Cardiac Arrhythmia: Review

by Carlo Raj, MD

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    00:01 So what we have here, quickly is an EKG. I am going to show you what components of this EKG would be the most important so that you can interpret it properly right. Ready? Now we can the X-axis and Y-axis. X-axis is what we are going to paying attention to. Is that clear? The X-axis represents or will show you the different types of waves, either positive deflection and negative deflection. Before we go on, I wish for you to take a look at a little bit of math up above so that you clearly see as to the difference between a little box and a big box okay.

    00:38 A little box is 1mm. It represents 0.040 memorize that if haven't already. You see that little box right there. The little box represents 0.04. So from henceforth, whenever I talk about little box, I am talking about 0.04. Is that clear? A big box is five little boxes.

    01:06 It cannot be any more dramatic. So if you take five of those little boxes, what is your time it took? Take a look. 0.020 seconds, is that clear? That you want to memorize. So so far, a little box 0.04, a big box is 0.2, why is that important? I want you to take that math that we just did please and I want you to come down and do you see where is this PR interval? I need you to memorize if you haven’t already, that that PR interval, the maximum amount of time normally speaking that PR interval should exist is 0.020 seconds maximum. What is the minimum? 0.120 okay. So if you take a look at the PR interval. What is the PR interval? The PR interval are the beginnings.

    01:54 "What does that mean Dr. Raj?" The PR intervals are the beginning of the P wave to the beginning of the QRS complex, is that clear? The PR interval represents what in your head? The PR interval you are thinking represents the time that requires an impulse to begin at the SA node making its way down to the AV node. Is that clear? Why is that important? Well, we could talk about how if your time of your PR interval is greater than how much? 0.2 seconds, which is the maximum time. You got a problem. Is that WPW or is that going to be AV nodal blocks. You see how we have taken the math that at some point maybe frustrated you and thought you so "Why do I need to know this?" I am telling you why right here. Clinical application. If you find you 0.2 seconds to be greater for PR interval and that is obviously AV nodal block because things are slowing down. And then we will talk about that upcoming.

    02:58 Whereas if it is less than 0.120 seconds, that brings us to a very well important diagnosis known as WPW. Now that's only one component, but do you see as to how that time becomes very important to us and how the little box and the big box will play huge roles? Let us continue on our X-axis, the P wave we all know means originating ever SA node, the electrical activity. You tell me when you mention this a bunch of times, what goes through the heart first? Electrical activity followed by the mechanical activity. What does the P wave represent? For mechanical activity. The A wave. Are you seeing it? Take a second. Okay.

    03:40 You saw it. In your head, P wave represents A wave. A wave represents atrial kick. Correct.

    03:46 That is the mechanical activity. What is that part of again? One more time, late diastole good. Let us continue. So now we have our QRS complex. We just discussed PR interval.

    03:56 The QRS complex represents only the ventricular depolarization. All it represents is ventricular depolarization. Now, if you talk about ventricular depolarization, then what are we referring to? It's the fact that we have, remember an actual potential way back basic concepts of physiology for cardiology. It is a fact that you have 0, 1, 2, 3, 4 okay. You tell me, with phases 0, 1, 2, 3, 4, which one of those represents ventricular depolarization? It is obviously phase 0 right.

    04:36 What does phase 0 mean to you? So I am really having you review your basics right now. So that phase 0 and how important is this? Really important. I say if you are not good with this, I highly recommend that you go back and take a look at your actual potentials for the heart and here specifically I am doing my mechanical activity okay. Why is this important? In a little bit in a lecture series we are going to antiarrhythmias and if you haven't understood this, things will get complicated. I don't want you to get frustrated. It is about really building upon your information okay. So that voltage-gated sodium channel is what that is? That phase 0 is a voltage-gated sodium channel, isn't it? And you have an ... gate giving more detail. Stuffs that you already should know. So that phase 0 is your voltage-gated sodium channel. It represents ventricular depolarization. How does that represent it on EKG? QRS complex. We will go as far as that right now. We will go into further detail as we go into phase 1, phase 2, which is plateau and phase 3. Right now we are focusing upon phase 0, voltage-gated sodium channel that has an activation gate, inactivation gate that is represented on your EKG by the QRS complex, ventricular depolarization.

    05:54 Let us move on to next portion. The all important ST segment. So ST segment bunch of things that we have talked about. If I told non-STEMI, non-ST elevation myocardial infarction, give me some differentials, please. If all that you see in a standard board question or an attending tells you, "Son or daughter, tell me about non-STEMIs." You are going to step up to the plate and you are going to tell them what? You are going to say maybe this is subendocardial type of myocardial infarction. What kind? Subendocardial myocardial infarction or this was a angina.

    06:32 Correct? "What kind of angina?" Is the attending asking you. You are not going to tell the patient, or you are not going to tell the attending that it is vasospastic angina. More likely you are referring to stable or perhaps unstable angina, right. And there you had ST depressions.

    06:52 Those were your non-STEMIs, is that clear? What if it was ST elevations? With ST elevation, the differentials would be transmural type of myocardial infarction or maybe vasospastic. Now, the attending or licensing exam is asking you, well how can you distinguish, how can you confirm? You're looking for cardiac enzymes. Cardiac enzymes are present, then you know your patient for sure had some type of myocardial infarction. If not, then your differentials are a little bit more. So, ST segment, we have spent a lot of time there. You know that normally it should be isoelectrical and then we have the T wave.

    07:29 Tell me about that T wave. Well that T-wave represents ventricular repolarization. So ventricular repolarization, now you tell me, if you are referring to actual potential, this could be a tricky question, if you haven't properly studied, if you haven't properly understood your pathophysiology. The T wave represents ventricular repolarization. If it is actual potential of mechanical type that I am referring to meaning phase 0, 1, 2, 3, 4, you tell me what phase of your actual potential is represented by your T wave? Phase 0, we already talked about was QRS depolarization. Phase 2 is plateau, that's your calcium influx and that actually is your ST segment, is that clear? How can you remember that? Plateau phase 2, ST segment flat. Here is phase 3. Have you ever put that into context? I hope you have because you know this is a beautiful thing. So if that potassium is effluxing during phase 3, isn't that repolarization? Of course, it is. So that is your T wave. Wonderful. Finally, we have our QT. That is important, isn't it? Why? I just got them talking to you about torsades de pointes. What did I say was the predisposing factor to torsades de pointes. It was a prolonged QT interval. So if that QT interval is prolonged, what caused it? Maybe drugs more commonly, antiarrhythmic such as your sodium-channel blockers class I, maybe you use antibiotics, maybe antipsychotics so on and so forth. Then also inherent such as romano-ward, Lange-Nielsen and such. Well, if you have a prolonged QT interval, you are predisposed to torsades de pointes.

    09:18 These are some of the most important points of this EKG. You are paying attention to X-axis, everything that I just went through here is just give you clinical application in the subsequent lecture series, we would dive into details further, further and further, but it all begins with knowing the foundation.

    About the Lecture

    The lecture Cardiac Arrhythmia: Review by Carlo Raj, MD is from the course Arrhythmias.

    Included Quiz Questions

    1. P wave
    2. QRS complex
    3. QT interval
    4. PS interval
    5. ST segment
    1. Sawtooth appearance
    2. Loss of P waves
    3. At least 3 distinctly different p wave morphologies
    4. Biphasic p wave
    5. Wavy P wave
    1. At least 3 distinctly different p wave morphologies
    2. Biphasic p wave
    3. Wavy p waves
    4. Loss of p waves
    5. Sawtooth appearance
    1. Hyperkalemia
    2. Quinidine
    3. Diphenhydramine
    4. Romano-Ward
    5. Lange-Neilsen
    1. WPW is a type of bradycardia
    2. WPW involves the presence of an abnormal pathway between the atria and ventricles
    3. WPW is associated with shortened PR interval
    4. WPW results in decreased filling of the ventricles
    1. Lengthening the PR interval decreases the amount of time available for ventricular filling
    2. Normal PR interval is between 0.12-0.2 s
    3. The PR interval represents late diastole to the start of systole
    4. PR interval indicates the time taken for the impulse to travel from the SA to the AV node
    5. AV nodal block presents with a PR interval that is greater than 0.2 s
    1. QRS complex
    2. P wave
    3. R-R segment
    4. QT interval
    5. ST segment
    1. Potassium efflux
    2. Sodium influx
    3. Sodium efflux
    4. Calcium efflux
    5. Calcium influx
    1. Late diastole
    2. Early diastole
    3. Closure of the atrioventricular valves
    4. Early systole
    5. Closure of the semilunar valves
    1. Calcium influx
    2. Sodium influx
    3. Calcium efflux
    4. Potassium efflux
    5. Potassium influx

    Author of lecture Cardiac Arrhythmia: Review

     Carlo Raj, MD

    Carlo Raj, MD

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