0:00 our especially our PG students they are not very comfortable with ECG wherever you handle it but today it will be made very easy by our own faculty Dr. sir but before that I'd like to request Shankana ma'am for presidential address >> thank you thank you Dr. Lea good evening everyone good evening I welcome Balu Praapati Shar I welcome our today's expert Dr. Resh I welcome Dr. I welcome everyone for this session. Uh ECG basically is not a synonym eco ECG never replace uh ecoard eco cardiography replace ECG. ECG is a very easily available handy
0:45 investigation in PIC and any emergency thing. So you can take a steps early and but ECG reading and knowledge of ECG is very essential and today Dr. Rites will make it perfect for us. Thank you Dr. Rites. Over to you lata please. Welcome Dr. Sitrii sir. >> Thank you ma'am for your kind words. Welcome Dr. Sep sir. >> Thank you. >> Miss Yogish sir and today we both are not present because of their prior commitments. So I'll like to straight away start the program. Uh I'll welcome a faculty for today Dr. Dhukram Walasa. He's consulted at Sri Ba Mahav Institute
1:30 Surat and uh he's going to say uh his uh show his knowledge on the topic named tiny hearts clear tracings pediatric ECG simplified over to you sir. >> Please before that few words from Dr. Prajapati Shabbald Praapati sir please. as why not sir everybody and it's a good to >> thank you thank you >> yes >> very good evening everyone uh uh in this forum I am I will be presenting the topic for the first time and I would like to thank all the
2:15 dignitaries for inviting me to talk on this difficult topic. >> Yes, >> being a pediatrician, I also know that ECG is extremely difficult as a pediatrician because our exposure while doing MD pediatrics or uh doing a child care program, we are usually afraid when somebody hands over ECG to us. Usually in case of MD medicine, those uh residents who are doing MD medicine, they are very much into looking at the ECG and uh they uh almost gets
3:01 significant amount of training in the ECG. But if we look at the pediatric ECG learning, we have not incorporated it in our MD programs to the extent and the reason is because it has not been incorporated by the senior faculties. Even our senior faculties are not very wellversed with the ECG because the only reason is we are not having a practice. We consider cardiology as a separate field rather than a part of pediatrics. Usually when we talk of nephrology, it's
3:46 usually an extension of pediatrics. When we talk of heology, it's an extension of pediatrics. when we talk of maybe uh neurology usually it's we consider it extension of pediatrics but when we talk of cardiology we usually do not consider it as an extension of pediatrics and that is the reason why we have a separate pediatric cardiac society of India but uh what I wanted to emphasize is that if we can incorporate the ECG in our MD uh pediatrics training then it becomes very very easy for our future generation to not only uh have free from fear but can
4:33 opt for cardiology also in the future. So uh in this particular uh session what I'm trying to going to explain is when a patient comes to us with some problem related to ECG how are we going to tackle it in our day-to-day practice clinically it is very easy the only thing is you should have courage to look at the ECG what are the important things that you should look into the ECG EG and once you look at those things your fear for looking at the ECG will get solved easily. So let us start with the learning of the ECG.
5:20 So what is ECG? ECG is basically the graphical presentation of the electrical activity of the heart on the paper. So we have already learned the action potential in our physiology in our second MBBS. So what is action potential? Action potential leads to excitation contraction coupling and this leads to contraction and relaxation of the muscles. So that contraction and relaxation of the muscles which happens inside the heart occurs because of the electrical current that passes through the conduction system of the heart. We have conduction system heart of the heart consisting of SA node the AV node
6:08 the bundle of his the right and the left bundle branches and the perkingi system. So we have the atrias which contract then the blood goes into the ventricles. By the time the blood reaches the ventricles the current also reaches the ventricles and now the ventricle contracts. So the atria and ventricle contraction occurs in tandem in such a way that the cardiac output is maintained. So to support the cardiac output which is the main function of the heart the electrical activity of the heart is extremely important and for that we represent it in the form of P
6:57 QRS and T waves. So when the action potential passes into the atrial cells it leads to the atrial depolarization and this atrial depolarization leads to atrial contraction and that atrial contraction or the atrial depolarization is seen as Pwave on the ECG. Then the current passes from the AV node. There is AV nodal delay and after which the current reaches the ventricle and then the ventricle contracts. After that delay that delay is the PR interval and after that PR interval delay you have a
7:42 ventricular depolarization what we call it as QRS wave. This QRS wave is synchronous with the ventricular contraction. Similarly, the Pwave is synchronous with the atrial contraction. So, atria contracts, you have a Pwave. The ventricle contracts, you have a QRS wave. Now, the ventricle relaxes. The ventricle relaxation occurs. Ventricular depolarization occurs and you have T-wave. Now again the next discharge starts from the SA node. You have another Pwave, another QRS and T-wave and this cardiac cycle goes on.
8:27 So this is how the atria contracts. You have a Pwave, you have the PR interval, the QRS wave and the T wave. So when you have seen the ECG we see that there are various leads on the ECG lead 1 2 3 AVR AVL AVF V1 V2 V3 why why we need to study so many leads. So these basically leads are the sensors which are placed on the body in different parts and these sensor will sense the direction of the electrical current that occurs in the heart. For example, if you
9:14 look at lead one, it is placed here. Lead two is placed here. Lead three is placed here. So now the current is moving in this direction. Uh I just wanted to know does everybody can see my mouse cursor also because I am explaining with the help of mouse cursor. >> Yes sir it's visible. >> Okay. Okay. Yes. So as the electric current moves from atria to the a node and to the ventricle. This is the direction of the electrical current in the heart. So anything which is moving in this direction and perceived by this
9:59 particular leads will be seen as positive. So if you look at lead one two this lead and one two we will see positive P wave positive QRS wave in lead one lead two but AVR you can look at the AVR. AVR is here. So the current is moving away from AVR. So it is perceived as negative. Okay. So the location of the leads on the body will determine the different morphology of the ECG QRS morphology. So now what is the importance of these limb leads and what is the importance of the precordial leads? The limb leads will
10:47 tell you about the axis of the heart. Will tell you about the Pwave axis will tell you about the QRS wave axis and the precordial leads. Precordial leads are placed on the chest from V_sub_1, V_sub_2, V3, V4, V5 and V6 like this above the chest. So that will tell you about the dominance of the heart. Which heart is dominant? The right ventricle is dominant or the left ventricle is dominant. If you look at here V_sub_1, V_sub_2, V_3, V4, V5 and V6, we can see that in lead V_sub_1 and V_sub_2 they are mostly negative and
11:32 later on it becomes bifphasic and later on in V5 V6 it becomes positive. So when the positive waves are seen in leftsided precordial leads so it's a left ventricle dominant. If the positive wave is seen in V_sub_1 and V_sub_2 it will suggest that the right ventricle is dominant. So when will be the right ventricle dominant? Right ventricle will be dominant in the fetal life and in the neonatal life. So that is important for us to know. So how do we read the ECG? Which are the first four things that we should know when we start looking at the ECG? The
12:18 most important thing that we start looking is the rate of the heart rate. So how are you going to calculate the heart rate? By counting the smallest number of squares between the two R waves. So when you count two small the smallest number of squares between the two R wave and divide it with with 1500 it will give you the accurate heart rate. So in this particular case this is Rwave this is Rwave subsequent consecutive Rwave and if you measure the smallest number of squares it is around 10. So when you divide 1500 by 10 it will come around 150 beats per minute. So the heart rate will be 150 beats per
13:03 minute. In this particular case there are only five small squares. So heart rate will be 300. In this particular case the heart rate is 100 15 small squares 5 five 1500 divid by 15 will be 100. This is the accurate way of measuring the heart rate. The crude way of measuring the heart rate is counting the large small square. This is the large small square. So this large there are two small squares. So you divide 300 by the large number of large small squares. So like here there are two large squares. So 300 divide by two will be 150. Here there is only one large square. So 300 divided by 1 will be 100
13:51 of 300. Here there are three large squares. So 1,500 uh 300 divided by 3 will be 100. So in that way also you can roughly calculate. But in actually the ECG will not have equal box presentation like this. It will be slightly one or two more than the what you see. Apart from the rate the another thing that we need to know is what is the rhythm? Whether the rhythm is a sinus rhythm or an ectopic rhythm. What is sinus rhythm? If the rhythm if the ECG the rhythm is arising from the sinus node SA node the conduction system the first most important part of the
14:37 conduction system is the SA node. The electrical discharge starts from the SA node. So when the electrical discharge start from the SA node that rhythm is considered to be the normal. Then you see at the Pwave axis and the QRS wave axis. To look at the Pwave axis and the QRS wave axis, what we need to do is whether the we look at the lead one and AVF. Why you will look at lead one and AVF? Because they are perpendicular to each other. Whether the waves are positive in V1 uh lead one and AVF or they are negative in lead one and AVF. So looking at this ECG let us calculate the heart rate that we have learned. So by crude method let us take
15:25 this two consecutive R views. By crude method we can see that there are three large squares. These three large squares you divide 300 by three large square it will come around 100. So by crude method and immediately very fast we can calculate the approximate heart rate in this ECG is 100. But now if you count extremely small squares we can see that these are 15 here 16 and 117. So these are 17 small squares. So 1500 divided by 17 will come around 90. So the actual heart rate of this ECG is 90. Now in this particular another case how to calculate the heart rate? Let us calculate the hard grid by crude method. We have two large squares. So 300
16:13 divided by 2 will be 150. But if you count the smallest number of squares, so there are 12 small squares. So 1,500 divided by 12 will give you heart rate of 125. So this is how you calculate the heart rate. After calculating the heart rate, try to find out whether the rhythm is a sinus rhythm or not. So how are you going to find out that the rhythm is sinus rhythm where the rhythm arising is from the essay node. So for that the characteristic finding are every Pwave should be followed by QRS with constant PR interval and the Pwave axis should be normal that is between 0 to 9.
17:00 How can you calculate that? It should be positive or upright in lead one and AVF. So when Pwave is followed by QRS and there is a constant PR interval with normal Pwave axis that is Pwave is positive in one and AVF then you can tell that this ECG is a normal sinus rhythm. Apart from SA node what are the other locations that the rhythm can arise the rhythm can arise from the AV node. When it the rhythm arises from the AV node, it is known as junctional rhythm where you won't see Pwave. If the rhythm arises from the atrial cells, not from the SA node, from the surrounding cells of the atria, then it is called as ectopic atrial rhythm.
17:47 When the rhythm arises from the ventricular cell, it is known as ventricular ectopic rhythm. So let us try to find out whether this ECG is normal sinus rhythm or not. So what we can see over here that this is the rhythm strip and we can see that there's a Pwave followed by QRS followed by T P QRS T P followed by QRS P followed by QRS P followed by QRS so there is a synchrony P always followed by QRS there is nearly constant PR interval there is no change in the PR interval PR intervals is constant in all the cycles and now it will find
18:32 the Pwave axis. The Pwave axis normally is positive in one lead one and AVF. So this is 1 2 3 AVR AVL AVF. So in AVF we see a positive Pwave and in one also we see positive Vwave. So when Pwave is positive in one and AVF and all Pwave are followed by QRS and PR interval is constant you tell that the rhythm is a sinus rhythm. So how are you find trying to find the QRS axis? QRS axis can also be found by looking at the QRS morphology in one and
19:18 AVF. So how are you going to do that in this particular see what is the direction of the QRS? The QRS is positive in one and here also the QRS is positive. The Rwave is prominent. The S wave is not prominent. The is wave is almost very negligible. So in one and af both are positive. So when one and af both are positive it is called a normal QRS axis. If the in lead one if the QRS is negative or the S wave is prominent and in AVF the R wave is prominent. So negative in one and positive in R. So here this is the
20:06 graph where we can see the lead one is here and AVF is here. So 0 to positive and this is negative. So this is positive and this is negative. So if lead one is negative so lead one negative will come this side and uh AVF positive will come this side. So it will form a graph in this direction. So the it will cause right axis deviation. So here will be the axis of the heart and that will call right QRS axis. Similarly for left QRS axis if lead one is positive and lead AVF is negative. So lead one is positive and lead AVF is negative. So the axis will be in this direction which is known as left axis
20:52 deviation. When both one and AVF are negative it is known as extreme left axis deviation. So it will tell you about the what is the QRS axis by this meimmonics. If one and AVF are reaching reaching each other so it is right axis deviation. If one and AVF are leaving each other it is left axis deviation. So now we will learn about what are the ECG changes that takes place with age. So let us start with the newborn. So newborn 12 lead ECG and the most important thing we need to have 12 lead ECG to interpret the ECG. We cannot have
21:38 a single lead taken from the monitor and try to find out what is there in the ECG. So we should always have a 12 lead ECG to find out the accurate diagnosis. So in a neonet what is the important finding of a normal newborn? In a normal newborn as we know in fetal life the right ventricle is the main ventricle which pumps twothird of the cardiac output to the fetal circulation. So the right heart is the dominant heart. So you have right axis deviation. So this is lead one and this is lead AVF. So lead one is negative and lead AVF is positive. So they are reaching towards
22:23 each other. So it's a right axis deviation. And apart from that the precordial leads will tell you about which ventricle is dominant. Here we can say that because there are positive wave in lead 1 2 3 the right ventricle is dominant. So it is right axis deviation positive R wave in right precordial leads and a negative T-wave this is QRS and then this is T wwave the T-wave negativity is suggestive of right ventricular dominance repolarization so in a newborn you will have right axis deviation upright Rwave in right precordial leads and T
23:10 inversion in right precordial needs. So once the child is born, you will see these three findings. After 1 month of age, what you are going to see that the right axis has changed to the normal axis. We have now upright uh QRS in one and AVF. So it's a normal QRS axis. However, the RV dominance continues beyond 1 month to 3 years of age and hence you will see upright Rwave in right precordial leads as well as T inversion in right precordial leads from 3 years to 16 years of age. You see the ECG which is almost like a normal adult
23:59 but the only single finding that is of clinical importance to you because there are many adult uh physician who will refer the patient to you that the patient is showing T inversion which is a sign of eskeemia. So that is important and very relevant for us. So in a child who is less than 16 years of age or 15 years of age though the Pwave uh QRS axis becomes normal the Rwave has gone in right precordal leads but the T inversion can be present physiologically till 16 18 years of age also. So when you see a chest pain child and ECG showing T
24:45 inversion in right precordial leads it is physiological because of the RV dominance and not suggestive of any eskeemia. And as soon as the child becomes adult, as soon as the child becomes adult, the T inversion will go away and you will see a normal ECG. So let us start with a case scenario commonly occurring in our practice. You have a 4-year-old boy coming to your OPD comes with a complaint of cuff. On examination there is throat uh throat congestion but on oscultation you find
25:32 that the heartbeat is irregular. Now you treat the child for URI again after one week you find that the heartbeat is still irregular on your oscultation. So what are you now going to do? The irregularity in heartbeat is there. We need to show it to our cardiologist. you do the ECG. So this ECG is done. So now looking at the ECG and with our knowledge till now what we have learned how are we trying to apply that knowledge and find out whether the ECG is normal or abnormal. So first what are the things which we are going to look at? We are going to
26:18 look at the whether the ECG is in sinus rhythm. whether the uh the ECG the rhythm arises from SA node or something else. So this is the rhythm strip where we can see that all Pwave is followed by QRS Pwave followed by QRS Pwave followed by QRS P followed by QRSP followed by QRS and the PR interval is fairly constant. If you look at the lead one, Pwave is positive and AVF the Pwave is positive. So positive Pwave in lead one AVF along with constant PR interval and P is
27:03 always followed by QRS. It suggest that this rhythm is a normal sinus rhythm. What we can see another thing extra is the RR variability. The distance between the R consecutive R is different. Here the distance between the two R is less. Here the distance between the R two R is more. And this RR variability is seen in relation with the respiration. During inspiration the RR distance increases and during expiration the RR distance decreases. Here during inspiration the RR distance increases during expiration the RR distance
27:50 decreases. So now the rhythm strip where we can we have confirmed that this RR variability is with the respiration and the PQRST morphology is suggestive of a normal sinus rhythm. So when you have irregular rhythm with normal sinus rhythm with variability related to the respiration that is known as sinus arhythmia. Sinus arhythmias are physiological and common in pediatric patients and they are suggestive of good cardiac reserve. So let us have another case similar case on oscultation. The child came for nocural aerunysis and we had rhythm
28:36 irregularity. So now you did the ECG and ECG showed this thing. Here we can see now try to identify whether it's a sinus rhythm or not. So let us take one lead. So here the lead there is a Pwave followed by QRS. Here we can see the QRS the QRS morphology of the second beat is different and we are not able to appreciate the P wave. Here we can see three waves. So this is P followed by QRS. Here also P followed by QRS but the wave between these two lead. There is no P wave. The QRS is slightly wider and the T is also inverted. So the QRST morphology is different from the
29:23 preceding QRS. So this is something different. So when there is an absence of Pwave with wide QRS and T inversion with a compensatory pause then that is known as ventricular premature contraction means this particular beat has arised from some ventricular cells and not from the SA node. So these are all SA nodal discharges but this particular discharge is from the ventricular cell because the morphology of QRS is same in a single lead it is known as monomorphic VPC. So now we made this child do exercise on doing exercise what
30:10 happened that there is teicardia and all the monomorphic VPCs disappeared. So when you have adrenalic discharge the node takes over and the suppresses the other ventricular or other uh discharges and this is called physiological and should not be considered for any treatment. So any occasional VPCs which disappear on exercise are considered to be physiological. So what you can do in your OPD without doing ECG also that you can make the child run when you hear a irregular sound on
30:58 running the child the there will be increase in the heart rate. If there is a malignant VPC or malignant rhythm problem that malignant irregularity will continue to come despite the child running despite causing the coroneropic effect. But if on running there is teicardian disappearance of the irregularity then probably you are dealing a benign condition and that child will not need any of the treatment. However, that has to be confirmed with the ECG also. Similarly, there is a premature atrial contraction which is slightly different from the ventricular premature contraction by way that in premature
31:46 atrial contraction the wave will come come early. the Pwave will be present but the morphology of Pwave will be different from the QRS and there will be a compensatory boss which will not be complete. So when you have a different morphology Pwave and the same morphology QRST wave with incomplete pause then it is a atrial premature contraction. But when you have a full compensatory pause with absent Pwave, wide QRS and inverted T-wave, then it is a ventricular premature contraction. So the irregular heartbeat seen on oscultation can be because of sinus arithmia, atrial premature
32:31 contraction and ventricular premature contraction. This we have now covered. What are the other disorder that we see in our OPD practice? extreme teicardia or extreme bradic cardia. So how are the child going to present to us? How one when one should think of rhythm abnormality? The symptoms range from completely asytomatic status to a significantly moribban condition like loss of consciousness, sudden cardiac death. Infants usually present to us as lethargic, poor feeding, irritable, excessive crying and with some form of underlying heart disease. Older children will have most important symptom of
33:18 palpitation, syncopy, chronic fatigability. The child was doing well but in since last few months the child is now extremely getting fatigued. So one should think of arhythmias which are not noticed in our clinical practice. We think of or suspect techythmia in a most common scenario where we are treating bronchilitis because a 2 to 3 month old kid comes to us with bronchulitis. The child is having teicardia. The heart rate is around 200 220 and now you are thinking SPT whether it's not an SVT you are already giving bronco dilators
34:04 also so whether that is attributing to the SVT or the bronospasm or the respiratory condition the infection responsible and there are two things simultaneously going on in their mind either it's an SPT or it's a myocarditis so how are you going to settle that apprehension by yourself before sending the patient for a cardiologist opinion. If there is heart rate variability, now the heart rate is 220 but later on it becomes 180 again it becomes 220. If the heart rate again goes to 160 and then again goes to 180 then to 200. If there is heart rate variability then it's very unlikely that it is SVT.
34:50 get the X-ray done. If there is no cardomegal on X-ray, it is unlikely that the child is having myocarditis. Another thing is baseline heart rate. Baseline heart rate variability of more than 20% during sleep. If the heart rate does not fall by more than 20% during sleep, then there is a possibility that you are dealing with the myocarditis. So there are different types of fast heartbeat problems based on the origin. Either it's an atrial cause means the cause is in the atria or the cause is in the ventricle. The fast beat heartbeat can be because of the atrial cause will have a narrow QRS because the cause is
35:37 in the atria the S AV node and the below conduction system is normal. So there will be a normal QRS but in case of ventricular the wide there will be a wide QRS. The causes of narrow QRS teicardia are sinus teicardia, supra ventricular teicardia, atrial flutter atrial fibrillation and multif focal atrial teicardia. In case of ventricular case you have a ventricular teicardia. But there are few exceptions in atrial teicardia which will have wide QRS unless prove otherwise all wide QRS should be considered and treated as ventricular teicardia if the child is critical. But
36:24 if the child is extremely stable then you can reconsider for other causes like bundle branch block or WPW syndrome. So when should one consider that teicardia as a sinus teicardia and not SVT? If Pwave is followed by QRS and constant PR interval and the Pwave axis is normal that is upright in one and AVF there is a sinus teicardio. take the ECG and ECG shows confirms this finding then that teicardia is a sinus teicardia means the heart rate the heart the uh rhythm is arising from the sin node. In newborn
37:11 you can have sinus teicardia as high as 220 and in infants and children you can have sinus teicardia as high as 180 beats per minute. But the pecularity is it gradually develops and over a minutes an hour and gradually comes down. The rate is variable with time. So it is not constant. In case of SVT if the heart rate is stuck on 212 then it is going to be 212 continuously irrespective of the time. But in case of sinus teicardia with exertion with relaxation of the child you can have heart rate variable from 180 to 200 to 220. So when that variability is there then it is more
37:58 likely that we are dealing with a sinus teicardia which is physiological. The causes of sinus teicardia we all know. So now let us try to understand few mechanism why this arhythmia occurs and based on this mechanism it becomes very much easy for us to find what is the morphology on the ECG and help us the diagnosis of that particular rhythm problem. So this is the cartoon picture of the SA node, the AV node, the bundle of his, the right and the left bundle branch. And in case of normal sinus rhythm, the rhythm originates from the
38:43 SA node. This will leads to a normal Pwave morphology with one and AVF positive. Then you have a nodal detail that is PR interval and then a QRS. So this is a normal ECG that happens in this particular pattern. But in case of ectopic atrial teicardia what is going to happen? Instead of P arising from this as node the P arises from other atrial cell because of the atrial automaticity. The this particular cells keeps on discharging the electrical signal at 200 or 250 rate and this will lead to PQRST at 200 or 250 rate. But the QRS will be
39:30 normal like the normal sinus rhythm but the Pwave will have a different morphology. In this case we have multif focal atrial degicardia. So there are three cells three atrial different cells which will keep on discharging the electrical signals. So this will also leads to similar type of pattern but all will have a different Pwave morphology. So when you have a different Pwave morphology, it is more likely a multif focal atrial teicardia. Sometimes you have a circus or the circular movement of the electric current between tuft of atrial cells. When this circular current moves in three or four cells continuously like
40:17 this, it leads to a flutter type of waves and this discharge this wave to the AV node maybe at the uh uh rate of around 250 to 300 not all the rate will be transmitted only 50% of the electrical impulse will be transmitted causing varying ° of block with the atrial flutter and this flutter will have a saw to type of F type of wave with the rate of around 250 to 200. In case of atrial ventricular nodal re-enton degicardia, you will have a circular movement of the
41:05 current inside the AV node and this will discharge on atrial side as well as on the ventricular side simultaneously and as a result of which you will see only QRS wave and the Pwave will be embedded in the QRS wave. Similarly, in a junctional rhythm, the current electric current starts from the AV node and will continuously discharge at around the rate of 250 to 300. In case of accessory pathway teicardia, this is the accessory pathway and this circuit keeps on moving like this. discharging the atria, discharging the
41:52 ventricle at the rate of 200 plus and this will lead to the uh AVRT type of teicardia. We will come uh to the ECG also in case of a PJRT type of teicardia. These are the different types of SVTs. These are different types of SVTs and that will this mechanism will help us understand the ECG based on this mechanisms here the there's a slow channel so it takes longer time for the Pwave to conduct so there will be a distance between the QRS wave and the Pwave in this particular case the distance will be more in this
42:39 particular case the QRS and the Pwave are very close to each other. So there are few things that you won't be understanding now but once I will show you the ECG you will be able to understand and identify these different types of arithmas. So in case of supraventicular teicardia all what we have learned ABRT atrial ventricular re-entrant teicardia atroventicular nodal reenter teicardia ectopic atrial teicardia PJRT these all are different types of supraventicular teicardia and these are the commonest type of pediatric arythmia. It is seen in two age group in the first few months of life 0 to 3 months it is extremely common and later on at 8 to 10 years of age it is common. The commonest
43:24 mechanism responsible is the AVRT. The second commonest mechanism responsible is the AVNRT. And ectopic atrial teicardia is also seen in less than 10% of cases. In older children, bigger children more than 10 years of age, it is the AVNRT mechanism. And in the younger children less than one year of age, it is the accessory pathway mechanism which are common. So this is age determination. So how are we going to classify that this particular uh rhythm is SVT and not sinus ticiardia. So when you have high heart rate with a narrow QRS complex and a constant RR
44:10 interval the heart rate may be as high as 150 to 250. The Pwave can occur before QRS. The Pwave can occur after QRS or Pwave may not be visible. When the Pwave is visible, it will always be abnormal means it will be it will not be positive in one and AVF. It is usually abrupt in onset. Abute means suddenly it is going to shoot up from 140 130 suddenly goes to 250. So these are the three different types of SVT with different Pwave morphology. So in this particular SVT what we can see that there is a Pwave which is
44:58 preceding the QRS wave. In this particular case we can see the Pwave which is following the QRS. This small indentation that we see between QRS and T-wave there is a small indentation over here. that this particular structure is the Pwave coming immediately after the QRS wave and in this particular case we are not seeing the Pwave. So not seeing Pwave means Pwave is Pwave absent? No, the Pwave is present but it is coming exactly at the same time of QRS. So it is embedded in the QRS and hence we are not able to see the Pwave. So in which condition you will see no Pwave? In which condition you will see Pwave after QRS and in
45:44 which condition you will see the Pwave before QRS? So when you see the Pwave immediately after QRS it is known as short RP teicardia but when you see the Pwave before the QRS it is known as long RP teicardia. So we classify for understanding of SVT as short RPI cardia and long rpicardia. So in this particular ECG this is a normal Pwave followed by QRS. In this particular case we do not see Pwave we see only QRS and T wave. QRS TE. So this is SBT with absent Pwave which is seen
46:31 in junctional teicardia and AV nodal re-entardia. Here we see Pwave immediately after the QRS wave between QRS and T. So this is called a short RP teicardia. This is seen in AVRT that is the SSR pathway teicardia. And this last case is the P abnormal P wave occurring immediately before the QRS wave. So this is a long RP teicardia which is seen in ectopic atrial teicardia which is seen in peroxisimal junctional reciprocating teicardia and AVRT where you have a slow conduction conducting P the atypical AVNRT.
47:19 So this there are few things you try to remember now but later on once you keep on practicing you will be able to understand and we will correlate well. So what is AV NRT? So when there is a reciprocating rhythm or the circular rhythm inside the AV node the current keeps on discharging moves continuously keeps on moving circulation circular way and discharge in the atria and the ventricle simultaneously. So this leads to high QRS rate and you can't see the Pwave because the Pwave occurs at the same time as the QRS. So you don't see the
48:06 Pwave. Sometimes you see a sudo Rwave like this a indentation on this at the end of the S wave. So if you see something like this at the end of QRS it is called sudo RV and there this finding is commonly seen in lead V1 is suggestive of AVNRT. In case of AVRT where you have a necessary pathway the current moves like this in this direction from the AV node in downward direction and accessory pathway in the upward direction. So this leads to QRS wave and then the P wave and the as the
48:54 current moves back it will lead to Pwave and you will see the Pwave immediately after the QRS wave. So when you see Pwave immediately after the QRS wave it is called short RP techicardia which is suggestive of AVR. Now you have condition where you have Pwave occurring before the QRS wave and that is known as long RP teicardia and the causes are sinus teicardia where the Pwave morphology will be normal that is one and AVF it will be positive and in rest of the cases ectopic teicardia peroxismal junctional teicardia and atypical AVNR you will have abnormal morphology of Pwave that will
49:40 differentiate between the sinus teicardia and the other three. So what is multif focal atrial teicardia? In case of multif focal atrial teicardia there are more than one focus and this will lead to more than one morphology of Pwave. So in this particular case this Pwave is similar to this Pwave. This Pwave similar to this Pwave. This Pwave is bifphasic. This Pwave is short. This Pwave is tall. So all Pwave are different and all QRS have the similar morphology because the Pwave occur at a different time. The RR interval is also variable. So in case of multif focal teicardia you will have more than three
50:25 different characteristics of Pwave with irregularly regular RR interval. So when the rhythm is irregular you can have multifogal atal teicardia also. In case of atrial flutter, you see a saw to pattern of fwave discharging at 250 to 300 beats per minute. But it is not possible for the AV node to accept all the 300 bits. So few beats are blocked and this will leads to atrial flutter with varying degrees of block. So this is a saw to pattern that we see. This is a flutter f waves sawtooth pattern waves. Here one wave is conducted, one
51:13 wave is not conducted. One wave conducted, one wave is not conduct. This is 2 is to one block type of atrial flutter which which be looks like a normal ECG. In this particular case there is 3 is to1 block and 2 is to one block alternatively. So this is a regularly irregular type of atrial flutter. And in this particular case 2 is to1 block 3 is to1 block 2 is to1 block 2 is to one block 4 is to1 block. So different blocks are occurring in tandem. So it's a irregularly irregular type of atrial flutter. So the important thing is the sawtooth fwave. This atrial flutter is common in fetal life and in the neonatal life.
52:02 Irregularly irregular rhythm atrial fibrillation waves. Atrial fibrillation is the arythmia of aging. It is usually seen in older age group but it is extremely important for us to know what how the atal flutter looks like. So we see R interval variability and instead of Pwave we see of indulating F small F waves we are not able to see the waves. So there are small small waves seen in between the F waves difficult to make out but we see wavy structures between the two R waves. So when you see R is variability the
52:49 distance between the two R is different and Pwave is difficult to identify then it is more likely at real fibrillation is more common in the adult ventricular teicardia white QRS complex because of the rhythm arising from the ventricular cells it is known as when three more than three ventricular premature contractions occur simultaneously it is known as vent particular teicardia when all the QRS have the same morphology it is known as monomorphic VT and all the QRS have different morphology it is known as polymorphic VT. So here this is QRST QRST QRST the all have similar morphology. So it is a
53:36 monomorphic ventricular teicardia. In this particular case the all QRS have a different type of morphology. It is called polymorphic witty. Polymorphic witties are dangerous and can lead to death. So with this all information how are we going to approach when we have ECG in our hand. So try to get the rate, what is the rhythm, whether the QRS is wide or narrow, what is the atrial activity, whether atrial activity is present or not. What is the relation of Pwave with the QRS? Whether it is abrupt or gradual. So asking these all five questions looking at the ECG will tell
54:23 you the diagnosis. So what is the rate? As we know that the newborns can have 220 as high as 220 sinus rhythm. Most SVT have heart rate of 150 to 200. Atrial flutter which is seen more common in the fetal life have a heart rate of around 300. Multif focal atrial teicardia has heart rate up to as less as 160 per minute. We have discussed the causes already. What teicardias are regularly regular? Regularly irregular. Sinus teicardia and spts are regular. Atrial flutter with fixed blocks are regularly irregular.
55:08 And what are irregular? Atrial fibrillation, multif focal atrial teicardia, polymorphic VT and atrial flutter with different blocks are irregularly irregular type of rhythm. Whether the QRS is narrow, when the QRS is narrow, it is more likely SVT. When the QRS is wide, it is more likely VT. What is the Pwave activity? So Pwave morphology will tell you whether the it's a sinus teicardia upright in one and AVL it is always sinus rhythm but if it is inverted then it is suggestive of supra ventricular teicardia or other
55:53 form of teicardia flutter waves they are best seen in 2 three and AVL there are few things which you have to learn only and once you keep on practicing then it will help you diagnose these things. When the atrial activity is absent, it is atrial fibrillation and there if it is regular then it is SVT or VT. So now coming to the relationship of Pwave with the QRS, we have already done this in the past. If Pwave is coming before QRS, after QRS, short RP and long RP we have done. And then we have done about the whether it's an approot the this is the normal heart rate variable and suddenly it shoots up and stays constant. If this is the scenario then
56:39 it is more likely SBTVt. If it is now less and later on the heart rate shoots up but it is variable then it is more likely irregularly irregular heart rate like atrial fibrillation multif focal atrial teicardia. So what are you going to do when you have a child with SVT? So veagal manover causes transient AV block. It are both they are both diagnostic as well as therapeutic. So it will culminate or terminate the re-entrant mechanism type of block. However, by transient AV block, it can also cause unmasking of the Pwave or the
57:25 flutter waves. So when you give adinosine or ve what are the likely things will tell you the diagnosis by giving adinosine if there is no change then either the dose is inadequate or you're dealing with the VT. By giving adinosine if there is transient decrease in the heart rate but again the heart rate increases then it is more likely sinus teicardia. If there is a prompt termination of the SVT then it is more likely a re-enter teicardia which is AVRT or AVNRT. And if there is uh unmasking of Pwave or
58:11 unmasking of flutter wave then is more likely at flutter or ectopic atrial teicardia. So in this particular case we have a sinus teicardia you did the kerotis massage or the adinosine what happened that we are now able to see the flutter F waves. So flutter F waves are seen which is unmasking the atrial flutter. So this is basically atal flutter and not the re-entrant teicardia. Here also there is sinus teicardia. This is supra ventricular teicardia where we cannot see the P wave. So it is more likely AVNRT thatin is given and it terminates with VPC and later on it converts into the sinus rhythm. So AVNRT
58:57 and AVRT gets converted to sinus rhythm with adinosine. So let us have some few ECG exercises. You have a 1 month old baby comes to us with heart rate of more than 200 and this is the ECG. So what is most important thing? Measure the rate. So what is the rate? Rate is around 6 to 7 small squares. So 6 to 7 small square 1500 divided by 6 to 7 small square it is around 250. So heart rate is around 250 and the QRS is narrow and RR interval is constant. So narrow QRS with RR interval constant with heart rate more than 200 is more likely suggestive of SVT. So this SVT can be
59:46 AVRT, AVNRT, ectopic atrial teicardia, PGRT, anything. Okay. So now try to find out whether we have a Pwave or not. So in lead V1 there is a small P possibility of Pwave which is seen. So Pwave seen immediately after the QRS is highly suggestive of SVT of AVRT type and adinosine was given. So AVRT type of SVT and adinosin reverted it to sinus rhythm. After reverting to sinus rhythm, we were able to see the delta wave which also confirmed that this is a accessory pathway teicardia or the WPW syndrome type of teicardia.
1:00:32 So what is the acute management? If the child is unstable, SVT synchronized cardio version. If the child is stable, try and attempt veagal maneuver by the time you get the IV line. In small babies, ice cold cloth on the face. It will help stimulate the vagus or some gentle splash of cold water on the face. In older children, unilateral kerotic massage can be done or can be asked to do veagal manovers. Walva manovers. Adinosin is the first drug of choice. 100 microgram per kg. Rapid bolus with flush rapid flush technique and can be
1:01:17 repeated as needed. If the patient responds to adinosine that is more likely AVRT, AVNRT. If the patient does not respondse to adinosine, you can give IV metrol considering the other diagnosis. In case of ectopic atrial teicardia, the child may respond with the metoprolol. If the child is not responding with the metroal, we can give in intravenous amodderon at 25 microgram per kg per minute as loading dose over 4 hours and then 5 10 micrograms per kg per minute at maintenance dose. If the child is a newborn is a infant then IV deoxxin can also be given considering ectopic atrial dicardia or atrial flutter in older children beyond
1:02:05 4 years of age veropill can also be given in svting if the child is not responding at all to anything then the synchronized cardio version can be given at 0.5 to2 jw per kg later on once the rhythm is retain to normal sinus rhythm then for prevention beta blocker deoxxins or calcium general blocker are recommended considering the recommendation from the cardiologist. So we have another case where we have 8-year-old boy who had dismant exertion for 3 to four months and not gaining weight. He was lethargic and is not able to cope up with the other children and he showed LVD dysfunction. So this is
1:02:52 the ECG. So in this ECG we can see there there is a clearcut teicardia. What is the rate? So there are around eight small eight to eight small squares. So heart rate is around 220 to 230 per minute. And the Pwave morphology you see the Pwave the Pwave in lead one is negative. So it's a ectopic atrial teicardia. So Pwave is morphologically of the Pwave is abnormal in lead one. So it's an ectopic atal teicardia which is responsible for teicardiommyopathy because there is a P wave followed by QRS wave. There is very high possibility that we may consider oh this is sinus
1:03:38 rhythm P followed by QRS P followed by QRS. So we may consider it as a sinus rhythm and may ignore the ECG but this ECG should be considered as abnormal and should be treated. This child actually uh was our patient and patient responded to uh beta blocker and because of the beta blocker response adinosin response uh uh the rhythm converted to sinus rhythm you can see that there is a tall pwave which is converted the pwave morphology has changed the inverted Pwave has now become upright. So on correcting the rhythm abnormality the
1:04:24 Pwave which was inver uh inverted this Pwave became upright. Now what can anybody try this ECG? What is this ECG presence? >> So let us go >> let us go step by step. So whether what is the rate? So we have around 17 we have around how many small we have around 12 13 small squares. So heart rate is around 110 to
1:05:11 120 120 heart rate. So heart rate is 120. Okay. So now heart rate of 120 you have a Pwave followed by QRS Pwave followed by QRS in each and every cycle. So Pwave is followed by QRS with constant PR interval and Pwave is positive in one and AVF. So this is basically the normal sinus rhythm. So we have we have been continuously seeing various SVTs. So I thought that I should put this ECG so that try to break the fear of looking at the ECG. So when you see at the ECG majority of the times you keep on looking at the
1:05:58 sinus rhythm many of the times you will become very much confident that this is sinus rhythm. When you see Pwave followed by QRS and Pwave is positive in one and AVF it's a normal sinus rhythm. So this one a wide QRS with T inverted it's a ventricular teicardia because all the QRS have similar morphology it is known as monomorphic VT. So in this particular case, anybody wants to try this case?
1:06:43 Can anybody appreciate this particular pattern? This is a saw to pattern of the flutter f waves where you have blocks. This is 4 is to 1 block, 3 is to 1 block, 2 is to 1 block. So this is irregularly regular atrial flutter waves with varying block. So this one is different morphology wide QRS complex is the polymorphic ventricular teicardia. So in this particular case the rhythm is
1:07:28 slow and suddenly it becomes fast. So what has happened is P followed by QRS, P followed by QRS, P followed by QRS and now there is an ectopic P wave which converts it into the teicardia when now the P wave is absent. So it's a SVT. So this is also tech arithmia where you can see that there is r variability that distance is more over here distance is less over here. So this is not sv this is something else. So what is something else? We can appreciate the pwave morphologies are different. So when you have a different pwave morphology the pwave here is similar to the pwave here.
1:08:15 This pwave is similar to the pwave over here. So like what I'm trying to explain that we have more than three different types of Pwave with RR var invariability. So which is suggestive of multif focal atrial teicardia. In multif focal atrial teicardia the heart rate is little bit on the lower SL side. So what is this? This is the disease of aging where you have RR variability and P wave are difficulty to see in small fibrillary waves atrial fibrillation. So heart blocks there are three types of hard blocks first degree hard block, second degree hard block and the third degree hard
1:09:01 block. When all the P waves are conducted but the PR interval is prolonged, it is first degree hard block. When some are conducted and some are not conducted, it is second degree hard block. When no P wave is conducted, it is third degree hard block. So in first degree hard block, there is increase in the PR interval. So first degree hard block is also the sinus rhythm. When the PR interval is prolonged but all P wave is followed by QRS, it is known as first degree hard block. In case of second degree hard block, not all Pwave are conducted. There of two types moits type one and type two. In type one there is gradual increase in the PR interval and later on the PR this
1:09:47 is this is small PR interval this is big PR interval and now this Pwave is not followed by QRS. So now there is a drop bit here the PR interval is short. This is large PR interval. Now the there's a drop bit. So this is called Wanky phenomenon which is called mobit's type one uh second degree hard block. In this particular case the PR interval is constant. There is no increase in the PR interval but there is all a non phenomenon. Few of them are conducted and few of them are not conducted. In this particular case every third beat is not conducted. So 3 is to1 block in this particular case
1:10:35 this P pave is conducted but this is not conducted. This is conducted this is not conducted. So it is 2 is to1 block. In case of third degree block not of not a single atrial beat is conducted. Hence the a synchrony is not there. the Pwave will beat at its own time and the QRS wave will beat at its own time. So this is in uh autonomic uh QRS waves and autonomic P waves. So the complete a dissociation that is suggestive of third degree heart block. So this was about the various understanding of the ECG which which I feel that we all should
1:11:20 know. I know that there are few areas which I have touched were little bit difficult but they are difficult for first- timers not for those who are going to practice in their day-to-day practice. Once you have a child with an irregular heartbeat and you make the child run and that irregularity goes away. Now you know that's a benign thing but you do the ECG and find out whether it was a sinus arithmia whether it was a VPC whether it was an APC that will give you confidence. Try to look at the ECG every time. Try to uh find out whether the Pwave is there or not. What is sinus rhythm?
1:12:08 Whether the Pwave is followed by QRS, whether the Pwave axis is normal or not. So uh what I personally feel that looking at each and every ECG looking for the sinus rhythm in the ECG is the first step to uh uh get uh used to ECG and later on once you are used to the ECG gradually you have a case of SVT. So you know that adinosine has worked. You know this is an SVT. You gave the adinosine. But now again you look at the ECG and try to find out what is the P wave. Whether the Pwave is before QRS, Pwave is after QRS. That will tell you the diagnosis of the uh uh
1:12:54 type of SVT. So uh this was the small effort made by me. I know many of them will find it little bit difficult and I want the uh feedback from the audience and questions are welcome. Thank you for patient listen >> sir one sir one question is has been already placed half an hour back >> uh how to know whether leads are placed correctly or not by reading ECG Dr. uh three has this session. >> Okay. So now let us go to the so for that we need to know what is the morphology of
1:13:41 QRS in each and every lead. Okay. Okay. So, uh what we need to understand is anything which is moving towards your particular lead has to be positive. So in case of AVR, you look at the AVR. AVR is over here. Okay. So AVR is in the
1:14:29 opposite direction of the electrical current of the heart. So AVR has to always be negative. Okay. If you place this AVR lead over here, it will become positive. So if AVR becomes positive, you now are able to find out that something wrong I have done. Okay. So instead of putting the red lead on the left side and yellow lead on the right side that will lead to AVR becoming positive. Similarly lead V_sub1 V2 V3 V4 if the patient is an adult where you expect there is LV dominance. So you will see a positive in
1:15:14 V5 V6 and negative uh QRS in V1 V_sub_2. So if those leads are also placed heazardly you will have positive in V1 V2 and negative in uh uh in V5 V6. So that will give you a clue that the uh chest leads have also been not placed correctly. >> Okay sir uh thank you for the answer. Next question. Why wait uh DRP has asked this question sir. Why wait till 1 year in case of AVRT and does fine cause incomplete right under branch block? >> Uh where are the questions asked? Can I just see the >> It is in chat. It is in chat. You can see
1:16:01 >> chat they put in chat. >> Are you able to see the questions? >> Okay. Okay. Okay. Third last question by D. >> Uh why wait till one year in case of AVRT? See AVRT is basically because of accessory pathway. So there are two phases where accessory pathway can cure on its own. That is the first 3 years of life and then between uh 8 to 10 years of life. Usually in major retro kids we see that the accessory pathway related delta wave disappears after first 2 to three years
1:16:47 of life. So that is the reason why we wait because if if the thing does not cure by uh speculated time then those kids may be have to subject to uh interventional sort of a treatment like radio frequency ablation and all those stuff. So it is better to wait and let it cure on its own. So they are self-curable. Avrts are selfcurable. That is why we wait for one year. And does fentanyl causes incomplete RBBP? I think it's a very uh difficult to answer. I have no idea about this thing. It it it may be the personal experience of the person who is asking. But I think
1:17:33 uh you need to go to the literature. I'm not sure about that sir. And in my two more questions I have not seen this happening. >> So two more questions. Please mention indications for RFA and if possible counseling for these AVR cases. Two questions. >> Yeah. Yeah. So in case of refractive arhythmias, refractive arhythmias which are not not uh uh not being cured or not being controlled by the medication. If the child is having uh recurrent AVR in a way that that is causing ventricular dysfunction then in those cases we need
1:18:20 to go for radio frequency ablation. But as far as the kids are small, it is difficult for these types of procedure to happen. So when the kids are really very small, we try to manage them medically. But if the kids are big and you have frequent episodes of a frequent episodes of uh tech ariththmias irrespective of what is the ethology, we refer them for uh radio frequency ablation. So there are no such specific guidelines related to when you should refer but it is a subjective criteria on individual to individual patient. If the patient is not responding to the maintenance therapy then you should
1:19:06 subject them for radio frequency ablation and if the ventricular functions are deteriorating you should subject them for radio frequency ablation. Any more questions? So >> I want more questions related to how to diagnose. I think this is these all are theoretical questions which you will get answered in the books. So like somebody wants to ask related to how to diagnose a particular thing. Retail sir. I'm Anand from Bhagat. Uh >> hello sir, how are you sir? >> Absolutely fine. Can I ask you a question because we have a patient in
1:19:53 which we had a dilemma. >> Okay. >> Uh sir, we have a six-year-old uh kid who is a down syndrome tricom 21 already operated for a transitional ABCD before 3 years. Now this child was fine. um he had an episode of gastroenteritis today and uh he was given granetron. So by mistake he was taken an overdose of granetron uh followed by which he had a brief seizure for about 7 to 8 seconds after an hour and thereafter the ECG which was taken in the ICU was showing a QTC prolongation. Uh that was after about 2 to 3 hours of injection of granetron.
1:20:38 So uh we were in a sort of dilemma whether it is granetron induced QTC prolongation it was almost 0.52 seconds um or whether it was a postabcd repair abnormality. So I mean uh should we spend time and repeat an ECG after 48 72 hours to just >> what we can do with this particular child because this long QT uh long QT interval whether it was there right from the beginning or it has happened after needs to be first differentiated and for that you can ask the parents to get any other ECG which has been done during the time of uh procedure. Usually the uh surgical uh surgical repair will
1:21:26 increase the interventricular current means it will it can cause bundle branch block. Long QT uh is usually not seen after the surgery. It's basically uh related to the ventricular relaxation. Uh QT interval is basically a ventricular relaxation process that is prolonged and that has nothing to do with the uh surgery. So usually surgery we don't see prolongation of the QT either the QT is long has to be because of the uh natural uh thing inside the heart or because of the medication. So that thing can be differentiated only by looking at the previous ECG whether it is there before the surgical ECG or it has happened now. If it changes to
1:22:13 normal QT after a few days then probably it is related to the uh medication. The another thing which you can take care in this particular child is maintenance of electrolyte imbalance that has happened because of the gastroenteritis so that it does not get triggered into the ventricular teicardia. So that is one thing which we need to take care of and uh uh uh avoid other medication list which can cause prolongation of QT. >> Fine sir. Thank you. >> Yeah. >> Uh sir we have got two more questions. >> Yeah. >> Danger signs to tell parents in SVT case and precautions to tell. And second question can you please explain this direction diagram again?
1:23:01 >> Okay. So uh actually uh there is a lot of theory pertaining to the understanding of the ECG where you have ethan triangle and all those stuff but just to make it simplified. So we have three uh limb leads lead one, lead two and lead three. Okay. And we have augmented limb leads AVR, AVL and AVS. So here we have the SA node. Here it's a AV node. And then you
1:23:49 have the uh uh bundle of his and the perkingi system. So this in this direction the whole depolarization and the repolarization of the heart occurs. The contraction and the relaxation of the heart occurs in this direction. So this is the axis of the whole uh electric current that passes through the heart. So now if uh this leads are the sensors which senses the direction of the electrical current. So if you're sitting here, how are you going to perceive the Pwave? Pwave is perceived that some Pwave is coming towards you. So when Pwave is coming towards you, you will see in lead one you will see a
1:24:36 positive Pwave. Now the QRS wave is also coming in this direction only. So it will be perceived as positive QRS. Now the relaxation also occurs in this direction like this and this. So it will be perceived as positive way. So now if you look at the AVR so AVR is here. So if the person sitting over here will perceive what is the direction of the current the P wave is going in this direction. So it is moving opposite to the AVR. So when it is moving opposite to the AVR it will be perceived as negative. So anything which is coming towards you is seen as positive. Anything which is moving away from the U is seen as negative.
1:25:22 So similarly that holds true for each and every location. So lead two will have all things positive. Lead AVL and a and lead three will depend upon the whether the heart is standing or lying down. You we all must have seen on X-ray that few hearts are standing and few hearts are lying down. So when the heart is lying down this AVL will show all positive and if heart is standing the lead three will be showing all positive views. So this is how you try to explain the different morphology of how the QRS will be there in uh the ECG.
1:26:09 Right. >> The uh one more question. Can you please make comment on ECG Pwave merry changes that can happen atrial dilotation also? Can you please comment briefly on VF? >> Okay. >> So uh Pwave morphology. So basically Pwave morphology is upright in one and AVF. Okay. But when the there is atrial dilation the Pwave morphology changes. So in this particular case like uh if the right atrium is dilated
1:26:56 the right atrium will take a longer duration of time and will leads to a tall Pwave. In case of left atrial dilation, you will have an Mshaped Pwave because the right atria has already contracted. Now the left atria is contracting. Left it takes more time. So these are all basically more sort of a theoretical things that is uh uh give you some clue whether the right heart is dilated or left heart is dilated. In case of atrial fibrillation uh ventricular fibrillation, ventricular fibrillation are chaotic indulatory movements that you see and these are the terminal events that you see on the ECG. you
1:27:44 don't see a characteristic morphologically wide QRS and T inverted
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