To the extend that I understand, this is basic cardiology and electrocardiogram interpretation. Please note that, as I am not a cardiologist, what I say here may be, at times, inaccurate, though I strive to do otherwise. Nothing in here shall be considered clinical advice. Figures without a license caption are public domain.
I have no idea on how much you know in cardiology, so please forgive me if I underestimate you. And, to apologize in advance, I’m writing this after I finished some homework in Study Hall, so my brain might be a bit messed up. If you notice any errors, please tell me. Thanks!
Firstly, here is an awesome playlist by Eric Strong, on his YouTube channel Strong Medicine.1 I’m too lazy to use bibliography management for a short document so please bare with me, but this playlist talks about the basics and advanced stuff of ECG interpretation, and was, and still is, a great help to me while investigating this topic.
In order to understand anything about the heart (we’ll focus on the human heart specifically), we need to look at the general structure of the heart. Please refer to the figure below. (Using the letter document-class so I can’t use real figures here.)
This is the frontal plane of the heart. The superior has the two artias/atriums, depending on how you want to say them, and the inferior has the ventricles.
Now you might be wondering why the heart beats. I cannot provide images on this for legal reasons, but I guess you could look them up yourself (something like “cardiac conduction system” on an image search). The middle of the right atria has something called the “sinoatrial node”, also called the “sinus node”, or simply the “sinus”. It’s in a relative superior location in the heart and acts as the heart’s primary pacemaker.
At the beginning a normal heartbeat, the sinus node fires, which propagates through and depolarizes the atria. Under normal circumstances (i. e. when the patient is having something other than Pulseless Electrical Activity or cardiomyopathies), depolarization will cause the muscles to contract, and thus, pump blood. The potential travels through the atria and reaches the atrioventricular node, which delays the conduction by a little bit. Then, the wavefront travels through the Bundle of His and to the Purkinje fibers, from where, it depolarizes the myocytes (basically cardiac muscles) of the ventricles and causes the ventricles to contract. Then, everything repolarizes (basically the sodium-potassium pump eating more ATP) and they wait for the next depolarization.
The normal rhythm of the human heart is called the “Normal Sinus Rhythm”. Look up the electrocardiogram, (and if you see multiple leads, mainly pay attention to lead II, I’ll explain why when we get to leads, nevermind for now) there’s a small bump (the “P wave”) indicating atrial depolarization, then there’s two to three spikes indicating ventricular depolarization (the “QRS complex”) consisting of a Q wave, R wave and S wave, in which the Q wave may be invisible in some patients and some leads. The R wave is usually the tallest one. And at last, we have the T wave, which indicates ventricular repolarization. You might ask where atrial repolarization is—they’re way to small to see on surface ECG, but may be detectable in an surgical/whatever electrophysiology study.
Note that lead II’s views a heart from a right-superior to left-inferior direction on a frontal plane. An electrical activity front that generally goes in the direction of a lead produces a positive bump on the lead, one that goes generally opposite from a lead produces a negative bump, and a perpendicular one produces nothing. Note that the heart is a 3D structure, and the “on a frontal plane” part that I mentioned just now is just so we can recognize the direction of the lead properly. The actual lead records in a line in 3D space, not a line in a plane, so adjust what you think of when hearing “perpendicular” and stuff.
The depolarization of the atria, which goes in a similar direction to the view of lead II, produces a positive little bump on lead II. The first part of the bump is generated by the right atria, and the second part is generated by the left atria. (There is no distinction on a normal ECG, but this will be apparent especially when dealing with atrial enlargement.)
The depolarization of the ventricles, the larger part of the heart, generates a QRS complex instead of simply one R wave because the ventricules first conduct inferiorly but then, through the Purkenje fibers, the wavefront travels superiorly.
The repolarization of the ventricles generate a wave, slightly larger than the P wave, indicating ventricular repolarization. The times of repolarization overlap with each other a lot because repolarization is slow, which (I remember?) is why we can’t see multiple T waves.
The relations between the waves, namely the segments and intervals, give us information in addition to the morphology of the waves themselves. Here are the most important ones.
The ST segment is the segment from the end of the the QRS complex to the start of the T wave. It is way too complicated to explain here, but basically, any sort of ischemia such as myocardinal infarctions or angina would likely, but not always, result in an elevated or depressed ST segment.
The QR interval is the time from the start of the QRS complex to the end of the T wave. A prolonged QT interval, with a QTc (QT interval corrected for heart rate, explained later) of more than around 450 ms, is abnormal, and may be at times considered long-QT syndrome, which is clinically related to a deadly tachyarrhythmia, Tosades de Points.
Literally the time between two adjacent R waves, indicating ventricular heart rate, which in normal circumstances is just the heart rate.
Look up “the cardiac action potential” and “the pacemaker action potential”. These should be fairly similar to the membrane potential diagrams for neurons, though repolarization looks slightly differnet. (That’s because even though the whole time we have outgoing potassium ions, but during the middle part where the membrane potential is decreasing slower, we have an influx of calcium ions (positive of course) and thus it cancels out some, but not all, of the voltage change that the outgoing potassium ions create.) If you compare the diagram of a normal cardiomyocyte to that of a cardiac pacemaker, you’ll see that the pacemaker cells don’t have a flat resting membrane potential—they upslope until they trigger the voltage-gated sodium channel (they upslope because there are open, but relative slow, sodium and potassium channels).
This weird pacemaker electrical activity is not only active in the sinus node, where we’d expect such activity, but they are also present in other areas of the heart. In case the sinus node fails, one or many of the “latent” pacemakers present across the heart will take over the heart’s rhythm, usually at a slower rate than the sinus node. These latent pacemakers have a gentler membrane potential upslope at their resting potential and thus spontaneously reach their threshold slower—normally during that process, it would have been already in the refractory period due to being polarized by the sinus node. But now as nothing is depolarizing it, it depolarizes by itself, thus causing the heart’s rhythm to be a “latent pacemaker rhythm” or “escape rhythm”. I’m sure you can figure out, at this point, why usually the fastest of the latent pacemakers take over when the sinus node fails.
(should list latent pacemakers here)
I guess it’s time to introduce abnormal rhythms! Look them up accordingly beause I can’t provide ECGs here. Note that these are abnormal rhythms. Many problems detected through ECGs are actually Normal Sinus Rhythm but with subtle (or significant if you have good eyesight) changes in the waveform. We’ll discuss the former here.
There is no electrical activity in the patient’s heart. It’s often called “flatline”, though “asystole” describes the activity of the heart while “flatline” describes the waveform on the ECG.
This “rhythm” is a big mess. The venticles’ electrical activity is completely messed up.
There’s (likely) an ectopic or a reentrant circuit in the ventricles, which fire rapidly, resulting in a wide QRS complex.
Ventricular Tachycardia, but slower. Although this is also a ventricular rhythm, it’s often due to a faulty pacemaker system, as the ventricles are one of the last latent pacemakers. Thus, rather than being an ectopic firing in the ventricles, it is likely a failed sinus node, conduction failure, or other issues that cause latent pacemakers to take over the heart.
The atrioventricular node (or tissue around it), instead of the sinoatrial node, is pacemaking the heart. The P waves may be hidden within the QRS complexes, as the impulse from the AV node is depolarizes the atria through retrograde conduction. The P waves are additionally inverted.
Normal Sinus Rhythm, except that the RR intervals are not constant. A variety of reasons may be responsible; the most common of which is “Respitory Sinus Arrhythmia”, i. e. normal changes in heart rate as a person respirates. (Faster rhythm while inhaling and vice versa.) More serious underlying problems may be responsible such as Sick Sinus Syndrome.
Including two common varients (AVRT and AVNRT), supraventricular tachycardia is caused by reentry somewhere superior to the ventricles but inferior to the atria or by ectopics in the region. Supraventricular Tachycardia, in a broader sense, refers to any tachycardia that originates outside the ventricles, including Sinus Tachycardia. But clinically it usually doesn’t include Sinus, AFib, AFlutter and ATach.
The atria has completely messed up electrical activity. The ventricles will respond irregularly, sometimes rapidly, in which case it’s called Rapid Ventricular Response.
The atria flutters constantly and rapidly, usually around 300 beats per minute, often varying depending on the size of the atria. Ventricular response is regular or regularly irregular (i. e. 2:1 then 3:1 then 3:1, loop etc. conduction).
Basically atrial flutter but slightly slower and 1:1 conduction. P waves must be somehow discernable to ATach this on ECG, otherwise we can only consider the ECG to be SVT. But nevertheless, if the atria is rapidly firing causing the tachycardia, it’s ATach.
These are the common abnormal rhythms that I can think of for now. Electrophysiology is complicated, many overlay rhythms or other weird stuff is possible. I might elaborate on rarer rhythms later but now I’ll turn the focus to “changes to the sinus rhythm”. Fun stuff is here like ischemia (including angina, myocardinal infarctions, etc.). Things here are much more complicated than basic arrhythmias so I’m using, well, paragraphs of text instead of description lists. I’ll try to be less boring than a standard cardiology textbook but I might have a hard time doing so. Also, when I say “Case n” or simply “(n)” where n ∈ ℤ+, please look up the case by its case ID on ECG Wave Maven2. In the below you need to start looking for pathologies in all leads. I’ll explain what the leads do in a bit—don’t worry too much if you don’t get “anterior lead” or something like that for now, come back here once we get to it for a bit of a review.
Myocardinal Infarction (e. g. 203, there are many possible locations and types of MI), commonly known as a “heart attack”, is when parts of the myocardium is going to die or has died due to ischemia (lack of bloodflow), usually caused by blood clots along with CAD. There are multiple types: Some have prominent/pathologic Q waves, some have ST depression, some have ST elevation, some have absurd T waves, some have a combination of those and others may have none (in which case ECG can’t help much).
Note to self: Dilated cardiomyopathy is 407.
Now you might be wondering what’s with the leads. Basically, different leads have different viewing angles/perspectives of the heart’s electrical activity.
We need to first take a look at the electrodes actually placed on the patient. For the limb leads, the right leg is ground, so we won’t care much about that. The left hand, right hand, and left leg have working electrodes recording our electrical activity. Look up “Einthoven’s Triangle”—I often also wonder why it’s labeled as a perfect 60∘ while human placement isn’t often that precise—turns out that Einthoven’s Triangle is actually pretty precise with its angles at the cardiac electrical level. Seems weird to me, I don’t get that part yet. Anyways, lead I is right-to-left (all these directions are from the patient’s perspective), lead II is from superior-right to inferior-left, and lead III is from superior-left to inferior-right. As explained before, an electrical front that goes with the direction of a lead produces a positive waveform and vice versa. If we take the center of the triangle, we have the “virtual terminal”. It’s basically the voltage average between the three electrodes. The central terminal to the verteces (I can’t spell) of the triangle create the aVR, aVL and aVF leads respectively for that to the right, left and left leg. It’s best to look it up to get a visual representation of the angles.
These are the three normal limb leads, three “augmented limb leads”, six in total. The other six leads on a normal 12-lead ECG, i. e. V1–V6
Yes, there are other electrical things especially the nervous system in the middle of all of this. But they seem to have a much smaller voltage than cardiac electrical activities, insignificant on the human surface, so we could usually safety ignore that.
Obviously still an unfinished document. Tired, see you later.
Sincerely,
Andrew Yu