Intervals and Segments

The PR interval runs from the start of the P wave to the start of the QRS, and it normally measures 120 to 200 ms. It contains two events stacked back to back. First the atria depolarize, which writes the P wave. Then the wavefront reaches the AV node and slows to a crawl, and this is where most of the interval is spent. The AV node conducts through slow, calcium-dependent tissue that deliberately holds the impulse for roughly 80 to 120 ms, giving the ventricles time to fill before they contract.

So a PR of 160 ms measures two things at once: atrial activation plus a deliberate pause. When the PR stretches past 200 ms, we call it first-degree AV block, and the name is slightly misleading because nothing is truly blocked: every P wave still conducts to a QRS. The impulse is simply taking longer to get through. The extra delay almost always lives in the AV node itself, where decremental, calcium-channel conduction can slow further without failing outright. That distinction matters, because delay in the node is usually benign, while delay below it behaves differently, and the surface PR alone cannot tell the two apart. We will see how the EP lab settles that question below.

The QRS duration times ventricular depolarization, and in a healthy heart it stays under 120 ms. That narrow window exists because the ventricles do not activate cell by cell; they activate almost simultaneously through the His-Purkinje system, a network of fast-conducting fibers that fans the impulse across both ventricles in under a tenth of a second. A wavefront racing down insulated Purkinje cables reaches the whole endocardium at once, so the muscle depolarizes as a near-synchronous flash and the QRS is crisp and brief.

A wide QRS means that fast delivery system failed and the impulse had to spread the slow way, muscle cell to muscle cell. There are two ways to arrive there. If one bundle branch is blocked, that ventricle no longer receives the fast signal; it depolarizes late, filled in by the wavefront creeping across the septum from the other side. That is bundle branch block, and the QRS widens past 120 ms because half the heart is waiting on cell-to-cell spread. The other route is a beat that starts in ventricular muscle itself, below the His-Purkinje entry points. It never boards the fast network at all, so it propagates entirely cell to cell and produces an even broader, stranger QRS. Both share one mechanism: when the impulse bypasses the His-Purkinje highway, conduction slows and the complex widens. The same widening appears whenever supraventricular impulses meet a bundle that has not recovered, the phenomenon of rate-dependent aberrancy.

The QT interval runs from the start of the QRS to the end of the T wave, and it captures the entire ventricular action potential written on the body surface: depolarization first, then the long plateau, then repolarization back to rest. The QRS marks the ventricles firing. The T wave marks them recovering. The stretch between the two is mostly the plateau, phase 2, where inward calcium current and outward potassium current sit in balance and the cells hold their voltage. The QT is therefore a direct read of ventricular action potential duration. Lengthen the action potential and the QT lengthens with it.

Because the action potential shortens at fast rates and lengthens at slow ones, a raw QT is only interpretable next to the heart rate. We correct it. The Bazett formula divides the QT by the square root of the RR interval in seconds; the Fridericia formula uses the cube root and holds up better at the extremes of rate. The result, the QTc, should stay under about 450 ms in men and 470 ms in women. A prolonged QTc means repolarization is dragging: the plateau outlasts its normal window, usually because outward potassium current (often I_Kr) is reduced by a drug or a channel mutation, leaving depolarizing current unopposed for too long.

A long QT is dangerous for a mechanical reason. When repolarization stalls, some ventricular cells can reactivate inward current before they finish recovering, firing an early afterdepolarization that rides up off the prolonged plateau. If one of those triggers a beat while the rest of the ventricle sits in a patchwork of recovered and unrecovered tissue, the impulse can spin into Torsades de pointes, a polymorphic ventricular tachycardia whose QRS axis twists around the baseline. The prolonged repolarization and its dispersion across the ventricular wall are what supply both the trigger and the substrate.

A segment is a flat stretch between waves, and each flat stretch has a cellular meaning. The PR segment runs from the end of the P wave to the start of the QRS. It is the electrically silent portion of the AV delay: the atria have finished depolarizing, the ventricles have not yet started, and the wavefront is inching through the node without generating enough surface voltage to move the pen. It sits on the baseline.

The ST segment runs from the end of the QRS to the start of the T wave, and it corresponds to the plateau, phase 2 of the ventricular action potential. During the plateau every ventricular cell is holding roughly the same voltage at the same time, so there is no gradient between one region and another and no current flows across the surface. The ST segment should therefore sit right on the baseline. When it does not, when it lifts or drops, the ECG is telling us that some region is at a different voltage from its neighbors during the plateau, and that voltage difference drives an injury current across the boundary. Ischemic or infarcting muscle repolarizes and depolarizes abnormally, so it sits at a different potential from healthy tissue, and the resulting current pushes the ST segment off the baseline. ST elevation and ST depression are that injury current, projected onto the leads.

The TP segment runs from the end of the T wave to the start of the next P wave. Every cell has finished repolarizing and the whole heart rests at its diastolic potential, so no current flows and the trace is genuinely flat. This is electrical diastole, and it is the true baseline of the ECG. When we judge whether an ST segment is elevated, we measure it against the TP segment, because that is the one stretch where we know the tissue is uniformly at rest.