Understanding Cardiac Electrophysiology and Arrhythmias: Key ECG Insights

Greetings to one and all on this  forum. I am Dr. Sanjay Andrew,   Professor of Physiology from Chettinad  Hospital and Research Institute in Chennai.   My topic for the discussion is From Action  Potentials to Arrhythmias. So, what I will  

be doing over the next half an hour is, I will be  using these objectives to update you on certain   core principles of electrocardiography. I shall  begin with the electrophysiology of the heart,   giving vi, giving you an overview of what  has already been discussed on this forum.

And then I will go on to certain  electrophysiological hallmarks.   First I will talk to about the electro, talk  to you about the electrophysiological hallmarks   seen in the ECG associated with the sinus rhythms.  And then I will follow it up with the same in  

certain conduction disorders of the heart. And  then I will give you a primary classification of   arrhythmias from where my clinicians will take  over and give you further inputs on the same.   So, we shall have a recap on the  electrophysiology of the heart.

The human heart is an electromechanical pump that  primarily has 5 core physiological properties.   Automaticity is the ability of the heart to  spontaneously generate an impulse. Conductivity   is the ability of the heart to generate this  impulse throughout the conducting system.  

Rhythmicity is the ability of the heart to make  sure that this impulse is conducted in a regularly   regular fashion. Contractility is the act in  mass and interaction within the cardiac myocyte. And this allows the heart to contract  as a whole or as a syncytium.  

There is another electrical property known as  refractoriness. Now, this is the duration of an   action potential where a second stimulus will  not be able to generate another impulse. Now,   as far as understanding the ECG is concerned, you  should know that most of the cardiac arrhythmias  

are because of a either an increase or a decrease  in the automaticity and conductivity of the heart.   Refractoriness is also essential to  understand how arrhythmias develop. I will be talking to you about  it later in the presentation.  

These are the 5 core physiological properties  which we had already discussed. Automaticity   is the ability of the heart to spontaneously  generate an impulse. Rhythmicity is the inherent   regularly regular discharge of a cardiac impulse.  Conductivity is the transmission of this impulse  

throughout the conducting system. Contractility  is contraction of the cardiac muscle as a whole. And refractin refractoriness is the  inability of cardiac muscle to respond to   electrical stimulation during a particular  interval in its action potential.  

So, this slide should gives you an overview of the  conducting system, which you might already know.   So, you can see, the SA node is  the primary pacemaker of the heart,   where your impulse is spontaneously  generated throughout the life of a person.  

From the SA node, you have 3 internodal tracts  which link up the SA node to the AV node. And the AV node continues as the bundle of His,  which in turn ca terminates as the Purkinje   fibres. The bundle of His is thrown into a left  bundle branch and a right bundle branch. And in  

this diagram, you can see, the left bundle branch  has an anterior division and a posterior division.   This slide shows 2 important electrical properties  of the heart, namely rate and rhythmicity,   and velocity of conduction of a cardiac impulse.  On this side, we can see that the rate and  

rhythmicity of a cardiac impulse is greatest at  the pace primary pacemaker or the sinoatrial node. And on this side, we can see that the fastest  uh the velocity of cardiac impulse conduction   occurs in the bundle of His  and the Purkinje system,  

and the slowest velocity of cardiac impulse  conduction occurs at the atrioventricular   node. This is an interesting slide which  gives you an histo historical update about   the discovery of the conducting system. So, you  can see that even though the conducting system  

terminates with the Purkinje fibres, the  Purkinje fibres were the were the part of   the conducting system that were first discovered  in 1845 and the internodal tracts were the last. The anterior, middle and posterior internodal  tracts, they were the last to be discovered in  

1963. Now, apart from the normal conducting system  which I just described, quite a proportion of the   population have certain abnormal bypass fibres,  also known as the paranodal tracts. And here in   this diagram, you can see the AV node and the  bundle of His which I will be referring to as  

the fascicle. Now, 5 of these abnormal  or paranodal tracts have been described. And here at 1, you have the  James atrio-fascicular bundle,   which extends between the atrium and the bundle  of His. At 2, you have the in intranodal bundle,  

which is present in the AV node. And at 3, you  have Mahaim's fasciculo-ventricular bundle,   which extends between the bundle of His and  the ventricle. And at 4, you have Mahaim's   nodo-ventricular bundle, which extends between  the AV node and the ventricle. And at 5,  

you have Kent's atrio-ventricular bundle, which  extends between the atrium and the ventricle. So, these paranodal tracts are sometimes  responsible for certain abnormal rhythms which   may be picked up in the ECG. In fact, one abnormal  rhythm which is known as accelerated conduction  

is due to these paranodal tracts, and I will be  describing about it later in this presentation.   Now, this slide shows the action potentials of  the various conducting tissues of the heart.   In physiology, whenever we describe  the classical cardiac action potential,  

we describe the ventricular action  potential with its 4 phases. However, stimulation of the different parts  of the conducting system give different types   of a waveforms. For example, in the SA node,  you have the classical pacemaker potential,  

which begins to evolve as we go down  the conducting system into the classical   ventricular action potential. So, this must be  kept in mind whenever we go about understanding   the electrophysiology of the heart. This slide  shows a classical ventricular action potential.  

And you can see that the ventricular  action potential has 4 phases. The first phase is the phase of depolarisation or  phase 0. And this is followed by the early repo   repolarisation or phase 1. And this is  followed by a plateau which is phase  

2. And then we have late repolarisation, which,  which is phase 3. And finally, we have phase 4,   which is returning back to the resting membrane  potential. The ionic basis of these phases   are described on this side, so, you you  can see that phase 0 is due to opening  

of the fast sodium channels and phase 1 is  due to closing of the fast sodium channels. Phase 2 is opening of the calcium channels and  phase 3 is due to closing of the calcium channels.   And finally, we have the return back to  the resting membrane potential or phase  

4. Now, antiarrhythmic pharmacotherapy is  widely used to manage cardiac arrhythmias.   And this slide shows there are 4 classes of drugs  which are used to manage cardiac arrhythmias,   and on the far corner, there  are some examples of each.  

But what I would like you to understand  is this section of the tabular column. So, you can see that each gra each group of drug  tends to act on the cardiac action potential and   try to control the arrhythmias. More on this will  be told to you by our pharmacologist in subsequent  

sessions. This slide correlates ventricular  action potential with a normal electrocardiogram.   And what we can see here is,  the P wave has no correlation,   because this is a ventricular action potential;  the P wave is due to atrial depolarisation. Now,  

the QRS complex corresponds with phase  0 of the ventricular action potential. And phase 2 or the plateau correspond with the ST  segment of the electrocardiogram. And the phase   of repolarisation corresponds with the T wave  of the electrocardiogram. Now, earlier in my  

presentation, I had described 5 core properties  of the heart; one of them was refractoriness.   So, we shall try to understand refractoriness  of the ventricular action potential,   because it is important for a for our  understanding of how arrhythmias are generated.

So, the refractory period, as you  might be knowing, is a period of the   action potential where a second stimulus will not  be able to generate another impulse. And there   are 3 types of refractory periods, namely,  the effective or absolute refractory period  

and the relative refractory period and  another phase known as the supernormal   phase. The absolute refractory period extends  from phase 0 up to the mid portion of phase 3.   During this period, even a strong second stimulus  will not be able to elicit an action potential.

The relative refractory period follows the  absolute refractory period in the ventricular   action potential. And during this period, a  very, very strong stimulus can bring about a   second action potential. Now, it is the last  portion of the refractory period also known  

as a supernormal phase, which is present in the  phase 4 of the action potential. It is this phase   from which most of the arrhythmias are generated.  So, during the supernormal phase, the cells of   cardiac muscle are hyper excitable with a single  stimulus capable of producing multiple responses.

I repeat, it is a supernormal phase from which  most of the cardiac arrhythmias are generated.   There is another classification of cardiac muscle  cells, namely the automatic cardiac muscle cells   and the non-automatic cardiac muscle cells.  The automatic cardiac muscle cells are located  

in the SA node and the AV node, and these  cells spontaneously gen generate impulses.   While the non-automatic cells are located  lower down in the conducting system,   and these cells depend on being  excited by the SA node and the AV node.

However, in certain abnormal states, the  non-automatic cells can become automatic.   This slide shows the core differences between  the automatic cells and the non-automatic cells.   So, here you can see, the pacemaker potential  which is primarily due to the automatic cells,  

and the ventricular action potential which  is primarily due to the non-automatic cells.   Now, here you will see, the pacemaker  potential has a slowly rising phase 4,   and phases 1 and 2 merge with each each other.

And this uh electrical activity is  predominantly calcium dependent.   And here you have the ventricular action potential  which is uh sodium de dependent predominantly.   And uh you can see the different phases; phase 0,  1, 2, 3 and 4 are very clearly defined. So, having  

told you about the um core electrophysiological  properties of the heart, I am going to go on to   certain electrophysiological hallmarks of  the ECG associated with the sinus rhythms. Now, a sinus rhythm is a, refers to a  rhythm in which the heart beats sequentially  

and normally described as regularly and regular.   The sinus rhythm usually exhibits a normal  rhythm with or without altered rates. So,   there are 3 important sinus rhythms which you  should be aware of, namely, sinus tachycardia,  

sinus bradycardia and sinus arrhythmia. So, sinus  tachycardia is a heart rate of regular rhythm with   a rate greater than 100 per minute. So, here you  can see, this is a tracing of a sinus tachycardia. And you can see, the rate has markedly increased.  And functionally or physiologically, a sinus  

tachycardia is seen during exercise and periods  of stress, while pathologically there are states   associated with the sinus tachycardia. And  a few examples of that is fever, anaemia   and hyperthyroidism. The sinus bradycardia  is the heart rate of regular rhythm  

with a rate less than 60 per minute. So,  the sinus bradycardia is usually seen when   the vagal tone has increased. And functionally,  it is typically seen in well-trained athletes. And there are certain pathological states where  a sinus bradycardia may occur. And uh disorders  

of the conducting system as well as hypothyroidism  are 2 examples of sinus bradycardia. So, here you   can see a classical sinus bradycardia where the  heart rate has markedly decreased. Now, the next   sinus rhythm is the sinus arrhythmia, which is  a heart rate of regular rhythm with alternating  

phases of fast and slow rates. From a functional  point of view or physiologically, a sinus   arrhythmia is usually seen in children and during  the different phases of the respiratory cycle. During inspiration, the heart rate increases,  and during expiration, the heart rate  

decreases. Sinus arrhythmia is also associated  pa pathologically with disordered generation of   impulses in the SA node. Here you have a tracing  of a sinus arrhythmia, and you can see the   heart rates being fast and then slowing down  and then becoming fast again. So, having  

told you about the 3 sinus rhythms, now I will go  through an update on certain electrophysiological   hallmarks which are seen in the ECG in  certain conduction disorders of the heart. So, we shall begin with aberrant conduction. So,  this is actually a refractoriness or a delay in  

conducting a supraventricular impulse into the  ventricles, and uh it should be kept in mind when   differentiating a supraventricular tachycardia  from a ventricular tachycardia. So, here you   can see an example of aberrant conduction. So,  here is the ECG strip in which you see the P  

wave occurring after the QRS complex, because of  aberrant conduction that is seen in this tracing. Next we have the accelerated conduction.  Previously, I had told you about the   paranodal tracts, and uh accelerate  accelerated conduction is usually seen  

when whenever there is a paranodal tract in which,  through which an impulse bypasses the AV node. So,   the classical finding of a accelerated  conduction is a shortened PR interval,   and uh this is seen in 2 important  syndromes which may be described later,  

namely the Wolff-Parkinson-White syndrome  and the lown Lown-Ganong-Levine syndrome. So, here you can see a tracing from a  patient with Lown-Ganong-Levine syndrome   and a accelerated conduction. And you can  see the PR interval trouble being shortened,  

because of accelerated conduction. Then we have  another disorder known as the atrioventricular   dissociation. So, this is actually a functional  block in the AV node; functional block of   conduction in the AV node. So, as a result, the  ventricles fire at a faster rate than the atria,  

since the AV is refract, AV node is refractory  to the passage of impulses from the SA node. So, here we usually see the P waves marching  towards and overtaking the QRS complexes,   and occasionally there will be a normal  rhythm known as the capture beat. So,  

here you can see a tracing of atrioventricular  dissociation. You can see the P waves marching   towards the QRS complexes and eventually  overtaking the QRS complexes. And this   may be followed by a normal rhythm or  isorhythmic pattern, known as the capture  

beat. There is another electrophysiological  disorder known as accrochage synchrony. Here what happens is, 2 adjacently situated  cardiac tissues may fire at the same rate,   even though they are stimulated at different rates  with a marginal difference. Now, this may be seen  

in AV dissociation, which I just now told you. And  usually accrochage synchrony is characterised by a   positive wave following the QRS complex, as you  can see in this tracing. Now, we come on to the   phenomenon of electromechanical dissociation,  or also known as pulseless electrical activity.

This is a phenomenon which usually precedes  death. And uh here what happens is, the   mechanical contraction of the heart does not occur  in spite of electrical activity being recorded.   And usually, the arterial pulse cannot be palpate  palpated in such patients. And there are quite a  

few causes of uh electromechanical dissociation  which is listed out in this slide. So, now we have   another rhythm where there is electromechanical  dissociation known as the agonal rhythm. So, here we, what we have is a slow rhythm with  wide and bizarre QRS complexes. And as I told you,  

it precedes cardiac arrest. And it is a classical  example of electromechanical dissociation. That   is, agonal rhythm is a classical exam example  of electromechanical dissociation. So, this is a   classical tracing of a agonal rhythm. Now, we come  to 2 uh closely related uh electrophysiological  

abnormalities, namely the ventricular  bigeminy and the ventricular trigeminy. So, the ventricular bigeminy is a  electrophysiological phenomenon in   which a sinus beat alter alternates with an  ectopic beat. So, here you can see a sinus  

beat alternating with a ectopic beat. And this is  a classical tracing of a ventricular bigeminy. So,   usually, these electrophysiological changes are  associated with certain arrhythmias, which the   clinicians will be talking to you about. And this  is the ventricular trigeminy which I told you.

So, here you see, 2 sinus beats may alternate with  an ectopic beat, or 2 ectopic beats may alternate   with a sinus beat. Here you have 2 ectopic beats  alternating with a sinus beat, in this tracing.   Now, the next uh electrophysiological  abnormality which I would like to tell you  

is the blocked atrial ectopic. Now, this occurs  as a consequence of digital digitalis toxicity.   As you all know, digitalis is a  drug used to manage cardiac failure.   So, what happens in the blocked atrial  ectopic is, the atrial premature beats,  

they are noted in the ECG as a single entity,  and uh are also known as isolated P waves. So, you can see this in this tracing. Now, we  come on to the congenital complete heart block.   It is a block in conduction of the impulses at  the upper part of the atrioventricular junction.  

So, usually, the ECG is characterised by a  normal rate with a narrow QRS complexes that   are dissociated from the P waves. So, you  can see the QRS complex, they narrow down   and the P waves are actually  dissociated from the QRS complex.  

Now, another type of a electrophysiological  disorder is a concealed conduction. What happens here is, certain impulses that are  conducted may not be picked up on the ECG at the   point where they are supposed to be picked up,  but they can be made out by analysing subsequent  

complexes. Atrial fibrillation is an example of  concealed conduction. And what happens here is,   the PR interval following a ventricular  premature beat is usually longer than normal. So,   here you can see, the PR interval forming  a ventricular ectopic can, is longer than  

normal. So, this is a example  of con concealed conduction. Now, decremental increment is noted to  occur in the second degree AV nodal block.   Here what happens is, there is a delayed  in conduction of impulses at the AV node  

and the P PR interval is initially widened but  gradually begins to narrow down. That is why it   is known as a decremental increment. And here you  can see this tracing. The PR interval is initially   increased, and as we go down, it  tends to narrow down or decrease.

Now, dissociated beat refers to a block in  conduction of impulses at the AV node, because of   a ventricular premature beat being generated  distally. So, the ECG shows a positive P wave   with a shortened PR interval. So, this tracing,  you can make out a positive P wave with a very,  

very short PR interval, and that is known as a  dissociated beat. An ectopic beat is an abnormal   beat that arises outside the SA node. This could  be either atrial, junctional or ventricular. So, the tracing on top is a tracing of a atrial  ectopic. So, here you have abnormal P waves.  

You can see the P waves being abnormal.  Then we have the junctional ectopic,   where the PVS are retrograde. And then the  ventricular ectopic, where the QRS complexes   are set to be bizarre. Now, when escape beat  occurs when the primary pacemaker of the heart,  

that is the SA node fails to fire, as a  result, usually a secondary pace pacemaker,   namely the AV node, takes over with a  single beat known as the escape beat. This can be seen in this tracing. These are  all sinus rhythms, and here you have the  

SA node failing to fire and the  secondary pacemaker taking over;   and this is the escape beat. Now, Wenckebach's  phenomenon is a commonly described entity,   and it usually occurs during heart blocks.  What happens here is, there is grouping of  

beats with an interval between the grouped beats.  So, here is a tracing of Wenckebach's phenomenon.   Here you can see 3 beats with an interval,  and then, grouping of beats again. And the last electrophysiological abnormality  that I will be describing to you is known as the  

Torsade de Pointes, which refers to a ventricular  arrhythmia with ventricular complexes of varying   shapes. So, here you can see a tracing of Torsade  de Pointes. You can see the ventricular complexes   are of different shapes. And usually this uh  electrophysiological disturbance is usually  

seen following the use of antiarrhythmic  drugs. So, now that I have given you a   update about certain electrophysiological  disturbances which can be picked up in the ECG,   I conclude this presentation by giving you  a primary classification of arrhythmias.

So, it is useful to classify arrhythmias;  a sino na sinoatrial node arrhythmias,   atrial arrhythmias, junctional or nodal  arrhythmias and ventricular arrhythmias.   So, you can see, I have listed  out few examples at each group,  

and uh this will be described by my clinicians in  the subsequent sessions. And as I conclude this   session, I would like to thank certain people  without whom this would not have been possible.   So, my heartfelt thanks goes  out to the flagbearers of NPTEL,  

for giving us this opportunity to share our  knowledge with one and all on this forum. The flagbearers of Chettinad Hospital and Research  Institute for always motiving motivating us to   excel in our endeavours of teaching and research;  my teachers and students all over the world for  

empowering me with the wisdom of Physiology and  Medicine. And last but surely not the least,   I would like to thank all the participants of  this learning exercise. Thanks to one and all.