Electrocardiography

The cardiac conduction system: SA node, AV node, bundle of His, right and left bundle branches, and the left bundle’s fascicles.

Three different populations of cardiac cells make an EKG possible, and almost everything else in this course is built on knowing what each one does. The first are pacemaker cells. Unlike ordinary tissue, they cannot sit quietly at a stable resting voltage — they drift toward threshold on their own and fire spontaneously, over and over. The sinoatrial (SA) node, a small cluster of these cells in the high right atrium, does this fastest, typically 60 to 100 times a minute at rest, with the exact rate tuned moment to moment by sympathetic and parasympathetic nerve traffic. The detail worth sitting with: the SA node is not the only tissue in the heart capable of spontaneous firing. Every cardiac cell, atrial or ventricular, carries some latent automaticity of its own. It simply never gets to show it, because the SA node always reaches threshold first and resets the rest of the heart before any slower, quieter pacemaker downstream gets the chance. Suppress the fastest clock and a slower one will eventually take over — that single fact is the entire logic behind escape rhythms, which a later module covers in depth.

The second population is essentially electrical wiring: the bundle of His, the right and left bundle branches, and the fine web of Purkinje fibers that reaches into the ventricular walls. These cells conduct current fast and with little resistance, the way insulated wire moves a signal better than the tissue around it. Their entire purpose is to get the depolarizing impulse to distant corners of both ventricles at nearly the same instant, so two large chambers of muscle contract together as a single unit instead of rippling from cell to cell the slow way.

The third population, by far the most abundant, is ordinary working myocardium — the muscle that actually does the squeezing. When an electrical impulse reaches a myocardial cell, it opens channels that let calcium rush in, and that calcium is what pulls the contractile filaments past one another. This handoff from an electrical signal to a mechanical contraction is called excitation-contraction coupling, and it is why every heartbeat you feel follows an electrical event that showed up on the EKG a fraction of a second earlier.

All of that activity reduces to two opposite electrical events, and every single wave on an EKG is one or the other. At rest, the inside of a cardiac cell sits well below zero relative to the outside, a voltage the cell's ion pumps work hard to maintain. Depolarization is the loss of that internal negativity as positive current rushes across the membrane — it is the trigger for contraction, and it is what produces the P wave and the QRS complex. Repolarization is the cell working its way back to that negative resting state afterward, resetting itself to fire again — it is what produces the T wave. Nothing more mysterious than that is happening on the page: tissue switching electrically on, then switching back off, recorded from a distance.

Before any of that electricity means anything, it helps to know exactly what the paper underneath the tracing is measuring. Standard EKG paper is a grid of small and large boxes, and each axis carries a fixed, unchanging meaning — there is no need to guess or calculate a scale each time you look at a strip.

The horizontal axis is time. At the standard paper speed, one small box equals 0.04 seconds, and since five small boxes make one large box, one large box equals 0.20 seconds. The vertical axis is voltage. One small box equals 0.1 millivolt, and one large box equals 0.5 millivolt. Those four numbers are worth memorizing cold, because every duration and every amplitude you will ever measure on an EKG is just a box count multiplied by one of them.

With that grid in hand, every wave you will ever encounter can be described along three independent dimensions: how long it lasts (duration, read off the horizontal axis), how big it is (amplitude, read off the vertical axis), and what shape it takes (configuration — upright, inverted, notched, biphasic, peaked, and so on). Learning to read an EKG is largely learning which combinations of duration, amplitude, and configuration are normal for each wave, and which combinations point to a specific problem.

The bundle of His highlighted — the sole electrical bridge between atria and ventricles.

Trace a single, ordinary heartbeat from start to finish and every wave on the tracing falls into place. The SA node fires first, but this discharge involves too little tissue to register on the surface EKG at all — the first thing you actually see is the wave of atrial depolarization it sets off, recorded as the P wave. The right atrium sits slightly closer to the SA node and begins depolarizing a moment before the left atrium, and it also finishes first, so the front half of a normal P wave is mostly a right-atrial signal and the back half is mostly a left-atrial one — a detail that becomes clinically useful once one atrium enlarges and starts distorting its half of the wave.

The impulse then reaches the AV node, and here it is deliberately delayed — about a tenth of a second passes before it is allowed through to the ventricles. That pause is not a flaw; it is the entire point. It gives the atria time to finish contracting and empty their contents into the ventricles before those ventricles begin contracting themselves. On the EKG, this delay is silent — it produces the flat line between the end of the P wave and the start of the QRS complex, because an entire chamber's worth of atrial muscle has already finished depolarizing and the AV node itself is too small to generate a visible signal.

Once released from the AV node, the impulse travels down the bundle of His, splits into the right and left bundle branches, and the left branch itself fans out into three fascicles — septal, anterior, and posterior — before the signal finally reaches the Purkinje network and ignites the ventricular muscle nearly all at once. This entire ventricular depolarization is what produces the QRS complex. One detail worth flagging early: the interventricular septum is actually the first part of the ventricles to depolarize, and it does so in a left-to-right direction. In some people this produces a small, normal "septal" Q wave in the leads that face the left side of the heart, and later modules will come back to why that small Q wave is reassuring rather than worrying.

Last comes the T wave, representing ventricular repolarization — the ventricles electrically resetting themselves after contracting. The atria repolarize too, but that signal is tiny and happens to fall right in the middle of the much larger QRS complex, so it is simply buried and never seen.

One full normal cycle in lead II: P wave, silent PR segment, QRS complex, then T wave — and it repeats.

The QRS complex can look strikingly different from lead to lead and from patient to patient, so electrocardiography uses a strict, position-based naming convention rather than fixed shapes. The rule only cares about the order in which deflections occur and which direction they point.

The first downward deflection of the complex, if there is one, is called a Q wave — but only if it truly comes first, before any upward deflection. The first upward deflection, whether or not a Q wave preceded it, is called an R wave. If a second upward deflection follows, it is labeled R′ ("R prime"). Any downward deflection that comes after an upward deflection is an S wave. And if the entire complex is negative from start to finish, with no upward deflection at all, the whole thing is called a QS complex rather than being broken into separate letters.

A couple of worked examples make the rule concrete. A complex that dips down, rises above the baseline, and returns to baseline is a Q wave followed by an R wave — described simply as "qR." A complex that rises first, dips below baseline, rises again, and then settles is "RSR′" — a pattern you will meet again when right bundle branch block produces its classic rabbit-ears shape in V1. And a complex that never crosses above the baseline at all, only dipping down and returning, is a QS complex, not a "Q wave" in isolation — the distinction matters because a QS pattern in the right leads can be an entirely normal variant, while the same pattern in the wrong leads can signal old infarction.

The PR interval (P onset to QRS onset) and the QT interval (QRS onset to T offset) bracketed on one normal beat.

Two words that sound interchangeable in casual conversation mean very different things on an EKG: a segment is a flat stretch of baseline between two named waves, while an interval includes one or more actual waves plus whatever segment sits next to them. Getting this distinction straight makes the standard measurements much easier to keep organized.

The PR interval runs from the very start of the P wave to the very start of the QRS complex, so it includes the P wave itself plus the flat AV-nodal delay that follows it. Normal is 0.12 to 0.20 seconds — three to five small boxes. The PR segment, by contrast, is only the flat part: from the end of the P wave to the start of the QRS, the silent stretch created by the AV-node delay described above.

The QRS interval (also called the QRS duration) is measured from the start to the end of the QRS complex itself, and normally falls between 0.06 and 0.10 seconds. Any wider than that means ventricular depolarization is taking an abnormal, slower route through the muscle rather than the fast bundle-branch highway — the subject of a later module on bundle branch block.

The ST segment is the flat stretch from the end of the QRS to the start of the T wave, representing the brief plateau between ventricular depolarization finishing and repolarization beginning. And the QT interval spans from the very start of the QRS all the way to the very end of the T wave — essentially all of ventricular depolarization plus all of ventricular repolarization together, which works out to roughly 40% of the entire cardiac cycle in a healthy heart at a normal rate.

The QT interval is unusual among these measurements because it is not a fixed number — it moves with heart rate, and for a good physiological reason. Repolarization has to finish preparing the ventricle to fire again before the next beat is due to arrive. When the heart speeds up, beats are due sooner, so the QT interval shortens to keep pace; when the heart slows down, the QT interval stretches back out. This is why every QT measurement in practice is compared against a rate-corrected value rather than the raw number — a subject the arrhythmia modules will return to.

A single wave of depolarization — here, the atria — can be summarized as one mean vector: a direction and a magnitude.

An EKG electrode does not "see" the whole heart at once the way an eye sees a room. At any given instant, it can only report the net direction and strength of the electrical current flowing through the heart at that moment — a single number that mathematicians would call a vector. Three simple rules follow directly from that fact, and they explain almost every deflection you will ever interpret.

If a wave of depolarization moves generally toward a positive electrode, that electrode records a positive (upward) deflection. If it moves generally away, the electrode records a negative (downward) deflection. And if the wavefront moves roughly perpendicular to the electrode's line of sight, the electrode sees positive and negative in quick succession, canceling toward the middle — a biphasic deflection. Repolarization follows the same three rules but produces the mirror-image result: a repolarization wave moving toward a positive electrode is recorded as negative, and one moving away is recorded as positive. This is exactly why a normal T wave, even though it represents the ventricles "turning off" rather than "turning on," still usually points the same direction as the R wave that preceded it — repolarization in the healthy ventricle sweeps backward, roughly opposite to the direction depolarization traveled, and the two negatives cancel into the same polarity.

None of this requires tracking every individual muscle fiber. Because an electrode only reports a net signal, an entire wave of depolarization — say, all of atrial depolarization, millions of cells firing over a tenth of a second — can be summarized as a single arrow: one average direction and one average magnitude, called the mean vector for that wave. The rest of this course leans on that simplification constantly, especially once axis calculations are introduced in the next module.

The frontal-plane hexaxial system: the six limb leads and their standard angles.

The six precordial leads in cross-section — V1/V2 face the right ventricle and septum, V4 the apex, V5/V6 the lateral left ventricle.

A standard EKG views the heart's electrical activity from twelve different vantage points, split into two groups that view two different planes of the body.

Six limb leads view the heart in the frontal (vertical) plane, as if looking at the body from straight ahead. Three are the original standard leads: I at 0°, II at 60°, and III at 120°. The other three are mathematically derived "augmented" leads: aVL at -30°, aVR at -150°, and aVF at +90°. Together, evenly spaced around the circle, these six angles form the hexaxial reference system used to calculate electrical axis.

Six precordial leads view the heart in the horizontal plane, as if looking down from above, and are placed directly on the chest wall at fixed anatomic landmarks: V1 sits in the fourth intercostal space just right of the sternum, V2 in the fourth intercostal space just left of it, V3 halfway between V2 and V4, V4 in the fifth intercostal space at the midclavicular line, V5 halfway between V4 and V6, and V6 in the fifth intercostal space at the midaxillary line. Their placement means each one has a natural anatomic "view": V1 sits closest to the right ventricle, V2 and V3 overlie the interventricular septum, V4 sits over the apex, and V5 and V6 look at the lateral wall of the left ventricle.

Because of where they sit, particular groups of leads are described together as viewing a shared territory of the heart — language that will come up constantly once ischemia and infarction are covered: the inferior leads are II, III, and aVF; the left-lateral leads are I, aVL, V5, and V6; the anterior leads are V2, V3, and V4; and aVR together with V1 are sometimes grouped as the right-sided view, looking at the heart from the opposite side of the rest of the panel.

A normal 12-lead pattern — small septal Q waves in the left-lateral leads, orderly R-wave progression V1→V6, and T waves following the polarity of the preceding R wave.

It is worth walking through what "normal" actually looks like, lead by lead, before spending the rest of this course learning to spot deviations from it.

A normal P wave lasts under 0.12 seconds and stands no taller than about 2.5 millimeters. It is upright in leads I, II, aVL, and aVF, is often biphasic in III and in V1 (reflecting those leads' more perpendicular view of the atrial vector), and is most positive in lead II and most negative in aVR — consistent with a normal P-wave axis of roughly 0° to 70°, pointing down and to the left, toward the electrode that faces the atria most directly.

A normal QRS complex often includes those small septal Q waves described earlier in certain left-lateral and inferior leads — the normal signature of the septum depolarizing first, left to right. Moving across the chest leads from V1 to V6, the R wave should grow steadily taller and the S wave steadily shallower, a pattern called R-wave progression; the point where R and S become roughly equal, called the transition zone, usually falls around V3 or V4. A normal QRS axis, in the frontal plane, falls roughly between 0° and 90°.

A normal T wave usually points the same direction as the R wave that came before it, for the repolarization reasons described in the previous section, with an amplitude somewhere between about a third and two-thirds the height of that R wave. Its shape is also distinctive if you look for it: T waves are more rounded and asymmetric than the sharp, angular QRS complex that precedes them.

Hold this normal picture in mind as a reference point — nearly every module that follows is really just describing a specific, named way that one part of this picture can change.