open up in that it leads reverses this depolarization that is caused by both the sodium calcium channels and you get repolarization as denoted by this downslope of this potential difference. 
• Now taking this within the context of the autonomic nervous system, you can see how the autonomic system affects this pacemaking ability of the cell. So the parasympathetic nervous system involves the acetylcholine coming from the post ganglion of the power to set the sympathetic nervous system binding to the amp to the muscarinic receptor, activating the G protein, which then subsequently activates this potassium-associated acetylcholine channel. 
• And because this is a potassium channel that goes in the direction that enhances the polarization, what it does is that during this stage of this slow leak of this ascending channel, it leads to this very slow rise of the peoples ation. Now, this is in the dashed line is what is considered a normal heart rhythm. So if there was no intervention from either the sympathetic or the vagal system or the parasympathetic system, you would have this type of automaticity of the electrical potential. 
• But with the vagal nerve, it slows this depolarization and subsequently leads to a slower heart rate. Essentially, you're not having firing of the cells happening more frequently. 
• The sympathetic nervous system, on the other hand, operates through norepinephrine or epinephrine that binds to the beta one receptors. The Vader on receptors then binds to general cyclase, which converts ATP to cyclic a&p. And the cyclic MP hastens or enhances this leaky current in the sodium channel. And this leads to a rise of this depolarization this steady leak, and then leads to a faster polarization or faster heart rate. The other thing that it does is that the cyclic a&p activates protein kinase a then activates potassium channels and calcium channels. So what it does is it increases the depolarization of fast depolarization and fast repolarization equalization so it enables a faster beating of the heart.
• So why am I harping on this and why am I bothering you with all this dTT Alice, because it's really important to know this physiology to understand what you're seeing when you're obtaining the heart rhythms that you get from your various devices. 
• The SA node is where both the parasympathetic nervous system and the sympathetic nervous system meet. And so we can gain insights in the activities of the autonomic nervous system based on heart rate over time. And what we look at is the inter between development for for the rbdigital. So this is an example of a EKG of a normal sinus rhythm. And we have we designate the our impulsive bar indicates the peak of this QRS segments. And then we identify the RR interval, the time between these intervals. And then we can obtain a calculation graph which I had shown before of the RPC for a good time to get a better sense of what is happening with a parasympathetic and sympathetic nervous system. 
• So what happens however, we have pre atrial contractions, where you have contractions that's happening at not only the se nos, but also in the other parts and topics sites that the right atrium, you will see that the R is designated here. 
• But does the RR interval actually provide any information about the autonomic nervous system? And what happens if you have a something called atrial fibrillation, where you have multiple ectopic sites throughout the right atrium, and sometimes the left atrium that leads to this erratic heart rhythm. 
• And what we recognize is that because a lot of these extra nodes occur outside the SA node, we consider them as noise and not reflective of what's happening in the autonomic nervous system. 
• So the important thing to know is that heartbeats originating from the SA know, are the only ones that provides sufficient insights into the parasympathetic nervous system and sympathetic nervous system. And to, to delineate what are sort of the normal rhythms through the essay notes, we change our into ends, or normal rhythms. And the way we know on an EKG, whether it's a normal rhythm or not, is we could see something called a P wave before this QRS you can see these P waves. And this P waves are the electrical contractions or electrical signals going through the right atrium. And we know through the access or the morphology, how it's shaped, that it's going through the right system. And the appear atrial contractions, we noticed that the normal sinus rhythms are occurring here, because we see the P waves here, we don't necessarily see the P waves that occur before these pre atrial contractions. And as a result, we eliminate these are ways. And sometimes what we do is we interpolate the end between the normal ones to get an idea of what the essay no would have done if it hadn't been for these ectopic beats. 
• For atrial fibrillation, on the other hand, it's so inundated by all these signals that are coming from these other parts of the right atrium, that we can't get enough information that say no, so we can't really get much of information in patients with atrial fibrillation is about their autonomic nervous system. So this is something that you can get from your EKG. 
• However, many of you were getting heart rhythms from use of watches and watches don't use, you know, obtain EKGs, what we obtained are the PVCs photoplethysmography, which measures the flow through and microvasculature is in your skin. And it has, you know, it doesn't have this rapid upstroke that you can see in the electric polarization, it's a slow rise. And the other thing to know is that you can't tell whether these things are normal sinus rhythms, or whether they are attributed to an ectopic beats honey, you can't directly because there isn't a P wave. And you don't have a P wave equivalent in the PPG signals. This actually is not a P wave is a reflective pulse wave. So it's not a P wave. 
• So this is one of the challenges that you may encounter as you do your research is that the PPGs won't give you information about what that were directly won't give you information about what kind of rhythm you have. And sometimes if someone has a lot of ectopic atrial beats or atrial fibrillation, it falsely gives you a higher heart rate variability and it doesn't give you a selection of your autonomic nervous system.
• Next thing I wanted to the reason that this diagram is really important is to really give you an understanding of the dynamics of the essay No. The in the essay knows the acetylcholine receptor operates very quickly. So the acetylcholine after it binds to the antigen receptor, the G protein acts literally in Heuss milliseconds to activate this potassium ion channel. 
• On the other hand, the sympathetic nervous system it has, its incubated through this enzyme called adenoidal. Sideways. And this cyclist operates at much slower timescales, approximately three seconds or lower, and as a result, is much slower to respond. 
• The other thing to note is that there are different dynamics in the neurotransmitters associated with each of these autonomic nervous system branches. The parasympathetic nervous system utilizes acetylcholine, and subnormal the sympathetic nervous system utilizes norepinephrine, or epinephrine. And the acetylcholine when it's released from this ball of the preganglionic neuron, it is quickly eliminated by abundant presence of acetylcholine esterase within the gap junction. On the other hand, the sympathetic nervous system has to not have to uptake these norepinephrine within the gap junctions. And the timescales are much different. So the parasympathetic nervous system removed these things about every 0.2 seconds, whereas the sympathetic nervous system removes it in 20 seconds. 
• And what this leads to is a very different is a very different dynamic for each of these branches of the nervous system. For the parasympathetic nervous system, they've done this and dance is they've stimulated the vagal nerve. And you can see the stimulation right here, they essentially give seven hertz electrical stimulation for about 22 seconds. And right away, you can see that the beats per minute or the heart rate significantly decreases. And almost immediately after you initiate the stimulation, and the moment it stops, you stop the stimulation, the heart rate jumps back up nearly close to its original heartbreaking rhythm. And the same after you do the second stimulation. And so the parasympathetic has a rapid onset, quick execution and a short recovery. 
• The sympathetic nervous system on the other hand, when you are delivering 20 hertz stimulation to the sympathetic nerve and take a look at the heart rhythm, you can see that it doesn't kick in right away, there's a little bit of a lag about seven seconds or so from the initiation of electro stimulation, and the the rise of apartments. And this rise in the heart rate is not immediate, like you see in the the vagal system, but it's very slow. And after you stop the stimulation, there's also a lag and it's a very slow recovery time. So the sympathetic has a delayed onset, slow execution and a long recovery time. 
• So what does this mean is that when we're breathing and our breathing that every, you know, three to seven seconds or nine to 24 cycles per minute. We're operating in the high frequency range. And as noted, parasympathetic nervous system is the only one that really is able to operate in the higher frequency range due to this dynamics, quick onset, quick execution, rapid execution, rapid recovery time, whereas the sympathetic nervous system is simply too slow. So when you have something like respiratory sinus arrhythmia, it changes in your heart rate with respirations is predominantly a parasympathetic phenomenon. 
• And it's simply due to the fact that the esino has a filter which inhibits the sympathetic nervous system to operate at a faster frequency.

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