What the PR interval measures
The PR interval is the time between the first atrial cell depolarizing and the first ventricular cell depolarizing. On paper that is the start of the P wave to the start of the QRS complex, measured to the Q wave if there is one and to the R wave if there is not. In some countries it is called the PQ interval; the name changes, the measurement does not.
Three things happen inside it, in order. The atria depolarize, which is the P wave itself and takes roughly 80 to 100 ms. The impulse then enters the atrioventricular node and slows to a crawl. Finally it races down the bundle of His, the bundle branches, and the Purkinje network until the first ventricular muscle fires. The flat stretch between the end of the P wave and the QRS is the PR segment: that is the AV node and His-Purkinje time made visible, and the reason the segment is flat is that the tissue conducting during it is too small to write anything on the surface.
In adults the normal range is 120 to 200 ms: three to five small boxes at 25 mm/s. It is shorter in infants and children and lengthens slowly with age.
Most of the interval is a pause
The PR interval is not the time it takes electricity to travel a distance. It is mostly the time the atrioventricular node holds the impulse before letting it through. Read it as a measure of that node, and the abnormal patterns below become predictable.
Why there is a delay at all
The atria and ventricles are separated by a ring of fibrous tissue that does not conduct. In a normal heart the only electrical route across it is the atrioventricular node and the bundle of His below it. That makes the node a checkpoint, and it is built to be a slow one.
Its cells resemble sinoatrial cells more than working muscle: small, sparsely coupled, and without the fast sodium channels that give atrial and ventricular muscle their sharp upstroke. They depolarize on a slow calcium current instead. A slow upstroke means a slow wave, and conduction through the node runs at about 0.02 to 0.05 m/s against nearly 1 m/s in the atrium and 2 to 4 m/s in the Purkinje fibers. The node also conducts decrementally: the earlier the next impulse arrives after the last one, the more slowly it gets through, because the cells have not fully recovered.
Two things depend on that slowness. First, the ventricles get time to fill. The atria contract during the PR interval and push a final top-up of blood into ventricles that have already filled passively; without the pause, atrial and ventricular contraction would overlap and that top-up would be lost. Second, the node protects the ventricles from the atria. In atrial fibrillation the atria fire several hundred times a minute, and it is the node's slow, decremental conduction that lets only a fraction of those impulses through.
Cell A
Cell B
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Watch the interval happen
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Same route, longer stall
A long PR interval is not a detour. The impulse takes exactly the same path; it just waits longer at the node. Compare the two animations: the only difference is how long the node stays lit.
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How to measure it
Measuring a PR interval on paper
- Choose the leadLead II usually shows the clearest P wave. Check a second lead, because the start of the P wave can be flat in one lead and visible in another.
- Mark the P onsetThe first point where the trace leaves the baseline, not the peak of the P wave. A caliper or a straight edge on the baseline helps.
- Mark the QRS onsetThe first deflection of the QRS in either direction, including a small Q wave. Do not wait for the R wave.
- Check the paper speedCount the boxesAt 25 mm/s each small box is 40 ms and each large box is 200 ms. At 50 mm/s, common on veterinary strips, halve those.
- Use the longest normal valueAcross leads, take the longest PR from a normally conducted beat. A lead that misses the start of the P wave reads short, never long.
- Check it beat to beatOne number is a measurement; a change across beats is a diagnosis. Look at every PR on the strip before deciding it is constant.
Three traps catch most learners. The first is measuring from the peak of the P wave rather than its start, which shortens every PR by 40 to 50 ms and turns a normal interval into a suspicious one. The second is a P wave whose first part is isoelectric in the lead you chose, which is why the longest PR across leads is the honest one. The third is a fast rate, where the P wave rides on the T wave of the previous beat and the onset has to be found by following the T wave's expected shape.
Want to practice on real paper with calipers you can drag? The intervals stage of the reading trainer checks your P onset and QRS onset against the answer key.
What moves it
| Input | What it does in the node | PR |
|---|---|---|
| Sympathetic toneexercise, fear, fever | More calcium current, faster nodal upstroke. The node conducts faster at the same time as the sinus node speeds up. | Shorter |
| Vagal tonerest, sleep, athletic conditioning | Acetylcholine slows the nodal upstroke and hyperpolarizes the cells. First-degree block in a sleeping athlete is this, not disease. | Longer |
| Premature atrial beats | An impulse arriving before the node has recovered conducts more slowly, by design. A premature P wave with a longer PR is decremental conduction, not block. | Longer |
| Digoxinvagomimetic | Increases vagal effect on the node. A therapeutic dose lengthens the PR; toxicity can block it. | Longer |
| Beta blockers, diltiazem, verapamil, amiodarone | Blunt the calcium current the nodal upstroke depends on, directly or by removing sympathetic support. | Longer |
| Hyperkalemia | Depolarizes resting cells and slows every upstroke in the heart. The PR lengthens along with the QRS. | Longer |
| Age and fibrosis | Scar in and around the node and His bundle slows conduction permanently. The usual cause of a long PR in older patients. | Longer |
| Accessory pathwaypre-excitation | A strand of muscle across the fibrous ring that skips the node entirely. The ventricles start early, so the PR is short and the QRS begins with a slur. | Shorter |
When the PR interval is wrong
Long and constant: first-degree AV block. A PR over 200 ms with every P wave conducted. The delay is nearly always in the node, from vagal tone, a nodal drug, or age. It causes no symptoms on its own and needs no treatment on its own. It is not quite as innocent as textbooks once said: in the Framingham cohort, people with a PR over 200 ms had about twice the long-term risk of atrial fibrillation, nearly three times the rate of eventual pacemaker implantation, and a modestly higher mortality than those with a normal PR. Treat it as a marker to note, not a disease to fix. One exception worth knowing: a long PR with a wide QRS may mean the delay is below the node, in the His-Purkinje system, which is a different risk.
Lengthening, then dropped: Wenckebach. The node's decremental conduction taken to its limit. Each impulse lands earlier in the node's recovery than the one before, conducts more slowly, and pushes the next one earlier still, until one fails to get through. The dropped beat gives the node a rest and the cycle restarts with a short PR. The largest jump in PR is usually between the first and second beats of the cycle, so the R-R intervals actually shorten as the PR lengthens, a detail that makes Wenckebach recognizable even when the P waves are hard to see. It is almost always in the node, and almost always benign.
Constant, then dropped: Mobitz II. Here the node is fine. The failure is in the His bundle or bundle branches, tissue that does not conduct decrementally; it either conducts normally or not at all. So the PR never lengthens, and then a beat is simply missing. Because the same diseased tissue can stop conducting altogether, Mobitz II is the second-degree block that leads to a pacemaker.
No relationship: third-degree block. When nothing crosses from atria to ventricles, an escape rhythm drives the ventricles on its own schedule and the P waves march through at their own rate. Any PR you measure is a coincidence. The tell is that the PR changes from beat to beat while both the P-P and R-R intervals stay regular.
Short: the impulse did not wait. A PR under 120 ms with a QRS that begins with a slurred upstroke, the delta wave, means an accessory pathway is pre-exciting the ventricles: Wolff-Parkinson-White. A short PR with a perfectly normal QRS is more often an impulse that started close to the node, such as a low atrial or junctional rhythm, in which case the P wave in lead II is inverted; the old label of Lown-Ganong-Levine for a short PR with normal QRS and a tendency to tachycardia is now rarely used. And a short PR in a small child is usually just a small child.
Depressed, not long. The PR segment can sag below the baseline while its length stays normal. With ST elevation across many leads and PR elevation in aVR, that is the signature of acute pericarditis. On its own it can mark atrial injury.
Each PR pattern is one thing happening at one place
Vagal tone, a nodal drug, or age-related fibrosis.
PR over 200 ms, constant, every P conducted.
Decremental conduction pushed until one impulse fails.
PR lengthens, a P is dropped, the PR resets.
Diseased bundle tissue conducts normally or not at all.
PR constant, then a P is dropped without warning. Often a wide QRS.
An accessory pathway crosses the fibrous ring.
PR under 120 ms, delta wave, QRS widened at its start.
Inflamed pericardium over the atria, or atrial infarction.
The segment sags; the interval length is unchanged.
Reason it out before you reveal
Each answer follows from how the node conducts. Try to build it yourself first.
Across species
| Species | Normal PR | What to expect |
|---|---|---|
| Human | 120 to 200 ms | Shorter in children, longer with age and in trained athletes at rest. |
| Dog | 60 to 130 ms | Varies with respiratory sinus arrhythmia as vagal tone rises and falls. Strips are often run at 50 mm/s, so halve the box values. |
| Cat | 50 to 90 ms | Short and fast. At 200 bpm the P wave can sit on the previous T wave, so find the onset carefully. |
| Horse | 220 to 500 mslonger in larger horses | Scales with body size; values that stay above 500 ms are probably abnormal. Second-degree block at rest is a normal vagal finding in fit horses and disappears with exercise. |
The two questions a PR interval answers
How long is the node holding the impulse? Read the length: normal, long, or short. Is it holding it the same way every beat? Read the pattern across beats: constant, lengthening, or unrelated to the QRS. The length tells you about the node's state; the pattern tells you where the problem is.
Key takeaways
The PR interval runs from P onset to QRS onset and times atrial depolarization, the AV node, and the His-Purkinje system together. The node is most of it and the only part that changes with autonomic tone.
The delay is deliberate: slow calcium-dependent nodal cells give the ventricles time to fill and shield them from fast atrial rhythms.
Measure from the start of the P wave to the first QRS deflection, in the lead with the longest normal value, at the right paper speed. Normal is 120 to 200 ms in adults.
Long and constant is first-degree block, in the node. Lengthening then dropped is Wenckebach, in the node. Constant then dropped is Mobitz II, below the node and more dangerous. Unrelated to the QRS is complete block.
Short with a delta wave means an accessory pathway; short with a normal QRS usually means the impulse started near the node.
Go deeper. The structure that sets the interval has its own page at atrioventricular node, and the exit below it at bundle of His. Each abnormal pattern is a rhythm page: first-degree AV block, Mobitz I, Mobitz II, third-degree block, and Wolff-Parkinson-White. Previous on this path: the P wave. Next: the QRS complex.
Sources this page draws on
Numbers and mechanisms above are taken from the following. Where sources disagree on a range, the page uses the more conservative figure.
- Burns E, Buttner R. PR interval. Life in the Fast Lane ECG Library. litfl.com/pr-interval-ecg-libraryNormal range of 120 to 200 ms, the definitions of long and short PR, and PR segment depression.
- Burns E, Buttner R. Pre-excitation syndromes. Life in the Fast Lane ECG Library.Short PR with delta wave in Wolff-Parkinson-White; the Lown-Ganong-Levine pattern.
- Burns E, Buttner R. Pericarditis. Life in the Fast Lane ECG Library.PR segment depression with PR elevation in aVR.
- Cheng S, Keyes MJ, Larson MG, et al. Long-term outcomes in individuals with prolonged PR interval or first-degree atrioventricular block. JAMA. 2009;301(24):2571-2577.Framingham follow-up: PR over 200 ms and the risks of atrial fibrillation, pacemaker implantation, and mortality.
- Josephson ME. Josephson's Clinical Cardiac Electrophysiology: Techniques and Interpretations. 5th ed. Wolters Kluwer; 2016.PA, AH, and HV intervals as the components of the PR interval, and their autonomic sensitivity.
- Electrophysiologic Study Indications and Evaluation. StatPearls, NCBI Bookshelf.Normal PA 25 to 55 ms, AH 50 to 140 ms, HV 35 to 55 ms.
- Klabunde RE. Cardiovascular Physiology Concepts. cvphysiology.com, Electrical Activity of the Heart.Slow calcium-dependent action potentials of nodal tissue, decremental conduction, and conduction velocities by tissue.
- Tilley LP, Smith FWK, Oyama MA, Sleeper MM. Manual of Canine and Feline Cardiology. 5th ed. Elsevier; 2016.Canine and feline PR reference ranges.
- Merck Veterinary Manual. Electrocardiography in animals. merckvetmanual.comSpecies intervals and paper speed conventions.
- Verheyen T, Decloedt A, De Clercq D, Deprez P, Sys S, van Loon G. Electrocardiography in horses, part 2: how to read the equine ECG. Vlaams Diergeneeskundig Tijdschrift. 2010;79:337-344.Equine PQ interval scaling with body size and the 500 ms upper limit.
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