In this video, Dr. Joshua Cooper, Director, Cardiac Electrophysiology, Temple University Hospital, reviews patterns of sinus node dysfunction, as well as fake-outs -- including hidden ectopic beats, vagal events, and accelerated junctional rhythm.
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This is Dr Joshua Cooper and this presentation is all about the sinus node. The reason this is important is that if a patient has symptoms related to sinus node malfunction resulting in either pauses or bradycardia. And there's no reversible cause. That is potentially an indication for a pacemaker. It's important to recognize when the sinus node is malfunctioning causing symptoms. And it is also important to recognize when there are other observations on telemetry that don't represent sinus node dysfunction. And a different treatment strategy is indicated. The sinus node also known as the sinoatrial node is a structure that sits in the top right part of the right atrium near the superior vena cava. It acts as the natural pacemaker spot of the heart and it sets the pace in response to what the body's needs are. If you're at rest or asleep, it fires more slowly and with adrenaline from activity or other causes, it speeds up every time the sinus node fires, it sends electrical signals across the right and the left atrium causing them to contract and resulting in a P wave on the EKG or telemetry. When the sinus node fires at slower than 60 beats per minute. That's defined as sinus bradycardia. That can be a completely normal phenomenon in younger people, athletic people, or those with higher vagus nerve tone to the sinus node. But it also may result if the sinus node itself is not functioning properly if there are symptoms and no reversible cause of sinus pericardia, such as this patient here who presented with fatigue and a heart rate of 34 beats per minute. That is potentially an indication for a pacemaker to speed up the heartbeat and alleviate those symptoms. Another potential manifestation of sinus node dysfunction is sinus pause or sinus node arrest. This can occur if the sinus node is firing just fine and then suddenly stops for no obvious reason, resulting in a pause. If this causes a pause in the heartbeat, that's long enough to cause lightheadedness or even fainting and there's no reversible cause. That's another indication for a pacemaker. Here's an example of that occurring where you have a patient having sinus rhythm followed by the sinus node stopping for no reason and then the heartbeat resumes. It's interesting to see in this case that the first beat after the pause is a junctional beat. That means there's no P wave in front of it. This beat was not generated by the sinus node, but instead by the A V node or the center of the heart, which creates a QR S with no P wave in front of it it's interesting to see that right after that happened, there's a little sinus beat, peeking out behind the QR S because the sinus node recovered slightly after the junctional beat kicked in. And the sinus node then continues to fire. After the pause, here's a slightly different version of that occurring where we have sinus rhythm, a more brief sinus arrest, but then prolonged evidence of a sinus arrest because the sinus node does not immediately kick in. And instead this patient remains in a slower rhythm that is initiated by the A V node mode or the center of the heart rather than the sinus node recovering. Notice that in this junctional rhythm, none of these QR S complexes are preceded by a P wave. So that means that each QR S is generated from lower down in the A V node rather than the sinus node. This can result in symptoms because of the bradycardia. Yet another manifestation of sinus node dysfunction can show up when the sinus node is suppressed by other atrial activities such as a premature atrial beat from another location. In this case, the sinus node can fire A PAC can suppress the sinus node and then it can take longer than normal for the sinus node to wake up after that suppression. Here's an example of that where we see a premature atrial beat occurring manifesting as an early P wave that has a different shape from the sinus node that tells us this early beat is coming from a different location, creating a P wave of a different shape. It suppressed the sinus node and it took a couple of seconds for the sinus node to wake back up and start firing again. If this pause is long enough again, it could cause lightheadedness or even fainting. And that is another manifestation of sinus node dysfunction and potentially an indication for a pacemaker. You can also see delayed sinus node recovery after an atrial arrhythmia such as atrial fibrillation. Here's an example of atrial fibrillation occurring and if it should stop on its own, you can see a little pause or a longer pause depending on the health of the sinus node before it kicks back in. Here's an example of atrial fibrillation occurring on the left a sinus pause and then sinus node recovery again, if this pause, sometimes called an offset pause or a conversion pause after spontaneous termination of atrial fibrillation is long enough to cause symptoms and there's no reversible cause. It's yet another indication for a pacemaker. This can also occur after an atrial tachycardia or atrial flutter or any atrial rhythm that's not coming from the sinus node. Here. In the bottom, we see an atrial tachycardia spontaneously terminating a sinus pause and then lack of sinus node recovery right away as this patient remains in an extreme bradycardic rhythm without P waves in front of these Q RSS. This is a junctional escape rhythm that persisted for a number of seconds before the sinus node finally recovered. Here's another example of an episode of Permal atrial fibrillation spontaneously terminating, resulting in a sinus pause and sinus bradycardia immediately following this event, you can see in the telemetry trend below that there's a period of atrial fibrillation lasting about an hour and a half and then it spontaneously terminates. And at the top here, we're seeing the telemetry recording at the time of that spontaneous termination. You can see that it takes two or three seconds for the sinus node to kick back in. And it's followed by a period of sinus periodic cardia. Several seconds later, we can see that the sinus rhythm has actually returned to a very normal rate of 83 beats per minute. It's interesting to note in this particular patient that their manifestation of sinus node dysfunction is not sinus brady cardia or fatigue during sinus rhythm. But in fact, simply pauses when the patient has atrial arrhythmias that spontaneously terminate, resulting in pre syncopy symptoms. There's another very specific form of sinus node dysfunction called sinoatrial exit block that can create very specific patterns on an EKG or telemetry strip. This type of sinus node dysfunction comes from the fact that there is a zone of fibrous tissue called perinatal tissue that surrounds the sinus node area. Every time the sinus node fires the electrical impulses must travel through this perinatal tissue to get to the right atrium and generate a P wave. And if there's extra fibrosis, then some of these signals from the sinus node which may continue to fire may not be able to escape through the perinatal tissue to even generate a P wave resulting in sinus bradycardia. For example, if every other beat can escape through the perinatal tissue, but every other beat blocks, then you might see sinus bradycardia and no evidence of these ineffective sinus node firings on the surface. EKG So how do we know that this is happening rather than just plain old failure of the sinus note to fire in the first place. Well, here's an example of a patient with sinoatrial exit block. Here, we see a normal sinus rate on the left and a bradycardic sinus rhythm on the right. And if you look at mathematically the rates of each, you'll notice that the bradycardic segment is exactly half the rate of the more normal sinus rate on the left. This is because every other impulse is failing to exit, resulting in an abrupt drop in heart rate, which is cut in half this same patient. On another part of the telemetry strip showed this clustering of sinus beats, three beats, followed by a pause, followed by another three beats. And this is another pattern of sinoatrial exit block. In this case, a 4 to 3 exit waky block pattern suggesting that this is not simply plain failure of the sinus note to fire, but failure of those impulses to exit in various patterns. It's rare and the treatment is the same if this patient has symptoms, a pacemaker is indicated. Let's review a few scenarios of changes in sinus node behavior that are not from sinus node dysfunction. Here's an example of a patient where the sinus rate is slowing down and speeding up back and forth throughout this telemetry strip. And here's another example of the same phenomenon where we see the sinus node speeding up and slowing down about two or three times for the duration of each of these recordings. This is a phenomenon known as sinus arrhythmia, which is a terrible term because we usually use the term arrhythmia to mean some abnormality. This is actually a very normal phenomenon and results from normal fluctuations in autonomic tone to the sinus node during breathing. That's why this is called Respi phasic sinus arrhythmia changes in vagus nerve and sympathetic tone to the sinus node during the course of breathing where different filling and emptying of the right atrium and different stretch on the wall of the atrium result during inspiration and expiration. Again, this is a normal phenomenon typically does not cause symptoms and does not require any treatment. Here's a telemetry strip of a patient who had Brady cardia while in the hospital and there are two main observations that you should make to figure out what's going on. The first is that the sinus node is slowing down, starting at the left of the screen with a rate of 62 beats per minute and then slowing down to the fifties and forties and even into the thirties. The second observation that is happening at the same time is that we see here, a P wave that fails to conduct down to the ventricles. If you look at the pr interval before and after that missed beat, which represents essentially second degree a V block, you can see that there's a big difference in the pr interval before and after which is classic for a Mobi one or Waky box type pattern signifying block at the level of the A V node. So what's going on here? We're seeing slowing down of the sinus node and a problem with the A V node occurring at the same time. These are very different anatomical structures in different locations at the A in the atrium. So why would they both malfunction or slow down at the same time? Well, there's one commonality between the two that can explain why this is happening simultaneously. And that commonality is the vagus nerve influence on each of these structures. The vagus nerve has a slowing effect on the sinus node as well as the A V node. And so what we're seeing here is a vasovagal reflex or a cardioinhibitory reflex resulting from high vagus nerve influence on the sinus node, slowing it down and also on the A V node resulting in a prolongation of the pr interval and even second degree or Mobi one A V block. This can be a very normal phenomenon and is self-limited. It can occur in particular with dehydration, pain or other stimuli that can provoke a vasovagal reflex or simply seen during high vagal tone during sleep in the hospital. Here's another patient with sinus node, dysfunction, sinus slowing occurring at night. This patient was asymptomatic at 3:12 a.m. because they were asleep. You can see here that the sinus node is progressively slowing to the point of a pause of over two seconds. And then the sinus node recovers and speeds back up. Notice that there's artifact associated with the acceleration in heart rate. And that isn't just a coincidence. This is a patient with obstructive sleep apnea and during the hypoxemia that results from the lack of breathing, there is a powerful vagal outpouring resulting in slowing of the sinus node. And as this patient shifts a little bit at the end of this particular APIC episode that results in a little movement of the telemetry wires and some artifacts seen on the telemetry strip. Here's another patient at 1:46 a.m. who had a period of sinus bradycardia asymptomatic because it was during sleep. And again, this was an APIC episode resulting in sinus node suppression from high vagal tone. During the apnea event. The patient partially woke up a little bit but was unaware of their APIC spells resulting in a little bit of a shifting and movement of the telemetry wires and artifact on telemetry. This is very classic for obstructive sleep apnea. There's no indication for a pacemaker. But instead this patient should have a formal sleep study and treatment of their sleep apnea. Here's a more significant example of a pause resulting from obstructive sleep apnea and a lot of the times we in electrophysiology will get a call uh asking if this patient should have a pacemaker again. This was another asymptomatic patient even though this was a pretty long pause of over five seconds, but the patient was asleep. This was occurring at 4:32 a.m. and notice like all vagal events. This episode was self limited and as soon as the patient started breathing again, no artifacts seen here. Uh there was an acceleration and in fact, back up to sinus tacho cardia signifying that this patient's sinus node works just fine. But this was a vague influence on the sinus node resulting in temporary suppression. The treatment again is to treat the sleep apnea itself. And these pauses go away when the patient stops having hypoxemic episodes at night. Here's another scenario that may mimic sinus node dysfunction but represents another phenomenon. If we look at the right side of this telemetry strip, we wonder where the P waves went suddenly. We have QR S complexes that don't have a P wave in front of them. If we look at the left side of the strip, there is the sinus rhythm occurring with a P wave in front of each QR S as expected. But as you then progress to the right side of the strip, you start to see the P waves vanish. In fact, they're moving into the QR S complexes and you can barely see them at all. There may be a couple little hints toward the end of the strip that maybe there's a P wave buried in the very front of the QR s. But otherwise, we really don't see them. So what's going on here? It's almost as if the Q RSS are being pulled forward into the P waves. And in fact, that's exactly what's happening. This is called an accelerated junctional rhythm. And what's going on here is that the A V node or the middle of the heart, the A V junction decided that it wants to join the show and start firing in a rate that is slightly faster and competing with what the sinus node was doing. So you have something called iso rhythmic activity between this accelerated junctional rhythm and the sinus rhythm. That means there's two things that are happening at about the same time and whatever is a little bit faster at that moment is going to win. And in this case toward the end of the strip, the junctional rhythm, the accelerated junction rhythm is a little bit faster and it kind of overrides the sinus rate which was slightly slower and you can see a little bit of a waxing and waning back and forth as one or the other may win the race. This is not a manifestation of sinus node dysfunction. But instead simply that there's a faster spot that decides to chime in. Here's a slightly different version of that where you can see over to the left sinus rhythm and then you have a premature junctional beat, not a premature atrial beat, but it's junctional because it's a narrow QR s but there's no P wave in front of it. In fact, there may be a retrograde P after it. And for a little period of time, we're in junctional rhythm where none of these beats have a P wave in front of them because they are generated from the A V node, the middle of the heart rather than the sinus node. And then the sinus node speeds back up, wakes up and then takes back over from this junctional rhythm. What's going on during this period of junctional rhythm? And why does it take this many seconds for the sinus node to kick back in after that premature junctional beat? Well, it's possible and likely in this case that these junctional beats are conducting backwards up to the atrium which essentially suppresses the sinus node over and over again. And it takes a little bit longer for the sinus node to finally wake up and start doing its job again. If a junctional rhythm successfully conducts retrograde. It's almost like having an ectopic atrial rhythm with P waves that are coming from a different place than the sinus node. Each one causing another repeat suppression of the sinus node activity until the sinus node says enough is enough. I'm going to kick back in speed up and take back over. And here's another example of iso rhythmic, accelerated junctional rhythm competing with sinus rhythm. You can see there's actually some sinus arrhythmia occurring probably Respi phasic sinus arrhythmia as the sinus rate is speeding up and slowing down with breathing between 50 62 beats per minute in this case. And that's competing with an accelerated junctional rhythm where the A V node decides that it wants to fire around 57 beats per minute. And depending on what the sinus node is doing at any given moment, either you're going to see a junctional beat with no P wave in front of it or a sinus beat where the P wave happens a little earlier and pulls in the QR S a little bit faster. And this competition back and forth again is called iso rhythmic rhythm between two different things. In this case, the sinus node and a junctional rhythm. This is not necessarily a manifestation of sinus node dysfunction. It's just normal sinus arrhythmia, but it's competing with an accelerated junctional rhythm for the next concept or mimic of sinus node dysfunction. We have to quickly review what premature atrial beats look like. And there are two main categories of premature atrial beats. Here, we're seeing the first one, there are two early beats here that are occurring and two things happen. Actually, with each one, number one, you're seeing an early P wave that is buried on top of the T wave. How do I know there's a P wave there because it looks different from the preceding T waves where there isn't a superimposed P. You can see an extra deflection in the bottom channel and an extra tall T wave because there's an upright P on top of it, making it taller than the other ones by comparison. And then you can see this pulls in an early QR S in this case conducting with a right bundle branch block apparent pattern because it comes early and the right bundle branch wasn't ready for this speed. So this is a PC that conducts with a right bundle branch block sort of two times in a row. Here. Again, you can see the P wave deforming the T wave. So you know it's there. And that's the explanation for the early QR S as well. Here in this bottom strip, we also have a PC but in this case, the AV node or the his Perini system or both are not ready to conduct that PAC down to the ventricles. So we call this a blocked PAC. It's a premature ATR complex that creates a P wave, but there's no Q that follows. Notice there's a little pause in the activity in the ventricular activity. Anyway, as we have sinus rhythm happening each one conducting with a long pr interval, probably delay in the AV node followed by A PC that you can see peeking in in this segment. And the beginning of the T wave very obvious compared to the preceding ones where there isn't any atrial activity. And this early beat comes early enough that the A V conduction cannot occur. It's refractory and there's no QR S a little pause and then back into sinus rhythm with the long pr interval. Let's apply those principles to this strip which is a mimic of sinus node dysfunction. At first glance, this looks like you have a normal sinus rate on the left at 76 beats per minute. And sinus bradycardia sinus node dysfunction on the right at 42 beats per minute. But let's look a little closer and let's initially focus on the transition between the faster and the slower rate. We can see that we have a couple extra early beats in there. And as we zoom in, we can see this is exactly what I showed on the previous slide. There are two PAC beats conducting with right bundle branch block. And we can see those P CS because they deform the T wave when you compare them to the previous T waves that don't have P waves on top of them. Let's now look more closely at the faster and slower sinus rates and look at the T waves in particular on the right. You now can see as I bring your attention to it, these little blips that deform the T waves on every single beat. And you can see that those little extra blips are absent on the left. When the sinus rate was faster, these little blips are blocked pcs happening in a Bi GEIN pattern. These are blocked pcs resulting in the appearance of sinus node dysfunction or sinus brady cardia. But in fact, it is normal sinus node suppression because of this frequent atrial ectopy. When you look at the heart rate, trend on the telemetry, it's very easy to see why you can be fooled that this patient might have sinus node dysfunction. You can see sudden drops, sudden bradycardic events down into the thirties. And in fact, the telemetry will alarm for bradycardia during these times. But if you click on these episodes, you'll see that there is uh evidence of blocked PAC S in a pattern of Bi Gey because these extra PAC beats deform the T waves. Very obvious when you compare them to another section where there isn't bradycardia where those little blips on the T waves are absent. Here is another area on telemetry where we can see the heart rate is faster. And if you click on there, you can see exactly the same phenomenon of atrial bi Gey. But in this case, the P waves are conducting with a right bundle branch block a bar but conducting nonetheless. So this patient has extraordinarily frequent atrial Opie. And when those beats conduct, you get a more normal heart rate on average. And when they fail to conduct, you have what mimics sinus brady cardia because those, those P waves are blocked. And here's another example of what appears to be sinus bradycardia with telemetry alarms going off because of heart rates in the thirties. But as you're learning through this presentation, your best conclusions are drawn when you look at all of the telemetry and make comparisons of one segment to another. And if you click on another part of the telemetry, in this case, you'll see this type of event where you'll see that after this one beat, there are two blips that look similar to the single blips that previously may have looked like part of the T wave, but it makes no sense for there to be two T waves after one QR s. And so you have to come up with a different conclusion. In this case, these are atrial events and looking back, you can say, oh my goodness, there's an atrial event after every single QR S here on top of the T wave. And these may be blocked PAC S with two in a row on one occasion. And if you click on yet another part of the telemetry you get a different type of clue here. We see that there are conducted pacs with that same shaped blip on top of the T wave. This time followed by a wide QS. This is a conducted QS with a left bundle branch block appar this time. And in addition, we can see in this bottom strip, there are T waves that don't have that additional blip on top of them because in the bottom strip, we actually have not a P wave after every other beat. This is Trigemini, it's a PC after two sinus beats rather than after every single one. And that finally gives us the opportunity to see what A T wave looks like without a superimposed P. And now we can go back and look at all of the other strips and see that in fact, every time we see this little bump, this double humped M shaped bump, that's in fact, a P wave that's not what a normal T wave looks like in this patient in those leads. And if you finally find an area where there isn't bradycardia, you can see the absence of atrial bi Gemini no P waves either conducted or blocked. And you can see this patient has normal sinus node function. And the treatment here is to try to eliminate the atrial ectopy if you can. Uh and this is not a scenario where the sinus node is having any problem at all. It is normally suppressed because of the very frequent atrial ectopy. And here's another example of a patient with bradycardic events with the telemetry alarms going off during periods of bradycardia. And you click on the bradycardic event and the novice might look at this and think aha that's sinus node, dysfunction, sinus bradycardia. But that no longer is you having watched the video up until this point and you see these little blips at the end of the T waves and you think to yourself, yes, those are blocked atrial events. This is another example of blocked PAC S and a pattern of bie. Uh and you go to the transition where the heart rate speeds back up. And you see, yep, I can see periods uh during bradycardia where you can see these extra P waves at the end of the T waves and those are gone when the sinus rate picks up and resumes its normal speed and you're away to the races. However, if you then look at another part of the telemetry where you have some early Q RSS as well, we can see there's a different order of things here. The P waves are after the early Q RSS. Here is a, an early QR S here and over here toward the end of the strip. And notice in this case, the QR S comes immediately in front of the early P wave. So these are not PAC S that either do or do not conduct but instead these are junctional beats. These are beats that are coming from the his bundle or maybe part of the EV node. And they are conducting either both forward and backward, creating an early QR S followed by the early inverted P wave in lead two, suggesting an upward vector or these junctional beats may block in the forward direction and and not create a QR s but only conduct retrograde, creating only a P wave. So you can see by gemini in the atrium. And you can see by Gemini in the junctional area in the his bundle or the A V node. And that also can block in the forward direction resulting in a simulation of sinus node dysfunction and in actual bradycardia. But again, not because of sinus node dysfunction, but because of suppression of the sinus node because of retrograde conduction to the atrium. In this pattern of bi gemini, here's another part of the telemetry strip which shows these premature junctional beats in a pattern of bi gemini. And in this case, we're seeing those bi Gein conducted beats in the forward direction, either have a narrow QS shape conducting like a sinus beat does or with a right funnel branch block A bar and C. So even junctional beats can forward with or without AC and here in the bottom, you don't have bradycardia because each of these are conducting both forward and backward. And in the top, we're seeing intermittent failure to conduct forward of these junctional beats resulting in retrograde ps suppression of the sinus node and essentially functional brady cardia. But again, from the toy, not from primary sinus node dysfunction. Yet one more example of a patient with bradycardia with telemetry alarms, here's a heart rate of 48 in the ventricles. But again, you're now getting good at finding the P waves on top of T waves. And you'll notice here that there is a 2 to 1 pattern uh with every other P wave not conducting. And in this case, the P waves that failed to conduct are not premature and they have a very similar shape to the P waves that do conduct. So this is sinus rhythm. But with 2 to 1 A V block, here's another example from another patient with the same phenomenon where we're seeing uh extra P waves of the same morphology. Interestingly, in this version, there is a slight change in rate when P waves are on either side of a QR S versus two P waves that are between Q RSS with no QS in between them. There's a slightly longer interval. In each of these cases, the top and the bottom, we're dealing with 2 to 1 a block with sinus rhythm. And in the bottom, the slight variation in sinus rate is another form of sinus arrhythmia, a slight speeding up and slowing down of the sinus node. In this case, not related to breathing or Respi phasic that we saw earlier in the presentation. But in this case, it's called ventricul phasic sinus arrhythmia, fluctuations in autonomic tone in Vegas versus sympathetic nerve tone to the sinus node that wax and wane on a beat to beat basis. Whether or not there's a QR s present or not, again, probably affecting stretch receptors or something else that modulates autonomic tone to the sinus node slightly speeding it up or slowing it down. And here's a patient who on the telemetry trend is having numerous countless excursions between a faster and a slower rate. You can see down here the continuous jumping up and jumping back down of the heart rate back and forth. And as we click on one of these transitions, we can see the telemetry strip up top that shows alternating 1 to 1 conduction on the right and 2 to 1 A V block in sinus rhythm on the left. And here's an example of each and you can see again on the left that these are, in fact, all sinus beats, the beats that don't conduct are not premature. They have the same morphology as the beats that do conduct. So this is not atrial ectopy or PAC S but simply sinus rhythm with 2 to 1 A V conduction resulting in a mimic of sinus no dysfunction if you didn't see every other P wave. But this is much easier to pick up than the blocked PAC S because in this case, usually the blocked P waves have the same shape as the conducted P waves and they're further out, not superimposed on a T wave. And so they're much easier to pick out. And so this usually is not confused with sinus node dysfunction. Um And if this again is an irreversible cause and the patient is symptomatic from Brady cardia or you worry about progression, a different type of indication for a pacemaker in this case, because of a V block, not because of sinus node dysfunction. So let's review some points that we covered during this presentation about sinus node behavior. Sinus node dysfunction can show up in different ways. Some patients can have sinus bradycardia or sinus pauses. And we'd reviewed this pattern of sinoatrial exit block, which gives you very specific patterns on telemetry, but nonetheless, is primary sinus node dysfunction. And if it is not reversible and causes symptoms is an indication for a pacemaker, you can have normal sinus rates when the person is in sinus rhythm, but you can have excessive sinus node suppression and a long sinus node recovery time after atrial ectopy, atrial fibrillation or other atrial arrhythmias. And if the pause uh is long enough that causes pre syncopy or syncopy and there's no reversible cause, that's another indication for a pacemaker. You can have temporary sinus node slowing, which is a self limited event. After high vagus nerve activity. This can come in the form of vasovagal events from dehydration, pain or other events that can occur in an IC U setting or it can occur during sleep from Apne episodes where you have low oxygen levels, prompting a vagal outpouring. These are also self limited and the treatment of course, there is to treat the sleep apnea. Uh and a pacemaker is not indicated for asymptomatic pauses during sleep, thought to be due to sleep apnea. There are other mimics of sinus node dysfunction that we reviewed. And those include accelerated junctional rhythm or ventricular rhythm, which I didn't review but accelerated rhythms that come from places other than the sinus node that compete with sinus node activity and overtake. It don't necessarily mean that the sinus node is malfunctioning. It just means that there's an alternate spot that's firing faster and competing. You can have blocked atrial by gemini or blocked junctional by gemini. And you have to look for those P waves on top of T waves to make this diagnosis. You can see 2 to 1 A V block in sinus rhythm. Again, not usually mistaken for sinus node dysfunction because those P waves are further out usually after the T wave and have the same shape as the conducted beats. But 2 to 1 A V block can occasionally if the P waves are of low amplitude, be mistaken for sinus node dysfunction in all of these circumstances. The key is to first identify P waves, both sinus P waves and P waves that come from some other source. And the best way to do that is to compare a bra aarti strip to an event that is not BRADA card where presumably there are no extra P waves on top of T waves. And you can see what a native T wave looks like and compare it to during Brady Cardia to identify whether or not there are extra P waves present. I hope you found this presentation helpful.
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